上海交通大学医学院诊断学双语教材
Clinical Diagnostics
（临床诊断学）
仁济临床医学院诊断学教研室
An Introduction to Clinical Diagnostics
After you finish your premedical courses, you are now going to touch patients. The
clinical diagnosis serves as a bridge between premedical and clinical medicine. It
includes physical diagnosis, Laboratory diagnosis and some instrumental examination.
Formerly these are taught separately but now our country they are combined to form
one course, which is now called clinical diagnosis.
The medical students are the physicians of tomorrow, and as such, you need
information from every source to unravel the mystery of the patients’ illness. Physical
diagnosis deals with such information through the two most fundamental skills, the
interrogation and physical examination.
Interrogation means to get the history in detail of a patient’s illness and the best
way as to let the patient tell his story in his own. As some crucial points might be
overlooked by the patients, you will ask many searching questions to make the history
complete and more informative.
Occasionally a patient will not or cannot give a straight story, you may interrogate
his (her)family members or friends to get more information date.
The next step is then to do a physical examination. The body of the patient will be
examined meticulously in every way possible by you, using all of your five senses. A
physical examination usually includes inspection, palpation, percussion, and
auscultation. Here our ancient doctors had given great contributions. Almost two
thousand years ago they had developed inspection, interrogation, smell and pulse
palpation to make diagnosis and develop many syndromes which are still useful
clinically today. After that you can make a preliminary analysis, correlating the
history with positive physical signs, determining the organs involved and even set
down a preliminary diagnosis, which we usually call it an impression but not a
definite diagnosis. A definite diagnosis will be made with the help of other special
investigative aids such as laboratory test, X ray films, EKG, endoscopy, ultrasonic
imaging, CT scanning etc, to add further clues or evidences to the first impression
obtained from physical diagnosis. Among them, only laboratory diagnosis and some
instrumental examinations are included in the course of clinical diagnosis as other
aids are too much specialistic and are usually taught separately.
Laboratory diagnosis is a science dealing with various kinds of laboratory
examinations and tests. As laboratory diagnosis is so complex that it is impossible to
apply all its contents to a single patient, you should select the proper ones according
to the impression you obtain from physical diagnosis. The laboratory diagnosis
usually contains two parts, the routine examination and the special tests. The routine
examinations include blood, urine and stool routine examinations and the special tests
usually direct to certain special organs.
The above are the general ways you will approach a patient when you go to the
ward. In fact this is a kind of bedside medicine. You should study hard and try to
master the technic. By this way you will understand what is health and what is disease.
By this way you will learn the procedures to do a clinical analysis which should be
fitting to dialectic materialism, that is, in an objective way. Further, you should always
keep in mind you are dealing with the diseased man but not the disease, so you should
give sympathy to the patient, and have a lofty mind of serving the people heart and
soul.
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Part I
Symptoms
Chapter 1
Fever
The core body temperature is kept constant (36.3-37.2o). Under normal
circumstances, it is tightly regulated, with circadian variations over a range that
usually does not exceed 1oC and a mean value of 37oC (the normal “set point”).
Fever is defined as an elevation of core body temperature above the normal range.
Pathogenesis
It is important to realize that fever is not equivalent to an elevated core
temperature but to an elevated set-point. The neuropathys responsible for
thermoregulation originate in the hypothalamus. A local sensing mechanism exists
wherein the temperature of blood is coupled to the development of autonomic
discharge.
Two types of pyrogen: exogenous pyrogen and endogenous pyrogen
1. Exogenous pyrogen: various microorganisms (such as endotoxin), mostly are
polysaccharides, can cause muscle contraction and rigor.
2. Endogenous: polymorphonuclear myelocytes and monocytes, activated by
exogenous pyrogen, synthesize cytokines, which cause liberation of PGE from
hypothalamus. The PGE is believed to reset the hypothalamic thermoregulatory
center by prompting an elevation in core body temperature.
Etiology and classification
1. Infective fever: After infection, metabolites from organism or pyrogen from
WBC cause fever.
2. Non-infective fever:
1). Absorption of necrotic substances: injury; ischemic necrosis; cell necrosis
2). Allergy
3). Endocrine and metabolic disturbances: hyperthyroidism and dehydration
4). Decreased elimination of heat from skin: heat failure
5). Dysfunction of central heat regulation:
a: Physical, as heat stroke;
b: chemical , as barbiturate poisoning;
c: Mechanical, as cerebral hemorrhage.
6). Dysfunction of vegetative nervous system; as the cases of sympathetic
overactivity.
Clinical manifestations:
1. The grade of fever
Low grade fever:
37.3~38oC
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Moderate fever:
38~39oC
High fever:
39.1~41oC
Hyperthermia fever: over 41oC
2. The clinical course and character of fever
The clinical courses of fever are consisted of the following three steps
1). Onset of fever
a: Sudden onset: fever rises within few hours, as pneumonia, up to
39~40oC
b: Gradual onset: fever rises gradually for few days, as typhoid
2). Persistence of fever: may be
a: continued
b: remittent
c: intermittent
d: recurrent
e: undulant
f: irregular type
3). Subsidence of fever: may be subside by crisis or lysis
Associated symptoms
1. Chills or rigor: as in septicemia and any acute infections
2. Congestion of conjunctiva: as in hemorrhagic fever
3. Herpes simplex: caused by herpes virus, frequently seen in cases of lobar
pneumonia
4. Bleeding tendency: in severe infection as hepatitis and blood dyscrasia as
leukemia
5. Lymph node enlargement: in cases of lymphoma, of metastasis of cancer
6. Enlargement of liver and spleen: in cases of hepatitis, leukemia
7. Arthralgia: in gout, rheumtic disease
8. Rash: drug rash, measles
9． Coma: in barbiturate poisoning, cerebral hemorrhage
Diagnostic points
Acute fever of less than two weeks are most of infectious origin, with an
inflammatory focus. Thus, either history or physical examination would show some
suggestive points about the cause of fever.
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Chapter 2
Pain
Pain is one of the common symptoms for which the physician is consulted.
Proper evaluation of pain depends largely upon knowledge of the various qualities of
pain, the significance of referred pain.
Pathological physiology
During injury of tissue, proteolytic enzymes are released which act on gamma
globulin to liberate irritating substances that stimulate nerve endings. Bradykinins,
serotonin, acetylchonie, 5-hydroxytypamine, histamine, prostaglandins, and other
similar polypeptides or acid metabolites cause pain by irritating the nerve endings,
from which the sensation is sent through posterior root of spinal cord, mostly cross to
other side, through spinothalamic tract, (lateral) medulla pons, and internal capsule,
spread diffusely into parietal and frontal lobe. The pain sensation is in segmental
distribution, as anterior part of head is through trigeminal, the thorax is through first
to fourth thoracic nerve, and upper abdomen the 6th-8th thoracic nerve.
Different organs may respond to different stimuli. Integumentary stimuli, at
lowest level of intensity, evoke sensations of touch, pressure, warmth, cold or tickle.
When noxious stimuli increased to the point approaching tissue destruction, pain is
added. The stimuli which skin is sensitive may not be true in case of GI system, which
is more sensitive to inflammation, ischemia, traction, spasm, while less to cutting,
needing and burn. The heart is sensitive to acute ischemia. The joint to hypertonic
saline, less to cutting.
There are two types of primary afferent nociceptors (pain receptors).
1. C fiber: 2-4μm in diameter, conducts slowly and causes a dull pain, as from
heart and viscera.
2. A-delta fiber: 6-8 μ m in diameter, as from skin, refers pain from
pericardium.
The referred pain is due to diseased internal organ, sending pain impulse through
spinal cord, which reflects the impulse to corresponding segment of integument,
coronary ischemic pain usually radiates to medial side of arm and fingers, which were
supplied by 6th –8th cervical, (or T1- 2) over the left side.
Clinical characteristics
1. Character of pain: spastic pain usually intermittent, and inflammatory persisting.
2. Localization of pain: usually in the diseased part, sometimes it may be referred,
as appendicitis with pain over epigastrium in early stage.
3. Quality and intensity of pain: The pain of a peptic ulcer may be “gnawing”,
“burning”. Anginal pain showed precordial distress or pain of dull, heavy quality.
If intensity of pain is getting worse, it means that the disease process is going on.
However, the severity, duration, frequency and special times of occurrence of pain
are also important.
4. Referred pain: The diffuse pain arising from deep somatic or visceral structures
tends to be projected to a more superficial region with the same segmental
innervation ---- so called referred pain. Pain of coronary insufficiency may be felt
along the inner aspect of the arm or in the left interscapular region
5. Aggravating and relieving factors: Anginal pain may be provoked by exertion,
cold, emotional upset and relieved by rest or nitroglycerine. Ulcer pain is relieved
by ingestion of food.
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Headache
Nearly everyone is subject to headache from time to time. Although most often a
benign condition, headache of new onset may be the earliest or the principal
manifestation of serious systemic or intracranial disease and therefore requires
thorough and systematic evaluation.
[Causes]
1. Intracranial diseases
(1) Infection: Meningitis, Encephalitis, Brain Abscess, etc.
(2) Vascular Disease: Acute Subarachnoid Hmorrhage, Cerebral Hemorrhage,
Cerebral Embolism, Cerebral Thrombosis, Hypertensive Encephalopathy,
Arterial Venous Malformation, etc.
(3) Intracranial Mass: Primary Brain Tumor, Metastatic Brain Tumor, Intra-cranial
Parasitic Infection, etc.
(4) Trauma: Cerebral Concussion, Cerebral Contusion and Laceration, Subdural
Hematoma, Epidural Hematoma, Intra-cerebral Hematoma, etc.
(5) Others: Migraine, Cluster Headache, etc.
2. Extracranial diseases
(1) Skull disease: Craniosynostosis, etc.
(2) Cervical Spine disease: Craniovertebral Junction Disease, such as, Chiari
Malformation, etc.
(3) Neuralgia: Trigeminal Neuralgia, Glossopharyngeal Neuralgia, etc.
(4) Ocular disorders, such as, Glaucoma, Acute Iritis; dental disease, or sinusitis.
3. Systematic disease:
(1) Acute infection: Influenza, typhoid, pneumonia or other fever diseases.
(2) Cardiac vascular disease: Hypertension, Heart Failure.
(3) Toxication: chemical or drug toxication.
(4) Others: Hypoglycemia, Anemia, Heat Stroke, SLE, etc.
4. Hysteric Headache
[Mechanism]
Headache is caused by traction, displacement, inflammation, vascular spasm, or
distention of the pain-sensitive structures in the head or neck. Isolated involvement
of the bony skull, most of the dura, or most regions of grain parenchyma does not
produce pain.
The pain sensitive structures within the cranial vault include venous sinuses, the
anterior and middle meningeal arteries, the dura at the skull base, the trigeminal,
glossopharyngeal, and vagus nerves, the proximal portions of the internal carotid
artery and its branches near the Circle of Willis, and the sensory nuclei of the
thalamus.
Extracranial pain sensitive structures include the periosteum of the skull, the skin,
the subcutaneous tissues, muscles, and arteries, the neck muscles, the second and
third cervical nerves, the eyes, ears, teeth, sinuses, and oropharynx, and the mucous
membranes of the nasal cavity.
[Clinical Features]
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1. Acute Headache: Headaches that are new in onset and clearly different from any
the patient has experienced previously are commonly a symptom of serious
illness and therefore demand prompt evaluation.
2. Subacute Headaches: Subacute headaches occur over a period of weeks to
months. Such headaches may also signify serious medical disorders, especially
when the pain is progressive or when it develops in elderly patients.
3. Chronic Headaches: Headaches that have occurred for years usually have a
benign cause.
4. Characteristics of Pain: Headache is most often described as throbbing; a dull,
steady ache; or a jabbing, lancinating pain. Pulsating, throbbing pain is
frequently ascribed to migraine. A steady sensation of tightness or pressure is
commonly seen with tension headache. The pain produced by intracranial mass
lesions is typically dull and steady. It is important to remember that the
character of the pain does not provide a reliable etiologic guide.
5. Location of Pain:
Unilateral headache is an invariable feature of cluster headache and most
migraine attacks.
Ocular or retroocular headache suggests a primary ophthalmologic disorder
such as glaucoma, optic nerve disease.
Paranasal pain localized to one or several of the sinuses.
Headache due to intracranial mass lesions may be focal, but will be bioccipital
and bifrontal when the intracranial pressure becomes elevated.
6. Associated Symptoms:
Fever or chills may indicate systemic infection or meningitis.
Visual disturbances suggest an ocular disorder, or an intracranial process
involving the visual pathways.
Nausea and vomiting are common in migraine and can be seen in the course of
mass lesions. Papilledema will be found when the intra-cranial pressure is
increased.
[History Taking]
1. It is important to know how the onset of the headache, its characteristic and
whether there are any precipitating factors.
2. If the headache is associated with vomiting, increased intracranial pressure must
be excluded.
[Case]
A 35 yrs old man has experienced headache in the past several years. He described it
as a “dull” headache. And his headache worsened in the past month.
During physical examination, severe papilledema was found.
A CT scan revealed a big brain tumor at sphenoid wing.
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So, his headache was caused by this large tumor and his intra-cranial pressure is so
high that papilledema was obvious.
Chest pain
Chest pain is usually related to diseases of the chest.
Etiology and pathogenesis
Any stimulus to intercostal nerve, nerves from heart, lung, diaphragm, bronchus
or esophagus, aorta will cause chest pain. Common causes are listed as follows:
1. Diseases of chest wall: such as Herpes zoster, costal chondritis, chest wall
tumors.
2. Cardiac and blood vessel causes: myocardial ischemia (angina pectoris,
myocardial infarction, aortic stenosis)，myocarditis, pericarditis
3. Respiratory diseases: pleuritis, pneumonia or lung cancer
4. Mediastinal disease: mediastinitis
5. Others: esophageal reflux
Clinical manifestations
1. Localization: herpes zoster cause blister along the intercostal nerve, chondritis
with local tenderness and elevation of bone.
2. Quality: intercostal neuralgia with prickling pain and local tenderness; angina
with precordial distress.
3. Factors related to chest pain: angina usually induced after effort or mental stress
and relieved by nitroglycerine.
4. Associated symptoms: bronchitis with cough, lung cancer with bloody sputum.
Diagnostic points
Detailed history: onset, quality, localization, provocating factors and associated
symptomns. P. E: especially neck lymph nodes and chest examination. Laboratory
and instrumental check up: especially sputum and chest X-ray film.
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Abdominal pain
Abdominal pain is one of the most frequent complaints for which patients seek
medical attention. It may be classified into acute and chronic.
Acute abdominal pain
Etiology and pathogenesis:
1. Parietal peritoneal inflammation: bacterial contamination (e.g., perforated
appendix) and chemical irritation (e.g., perforated ulcer, pancreatitis).
2. Acute inflammation of abdominal organs: gastritis, enteritis.
3. Mechanical obstruction of hollow viscera: obstruction of the small or large
intestine.
4. Vascular disturbances: embolism, vascular rupture, torsion of the organs.
5. Referred pain: pneumonia, coronary occlusion.
6. Abdominal well: trauma
7. Metabolic and toxic causes: allergic factors etc.
Clinical manifestations
1. Localization: usually with tenderness over the diseased organ
2. Quality and severity: perforation with severe dull pain over upper abdomen.
Renal colic with severe pain over back radiating to lower abdomen.
3. Provocation and relief: acute gastritis and enteritis are induced by eating unfresh
or raw foods, and ameliorated after vomiting or discharge.
4. Associated manifestations: jaundice favors liver, gallbladder or pancreatic
disease. Hematuria is usually due to renal stone.
Diagnostic points:
The history should be emphasized on the onset, location, quality and possible
etiologic factor of the abdominal pain. Detailed physical examination of chest and
abdomen is important. Echo and X-ray examination, gastroscopy and intestinal
fibroscopy are sometimes needed. If the diagnosis remained indefinite, laparotomy is
indicated.
Chronic abdominal pain
Etiology and pathogenesis:
1. Chronic inflammation of abdominal organs:
reflux esophagitis, chronic
ulcerative colitis.
2. Peptic ulcer
3. Distention of visceral surfaces: hepatic or renal capsules.
4. Metabolic and toxic causes: uremia
5. Infiltration of tumor
6. Neurogenic: irritable colon, neurosis.
Clinical manifestations:
1. Past history: Acute inflammation of abdominal organs may cause adhesion and
chronic inflammation of the organs.
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2. Localization: Pain is usually consistent with the diseased organ.
3. Quality: Duodenal ulcer is related to hunger, liver cancer is with persistent
pain.
4. Pain and position of the body: Ptosis of stomach or kidney shows pain when
standing for long time.
5. Associated symptoms: When associated with fever, they are usually due to
chronic infection, lymphoma or malignant tumor of abdominal organ. When
associated with vomiting, diseases of esophagus, stomach, billary tree may be
indicated.
Diagnostic points:
Same as in acute abdominal pain.
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Chapter 3 Edema
1. Definition
Edema is defined as a clinically apparent increase in the interstitial fluid volume.
Depending on its cause and mechanism, edema may be localized or have a
generalized distribution. Ascites and hydrothorax refer to accumulation of excess
fluid in the peritoneal and pleural cavities, respectively, and are considered to be
special forms of edema.
2. Pathogenesis
The hydrostatic pressure within the vascular system and the colloid oncotic pressure
in the interstitial fluid tend to promote a movement of fluid from the vascular to the
extravascular space. In contrast, the colloid oncotic pressure contributed by the
plasma proteins and the hydrostatic pressure within the interstitial fluid ,referred to
as the tissue tension, promote the movement of fluid into the vascular compartment.
As a consequence of these forces there is a large movement of water and diffusible
solutes from the vascular space at the arterial end of the microcirculation and back
into the vascular compartment at the venous end. These forces are usually balanced
so that a steady state exsits in the sizes of the intravascular and interstitial
compartments,and yet a large exchange between them is permitted. However,should
any one of the hydrostatic or oncotic forces be altered significantly, a net movement
of fluid between the two components of the extracellular space will occur. The
development of edema then depends on.
3. Etiology and Clinical Appearances
(1) Generalized Edema
a. Cardiogenic edema：especially the manifestation of right heart failure. It’s been
evidenced that a reduction of the effective circulatory blood volume and renal
blood volume, as well as the decreased glomerular filtration rate occur in this
condition with secondary elevation of the aldosterone secretion, tubular Na
reabsorption and sodium and water retention. The increment accumulates in the
venous circulation, and the increased capillary and lymphatic hydrostatic
pressure leading to reduction of fluid reabsorption promotes the formation of
edema. It could be first found in the legs symmetrically. Patients commonly have
the evidence of heart failure, such as dyspnea, basilar rales, venous distention
and hepatomegaly, etc.
b. Nephrogenic edema：The primary alternation in this disorder is a diminished
colloid oncotic pressure due to massive losses of protein into the urine and
retention of sodium and water by the kidney. Edema usually starts from the
eyelids and face and tends to be most pronounced in the morning, accompanied
by abnormal urinalysis, hypertension or renal insufficiency.
c. Hepatogenic edema：Ascites and biochemical and clinical evidence of hepatic
cirrhosis suggest the edema of hepatic origin. Edema may occurs from the ankle
and extends upwards, but scarcely involving the head, face and upper extremities.
This condition is characterized by hepatic venous outflow blockade, which in
turn causes expansion of the splanchnic blood volume and increased hepatic
lymph formation. These alternations are frequently complicted by
hypo-albuminemia secondary to reduced hepatic synthesis and reduce the
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effective arterial blood volume even further leading to activation of the RAA
system.
d. Malnutrition：A diet grossly deficient in protein over a prolonged period ,
protein-losing enteropathy and severe burn may produce hypoproteinemia and
edema. Before edema occurs from the lower extremities, there may be a history
of weight loss.
e. Idiopathic edema：This syndrome, which occurs almost exclusively in women, is
characterized by periodic episodes of edema(unrelated to the menstrual
cycle),frequently accompanied by abdominal distention. Etiology is unclear.
f. Miscellaneous：These include hypothyroidism, in which the edema(myxedema)
may be located typically in the pretibial region and which may also be associated
with periorbital puffiness. Exogenous hyperadrenocortism, premenstrual nervous
syndrome, pregnancy, and administration of estrogens and vasodilators,
particularly the calcium antagonist nifedipine, may also all cause edema.
(2) Localized edema：Edema originates from local venous or lymphatic obstruction
or increase of the capillary permeability, such as local inflammation, thrombosis,
thrombophlebitis, filariasis, etc.
4. Approach to the Patient
An important first question is whether the edema is localized or generalized. If it is
localized, those phenomena that may be responsible should be concentrated upon.
Hydrothorax and ascites are forms of localized edema. Either may be a consequence
of local venous or lymphatic obstruction, as in inflammatory or neoplastic disease.
If the edema is generalized, it should be determined, first, if there is serious
hypoalbuminemia, e.g.serum albumin<2.5g/dl. If so, the history, physical examination,
urinalysis, and other laboratory data will help evaluate the question of cirrhosis,
severe malnutrition, protein-losing gastroenteropathy, or the nephrotic syndrome as
the underlying disorder. If hypoalbuminemia is not present, it should be determined if
there is evidence of congestive heart failure of a severity to promote generalized
edema. Finally, it should be determined whether the patient has an adequate urine
output, or if there is significant oliguria or even anuria.
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Chapter 4
Mucocutaneous Hemorrhage
Mucocutaneous hemorrhage is due to the dysfunction of hemostasis blood
coagulation. The clinical feature is, spontaneous bleeding in general or regional
mucocutaneous, or maintainable hemorrhage after mild damage.
Etiology mechanism and Pathogenesis The basic mechanism of mucocutaneous
hemorrhage as follows: 1 Capillary wall defect. 2 abnormal of platelet number or
function. 3 Coagulation factors absence or activities reduce. 4 Anticoagulation factors
increase within the blood. The defect of one of above factors will cause the
deficiencies of hemostasis and coagulation functions, lead mucocutaneous
hemorrhage.
1 Capillary wall defect Normally, the local vascular constricts reflexly to
seal the damaged vascular endothelium and reduce blood flow as soon as the
capillary trauma. Then, the capillary is constricted continuously to play the role of
hemostasis which acted as the platelet secretion of serotonin as the
vasoconstrictor. When the capillary wall has congenital defect or camage, it can’t
normally play the role of hemostasis by constriction, and then lead to
mucocutaneous hemorrhage. It’s usually seen in:
(1) Hereditary hemorrhagenic capillary dilatatasis,
(2) Anaphylactoid purpura, non-thrombocytopenic purpura, purpura senilis
and methanical purpura.
(3) Severe infection, chemical agents or drugs toxicosis and abnormal
metabolism such as vitamin C or deficiency, uremia, arteriosclerosis.
2 Platelet abnormality Platelet play the main role in hemostaic process.
Platelets adhere and aggregate in the injured vessel, form the white thrombi to
block wound. The enzyme system of platelet membranes can actuate to form
thromboxane A2 which further aggregates platelets and enhances vasoconstriction
to amplify local hemostasis. Platelet also release the platelet factors and
thrombocytin to serve the clotting process or clot constriction, promote the
hemostasis effection. The abnormalities of platelet number or function will cause
the mucocutaneous hemorrhage. It’s often seen:
(1) Thrombocytopenia: ① primary thrombocytopenia: such as primary
thrombocytopenic purpura, neonatorum thrombocytopenia. ② secondary
thrombopenia: like drugs, infection, aplastic anemia, leukemia, hypersplenia,
etc.
(2) Platelet dysfunction: by congenital thrombasthenia, giant platelet
syndrom, and also acquired as drugs, hepatic disease, uremia.
(3) Thrombocytosis: there are primary thrombocythemia and secondary due
to affection of infection, post splenectomize, chronic mylocytic leukemia.
3 Coagulation abnormality Hemostasis process is much complex, in
which there are many coagulation factors. It’s the chain reaction activated by
pre-enzyme. It’ll cause coagulation disorder then mucocutaneous hemorrage that
any one of coagulation factors defect or dysfunction. Which often been seen in
clinic are: ① congenital: hemophilia, hypofibrinogenemia, deficiency of factor
V, hypoprothrombinia. ② secondary, deficiency of vitamin K, severe hepatic
disease.
4 Anticogulant agents increased in blood circulation
abnormal
proteinemia, heparan anticogulants increased or over-dose of anticoagulant.
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Clinical manifestation Red of dark red blotch is formed by mucocutaneous
hemorrhage. Usually, it isn’t above skin and not fade after stressed. That’s called
purpura.
In vascular defects and platelet abnormalities, hemorrhage is usually cutaneous
and/or mucosal, which presences petechiae, ecchymosis. While tissue hematoma and
internal organs bleeding are rare. In clotting factors deficiency, hemorrhage is often
internal organs, intra-muscle or soft tissue hematoma, and also intra-anticular. There
are family history or hepatic disease history in hemorrhage of coagulation disorders.
Accompaniment symptom
1 symmetric purpura of limb with arthralgia of abdominalgia, hemuresis,
is usually in anaphylactoid purpura.
2 General cutaneomucous purpura with ulemorrhsagia, nosebleed or
hemafecia, hemuresis is common in primary thrombopenic purpura.
3 Purpura with jaundice is often seen in coagulation disorder of hepatic
diseases.
4 Hemophilia and congenital platelet dysfunction should be considered
when with excessive bleeding after microtrauma from a child, joint hemorrhage
and having family history.
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Chapter 5
Dyspnea
Dyspnea is defined as an awareness of difficulty in breathing. It is therefore a
symptom, usually described by the patient as “shortness of breath,” whether the
sensation is due to actual difficulty in breathing or is essentially an awareness of
hyperventilation. If the symptom becomes striking, it always companies with
dilatation of nares, cyanosis, use of accessory muscles of respiration and
abnormalities of respiratory rate, depth or rhythm.
Etiology
The most frequent causes of dyspnea are cardiorespiratory disease. It also can be
initiated by the other factors. Such as toxic, neuropsychogenic, hematologic. In
addition, the increase of abdominal pressure (massive ascites, pregnancy etc) can
develop dyspnea too. Normal person may experience the physiologic dyspnea during
heavy exercise.
Mechanism and clinical feature
Dyspnea can be classified according to the etiology as follows:
1. Respiratory dyspnea:
Respiratory dyspnea is caused by abnormal ventilation and gas exchange,
reduction in ventilatory capacity, hypercapnia and hypoxemia resulting from
respiratory disease.
Respiratory dyspnea can be divided into three clinical types.
(1) Inspiratory dyspnea
Inspiratory dyspnea tends to occur primarily when there is obstruction, such as
inflammation, edma, tumor and foreigh body in larynx, trachea and major bronochi. It
is characterized by the depression sigh, in which visible indrawing over the sternal
notch, the supraclavioular spaces, the intercostal spaces and the epigastrium in the
inspiration can be seen often this accompanied by a coarse, low pitched inspiratory
wheezing and dry cough. It is commonly present in stenosis and obstruction of larynx,
trachea, and bronchi.
(2) Expiratory dyspnea
Expiratory dyspnea is due to the decrease of lung elasticity and spasm narrowing
of the bronchioles and smaller bronchi as in emphysema, bronchial asthma and
asthmatic bronchitis, Expiration is prolonged and laboured with wheezing.
(3) Mixed dyspnea
Mixed dyspnea occurs with the extensive lung disease, such as severe pneumonia,
pulmonary fibrosis, massive atelectasis, pleural effusion and pneumothorax, resulting
in the decrease of ventilators and gas exchange capacity. Breathing is difficult during
both inspiration and expiration.
2. Cardiac dyspnea
Cardiac dyspnea is usually attributable to pulmonary vascular congestion
resulting from the left and/or right heart failure.
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The dyspnea caused by right-sided heart failure is less severe than that one caused
by left-sided. Left-sided heart failure leads to impaired gas exchange. Compliance is
reduced, and therefore, ventilation is decreased to the edematous lung regions and
vital capavity reduced. Alveoli are stiff and more work is needed to overcome elastic
recoil, the high alveolar pressure will stimulate stretch receptor and initiate the
inflation reflex resulting in early turning off of inspiration and an increase in
respiratory rate.
Right-sided heart failure causes stasis systemic circulation. The mechanism
includes (1) the pressure of right atrial and superior vena cava is the natural stimulus
of respitatory center. (2) The decrease of oxygen content and the accumulation of the
acid metabolites, such as lactic, stimulate respiratory center. (3) The restriction of the
respiratory movement caused by enlargement of liver resulting from congestion,
ascites and pleural effusion.
Symptoms of congestive heart failure can cause orthopnea and paroxysmal
nocturnal dyspnea when elevated-filling pressure is present. Orthopnea is difficulty in
breathing in the supine position, this may be relived by sitting up, which reduces the
degree of pulmonary congestion by pooling blood in the lower extremities and
lowering left ventricular filling pressures, improving the diaphragmatic movement,
increasing vital capacity.
Paroxysma nocturnal dyspnea is a specific symptom. The patient awakes short of
breath at night, but often obtain relief by sitting up for a period of time. It is belived in
that assumption of supine posture for sleep result resorbtion of extracellar fluid into
the intravascular space, causing arise in filling pressure. In the most advanced cases,
the patients become acutely dyspneic, cyanotic and very frequently produce foany
sputum tinged with blood. On physical examination, their are moist rales at the both
lung bases, tachycardia, wheezing and bronchospasm. The markedly accentuated
second heart sound in the pulmonic area. The paroxysmal dyspnea is termed as
cardiac asthma, which can be seen in the hypertensive heart disease and coronary
heart disease.
3. Toxic dyspnea.
In the metabolic acidosis (uremia and diabetic ketosis), the acid metabolites
stimulate the respiratory center, causing deep and regular respiration with snoring.
The overdose of morphine and pentobarbital can depress respiratory center
causing deep respiration or Cheyne-Stokess respiration.
4. Neuro-Psychogenic dyspnea.
Dyspnea may occur in the patients suffering from cerebro vascular diseases (intra
cranial hemorrhage, elevated intracerebral pressure). The respiratory center loses the
blood supply or is compressed. The respiration becomes deep, slow and irregular. In
some cases the dyspnea may be psychogenic, which is characterized by repetitive
deep, signing respiration with numbness of extremities or lips, cheiropedal spasm.
These are also manifestations of acute hypocapnia and respiratory alkalosis.
5. Hematologic dyspnea
In severe anemia, sulfhemoglobinemia, methaemoglobinemia or carbon
monoxide poisoning the decrease of oxygen-carrying capacity and oxygen content
15
develop abnormal respiration and increased heart rate. The respiration rate also
increases in shock which stimulates respiration center because of hypotension.
Accompanying symptoms
1. Paroxysmal dyspnea with wheezing. It is present in bronchial asthma and cardiac
asthma. Paroxysmal severe dyspnea is often seen in acute larynx edema, foreign
body in bronchi, massive pulmonary embolism, and spontaneous pneumothorax.
2. Dyspnea with chest pain. It is frequently observed in lobar pneumonia,
pulmonary infarction, spontaneous pneumothorax, acute exudative pleurisy, acute
myocardial infarction, and bronchial carcinoma.
3. Dyspnea with fever. It is commonly noted in pneumonia, lung abscess,
pulmonary tuberculosis, pleurisy, acute pericarditis, and nervous system diseases.
4. Dyspnea with cough and purulent sputum. It is often present in chronic bronchitis,
obstructive pulmonary emphysema with infection, purulent pneumonia, and lung
abscess; Dyspnea with large amount of foany sputum is often seen in acute left
ventricular heart failure and organophosphorus poisoning.
5. Dyspnea with coma. It suggests cerebral hemorrhage, meningitis, pneumonia
with shock, uremia, diabetic ketoacidosis, and acute poisoning.
16
Chapter 6 Cough and Expectoration
Cough is undoubtedly the commonest of respiratory symptoms. It is a reflex act
that may be initiated voluntarily or involuntarily against infection of dust, noxious
gases, and may vary in severity from the occasional “clearing of the throat” that
everyone performs several times daily to a severe, hacking, harassing paroxysmal
cough that may incapacitate the afflicted individual and even threaten life itself.
Coughing per se may cause complications, including posttussic emesis, tussic syncope,
tussic rib fractures, pneumomediastinum, spontaneous pneumothorax, bullous
emphysema, and abdominal hernias. A protracted cough interferes with rest and sleep,
aggravates bronchial asthma, and causes irritation to bronchial mucosa and larynx so
that the cough tends to become self-perpetuating.
Cough arises from stimulation or irritation of the pharynx, larynx, trachea, or
bronchi. The stimuli which produce cough may be inflammatory, mechanical,
chemical, or thermal. Occasionally, cough results from pleural irritation in the absence
of tracheobronchial disease, and is even reputed to arise from stimulation of the
auricular branch of the vagal nerve.
Etiology
The cough reflex can be initiated by a wide variety of stimuli.
1. Respiratory disease: Sensatory points initiating a reflex cough are located in
the respiratory tract from the pharynx to the small bronchi, especially in the main
carina. The smaller bronchiele and alveoli are relatively insensitive to irritants. The
irritation is usually caused by irritating gas inhalation, foreign body, inflammation,
tumor, bleeding etc.
2. Pleural disease:
Cough may also be stimulated by impulse resulting from pleurisy or irritation of
pleural membrane.
3. Cardiovascular disease:
Left ventricular failure, which causes pulmonary congestion and alveolar
transudation of fluid is often associated with cough. Sometimes right-side heart failure
and pulmonary embolism also develop cough.
4. Central factor:
Cough can also originate from the cortex (voluntary cough), the impulses are
transmitted from cortex to the medulla cough center, which sends impulses to the
muscular system of chest and the larynx, and a cough results.
Expectoration:
Ciliary activity carries particles and macrophages on the mucous lining layers of
the respiratory epithelium to larger bronchi where the cough reflex is important in
their clearance, mucus is propelled upward to the glottis.
Covering the cilis there is a thin layer of secretion the mucous blanket which is
produced by the submucosal bronchial glands and to somewhat lesser extent by the
goblet cells, mucus can keep the airway membrane moist. An increase in the volume
and viscosity of tracheobronchial secretions occurs in association with infection or
irritation of the lungs, which induce the congestion of membrane, edema, increase of
the permeability of capillary. In the respiratory infection of parasitic lung disease,
virus, mycoplasma, pathogenic bacteria, amebia can be detected from the sputum.
In the pulmonary congestion or edema, the escaped blood from pulmonary
17
capillary can initiate cough and expectoration. Frothy, pink watery secretion is
characteristic for the pulmonary edema.
Clinical presentation
1. Character of cough.
Cough without sputum is called as dry cough or unproductive. It is usually caused
by acute pharyngitis, early stage of acute bronchitis, pleurisy, and mild tuberculosis.
Cough with sputum is called as productive cough. It is caused by pneumonia,
chronic pharyngitis, chronic bronchitis, broncheactasis, lung abscess, and cavitious
tuberculosis.
2. The duration and pattern of cough:
Cough initiated suddenly is mostly developed by acute upper airway infection or
foreign body in the trachea or bronchi. Chronic cough is often associated with chronic
bronchitis, bronchial asthma and tuberculosis. Paroxysmal cough is seen in the
whooping cough, tuberculous adenopathy or the broncus impressed by tumor.
Periodic cough is seen in the chronic bronchitis or bronchiectasis. It is always related
to the change of body position. Nocturnal cough particularly associated with asthma,
tuberculosis, chronic loft heart failure. It has possible association with the vagal
excitation at night.
3. The tone quality of cough:
It means the change of the sound and may suggest the location of the pathology.
For example, a "breaking" cough suggests epiglottal disease, a "brassy" cough is
associated with tracheal airway, and “Hacking" or "cleaning of throat" is often caused
by a postnasal discharge. A “hoarseness" with coughing suggests larynto-tracheal
bronchitis or impaired function of the recurrent laryngeal nerve, as from aneurysm of
the aorta, left atrial enlargement, or mediastinal malignancy. Inspiratory stridor
suggests an upper airway obstruction.
4. The character and volume of sputum:
Clear, white, or gray sputum is characteristically present in cases of chronic
bronchitis. In “pure” cases of emphysema, the cough is often nonproductive.
Tenacious sticky mucoid sputum, occasionally with bronchial casts, is commonly
noted in asthmatics. Foul-smelling purulent sputum suggests bronchiectasis.
Expectoration of calcific particles (broncholithoptysis) is diagnostic of
broncholithiasis.
Associated hemoptysis also raises the possibility of a malignant process,
bronchiectasis, lung abscess, or chronic bronchitis.
(Accompanying symptom)
1. Cough with fever: It is indicative of acute or active infection in the respiratory
system such as measles, pneumonia, influenza, lung abscess, tuberculosis, pleurisy
etc.
2. Cough with chest pain: It suggests the plural cavity be involved and may be
seen is the heart disease and coronary heart disease, such as pneumonia, pleurisy,
bronchial carcinoma.
3.Cough with dyspnea
It is often present in the edema of larynx, larynx tumor, chronic obstructive
pulmonary diseases, severe pneumonia, tuberculosis, massive pleural effusion ，
18
pneumothorax pulmonary congestion, and pulmonary edema.
4. Cough with large amount of purulent sputum
It is commonly noted in bronchiectasis, lung abscess, and bronchi-pleural fistula.
5. Cough with hemoptysis
It suggests pulmonary tuberculosis, bronchiectasis, bronchial carcinoma, lung
abscess, or mitral stenosis.
6. Cough with clubbed fingers
It is commonly seen in bronchiectasis, lung abscess, bronchial carcinoma, and
thoracic empyema.
7. Cough with wheeze
It is often seen in bronchial asthma, cardiac asthma, and foreign body in trachea
and bronchi.
19
Chapter 7
Hemoptysis
Hemoptysis is the expectoration of blood from the airway below larynx. When
patients complain of coughing up blood, the nose, mouth and upper respiratory tract
must be searched carefully by the mirror examination to rule out the possibility that
blood may come from those areas.
Although the quantity of blood produced may vary in quantity from streaks and
flecks in the sputum to massive hemorrhages, even minimal bleeding may be an early
indicator of the presence of serious bronchopulmonary disease. Hemorrhages of even
moderate degree may be life threatening.
In approximately one-half of patients with hemoptysis, the standard chest
roentgenogram shows no abnormalities or only minimal nonspecific changes.
Hemoptysis may be the initial or the sole symptom of bronchopulmonary disease, and
the determination of its cause is a common diagnostic problem.
Etiology
1. Bronchial disease:
Hemoptysis may occur in bronchiectasis (TB or non-TB), chronic bronchitis,
endobronchial tuberculosis disease, bronchogenic carcinoma. It can be seen in the
benign bronchogenic tumor, broncholithiasis, foreign body, bronchogenic nonspecific
ulceration. The inflammatory processes leads to the increase of permeability of
capillary and rupture of vessels in the bronchial mucosa. Blood-streaked sputum
occasionally occurs in the course of acute bronchitis.
2. Lung diseases:
The sputum of pneumococcal pneumonia is classically described as "rusty" in
appearance. Pulmonary tuberculosis was formerly the most common cause of
hemoptysis and is still an important etiology. Pulmonary tuberculosis may cause the
expectoration of frank blood from pulmonary cavity. Lung abscess may be associated
with putrid smelling sputum and expectoration of blood. Hemoptysis occurs in
approximately 25% of patients with pulmonary embolism and infarction. Pulmonary
fungi and parasite infection may also serve as the sources of hemoptysis.
3. Cardiovascular diseases:
Pink,frothy sputum is frequently associated with acute pulmonary edema.
Blood-streaked sputum may occur with acute pulmonary congestion when the classic
findings of acute pulmonary are not fully developed. The blood comes from
pulmonary capillaries, which have ruptured under high intravascular pressure.
Hemoptysis due to mitral stenosis is frequently induced by physical exercise, by
sexual intercourse, or in the presence of excitement. The blood comes from a break in
the pulmonary veins which have ruptured under very high pressure. The bleeding is
due to rupture of endobronchial vessels that form collateral channels between the
bronchial veins and pulmonary venous system. Episodes of pulmonary hemorrhage of
this type tend to subside as the veins adapt to the high pressure and as pulmonary
arteriolar disease develops. Many pulmonary emboli do not lead to pulmonary
infarction, and when they do, frank hemoptysis occurs in the minority of instances.
Despite this, when hemoptysis occurs in a patient with heart failure, pulmonary
infarction is likely. The bloody sputum usually appears within a few hours to a day
20
after the embolus and is due to necrosis and hemorrhage into the alveoli.
hemoptysis is also associated with congenital cardiac disease and aortic
aneurysms..
4. Constitutional diseases:
Blood spitting may also occur in the patients suffering from certain blood
dyscrasias, such as hemophilia, leukemia, and infectious disease, connective tissue
disease.
Clinical manifestations
1. The patient’s age.
Hemoptysis is often seen in pulmonary tuberculosis, bronchiectasis, and
rheumatic heart disease (mitral stenosis) for most youth. Cancer is now the disease
that patients think of when they expectorate blood, just as it was tuberculosis 50 years
ago. If an elder people complain of coughing up sputum tinged with blood or streaks
of blood in sputum, especially in the male patient with long history of smoking, the
possibility of suffering cancer must be taken into account. If the patient is in close
contact with tuberculosis suffer, the pulmonary tuberculosis should be considered.
The diagnosis of paragonimialsis may be suspected in the man with the history of
eating raw or improperly cooked crabs or crayfish.
Epidemic hemorrhagic fever, leptospirosis also can cause hemoptysis, they are
endemic
diseases.
2. The amount of coughing up blood
Hemoptysis can be classified into three groups according to the amount of
coughing blood, massive, moderate and minimal. Massive hemoptysis may be defined
in various ways, but is usually taken to include cases in which there is expectoration
of 500 ml or more with 24-hour period. Massive hemoptysis often occurs in the
patients with pulmonary tuberculosis cavity, chronic lung abscess or bronchiectasis.
Minimal means the amount of coughing up blood less than 100 ml, and moderate is
between them.
3. Color and character.
When a patient gives a history of “coughing blood,” it is necessary to ascertain
the exact nature of the sputum. The sputum must be examined both grossly and
microscopically. It is useful to determine whether the material that is coughed up
contains large volumes of liquid blood, which indicates brisk bleeding, or whether it
contains smaller quantities of dark or clotted blood, which would indicate slow
bleeding from low-pressure vessels or subsiding bleeding. Brisk bleeding, for
example, is commonly associated with specific focal ulceration of the bronchus, such
as bronchogenic carcinoma, a foreign body, bronchiectasis, or a bleeding aortic
aneurysm. Slow bleeding strongly suggests venous bleeding which is more likely to
be the result of increased in blood flow through the bronchial venous system such as
may occur as a result of mitral stenosis or bronchiectasis.
Accompanying Symptom
1.Hemoptysis with fever: Pulmonary tuberculosis, pneumonia, lung abscess and
leptospirosis, epidemic hemorrhagic fever, bronchogenic carcinoma.
21
2. Hemoptysis with chest pain: Lobar pneumonia, pulmonary infarction, and
pulmonary tuberculosis cancer.
3. Hemoptysis with putrid sputum: lung abscess, cavitious tuberculosis, and
bronchiectasis.
4. Hemoptysis with irritating cough: bronchogenic carcinoma, mycoplasma
pneumonia.
5. Hemoptysis with skin and mucosa bleeding: hematologic disease, epidemic
hemorrhagic fever, rheumatism, leptospirosis.
6. Hemoptysis with jaundice: leptospirosis, lobar pneumonia, pulmonary
infarction.
The distinction between hemoptysis and hematemsis
Hemoptysis
hematemesis
History:
T.B, bronchiectasis
Ulcer, cihrrosis
Presymptom:
Cough,
chest Vomit,
nausea,
epigastric
discomfortable
discomfort
mode of expectoration:
blood spitting
vomiting
color of blood:
bright red
dark red and black
Material mixed with
mixed with air bubble contain food debrits gastric juice
blood
and sputum
pH
alkaline
acid
melena
No
Yes
occasionally swallowed may continue for several days
22
Chapter 8
Cyanosis
Cyanosis is a bluish discoloration of the skin and mucous membranes resulting
from and increased amount of reduced hemoglobin or of abnormal hemoglobin
pigments in the blood perfusing these areas.
Mechanism
In general, unsaturated oxygen of arterial blood is 1 vol/100ml, unsaturated
oxygen in venous blood is 6 vol/100 ml, and in capillary the unsaturated oxygen
probably in the mean value of arteral and venous blood (1+6/3=3.5 vol/100 ml). When
fully saturated with oxygen, each gram of hemoglobin binds 1.34 ml of oxygen.
Cyanosis becomes apparent at a mean capillary concentration of 5 gm/100 ml reduced
hemoglobin (or blood unsaturated oxygen 6.7 vol/100 ml).
Since it is the absolute quantity of reduced hemoglobin in the blood that is
responsible for casnosis the higher the total hemoglobin content, the greater the
tendency toward cyanosis; thus patients with marked polycythemia become cyanotic
at higher levels of arterial oxygen saturation than patients with normal hemotocric
values, and cyanlsis may be absent in patients with severe anemia despite marked
arterial desaturation.
Etiology
There are four principal forms of cyanosis
1. Central cyanosis, characterized by decreased arteria oxygen saturation due to
right-to-left shunting of blood or impaired pulmonary function. It includes pulmonary
cyanosis and cardiac cyanosis. Pulmonary cyanosis is often seen in severe respiratory
diseases, such as pneumonia, obstructive pulmonary emphysema, and primary
pulmonary hypertension. Cardiac cyanosis is commonly present in congenital heart
disease when the volume of a right-to-left shunt exceeds 30 per cent of the left
ventricular output.
2. Peripheral cyanosis, most commonly secondary to cutaneous vasoconstriction
due to a low cardiac output or exposure to cold air or water if peripheral cyanosisis
localized to as extremity arterial or venous obstruction should be suspected. It also
includes congestive peripheral cyanosis and ischmic peripheral cyanosis. Congestive
peripheral cyanosis is often seen in right-side heart failure, constrictive pericarditis,
local venous diseases. Ischmic peripheral cyanosis is often seen in severe shock.
3. Mixed cyanosis, central cyanosis and peripheral cyanosis occur in the same
time, the blood is insufficiently oxygenated because the lung is congested or more
deoxygenation due to slow peripheral circulatory blood flow in peripheral capillary
vessels.
4. Cyanosis resulting from abnormal hemoglobin pigments in the blood.
a. Methemoglobinemia due to drugs or chemical poisoning (methemoglobin 3
gm/100 ml) such as nitrite salt, sulfa drugs or phenacetin etc.
b. Hereditary methemoglobinnemia.
c. Sulfhemoglobinemia (sulfhemoglobin 0.5 mg/100 ml).
23
Diagnosis
A history of cyanosis beginning in infancy suggests a congenital cardiac
malformation with a right-to-left shunt hereditary methemoglobinemia is another
cause of congenital cyanosis; the diagnosis of this condition is supported by a family
history of cyanosis in the absence of heart diseases. If cyanosis appears at the age of 6
months or later in childhood it may be due to the development of progression of
obstruction to the right ventricular outflow in patients with ventricular septal defect.
Development of cyanosis between age 5 and 15 years suggests an Eisenmenger's
reaction with right-to-left shunting as a consequence of a progressive increase in
pulmonary vascular resistance.
A history of cyanosis localized to the hand suggests Reynttd's phenomenon
central cyanosis due to congenital heart disease or pulmonary disease
characteristically worsens during exertion, whereas peripheral cyaonsis of congestive
heart failure at rest may be accentrated only slightly, if at all, during exertion.
If cyanosis is caused by methemoglobinemia there is a history of contact of drugs
or chemical material. Spectroscope is helpful to diagnose methemoglobinemia. If
cyanosis is due to congenital heart diseases, echocardiography, right heart
catherixation and angiocardiography should be performed.
Accompanying symptoms
1. Cyanosis with dyspnea: severe cardiopulmonary diseases, pneumothorax.
2. Cyanosis with clubbed fingers: congenital heart disease, chronic pulmonary disease.
3. Acute cyanosis with conscious disturbance: medicine or chemicals poisoning,
shock, acute pulmonary infection.
24
Chapter 9
Palpitation
Definition:
Palpitation may be defined as an awareness of the beating of the heart, an
awareness moat commonly brought about by a change in the heart's rhythm or rate or
by an augmentation of its contractility. Palpitation is not pathognomonic of any
particular group of disorders; indeed, often it signifies not a primary physical disorder
but rather a psychio disturbance. Even when it occurs as a more or less prominent
compliant, the diagnosis of the underlying disease is made largely on the basis of
other associated symptoms and the data. Concern is al the more pronounced in
patients who know or who have been told that they may have heart disease; to them
palpitation may seem to be an omen of impeding disaster. Since the resulting anxiety
may be associated with increased activity of the autonomic nervous system, with
consequent increases of the cardiac rate and rhythm and the vigor of contraction, the
patients awareness of these changes may then lead to a vicious cycle, which
ultimately be responsible for this incapacitation.
Palpitation may be described by the patient in various terms, such as "fluttering",
"flopping", and "skipping", and in most cases it will be obvious that the complaint is
of a sensation of disturbed heartbeat. The wide variability in the sensitivity to
alteration in cardiac activity among different individuals must be appreciated. Some
patients seem to be unaware of the most serious and chaotic dysrrhythmias; other are
seriously troubled by and occasional extrasystole. Patients with anxiety states often
exhibit a lowered threshold at which disorders of rate and rhythm result in palpitation.
Indeed, it is not unusual for palpitation to be the major manifestation of the emotional
disorder. The awareness of the heartbeat also bends to be more common at night and
during introspective moments, but is less marked during activity. Patients with organic
heart disease and chronic disorders of cardiac rate, rhythm, or stroke volume tend to
accommodate to these abnormalities and are often less sensitive than normal persons
to such events. Persistent tachyeardia and/or atrial fibrillation may not be
accompanied by continual palpitation, in contrast to a sudden, brief alteration in
cardiac rate or rhythm which often causes considerable subjective discomfort. Thus,
palpitation is particularly prominent when the precipitating cause for increased heart
rate or contractility or arrhythmia is recent, transient, and episodic. Conversely, in
emotionally well-adjusted individuals palpitation becomes progressively less
disconcerting as the cause (e. g. anemia, frequent extrasytoles, complete A-V block)
persists.
Under ordinary circumstances the rhythmic heartbeats is imperceptible to the
healthy individual of average or placid temperament. Palpitation may be experienced
by normal persons who have engaged in strenuous physical effort or have been
aroused emotionally. This type of palpitation is physiologic and represents the normal
awareness of an overactive heart-i.e. a heart that is beating at a rapid rate and with an
increased contractility. Since palpitation due to overactivity of the heart may occur
also in certain pathologic states, e. g., high fever, severe anemia, or thyrotoxicoxix, it
is commonly assumed that it is the overactivity person that is responsible fore the
symptom. However, overactivity of the heart is generally associated with several other
alterations in cardiac function including acceleration of heart rate, more rapid
development of intraventricular pressure during isometric contraction, increased
intensity of the heart sounds, especially of the first sound, a short duration of systole,
25
and a greater ejection velocity.
When palpitation is heavy and regular, it is usually caused by an augmented
stroke volume, and it should raise the question of aortic or mitral regurgitation,
ventricular septaldefect, or of a variety of hyperkinetic circulatory states (anemia,
arteriovenous fistula, thyrotoxicosis, and the so-called idiopathic hyperkinetic heart
syndrome.) It may also occur immediately after the onset of cardiac slowing, as with
the sudden development of heart block, or upon the conversion of sinus rhythm from
atrial fibrillation. But unusual movements of the heart within the thorax are also
frequently the mechanism of palpitation. Thus, the ectopic beat and/or the
compensatory pause may be appreciated, since both are associated with alteration in
cardiac function.
Important causes of palpitation:
1. Disorders of the mechanism of the heartbeat.
1) Extrasystole: In most cases the dianosis will be suggested by the patient history.
The premature contraction and postpremature patient may say that he feels if "the
heart turns over". The pause following the premature contraction may be felt as an
actual cessation of the heartbeat, in contrast with the complete unawarness of pauses
of similar duration when atrial fibrillation with a slow ventricular rate occurs. The
patient's apprehensions seem to magnify the duration of the interval and sometimes
may make him wonder if the heart will ever resume its beat. The first ventricular
contraction succeeding the pause may be felt as an unusually vigorous beat and will
be described as "ourding" or "thudding".
Usually the identification of the extrasystole as the cause of palpitation is a
simple matter. When extrasystoles are numerous, clinical differentiation from atrial
fibril action can be made by any procedure that will bring about a definite increase in
the ventricular rate; at increasingly rapid heart rate, the extrasystoles usually diminish
in frequency and then disappear, whereas the irregularity of atrial fibrillation increases.
A-V block with dropped beats, is the only other common arrhythmia with which the
premature contraction is likely to be confused; but simple ausculatation will reveal the
difference.
2) Ectopic tachycardias: These conditions are common and medically important
causes of palpitation Ventricular tachycardia, one of the most serious arrhythmia,
rarely is manifested as palpitation; this may be related to the abnormal sequence, and
hence impaired coordination and vigor, of ventricular contraction. If the patient is
seen between attacks, the diagnosis, of ectopic tachycardia and its type will have to
depend upon the history, but of course the precise diagnosis can be made only when
an ECF and observations on the effect of carotid sinus pressure are made during the
episode. Monitoring of the ECG with a portable tape recording system and asking the
patient to record the time of onset and cessation of the palpitations are extremely
helpful in determining their cause. The mode of onset and offset gives the most
important lead in distinguishing sinus from one of the various forms of ectopio
tachycardias; sinus taohycardia commences and ceases over the course of minutes or
seconds, but not instantaneously as is characteristic of ectopic rhythm.
2. Organic or functional disturbance origination outside the circulatory system:
1) Thyrotoxicosis: In its fully developed form, thyrotoxicosis will usually be
evident and offers little difficulty in the may of diagnosis except in the elderly, in
whom so-called apathenichyperthyroidism may be present. Thyrotoxicosis is
particularly likely to be over-looked in the presence of myocardial failure.
2) Anemia: when mild, anemia may cause palpitation during exertion; when
severe, palpitation may be present at rest. Appropriate studies of the blood will clarify
26
the situation.
3) Palpitation may be present in acute infections, particularly in the early stages.
4) Hypoglycemia: Palpitation is often a prominent feature of the condition and
appears to be related to release of catecholaminels. The diagnosis is confirmed by
appropriate blood sugar estimations, by reproduction of the symptom when hsulin is
administered, and by prompt relief of symptoms on the administration of glucose.
5) Drugs: The relationship between the development of palpitation and the use
tobacco, tea, alcohol epinephrine, ephedrine, aminophylline, atroping, or thyroid
extract is obvious.
6) Tumors of the adrenal medulla (pheochromecytoma).
Palpitation as a manifestation of the anxiety state
27
Chapter 10
Gastrointestinal Hemorrhage
Gastrointestinal bleeding may be obvious efflux of blood from the
gastrointestinal tract (gloss blood) or no external manifestation (occult blood).
【Causes of GI bleeding】
Upper Gastrointestinal Diseases
I.
Digestive diseases
1. Esophageal:
Varices,
esophagitis,diverticulitis,cancer,injury,Mallory_Weiss
tear,hiatal hernia.
2. Gastric/duodenal: Ulcers,cancer, acutemucosalesion, (hemorrhagic / erosive
gastritis),vascular lesions.(arteriosclerotic vessel dysplasia)
3. Hepatobiliary: Esophagogastric varices (due to cirrhosis) and
Acute hemorrhagic cholangitis,
4.Pancreatic : Pancreatic cancer of Vater's Ampulla.
II. lower gastrointestinal diseases
1. Intestinal:
T.B.,
Chron's,
ulcerative
colitis,tumour,angioma,meckel's
diverticulitis,acute hemorrhagic_necrotic enteritis.
2. Colonic: Dysentery (bacterial ,Amebic),Inflammatory bower disease,
Cancer,polyps, schistomiasis,angiodysplasia.
3. Rectal and anal: trauma,proctitis,cancer,hemorrhoids,fissures,fistulae
Hematemesis
Hematemesis is vomiting of blood
Bright red
Coffee_grounds
in a appearance
[Causes]
The most common causes of hematemesis
1. peptic ulcer
2. esophagogastric varices
3. acute mucosal lesions
4. benign and malignant neoplasms
5. Mallory_weiss tear
[Symtoms]
1. Nausea
Retching
vomiting
melena
2. The colon of the blood depends on the magnitude and the length time the blood
has remained in the stomach.
stomach
3. Small amount of blood
dark brown
acid secretion
coffee grounds
in
appearance
acid hematin
4.Massive/rapid bleeding
bright red /brisk bleeding
5.Blood loss >1000ml
hypovolemia manifested by
shock
Tachycardia vs Hypotension
Hematochezia
Hematochezia is bleeding per anum
[Causes]
The most common causes
28
1. peptic ulcer, acute mucosa lesions
2. Dysentery ,inflammatory bowel disease
3. Cancers,polyps
4. Hemorrhoids,angiodysplsia
5. Diverticulae
[Symptoms]
The color of the blood is related to the followings:
I. The site of bleeding (UGI,LGI)
The ligment of Treitz is the dividing point for UGI and LGI lesions.
△ Hematemesis: it is the vomiting of blood (bright red or coffee_grounds
in appearance and contain a source of bleeding above the ligament of Treitz.
△ Three different types of bleed per annum can be distinguished.
1. Melena____ The passage of black,tarry,sticky stool. RBC destroyed iron
mucus
sulfide
tarry stool.
intestine
2. Occult blood stool______ blood may not be appear glossly in the stool,but can
be detectable only by chemical tests. It may be manifestations of either UGI or
LGI bleeding .
3. Hematochezia____The passsage of bright red stool per rectum. It represents
either a very rapid massive UGI bleeding or more likely a lower intestinal
source.
II. The color of the stool only reflects the length of time the blood has remained
to be digested in the intestinal lumen. The longer the blood remains in the
GI tract, the more likely melena will occur.
III.
The rapidity of bleeding
GI transit blood rapidly____ the stool may be bright red or maroon
Ⅳ. The magnitude of bleeding
Hematemesis
often suggest>100ml of blood loss
Hematochezia
Melena: >500ml of blood loss
Occult blood stool: indicates bleeding of >500ml from any levels of GI tract
Massive bleeding
Hypovolemia
Shock
Tachycardia and
hypotension
[Diagnostic Procedures]
1.Helpful information: Age,prior episode of bleeding,associated illness,medicaton
take,prior abdominal surgery,recurrent bloody diarrhea,recent change in stool caliber.
3. Physical examination: T.P.R.Bp., jaundice, anemia, skin and mucous bleeding,
hepatosplenomegaly, abdominal mass, ascites, loss weight, epigastric tenderness,
digital
rectal
examination,spider,angioma,pulmar
erythema,lymphnode
enlargement.
4. Lab findings: liver function tests,occult blood test,diagnostic hematology.
5. Imagin
techniques:
Barium
X-ray
series(meal
lemena),ultrasonography,CT,endoscopic examination.
Chapter 11
29
Chapter 11
Diarrhea
[Definition]
1. Increase in the frequency of bowel movements
2. Increase in stool liquidity
3. In some cases,increase in daily stool weight (>200g/d)
[Etiology]
Ⅰ.Acute Diarrhea
1. infection:
(1) viral,
(2) bacterial(campylobateria,shigella,E.Coli,Salmoneila,etc)
(3) fungal
(4) parasitic (amebic trophozoites,Giardia)
2. food poisoning:bacterial,plants,chemical poison(arsenic)
3. systematic diseases (Influenza,sepsis,measle,etc.)
4. Miscellanous: (1)Allengic diseases(Allergic purpur……)
(2)endocronic diseases (ZES,etc.)
(3)Drugs: laxatives,5-FU,etc.
Ⅱ.Chronic Diarrhea
1. Intestinal: (1)Infections(T.B.,chronic bacteria dysentery,etc.)
(2)parasitics(Amebia dysentery,giardiasis,etc.)
(3)IBD(ulcerative colitis,Chron's,etc.
(4)malabsorption syndrom.(lactase deficiency,etc.)
(5)Tumors.
2. Gastric (chronic gastritis,subtotal gastrectomy,etc.)
3. Pancreatic(chronic pancreatitis,pancreatic cancer,etc.)
4. Hepatobiliary(liver cirrhosis,obstructive jaundice)
5. Endocronic (Hyperthyroids crisis,ZES,Carcinoids)
6. Drugs(Reserpin,Ismelin,laxatives,etc.)
7. Others (Uremia,hypogammaglobulemia,etc.)
30
[Pathophysiological mechanisms]
Ⅰ.Secretory diarrhea (increased intestinal secretion)
Agents
1.infections(cholera toxin,E-coli,salmonella,staphylococcal)
2.hormanal(guthormones,ZES,VIP),cancer(calcitonin,prostaglandins)
3.miscellaneous(laxatives abuse,villus adenoma of the rectum)
active
Adenylate cyclase
cAMP system
Nacl ↑
secretory
diarrhea.
Ⅱ.Osmotic diarrhea
It caused by accumulation of the followings in the gut lumen.
being osmotically active
Poorly absorble solutes
Maldigestion of ingested food
Failure to transport an osmotically
Active dietary nonelectrolyte (ei,glucose)
water
diarrhea
salts
Intestinal lumen
III.Decreased intestinal surface area and/or intestinal absorption
Ex: surgical removal, malabsorption syndrome
Ⅳ. Rapid transit of intestinal contents (shortened transit time)
contents
increase in intestinal motility (intestinal hurry)
reduce
contacts time
small
bowel mucous
increase
volume
stool
liquidity
Ex: irritable bowel syndrome (Functional diarrhea)
Laxatives abuse
Post vagotomy diarrhea
Post gastrectomy dumbing syndrome.
[Symtoms]
Ⅰ. Acute diarrhea (duration less than 2 weeks)
1.onset: Abrupt frequent small fecal discharge
cramping abdominal pain,tenesmuse
2.stool: increased in volume and liquidity
routin examinition: fleck of blood,mucus
31
WBC,RBC,pus ,destroyed epithelium
3.sever cases: dehydration,electrolyte disturbances,metabolic acidosis,
collapse hypovolemia,tetany.
Ⅱ.chronic diarrhea( duration more than 2 months)
1.onset: gradual /insidious
diarrhea of variable severity
diarrhea alternate with constipation
colicky abdominal pain, distention
2.stool: watery,bloody,steatorrhea
contains:inflammatory cells /mucus/pus/indigested food
3.severe /long_standing cases:weihgt loss,malnutrition,edema,malabsorption
wasting, bone pain,multy vits deficiency.
Ⅳ.Accompanied symptoms
1. severe dehydration (cholera,pancreatic cholera—WDHA,etc.)
2. fever(Acute bacillery dysentery,Thyphoid,T.B.enteritis,etc.)
3. tenesmus (Acute dysentery,proctitis,etc.)
4. markedly weight loss (cancer of gut,malabsorption,etc.)
5. arthralgia/arthritis(IBD,cnnective tissue diseases,etc.)
6. masses(malignant cancer of GI,T.B.peritonitis,etc)
[Diagnostic procedures]
Ⅰ.Informmation:
1. in epidemic (dysentery,v.cholerae,thyphoid,food poisonning,enteritis)
2. food allergy
3. past illness(antibiotic related diarrhea,etc.)
4. medication take(corticosteroids,laxatives,etc.)
5. predisposing conditions (surgical resection,parasitic infection,etc.)
II.Physical Examination
Fever,dehydration,manutrition,anemia,ulticaria,jaundice,arthralgia,abdominal masses,
Tenesmus,digital rectal examination.
III.lab findings
1. blood
⑴ RBC ⑵WBC,⑶culture,⑷specific antigen/antibody (widal test,etc.)
⑸serum testings(carotin/iron,ferritin/albumin/folic acid,vitB12/glucose/
gut hormone/Ca2+,K+,Cl-,Na+)
2. Urine: protein,cast
3. Stool: (1) appearance(watery,bloody,bulky,sticky,malodorous,steatorrhea,foul_
Smelling)
(2) Microscopy____PMNC (in shigella,salmonella and E.coli)
____ E.Coli.
_____mononuclear(M)
_____motile amebic trophozoites
(3)Gram's Stain(+): in staphylococcal enteritis
(4)culture: salmonellae,shigella,v.cholera
(5)fat determination
4. Tolerance tests: d_xylose,Glucose/lactose/sucrose
5. Breath tests:14c glycine_cholate,xylose
6. Culture of jejunal aspirates: Bacteria overgrowth,increased bile and deconjugation.
7. 5 HIAA: Urinary excretion.
8. VitB12 absorption test
32
9. X_ray barium (meal /enema)
10. Endoscopy:duodenoscopy(ERCP),colonoscopy,sigmoidoscopy.
11. Suction biopsy technique( Jejunal mucosa histology
33
Chapter 12
Nausea and Vomiting
Nausea and Vomiting are common clinical symptoms. Nausea is a sensation of
upper abdominal discomfort and having an urge to vomit. It goes with the symptom of
vagus exciting, such as paleness, sweatiness, salivation, low blood pressure and
bradycardia. Nausea is a prelude of vomiting, but sometimes vomiting occurs without
nausea or nausea occurs without vomiting. Vomiting is forcing the contents of the
stomach and small intestine up through the esophagus and out of the mouth. They are
complex reflex caused by multiplicate reasons.
【Causes】According to the pathogenisis, the causes of nausea and vomiting can be
devided into several sorts as follows:
1. reflexible vomiting
(1) irritation of pharynx: smoking, severe cough, nasopharyngitis and so on.
(2) Gastroduodenal diseases: acute and chronic gastroenteritis, peptic ulcer, acute
gastric dilatation, pyloric obstruction, duodenal stasis and so on.
(3) Intestinal diseases: acute appendicitis, intestinal obstruction, acute necrotizing
enterocolitis, abdominal type of allergic purpura and so on.
(4) Hepatic, biliary and pancreatic diseases: acute hepatitis, liver chirrosis, hepatic
congestion, acute and chronic cholecystitis, pancreatitis and so on.
(5) Diseases of peritoneum and mesentery: such as acute peritonitis.
(6) Systemic diseases: nephrolithiasis, acute pyelonephritis, acute inflammation of
pelvic cavity, rupture of ectopic pregnancy and so on. Myocardial infarction,
heart failure, diseases of labyrinth, glaucoma and inappropriate refraction also
can lead to nausea and vomiting.
2. central vomiting
（1） Encephalic inflammation, all kinds of cephalitis and meningitis.
（2） Cerebral vascular disease such as cerebral hemorrage, cerebral infarction,
cerebral thrombosis, hypertentional encephalopathy and migraine.
（3） Skull and intracranial injury: brain contusion or intracranial hematoma.
（4） Epilepsies, especially status epilepticus.
（5） Systemic diseases: hydrocephalus and elevated intracranial cavity pressure
(ICP) caused by uremia, hepatic encephalopathy, diabetic ketoacidosis
(DKA) and hypoglycemia.
（6） Drugs: such as antibiotics, many chemotherapy drugs, digitalis and morphia,
these drugs stimulate vomiting center and lead to vomiting.
3. Neuropathic vomiting：gastrointestinal neurosis and anorexia nervosa.
【Pathogenesis】Vomiting is a complicated reflex including three stages: nausea,
vomiturition and vomiting. In the stage of nausea, tensility and peristalsis of stomach
decrease, while tensility of duodenum increases with or without reflux of duodenal
fluid. In the stage of vomiturition, upper part of stomach relax with transient
contraction of gastric antrum. In the stage of vomiting, the abdominal muscles tighten
34
against a relaxed stomach with an open sphincter. The contents of the stomach are
propelled up and out. Vomiting is different from countercurrent regurgitation, in
which the contents of the stomach reflow up through the esophagus and out of the
mouth without nausea and contraction of diaphragm.
The center of vomiting is located in the medulla consist of two parts with different
function. One is neural reflex center----vomiting center, which located in the lateral
medullary reticular formation in the medulla. The other is chemoreceptor trigger zone
at the base of the fourth ventricle of the brain. Vomiting center receives afferent
impulsion from digestive tract, pallium, inner ear vestibule, coronary artery and
chemoreceptor trigger zone, and administrates the vomiting action directly. The
chemoreceptor trigger zone has numerous dopamine D2 receptors, serotonin 5-HT3
receptors, opioid receptors, Acetylcholine receptors, and receptors for substance P.
Stimulation of different receptors are involved in different pathways leading to
vomiting.
【Clinical Manifestation】
1. the time of vomiting: vomiting which occurs upon waking is often induced by
morning sickness, uremia, chronic alcoholism, functional dyspepsia or sinusitis. If
the vomiting occurs at night, the common cause is pyloric obstruction.
2. the relation with eating: the vomiting occurs some time after dinner is always
caused by food poisoning, especially for the collective pacients. Vomiting just
after dinner may be neuropathic vomiting. Lingering vomiting (deferred vomiting)
is defined as the vomiting occurs more than 1h after dinner, which indicates
decline of gastric tensility. Vomiting after several meals is often cuased by pyloric
obstruction.
3. the features of vomiting: neuropathic or ICP vomiting are lack of nausea.
Projectile vomiting always indicates ICP.
4. character of vomitus: The barmy or septic smell indicates retention of gastric juice
and food. Feculent vomitus occurs with low-intestine obstructive lesions. When
the vomitus contains bile it suggests the obstruction located under duodenal
papilla. If the vomitus contains no bile it suggests the obstruction located upon the
duodenal papilla. Vomitus with plenty of acid fluid indicates duodenal ulcer or
gastrinoma. Vomitus without acid fluid is always due to cardiac stenosis.
Obstruction of upper digestive tract can be determined according to the quantity of
vomitus, and the amount of liquid loss can be estimated.
【Associated manifestations】The associated manifestations followed are helpful to
the diagnosis of nausea and vomiting. (1)When vomiting is associated with abdominal
pain and diarrhea it maybe a result of acute gastroenteritis, bacterial food poisoning,
cholera, paracholera and acute toxicosis. (2) Vomiting associated with right upper
abdominal pain, fever, chill or jaundice suggests cholecystitis or gallstone. (3)
Projectile vomiting with headache is due to ICP or glaucoma.(4) Vomiting with
35
vertigo and nystagmus may occur in vestibule lesion.(5) When vomiting occurs
during the treatment of antibiotics and chemotherapy, it maybe due to the side
effect.(6) If a woman develops vomiting which occurs upon waking and menopause,
it often indicates morning sickness.
【Keypoints】
1. Beginning of vomiting: with or without inducement, rapid or slow initiation,
association with food, history of abdominal surgery, menstrual history and so on.
2. Time of vomiting: in the morning or at night, intermittent or persistent, associated
with food and activity or not.
3.
Feature of vomitus: its color, contents and odor.
4.
Inducment: such as position, eating and stimulation of pharynx.
5.
Associated menifestations mentioned before.
6. Examination and treatment: X-ray of barium meal, endoscopy, ultrasonic exam,
blood sugar, BUN and so on.
36
Chapter 13
Jaundice
Accumulation of bilirubin in the bloodstream causes yellow pigmentation of the
plasma,leading to discoloration of heavily perfused tissues. Clinically ,
hyperbilirubinemia appears as jaundice or icterus ,yellow pigmentation of the skin and
scerae .
【Bilirubin Metabolism】
normal serum bilirubin concentrations range from 5 to 17 μmol/L (0.3 to 1.o
mg/dl).More than 90 percent of serum bilirubin in normal individuals is in the
unconjugated form . The remainder is conjugated to a polar group (primarily
glucuronide ),rendering it water-soluble and thus able to be filtered and excreted by
the kidney.
Approximately 90 percent of circulating bilirubin in derived from senescent red
blood cells.When circulating erythrocytes reach the end of then normal life span of
approximately 120 days,they are destroyed by reticuloendothelial cells . Oxidation of
the heme moiety dissociated from the hemoglubin within these cells generates
biliverdin ,which is than metabolize to bilirubin .Approximately 15 to 20 percent of
circulating bilirubin is derived from other sources ,including (1)ineffective
erythropoiesis resulting from destruction of maturing erythroid cells in the bone
marrow,and , (2) the metabolism of other heme-containing proteins , most notably
hepatic cytochromes, muscle myoglobin ,and widely distributed heme-containing
enzymes.
Unconjugated bilirubin liberated into the plasma is bound tightly,but
nonconvalently, to albumin. Certain organic anion , such as sulfonamide and
salicylate , compete with bilirubin for binding sites on albumin ,permitting the
released pigment to enter tisssues. Conjugated bilirubin is bound to albumin in two
forms reversible and irreversible . Reversible , noncovalent binding is similar to that
of unconjugated bilirubin , although the complex is less stable . When present in
serum for extended periods of time (e.g. , with cholestasis ), conjugated bilirubin can
form an irreversible,covalent complex with albumin referred to as delta bilirubin or
biliprotein . Because of the irreversibility of binding , this complex is not excreted by
the kidney .
Hepatic metabolism of Bilirubin: The liver has a central role in the metabolism of
the bile pigments . This process can be devided into three distinct phases: (1) hepatic
uptake: unconjugated bilirubin bound to albumin is presented to the liver cells. The
uptake and subsequent hepatocyte storage of bilirubin involve binding of bilirubin to
cytoplasmic anion-binding proteins,especially ligandin (glutathione-s-tansferase
B),that prevent efflux of bilirubin back into the plasma; (2) conjugation: unconjugated
bilirubin is water-insoluble unless complexed to an amphipathic molecule such as
albumin . Since albumin is absent from bile,bilirubin must converted to a
water-soluble derivative before biliary excretion. The process is accomplished
predominantly by conjugation of bilirubin to glucuronic acid , generating bilirubin
glucuronide . The conjugation reaction occurs in the endoplasmic riticulum of
hepatocytes and is catalyzed by bilirubin glucuronozyl transeferase ; (3) Excretion: In
normal circumstances, only conjugated bilirubin can be excreted into bile . Impaired
excretion lends to decreased bilirubin concentrations in the bile and concomitant
efflux of conjugated bilirubin through the sinusoidal menbrane of the hepatocyte into
37
the blood stream .
Intestinal phase of Bilirubin Metabolism: after secretion into the bile,conjugated
bilirubin is transported through the biliary ducts into the duodenum .Conjugated
bilirubin is not reabsorbed by the intestinal mucosa . It is either excreted unchanged in
the stool or metabolized by ileal and colonic bacteria to urobilinogen and related
products. Urobilinogen can be reabsorbed from the small intestinel and colon and
enters the portal circulation .Some of the portal Urobilinogen is taken up by the liver
and reexcreted into the bile,and the remainder by passes the liver and is excreted by
the kidney . Under normal conditions,the daily urinary excretion of urobilinogen does
not exceed 4 mg.When the hepatic uptake and excretion of urobilinogen is impaired
(e.g.in hepatocellular disease)or the production of bilirubin is greatly increased
(e.g.with hemolysis),daily urinary urobilinogen excretion may increase
significantly .In contrast,cholestasis or extrahepatic biliary obstruction interferes
which the intestinal phage of bilirubin metabolism and leads to markedly decreased
production and urinary excretion of urobilinogen,measurement of urinary
urobilinogen can thus be a useful tool in distinquishing possible cause of
hyperbilirubinemia .
Renal Excretion of Bilirubin : The urine normally contains no detectable bilirubin
by usual clinical assays. Unconjugated bilirubin ,being tightly bound into albumin,is
not filtered by the renal glomeruli. Because there is no tubular secretory process for
bilirubin,unconjugated bilirubin is not excreted in urine. In contrast ,conjugated
bilirubin is a polar molecule less tightly bound to albumin,and is filtered by the
renal glomeruli and appears in the urine.The presence of bilirubin in the urine is
evidence of conjugated hyperbilirubinemia and can be a useful differentiating point
early in the evaluation of jaundice .
【Classification of Jaundice 】
Hemolytic Jauandice:
1.Overproduction of bilirubin: An increaced amount of hemoglobin released from
senescent or hemolyzed blood cells leads to increased bilirubin production.
Erythrocyte destruction leading to hyperbilirubinemia most commonly results from
intravascular
hemolysis.(e.g.autoimmune
,microangiopathic
,or
hemoglobinopathy_associated),or reabption of a large hematoma . Excess bilirubin
production is reflected in increased serum bilirubin levels of up to 51 to 68
μmol/L (3 to 4 mg/dl),with a predominance of unconjugated bilirubin.
2.Impaired hepatic uptake of bilirubin: The uptake of bilirubin by hepatocytes
requires dissociation of the nonpolar pigment molecule from albumin,transport across
the cell menbrane,and binding to ligandin .In rare cases of drug_induced jaundice and
possibly in some Gilbert's Syndrome ,there may be disruption of this phase of
bilirubin.
3.Impaired glucuronide conjugation : Deficiency in glucuronide transferase
activity can occur as a result of both acquired and genetic defects. In the fetus and
neonatal,glucurononocyl transferas activity is normally low. Although
transiet,together with increased neonatal intestinal absorption of unconjugated
bilirubin,contribute to the development of neonatal jaundice that occurs between the
second and fifth days of life. The significant of inherited deficiencies of
glucucoronosyl transferase depends on the level of residual enzyme activity. Gilbert'
Syndrome
associated
with
mild
decrease
in
activity,produces
mild ,asymptomatic ,unconjugated hyperbilirubinemia. Moderately decreased activity
occurs in Crigger_Najjar Syndrome typeII,this enzyme is totally absent in
Crigger_Najjar Syndrom typeI,an autosomal recessive disorder associated with
38
kernicterus and childhood mortality from central nervous system dysfunction.
Acquired defects in glucuronosyl transferase activity may be induced by drugs
(i.e.direct enzyme inhibition),or be associated with liver disease generally.
Jaundice with prodominantly conjugated bilirubiemia:
I. Obstructive Jaundice:
Pathogenesis: 1.it is due to intra_and_extrahepatic Obstruction of bile ducts.
2.Intrahepatic Jaundice: Hepatitis,PBS,Drugs.
3.Extrahepatic
Biliary
obstruction:
stones,stricture
inflammation,tumors(Ampulla of vater)
Symptoms: Pruritis;
Jaundice may vary in intensity;
Chill+fever+gall bladder enlargement;
Stone +cholangitis.
Lab findings: Serum bilirubin↑,
Fecal urobilinogen↓(incomplete obstruction)
Urobilinogen absence (complete obstruction)
Urobilinogenuria is absent in complete obstructive Jaundice
Bilirubiriuria↑
Serum ALP↑
Serum Cholesterol
II.Hepatic Jaundice
Pathogenesis: due to a disease effective hepatic tissue either congenital
or acquired diffuse hepatocellular injury.
1. In paired or absent hepatic conjugation of bilirubin.
△ decreased GT activity (Gilbert's syndrom)
△ hereditary
absence
or
deficiency
of
UDPGT(Grigler_Najjar Syndrom)
2. Familiar or hereditary disorders
△ Dubin_Johson Syndrom
△ Rotor Syndrom
3. Acquired disorders
△ hepatocellular necrosis
△ Intrahepati cholestasis (Hepatitis,Cirrhosis,
Drug_related)
Symptoms: weakness, loss appetite, hepatomegaly palmar erythema, Spider
Lab findings: 1.liver function tests are abnormal
2.both CB and UCB↑
3.bilirubinuria
【Diagnosis procedure 】:
1. History
2. Physical examination
3. Familia occurrence of jaundice
4. Duodenal biliary drainage
5. Imagine techniques: Ultrasonography,CT,Pandaendoscopy ERCP,PTC,X_ray(GI
series,Angiography) etc.
【Differential diagnosis 】:
1. Once jaundice is recognized,it is important to determine whether
Hyperbilirubinemia is predominantly CB or UCB?
39
2. Diferentiation of hemolitic from other types of jaundice is usually not difficult.
3. The laboratory findings are inconstant in partial biliary obstruction and
differentiation from intrahepatic cholestasis is particularly difficult.
40
41
Chapter 14
Vertigo
Vertigo implies the illusory sensation of turning or spinning-either of the patient
himself or his environment.Dizziness is less easily defined as lighthead. Although
vertigo may be distinguished from dizziness by demanding that unmistakable whirling
or turning be present, these two symptoms often are clinically indistinguishable and
may be approached as one entity. Conditions that involve vestibular funtion can be
separated into peripheral ( otological vertigo) and central subgroups. Patients with
these syndromes present clinically with a combination of vertigo and ataxia.
Practically, there are far more cases of otological vertigo than central vertigo, and for
the reason in clinical practice, a detailed understanding of otological vertigo is
essential.
[ Etiology and clinical manifestation ]
1. Periphral Vertigo ( otological vertigo)
(1) Benign Paroxysmal Positional Vertigo: Benign Paroxysmal Positional Vertigo
(BPPV) is the cause of half of all cases of otological vertigo; it accounts for
about 20% of all patients with vertigo. BPPV is diagnosed by the history of
positional vertigo with a typical nystagmus pattern ( a burst of upbeating/
torsional nystagmus) on positional testing. Symptoms are precipitated by
movement or a poison change of the head or body. Getting out of bed or
rolling over in bed are the most common” problem” motions.
(2) Vestibular neuritis : Vestibular neuritis is a self-limited otological condition.
Patients present with vertigo, nausea, ataxia, and nystagmus. Mossst cases of
vestibular neuritis are monophasic . Hearing is not impaired, and when there
are similar symptoms with abnormal hearing, the symdrome is termed
labyrinthitis. A strong nystagmus is seen acutely. Vestibular neuritis is thought
to be caused by viral infections involveing the vestibular portion of the eight
nerve. It usually happens with fever or after the infection of upper respiratory
tract. In vestibular neuritis, severe distress associated with constant vertigo,
nause, and malaise usually lasts 1 to 3 day, and less intense symptoms
ordinarily persist for 2 weeks. Roughly 10% of patients may take as long as
2 months for the condition to improve substantially.
(3) Meniere’s Disease: Classic meniere’s disease presents as a quadrad of
paroxysmal symptoms, including tinnitus, nausea and vomitting, fluctuating
hearing, and episodic vertigo and nystagmus..
(4) Cerebellopontine Angle Syndrome: Acoustic neuromas and other tumors such
as menigiomas, which can appear at the cerebellopontine angle, usually
display asymmetrical sensorineural hearing loss, usually, patients in the fifth
or greater decade present with mild vertigo or ataxia, accompanied by a
significant asymmetrical hearing loss.
2. Central Vertigo
In neurological practice, central vertigo typically makes up only 25% of diagnosis of
patients
presenting with vertigo, because otololgical vertigo and vertigo of unknown cause are
much more frequent. Stroke and TIAs account for one third of cause of central vertigo.
Vertigo attributed to vertebrobasilar migraine accounts for another 15% cases. A large
number of individual miscellaneous neurological disorders such as seizures, multiple
sclerosis, and the Arnold-Chiari malformation make up the reminder
42
(1) Stroke and TIA
Cerebellum
AICA distribution
PICA distribution
(2) Vertebrobasilar migraine
Adult form
Childhood variant ( benign paroxysmal vertigo of childhood
(3) Others
Seizure ( temploral lobe)
Multiple Sclerosis, post-infectious demyelination
Arnold-Chiari malformation
Tumors of eight nerve, brain stem or cerebellum
Paraneoplastic cerebellar degeneration
Wernick’s syndrome
[Accompanying symptoms]
Ask about symptoms specific to brain stem, such as diplopia, dysarthria, and ataxia.
Tinnitus may localize the problem to the inner ear. If there is posterior neck or head
pain, consider vertebral dissection and stroke.
43
Chapter 15
Tic and Seizures
Tics are patterned sequences of coordinated movements that appear suddenly and
intermittently. The movements are occasionally simple and resemble a myoclonic jerk,
but they are usually complex, ranging from head shaking, eye blinking, sniffing, and
shoulder shrugging to complex facial distortions, arm waving, touching parts of the
body, jumping movements, or making obscene gestures. Most often, tics are rapid and
brief, but occasionally they can be sustained motor contractions.
One feature of tics is the compelling need felt by the patient to make the motor or
phonic tic, with the result that the tic movement brings relief from unpleasant
sensations that develop in the involved body part. Tics can be voluntarily controlled
for brief intervals, but such a conscious effort is usually followed by more intense and
frequent contractions.
A seizure is a transient disturbance of cerebral function caused by an abnormal
neuronal discharge.
[Etiology]
1. Cerebral Disease
(1) Infection: Encephalitis or encephalitis caused by bacterial, fungal, or
parasitic infections can cause serzures.
(2) Trauma: Head trauma is a common cause, particularly when it occurs
perinatally or is associated with a depressed skull fracture or intracerebral
or subdural hematoma.
(3) Tumor: Both primary and metastatic brain tumor can be the cause.
(4) Vascular Disease: Cerebral hemorrhage, spontaneous subarachnoid
hemorrhage, hypertensive encephalopathy, global cerebral ischemia, etc.
2. Systemic Disease:
(1) Infection:
(2) Electrolyte Disorders: Hyponatremia and hypocalcemia can cause seizures.
(3) Hypoglycemia can produce seizures, especially with serum glucose levels
of 20-30 mg/dL.
(4) Uremia can cause seizures, especially when it develops rapidly.
(5) Hyperthermia can result from infection, heat stroke, and hypothalamic
lesions.
[Mechanism]
It’s mechanism is still not clear. Very probably it is related to abnormal discharge of
neuron.
[Clinical Features]
Tics can be classified into 4 groups depending on whether they are simple, or multiple
and transient or chronic.
1. Transient simple tics are very common in children, usually terminate
spontaneously within 1 year.
2. Chronic simple tics can develop at any age but often begin in childhood.
Treatment is unnecessary in most cases.
44
3. Persistent simple or multiple tics of childhood or adolescence usually begin
before
age 15.
4. There is a specific syndrome called Chronic Multiple Motor and Vocal Tics.
Seizures can be classified as Generalized Seizures and Partial Seizures.
Tonic-Clonic (Grand Mal) and Absence (Petit Mal) are the most two regular types of
generalized seizure. While Simple Partial, Complex Partial and Partial Seizure with
secondary generalization are the most types of partial seizure.
[History Taking]
At what age did the tic or seizure first occurred, its clinical course, and its
predisposing factors are all important. The tonic is generalized or partial. It is tonic or
clonic. What is the conscious level during the attack?
A thorough neurological and systemic examination is important.
45
Chapter 16
Disturbances of the Level of Consciousness
Abnormalities of the level of consciousness are characterized by impaired
arousal or wakefulness, and they result from lesions of the ascending reticular
activating system or both cerebral hemispheres.
[Causes]
1. Brain Lesions:
(1) Supra-tentorial or infra-tentorial Subdural Hematoma: It is a consequence of
trauma. Chronic subdural hematoma is more common in older patients. Sometimes
the trauma is so slight, that the patient even has forgotten it.
(2) Epidural Hematoma: Epidural hematoma typically results from head trauma
associated with a lateral skull fracture and tearing of the middle meningeal artery
and vein.
(3) Cerebral Contusion: Cerebral contusion caused by head trauma is associated
with initial unconsciousness from which the patient recovers. Edema surrounding
the contusion may cause the level of consciousness to fluctuate, and focal
neurological signs may develop.
(4) Intracerebral Hemorrhage: It can be a consequence of cerebral contusion or a
result of chronic hypertension.
(5) Brain Abscess: Blood-borne metastasis from distant systemic infection, direct
extension from parameningeal sites, infection associated with recent or remote head
trauma or craniotomy, and infection associated with cyanotic congenital heart
disease may all cause brain abscess.
(6) Cerebral Infarction: Cerebral edema following massive hemispheric infarction
can produce contralateral hemispheric compression or transtentorial herniation that
will result in coma.
(7) Pontine Hemorrhage: The apoplectic onset of coma is the hallmark of this
disease.
(8) Cerebellar Hemorrhage or Infarction: The clinical presentation of cerebellar
hemorrhage or infarction ranges from sudden onset of coma, with rapid evolution to
death, to a progressive syndrome developing over hours or even days.
(9) Brain Tumor: Usually coma occurs late in the clinical course of primary or
metastatic tumors of the central nervous system. If there is hemorrhage into the
tumor, the patient’s conscious level may deteriorate suddenly.
2. Diffuse Encephalopathies
(1) Meningitis and Encepahlitis: Meningitis and encephalitis may be manifested by
an acute confusional state or coma, which is associated with fever and headache.
(2) Spontaneous Subarachnoid Hemorrhage: In spontaneous subarachnoid
hemorrhage, symptoms are sudden in onset and include very severe headache.
Consciousness is frequently lost at onset.
3. Systemic Disease:
(1) Hypoglycemia: In most cases, hypoglycemic encephalopathy is insulin
overdose.
(2) Global Cerebral Ischemia: Global cerebral ischemia produces encephalopathy
46
which culminates in coma; it most often occurs following cardiac arrest.
(3) Drug Intoxication: Sedative-hypnotic drug overdose may cause coma. Coma is
preceded by a period of intoxication marked by prominent nystagmus in all
directions of gaze, dysarthria and ataxia.
(4) Hepatic Encephalopathy: In patients with sever liver disease, hepatic
encephalopathy can lead to coma.
(5) Electrolyte disorders: When serum sodium levels fall below 120 meq/L, the
patient’s conscious level will be impaired.
(6) Hypothermia and Hyperthermia: When the temperature is below 26 degrees
centigrade, or
above 42 degrees centigrade, the patient is comatose.
[Mechanism]
Consciousness, the awareness of self and environment, requires both arousal and
mental
content; the anatomic substrate includes both reticular activating system and cerebral
cortex.
[Clinical Features]
The level of consciousness is described in terms of the patient’s apparent state of
wakefulness and response to stimuli.
Mild impairment of consciousness may be manifested by sleepiness from which the
patient is
easily aroused when spoken to. As consciousness is further impaired, the intensity of
stimulation required for arousal increases, the duration of arousal declines, and the
responses elicited become less purposeful.
The most severe degree of depressed consciousness is coma, in which the patient is
unresponsive and unarousable. Less severe depression of consciousness results in an
acute confusional state, or delirium, in which the patient responds to at least some
stimuli in a purposeful manner but is sleepy, disoriented, and inattentive.
In patients with impaired conscious level, abnormalities during physical
examination may suggest the underlying cause.
Papilledema suggests increased intracranial pressure. An intracranial mass should
be considered.
Pupillary constriction suggests opiate ingestion.
Dilated pupils suggest anticholinergic intoxication.
Small, irregular pupils that react poorly to light---but better to
accommodation---can be seen in neurosyphilis.
Systemic signs of liver disease and tremor may suggest hepatocerebral
degeneration.
Abnormally high blood pressure may suggest hemorrhagic stroke.
Tachycardia, sweating, and papillary dilation are early signs of hypoglycemia.
Fever, neck stiffness and signs of systemic or parameningeal infection, such as
otitis suggest meningitis or encephalitis.
Neck stiffness is also seen in spontaneous subarachnoid hemorrhage patient.
[History Taking]
47
1. How is the consciousness impairment occurred and progressed.
2. To see whether there are concomitant signs, such as fever, vomiting, change
in blood pressure, etc.
3. Past History: Diabetes Mellitus, Chronic Hepatitis, etc.
[Case]
A 57 yrs old woman experienced excruciating headache when she was rest at home
and she lost her consciousness very soon.
After she was transferred to the hospital, a physical examination revealed neck
stiffness. And a CT scan revealed acute subarachnoid hemorrhage. And later,
angiography revealed the hemorrhage was caused by a ruptured intra-cranial
aneurysm.
So when this aneurysm is ruptured, it cause severe subarachnoid hemorrhage.
And this was the reason why the patient lost the consciousness and the neck was so
stiff.
48
Chapter 17
Hematuria
1. Definition
Hematuria is defined as more than three red blood cells per high-power field in a
centrifuged specimen of urine. It may be gross or microscopic, according to the
amount of red blood cells in the urine.
2. Etiology
(1) Diseases of the urinary system：which is the most common cause. For example,
glomerulonephritis, neoplasm, stone, tuberculosis, trauma, etc.
(2) System disorders：
a. Hematological disorders：ITP, aplastic anemia
b. Infection：infective endocarditis, septicemia
c. Connective tissue diseases：SLE, polyarteritis nodosa
d. Cardiovascular disorders：hypertensive nephropathy, chronic heart failure
e. Endocrine and metabolism diseases：gout, diabetes mellitus
(3) Diseases of adjacent organs to urinary tract：prostatitis, appendicitis, etc.
(4) Drug and chemical agents：sulfanilamides, anticoagulant, etc.
(5) Miscellaneous：exercise, “idiopathic” hematuria
3. Clinical Feature
The colour of the hematuria depends on the amount of red blood cells in the urine
and the PH. When the urine is acidic, the colour may be more darker than it is
alkalized. A single urinalysis with hematuria is common and can result from
menstruation, drug, porphyrin, etc. Hematuria must be differentiated from
hemoglobinuria, the latter is caused by hemolysis, soy-like, and has very few red
blood cell under the microscope. It is very important to identify the origin of the
hematuria . Gross hematuria with blood clots is almost never indicative of glomerular
bleeding but rather suggests a postrenal source. Collecting the three stage of urine of a
patient during micturition, if the initial specimen contains red blood cell, the origin
may be urethra. If bleeding occurs mainly at the end of micturition, the bladder neck
and triangular area or posturethra should be examined carefully. Total hematuria,
which occurs throughout voiding, means that blood comes from the upper urinary
tract or bladder. To evaluate the red blood cell is glomerular origin or not needs to
make a phase-contrast microscopy examination. Due to press and PH, osmolarity
changes in the distal tubule, the red blood cells of glomerular origin are often
dysmorphic.
4. Approach to the Patient
49
HEMATURIA
proteinuria(>500mg/24h)
dysmorphic RBCs or RBC casts
(-)
(+)
(+)
pyuria, WBC casts
urine culture
urine eosinophils
(-)
hemoglobin electrophoresis
urine cytology
UA of family numbers
24h urinary calcium/uric acid
(-)
IVP +/- renal
ultrasound
(+)
(-)
as indicated:
retrograde
pyelography or
arteriogram,
or cyst aspiration
serologic and
hematologic
evaluation: blood
culture, anti-GBM
antibody, ANCA
complement level
cryoglobulin,
hepatitis B and C
serology, VDRL
HIV, ASLO
renal biopsy
(+)
cystoscopy
biopsy and
evaluation
(-)
(+)
renal CT scan
(-)
open renal biopsy
follow periodic
urinalysis
RBC, red blood cell; WBC, white blood cell; GBM, glomerular basement membrane
ANCA,antineutrophil cytoplasmic antibody; VDRL, venereal disease research laboraTory; HIV,human immunodeficiency virus; ASLO,antistreptolysin O; UA,urinalysis;
IVP, intravenous pyelography; CT,computed tomography.
(Adapted from Harrison’s Principles of Internal Medicine, 14th edition)
50
Chapter 18
Incontinence of Urine
1. Definition
Incontinence, the inability to retain urine in the bladder, result from neurologic or
mechanical disorders of the system that control normal micturition. Loss of urine
through channels other than the urethra(ectopic ureter, fistulae) and severe tubercular
cystitis(contracture of bladder) are rare but cause total or continuous incontinence.
2. Etiology and Clinical Appearances
(1) True incontinence：In this condition, the sphincter of the bladder and urethra
becomes prone to uncontrolled because normal neural pathways are damaged. It
often arises from diseases of the central nervous system such as cerebrovascular
accidents, Alzheimer’s disease, neoplasm, etc.
(2) Overflow or paradoxical incontinence ：This form of incontinence arises from
large residual volumes of urine secondary to obstruction at the bladder neck or the
urethra(urethral stricture). Benign prostatic hyperplasia afflicts upward of 75
percent of old man.
(3) Stress incontinence：This condition is common in postmenopausal parous woman.
Parturition may damage the pelvic support of the bladder so that the bladder and
urethra can slip downward from their normal position above the pelvic diaphragm.
As they do, the urethra shortens, and the normal urethrovesical angle, important in
closing the urethral sphincter, is lost. Many women become unable to resist the
passage of urine under the stress of increased intra-abdominal pressure during
coughing, sneezing, climbing strains and other physical activity, so small amount
of urine escape.
(4) Urge continence：It is an involuntary loss of urine associated with a strong desire
to void. Bacterial cystitis or bladder cancer, bladder outlet obstruction and
neurogenic bladder must be excluded.
3. Approach to the Patient
The history should define the onset, duration, evolution and triggering events of
leakage. Severity of incontinence is denoted by recording the type and number of pads
used per day and how the incontinence affects daily activities. The amount and type of
fluid consumed, sexual history(hormonal status, deliveries, venereal diseases),
gastrointestinal function(fecal incontinence, constipation), and past urologic
history(bed-wetting, surgeries) must also be documented. The physical examination
should place special emphasis on the abdominal, genital, pelvic and neurologic
system. Stress incontinence must be demonstrated by asking the patient to cough,
strain , or even stand or squat. More complex testing is needed to determine whether
the urethral anatomy is normal(evaluation of urethral mobility, lateral view of the
urethra on the voiding cystourethrogram, cystoscopy), whether urethral function is
normal with adequate closure(leak point pressure, urethral profilometry,
videourodynamics) or whether bladder function is normal(bladder volume based on
home diary, filling cystometrogram).
51
Chapter 19
Urinary Frequency, Urgency and Dysuria
1. Definition
Urinary frequency means voiding at frequent intervals, due to a sense of bladder
fullness. Urgency is an exaggerated sense of needing to urinate, due to an irritable or
inflamed bladder. Dysuria refers to pain or a burning sensation during micturition.
2. Etiology and Clinical Appearances
(1) Frequency
i. micturition increased but the volume each time is normal
such as diabetes mellitus, diabetes insipidus, polyuria period of acute renal failure
ii.micturition increased and the volume each time is decreased
a. bladder and urethral irritation：inflammation, tuberculosis, stone
b. diminished capacity of bladder ： neoplasm, contracture of the bladder,
pregnant uterus
c. obstruction of the lower urinary tract：for example, prostatic hyperplasia, often
seen in man after age 40 accompanied by force of the urinary stream, hesitancy in
initiating voiding , postvoiding dribbling and the sensation of incomplete
emptying.
d. neurogenic bladder：history of neurologic disease
e. psychogenic cause：nervous, worry, dread
(2) Urgency：acute cystitis, urethritis, prostatitis, stone, bladder cancer, neurogenic
bladder, etc. Urgency is commonly associated with frequency and dysuria.
(3) Dysuria：urethritis, cystitis, prostatitis, bladder tuberculosis, stone, foreign body,
end-stage bladder cancer, etc. Dysuria occurs at the beginning of micturition in
urethritis. Cystitis can aggravate the pain at the end of micturition, and is often
accompanied by fever and pyuria. Prostatitis in men can also cause discomfort in
the lower abdomen, groin, perineum, rectum, testes, or penis. If patient is
concomitant with evidence of TB infection and hematuria, it is necessary to
consider bladder tuberculosis.
3. Approach to the Patient
The history should focus on past as well as present urinary problems. A pelvic
examination in woman and prostatic examination in men are necessary components of
the physical examination. Urinalysis in all patients , leukorrhea in women and the
prostatic fluid in men obtained by prostatic massage, should be examined by
microscopy. Prostatic fluid is an important clue to prostatitis and may, when prostatitis
is chronic, be the only detectable abnormality. Additional evaluation, when the cause
is not evident, may include cultures of urine and prostatic fluid for aerobic and
anaerobic bacteria, tubercle bacilli, and mycoplasmas; ultrasound, excretory
urography, and voiding cystourethrography. If these examinations do not reveal the
diagnosis but syndromes are troublesome, urologic evaluations, including cystoscopy,
urethroscopy, endoscopic biopsy and dynamic urinary tract studies may be useful.
52
Chapter 20
Retention of Urine
1. Definition
A variety of lesions can lead to interference with the normal ability to empty the
bladder and to retain large amount of urine in the bladder, which is referred to the
retention of urine. Overflow or paradoxical incontinence can occur with prolonged
overdistention of the bladder. Retention of urine requires to be relieved as soon as
possible to prevent progressive renal damage.
2. Etiology and Clinical Appearances
(1) Acute retention of urine
A. mechanical obstruction
caused by obstruction at the bladder neck or the urethra, such as prostatic
hyperplasia, urethral injury and stricture, stone, neoplasm, foreign body, pelvic
mass, etc.
B. dynamic obstruction
caused by the dysfunction of micturition without obstruction of the urinary tract,
such as anesthesia, neurologic disorders, excessive smooth muscle relaxation from
drugs(anticholinergic medications), etc.
C. miscellaneous
hypokalemia, fever, coma, stay in bed, etc.
(2) Chronic retention of urine
It develops slowly , also produces a dilated and palpable bladder, but the patients
feel less painful, such as benign prostatic hyperplasia, prostatic carcinoma and
bladder cancer.
3. Approach to the Patient
A history of difficulty in voiding, pain, hematuria, operation, drug or coma is very
important. Evaluation for distention of bladder often can be obtained by palpation and
percussion of the abdomen. A careful rectal examination may reveal enlargement or
nodularity of the prostate, abnormal rectal sphincter tone, or a rectal or pelvic mass. In
the female, vaginal, uterine, and rectal lesions responsible for urinary tract obstruction
are usually revealed by inspection and palpation. The nervous system examination
should also be done if necessary. Laboratory testing needs the electrolyte analysis to
exclude hypokalemia. If retention has been a long duration, abdominal ultrasound
should be performed to evaluate bladder and ureter size, as well as pyelocalyceal
contour. If urinary tract obstruction is suspected, intravenous pyelography, cystoscopy,
urethrography, or computed tomography are indicated until the site of obstruction is
determined.
53
Part II
Inquisition
Chapter 1
Importance of inquisition (asking histtory)
1. Inquisition is an important part of diagnostic procedure through the conversation
between the patient and doctor.
2. It is useful to understand the actual history of an illness, no other diagnostic
technology can take its place.
3. For an experienced physician with profound knowledge, diagnosis or impression
can be made simply by inquisition. As the diseased organ would give some clue by
its pathophysiological changes.
4. An inaccurate or rough history would lead you to make a wrong diagnosis.
Method of inquisition
1. Physician should be patient and kind to the patient and treat him as one of his/her
family member. The atmosphere should be invariably benevolent. Therefore, the
patient can trust him/her.
2. Inquisition usually begin with the patient’s chief complain. It is approached
gradually and systematically.
3. Ask questions in the most direct and simple language. After the patient has related
in his own way the story of his illness, it will be necessary to ask more specific
questions to elicit further information or to clarify the exact nature of his
complaints.
4. Never force the patient to related symptoms, which is difficult to answer. Ask some
easy questions first, such as “how is your feeling when the illness starts? ”. And
then, add some questions such as “ anything happened before the illness? ”.
5. Hints to the patient such as “did you vomit during headache” are avoided. Instead,
just ask “ anything happened during your headache?”. Questions should be
objective.
6. The following aspects should be noted:
(1). For a critical case, the inquiry should be short and emergency treatment
started as early as possible.
(2). Words used during inquiry should be understood by the patient. Try not to use
medical terms such as occult bleeding, tonesmus, opistaxis.
(3). History should be taken from the patient himself, from his relatives or friends
only when patient is in critical status and/or unable to talk.
54
Chapter 2
Contents of inquisition
1. General data: such as name, sex, age，native, birth place, profession, marital
status, source of history and estimate of reliability etc.
2. Chief complaints: It should constitute in a few simple words the main reasons
why the patient consulted his physician, which usually includes symptoms or sign
the patient is suffering.
3. History of present illness: It should be a well-organized, sequentially developed
elaboration of patient’s chief complaint or complaints. A good history will reflect
the facts that your diagnosis or impression is going to be made.
It includes the following aspects:
(1). Onset and duration of the disease.
(2). Main symptoms, location and their character.
(3). Etiology and provoking factors.
(4). Evolution of disease
(5). Associated symptoms.
(6). Treatment and its effects.
(7). General condition, especially the dietary habit.
4. Past history:
Health condition and disease which the patient suffered before
the present illness. Infectious disease, surgery, allergy are essential part of the
case history.
5. Systems review:
The purpose of this review is twofold:
(1): A thorough evaluation of the past and present status of each body system.
(2): A double check to prevent omission of significant data relative to the
present illness.
6. Personal history:
It includes those relating to smoking and alcoholic
beverages (duration and amount), sedatives, social history, profession and
working condition.
7.
Marital history: This review includes data concerning the health of the
mate, the number of children and their physical status.
8. Menstrual history
9. Childbearing history
10.
Family history: Inquire the disease of patient’s first relative which might
be hereditary, such as heart disease, hypertension, diabetes etc.
55
Chapter 3
History Writting
History writing is the most important part of diagnosis of a disease. It is the
systematic record of the onset, progression, diagnosis and treatment of disease. It
includes symptoms, signs, laboratory, instrumental studies, impression of the disease,
changes of the clinical manifestations, response to the treatment and prognosis. Not
only it is the true record of the state of an illness, but also it reflects the quality of
medical treatment and scientific level. A doctor should always write a good history
through his incessant study of medicine.
Basic requirement
1． The content of history should be genuine.
2． The history should be written according to the form described in the textbook.
3． The description of the history should be refine. The words used should be
appropriate.
4． The history should be written in a systemic, complete and clear way.
Forms and contents of the history
1. Outpatient history： Brief, main points of disease, including main symptoms and
signs, laboratory tests, initial diagnosis and treatment.
Emergency and critical patients: Their history should be further recorded with
BP, Temp, mental status, methods, processes and precise time of the treatment.
2. Admission history:
Two types of admission history: complete history and admission note.
1). Complete history: written by intern and/or junior resident
2). Admission note: written by senior resident
3). Progressive note: It is very important. For severe patient, it should be
written according to the progression of the disease at any time of the day. For mild
patient, it may be written every 2~3 days. It includes the following:
a: Change of main symptoms and signs
b: Lab findings --- analysis of the result.
c: Noninvasive and invasive findings.
d: Reason of treatment.
e: diagnosis and plain of treatment
f: Patient’s and his/her relative’s idea and suggestion.
The first progressive note should be written at the same day of patient’s
admission.
4). Consultation note.
5). Transfer note.
6). Preoperative, operative and postoperative notes
7). Discharge note.
8). Death note.
9). Readmission note. A:
Past history and history detailed after last
discharge
56
B:
Previous history should be put in the chart
General steps in history writing
1. An accurate and comprehensive description of patient’s complaint.
2. List the possible diagnosis from the description.
3. Ask the questions to patient which are designed to confirm or exclude the
tentative diagnosis.
4. A thorough physical examination.
5. Reassemble the history and findings into a well organized record according to
the principles mentioned above.
Example
Name: Guo Yi
Sex: male
Age: 20 years old
Nationality: Han
Birthplace : Shanghai
Marital status: Unmarried
Medical history
Occupation: student
Address: No 852,Beijin Road, Shanghai
Time admission: 5PM Feb 14 2003
Time recording: 5PM Feb 14 2003
Reliability: Reliable
History offer :Himself
Chief complaint :
Epigastric pain and melena for two days
Present illness :
The patient presents with an 8-year history of duodenal ulcer. Two days ago he felt
abdominal pain, the pain was located in the epigastric area and was burning in quality.
The pain occurred on an empty stomach 2 to 4 hours after meals and/or at night, was
relieved by antacids and accompanied with the symptoms of epigastric fullness,
belching, bloating and early satiety. After the pain he emptied the bowels
characterized by dark black, liquid, tarry, metallic-smelling stool, it was about 5oo ml,
2-3 times per day. The patient also reported vomiting 50 ml “coffee grounds” material
once. After then he felt palpitation, cold sweating and dizzy, and syncoped for 10
minutes. So he was presented to emergency room. Occult blood test +, skull CT scan
(-) , emergency endoscopy showed duodenal ulcer (A1stage), blood routine: WBC
11*109, GN 75% ,Hgb 9.5g/l ,hematocrit value 29%.He was then admitted to the
hospital for evaluation and treatment.
He denied having taken Non-steroidal Anti-inflammatory drugs before
hemorrhage.
Past history :
prior major illnesses and injuries : The patient has a 3-year history of Hypertension.
he denied the history of Diabetes Mellitus.
prior operations :No prior operations
prior hospitalizations : No prior hospitalizations
allergies : No food, medications, chemicals allergy.
57
age appropriate immunization status : Unknown
Social history :
marital status : Unmarried
current employment : student
use of drugs : No medications were daily used
use of alcohol : No drinking
use of tobacco : No smoking
level of education : Middle school
sexual history : Denied perverted sexual history
Family history :
Health status or cause of death of parents, siblings, and children : All are healthy
Specific diseases related to problems identified in the chief complaint or history of the
present illness and/or system review : None
Diseases of family members which may be hereditary or place the patient at risk : No
hereditary diseases
Review of systems :
Respiratory system : Denied dyspnea, hemoptysis, asthma, bronchitis, orthopnea,
emphysema.
Cardiacvascular system : Denied dyspnea ,paroxysmal nocturnal dyspnea, orthopnea,
edema ,but chest pain, palpitations
Gastrointestinal system : Denied rectal bleeding, vomiting blood, black tarry stools,
abdominal pain,jaundice, hepatitis, diarrhea, change in bowel
habits, constipation.
Urinary system : Denied polyuria, dysuria, hematuria, incontinence, urinary infections,
stones.
Hematologic system : Denied anemia, easy bruising or bleeding.
Endocrine system : Denied thyroid trouble, heat or cold intolerance,excessive
sweating,diabetes;excessive thirst,hunger or urination.
Musculoskeletal system : Denied joint pains or stifness,srthritis, gout, backpain.
Denied muscle pains and cramps.
Neurological system : Denied seizures,paralysis,local weakness, numbness, tremors,
memory problems
Physical examination
Vital signs :
T:36.3℃; P:72/min ; R:18/min ; BP:140/80mmHg
General appearance:
Well developed and nourished male, pleasant and cooperative.
Skin and Mucosa:
No edema, jaundice. No rashes , ecchymoses present, no ticks noted. Slight anemia
countenance.
58
Lymph Node:
No pathological enlargement of superfical lymph nodes.
Head:
Eyes: Conjunctiva is pale, no other obvious abnormity
Ears: No obvious abnormity
Nose: No obvious abnormity
Neck:
soft, no venous engorgement. thyroid glands not palpable, and no thrill or brunt.
trachea in midline.
Respiratory:
symmetrical chest and respiratory movements. no abnormal dullness , rales or rhonchi
heard.
Cardiovascular :
maximal impulse (PMI) not visible but palpable in the 5thcostal interspace, 8cm form
the middle line, no thrill. the cardiac dullness as follows:
Right （cm）
Interspaces
Left (cm)
2.0
Ⅱ
2.0
2.0
Ⅲ
4.0
3.0
Ⅳ
6.0
Ⅴ
8.0
midsternal line to midclavicular line 8.5cm
heart rate 72/min, regular. No obvious heart murmur, no pericardium friction
sound.
Peripheral vascular:Pulses intact in all extremities. No irregular pulse.
Abdomen: Soft, Liver, spleen not palpable, no shifting dullness, tenderness in
epigastric arer without rebound tenderness, Bowel sounds active 10-12/min,
Genitoreproductive:Normal.
Extremities: No cyanosis, clubbing, or edema.
Neurological/mental: Kerning sign negative, Brudzinski sign negative.
Motor: No obvious abnormity
Sensory: No obvious abnormity
Reflex: Biceps reflex normal, triceps reflex normal, knee jerk normal, Babinski’s sign
59
not present .
Laboratory data
Occult blood test +
skull CT scan (-)
emergency endoscopy showed duodenal ulcer (A1stage)
blood routine: WBC 11*109, GN 75% ,Hgb 9.5g/l ,hematocrit value 29%
.Diagnosis
Duodenal ulcer accompanied by hemarrhage
Differential diagnosis
1. Acute erosive gastritis :The patient has not a history of stress and denies taking the
Non-steroidal Anti-inflammatory drugs before hemorrhage, emergency endoscopy
does not find the erosive lesions. So we can exclude it.
2. Rupture of oesophago- gastric varices: The patient has not a history of liver
disease, no sign, symptom and lab experiment indicate liver cirrhosis. All
evidence do not support the diease.
3. Gastric tumor: It always occurs in elder people, makes the patients in bad
condition. Occult blood test persistent positive, antacids usually can not relieve
the symptom. Endoscopy and GI may help the diagnosis.
60
Part III
Physical Examination
Chapter 1 Basic methods of Examination
A systematic approach to the bedside examination of a patient is essential to
determine the significance of an abnormal physical finding. It includes five basic
methods-namely, inspection, palpation, percussion, auscultation, and olfactory
examination.
Inspection
Inspection is seeking physical signs by observing the patient. Of the several
methods of examination inspection is the least mechanical the hardest to learn, but it
yields most physical signs. More diagnoses are probably made by inspection than by
all other methods combined. The method is the most difficult to learn because no
systematic approach can encompass the variety of signs. More than any other method,
inspection depends entirely upon the knowledge of the observer; we tend to see things
that have meaning for us.
The layman looks at a person and concludes that there is something “peculiar”
about him; the physician gives a glance and diagnoses acromegaly. From his study of
disease, he can dissect the “peculiarity” and recognize the diagnostic components,
such as the enlarged supraorbital ridges, the widely spaced teeth the macroglassia, the
buffalo hump, the huge hands and feet. Practice is required to learn inspection.
1. General inspection. The initial act of physical examination is the inspection of
the body as a whole. Most clinicians believe that composite pictures of disease,
although composed of many sighs, strike them at a glance; they attempt to teach
others perceive likewise.
In looking at the patient as a whole, many facts are noted methods in physical
examination/inspection.
General inspection about motor activity, body builds, outstanding anatomic
malformation, behavior, speech, nutrition, and appearance of illness.
2. Local inspection. Focusing observation on a single anatomic region yields
hundreds of physical signs. Since only signs perceived by inspection can be illustrated,
the myriad of pictures used in books on surgical diagnosis hint the importance of the
method in that field. The dermatologist relies almost entirely on the appearance of
skin lesions to make a diagnosis.
3. Usage more or less confines the term inspection to observation with the
unaided eyes. Actually, visual, visual signs are the chief or only rewards in the use of
the ophthalmoscope, slit lamp, gonioscope, otoscope nasoscope, laryngoscope,
bronchoscope, gastrocope, thoracoscope, peritoneoscope, cystoscope, anoscope, and
sigmoidoscope. The pathologist uses the microscope; the radiologist inspects the
fluoroscopic screen and photographic films.
61
Palpation
The usual definition of palpation is the act of feeling by the sense of touch. But
this is too limited; when the physician lays his lands upon the patient, he perceives
physical signs by his tactile sense, temperature sense, and his kinesthetic sense of
position and vibration. Palpation is widely used in the physical examination especially
in the abdomen examination.
1. Sensitive parts of the Hand: Tactile sense. The tips of the fingers are the most
sensitive for fine tactile discrimination, and temperature sense. Use the dorsa of the
hands or fingers; the skin is much thinner than elsewhere on the hand. Vibratory sense.
Palpate with the palmar aspects of the metacarpophalangeal joints rather than with the
finger tips to perceive vibrations such as thrills or the precordial cardiac thrust. Probe
the superiority for yourself by touching first the fingertip, then the palmar base of
your finger, with a vibrating tuning fork. Sense diagnostic Mode: Symptoms and
signs.
Use the grasping fingers, so you perceive with sensations from your joints and
muscles.
2. Structures Examined by palpation. Palpation is employed on every part of the
body accessible to the examining fingers: all external structures, all structures
accessible through the body orifices, the bones, the joints, the muscles, the tendon
sheaths, the ligaments, the superficial arteries, thrombosed or thickened veins,
superficial nevers, salivary ducts, spermatic cord, solid abdominal viscera, solid
contents of hollow ivccera, accumulations of body fluids, pus, or blood.
3. Quality Elicited by palpation: Texture. The skin and hair, Moisture. The skin
and mucosa. Skin temperature. At various levels of the body. Masses. The size, shape,
consistency, mobility, pulsation (expansile or transmitted) precordial cardiac thrust.
Crepitus. In bones, joints, tendon sheaths, pleura, subcutaneous tissue. Tenderness. In
all accessible tissues. Thrills, over the heart and blood vessels. Vocal fremitus.
4. Special Methods of palpation: Light palpation. Deep palpation. Ballottement.
Fluctuation. Fluid wave.
Percussion
In physical diagnosis, percussion is the method of examination in which the
surface of the body is struck to emit sounds that vary in quality according to the
underlying tissues.
Methods of percussion: Immediate or indirect percussion. In the method the left
middle finger is laid upon the body surface to serve as a pleximeter; it is struck sharp
blow with the tip of the right middle finger, the plexor immediate or direct. The body
surface is struck directly with one or more fingers of a hand.
1. Sonorous percussion. This term is applied to any method of percussion when
its purpose is to ascertain the density of the tissue by the sound emitted when struck.
Various densities emit sounds given special meanings. The percussion notes may be
arranged in sequence according to the density that produces them, from least to most
dense: tympany hyperresonance, resonance, impaired resonance, dullness, flatness.
Certain steps in normal tissues. Tympany is the sound emitted by percussing the
air-filled stomach; resonance is produced by striking the air-filled lungs; flatness
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results from the thigh. In general the pitch or frequency of the sounds progresses
through the series from lowest for tympany to highest for flatness; the duration of the
sound ranges in the series from long to short.
Sonorous percussion is employed to ascertain the density of the lungs, the pleural
space, the pleural layers, and the hollow viscera of the abdomen.
2. Definitive percussion, where two structures in apposition have greatly
contrasting densities, as demonstrated by their percussion notes, mapping of area of
greater density furnishes a concept of the size of the structure or the extent of its
border. Any method of percussion used for this purpose is termed definitive
percussion.
Definitive percussion is commonly employed to ascertain the location of the lung
bases, the width of the lung apices, the height of fluid in the pleural cavity the width
of the mediastimum, the size of the heart, the outline of dense masses in the lungs the
size and shape of the liver and spleen, the size of a distended gallbladder and urinary
bladder, the level of ascitic fluid.
Auscultation
Although auscultation might literally imply the act of hearing to obtain physical
signs, usage restricts it almost solely to hearing through the stethoscope. Rales and
friction rubs. Crepitus can be heard in joints tendon sheaths, muscles, fractured bones,
and in subcutaneous emphysema. The heart makes its various valve sounds with their
splitting, murmurs, rhythm disturbances, pericardial rubs and knocks. Auscultation of
the abdomen reveals bowel sounds, murmurs from aneurysms and stenotic arteries,
especially the renal. The stethoscope is applied to the scrotum to detect bowel sounds
in a scrotal hernia.
As every musician knows, the ear can be trained to recognize sounds more
accurately. Each person learns to recognize the voices of many associates by patterns
of pitch and overtones.
Olfactory examination
In olfactory examination physician makes use of his sense of smell to obtain the
abnormal odors of the patients and identify the signs of diseases.
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Chapter 2
General Inspection
General inspection is a series of accurate and meaningful observations. It
includes a general survey of the patient’s sex, age, mental status, mood, posture, body
movements, gait speech, breath odor, state of nutrition, stature, temperature and skin.
General inspection begins with history taking.
General appearance
Even before the formal physical you will begin making observations that may
alert you to disease. Throughout the history and physical, these cumulative
observations form the basis for logical diagnostic deductions.
As the patient moves into the examining room, you might note the gait. Is it
painful? Is there evident favoring of one side of the body, as in stroke?
A wealth of information can be gained by shaking hands with the patient. Warm,
moist hands may suggest hyperthyroidism.
When the patient speaks, does the tone of his voice suggest the hoarseness of
laryngeal cancer, the weakened, thickened, and lowered voice of hypothyroidism; the
“vocal ataxia” or “scanning speech” of multiple sclerosis or cerebellar disease?
The face has always been the mirror or the mind. It shows pain, fear, anxiety, and
sadness. It is in the face that we first notice whether our patients are pale, ruddy,
cyanotic, or icteric. Thickened features suggest hormonal imbalance-e.g., of the
thyroid or growth hormone. Fullness may be a consequence of edema, obesity, or a
result of excess corticosteroids. A malar flush may signal lupus or mitral stenosis.
Shiny skin and tight features first alert us to possible scleroderma. Cranial nerve
dysfunction may be manifested by ptosis, strabismus, or facial asymmetry.
Habitus refers to your patient’s general shape-his or her body build. Cachexia is
an extreme thinness and debility caused by some serious disease, such as cancer or
chronic infection. Signs of recent weight loss, such as loose clothes, newly punched
belt holes, and redundant skin folds, clue the clinician to a loss of flesh or fat that may
or may not have been noticed by the patient.
Simple obesity is a deposition of body fat in excess of some arbitrary standard.
Pathologic obesity is deposition of body fat to the point of physiologic compromise of
the individual, who may have respiratory, cardiac, or orthopedic difficulty. In these
conditions excess fat is apportioned generally around the body-face, trunk, buttocks,
and extremities. Deposition of fat around the trunk, with thin extremities in which
muscle wasting is evident, may suggest hypercorticosteroidism.
Vital Signs
Because a heartbeat, breathing, and body warmth are the clinical signs of life (the
absence of which signaled death in the era before the advent of modern laboratory
aids such as the electroencephalogram), the so-called vital signs (pulse, respiratory
rate, temperature, and blood pressure) continue to be the most frequently examined of
all physical findings.
Temperature
The temperature is generally taken by placing the thermometer under the patient’s
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tongue for 3 minutes. The temperature may be taken orally or rectally, and in the
United States the Fahrenheit scale is usually used. Falsely low levels may result from
incomplete closure of the mouth, breathing through the mouth, leaving the
thermometer in place for too short a time, or the recent ingestion of cold substances.
Falsely elevated levels may result from inadequate shaking down of the thermometer,
previous ingestion of warm substances, smoking, recent strenuous activity, or even a
very warm bath.
In most persons there is a diurnal (occurring every day) variation in body
temperature of 0.3~1C. The lowest ebb is reached during sleep, at which time the
temperature may fall as low as 35.7~36.1C. As the patient begins to awaken, the
temperature slowly rises.
You will note that the upper limit of normal on the standard thermometer is 37C.
Rectal temperatures are usually 0.3 to 0.5C higher than oral temperatures, but
they tend to be less subject to alteration by the oral factors mentioned above and are
generally more constant and reproducible.
Pulse
The radial pulse is best taken at the base of the patient’s thumb. If the examiner
uses two of three fingers along the course of the artery, he or she may determine the
pulse contour as well as the rate.
Initially, and always if the pulse is irregular, the examiner should count the pulse
for a full 60 seconds. If the pulse rate is between 60 and 100, and the rhythm is
absolutely regular, many physicians will “shortcut” and count the pulse for 30 seconds,
then multiply by two.
If the radial pulse is poor or irregular, the pulse may be taken by listening to or
palpating the apex of the heart (the apical pulse). The normal resting pulse rate ranges
from 60 to 100. It may b in the 50 in a conditioned athlete, or 100 or over in an
excited patient. Rates less than 60 are often referred to as bradycardia, and rates over
100 as tachycardia.
The pulse rate and rhythm should be recorded, and if abnormal contour is
discovered, that too must be noted.
Respirations
Many physicians find it of value to count the respirations while appearing to take
the pulse, since the natural tendency of the patient is to breathe awkwardly under
observation. Normal respiratory rate is between 8 and 14 per minute in adults and is
somewhat more rapid in children.
Note abnormalities of respiratory rate and rhythm. Extremely slow respiration
usually indicates central nervous system respiratory depression due to disease or drugs.
Periodic or Cheyne-Stokes respiration occurs with serious cardiopulmonary or
cerebral disorders. Deep slow breathing (Kussmaul’s respiration) characterizes
acidosis, a state in which the physiologic response to increased metabolic acid in the
blood is a compensatory “blowing off” of carbon dioxide. Extreme tachypnea is
present during many acute illnesses. It may be due to chronic or acute pulmonary or
cardiac disease or systemic disorders, such as shock, severe pain, and acidosis;
although it may represent undue excitement or nervousness, especially when
accompanied with sighing, an organic cause should be excluded.
The patient’s preferred position is important. Can he lie flat comfortable? Patients
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with congestive heart failure prefer the sitting position, as do patients with pulmonary
disease during acute attacks of infection or bronchospasm. Patients with pericarditis
often sit and lean forward.
Blood pressure
The normal adult blood pressure varies over a wide range. The normal systolic
range varies from 95 to 140 mm Hg, generally increasing with age. The normal
diastolic range is from 60 to 90 mm Hg. Pulse pressure is the difference between the
systolic and diastolic pressure. Mean pressure can be approximated by dividing the
pulse pressure by three and adding the value to the diastolic pressure. Routing
measurements should be made with the patient sitting and recumbent.
Skin
The skin has been called the “mirror” of an individual’s health, since diseases of
any organ system is often reflected from it. Inspection is the most important part of
the examination of the skin. Color, shape, skin eruption, muculae, roseolae papulaes
wheals, maculopqpulaes wheals, maculopapulaes spider angioma, petechia, purpura,
ecchymosis, hematoma are noted.
Obviously, skin color varies greatly from person to person and even from area to
area on the same person. If possible by use of photographs or findings from earlier
examinations, the previous skin pigmentation should be ascertained so that the present
coloring can be evaluated more precisely. Usually, an area of increased or decreased
pigmentation in skin that is otherwise normally pigmented signifies some
abnormality-for example, postinflammatory hyperpigmentation or vitiligo.
The normally occurring skin pigments are melanin, hemoglobin, and carotenoids.
Diffuse or localized melanin hyperpigmentation can be seen in such conditions as
Addison’s hypoadrenocorticism, hyperthyroidism, pregnancy, hemochromatosis, and,
most commonly, after exposure to sunlight. Melanin pigment is lacking in albinism
(diffuse) and vitiligo (patchy). Erythema of the skin results from increased amounts of
oxygenated blood in the dermal vasculature, such as might occur with fever or
sunburn. Increases in deoxygenated blood hemoglobin result in a bluish tint to the
skin (cyanosis) in such conditions as congestive heart failure, pneumonia, and
congenital heart disease with right-to-left shunts. Localized red or purple changes
result from vascular neoplasms, birthmarks, and hemorrhage into the skin (petechiae
and ecchymoses). Pallor results if the hemoglobin content of the skin is decreased, as
in anemia or shock.
Changes in the color of the skin may result from the deposition of pigments
normally not found in significant quantities in the skin. Thus, the yellow or even
greenish hue of jaundice results from increases in tissue bilirubin in the skin and
sclerae. Carotenemia also results in yellowing or the skin but, unlike jaundice, the
sclerae are not involved. This pigment change is caused by increased amounts of
carotenoids in the skin and results from myxedema, diabetes, or ingestion of excess
amounts of foods containing these pigments, principally carrots. Carotenemia is
occasionally present during pregnancy. Certain metal salts, such as silver, gold, and
bismuth, when administered over prolonged periods as mediacations, may be
deposited in the skin and cause a greyish discoloration. Foreign bodies such as
carbon-containing particles can also cause localized pigmentation of the skin-for
example, tattoos.
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Generally, palpation of the skin is used to confirm and amplify the findings
observed on inspection. Inspection and palpation are inseparable interrelated and the
examiner often uses them synchronously. Such findings as temperature, moisture,
texture, elasticity, and presence of edema in the skin are detected by palpation.
Although the skin temperature is a poor gauge of the temperature of the inner
body care, it may reflect a maladjustment in the thermoregulatory mechanism of the
body. Thus, if a febrile person’s skin is warm and dry, one knows that sweat
evaporation is not cooling the body and that the patient’s temperature is probably
rising. On the other hand, if the skin is warm and wet, then the sweating is probably
acting to reduce the temperature. Skin temperature depends on the amount of blood
circulating through the dermis. Thus, localized hyperthermia indicates localized
increased blood flow, as noted in localized burn or furuncle. Generalized skin
hyperthermia suggests increased blood flow in the entire integument-for example,
generalized sunburn and hyperthyroidism. Localized reduced blood flow results in
coolness of that area-for example, peripheral arteriosclerosis and Raynaud’s
phenomenon. Generalized cutaneous hypothermia signifies a generalized reduction of
skin blood flow-for example, shock.
Sweating results from autonomic discharge arising from stimulation of either the
central nervous system or the peripheral nervous system. Various combinations of
skin moisture and temperature findings can be evaluated on the basis of the previously
described physiologic principles. Thus, cool wet hands in indicate vasoconstriction
and adrenergic sweating-a combination often resulting from autonomic nervous
system stimulation caused by anxiety.
“Skin texture” refers to the quality and character of its surface. Is it rough and dry
as it may become in hypothyroidism, the postmenopausal state, or “winter itch?” Is it
velvety smooth, as seen in hyperthyroidism?
Loss of elasticity of the skin refers to its inability to return promptly to its normal
position when stretched or pulled. This occurs most commonly in such areas of
chronic actinic damage as the backs of the hands and the face. Increased elasticity of
the skin and joints occurs in the Ehler-Danlos syndrome (cutis hyperelastica). Laxness
or laxity of the skin refers to sagging or looseness of the integument and is seen
following rapid weight loss and in the aged as the result of a lifetime of gravitational
pull on the loose tissues of the face, buttocks, and other areas of the body.
Since the skin is a large depot for body water and electrolytes, much can be
learned about the state of total body hydration by careful palpation. Thus, if the skin is
loose, wrinkled, and lax in areas not previously subjected to chronic sun-damage, this
suggests dehydration of the entire body. On the other hand, excess body water may
also be stored in the skin and may be manifested by pitting edema, wherein firm
pressure against the fluid-filled area results in an indentation in the skin.
Edema
Generalized edema is easily detected during inspection and usually results from
nephrotic syndrome and sepsis and rarely from severe heart failure. Dependent edema
involving the inferior extremities, on the other hand, is a consequence of systemic
venous hypertension associated with right heart failure and can be detected by
inspection.
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Hair
Normal hair distribution is well appreciated by most examiners and need not be
considered here. However, it should be remembered that facial, axillary, and public
hair depend on the presence of sex and other hormones and thus is related to both the
sex and the age of the patient. Scalp hair should be specifically examined for length,
texture, fragility, sheen, and the ease with which hairs can be manually removed from
their follicles.
Lymph node
Lymph nodes are distributed throughout the body but for most purposes can be
divided into five major groups: cervicofacial-supraclavicular, axillary, epitrochlear,
inguinal, and femoral. Other lymph node groups that occasionally become
pathologically enlarged are the suboccipital, postauricular, suprasternal, and popliteal.
Evaluation of the numerous lymph nodes of the mediastinum, abdomen, plevis, lymph
nodes of the mediastinum, abdomen, pelvis, and lower extremities must be done by
computed tomography (CT) or lymphangiography.
Lymph nodes are examined by palpation. In general the tips of the first four
fingers are sued, and five major qualities of the nodes are noted: location, size in
centimeters (using a ruler), degree of tenderness, fixation to underlying tissue, and
texture (hard, soft, etc.).
Normal lymph nodes are not palpable. However, mild enlargement (<1 cm) of the
inguinal nodes is quite common, and probably results from repeated superficial
infections of the fee and legs. These nodes are soft, nontender, and movable, with
normal overlying skin. Femoral node enlargement, in contrast, is more likely to be of
clinical significance. Similar small, soft, movable nodes are also found in children in
the cervicofacial and axillary areas as a result of exposure to upper respiratory
pathogens and superficial infections of the upper extremities.
Lymphadenopathy may be either localized or generalized. The former is generally
associated with a local infectious process in the anatomic area drained by the nodes in
question, or neoplasm. Texture, size, tenderness, and fixation can all weigh in favor of
one or the other of these possibilities; hard nodes favor neoplsms, as do greatly
enlarged (>3 cm), nontender, and fixed nodes. Small, soft, tender, red, and movable
nodes are more often a result of inflammation or some other type of antigenic
challenge. Location is also of importance; isolated occipital, postauricular, or
epitrochlear lymphadenopathy is unusual in primary lymphoma and more commonly
results from locallized inflammation. Posterior or anterior cervical, supraclavicular,
mediastinal, or intraabdominal adenopathy is more commonly associated with
neoplasia.
Posture
The patient’s position or posture may reveal significant information. (for example:
arthritis, congestive heart failure, carcinoma of the body or tail of pancreance) thus,
the position of the patient at the time of examination may suggest certain disease
possibilities.
Body movements
Body movements are classified as voluntary and involuntary. Involuntary
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movements are usually abnormal and may occur in either conscious or comatose
states.
1. The tics: These are habit spasms and usually involve the muscule of the eyes,
face neck. They generally occur in tense or emotional persons.
2. Convulsive movements
Convulsive movements are a series of violent involuntary muscule contractions.
(1) Tonic convulsions are custained contractions.
(2) Clonic ones are characterized by intermittent contraction and relaxation.
(3) Tremors are trembling movements that are result of various causes such as
fatigue, alcoholic intoxicaton. Certain drugs, thyroxicosis, parkingsonism, hysteria
and nervous.
(4) A flapping tremor can frequently be seen in the presence of hepatic cama. This
is best seen in the hands, although it may occur in the feet or tongue, with the arms
outstretched on the bed, the wrists dorsiflexed and the fingers spread apart, there
occurs episodes of rapid alternating flexion and extension movements at the patient’s
wrists and the metacarpophalangeal joints.
Gait
Abnormalities of gait are also noted during inspection. Neurologic deficits
resulting from cardioembolic strokes or hypertensive cerebrovascular disease may be
associated with abnormalities of gait. A parkinsonian gait may indicate Shy-Drager’s
syndrome, which may be associated with orthostatic hypotension. Certain metabolic
disorders such as hyperthyroidism, hypothyroidism, Cushing’s syndrome, and
acromegaly can be suspected during inspection, and these metabllic diseases may be
associated with various cardiovascular abnormalities including systemic and
pulmonary hypertension and myocardial and pericardial diseases.
Speech
The character of a patient’s voice and the manner of his speech may be of
considerable diagnostic aid, involvement of larynx by inflammation. TB or
malignancy may result in hoarseness. In cerebral vascular accidents, the speech is
often thick, and words are enunciated with considerable difficulty. In paralysis of
recurrent laryngeal nerve the voice is weak and loss its normal resonating quality.
Three different basic speech defects are encounteaed: pphonia, aphasia, and anarthria.
Breath odors
Nutrition
As part of every P. E. the physician should record the patient’s sex, age, weight,
height, temperature, pulse and respiratory rate.
1. Overweight or obesity may be either exogenous or endogenous in origin.
Edema must be differentiated from obesity, in edema the tissues pit (indent) when
pressed with finger. This phenomena is not present in obesity.
2. Underweight. The examiner should evaluate the patient’s present weight in
term of his average weight; that is , has patient always been slender or has been lost
weight, pepople may lost weight as the result of voluntarily decreased calaric intake
or because of various wasting diseases, such as pulmonary TB, malignancy and
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hyperthyroidism.
Stature
“Stature” here refers to height and build.
People’s height is below normal. Gigantism is of two essential types, both of
which are caused by hypersecretion of the anterior pituitary growth hormone. This
overactivity of anterior lobe gegins before the body epiphyses fuse, there results an
individual of abnormally large stature with absent or retarted sexual development.
On the other hand, the anteriar lobe becomes overactive following fuse of
epiphyses, acromegaly results.
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Chapter 3
Head and Neck
A. Head: HAIR AND SCALP
The character and the color of the hair should be noted.Alopecia,a thinning of the hair
or actual baldness,is the result of injury or death of the hair follicles.Although a
number of conditions may cause loss of scalp hair,the most common is hereditary
alopecia.Hereditary male baldness usually begins with a generalized thnning of the
hair associated with recession of the anterior headline,particularly in the area of the
temples.Other forms of alopecia are toxic or symptomatic alopecia and alopecia
areata.Presently the most common cause of sudden hair loss among hospital patients
is the side effect of drugs used for palliation of malignant tumors and leukemia.In
hypothyroidism(myxedema) the hair is commonly coarse,dry,and brittle.
SKULL(CRANIUM)
The examiner palpates the entire skull using both hands and simultaneously examines
symmetrical areas.The examiner parts the hair to observe the scalp,noting any
scaliness,deformities,lumps,tenderness,lesions or scars.
The size and shape of the cranium vary considerably from patient to patient.Certain
deformities of the skull result from congenital malformations.Microcephaly is a
congenitally small skull resulting from failure of the brain to develop normally in size
and function.The result ,a skull much smaller than normal,is always accompanied by
severe mental retardation.In contrast,oxycephaly or steeple skull ,which results from
premature union of the cranial sutures that leads to grotesque malformations of the
calvarium ,is not ordinarily accompanied by mental retardation.An abnormally large
head(macrocephalus) may occur with several conditions:Hydrocephalus,Osteitis
deformans(Paget’s disease of bone),Acromegaly.Vitamin D deficiency (rickets) causes
enlargement of the frontal and parietal prominences,producing a somewhat square
head.
FACE and its ORANGANS
General appearance(facies).Cetain individuals possess a gifted ability to look at
another’s face and,almost instinctively,sense a great deal of information.
ThyrotoxicosisOne form of thyrotoxicosis ,caused by Grave’s disease,is also
characterized by protrusion of one or both eyes(exophthalmos),and some signs:Graefe
sign,Stellwag sign,Mobius sign,Joffroy sign.
EYES
Lids.Faults in position include outward rolling of the lids(ectropion) and inrolling
(entropion). Systemic disease(for example nephrosis,heart failure,allergy,or thyroid
deficiency ) may be suspected in the presence of lid edema, provided purely local
inflammation and the slight bulging of lid skin commonly caused by aging are
excluded.Ptosis (drooping of the upper lid ) may be an early sign of involvement of
the third nerve by any cause.Congenital defects rank high among causes of ptosis.
Conjunctiva The conjunctiva is divided into two portions,palpebral and
bullbar.Palpebral conjunctiva lines the posterior lid surface.Bulbar conjunctiva covers
the eye up to the limbus.Conjunctiva is normally quite transparent,and the white color
of the eye is caused by the underlying white sclera.
Cornea.Good vision requires a perfectly smooth and transparent cornea.Two of the
most common abnormalities of the cornea are abrasions and opacities.Corneal
sensitivity(fifth nerve) is tested by touching a wisp of cotton to the center of the
cornea and noting the brisk lid closure.This lid closure is a normal and important
protective reflex.
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PupilNormal pupils are perfectly round,equal in size,and constrict visibly to light and
during accommodation.The direct reaction to light refers to constriction of the pupil
receiving increased illumination.Constriction of the opposite pupil is termed
consensual pupil reaction. The reaction to accommodation is best tested by holding
one fingertip about 4 inches from the eye being tested.If the pupil reacts to light,it
ordinarily may be assumed that reaction to accommodation will be present.Failure to
react to light with preservation of convergence is very characteristic of central nervous
system syphilis.
Pupils are normally smaller in infancy and old age.Enlargement of the pupil may be
caused by ocular injury,acute glaucoma,systemic poisoning by parasympatholytic
drugs,and local use of dilating drops.Constriction of the pupil is seen in iris
inflammation ,in glaucoma patients treated with pilocarpine,as an effect of
morphine,and physiologically in sleep.
Intraocular pressure.By indentation of the eye with the examining fingers,a crude
estimate of intraocular pressure may be made.Pressure measurement is important
because elevated intraocular pressure,known as glaucoma, causes slow death of nerve
fibers and is responsible for 12% of blindness in American.
EARS
Inspection of the external ear is so obvious that it is frequently neglected.It should
require only a few seconds.Occasionally tophi,which are small white deposits of uric
acid crystals caused by gout,are seen along the margins of the auricle.
Next the examiner inspects the external auditory canal and the tympanic membrane.
In physical diagnosis the tympanic membrane or eardrum may be regarded as a
translucent membrane through which the otologist views normal anatomy and also
pathologic processes in the middle ear.
Examination of hearing
A hearing test should be part of every physical examination.A reasonably accurate
estimate of hearing can be made by any physican who understands a few basic
principles.For testing hearing in the office or at the bedside the only instruments
needed are one or two tuning forks,a masking device,and the examiner’s own voice.
NOSE
There is an anterior plexus of blood vessels in the mucosa of the nasal septum,and the
examiner can often see small arteries and veins here.This is the most common site for
epistaxis(nosebleed) .
Examination of the paranasal sinuses is done more indirectly than other otolaryngic
procedures.The examiner cannot see into any of the sinuses and only rarely can he see
a sinus ostium.Information about the condition of the sinuses is gained(1)by
inspecting and palpating the overlying soft tissues(maxillary and frontal sinuses)(2)by
noting secretions that may drain from the sinuses ,and (3)by transillumination .
ORAL CAVITY
Observe lips, buccal mucosa,teeth,gums and tongue
The examiner inspects the lips,all surfaces of the tongue,gums,roof of mouth,and the
buccal mucosa(the tissue lining the cheeks) by asking the patient to open his mouth
and by shining a light into the area to be examined.The examiner may use a tongue
depressor to aid inspection.
Lips-The healthy lips are wet and red in color.This is caused by a rich capillary
network.
Buccal mucosa-To examine the buccal mucosa it is necessary to shine a light into the
patient's mouth.The healthy buccal mucosa is pink and smooth.The duct of the parotid
gland opens onto the buccal mucosa opposite the upper second molar.
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Tongue The tongue is examined by both inspection and palpation for its shape ,motion
and ulceration.
Teeth and gingiva There are 32 teeth in the full adult dentition.The teeth are inspected
for evidence of caries and malocclusion.
Pharynx is devided into three parts:nasol pharynx,oral pharynx and laryngeal
pharynx.When the tonsils become enlarged,they may extend considerably beyond the
anterior tonsillar pillars,at times even to the midline .At other times white spots on the
tonsils may indicate follicular tonsillitis.
Larynx Tumors of the true cords prevent accurate approximation during phonation
and therefore cause hoarseness.For that reason malignant tumors arising on the true
cords have a very favorable prognosis if the patients sees a physician as soon as he
becomes hoarse and if the physician examines the larynx.
MOVEMENTS OF THE HEAD
The head may be tilted to the side as the result of shortening of the sternomastoid
muscle.This condition is known as torticollis.Although this is usually a congenital
defect,it may be caused by inflammation of the muscles.
A not uncommon observation in elderly people is the constant rhythmic tremor of the
head and its attendant degenerative changes in the brain.
Bounding(a slight up-and-down movement) of the head that is synchronous with the
pulsation of the heart may be noted in patients with aortic regurgitation as the result of
the widened pulse pressure.
B. NECK
Blood vessels Auscultation over the carotid arteries may reveal bruits that indicate
stenosis of major arteries in the neck. These changes are usually caused by
atherosclerosis and may produce serious brain damage. Most significant is the
high-pitched bruit heard over the bifurcation of the carotid artery. It usually indicates
a stenosis of the internal carotid artery that is remediable by surgery. The low-pitched
murmurs heard over the base of the neck are commonly cause by artherosclerosis of
the subclavian artery.
The jugular veins are ordinarily not distended when the patient is in a sitting
position, although filling of these veins will be seen as he reclines. When there is
distention of these veins in the upright position, it usually indicates congestive heart
failure. On the other hand, it may be the result of any obstruction to the return flow of
blood from the head and neck into the thorax, such as constrictive pericarditis, tumor
of the mediastinum, or obstruction of he superior vena cava.
Thyroid gland.Palpation. Seat the patient in a chair and stand behind him. He must be
relaxed and comfortable with his chin lowered and the back of his head resting against
your body. Place your fingers anteriorly with their tips over the patient’s thyroid, and
the thumbs resting on the patient’s posterior neck. Throughout the examination,
repeatedly ask the patient to swallow to facilitate identification and delineation of the
gland.The examiner should feel as much of the thyroid gland as possible.The
size,configuration,consistency,presence,and number of abnormal nodules should be
carefully recorded.
Trachea. First, the trachea is palpated for evidence of deviation. The trachea is
probably best palpated just above the suprasternal notch. The trachea may be
displaced laterally by an aortic aneurysm, a mediastinal tumor, or a unilateral thyroid
enlargement. In similar fashion, a large amount of fluid or air in the pleural space will
push the trachea and other mediastinal structures toward the opposite side. If there are
pleural adhesions, fibrosis within the lungs, or atelectasis, there may be displacement
of the trachea toward the affected side. Second, the trachea is palpated for evidence of
73
trachea tug.
Cervical lymph nodes
Palpate lymph nodes bilaterally.The examiner may be positioned in front of or behind
the patient and examine the lymph nodes with the pads of his index and middle
fingers.This should be done slowly and carefully to make certain that there aren’t any
abnormalities present.It is better if the examiner moves the skin over the underlying
tissue rather than move his fingers over the surface of the skin.The examiner may
have the patient position his head with his neck slightly flexed forward.The examiner
palpates all nodes bilaterally.
For palpation of lymph nodes,be sure to keep the skin and muscles relaxed.If the
lymph
nodes
are
enlarged
,
note
their
location,size,number,hardness,mobility ,tenderness,adhesion,fusion,swelling ,fistula
or scars.
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Chapter 4
Physical Examination of the Chest
The chest indicates the region that lies under the neck and above the abdomen.
Chest wall is composed of sternum, ribs, and vertebras. The anterior part is a little
shorter than the posterior part. Chest examination includes many components: chest
shape, chest wall, breasts, vessels, mediastinum, bronchus, lung, pleura, heart, and
lymph nodes, etc.
In addition to general physical examination, the following check methods have
been widely used in clinical work: X-ray topography, lung function test, blood-gas
analysis, aetiology, histology, and relevant bio-chemical tests. These methods can
provide early stages of abnormality and pathogens, even give out exact diagnosis on
pathology and pathogenesis, but, many changes in palpation, percussion and
auscultation for all kinds of rales, can not be detected through these methods so they
can’t completely replace the basic physical examinations till now. The basic physical
examination has long been used clinically, which doesn’t need high-quality
equippment, handy for use to provide important information and signs for the
diagnosis of the chest diseases. Of course, a correct diagnosis depends not only on the
basic physical examination, but also other supplementary examinations and the ill
history should be emphasized in synthetical consideration.
Traditional physical examination of the chest includes four methods, inspection,
palpation, percussion and auscultation. The examination should be performed in warm
circumstance with well light. The patient should expose the chest to the full, in sitting
or supine position according to the need for the examination or the ill condition, and
be examined thoroughly with the sequence of inspection, palpation, percussion and
auscultation. In general, the anterior and the lateral part is examined first, then the
posterior part, this may overcome the tendency that only percussion and auscultation
be cared but inspection and palpation be overlooked and avoid omission of any
significant sign.
A.. Landmark on chest wall
The chest contains important organs such as lung and heart. Examination of
chest aims to determine the physiologic and pathophysiologic situations of these
organs. The position of each organ inside the chest can be determined by examining
the surface of the chest. To mark the underlying organ, and detect the position and
range of the abnormalities, it is quite important to make well aquaintance with the
natural landmarks and artificial lines, with which the underlying structure and
abnormalities can be exactly located on the chest wall.
I Bone landmark
Suprasternal notch: Above the manubrium sterni. In normal condition trachea is
in this notch.
Manubrium sterni: a piece of hexagon bone at the top of the sternum. Its upper
part connects bilaterally to the sternal end of each clavicula, while its base part
connects to the sternum.
Sternal angle: Also termed Louis angle. It is formed by the protrusion of the
conjunction composed of sternum and manabrium sterni. It connects bilaterally to
each of the right and left second costal cartilage. It acts as an important landmark for
counting rib and interspace, and indicates the bifurcation of the trachea, the upper
level of the atria of heart, the demarcation of upper and lower part of mediastinum,
and the fifth thoracic vertebra as well.
Suprabdominal angle: also termed infrasternal angle, denotes the angle formed by
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the bilateral rib rows (composed of the seventh to tenth costal cartilage joining
bilaterally) which meet at the lower end of the sternum. It corresponds to the dome
part of the diaphragm. Normally this angle is approximately 70°- 110°,narrower in
slender and wider in dumpy persons, and it also widens slightly during deep
inspiration. The underlying region contains the left lobe of liver, stomach and
pancreas.
Xiphoid process: the protrusive triangular part of the lower end of the sternum
with its base connects to the sternum. The length of xiphoid process in normal subject
varies widely.
Rib: a total of 12 pairs. Each connects to the corresponding thoracic vertebra with
its posterior end. The ribs run obliquely to the lateral and then to the anterior direction,
with smaller oblique angle above and larger angle lower. Each of the 1-10 rib
connects to the relevant cartilage and the sternum, constructing the bony framework
of the chest. The eleventh and the twelfth rib do not connect to the sternum and thus
are called free ribs.
Intercostal space (interspace): The space between two adjacent ribs, used to
mark the position of any lesion. Beneath the first rib is the first interspace, beneath the
second rib the second interspace, and so forth. Most ribs are palpable over the chest
wall except for the first one because its anterior portion is overlapped by the clavicula
and usually unpalpable.
Scapula: lies between the second and the eighth rib on the posterior chest wall.
The hillock and shoulder ridge of the scapula is palpated easily. Its inferior end is
called inferior angle. When the patient is in standing position with his arms hanging
naturally, the inferior angle acts as the mark of the seventh or the eighth rib, or
corresponds to the eighth thoracic vertebra.
Spinous process: marks the posterior midline. The seventh cervical spinal process
at the base of the neck is most prominent, usually serves as the hallmark for counting
the thoracic vertebrae which start just following it.
Costolspinal angle: constructed by the twelfth rib and the spine. The kidney and
ureter lies in the region in front of this angle.
II Vertical line landmarks
Anterior midline: namely midsternal line, a vertical line through the middle of the
sternum running from its top at the middle point of the upper ridge of the manubrium
sterni and running down vertically through the middle of the xiphoid process.
Midclavicular line (left, right): vertical line drawn through the middle point of
each clavicula, e.g. the vertical line running through the middle point of the clavicula
between its shoulder end and sternal end.
Sternal line (L, R): vertical line runs along the vertical edges of the sternum and
parallels to the anterior midline.
Parasternal line (L, R): Vertical line at the middle of sternal line and
midclavicular line.
Anterior axillary line (L, R): vertical line drawn downward through the anterior
axillary fold along the anteriolateral aspect of the chest.
Posterior axillary line (L, R): vertical line drawn through the posterior axillary
fold along the posteriolateral wall of the chest.
Midaxillary line (L, R): running downward vertically from the apex of the
axillary and between anterior axillary line and posterior axillary line.
Scapular line (L, R): vertical line drawn through the inferior angle as the arm
hanging naturely, parallels to the spine.
Posterior midline (L, R): namely midspinal line, running vertically downward
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through the posterior spinal process, or along the middle of spine.
III Natural fossa and anatomic region
Axillary fossa (L, R): the depressed region formed from the inside aspect of the
upper arm connecting to the chest wall.
Suprasternal fossa: a depressed region above the manubrium sterni, behind it lies
the trachea in normal condition.
Supraclavicular fossa (L, R): the depressed region above the clavicula,
corresponds to the upper part of each lung apex.
Infraclavicular fossa (L, R): a depressed region beneath the claviculae with its
lower margin at the third rib, corresponds to the lower part of each lung apex.
Suprascapular region (L, R): the region above the scapular hillock with the upper
lateral margin at the ridge of the trapezius, corresponds to the lower part of the lung
apex.
Infrascapular region (L, R): the region that between the line through two inferior
angles and the horizontal line through the twelfth thoracic vertebra. The
posteriormidline departs it into two parts.
Interscapular region (L, R): The region between the inside ridges of both scapulae,
is departed by the posteriormidline into two parts.`
IV The boundary of lung and pleura
Trachea runs down along the anterior part of the neck into the thorax at the front
of esophagus, bifurcates into the left and the right primary bronchus at the sternal
angle level, then enters into the left and right lungs, respectively. The right primary
bronchus is wider, shorter and steeper, while the left one is slender and oblique. Right
primary bronchus departs into three branches, enter the upper, middle, and lower lobe
of the right lung, respectively. Left primary bronchus bifurcates and enters the upper
and lower lobes, respectively. Two lungs resemble in shape, except for that the
anterior part of the left lung is occupied by the heart. Each lobe has a topographic
position on chest wall. To know the topographic position is of importance for location
diagnosis of lung diseases.
Lung apex: protrudes about 3 cm above the upper edge of the clavicula with its
apex point near the sternal end of the clavicula, approaches the level of the first
thoracic vertibra.
Upper boundary of the lung: its projection on the anterior chest wall forms an
upward arc. It begins at sternal-clavicular junction, runs upward and outward to the
level of the first thoracic vertebra, then downward and outwardly, ends at the border
point of middle and inner one third of the clavicula.
Outer boundary of the lung: runs downward from the upper boundary, quite
approaches the inner surface of lateral chest wall.
Inner boundary of the lung: runs down from the sternal-clavicuar junction, the
two sides nearly meet each other at the sternal angle, then runs down along each side
of the anterior midline, then separates at the fourth costal cartilage level. The right
boundary continues almost vertically downward, turns rightward at the sixth costal
cartilage, runs down to meet the lower boundary. The left boundary turns leftward to
the anterior end of the fourth rib, along the anterior ends of 4-6 ribs downward, then
turns left again to meet the lower boundary.
Lower boundary: two sides of the lower boundary are in analogy position. The
anterior part begins from the sixth rib, runs downward and laterally to the
midclavicuar line at the level of the sixth interspace, and to the midaxillary line at the
level of the eighth interspace. The posterior part of the lower boundary approaches
horizontal at the tenth rib level by the inferior angle line.
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Boundaries between lobes: called fissure. Lobes of the two lungs are separated by
visceral pleura between lobes. The fissure between the upper lobe and the middle and
lower lobes of the right lung, and that between the upper and lower lobe of the left
lung, is called oblique or diagonal fissure. Both begin from the third thoracic vertebra
at posterior midline, run outward and downward, meet the fourth rib at
posterioraxillary line, then run downward anteriorly, end at the sixth chondrocostal
junction. The anterior upper aspect of the right lower lobe attaches to the lower aspect
of the middle lobe. The boundary between the upper and middle lobe is horizontal,
called horizontal fissure, begins from the forth rib at posterior axillary line, ends at the
right edge of sternum at the level of the third interspace.
Pleura: the pleura covering the surface of the lung is termed visceral pleura, and
that covering the inner surface of the chest wall, the diaphragm, and the mediastinum,
is called parietal pleura. The visceral part and the parietal part of pleura turn over each
other successively, make up the right and the left thoracic cavity two wholly closed
spaces. Intrathoracic pressure is negative, which makes the two layer of pleura adhere
closely together, forming a latent cavity. In the cavity there is a little plasma, which
lessons the rub between pleura during respiration. At each side, the costal part and the
diaphragmatic part of the parietal pleura beneath the lower boundary of lung turns
over and compose a place about 2-3 interspace height, called sinus phrenicocostalis.
Because of its lowest position, even at deep inspiration, it can't be brimmed by the
expanded lung.
B. Chest wall, chest framwork, and breast
I Chest wall
In examining chest wall, the examiner should pay attention to the following
aspects in addition to the nutrition, skin, lymph nodes, and the development of
skeleton muscle:
1. Vein: Normally the vein on chest wall is not obvious. When superior or inferior
vena cava and their branches are blocked, collateral circulation will be built up, veins
on chest wall become full form varicose. The blood flow in the varicose vein is
downward when superior vein is obstructed, and upward when inferior vein
obstructed.
2. Subcutaneous emphysema: Indicates the condition when air enters and stores
in subcutaneous tissue. Pressing the skin with fingers will lead to motion of stored air
in the subcutaneous tissues, and produce crepitation, a sensation like rolling a lock of
hair between the thumb and fingers or grasping snow. When pressing the stethoscope
on the involved skin, the sound can be heard that resemble to rolling hair, called
crepitus. Subcutaneous emphysema at chest is commonly the result of injuries of lung,
trachea or pleura, free air escapes from injured part into subcutaneous tissues.
Occasionally subcutaneous emphysema can be caused by local infection of bacillus
aerogenes. In severe cases air may spread to neck, abdomen and other position of
subcutaneous tissues.
3.Tenderness: Normally there is no tenderness on chest wall. In intercostal
neuritis, costal cartilagitis, chest wall soft tissue inflammation and rib fractures, the
involved portion may be tender. Tenderness and pain on percussion on sternum
usually exist in leukemia patients when myelodysplasia occurs.
4.Interspace: It must be mentioned whether there is any retraction or bulging of
interspace. Retraction of the interspace during inspiration indicates the obstruction of
free air flowing into the respiratory tract. Bulging of interspaces may be seen in
patients with massive pleural effusion, tension pneumothorax, or severe emphysema.
In addition, the corresponding interspace bulging may be noted in the thoracic wall as
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the result of tumor, aortic aneurysm, or marked cardiac enlargement in infancy and
childhood.
II Chest framwork
In normal subjects, there is some variation in size and shape of the thorax. In
general, the two halves of the thorax are grossly symmetric, present elliptical shape.
Shoulders are at nearly horizontal level. The clavicula is a little prominent and there is
a little depression of both the supraclavicular and infraclavicular areas. Though, in
right-handed person, the greater pectoral muscle at the right side is usually more
developed than that of the left side. The opposite would apply for those who are
left-handed. In adult, the anterioposterior(AP) diameter of the thorax is shorter than
the transverse diameter, present a ratio of 1:1.5. In elder and childhood, the AP
diameter is a little shorter than or nearly equals to the transverse diameter, makes the
thorax cylindric.
1. Flat chest: The thorax framework is flat, the AP diameter is less than half of the
transverse diameter. This can be seen in slender adult, and in patients with chronic
hectic diseases as well, such as tuberculosis.
2. Barrel chest: The AP diameter is increased to as large as, or even greater than
the transverse diameter, resulting in cylindric thorax. The oblique degree of the rib
becomes small, the rib angle with spine is larger than 45°. Interspace becomes wider
and full. The infrasternal angle becomes wider with less respiratory variation. This
situation can be seen in severe emphysema patient, or elderly or obese subject.
3. Rachitic chest: a deformed chest caused by rachitis, seen mostly in childhood.
Along each side of the sternum, chondrocostal junctions usually bulge like rosary,
termed rachitic rosary. The lower anterior part of ribs turns outward, the part of chest
wall attaching with diaphragm depress, form a sulciform band, called Harrison groove.
The xiphoid process is depressed, making the thorax funnel-like, called funnel chest.
If the AP diameter is a little longer than the transverse diameter, the vertical span is
smaller, the lower part of the sternum bulges, and the adjacent ribs depress, the
resultant deformed chest is called pigeon chest.
4. Unilateral deformation of the thorax: Bulging of hemithorax is noted most in
massive effusion, pneumothorax, or unilateral severe compensatory emphysema.
Unilateral flat or retraction of the thorax is usually seen in atelectasis, pulmonary
fibrosis, extensive thickening fibrotic pleura, etc.
5. Local bulge of chest wall: Seen in obvious heart enlargement, massive
pericardial effusion, aortic aneurysm and tumors inside or on the chest wall. Besides,
bulging can also be noted in costal cartilagitis and rib fracture, the former usually has
tenderness on the bulged cartilage, the latter often reveals severe pain as the chest wall
being pressed, in addition to bone fremitus of the broken ends of ribs.
6. Thoracic deformation caused by deformed spine: Severe kyphoscoliosis,
kyphosis, or protrusion of spine, can lead to asymmetric thorax, with widened or
narrowed interspaces. The relation between the landmark and the position of
underling organ changes. In severe cases of spine deformation, the deformed thorax
may cause respiratory and circulatory dysfunction. This is common in spinal
tuberculosis.
III Breast
Normally the breast is not obvious in childhood and man, with the nipple located
in the fourth interspace at midclavicular line. In normal female the breast begins to
develop during adolescence, assumes hemispherical. The nipple also develops to
cylidric shape.
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Breast examination should be conducted in systemic sequence rather than only
the position complained by patient, lest any misdiagnosis. Besides breast, the
lymphatic drainage sites must be examined as well. When examined, the patient
should stripped to waist for adequate exposure of the chest, and plenty of light is
essential. The patient is usually in sitting or supine position. Normally the first step is
inspection, then palpation.
1．Inspection
1) Symmetry: two breasts are generally symmetrical in healthy female in erect
sitting position. Mild asymmetry can also be seen as the result of difference in
development of two breasts. Obvious enlargement of one breast may denote
congenital deformation, cyst formation, inflammation, or tumor. Shrinkage of one
breast usually indicates maldevelopment.
2) Superficial appearance: Skin erythema of the breast may indicate local
inflammation, or breast cancer involving the superficial lymphatic tube and causing
carcinous lymphadenitis. The former is commonly associated with local swelling,
hotness, and pain, whereas the latter presents scarlet skin without pain, this provides a
differentiation. When breast tumor is present, the superficial vessels are usually
visible. Moreover, ulceration, pigmentation and scars on the breast skin should be
mentioned.
Edema of the breast makes the hair follicles and follicular openings easily seen,
which may be obvious in breast carcinoma and inflammation. The edema associated
with carcinoma is caused by mechanical blockage of cancer cells in the lymphatic
channels beneath the skin, termed lymphoedema. In this situation, the hair follicles
and follicular opening depress obviously, so that theinvolved skin looks like “ orange
peel” or “ pig skin”. Inflammatory edema is caused by inflammatory irritation, which
increases the capillary permeability, results in the extravation of plasma into the
intercellular space, usually associated with skin redness. Notations should be given as
to the exact location and range of the edema on the breast skin.
During pregnancy and lactation period, the breast will enlarge obviously, protrude
and prollapse, with larger areola and more pigmental. The axillae becomes full,
superficial vein in breast skin can also be seen. In some instances the breast tissue
extends to the apex of the axillae, because of the hypertrophy of the breast tissue in
preparation for lactation.
3)
Nipple: The size, location, symmetry of two sides and whether or not
inversion of the nipple must be noted. Nipple retraction since childhood indicates
mal-development; if it appears recently, it may implies malignancy. Secretion
appearing at the nipple indicates abnormality along ductal system. The secretion may
be serous, purple, yellowish, greenish or sanguineous. Bleeding is most often caused
by the presence of benign infraductal papilloma, but also by the presence of breast
carcinoma. Clear nipple secretion becomes purple, green, or yellow, usually indicates
chronic cystic mastitis. During pregnancy the nipples become larger and more mobile.
In condition with hypoadrenocorticism, there may be obvious pigmentation on areola.
4) Skin retraction: Breast skin retraction may be due to trauma or inflammation
which cause local fat necrosis and fibroblastic proliferation, leading to shortening of
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the ligamentous fibers between the superficial layer and the deep layer in the involved
area. It should be mentioned that if there isn't any definite evidence of acute breast
inflammation, skin retraction often indicates the presence of a malignant tumor.
Especially when advanced appearance of carcinoma such as tumor mass, skin fixation
or ulceration does not appear, the mild degree of skin retraction may be the physical
sign of early stage of breast carcinoma.
In order to find skin or nipple retraction, the patient should be instructed to do
such upper limb movements that cause the contraction of anterior chest muscles to
stretch the breast ligament, such as raising arms over head, pressing palms together, or
exerting pressure on both hips with her hands.
5) Axilla fossa and supraclavicular fossa: Thorough inspection of the breasts
includes observation of the most important lymphatic drainage areas. Detailed
observation of the axillary and supraclavicular regions must be conducted to find if
there are any bulging, redness, mass, ulceration, fistula or scars.
2. Palpation:
The upper margin of the breast is at the second or the third rib, its lower margin
at the sixth or seventh rib, the inner margin at the sternal ridge, and the outer margin
ends at anterioaxillary line.
When the breast is palpated, the patient may take sitting position, with her arms at
side first, then overhead or pressed on both hips. In supine position, the shoulders can
be elevated by a small pillow putted under them to allow the breasts rest more
symmetrically on the chest wall for more detailed and convenient examination. Take
the nipple as the central point, a horizontal line and a vertical line through the central
point departs the breast into four quadrants. This makes it convenient to locate the
lesion.
The palpation should begin from the healthy breast, then the ill one. The
examiner should place his palm and fingers flatly on the breast, press gently with the
palmar aspect of fingertips, with a rotary or to-and-fro motion. The left breast should
be palpated from the upper lateral quadrant, with a procedure of clockwise direction
for thorough examination, each quadrant is palpated superficially and then deeply, and
the nipple is palpated finally. The same procedure is adopted for palpation of the right
breast with anti-clockwise direction. Attention must be paid to any redness, swell,
hotness, tenderness and lump while palpation being performed, as well as induration,
mis-elasticity and secretion.
The normal breast is felt like vague granular and pliable. The amount of
subcutaneous fatty tissue will affect the “feel” of the breast. The breast of younger
woman is softer and more homogeneous, whereas in older woman it will be more
stringy and nodular. The breast is made up of lobules of glandular tissue, which
should not be misconstrued as tumor mass when palpated. During menses the breast
becomes tight with congestion and the loose with decongestion thereafter. During
pregnancy the breast becomes larger and more pliable, whereas during lactation
period it is more nodular. Upon palpation of the breast the following physical qualities
should be noted:
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1)
Consistency and elasticity: Increase in firmness and lost of elasticity
suggests infiltration of the subcutaneous tissue by the presence of an inflammation or
neoplasm. In addition, the consistency and elasticity of the nipple must be noted.
When subareolar carcinoma exist, the elasticity of the skin of involved region is
usually lost
2)
Tenderness: The presence of tenderness in a position of the breast
usually indicates an underling inflammatory process. The breast is prone to be
sensitive during menstruation, however, tenderness is seldom in present with
malignant lesions.
3) Mass: If a mass exist, it should be characterized as the following features:
① Location: The exact location of the mass must be designated. General method
is to take the nipple as the central point, describe the mass according to the clock
numbers and axis. Furthermore, the distance of the mass from the nipple must be
recorded for the sake of accurate location of the mass.
② Size: The mass must be described in length, width and thickness, for the
comparison in the future to determine if it progresses or regresses.
③ Contour: pay attention to whether the mass is regular or irregular, the margin
is dull or acute, and whether it adheres to surronding tissue or not. Most benign
tumors have a smooth, regular contour, whereas most malignant masses are
convavoconvex, with firmed margin. However, it must be mentioned that
inflammatory lesions may also have an irregular contour.
④ Consistency: The hardness must be described clearly. It may be described
generally as soft, cystic, moderately firm or extremely hard. A benign tumor is usually
felt soft, cystic; while a firm consistency mass with irregular contour usually denotes
a malignant lesion. However, a hard region may also be caused by inflammation.
⑤ Tenderness: It should be ascertained whether or not the lesion is tender, and,
if so, to what degree. An inflammatory process is usually moderately or markedly
tender, whereas most malignant lesions are not obviously tender.
⑥ Mobility: The examiner should determine whether the lesion is freely
movable. If it is movable in certain directions, or fixed, he must determine wether the
mass is fixed to the skin, to the deep structures, or to the surrounding breast tissue.
Most benign lesions have a large mobility, inflammatory lesion is considerably fixed,
and a malignant lesion in early stage is movable, however, as the process developes, it
becomes fixed because other structures are invaded.
After palpation of the breast, the axilla, supraclavicular region and neck should be
palpated carefully, to detect any enlargement of lympho nodes or other abnormalities,
because these areas are usually involved in inflammatory lesion or invaded by
inalignancy.
3. Common breast lesions:
1) Acute mastitis: The breast is red, swollen, hot and painful, inflammation is
82
usually restricted in one quadrant of one breast. Induration or mass is palpable,
associated with general toxic symptoms such as shiver, fever, and sweat. This disease
occurs commonly in lactation women, sometimes also in young women and men.
2) Breast tumors: One must differentiate benign from malignancy. Breast
carcinoma is lack of inflammatory appearance, most are solidate and adherent to
subcutaneous tissue, the local skin appear as orange peel, the nipple is usually
retracted. It is most seen in female of middleaged or older, usually associated with
axillary lymphatic metastasis. Benign lesions are soft, clear of margin, and somehow
movable, usually seen as cystic mastoplastia, intracanalicular fibroma, etc.
Gynecomastia in male usually occurs with endocrine disorders, such as estrogen
intak, hyperadrenocorticism, and liver cirrhosis, etc.
C. Lung and pleura
When chest is examined, the patient is generally in sitting or supine position with
upper garment stripped off for adequate exposure of the chest. The room should be
comfortably warm, because shivering of the muscle caused by cold may lead to
unsatisfactory inspection, or make auscultation misunderstood. Good lightening is
quite important. When the patient is supine for the examination of the anterior thorax,
the light should be above and directly in front of the anterior thorax, above and behind
when the posterior thorax being examined. The lateral walls can be examined with the
same light, if the examiner rotates the patient from front to back. The examination of
lung and pleura routinely includes inspection, palpation, percussion, and auscultation.
I Inspection
1. Breath movement: The breath movement in healthy subject at rest is steady and
regular. This is controlled by the breath center and regulated by the nerve reflex.
Some serum factors, such as hypercapnia, may directly inhibit the breath center and
make the breath shallow. Hypoxemia can stimulate the carotid sinus and the aortic
body chemo-receptor, thus quicken the respiration. In condition of metabolic acidosis,
the blood PH drops, and respiration become deeper and slower to remove CO2 out of
the lungcompensately. In addition, pulmonary stretch reflex can also change the
rhythm of respiration, seen in conditions like pneumonia or pulmonary congestion
caused by heart failure, thus breath becomes superficial and quick. Furthermore, the
breath rhythm can also be controlled by consciousness.
The respiratory movement is accomplished through the contraction and relaxation
of the diaphragm and intercostal muscles. The thorax expands and relaxex with the
respiratory movement to bring about the expansion and collapse of the lung. In
normal condition, inspiration is an active movement, leading to the expansion of the
thorax, increasing the intrathoracic negative pressure and expansion of the lung,
resulting in the air flowing into the lung from the upper respiratory tract. The average
tidal volume in adult with quiet breath at rest is about 500 ml. Expiration is a passive
movement depending on the elastical recoil of the lung and chest, accompanied by the
decretion of negative intrapleural pressure, then the air in the lung is exhaled
accordingly. Therefore, inspiration and expiration are closely related to the negative
intrapleural pressure, the air flow into and out of the lungs, and the changes of
intrathoracic pressure. During inspiration, the anterior parts of the ribs move outward
83
and upward, while the contraction of diaphragm leading to bulging of the abdomen,
whereas during expiration, the anterior parts of ribs move inward and downward,
while the relaxation of the diaphragm leading to retraction of the abdomen.
Respiration in healthy males and children tends to be predominantly
diaphragmatic, the lower part of thorax and the upper abdomen move up and down
substantially, and form abdominal respiration. Whereas in female, the respiration is
mainly dependent on intercostal muscles, this is thoracic respiration. Actually, both
forms of respiration exist simultaneously with different degrees. Some diseases can
change respiratory patterns. Pulmonary or pleural diseases such as pneumonia, severe
tuberculosis and pleurisy, or chest wall diseases such as intercostal neuralgia, rib
fracture, can all weaken the thoracic respiration and strengthen the abdominal
respiration. Peritonitis, massive peritonal effusion, extreme enlargement of the liver or
spleen, tremendous intraperitonal tumor and advanced pregnancy, can all limit the
downward movement of the diaphragm， resulting in weakened abdominal respiration
and compensatory strengthened thoracic respiration.
In patients with partial obstruction of the upper breathing tract, air flow into the
lung is impedent, thus the inspiratory muscle contraction may lead to extremely high
negative intrathoracic pressure and cause the depression of supersternal fossa,
superclavical fossa and interspaces, termed “ three depression sign”. On such
occasions inspiration is prolonged, hence called inspiratory dyspnea. It usually occurs
when trachea is obstructed, by foreign body, for example. On the contrary, in patients
with lower respiratory tract is obstructed, because the airflow out of the lung is
impedent, exhalation with exertion may lead to bulging of the interspaces. This is
associated with prolonged expiration, called expiratory dyspnea, it usually occurs in
asthma and obstructive emphysema.
Litten Phenomenon: Also named as wavy diaphragmatic shadow, a phenomenon
of diaphragm movementdemonstrated by the oblique projection of light. When the
phenomenon is detected, the light should be placed at head or foot side, the examiner
is in front of or at the side of the light with his vision line at the upper abdomen level.
During inspiration, a narrow shadow begins from the anterioaxillary line in the
seventh interspace and shifts to the tenth interspace, whereas during expiration, the
shadow regresses upward to the original position. This phenomenon is due to the
diaphragmatic movement corresponding to respiration. The normal shift range of the
diaphragm is 6cm, which has the same clinic significance as the lower margin of lung.
1. Respiratory rate: In the normal adult at rest, the respiratory rate is 16 to 18 per
minute. The ratio of respiratory rate to pulse rate is 1:4. The respiratory rate in
newborn is about 44 per minute, and decreases gradually upon growing up.
1) tachypnea: Indicates the increased respiratory rate that over 24 per minute,
usually seen in fever, pain, anemia, hyperthyroidism and heart failure. Usually the
respiratory rate increases approximately four additional cycles per minute for each
1°above the normal temperature.
2) bradypnea: Indicates the decreased respiratory rate that less than 12 per minute.
The respiration becomes superficial, seen in over dose of anesthetics or sedatives and
elevated intracranial pressure.
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3) Change of the breath depths: Hypopnea (fig.3-5-8),could be seen in respiratory
palsy, ascites and fatness, etc. And also could be seen in pneumonia, pleurisy, pleural
effusion and pneumothorax. Hyperpnea (fig.3-5-8), could be found during strenuous
exercises, for increased body oxygen supply needs more air exchange through the
lung. It can also appear when one is excited or nervous, because of over ventilation.
Decreased PaCO2 ensues and could induce respiratory alkalosis.
Patients often feel numbness around the mouth and at the tips of the limbs. Tetany
and apuea may happen in severe cases. Deep and slow breath could appear during
serious metabolic acidosis. This is because the HCO3 in the extracellular fluid is not
enough, and PH is lower, for compensation, CO2 is eliminated by the lung to maintain
the acid-base balance. This kind of deep and slow breath is also named as Kussmaul
breath, seen in diabetic ketoacidosis and uremic acidosis.
(3) Rhythm of the breath
Normal adult respiration is basically regular and smooth in testing status. The
rhythm of the breath usually changes in diseases.
1. Tidal breathing Also called as cheyne-stokes respiration. Respiration waxes
and wanes cyclically so that periods of deep breathing alternate with periods of
apnea(no breathing). The periods of the tidal breath can last from 30s to 2min. The
periods of apnea can persist 5-30s. So only through carefully and long enough
observation, the whole process could be realized.
2. Ataxic breathing
Also called Biot’s breahting. Ataxic breathing is
characterized by unpredictable irregularity. Breaths may be shallow or deep, and stop
for short periods (fig. 3-5-0).
The mechanism of the upper two rhythm is that the respiratory central excitability
is depressed, the feedback system of the breath can’t work normally. The respiratory
center can only be excited when anoxia is severe, and CO2 concentration in the blood
reaches a certain degree; when the CO2 is exhaled, the center lost the effective
excitability again, the breath weakened and suspended.
Causes include heart failure, uremia, drug induced respiratory depression and
brain damage(typically on both sides of the cerebral hemispheres or diencephalon).
Ataxic breathing is more severe than the tidal breathing, the prognosis is worse,
often happening before demise. Aging people normally may show tidal breathing in
sleep, this is a sign of cerebrovascular sclerosis.
3.Inhibitory breath
The inspiration is suspended while a severe pain in the chest happened, the
respiratory movement restrained suddenly and momently. The expression of the
patient is suffering, breath become shallow and frequent. Causes include acute
pleurisy, tumor, costal fracture and severe trauma of the thorax.
4. sighing respiration
Breathing punctuated by frequent sighs should alert you to the possibility of
hyperventilation syndrome – a common cause of dyspnea and dizziness. Occasional
sighs are normal.
2. PALPATION
(1) Thoracic expansion
It is the movement range of the thorax during respiration. Easy to obtain when
examine the antero-inferior part of the thorax, where the respiratory movement is
much obvious. Place your thumbs along each costal margin, and your hands along the
lateral rib cage. When the patient inhales deeply, watch the divergence of your thumbs
as the thorax expands, and feel the range and symmetry of respiratory movement.
Causes of unilateral diminution of or delay in chest expansion include huge pleural
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effusion, pneumothorax, pleural thickening and atelectasis etc(fig. 3-5-10).
(2) Vocal fremitus
Also called tactile fremitus. Vocal fremitus refers to the
palpable vibrations transmitted through the bronchopulmonary system to the chest
wall when the patient speaks. Ask the patient to repeat the words “yi—“. If fremitus is
faint, ask the patient to speak more loudly or in a lower voice.
Palpate and compare symmetrical areas of the lungs using either the ball of your
hand (the bony part of the palm at the base of the fingers) or the ulnar surface of your
hand.
In either case you are using the vibratory sensitivity of the bones in your hand to
detect fremitus.
Identify, describe, and localize any area of increased or decreased fremitus.
Fremitus is typically more prominent in the interscapular area than in the lower lung
fields, and is often more prominent on right side than on the left. It disappears below
the diaphragm.
Fremitus is decreased or absent when the voice is soft or when the transmission
of vibrations from the larynx to the surface of the chest is impeded. Causes include an
obstructed bronchus, chronic obstructive pulmonary disease, separation of the pleural
surfaces by fluid (pleural effusion), fibrosis ( pleural thickening), air (pneumothorax)
or an infiltrating tumor; and also a very thick chest wall.
Fremitus is increased when transmission of sound is increased, as through the
consolidated lung of lobar pneumonia.
(2) pleural friction fremitus
During acute pleurisy, the fibrin deposit between the two layers of the pleura, the
visceral pleura and the parietal pleura rub with each other, this can be felt by the
examiner’s hand, so it is called pleural friction fremitus. It can be palpated both in
inspiration and expiration. It is most obvious at the lower part of the thorax for the
movement range here is the greatest.
When the air passing through the narrow trachea and bronchus or through thick
exudate in the airway, a kind of fremitus could also be produced. Differentiated,
usually the former could disappear after coughing while the latter will not.
3 PERCUSSION
(1) The method of percussion
1) Mediate percussion
Hyperextend the middle finger of your left hand(the
pleximeter finger). Press its distal interphalangeal joint firmly o the surface to be
percussed.Avoid contact by any other part of the hand, because this would damp the
vibrations. Put your right forearm quite close to the surface with the hand cocked
upward. The right middle finger should be partically flexed, relaxed, and poised to
strike.
With a quick, sharp, but relaxed wrist motion, strike the pleximeter finger with
the right middle finger (the plexor). Aim at your distal interphalangeal joint.
Use the tip of your plexor finger, not the finger pad. Your striking finger should
be almost at right angles to the pleximeter.
Withdraw your striking finger quickly to avoid damping the vibrations that you
have created.
Use the lightest percussion that will produce a clear note. A thick chest wall
requires heavier percussion than a thin one. In comparing two areas, however, keep
your technique constant. Thump about twice in one location and then move on. You
will perceive the sounds better by comparing one area with another than by repetitive
thumping in one place(fig.3-1-2).
2) Immediate percussion
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Percuss the thorax by the tip of your plexor finger or the united finger pad
directly to show the changes of different places.
When percussed the patient should be in a sitting or dorsal position, relaxed, and
breathing homogeneously. First, examine the anterior chest, percuss each intercostal
space one by one from supraclavicular fossa. Second, the lateral chest wall, ask the
patient raise the arms and put them on the head, percuss from the axilla down to the
costal margin. And last percuss the posterior chest. Ask the patient lower the head
slightly, keep both arms crossed in front of the chest, shift their scapulae lateralwards
as obviously as possible. The upper body leans slightly anteriolly, percuss from apices
to the lung bases, after the width of apics be decided, then percuss each intercostal
space from up to sown, until the movement range of the diaphragm be identified.
(2) Influencing factors
Dullness replaces resonance when fluid or solid tissue replaces air-containing
lung or occupies the pleural space beneath your percussing fingers. Examples include:
lobar pneumonia, in which the alveoli are filled with fluid and blood cells; and pleural
accumulation of serous fluid (pleural effusion), blood (hemothorax), pus (empyema),
fibrous tissue, or tumor. Generalized hyperresonance may be heard over the
hyperinflated lungs of emphysema or asthma, but it is not a reliable sign. Unilateral
hyperresonance suggests a large pneumothorax or possibly a large air-filled bulla in
the lung.
(3) Classification of the percussion notes
1) Resonance
It is the normal sound of the lung, not very loud but could be
heard easily , and have a long duration, shown as a low pitched sound.
2) Hyperresonance
Lower and longer than the resonance, very loud and very
easy to be heard.
3) Tympany The pitch is higher than resonance, the duration is moderate,
intensity is moderately loud, e.g. percussion on a stomach filled with gas produces
such a sound.
4) Dullness Opposite to resonance, duration is not so long, pitch and intensity
are both of medium degree, senses of vibration beneath the pleximeter finger is not so
obvious, but sense of resistance is increased.
5) Flatness
It refers to the lacking of resonance, bery similar to the sound of
knocking a water-filled container. It is also considered as the extreme dullness. It is
high and soft in quality. Duration is short.
(4) Normal percussion notes
1)
Normal percussion notes of the lung: resonance is the normal notes of
the lung. It is influenced by the air containing, the thickness of the chest wall, and
the organs around. Influenced by muscle and skeleton, the sound is duller in the
upper part of the anterior thorax than the lower part; duller in the upper part of the
right thorax than of the left side; duller in the posterior chest than the anterior chest.
And the sound of right infra-axilla is duller for the liver is near, though in the left
side at the comparable part, the percussion soud is tympany for the gastic air
bubble over there, this part is also called Tranbe tympany region.
2. Percussion of the pulmonary boundary
(1) Upper pulmonary boundary, that is the width of the apics, posterior part
of the cervical muscle is its inner side and shoulder girdle is at its lateral side. The
method is: percuss from the middle trapezius muscle outwards to lateral side little
by little, when the sound turns from resonance to dullness gradually, the lateral
termination of the upper border is identified. And then, percuss from the same
middle part to inner-side, when the resonance turn to dullness again, the inner
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termination of the border comes out. The width of this resonant boundary is the
width of apics, 5-8cm regularly, it is also named as Kronig isthmus. The width of
right side is narrower than left, for right apics is located lower and the muscle of
right shoulder girdle is stronger. The boundary is narrowed or sounds dull when
tuberculosis infiltrates the apics and fibrosis or atrophy is formed. The upper
boundary widened or changed to hyperresonance when there is emphysema.
(2) The anterior pulmonary boundary
The heart normally produces an area of dullness to the left of sternum. The right
anterior pulmonary boundary is at the sternal line, and the left one is at the parasternal
line from 4th to 6th interspace. It is influenced by the size of heart, pericardial effusion,
aortic aneurysm, enlarged lymph nodes of the pulmonary portal and also by the
emphysema.
(3) The inferior pulmonary boundary
It is about the same of two sides, located at the 6th intercostal space at the
midclavicular line, 8th interspace at the midaxillary line, 10th interspace at the scapular
line. It is different in different body type. In fat person, the boundary could be
elevated about one intercostal space and in thin person descended about one
interspace. Pathologically, the boundary descends with emphysema, celiac organ
declined. It elevates with a atelectasis, celiac hypertension.
3.movement range of the lower pulmonary boundary
That is equal to diaphragmatic movement. Method is: identify the level of
diaphragmatic dullness during quiet respiration. With the pleximeter finger held
parallel to the expected border of dullness. Percuss in progressive step downward until
dullness clearly replaces resonance. Diaphragmatic excursion may be estimated by
nothing the distance between the levels of dullness on full expiration and on full
inspiration, normally around 6-8cm.
An abnormally high level suggests pleural effusion or a high diaphragm, as from
atelectasis or diaphragmatic paralysis.
4.Percussion of thorax in a lateral decubitus.
Influenced by the bed, we can percuss out a comparative dull zone alone the near
–bed-side thorax. The diaphragm elevated caused by the celiac pressure. An the
near-bed-side intercostal space, we can percuss out a comparative dullness region at
the tip of the subscapular angle on the upper side, when pillow is removed, the spine
stretched, this dull region then disappeared. Change the position, examine again to
prove the influence of the posture(fig 3-5-13)
5. Abnormal percussion sound of the thorax
The percussion sound can be changed at least the focus is larger than 3cm and the
distance between the surface less than 5cm.
The note will be dullness or flatness when air contain decreased, such as
pneumonia, atelectasis, pulmonary infarction, pulnomary edema, tumor, pleural
effusion, pleura thickening etc.
The note will be hyperresonance when the pulmonary tension decreased and air
contain increased. Such as emphysema.
If the diameter of the cavity lesion is larger than 3-4cm, and close to the chest
wall, such as cavernous lung tuberculosis, liquefacient pulmonary abscess and cysts,
the note will be tympany. If cavity is very large and located shallow, or patient with
hypertonic pneumothorax, the percussion note will be tympany locally. For its
metalloid reecho, the note is also called Amphorophony.
When pulmonary air contain decreased, such as atelectasis, congestion and
dissolution stage of pneumonia, pulmonary edema, the local percussion note can be a
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mixed sound which has the character of both dullness and tympany, we name it as
dulltympany
Dullness replaces resonance when fluid or solid tissue replaces air-containing
lung or occupies the pleural space beneath your percussing fingers. Examples include:
pleural effusion. If the effusion is moderate, without pleural thickening or adhesion,
patient in a sitting position, there will have a Damoiseau curve formed by the effusion,
Show as figure 3-5-14. Also show as the same figure, there are Garland and Grocco
triangle region of dulltympany formed by the effusion, spine, and pulmonary lower
boundary. The size of this region is influenced by the quantity of effusion.
4. AUSCULATION
Listen to the breath sounds with the diaphragm of a stethoscope as the patient
breathes somewhat more deeply than normal through an open mouth. Using locations
similar to those recommended for percussion and moving from one side to the other,
compare symmetrical areas of the lungs. Listen to at least on full breath in each
location. If the breath sounds seem faint, ask the patient to breathe more deeply. You
may then hear them easily.
(1) Normal breath sounds
1)
vesicular breath sound
It is soft and low pitched. They are heard through inspiration, continue without
pause into expiration, and then fade away about one third of the way through
expiraton(fig.3-5-15).
The strength of the sound is associated with sex, age, respiratory deepth,
pulmonary elasticity, and the thickness of the chest wall.
2). Bronchial breath sound: is the sound of turmoil flow produced by the
inspirated air through glottis, trachea or major bronchi, similar to the sound of “ha”
when one lift tongue to make the expiration through mouth. Its pitch is high,
inspiration is shorter than expiration because inspiration is of active movement, the
glottis widens, inflow is rapid, while expiration is of passive movement, the glottis
gets narrower, and out flow is slow. Besides, the expiration is more exaggerated and
higher pitched, there is a very slow silent pause between inspiration and
expiration(Fig.3-5-15).
In normal persons, bronchial breath sound could be heard over the laryngus
suprasternal, notch the areas near the 6th and 7th cervical vertibra, and around the 1st
and 2nd thoracic vertebra. The louder and the lower pitched is the sound, the nearer to
the trachea one listca to.
3. Bronchovescicular breath sound: is a mixed sound composed of bronchial
breath sound and vescicular breath sound, higher pitched and louder. While its
expiratory component is similar to bronchial breath sound, with lower loudness and
pitch, and sith less tubular characteristc and shorter expiratory phase, there is a very
short gap between inspiratory and expiratory phase, durations of two phases are
almost the same(Fig.3-5-15).
Bronchovescicular breath sound could be heard in the 1st and 2nd intercostal space
near the sternum, around the intrascapular region at the 3rd and 4th thoracic vertebrae,
and around the lung apex. If such a sound is heard at other location than those
mentioned above, it is usually abnormal, a disorder should be suspected of.
(2) Abnormal breath sounds
1. abnormal vesicular breath sound
1) Decreased or absent vesicular breath sound: This is associated with decreased or
slower air flowing ito the vesicls and also with impaired conduction of breath
sound. This sign on the lung could appear localized, unilateral or bilateral, the
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causes may be the followings: a).restricted movement of the thorax due to chest
pain, ossification of rib cartilages and resection of ribs etc. b) respiratory muscle
diseases, such as myasthenia, grakis, diaphrmatic paralysis and diaphramatic
muscular spasm etc. c) bronchial obstruction, like chronic bronchitis, bronchial
stricture etc. d) oppressive under-expansion of the lungs, such as pleural effusion,
or pneumothorax etc. e) abdominal disorders, like massive ascitis, huge tumor in
the abdomen etc.
2) Increased alveolar breath sound: Alveolar breath sound accentuated on both sides
is associated with exaggerated respiratory movement and vetilation, on such
occasion, there is more and faster air flow into the lunge. The causes are as follows:
a) body oxygen demand increases and makes respiration deep, long and faster, eg.
Exercise, fever and high metabolism rate etc; b) anoxia stimulattes respiratory
center, makes respiration accentuated, eg, anemia c) blood acidity increases.
Stimulates respiratory enter, eg, acidosis; unilateral accentuated alveolar breath
sound could been seen in patients with unilateral thoracic pulmonary diseases; then
there is diminished alveolar breath sound on the involved side, and compensatory
accentuated breath sound on the normal side.
3) Elongated expiratory breath sound. Occurs because of partial obstruction, spasm or
stricture of the lower respiratory tract, happening in bronchitis, bronchial asthma
etc. Leading go elevated expiratory impedence, or because of lowering elasticity of
pulmonary tissue, resulting in decreased expiratory power, happening in COPD etc.
4) Interrupted breath sound: Segmental pulmonary inflammation or bronchial
structure makes the air enter alveoli unharmoniously and thus results in interrupted
breath sound. It is also called cogwheel breath sound because of short irregular
pauses, often seen in pulmonary TB and pneumonia. It must be noticed that
interrupted adventory sounds due to muscular contractions may be produced when
one feels chilly, painful or nervous, but they are not related to respiration, and
differentiation is easy.
5) Hoarse breath sound: heard in the early stages of bronchial or lung inflammations,
due to smoothlessness or stricture produced by mild bronchial membranous edema
or inflammation.
2. Abnormal bronchial breath sound, bronchial breath sound heard at the locations
where vesicular breath sound should be heard is abnormal, and is also called
tubular breath sound, the reasons are as follows:
1) Consolidation of lung tissue: This makes bronchial breath sound conducted easily
through the dense consolidated lung tissue to body surface, its location, area and
loudness is related the location size and depth of the lesion, the larger and the
shallower the lesion, the louder the sound, and the vice versa. At consolidation stage
of lobar pneumonia, bronchial breath sound is often louder and high pitched near
the listening ear.
2) Big cavity in the lung, when there is a cavity in the lung surrounded by
consolidated lung tissue, communicating with the bronchus. The breath sound
harmonicates in the cavity, and conducts well through the consolidated tissur,
bronchial breath sound could be heard clearly, often seen in pulmonary abxcess or
cavity-formed pulmonary TB.
3) Pressed atelactesia: pleural effusion may press on the lung, make underlying lung
tissue more dense and cause atelactesia. Because of better conduction through the
consolidated past of the lung, bronchial breath sound could be heard clearly. This
condition is often seen in lung abscess and cavitous pulmonary TB.
3. Abnormal bronchoalveolar breath sound: heard over the area where only normal
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alveolar breath sound is heard. It is produced because consolidated part is smaller
and mixed with normally air contained pulmonary tissues or the consolidated part is
deep and covered by normal lung tissue, often seen in bronchopneumonia,
pulmonary TB early stage of lobar pneumonia or over the underexpanded lung area
above pleural effusion.
(3) Rales, the adventitious sound, not present in normal situation, not due to the
change of breath sound. Several kinds of rales could be discerned according to
their characteristics.
1. moist rale: produced due to passage of air through thin secretions in the respiratory
tract, such as exudate, sputum, blood, mucus, or pus etc. The sound could also be
regasded as crackles produced by reopening of the bronchials at inspiration when
bronchiolar wall adheres and closes because of tenacious secretion at expiration.
1) The characteristics of rales: adventious sounds besides breath sound, discrete and
short in time, often series of jeveral sounds appear, siginificant in inspiration or in
the terminal phase of inspiration, present sometimes in the early phase of expiration,
the location is rather fixed, quality not variable, medium and fine rale could be
present simultaneously, it may diminish or disappear after cough.
2) Classification of rales: 1.loud or unloud rale according to its louderness (1) loud
rale: rales sonorous, heark in pneumonia, lung abscess or cavitous pulmonary TB,
produced due to surrounding tissue with better conduction. Consolidation or
harmony in the cavity lead to loud rale. If the cavity wall is smooth, sonorous rale
may mix with somewhat metalic pitch. (2) unloud rale, the sound is low and for to
ear because there is still much normal lung tissur around the lesion, sound becomes
gradually lower during conduction.2. Rales could be divided into coarse, medium
and fine ones and even crepitations according to the size of respiratory tract lumen
the amount of secretion(Fig.3-5-16). (1) coarse rales: also named as large bubble
sound, often happening in the early phage of inspiration(Fig 3-5-17), heard over the
areas of trachea major bronchi and cavitation, such as bronchiectasis, lung edema,
pulmonary TB or lung abscess cavitation. Comatose and death impending patients,
are too weak to excrete secretion in the respiratory tract. Coarse rale could be heard
over the trachea, even without usage of stethoscope, it is then called death rattle on
this occasion.(2) Medium rales: or medium bubble sound, produced in the medium
bronchi, at the middle phase of inspiration(Fig 3-5-17), heard in bronchitis,
bronchopneumonia etc. (3) fine rale also named small bubble sound, produced in
bronchioles, at the late phase of inspiration(Fig3-5-17), met in bronchiolitis,
bronchopneumonia pulmonary congestion and pulmonary infarction etc. (4)Crepitus:
a very fine and harmonious rale, often occussing at the terminal phase of
inspirationlike the sound when one hold a lock of hair near your ear and sub it, they
are the result of presence of secretion in the bronchioles and alveoli, haking them
adhere one another, when the patient inhales, these bronchiole and alveoli open
again and result in high- pitched fine crackling rales with high frequency.
They are often met in inflammation of brochioles and alveoli or pulmonary
congestion, early phase of pneumonia and alveolitis etc. However in normal old
people or patients with prolonged bed rest, crepitus alsocould heard over two lung
bases, it disappears after several deep breaths or coughing, with no clinical
significance.
Localized lung rales only indicate localized lesions of the same plase, like pneumonia,
pulmonary TB, or bronchiectasis etc. Rales over two lung bases are often met in
pulmonary congestion due to heart failure and bronchopneumonia etc. Rales over the
whole two lung fields are often met in acute lung edema and severe
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bronchopneumonia.
2. Rhonchi: produced because there present stricture or partial obstruction of the
trachea, bronchi or bronchioles, air through these passways becomes turbulent, the
pathologic basis for which is inflammatory membranous congestion and edema
oversecretion, bronchial muscular spasm, obstruction due to tumor and foreign bodies
in the bronchial lumen, and stricture due to oppressian of extraluminal enlarged lymph
nodes or mediastinal tumors. 1) Characteristics of bronchi: they are continuous,
relatively long, and musical adventious breath sound. Rhochi are rather high-pitched
with the basic frequency of about 300-500 Hz. Audible both during inspiration and
expiration, in general more prominent during expiration. Rhonchi are easily variable
in intensity, quality and location, sometimes they change obviously instantly. Some
rhonchi, which occur in the large air passages above main bronchi, may be very loud,
audible easily even without stethoscope.
3) classification: (1)sibilant rhonchi: high pitched, basic frequency may be over 500
Hz, short like “zhi-zhi” sound, or musical in character. Sibilant rhonchi are often
produced in smaller bronchi or bronchioles(Fig3-5-16), and often accentuated by
forced expiration.(2) sonorous rhonchi: are low pitched, the basic frequency is about
100-200 Hz, like moaning or snore in character. They often occur in trachea or
major bronchi(fig3-5-16).
Rhonchi heard on both sides of lungs, are often met in bronchial asthma, chronic
bronchitis and cardiogenic asthma etc. Localized rhonchi are often heard in bronchial
membranous TB or tumor because of localized bronchial structure.
(4) Vocal resonance : is produced in the same fashion as vocal fremitus. It is elicited
by having the patient repeatedly say “yi” with ordinary voice loudness, sound
vibration at laryngus will conduct through trachea, broncho alveoli and chest wall
to the stethoscope. Normally, the word spoken are not as loud and clear as when
heard directly, and the syllables are not distinguishable. It is heard loudest near the
trachea and major bronchi and is less intense at the lung bases. Vocal resonance is
decreased in bronchial obstruction, pleural effusion, pleusal thickening, chest wall
edema, obesity and emphysema etc. Vocal resonance changes when there present
pathologic conditions, it is classified as follows according to auscultation
differences.1. Bronchophony: This indicates vocal resonance that is increased both
in intesity and clarity, it is usually associated with increased vocal fremitus,
dullness to percussion and abnormal bronchial breathing, and indicates the
presence of pulmonary consolidation.2. pectorilogny: a kind of bronchophony that
is more intense and clear and near to ear. The syllables may be understood when
the patient whispers. Its presence always indicates large area of consolidation.
Occasionally, pectriloging may be obvious before bronchial breath sounds
develop.3. eqophony: not only there is an increase in intensity of the spoken voice
but its character is also altered so that there is a nasal or bleating quality. Ask the
patient to say”yi-yi-yi”, if egophony is present, they will sound as “a-a-a”.It is
often heard over the upper portion of a moderately pleural effusion or where there
is a small amount of fluid in association with pneumonic consolidation.4.
“whispered” pectoriloguy, the sounds must actually whispered as :yi yi yi”,In the
normal subject the whispered voice is heard only faintly in the areas where
bronchovesicular breath sounds are normally heard. Accentuated and
higher-pitched pectoriloguy could be clearly heard when there is pneumonic
consolidation, thus this sign is of value for the diagnosis of pulmonary
consolidation.
(5) Pleural friction rub: Normally the visceral and parietal surfaces of the pleura glide
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quietly during respiration because of the presence of a little amount of fluid in the
pleural cavity. However, when these surfaces become inflammed and there is
exudated fibrin, the subbing of the roughened surfaces during respiration produces
such pleural friction rub. The characteristics of a friction rub can be imitated by
pressing the palm of one hand over the ear and then rubbing the back of the hand
with the fingers of the other hand. It is often heard during both phases of
respiration, relatively superficial, more clearly at the end of inspiration or at the
beginning of expiration. Friction rub disappears when breath is held. An increase
in intensity of the friction sub may be noted with pressure of the stethoscope over
the chest wall.
The most common site for a friction rub to be heard is the lower anterolateral chest
wall, the area of greatest thoracic mobility. It is seldom heard over the apex because
its respiratory excussion is less than the laver portion of the thorax. Friction rub may
disappear or reappear with the changes of body position. It also disappear when there
presents moderate amount of pleural effusion, and two layers of pleura separate, but
reappears when effusion is absorbed and two layers contact again. If mediastinal
pleura becomes inflammed, pleural friction rub could be heard both with respiration
and heart beat. Pleural friction rub often occus in fibrioous pleusisy, pulmonary
infarction, pleural tumor and uremia etc.
(6) Coin sign: press a coin on the patients’ one side of middle of front chest, then tap it
with another coin. On the comparable part of the back of the ipsilateral thorax, one
could hear a tympany with a kind of metal tone, this is the positive coin sign,
which could be met in pneumothorax.
(7)
D The major symptoms and signs of common respiratory diseases
(1) Lobar pneumonia
Lobar pneumonia refers to lobar distribution of pulmonary inflammation, the main
pathogen is streptococcus pneumoniae. Pathologically, three stages could be
discovered, they are congestion, consolidation and dissolution. Clinical manifestations
are different with different stages, however there are no clear demarcation among
three stages.
[symptom] the patients usually are adolescent with the occurrence after tiredness,
wine drinking, exposing in the coldness.
The disease often starts abruptly, with chill and then high fever, the temperature could
be up to 39-40°C , as sustained fever, they usually complain of headache, muscular
pain, chest pain on the affected side, tachypnea, cough, rusty brown sputum, the
temperature may drop drastically several days later, and accompanied by massive
sweating, the patient then may feel much better.
[signs] The patient appears acute faces, with flushed cheeks, alae nasi fans, dyspnea,
cyanosis, rapid pulse, and perioral herpes is also common, signs of congestive stage
may be present, including increased vocal fremitus. Crackles are localized to the
involved region. When pneumonia involving a whole lobe progresses, signs of
consolidation appear, as significantly increased , vocal fremitus and resonance,
dullness or flatness to percussion, and bronchial breath sounds, pleural friction rub
could be heard if pleura is involved, During resolution stage, all the above signs
gradually disappear.
(2) chronic bronchitis complicated with emphysema
Chronic bronchitis is a non-specific inflammation involving membrane of the brachea
and bronchials and the surrounding tissues, It occurs insidiously and progresses
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slowly, worsens to become chronic obstructive emphysema in the late stage, and even
leads to pulmonary hypertension and cor pulmonale. Its etiology is variable, most
propably associated with prolonged smoking, repeated respiratory tract infections,
long time contact with toxic gas and dust, air pollution, bad weather conditions,
allergic tendency, deficiency of local defense mechanism and immune function and
unbalance of autonomic nervous system, etc.
In the lesion, there are bronchial membranous congestion, edema, oversecretion of the
glands, resulting in bronchial spasm, bronchial membranous atrophy, rupture and
damage of bronchial smooth muscle, hyperplasia of peribronchial fibrous tissue, and
finally bronchiolar and alveolar dilatation.
[symptoms] Chronic cough is the main symptom in winter, and often lasting longer
than 3 months, the cough is often more severe in the morning and is associated with a
lot of white mucoid or serous frothy sputum, the sputum becomes purulent when the
patient has infection. The patient often feels dyspnea and chest dicomfort, which
worsens during exercise, and dyspnea gradually progresses.
[Signs] No obvious signs are found in the early stage,in acute exacerbations one could
hear sparse dry or moist rales. often located at the lung bases, decreased or
disappeared after cough. The amount and location of the rales are often variable. More
rhonchi associated with elongation of expiratory phase could be heard for the
asthmatic pattern of chronic bronchitis.
In patient with obstructive emphysema, one could find barrel-shaped thorax,, narrow
intercostal space, decreased respiratory movement, weakened vocal fremitus and
resonance, hyperresonance over the lungs to percussion, lowerness and the diminished
movement of the lower lung margins. Heart dullness area is smaller, the lower liver
margin is displaced downward. Alveolar breath sound with elongation of expirtory
phase is diffusely distributed, moist rales could be heard on two lung bases.
(3) bronchial asthma
Chronic bronchial inflammation is mainly caused by allergic reaction. Airways are
highly sensitive to various stimuli, and this can lead to diffuse reversible airway
obstruction for the vulnerable ones. At the attack, bronchial smooth muscle is spastic,
mucous membrane is congestive and edematous, and the gland oversecretion is
common.
[symptoms] Majority patients start in young or adulthood, repeatedly occur with the
change of seasons. Contact with allergens are often present before the attack, patients
often have symptoms associated with respiratory infection or allergic manifestations,
such as nose tickling, sneezing, snivel or dry cough. Then chest discomfort and
shortness of breath quickly appear, lasting hours or even days, the asthma usually
relieves gradually after more or less thin sputum was spit out.
[signs]
Patients usually have no obvious signs during resolution stage, while
during the attacks, they appear severely expiratory dyspnea, showing orthopnea, with
the recruitment of respiratory ancillary muscles. The grave patients may show
cyanosis, massive diaphoresis, full thorax, diminished respiratory movement with the
chest almost at the inspiratory position, diminished vocal fremitus and
hyperresonance on percussion, dry rales and wheezing sound could be heard on both
lungs. Patients with prolonged duration and multiple recurrence may be complicated
by obstructive emphsema, and will show related symptoms and signs.
(4)pleural effusion
Pleural effusion is produced because the static pressure of the pleural capillaries are
elevated (eg. heart failure), lower osmotic pressure (hypoalbuminemia due to liver
sclerosis, nephropathy) or higher capillary wall permeability(eg. TB, pneumonia and
94
tumor etc.), resulting in increase of production or decrease of absorption of fluid in
the pleural cavity. Besides, impaired drainage of pleural lymph and trauma also could
lead to pleural effusion or hemothorax. Pleural effusion could be classified into
exudate and transudate due to different etiologies.
[Symptoms] Symptoms are often not obvious if effusion is less than 300 ml, however,
patients with small amount inflammatory fibrous exudation often complain of
irritative unproductive cough, worsened on inspiration, and accompanied by chest
pain on the affected side. Patients would rather lie on the affected side to restrict
respiratory movement of this side in order to alleviate pain. When effusion increases,
parietal and visceral layers of the pleura separate, pain may become milder or even
disappeare. Patients with more than 500 ml effusion often complain of dyspnea and
chest discomfort. Huge effusion may press or even displace mediastinal organs to
cause palpitation, dyspnea, orthopnea or even cyanosis, besides the symptoms due to
pleural effusion itself, patients often have symptoms of the orginal diseases, for
example, they have fever and toxic symptoms because of exudate due to inflammation,
and have symptoms of HF, ascites, edema etc if the effusion is of non-inflammatory
transudate.
[Sign] Patients with small amount of effusion often have no obvious signs, or they
may only show diminished chest wall movement on the affected side. In the patients
with moderate or large amount of effusion, there could be seen shallow respiration,
restricted movement of affected side, wide intercostal space, displacement of apex
beat and trachea toward the opposite side, or absent apex beat.
In patients with moderate amount of effusion without thickening and adhering of the
pleura, one could percuss out Damoiseau line of the upper margin of effusion.
Garland triangle on the upper and back area of the effusion, Scoda hyper-resonant
area above and in front of area on the normal side.(Fig. 3-5-19). In patients with
huge effusion or effusion with thickening and adhering of the pleura, flatness on
percussion is common, over the effusion areas, breath sound and vocal resonance are
diminished or absent, bronchial breath sound sometimes could also be heard. Pleural
friction rub is often heard in fibrinous pleuritis.
(5) pneumothorax
Pneumothorax means that the air enters the pleural cavity. If the pneumothorax is
caused by rupture of visceral layer of the pleura, due to bleb beneath the surface of the
normal lung, chronic respiratory emphysema, or pulmonary TB, it is called
spontaneous pneumothorax.
Sometimes doctors inject filtered air into the pleural cavity artificially to treat some
diseases, such pneumothorax is called artificial pneumothorax. Besides, those caused
by thoracic injury or acupuncture are called traumatic pneumothorax.
[symptoms] Inducing factors are often as follows, holding heavy things, holding
breath, strenuous exercises or cough. Patients feel ipsilateral chest pain suddenly and
progressive dyspnea, sometimes, they can’t lie supine and so have to lie on the normal
side, let the affected side upward in order to alleviate pressing symptoms.
Patients could have cough, with or without sputum. In mild closed pneumothorax only
mild dyspnea is present, and patients may calm down several hours later. Severe
tension pneumothorax patient, may show nervousness, restlessness, diaphoresis,
rapid pulse, syncope, cyanosis and even respiratory failure besides dyspnea.
[Signs] Patients with mild pneumothotax often have no obvious signs. When air
trapped in the pleural cavity is voluminous, then on the affected side appear fullness
of the chest, wide intercostal spaces, diminished respiratory movement, and
diminished or no vocal fremitus or resonance. Trachea and heart displace toward the
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Cons
olidat
ion
Emph
ysem
a
Atele
ctasis
Pleur
al
dffusi
on
Thick
ened
pleura
pneu
moth
orax
healthy side, tympanic sound on percussion, liver dullness edge displaces downward
when pneumothorax is on the right side. Breath sound is diminished or disappeared on
the affected side. Coin sign is positive.
The signs of common pulmonary and pleural diseases are listed in table 3-5-1
Table 3-5-1
inspection
palpation
Percussio
Auscultation
n
Chest
Respirato
Trachea
Vocal
Note
Breath
rale
Vocal
appearance
ry
location
fremitus
sound
resonance
movemen
t
Symmetrica Diminish
Central
Increased Dullness Bronch Moist
Strengthened
l
ed on the
on the
or
ial
rale
affected
affected
flatness
breath
side
side
sound
Barrel-shap Diminish
Central
Diminish Hyperres Dimini Always
Diminished
ed
ed on
ed on
onance
shed
without
both sides
both sides
Denting of Diminish
Deviate
Diminish Dullness Disapp Withou Disappeared or
the affected ed on the
toward
ed or
eared
t
diminished
side
affected
the
disappear
or
side
affected
ed
diminis
side
hed
Fullness of Diminish
Deviate
Diminish Flatness Dimini Withou Diminished or
the affected
ed or
toward
ed or
shed or
t
disappeared
side
disappear
the
disappear
disappe
anced on
normal
ed
ared
the
side
affected
side
Denting of Diminish
Deviate
Diminish Dullness Dimini Withou
Diminished
the affected ed on the
toward
ed
shed
t
side
affected
the
side
affected
side
Fullness of Diminish
Deviate
Diminish Tympany Dimini Withou Diminished or
the affected
ed or
toward
or
shed or
t
disappeared
side
disappear
the
disappear
dissape
anced on
normal
ed
ared
the
side
affected
side
E . The Heart
In the present era of technological advances, particularly in the various imaging
modalities, there is a growing conception among practicing physicians in
cardiovascular medicine that bedside physical examination is unnecessary and does
not provide useful information. It should be emphasized, however, that for proper
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application and interpretation of various new and old tests that are available for
cardiovascular evaluation in a given patient. Bedside clinical examination should be
performed and practiced in the same way following similar sequences.
Preparing the patient
The heart examination should be made as easy as possible for the patient, who
usually expects it to be a relatively distasteful experience. If the physician is
considerate and gentle, the patient should feel when it is all over, that most of his or
her fears on that score were unfounded. The ideal examining room is private, warm
enough to avoid chilling, and free from distracting noise and sources of interruption.
Adequate (preferably fluorescent or natural) light is essential. The examining table
may be placed with its head against the wall, but both sides (particularly the right) and
the foot should be accessible to the examiner. And the results should be recorded
carefully.
Inspection
1. Observe precordium
Inspection of the precordium should begin at the foot of the bed. The subject
should be supine with the legs horizontal and the head and trunk elevated to
approximately 15-30 degrees. Asymmetry of the thoracic cage due to a convex
bulging of the precordim suggests the presence of heart disease since childhood, such
as congenital heart disease and rheumatic heart disease, with skeletal molding to
accommodate cardiac enlargement. In the adult, precordial bulge may be produced
from the massive pericardial effusion.
2. Apical impulse
The apical impulse is occurring early in systole. In adults the apical impulse
normally is located in the left fifth intercostal space, either at or medial to the mvl
and about 2-2.5 cm diameter, it serves the examiner as a marker for the onset of
cardiac contraction.
Displacement of the apical impulse:
a) Heart disease:
Some heart diseases cause the left ventricular hypertropy dilatation or both, the
apical impulse is displaced laterally and inferiorly and sustained, and it may be
shifted to the left and upward in right ventricular hypertrophy, dilatation or both. It
can be found at the right fifth intercostal space in dixtrocardiac and can not be
found in massive pericardial effusion.
b) Thoracic disease: pneumothorax and pleural effusion will displace the apical
impulse to the normal side. Pleuraladhesion and ateleotasis will result in a
displacement of impulse toward the diseased side.
c) Abdominal disease: The apical impulse also can be displaced by large mass,
massive ascites.
d) The apical impulse may have increased amplitued and duration in those persons
with a thin chest, anemia, fever, hyperthyroidism and anxiety. The examiner
should always observe the shape and contour of patint’s chest. Depressions of the
sternum, Kyphosis of dorsal spine, scoliosis often alter the shape and position of
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the apical impulse.
Abnormal pulsations in the other areas.
a) Right vertricular hypertophy (RBH). The impulse is clearly seen in left third
fourth intercostal space.
b) Pulmonary emphysema with RVH, usually the pulsation can be found inferior
the xiphoid process.
c) In asending or arch aortic aneurysm, one may detect abnormal pulsations in
aortic area, with bulging or pulsation in systole.
d) Pulmonary hypertension with dilatation the pulsation in systole may be detected
in left second intercostal space to the edge of sternum.
palpation
Usually inspection and palpation are discussed together because there is an
intimate relationship between these two processes in the heart examination. Palpation
not only confirms the results in inspection, but also discovers diagnostic signs.
Through careful palpation, the examiner should aim to determine the location and size
of the cardiac apex impulse, characterize its contour, and identify any abnormal
precordial pulsations. The palm of the hand, ventral surface of the proximal
metacarpals, and fingers should all be used for palpation because each is useful for
optimal appreciation of certain movements.
1) Usage of the palpation confirms the precordial pulsation’s location. Amplitude,
duration and intensity. In left ventricular hypertrophy (LVH) the impulses are very
forceful, sustained throughout systole and has a great amplitude. The apical
impulse may have decreased amplitude and duration in those patients with
myocarditis. In massive pericardial effusion the impulse cannot be palpable.
2) Thrills are actually palpable fine vibrations, most commonly produced by blood
from one chamber of the heart to another through a restricted or narrowed orifice, it
may occur in systole, diastole, presystole and at times may be continuous. Any
thrill should be described as to its location, its time in cardiac cycle, and its mode
of extension or transmission. The intensity of the thrill varies according to the
velocity of the blood, the degree of narrowing of the orifice and which it is
produced and difference in pressure between the two chambers of the heart. Quality
of a thrill depends on the frequency of vibration producing it, rapid vibrations result
in fine thrills whereas slower vibrations produce coarser thrill.
3) Pericardial friction rub is a to-and-fro grating sensation, which is usually present
during both phases of cardiac cycle, often rubs are more readily palpated with the
patient sitting erect and leaning forward during the end period of deep inspiration.
The rub is caused by a fibrinous pericarditis. In the presence of pericardial effusion
the rub will usually disappear because of the separation of visceral and parietal
layers by the accumulated fluid.
Percussion
The chest is percussed to confirm the cardiac borders, size contour and position
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in the thorax, patient should lie supine on an examining table or sit on the chair, with
the physician at his right side. Usually we employ indirect percussion for percussing
heart borders. It is outlined by percussing in the 5th, 4th, 3rd and 2nd interspace on the
left sequentially, starting near the axilla and moving medially until cardiac dullness is
encountered. The beginner should mark with a skin pencil where the note changes.
The distance from left midsternal line to the left border should be measured and
recorded, measurement should be made along a straight line paralleled to the
transverse diameter in the thorax.
1) The heart borders
(1) The base of the heart, formed by both atria, corresponds to a line crossing the
sternum obliquely, from the lower border of the second left costal cartilage, at a
point just to the left of its juction with the sternum, to upper border of the third
right costal cartilage, at a point 2 cm lateral to its sternal junction.
(2) The right border of the heart: It confirms with a curved line with its convexity
toward the right, extending from the upper border of the third right costal cartilage
2 cm lateral to its junction with the sternum, to the sixth right chondrosternal
articulation.
(3) The left border of heart. It is formed by the left ventricle and the atrium and is
represented by a curved line with its convexity directed upward and toward the
left, extending from the 5th left interspace 1.5 cm medial to the Mvl, to the
lowerborder of the second left costal cartilage 1-2 cm, to the left of its articulation
with the sternum.
(4) The inferior border: It is formed by the RV and a lesser extent by the L V, is
represented by a line drawn from the 5th chondrosternal articulation to the site of
the cardiac impulse in the left 5th intercostal space 1-2 cm to the M. V. I.
2) Normal relative dullness of the heart
Right
Intercostal space
Left (cm)
2-3
II
2-3
2-3
III
3.5-4.5
3-4
IV
5-6 (cm)
V
7-9
In normal person the distance from the 5th to the midsternal line is about 7-9 cm.
3) Changing cardiac dullness
Heart disease
Left ventricular enlargement, the cardiac dullness will be extended to the left and
downward, the heat silhouette is like a shoe. It is frequently seen in aortic
regurgitation and called aortic heart.
Right ventrucular enlargement, the cardiac dullness will extended to left and upward.
The right ventricular is severely enlarged the right border of the hert will extended to
the right.
Left atrium and pulmonary dilatation
Both the left artrium and pulmonary artery enlarged, the pulmonary artery will be
exaggerated to leftward. The cardiac silhoutte is like a pear and called mitral heart,
it is frequentlyseen in mitral valve stenosis. Aortic dilation, aneurysm of aorta,
pericardial effusion, all those diseases may cause the base border of heart
enlargement, so that the base border of the heart will be widened.
Congestive heart failure, myocarditis, myocardiopathy and pericardial effusion
may cause the heart silhouette extending both to right and left. Especially in presence
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of pericardial effusion, percussion at times may be helpful in outlinging the changing
cardiac silhouette resulting from a change in the patient’s position.
AUSCULTATION OF THE HEART
The purpose of auscultation of the heart is to find the normal and abnormal
sounds of the heart. It plays a very important role in the diagnosis of heart disease. It
is a very interesting thing to master the auscultation, but it is difficult.
For a thorough examination, auscultation must be done with the patient in a
sitting, lying, and left lateral recumbent position, and change the position of patient in
order to detect some abnormal sounds and murmurs. while the patient roll onto his left
side, the murmur at the apex will be hear more clearly. Exercise is valuable for
increasing the intensity of faint murmurs. In auscultation, sometimes let the patient
holding the breath at the end of expiration, the murmur will be hear easier.
I. Auscultatory Valve Areas
Sounds produced by each valves of the heart may propagate to different area at
the pericardial area following the blood stream. At this area, one can hear the sound
clearest in auscultation. It is called “auscultatory valve area”. The auscultatory valve
area does not correspond with the anatomic location of the valve themselves.
l. Mitral valve area: it is at the apex, in the fifth left intercostal space, medial to
the midclavicular line.
2. Aortic valve area: there are two auscultatory area of AV, one is located in the
second right intercostal space, just lateral to the sternum. The other is at the third or
fouth intercostal space, left to the sternum border. We call it the second auscultatory
area of AV.
3. Pulmonary valve area: in the second intercostal space just lateral to the sternum.
;
4. Tricuspid valve area: at the lower part of the sternal near the xiphoid.
.
The physician should adopt a systematic way of listening: start at the apex, then
move to the PV area , AV area, second AV area, TV area. Beside, according the
clinical feature, the other part of pericardium, neck, axilla, and back may be
examined.
Ⅱ. The Content of Auscultation
It includes rate, rhythm, heart sound, murmur and pericardial friction sound.
1. Heart rate: It means how many beats per minute. It normally varies with age,
sex, physical activity and emotional status.
In normal adults: 60-80/min
Sinus tachycardia : >1OObeats/min in adults;
Sinus bradycardia : <=60 beats/min in adults.
2.Heart rhythm: It is regular in Normal adults, but young adult and children
may sinus arrhythmia. The most common arrhythmias in clinical practice are:
100
premature beat (extrasystole) and atrial fibrillation.
Premature beat is a sudden extrasystole of the heart in the basis of normal heart
rhythm ,and followed by a longer compensatory pause.
The characteristic auscultation of extrasystole is:
(l) The intensity of S1 is increased;
(2) The intensity of S2 is decreased or even disappeared;
(3) The peripheral arterial pulse is absent.
Atrial fibrillation: It is the common arrhythmia in clinical. It is caused by a very
high frequency impulse coming from the atrial ectopic point or caused by the circus
movement of the ectopic impulse. The clinical auscultatory characters are “three
inconsistence”;
(1) The ventricular rhythm has absolutely no regularity;
(2) The intensity of S1 is inconsistence;
(3) The rate of heart and pulse are unconcerned.
3. Heart sound
A. Normal heart sounds
In most of normal individuals there are four heart sounds. The first and second
sounds can be heard with ease in normal subjects. However, the third sound only can
be heard in young person and children. The fourth sound is frequently inaudiable.
The producing mechanism of heart sound
1) S1: Although several cardiac events play a part in the production of the S1 ,
the vibration of the closure of the atrioventricular valves is the most important and
accounts for most of the sounds that are heard. The S1 indicates the beginning of the
ventricular contraction. Phonocardiographic analysis shows four components in the S1,
which have been related to the various events occuring at the onset of systole:
(a) Development of tension in the ventricular musculature;
(b) Closure of the Atrioventricular valves;
(c) Opening of the semilunar valves and the onset of ventricular ejection;
(d) Acceleration of the blood in the arteries during maximum ejection.
Often some residual vibrations of auricular origin occur at the very beginning of
the S1.Normally, only the components due to the closure of the AV valves and the
opening of the similar valves are heard, but the either components may be heard under
abnormal circumstance.
S1 can be heard at any part of pericardium, loudest at apex, lower in pitch than
those of the S2,with 55-58 Hz in frequency, last about 0.1 second, longer than those
of the S2.
2) S2: The second heart sound is mainly produced by the vibration of the
closure of the semilunar valves during the beginning of the ventricular diastole. It is a
composite sound result from closure of both the aortic and pulmonary valves. The
vibration of the relax of ventricular muscle in diastole, the moving of blood flow
within the great vessels, the opening of MV and TV, are taken part in the formation of
S2. The exist of S2 is an indicator of the beginning of ventricular diastole. It can be
heard at any part of pericardium and loudest at the basic. The S2 is high in frequency
and shorter in lasting duration than the S1 It has a snapping-like tone.
101
3) S3: The third heart sound is heard in most children and some adults. It occurs
in early diastole approximately 0.12-0.18 second after the S1. Being lower in both
frequency and intensity. It occurs during the phase of early diastolic filling, the blood
moves into ventricle rapidly from atrium, produces the vibrating of ventricle wall.
Usually it is heard clearly at the apex or superinternal of the apex.
4) S4: The fourth heart sound occurs late in diastole or just prior to the S1 about
0.l second , produced in the ventricle during the ventricular filling associated with an
effective atrial contraction. It is also low in frequency and intensity and rarely heard
under normal conditions.
b. The differentiate between S1 and S2:
1) The S1 has a lower pitch, a longer lasting time. It is maximal in intensity at
the apex. The S2 has a higher pitch, a shorter lasting time. It is maximal in intensity at
the basic;
2) The duration between the S1 to S2 is shorter (has a shorter pause) than the
duration between the S2 to the S1 of next cardiac cycle (has a longer pause);
3) The S1 is synchronized with the apical pulse. and is mimic coincident to the
aortic artery pulse. The S2 is produced after the apical impulse.
B. Abnormal Heart Sounds
Change in loudness
1) Both the S1 and S2 are affected simultaneously: Both increased; both
decreased;
2) Change of S1:It depends on the myocardial contraction, the filling degree of
ventricle, the elastic and position of the valve.
S1 increased:
(1) In the situation of high fever, hyperthyroidism and ventricular hypertrophy,
(2) In MS
(3) In complete AV block
S1 decreased:
(1) It occurs in myocardial infarction;
(2) In mitral insufficiency;
(3) In aortic insufficiency.
In arrhythmia, the S1 at apex may be louder or weaker.
3) Change of the S2:It mainly depends on the pressure within the aorta and
pulmonary artery and the situation of semilunar valves.
(1) S2 Increased at aortic valve area :It is due to the pressure increased within
the aorta.
(2) S2 increased at pulmonary valve area: It is due to pulmonary hypertension.
(3) S2 decreased at aortic valve area: It is due to aortic pressure diminished.
(4) S2 decreased at pulmonary valve area: It is due to the pressure diminished
within the pulmonary artery.
b. Change of the quality of the heart sound
If the myocardial muscle is damaged severely, the heart sound like a pendular, it
is called pendular rhythm. If accompany with tachycardia, like the heart sound of
embryo, it is called embryocardia.
102
c. Splitting of heart sounds.
Splitting of S1 :It is due to the closure of MV and TV asynchronously, loudest
over the apex. It may occur in normal children and young person, and usually occur in
right bundle branch block.
Splitting of S2:It can be heard in following conditions.
(1) In normal person;
(2) In pathological situation: conditions that cause an over volume to empty or
delay of emptying time of one side of the heart will produce splitting of the S2.
(3) The influence of respiration: in inspiration, the pressure within the thorax is
decreased and the venous return to right heart is increased. The RV require a slightly
longer period to empty it itself, the PV closure does not occur until the ventricle has
emptied itself, so make the S2 splitting slightly in normal condition. In pathological
situation, if the splitting of S2 is due to the abnormal of right side of the heart,
inspiration will produce the S2 splitting more.
If the abnormal is within the left side of the heart, such as AS, the emptying
time of left ventricle is delayed. The order of valve closure may be reversed, the two
components then more closer together or may be single, this is referred to as
paradoxical splitting of S2.
(4) Fixed splitting of S2: in the usual case of ASD, the S2 over the PV area is
widely split, with little or no change in .the degree of splitting during either phase of
respiration. This is referred to as fixed splitting.
d. extra sounds:
The extra sounds in systolic period
1) Early systolic ejection sound:
In the presence of dilatation of the aorta or pulmonary artery, or in the
hypertension of aorta or pulmonary artery, it can be heard.
(1) Pulmonary early systolic ejection sound : It can be heard after S1 with a
high pitch sharp. They are best heard at the left side of the sternal border, in the 2-3
intercostal space. These sound are not transmit to the apex. It can be heard in obvious
pulmonary dilation and pure PS.
(2) Aortic early systolic ejection sounds: It appear after the S1, have the equal
quality of pulmonary artery early systolic click. They are heard over the base of heart
as well as at the apex.
2) Mid and late systolic click:It occurs in MVP. The redudent and floppy of the
tandae chordea can not control the mitral valve at annul level and prolapse into the LA
at late systolic period. In systolic period the pathological tandea chordea suddenly be
tight, produce vibration, so the click occurs. Sometime it may produce MI, so there is
SM after the click.The click usually occurs after the S1 close to the S2, best heard at
apex. The pitch is lower that in early systolic click.
The extra sounds in diastolic period:
1) Gallop
(l) Protodiastolic gallop rhythm:
It is termed S3 gallop orS3 gallop. It is the pathologic counterpart of the S3 and
occurs at the time of rapid diastolic ventricular filling.It is a brief low-pitched sound It
occurs at middle diastole at the end of rapid filling phase of diastole. In the early
diastole, the blood through into the ventricle from the atrium in failing myocardium,
103
the tension is poor, produce the vibration of the ventricular wall.. It reflexes that the
LV function is decreased.
(2) Presystolic gallop:
The extra sound in prespstolic gallop is pathological S4.It is termed as S4 gallop or
atrium gallop.It occurs in late diastole and is temporally related to atrial contraction .
It is due to the increasing contraction of atrium.It occurs precede the the S1. It is
low-pitched, best heard at the apex or 3-4 intercostal space, left to the sternal border.
(3) Summation gallop:
It is termed the middle diastolic gallop, produced by the overlapping of early
diastolic gallop and presystolic gallop while the heart rate is quite faster.
2) Opening snap of MV:
It occurs after the S2 in MS. This sound is brief in duration and high in pitch than
other gallop sounds. It is due to the vibration of the opening AV valve suddenly
stopped during the blood from LA into LV in early diastole of the ventricle. The
opening snap of the MV usually indicates a flexible valve, and its presence is, an
evidence that the valve is probably suitable for mitral commisurotomy operation.
3) Pericardial knock:
In the presence of constrictive pericarditis, at time an extra sound is heard in
diastole, occuring shortly after the second heart sound. This is reffered to as the
pericardial knock. It may be heard all over the precordium and loudest at the apex and
left side at lower part of the sternal. It is due to the constriction of the pericardial after
inflammation, the diastole of ventricle are eliminated at the ventricular rapid filling
phrase in early diastole, the ventricular diastole has to stop suddenly produces the
vibrate of ventricular wall.
Quadruple rhythm
In some pathological situation, when the presystolic gallop and protodiastolic
gallop both sounds are present, a quadruple rhythm results. The heart rate usually
increased , the presystolic gallop and protodiastolic gallop usually summate together,
this is the summation gallop.
In the therapy of pacemaker, there are some abnormal heart sounds, murmur
and extra sounds. The pacemaker sound is produced by the contraction of the local
intercostal muscle due to the leakage of the electric current stimulate the intercostal
nerves.
In the patients suffering from valvular disease, after the operation of valvular
replacement, the prosthetic valve as in mechanical valve, the abnormal heart sound
are produced by the crush of metal stent or metal annuls of the valve, such as the click
sounds.
Heart Murmurs
1. General considerations
l) Heart murmurs are an abnormal sound;
2) It should be differentiate from the heart sounds;
3) It has a very important clinical value.
2. Mechanism of production:
Mechanism of production:
Heart murmurs are abnormal sounds produced by vibrations within the heart
itself or in the walls of the large arteries. It usually caused by one of the following
mechanisms:
l). Increased velocity of blood flow though normal valves;
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2). Forward flow though narrowed or deformed valves;
3). Backward or regurgitant flow through incompetent valve;
4). Abnormal connection;
5). Vibration of loose structure within the heart;
6). Increase with diameter of a major vessels.
3.Characterized of murmurs:
1. Location: murmurs of valvular origin are usually best heard over their
respective auscultatory valve area.
2. Timing: murmurs are timed according to the phase of the cardiac cycle
during which they occur. There are three basic types of murmurs: systolic, diastolic
and continuous.
3. Quality: the quality of murmur depends on the frequency and intensity of the
sound wave, and related close to the pathology and hemodynamic changes of the heart.
We usually describe the SM as blowing, harsh or musical. About the DM, it may be
describe as blowing, sigh-like and rumbling. The CM are described as machine-like
and hum.
4.Radiation: some murmurs are transmitted with the direction of the
bloodstream by which they are produced, other murmurs are propagated from their
point of origin in many directions.
5.Intensity: the intensity of murmurs are related to several factors:
(1) the severity of abnormal;
(2) the velocity of blood flow;
(3) the pressure gradient of crossing valve.
The most widely used system (Levine and Harvey)for grading the intensity of
heart murmur is six-point scale: grade 1 murmur is barely audible and is often missed
on the first cardiac examination, grade 2 is usually readily heard and slightly louder
than grade 1, grade 3 and 4 are quite loud and grade 5 is even more pronounced, grade
6 may be heard with the stethoscope just removed from the chest wall.
.
A murmur that increases in intensity after its onset termed “crescends”. If it
decreases in intensity, it is referred to as “decrescends”. If the first portion of a
murmur is increases in character and the latter portion is decreased it is then referred
to as a “diamond-sharped” murmur.
6.Physiological maneuver : The examiner may intervene in several ways to
modify sounds and murmurs for the purpose of better recognition and differentiation.
Some of the most helpful maneuver are discussed below:
1.Change the body position: it may produces some heart sound or murmur
increase or decrease. The murmur of mitral stenosis is more evident in left
recumbent position. In sitting position, leaning forward, held respiration in the
end of deep expiration, is useful to the ausculation of aortic insufficiency murmur.
Prompt squatting from standing position or raising two legs at supine position
may increase venous return, therefor increase the strock volume and cardiac out
put, increase the murmur of MI and AI .The murmur of hypertrophic obstructive
cardiomyopathy is decreased in squatting and increased in standing position.
2.Respiration: respiration may change the output volume of left and right
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ventricle, then inflence the tensity of the murmur. During deep inspiration, the
pressure with in the thorax decreased, the venous return increases, the blood
volume of pulmonary circulation increases, therefore the output volume of right
side heart is large than those of left side heart and the heart has a clock wise
rotation along long axis ,the tricuspid valve closes to the chest wall more, produce
the murmur of TI,TS,PI increase in intensity. It is in the opposite way during
expiration.
3.Exercise: exercise increases heart rate, blood volume of circulation and blood
velosity, so the murmur due valvular stenosis will increase.
Ⅳ.The clinical value of murmur in each valve area of auscultation.
Heart murmur usually is a feature of the disease of cardiac or vessels. It may
appear in rare normal individuals. The abnormal which produce the murmur may
be organic, relative, and functional.we call it organic, relative, and function
murmur. The term “relative M” indicates the valves itself is not involved but the
supporting tissues of the valves are abnormal. It consist the dilation of the valve
annulus, the damage of chordae tendineae, the enlargement of cardiac chamber or
great vessels, and produce a relative stenosis or insufficiency of the orifice of the
valve. The functional M usually reveals in systolic period in part of healthy child
or young person or in the situation due to increasd flow across a normal valve.
(1) Systolic murmur
1) MV area: the murmur at apex is produced by mitral insufficiency. Its origin
and cause may be organic, relative or functional.
Organic MI most are due to rheumatic heart disease, MVP and dysfunction of
papilly muscule. It is a pansystolic M,overlap the S1,high-pitched, blowing in
charter, more harsh, louder than 3/6 degree in decresento type and frequently
radiate toward the left axilla. It is diminished in inspiration, increased in
expiration. It is best heard in left supine position.
Relative MI: It is due to the dilated LV. It is heard in hypertensive heart
disease,acute rheumatic fever, dilated cardiomyopathy and severe enemia.The M
is in soft charter and less in radiation.
Functional MI: the valve is normal but the blood flow is quite faster. It is heard in
high fever, enemia in middle degree, hyperthyroidism, usually is less than 2/6
degree, in soft charter, more local in area, does not radiateto other part. The M
will disappear when the cause producing faster velosity of the blood flow
disappeared. It is heard in part of the normal adult.
When valvular insufficiency exists, the ventricular pressure remains above atrial
pressure throughout systole. When the aortic and pulmonary valves close, the
ventricular pressure is still well above the atrial pressure, thus the murmur of Mi
is heard throughout systole and for a brief period following the S2.
2) AV area: it is heard in organic AS. The murmur is harsh in charicter,
cresendo-decresendo type, radiate toward the neck following the great vessels, usually
are accompanying with systolic thrill and S2 is diminished at AV area.It is also heard
in relative lesion of AV, such as dilation of aorta due aortic arteriosclerosis,
hypertensive heart disease.
3) PV area: it is an ejection murmur, most of them are functional.It can be
heard in part of normal children and young person. It is soft and weakness in
charter. This murmur may exist in relative stenosis of the orifice of pulmonary
artery, due to pulmonary artery dilation in pulmonary hypertension,such as ,MS,
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ASD.The organic murmur in this area are produced in congenital PS. It is louder
in intensity, harsh in quality, diamond-shaped, usually accompanying with
systolic thrill. The S2 decreased in this area.
4) TV area: The systolic murmur in this area indicates Ti, most are relative TI
due to dilate of right ventricle. It is a blowing SM, increased in inspiration. The
organic SM are very rare here. .
5) Other position: In VSD, a loud and harsh SM can be heard at third and fourth
intercostal space, left to the sternal border, usually are accompanying with systolic
thrill.
(2) Diastolic murmur:
1) MV area:
Most of them are produced by organic lesion of the valve. In rheumatic
MS,an mid-late rumbling diastolic murmur can be heard at the apex,
cresendo-sharped, in low-pitch. It is generally confirmed to a rather
small area, best hears in left recumbent position at the end of expiration,
usually are accumpanying with louded S1, OS of MV and diastolic thrill.
The DM of relative MS may occurs in AI.It is termed Austin Flint
murmur. Do not accompanying with louding S1 or OS.The
mechanism are the blood regurgitating from the aorta into LV
stricking the MV area up,produce relative stenosis of MS.
d.
2) AV area: The murmur begins immediately after the AV closure sound.It is
usually heard in rheumatic AI. The murmur are sigh-like, decresedo, may radiate to
the left side of the lower part of sternal. It is best heard at the aortic second area,
3) PV area: The diastolic murmur at this area, most are produced by relative Pi.
The Grahan Steell murmuris also a relative murmur.
4) TV area: It is rare in clinical.
(2) Continuous murmur: Murmurs which extend from systole into diastole are
called continuous murmur, such as in Patent Ductus Arteriosus. It is a
continunous murmuur, harsh in quality, mimic the sound of machine
rotating.It is best heard at second intercostalspace, left to the sternal border.
The murmuer begins after S1, middle pitch,cresendo type, recher peak
intensity at late systole, envelop the S2 and decreased at early-middle diastole,
produceing a large diamond sharp, persistent from systole to diastole, the peak
of diamond is at the top of S2. Continuous murmur can also be heard in
arterio-vein fistula.
Pericardial friction rub
The pericardial friction rub is produced by the rubbing on each other of the
parietal and visceral surfaces of the roughened pericardium during pericadiatis.
The sound is usually in both systolic and diastolic, with a to-and-fro character, but the
systolic component predominates, and sometime the sound is heard only during
systole. In general, the sound is harsh, resemble massage the ear using the finger. At
times, it is soft, it seems closer to the ear than the heart sounds. The rub is most
commonly heard at the third to fourth intercostal space left to the sternal border. It is
best heard in the sitting position leaning forward and held breath.The common cause
of pericardial friction rub is pericarditis(TB,non-spicific, rheumatic). It also can be
seen in acute myocardial infarction, uremia and SLE.
107
F. THE BLOOD VESSELS
ⅠPulse
The palpation of artery is an important step in the cardiovascular examination.
From here We can get data of the patient above the general condition, the function of
circulation, and some cardiovascular abnormalities. So it has an important value in the
clinical diagnosis.
The arterial pulse can be papated at any point where the arteeainst a firmer surface
usually bone.
l. First pay attention to the intensity and the beginning time of the radial A. and
compare the radial A. in both sides if it is equal or not.
2. The pulse intensity may not be equal between the upper and lower
extremitries.
3. Compare the pulse of artery of both lower extremtries at the relevant
position.
In examining the pulse, It Is important bear In mind the following points:
rate, rhythm, consistency, intensity, wave form and condition of the arterial wall.
a. rate
b. rhythm
c. tention: The tention of pulse depends on the level of the arterial systolic
pressure.
d. Intensity: The intensity depends on the arterial filling degree and the
resistance of peripheral vessels, it also depends on the cardiac output and pulse
pressure.
e. Wave form
The arterial pulse starts at the instant the valve opens and left ventricular ejection
begins. This results in an abrupt sharp rise in aortic pressure, since blood enters the
aorta much faster than it flows to the more distal arteries. During the systolic phase of
left ventricular ejection a large portion of the blood is temporarily stored in the
proximal aorta. Once the aortic pressure reaches a peak it begins to fall as ventricular
ejection slows, and blood continues its flow in the peripheral arteries. As the ventricle
relaxes there is a transient reversal of flow from the central arteries to the ventricle
and the aortic valve closes. The aortic pressure continues to decrease during diastole
as blood flow continues to the peripheral vessels.
The pulse wave is composed of an ascending limb, peak, and descending limb.
There is a small notch near the peak of the ascending limb and a similar notch on the
descending limb.
l. Water hammer pulse.
A strong bounding pulse with a tall rapid ascending limb and an equally rapid
decending limb .It is called a water-hammer or collapsing pulse.
2. Pulsus alternans.
Pulsus alternans is charterized by a regulary alternating pulse, in which every
other beat is weaker than the preceding beat. Actually, there is an alternating series of
high and low pulse waves caused by an alternating contractile force of the left
ventricle. Since the weak beats are but slightly weaker than the strong beats, this
arrhythmia may be overlooked unless the examiner is skilled or alerted to its
possibility. It is more likely to be detected when the patient is sitting or standing. It
must be distinguished from bigeminy.Consequently it is a valuable indication of left
ventricular failure .
3. Dicrotic pulse.
In dicrotic pulse there are two impulses that are palpable during diastole. It
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usually occurs in the presence of high fever and may be palpated in both the carotid
and peripheral arteries.
4. Paradoxical pulse.
Paradoxical pulse is charterized by a decrease in the amplitude or an actual
imperceptibility of the pulse that occure during the inspiratory phase of respiration.
This phenmenon is caused mainly by pooling of blood in the pulmonary circuit
during inspiration resulting from the expansion of the lungs and an increase in the
negative intrathoracic pressure. In turn this results in a decrease in the return of
blood to the left side of the heart, a decrease in left ventricular output, and thus a
decrease in arterial blood pressure. When the systolic blood pressure falls more
than 10 mm.Hg during inspiration the pulse is refferred to as paradoxical. The
most accurate means of identifying a sphygmomanometer, since it can be easily
overlooked while palpating the radial artery. The presence of a paradoxical pulse
should suggest the possibility of massive pericardial effusion, constrictive
pericarditis. f.Consistency of the arterial wall.
This is best accomplished by expressing the blood from a distal segment of
the radial artery that has been ocluded by digital pressure. The trun consistency of
this vessel can then be determined by means of palpation. Normally the wall of an
artery under these circumstances is soft and pliable. In arteriosclerosis the wall
offers more resistance to compression by the palpating finger, and the vessel may
be rolled easily between the examining digits. This is often referred to as a “pipe
stem” artery may be beaded in consistency and tortuous in its couse. In elderly
persons the examiner may actually visualize these snakelike pulsating arteries
under the skin of the arms and forearms.
2. Pistol-shot sound
3. Duroziez's sign.
4. Pathological sound: including systolic murmur and continuous murmur.
Measurement of Arterial Blood Pressure
For routine measurement, the patient may be either sitting or lying in the supine
position. The patient should have been resting for some time. Bare the arm and affix
on it the collapsed cuff smoothly, so the distal margin of the cuff is at least 3 cm
proximal to the antecubital fossa. The cuff is evenly and firmly wrapped about the
arm with the center of the inflatable portion over the brachial artery, place the
chestpiece of the stethoscope over the brachial A. at the antecubital fosse. The radial
pulse is palpeted and inflate the cuff to a pressure about 30 cm of mercury about the
point where the palpable pulse disappears. Open the valve slightly ,so the pressure
drops gradually(2 mm/second). From this point, observation may be made by either
auscultation or palpation. Press the bell of the sterhoscope hightly over the brachial A.
and note the pressure reading at which sounds first become audible, this reading is
taken as the systolic pressure. As the blood pressure cuff is further deflated, the
sounds undergo changes in intensity and quality. As the cuff pressure approaches
diastolic, the sounds often quite suddenly become dull and muffled and then cease.
The point of complete cessation of sounds is the best index of the diastolic pressure.
The systolic pressure is depended on the myocardial contractility and the
cardiac output. The diastolic pressure is depended on the resistance of peripheral
vessels. The cardiac output decreasing or the peripheral vesseular resistance
decreasing may produces the blood pressure drop.
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Under normal circumstances there is little or no significant difference in the blood
pressure in the two upper extremities. In certain instances-for example, aortic
aneurysm or obstruction of the innominate artery-there may be a significant
discrepancy in the blood pressure in the upper extremities.
Blood pressure is somewhat variable and depends on sex, race,and climatic conditions.
Some serious causes of low blood pressure(hypotension) include Addison’s disease,
acute myocardial infarction, hemorrhage, and shock. Among the causes of high blood
pressure(hypertension) are essential hypertension, chronic glomerulonephritis,
pheochromocytoma, renal artery stenosis, and coarctation of the aorta.
G. MAJOR SYMPTOM AND SIGN
OF COMMON DISEASE IN CIRULARORY SYSTEM
Mitral stenosis
Mitral stenosis(MS) results from recurrent rheumatic activity. During the course
of M.S., the flow of blood is damped from left atrium to left ventricle in diastole, left
ventricle filling is then decreased, and the left atrial pressure is increased, left atrium
is overfilled, causing dilatation and hypertrophy of it. The high atrial pressure induces
a dilatation and stasis of pulmonary vein and capillary. Then pulmonary artery
pressure increased gradually due to the increased pulmonary circulatory resistance
and pulmonary arterial sclerosis developed later on. The right ventricle is overloaded
and then the compensatory hypertrophy and dilatation occur. Right ventricular failure
may be present finally.
Symptoms
There is no symptom, or only a slight in a case of mild or moderate M.S. Major
symptoms (due to left atrial dysfunction)are as follows. Exertional dyspnea, cough,
hemoptysis and occasional paroxysmal nocturnal dyspnea.
Signs
Inspection: The so-called “Mitral Facies” May be present. The apical pulse may
extend to left side.
Palpation: diastolic thrill may be felt at apex.
Percussion: The cardiac dull area extend to left in early stage and later on to
right. A prominence of “cardiac waist” may be present, making the heart to form a pea
–shaped dullness.
Ausculation : A loud snappy first sound and a localized cresendo rumbling
diastolic murmur in the mid-late stage may be hear at apex, which can be clearer
when the patient in lying in left lateral position. The opening snap may be present.
The pulmonary second sound may be accentuated or splitting. Moist rales at the base
of lung may be appeared.
X - ray. The lung markings are increased. The heart shadow showed a
“ Mitralized contour”. Barium meal of esophagus may show an enlargement of the
left atrium which compresses the esophagus backwardly. Enlargement of right
ventricle may be present in late stage.
EKG: A broad p wave with a notch “Mitral P” and enlargement of right
ventricle may be present.
Echo: Double -spike of mitral anterior leaflet disappeared and flat curve may be
seen. Anterior and posterior leaflets move in same direction. Right ventricular
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enlargement may be seen in late stage.
Mitral Insufficiency (MI)
The main cause of MI is rheumatism, and MI may be produced by left
ventricular dilatation due to any cause. During left ventricular contraction the blood
regurgitates into the left atrium, so that the filling degree and pressure were
augmented for the left atrium and them the compensatory dilatation of left atrium
occurs. During the left ventricular diastole the left ventricle accepts more blood flow
from left atrium and from left ventricle regurgitate. Consequently, the left ventricle
bears blood volume so heavily during the left ventricular contraction that the
compensatory dilatation and hypertrophy of the left ventricle occur gradually.
Symptoms:
The patient has fatigue, palpitation in the early stage. If without heart failure,
the patient feels no symptom for a long time.
Signs:
Inspection: The apical beat is displaced to left and lower.
Palpation: The apical beat is heavy.
percussion, cardiac dullneus enlarged toleft, or right in late stage. Auscultation:
a grade Ⅲ or more pansystolic blowing murmur may be heard and transmitted to the
left axilla and supscapular region. The first heart sound was decreased and masked by
the murmurs. The pulmonary second heart sound was accentuated.
X-ray shows dilated left ventricle and left atrium and pulmonary congetion.
EKG shows left ventricular hypertrophy.
Aortic Atenosis
The valvular deformity in aortic stenosis may be the result of rheumatic fever but
also occur on the basis of a congenital defect or atherosclerosis. Calcific stenosis may
occur when the underlying pathologic condition is either rheumatic or sclerotic.
In aortic stenosis blood is forced under great pressure by the left ventricle
through a narrowed aortic valve into the aorta. The resistance of output the blood in
left ventricle is increased. The wall thickening of LV gatting high and high due to the
constraction of LV increased. The mean pressure of aorta is decreased, the blood flow
in coronary artery and periphelow artery is decreased.
The main symptom are palpation, fatigue,,angina, even syncope.
Signs: The apical impulse is increased,and displaced laterally.A systolic thrill
may palpable at the second intersapace lateralal to the sternal with a pulsus parvus..In
auscultatioin, there is a murmur , systolic in time, loud, harsh, and usually has a
crescendo-decrescendo charter. The murmur is ejection in nature, beginning shortly
after the first heart sound and ending just before the aortic component of the second
sound. The murmur is heard over the right second interspace lateral to the sternum
and radiated widely, frequently to the right side of the neck and especially to the apex.
The aortic component of the second sound is delayed in most cases and is absent in a
few. Consequently, there is either a single second heart sound, or a reversed splitting
of the second sound, the aortic component occurring after the pulmonary.
Aortic Insufficiency
Etiology: The cause of aortic insufficiency are rheumatic fever, the commonest,
and arteriosclerosis and infective endocarditis. Syphilis is a less common cause of A.I.
in our country now.
In aortic insufficiency, the left ventricle receives both blood from left atrium
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and aortic regurgitation, the augmentation of stroke volume leads to compensatory,
left ventricular dilatation and hypertrophy and relative M.I. The regurgitant jet from
aorta hits the anterior mitral leaflet and causes it moving toward left atrium during
diastole, result in relative mitral stenosis, Because the blood leaks to the left ventricle
in diastole, the diastolic pressure is decreased causing an increase in pulse pressure
and other signs of peripheral vessels due to A.I.
Symptom: The patient may be free symptom or only feels palpitation in the
early signs:
Signs:
Inspection: Patient looks pale, the apical impulse is diffuse and displaced
laterally or inferiorly.
Palpation: The apical impulse is displaced laterally and inferiorly, lifting
impulse may be felt.
Percussion: cardiac dullness is enlarged laterally and inferiorly. The “cardiac
waist” is decreased. The cardiac dullness shows a boot-shaped shadow.
Auscultation: First heart sound is decreased at apical area and the aortic second
heart sound decreased or disappeared. A blowing diastolic murmur is audible in the
aortic area or third intercostal space left to sternum and transmitted to apex. A soft
blowing systolic murmur at apex may be heard due to the relative mitral insufficiency.
If there is relative mitral stenosis, a rumbling murmur in early-mid diastole at
apex may be heard, it is called “Austin-Flint” murmur.
Peripheral varcular signs due to increased pulse pressure are as follow: (l)
Moving of head with each heart beat, i.e. Musset sign; (2)Carotid pulsation;
(3)Capillary pulsation; water hammer pulse; pistolshot sound; Duroziez dicrotic
murmur etc.
Pericardial Effusion
The commonest causes of pericardial effusion are inflammatory( tubercurosis or
purulent disorders)and noninflammetory ( Rheumatism, nephrosis). For a slight
effusion, there is no effect on heart and hemodynamics. If pericardial effusion
increased rapidly or gradually but massive, the elevated pressure of pericardial cavity
limit the dialate of the heart,influnce the blood flow retun from systemic venus to
the right ventricle, the ventricular filling and out put were reduced, produceing a
serious hymodynsmic changes.
Symptom:
The severity of symptom depends on the pericardial effusion volume and the
velosity of effusion producing.patients may complainpericardial compression,
dyspnea. If the effusion compresses the neighboring organs, cough, hiccup, dysphagia
may be present. In addition, there are inflammatory symptoms of fever, sweating,
fatigue and pericardial pain.
Signs:
Inspection: It is dyspnea in a sitting, leaning forwarl posture. The cardiac
impulse decreased or disappeared.
Palpation: Apical pulsation reduced or absent, with fast and small pulse,
paradoxlcal pulse may be present.
Percussion: Cardiac dullness is enlarged and almost coincide with posture.
Auscultation: A faint heart sound and sometimes pericardial friction rub may be
112
heard. Ewa's sign with dullness below the angel of left scapula as associated with the
increased vocal fremitus , broncbial breath. Elevated venous pressure, small pulse
pressure and positive hepatojugular reflex may be present.
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Chapter 5
Abdomen
1.Introduction
Advances in scientific medicine have, on occasion, threatened to displace the
history and physical examination in the evaluation of the patient. However, we
usually discover that technologic advances serve to make the physical examination
more rational and provide new understanding or objective documentation of
long-appreciated physical finding. New techniques for evaluation of the
intra-abdominal contents include many biochemical, isotopic, ultrasonic, and
angiographic methods. These advances, although improving our ability to detect,
document, and interpret physical finding, have not superseded the need for the
skills of the medical interview and physical examination. An orderly approach to
the examination of the abdomen will make possible the analysis of the symptoms
arising from the many organs of the digestive and genitourinary systems found in
this region.
Certain features of the abdominal examination differ from those of other areas.
Although most of the information acquired is obtained from palpation, there are
many exceptions. Palpation may be very difficult in the obese, very muscular, or
tense patient. For reasons to be described later, palpation is performed last. The
order of other techniques is also changed, but it must be recalled that the same basic
steps of inspection, percussion, palpation, and auscultation are used in this area as
in other areas.
Although a detailed analysis of abdominal pain is beyond the scope of this
chapter, a few common examples that demonstrate the variable usefulness of
different sources of information are worthy of note. The physical findings may be
entirely negative in the presence of peptic ulcer disease, whereas a typical history of
pain relieved by food will suggest the diagnosis. In the patient with jaundice, right
upper quadrant pain, and tenderness, the physical findings may not enable
distinction between obstructive jaundice or hepatitis, but the history may be
virtually diagnostic. Finally, when abdominal pain is referred from thoracic or
vertebral sources, neither history nor physical examination, confined to the
abdomen, will help unless integrated into the total clinical context.
2.Topographic anatomy
There have been several systems devised for dividing the abdomen into
topographic segments, but only the one in most general use will be described here.
Other systems may be found in any standard textbook of anatomy. Secting lines,
one extending vertically from the xiphoid to the symphysis pubis and the other
extending horizontally across the abdomen at the level of the umbilicus. This
divides the abdomen into the right upper, right lower, left upper, and left lower
quadrants. The term epigastrium, which is included here because of its frequent use
in clinical medicine, is composed of the medial halves of the right and left upper
quadrants. The student must know the structures located in each of these areas, the
most important of which are the following.
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Right upper quadrant






Liver
Gallbladder
Duodenum
Pancreas
Right kidney
Hepatic flexure of colon
Left





upper quadrant
Stomach
Spleen
Left kidney
Pancreas
Splenic flexure of colon
Right



lower quadrant
Cecum
Appendix
Right ovary and tube
Left lower quadrant
 Sigmoid colon
 Left ovary and tube
Midline
 Bladder
 Uterus
3.Position of patient
Before any attempt is made to examine the abdomen, care must be taken to see
that the patient is relaxed and in a proper position. With the attaint in a supine position,
the head should be elevated on a pillow and the arms should be placed across the
chest. The patient should be assured that no sudden manipulation or painful procedure
will be carried out.
Since the structures under investigation are separated from the examiner’s hand
by a rather thick abdominal wall, an adequate relaxation of the abdomen must be
obtained before satisfactory examination can be performed.
4.Physical Examination

INSPECTION
The examiner should resist the temptation to begin palpating the abdomen before
adequate inspection is carried out. This is an excellent opportunity for the experienced
clinician to make small talk to aid in the relaxation of the patient, or even to restate
briefly the digestive history to assure his own orientation to the examination. The
patient should be suitably draped with the skin exposed from sternum to pubis. There
115
should be adequate lighting and occasionally oblique illumination will reveal features
otherwise missed. The abdomen is observed first for general symmetry, visible masses,
and the status of nutrition. The skin normally is the same as that noted elsewhere in
the body. Silver striae (vertical, often, wrinkled, streaks) are frequently seen in the
lower quadrants of the abdomen following a large gain of weight or after pregnancy.
Tight, glistening skin is often associated with ascites and edema of the abdominal wall.
Exanthematous rashes and petechiae may be observed. The presence and location of
any surgical scars should also be noted at this time, as well as any obvious pulsation’s.
Frequently in slender patients, pulsation’s transmitted from the aorta may be seen in
the epigastrium. Such pulsation’s may also represent masses in contact with major
vessels or abnormalities of the vessels themselves.
Obvious asymmetry of contour may be an important finding. Lateral asymmetry
will be noted only if one remembers to examine from above as well as from the side.
The presence of masses or hernias may be suspected from this observation and
confirmed later by palpation. When observed from the side, the abdomen is usually
flat from xiphoid to symphysis pubis, or symmetrically protuberant or scaphoid,
depending on the nutritional status of the patient. The umbilicus is usually centrally
located in the abdominal contour. Supraumbilical fullness may represent a mass
originating in the upper abdominal structures, such as in the liver, pancreas, stomach,
or trans verse colon. Similarly, fullness in the lower abdomen may result from bladder
distention, pregnancy, or masses arising from the ovaries, uterus, or colon.
Generalized symmetrical abdominal fullness is a more frequent and often difficult
diagnostic problem. This fullness is usually caused by ascites (free fluid within the
abdomen), obesity, or distention of the bowel with trapped gas. The distinction usually
can be made from the history and related physical finding. Helpful information from
inspection include the overall nutritional status of the patient, bulging of the flanks
caused by fluid accumulation, and the appearance of the umbilicus. The umbilicus is
usually deeply inverted in obesity and flat or everted in long-standing ascites. When
abdominal distention is accompanied by visible peristaltic contractions, it is almost
diagnostic of intestinal obstruction. This finding is made more obvious when the
abdomen is viewed by cross illumination.
Next the examiner may note the presence of distended abdominal veins.
Prominence of these vessels indicates increased collateral circulation as a result of
obstruction in the portal venous system or in the vena cava and may coexist with
ascetics in the patient with cirrhosis. It is helpful to remember that the normal
direction of flow in these vessels is away from the umbilicus, that is, the upper
abdominal veins carry blood upward to the superior vena cava and the lower
abdominal veins drain downward to the inferior vena cava. The direction of blood
flow in these collateral veins is easily assessed by a simple maneuver. A segment of
vein in the epigastrium is emptied between two fingers to a distance of a few
centimeters. One then allows blood to refill the vein from one direction by removing
the rate of refilling. The same segment is again emptied and filling from the opposite
direction is estimated. Usually the rate of filling is obviously faster in one direction
than in the other, indicating the direction of flow in that portion of the collateral
venous system. The process is repeated in the hypogastrium and the direction of flow
in the lower abdominal veins is observed. In portal hypertension normal flow
direction is maintained. In contrast, obstruction of the vena Cava alters the flow
direction in these veins. In obstruction of the superior vena Cava, the flow direction in
the upper abdominal venous collaterals is reversed or downward. In the inferior vena
Cava obstruction the direction is reversed in the lower abdominal veins, and they will
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drain upward.
When portal hypertension is present or when there is other reason to suspect liver
disease, the examiner should make a careful inspection of the upper extremities, face,
neck, and chess for the presence of coetaneous enigmas (spider nevi), which are found
in association with liver disease. These may be distinguished from petechiae and other
lesions by the fact that they blanch, not only by pressure on the nevus but also by
gentle pressure over the central arteriole that feeds this clump of dilated blood vessels.
The abdomen is inspected for evidence of unusual pigmentation, such as jaundice.
Disorders accompanied by hyperpigmentation also may be more notable on inspection
of the skin of the abdomen, where changes caused by exposure of the skin to sunlight
are readily separated from those caused by generalized increase in pigment. The
tendency of these disorders to manifest increased pigmentation in areas of minor or
persistent trauma to the skin may be especially evident at the belt line. Other pigment
changes caused by intra-abdominal hemorrhage may be found. A bluish discoloration
of the umbilicus occasionally is seen after major intraperitoneal hemorrhage. A similar
discoloration of the flanks, in the absence of trauma, occasionally is seen following
the extravagation of blood from intra-abdominal organs into extraperitoneal sites, as
in hemorrbagic pancreatitis.
Finally, hair distribution should be noted. In the normal female, the pubic hair is
roughly triangular with the base above the symphysis, whereas in the male it is in the
shape of a diamond, often with hair continuing to the umbilicus. The distribution and
quantity of hair may be altered by chronic liver disease and various endocrine
abnormalities.
 PALPATION
The second step in the abdominal examination is palpation. This procedure is usually
the most important and often the most difficult to perform accurately. Proper
preparation of the patient and systematic application of the principles outlined will
result in a satisfactory examination. Several different kinds of information may be
obtained by palpation. One may elicit pain or discomfort upon abdominal pressure,
the nature of which may be of considerable value in arriving at a diagnosis. A related
finding is a change in the tone of the abdominal wall , often caused by intrabdominal
irritative processes. One also may detect masses or organ enlargement , findings that
ordinarily are of great importance in the evaluation of the patient.
Relaxation and positioning of the patient. During palpation the patient should
continue to lie supine with arms relaxed on the chest or at the sides. The examiner
should make certain that his hands are warm. He should assure the patient that he will
make an effort not to cause discomfort and follow up this assurance by avoiding at the
outset an area already described as painful. If the patient exhibits ticklishness, the
examiner should disregard it and try to continue. If this proves unsuccessful, it is
useful to have the patient place his own hand on his abdomen, since this never tickles.
The examiner may tentatively exert pressure on the abdomen through the patient’s
own hand, and gradually increase the pressure, while assuring the patient that the
examination will cause no discomfort. When the patient has relaxed, the examiner
again places his own hand on the abdomen and allows the patient to maintain contact
with his hand. This usually complete the relaxation of the ticklish patient, and the
examination proceeds as usual.
The examination is begun with gentle exploration of the abdominal wall with no
effort made to palpate deeply. The patient may be further relaxed by instructing him to
breathe slowly and deeply. As with inspection ,the initial step in palpation may be
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facilitated by distracting conversation or questions regarding the history. If the patient
remains tense or if the abdominal wall is very muscular ,better results may be
obtained by having the patient flex the thighs and knees.
It should be emphasized again that during the preliminary stages muscle
relaxation is the goal. At this time no attempt should be made either to elicit
discomfort or to palpate for a mass or enlarged viscous. By light palpation some
estimate may be made of the degree of muscle rigidity or resistance. If these are
present, the examiner should determine whether the abdominal wall exhibits
voluntary muscle.
Tightening or actual rigidity. Rigidity of the abdominal muscles is manifested by
increased tonus, which is reflex in nature and produced by irritative lesions involving
the peritoneum. This muscle spasm cannot be relaxed by voluntary effort. Voluntary
tensing of the muscles, on the other hand, is brought about through fear or
nervousness and is not necessarily associated with an intra-abdominal lesion. This
type of muscle tension can be overcome by roper technique, reassurance, and an effort
to relax on the part of the patient.
A maneuver occasionally useful for confirming that increased muscle tone is
caused by voluntary tension is to use the stethoscope for palpation. Having carried out
auscultation without exerting pressure, the examiner may reapply it to several areas of
the abdominal wall without comment. The patient does not associate the instrument
with pain or pressure and will not react to it with muscle guarding. The examiner
applies the head of the stethoscope lightly at first, then with increasing pressure. In
voluntary tension, one may apply considerable pressure in this way, often to find a
much more relaxed abdominal wall. On the other hand, true increased tone caused by
peritoneal irritation will be manifest by a response equal to that produced by manual
palpation.
During deep palpation in the midepigastrium, almost all patient will complain of
tenderness, which accompanies pressure on the abdominal aorta. It is well to reassure
the patient that this sensation is normal during deep palpation of this area.. In fact, if
the examiner is able to palpate the aorta and the patient does not experience some
discomfort, this would probably be abnormal.
Locating painful area. After relaxation is obtained, the examining hand is first
moved gently over the entire abdomen, and an estimate of the muscle tone in the
various quadrants is made. Following general palpation, an attempt should be made to
detect and localize any painful area within the abdomen. Two types of pain may be
elicited by palpation.
1. Visceral—This is pain that arises from an organic lesion or functional disturbance
within an abdominal viscus. For example, it is the type seen in an obstructive lesion of
the intestine in which there is a buildup of pressure and distention of the gut. This type
of pain has several characteristics: it is dull, poorly localized, and difficult for the
patient to characterize.
2. Somatic—This is similar to the distress noted in painful lesions of the skin. It is
sharp, bright, and well localized. It is sharp, bright, and well localized. It is not caused
primarily by involvement of the viscera; rather it indicates involvement of one of the
somatic structures, such as the parietal peritoneum or the abdominal wall itself. It
should be pointed out that an inflammatory process originating in a viscus will
produce visceral pain that may extend to involve the peritoneum. Inflammation of the
peritoneum would then result in somatic pain. This is best illustrated by appendicitis
in which the pain is at first poorly localized, dull, ill defined, and primarily midline
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(when it is entirely visceral in origin). Later, as the inflammation spreads to the
peritoneum, the pain becomes sharp, bright, and well localized in the right lower
quadrant over the involved region.
After a painful area is located, the examiner should determine whether the pain is
constant under the pressure of the examining hand or if it is transient, tending to
disappear even though pressure is continued over the area. Pain caused by
inflammation usually remains unchanged or increases as pressure is applied. Visceral
pain as the result of distention or contraction of a viscus tends to become less severe
while pressure is maintained.
Occasionally the examiner may have difficulty in distinguishing visceral pain
from that arising in somatic structures, such as the spine and abdominal wall. An
example of abdominal wall discomfort is seen in patients with fibrositis. These types
of pain may be differentiated by having the patient tense his abdominal muscles,
which may be accomplished by forcefully elevating his head while keeping his
shoulders flat on the table. Under these conditions increased tension of the abdominal
wall will accentuate the pain if it originates in somatic structures. On the other hand,
discomfort from intra-abdominal sources will be less severe with the abdomen tense
than when relaxed.
Rebound tenderness. When pain has been elicited, the examiner should test for
the phenomenon of rebound tenderness. This is found only when the peritoneum
overlying a diseased viscus becomes inflamed. Although it may be produced in
different ways, the most common is to press firmly over a region distant from the
tender area and then suddenly release the pressure. The patient will feel a sharp stab
of pain in the area of disease if true rebound tenderness is present. For example,
pressure applied in the right lower quadrant and then suddenly released will cause a
marked increase in pain over an area of diverticulitis in the left quadrant. Rebound
tenderness may also be elicited by having pressure over the tender area and having the
patient cough or strin. Marked tenderness to percussion in the area is usually seen in
this situation. This type of tenderness indicates widespread inflammation of the area
involved is small, and rebound tenderness may be elicited only over the most tender
area of the abdomen.
Palpation of organs and masses. The examiner should palpate for enlargement of
intra-abdominal organs, principally the spleen, liver, and kidneys. In examining for
splenic enlargement, the examiner should stand at the patient’s right side. His left
hand is placed over the patient’s left costovertebral angle, exerting pressure to move
the spleen anteriorly. At the same time his right hand is worked gently under the left
anterior costal margin. With the examiner’s hands stationary in this position, the
patient is instructed to take a deep breath. If there is significant enlargement of the
spleen, it will be palpated as a firm mass that slides out from under the ribs, bumping
against the finger of the examiner’s right hand. The spleen normally moves down with
inspiration. If splenic enlargement is suspected from previous percussion but cannot
be felt by the technique just described, the patient should then be rolled slightly
toward the right so that the spleen may fall anteriorly . The examining hands are again
placed as described and the procedure is repeated. Occasionally a spleen that cannot
be felt with the patient in the supine position may be palpated by this maneuver. When
the spleen can be felt, it must be considered abnormal, sine the normal spleen is not
palpable.
One must be careful to avoid missing a spleen so large that the edge is well
below the costal margin. Previous percussion of the left upper quadrant should
prevent this error. If the edge is not felt under the left costal margin but splenomegaly
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is suspected, the examiner should palpate more medially, than in the midaxillary line,
and finally explore the inferior portion of the left abdomen. A technique used in the
obese or heavily muscled patient is for the physician to move to the patient’s left side
and face the lower abdomen, while the patient rests the small of the back on his left
forearm. The examiner then may palpate with both hands over a large portion of the
left abdomen while the patient takes deep breaths.
Next, palpation for enlargement of the liver is performed. The right hand may
be held either parallel or perpendicular to the long axis of the patient. The fingers are
gently worked deep into the right upper quadrant. With the examiner’s fingers in place,
the patient is again requested to take a deep breath. Ordinarily the liver is not palpable,
although not infrequently the examiner may feel the edge of the normal live at or
slightly below the right costal margin. When the liver is palpated, a firm edge will
strike the fingers upon inspiration. When felt more than 1cm below the costal margin,
however, the organ should be considered abnormally large. An exception is a
congenitally large right lobe of the liver, which occasionally extends quite far into the
right flank. Another exception is seen in severe, chronic emphysema, in which the
diaphragms are depressed by the over expanded lung, displacing the liver below the
costal margin. In both instances, the total mass of the liver is within normal limits.
The findings on palpation should be predictable from the estimates made during
percussion. The character of the surface of the liver should be described. Not
infrequently large metastatic masses may be present and palpable in the liver . In
some persons with cirrhosis, the anterior surface of the liver will have a granular feel.
This is easily felt in the thin individual.The same precautions mentioned in the
examination of the spleen also apply to the palpation of the liver. In some conditions,
the left lobe is predominantly enlarged and palpation must include the epigastrium to
appreciate that portion of the liver. If percussion suggests massive enlargement, one
may need to explore a large area of the right abdomen to find the lower border of the
liver, which occasionally may extend below the level of the umbilicus or even to the
iliac crest. As in palpation of the spleen, it may be helpful to palpate from above using
the palmar aspects of both hands in an attempt to feel the liver through the obese or
very muscular wall.
Occasionally other normal structures may be felt in the abdomen. In thin
persons, the lower poles of the kidneys may be felt high in either flank by deep
palpation. The kidneys will descend with inspiration. A distended bladder may be
palpated in the suprapubic region. Often this is more readily detected by percussion.
Confirming that a mass is felt in the suprapubic region lower quadrant, it is easily
manipulated by the examining fingers, and the gas may be expressed into the colon.
By deep palpation in the left lower quadrant, the examiner may feel the sigmoid colon
as it rolls over the pelvic brim, where it is felt as a sausage-shaped mass that is freely
movable and frequently tender.
It should be emphasized that careful palpation of the vascular structures of the
abdomen has become an important part of the physical examination. In patients who
are thin or have some anterior curvature of the spine, the abdominal aorta is normally
felt as a soft pulsatile structure in the midepigastrium and extending down to the brim
of the pelvis. Tenderness is elicited from pressure on this structure. In older
individuals, aneurysms frequently occur in this vessel. These aneurysms are saclike
enlargements of a segment of a segment of the abdominal aorta, are felt as pulsatile
masses in the midportion of the abdomen, and are frequently associated with pain in
the abdomen. If a pulsating mass is noted, the examiner must first decide whether this
is a pulsation transmitted through an overlying structure from the aorta. If the aorta
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appears to be the site of the enlargement, then its width should be estimated.
Aneurysms may be multiple and involve not only the abdominal aorta but also the
internal iliac vessels. Consequently, if the examiner discovers a pulsatile mass in the
aorta, he also should palpate carefully in the region of the pelvic brim for other similar
lesions.
Under normal circumstances, the gallbladder cannot be palpated. However, in a
jaundiced patient, the right upper quadrant should always be carefully palpated for a
soft, cystic mass, approximately 6 to 8 cm in diameter , which appears to be attached
to the liver and moves with respiration. This is an exceedingly valuable sign in
differentiating jaundice caused by cancer of the head of the pancreas or the common
bile duct from that caused by gallstones. In the presence of tumor of the common bile
duct or head of the pancreas, the wall of the gallbladder is normal, and consequently
the organ is capable of distending to the point that it is palpable .On the other hand, if
the obstruction is caused by gallstones, the gallbladder wall is inflamed, and this
diseased organ is not capable of distention. Therefore, the gallbladder will not become
palpable.
Exceptions to this rule occur in nonjaundiced patients with inflammatory
gallbladder disease. Patients with gallstone obstruction of the cystic duct and
cholecystitis may develop hydropic distention of the infected gallbladder, which is
palpable as a tender right upper quadrant mass.The gallbladder may also become
transiently palpable early in the course of an attack of biliary colic, only to recede
with subsidence of the attack.
When one can palpate an abdominal mass that is not clearly an enlarged organ, it
should be characterized as to size , location ,consistency, contour, mobility , and
tenderness. Masses in the abdominal wall may be distinguished from those of visceral
origin by palpation during voluntary tensing of the muscles. When the patient lifts his
head from the examining table, abdominal wall masses will remain palpable and even
may become more evident as they are elevated by the tensed muscle. In contrast,
intra-abdominal masses will be more difficult to discern after the wall is tensed.
Finally, one should palpate the umbilicus for evidence of nodularity or a mass,
the presence of which implies peritoneal seeding from an intra-abdominal neoplasm.

PERCUSSION
Percussion of the abdomen is primarily used to establish the presence of distention,
tumors, fluid, and enlargement of solid viscera. Light percussion is preferable, since it
produces a clearer tone. It is well to establish an orderly procedure for percussion.
With the patient recumbent, the examiner should stand at the patient’s right side. First,
percuss down the lower left thoracic wall in the midamillary line. This should produce
a resonant note over the underlying lung in this area. Below the level of the left
hemidiaphragm there is normally a tympanitic note caused by the splenic flexure of
the colon. Any dullness extending above the ninth interspace in the left midaxillary
line should make the examiner suspicious that there is enlargement of a solid organ in
this area. This is most likely caused by the spleen, but occasionally may be mimicked
by enlargement of the kidney or by marked enlargement of the left lobe of the liver.
Consolidation of the left lower lobe of the lung or pleural effusion will invalidate this
observation.
In the presence of lesser degrees of splenomegaly, another technique for
processing the spleen has been of value. Following percussion in the left midaxillary
line, the procedure is repeated in the lowest intercostal space in the left anterior
axilary line. Normally the percussion note here also is resonant. Percussion is
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continued while the patient takes a deep breath. In the absence of splenic enlargement,
the percussion note should not change. With modest degrees of splenomegaly, the
lower pole of the spleen moves inferomedially and is brought forward during
inspiration. As it moves under the lowest intercostal space with inspiration, it will
produce a change in the percussion note from resonance to dullness.
Next, percussion of the liver should be performed in the right midaxillary and
midelavicular lines. The normal upper limit of liver dullness in the midaxillary line
varies from the fifth to the seventh interspace. Because of this variation, determination
of the actual extent of liver dullness is more reliable. This is done by percussion in the
right midelavicular line until the upper border is determined. One then percusses
downward over the liver until the lower border of liver dullness is found. The lower
border of liver dullness is at the costal margin. Dullness extending into the normally
tympanitic right upper quadrant indicates hepatic enlargement, a mass adjacent to the
liver, or downward displacement of the liver. Measurement of the actual extent of
liver dullness will help define these findings. The diameter may be checked by
repeating percussion during full inspiration and again during full expiration, which
should yield a range of about 2 to 4cm. Movement of both borders. The mean
diameter of liver dullness is about 10cm, with the normal upper limit being about
12cm. Since these values vary somewhat with the sex, height, and body build of the
patient, the overall size of the patient must be taken into account when using this
method. Since estimates of liver size vary somewhat with the force of percussion, the
student must learn that light percussion is most accurate.
The remainder of the normal abdomen is more or less tympanitic to percussion,
depending on the amount of gas in the intestine. After percussion of the liver and
spleen, one may percuss over any visible masses to determine whether they are dull
(as with tumor or fluid-filled spaces) or tympanitic (as with distended bowel).
Distention of the urinary bladder may yield an area of suprapubic dullness. If other
masses are detected by palpation later in the examination, percussion may help to
characterize them further.
The last thing to be noted on percussion is the presence or absence of free fluid
in the abdominal cavity (ascites). This may be detected by several maneuvers(1) fluid
wava, (2)shifting dullness , and (3) elbow-knee position.
Fluid wave. With patient lying on his back, the examiner’s left hand is placed
against the patient’s right flank. An assistant or the patient places the ulnar edge of
one hand lightly against the middle of the abdomen to prevent the transmission of any
wave through the tissues of the abdominal wall. The examiner’s right hand then
lightly taps the left flank of the patient. In the presence of a siguificant amount of
ascites, a wave will be transmitted through the fluid that will be felt against the
examiner’s left hand as a sharp impulse. This finding is present only when there is a
reasonably large amount of fluid.
Shifting dullness. When the patient with ascites lies on his back, the fluid will
migrate into the flanks, producing dullness laterally. At the same time the
midabdomen is tympanitic because of the underlying bowel. When dullness is found
in the flanks, a mark is made on the skin at the appropriate level. The patient is then
rolled onto his right side, and the percussion is aagain carried out toward each flank.
In the presence of ascites, the fluid will gravitate toward the midline and that the
bowel, which has been displaced upward by the fluid, results in a tympanitic note in
the upper flank. This is repeated after rolling the patient to his left side. By this means,
an estimate of the amount of free fluid can be made.
Elbow-knee position. The presence of small amounts of fluid may be readily
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detected by placing the patient in an elbowknee position and percussing from the
flanks toward the most dependent portion of the abdomen. Free fluid, if present, will
run from the pelvis into the most dependent area, which, if the patient is in the proper
position , is located in the periumbilical region. The finding of dullness in this area
indicates the presence of ascitic fluid. This technique is more sensitive for detecting
small amounts of fluid than are the previously described methods.

AUSCULTATION
The diaphragm of the stethoscope should be placed lightly against the abdominal
wall in order to avoid artifacts resulting from friction and compression of vessels.
First, one should listen to the sounds produced by intestinal peristalsis. These sounds
are difficult to describe and are best appreciated from the experience of listening to
the abdomen of many normal individuals. Also, this exercise permits understanding of
the normal wide variability of bowel sounds, which may be interpreted as evidence of
disease by the inexperienced examiner. The recording of “slightly hypoactive” bowel
sounds by the student usually represent an attempt to give significance to a normal
finding.
Two abnormalities of the bowel sounds are significant. The absence of any
sound or extremely weak and infrequent sounds heard after several minutes of
continuous auscultation ordinarily represent the immobile bowel of peritonitis or
paralytic ileum. In contrast, increased sounds with a characteristic loud, rushing,
high-pitched tinkling quality often occur in mechanical intestinal obstruction and may
be accompanied by waves of pain. The latter findings are caused by distention of the
bowel and increased peristaltic activity proximal to the site of the obstruction.
Another sound that is unrelated to peristalsis may be heard in the appropriate
setting and is known as a succession splash. In cases of pyloric obstruction, with
increased air and fluid in the stomach, this sound may be produced when the abdomen
is rocked from side to side with one hand. A similar sound may be heard over the
inferior sternum and epigastrium in the presence of a large hiatus hernia.
The most important physical finding indicating vascular disease is a bruit. A bruit
in the abdomen is a systolic sound created by turbulence in the flow of blood through
a partially occluded or diseased artery. One type of bruit is that which is heard over
the aorta and is produced by atherosclerotic plaques or an aneurysm. Partial occlusion
of other major abdominal arteries, either by congenital bands or by atherosclerotic
plaques, may be detected by auscultation. Examples of these types of lesions are
found in the celiac artery and superior mesenteric artery. Also, a bruit may be heard
over diseased renal arteries. To be of significance a bruit must be heard consistently in
the area if the patient is moved into various positions, and it must be heard with
extremely light pressure on the diaphragm of the stethoscope.
Other sources of bruits in the abdomen include vascular malformations of
congenital origin or those produced by distortion of vessels by tumor, cysts, or severe
inflammation. Rarely one may hear a bruit caused by an intra-abdominal
arteriovenous shunt. Adequate auscultatory practice of them must include listening in
the epigastrium, above and lateral to the umbilicus on both sides, and over the liver. It
is worth emphasizing that bruits often are soft and high pitched and require the same
intensity of concentration as that required for the detection of grade I cardiac murmurs.
Obviously, if the bowel sounds are very loud, significant bruits may be missed on
casual examination.
Another vascular sound that may be heard is that of a venous hum. This is
usually heard over the upper portion of the abdomen or liver and is associated with
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enlargement of the anastomotic veins most frequently associated with liver disease or
with portal or splenic vein thrombosis. Congenital abnormalities of the umbilical vein
will also produce this finding. This sound is softer than the arterial bruit and tends to
be a continuous humming sound rather than systolic in time.
Occasionally, friction rubs may be heard over parts of the abdomen. A definite
friction rub may be heard over the spleen in cases of inflammation of the spleen or
with splenic infarction. Friction rubs may also be heard over the liver and almost
always indicate either a primary or metastatic tumor to the liver. Since these sounds
are quite, soft and are associated with respiration, they must be separated from normal
breath sounds. Care must be taken to avoid sounds from the skin.
Major Symptoms and Signs of Common Abdominal Diseases
1.Gastric and Duodenal Ulcer
Gastric and duodenal ulcer is a common and chronic disease. Peptic ulcer is termed
depending on the aggressive action of hydrochloric acid and pepsin on the mucosa.
Peptic ulcer usually occurs in the stomach, pylorus, or duodenal bulb but also can
develop in the lower esophagus and upper jejunum after gastroenteroanastomosis.
Symptoms
The major symptom of peptic ulcer is chronic recurrent painful upper abdominal
disorder. The cause of ulcer pain may be due to: (1) increased acidity at the ulcer site
and the relief of pain to a decrease in luminal acidity. Pain threshold to the stimulation
of acid is decreased; (2) hypertension of mero-muscle; (3)stimulation of acid to ulcer
surface.
1. Upper abdominal pain has some characters as follows:
(1) location: The most common location of ulcer pain is left and epigastrium in
gastric ulcer, and right and epigastrium in duodenal ulcer.
(2) Property: The property of ulcer pain is usually persistent, dull, burning,
distending, or hungry sensation lasting for 1-2 hours or 3-4 hours.
(3) Periodic and seasonal change: In gastric ulcer episodes of ulcer pain usually
occur 1/2-2 hours after meals and disappear before next meal. On the contrary, in
duodenal ulcer the episodes of ulcer pain usually occur 3-4 hours after meals and
can be relieved by ingestion of food. Thus, the duodenal ulcer pain is also termed
empty pain.
The comose seasons of gastroduodenal ulcer are times between fall and winter, or
winter and spring, strongly associated with cold climate.
(4) chronic and recurrent episodes: The episodes of annual recurrences during
particular seasons may last weeks to months.
2. other accompanied symptoms
Acid regurgitation, belching, nausea, vomiting, anorexia, constipation, and weight
loss are often accompanied with ulcer pain.
Signs
The physical examination is usually not helpful in uncomplicated peptic ulcer
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disease. Epigastric tenderness is an insensitive and nonspecific finding and correlates
poorly with the presence of an active ulcer crater. Rarely, peptic ulcer is associated
with multisystem syndromes that may produce physical findings.
Complications
1. bleeding: Bleeding is the most common complication of peptic ulcer disease, and
peptic ulcer is the most common source of acute upper gastrointestinal bleeding.
Risk of bleeding is unrelated to duration of ulcer disease. Hemorrhage results from
erosion of the ulcer into a blood vessel. The most common sign of acute bleeding is
melena, with or without hematemesis. Major blood loss (1500ml) can result in
circular failure. The ulcer pain may be relieved after bleeding.
2. Perforation: An ulcer may penetrate the wall of the duodenal or stomach, resulting
in sudden, severe, constant abdominal pain that reaches maximal intensity rapidly.
The pain may quickly becomes generalized. Marked abdominal tenderness to
palpation and diffuse, boardlike rigidty of the abdominal wall musculature are
present. Hypotension and tachycardia usually occur owing to intraperitoneal fluid
loss. Patients with penetration into solid organs usually present with intractable
ulcer pain.
3. Obstruction: Gastric outlet obstruction is caused by edema, smooth muscle spasm,
fibrosis, or a combination of these processes. Obstruction delays gastric emptying
and commonly causes nausea, vomiting, epigastric fullness or bloating, anorexia,
early satiety, and a fear of eating. Epigastric pain is frequent and may be relieved
temporarily by vomiting. Vomiting is often copious and may contain undigested
food but usually no bile. Physical examination may reveal visible peristalsis in the
epigastrium, or a succussion splash over the stomach.
4. Cancer transformation: Cancer foci may be present in association with an ulcer,
especially gastric ulcer. Thus, all gastric ulcers must be suspected of having small
areas of malignancy even when the ulcer appears benign by radiography or
endoscopy. Biopsy and cytologic examination reveal the true nature of the lesion.
2.. Acute Peritonitis
Bacterial peritonitis most commonly results from perforation of an abdominal
viscus caused by trauma, obstruction, infarction, neoplasm, foreign bodies, or primary
inflammatory disease. It can be classified as:
1. generalized and localized peritonitis, based on the inflammation range.
2. Primary and secondary peritonitis, based on the source of disease.
3. Nonbacterial and infected peritonitis, base on the character of first stage of
inflammation.
Symptoms
Regardless of etiology, abdominal pain, nausea, vomiting, tachycardia, and fever
are usually present. The severity of these symptoms is related to the extent of
contamination: in generalized peritonitis, shock is often present and may be profund,
whereas signs and symptoms may be minimal if infection is localized.
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Signs
In severe cases, there may be exquisite, diffuse, direct, and rebound tenderness and
rigidity of the abdomen; bowel sounds are usually diminished or absent, and
distention may be present. Tachycardia or unexplained hypotension may herald
peritonitis in elderly patients or those receiving corticosteroids in whom the clinical
manifestations are masked or suppressed.
3．Liver Cirrhosis
Cirrhosis is an irreversible alteration of the liver architecture, consisting of hepatic
fibrosis and areas of nodular regeneration. So it is a pathological diagnosis. Identified
causes include viral hepatitis, alcoholic hepatitis, schistosomiasis, malnutrition,
chronic severe heart failure, and a fen drugs and toxins. Based on pathological
characters, it can be classified into several types as micronodular, macronodular,
mixed, and nodular undistinct.
Symptoms
Compensatory cirrhosis may remain clinically silent for many years and frequently
is discovered unexpectedly, often during the evaluation of an unrelated condition.
When the disease becomes clinically manifest, its symptoms are usually nonspecific
(malaise, lethergy) or related to portal hypertension and include ascites, splenomegaly,
hypersplenism, or bleeding esophageal varices. Fever, jundice, testicular atrophy and
gynnecomastia(men), menstrual irregularities (women), and muscle wasting are found
frequently.
Signs
The liver may be large or small and usually has a firm consistency. Spider
angiomas, palmar erythema, parotid enlargement, splenomegaly, and edema are found
frequently.
In discompensatory stage, presentation due to portal hypertension are very common as
follows:
1. ascites: It is the most notable clinical manifestation of liver cirrhosis.
2. Portal collateral circulation: The portal-systemic collaterals may be formed as:
(1)The veins that lie in the mucosa of the gastric fundus and esophagus are of
greatest clinical interest because, when dilated, they form gastric and esophageal
varices. (2)The remnant of the umbilical vein may also dilate. If flow through this
vessel becomes great enough, a loud venous hum may be audible over the path of
the umbilical vein. Dilated abdominal wall veins are common and are especially
prominent when the patient stands. (3) The hemorrhoidal veins may also act as
collaterals.
3. Splenomegaly and hypersplenism: Hypersplenism may lead to thrombocytopenia,
leukopenia, and/or anemia.
4．Acute Appendicitis
Acute appendicitis is termed as acute bacterial infection of appendix. It is the most
common disease in acute abdomen.
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Symptoms
Typically, the illness begins with vague abdominal discomfort followed by slight
nausea, anorexia, and indigestion. The pain is persistent and continuous but not severe.
Within several hours the pain shifts to the right lower quadrant, becoming localized
and causing discomfort on moving, walking, or coughing. The patient often has a
sense of being constipated.
Signs
Examination will show cough tenderness localized to the right lower quadrant.
There will be well-localized tenderness to one-finger palpation and possibly very
slight muscular rigidity. Rebound tenderness is classically referred to the same area.
Peristalsis is normal or slightly reduced. The temperature is only slightly elevated in
the absence of perforation. Poorly localized epigastric pain heralds the onset of
appendicitis in a retrocecal or retroileal appendix. At this point, the psoas sign may be
positive.
Perforation is a accompanied by more severe pain and higher fever than in
appendicitis. It is one of the complications of acute appendicitis, unusual for the
acutely inflamed appendix to perforate within the first 12 hours.
5．Intestinal Obstruction
Intestinal Obstruction is a common acute abdomen. It can be classified into 3 types
according to the causes:
1. mechanical obstruction: Clinically this condition is most common. The cause of it
may be adhesion, intussusception, strangulated hernia, et al.
2. dynamic obstruction: It can be further classified into paralytic and spastic
obstruction. The former is more common, as seen in acute generalized peritonitis or
after surgery.
3. Vascular obstruction: The cause usually is thrombosis in mesenteric vein,
resulting in intestinal ischemia.
Furthermore, intestinal obstruction can be classified into simple and strangulated
obstruction, complete and incomplete obstruction, or acute and chronic obstruction.
Symptoms
Deep, visceral, cramping pain is usually referred to the gastrium. Severe,
continuous abdominal pain suggests intestinal ischemia or peritonitis. The degree of
pain is much more severe in small intestinal obstruction than in large intestinal
obstruction. In the latter, vomiting is a late finding and may not occur at all if the
ileocecal valve prevents reflux. The onset and character of vomiting may indicate the
level of the lesion. Recurrent vomiting of bile-stained fluid is typical early sign of
proximal small bowel obstruction. Feculent vomiting is a late manifestation.
Constipation or obstipation is a universal feature of complete obstruction, although
the colon distal to obstruction may empty after the initial symptoms begin.
Constipation itself is hardly an absolute indicator of intestinal obstruction. However,
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obstipation (the absence of passage of both stool and flatus) strongly suggests
mechanical bowel obstruction if there is progressive painful abdominal distention or
repeated vomiting.
Signs
Painful aspects, breathless, tachycardia, and even shock may be present in patients
with bowel obstruction. The abdomen should be carefully inspected before palpation.
Signs may include tensely distended abdomen, visible peristalsis occurring in
advanced bowel obstruction, soft doughy fullness in early paralytic ileus or
mesenteric thrombosis, peristaltic rushes synchronous with colic, infrequent tinkly or
squeaky sounds, muscular tautness and rigidity, and tenderness.
Case and Problem Based Larning Approach
Ascites
Case history:
A 57-year-old female patient was admitted on Jan. 20th 2003 because of
“fatigue and anorexia for 2 months, abdominal swelling and oliguria for half a
month”. Two months ago, the patient began to feel fatigue, decreased tolerance of
physical activities and anorexia without any identifiable causes. She used to eat
100g rice every meal, but now she could only eat 50g. She also had low fever and
felt better after taking anti-cold medications.
Half a month ago, the patient began to feel abdominal swelling. Her pants’
waist belt became tight for her. Urine volume decreased to 500 ml everyday and
its color was dark. Then the patient went to the nearby district hospital and took
the abdominal ultrasound examination. The result showed she had liver cirrhosis,
splenomegaly, and large volume of ascites. The patient had acute hepatitis B 20
years ago. During the years after the acute infection, her liver function was
abnormal intermittently.
She had no habit of smoking or drinking alcohol. She was married and had one
son and one daughter. Her daughter and husband were both healthy. Her son had
hepatitis B infection. Her father died of primary hepatic cancer. Her mother is still
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alive.
Physical Examination: T: 37.5C, BP:16/10KPa, R:18/min, HR: 100/min.
Consciousness, hepatic face, mild jaundice of sclera, liver palm(+), spider
angioma on left neck, no palpation of lymph nodes, lung auscultation negative,
heart (-). Abdominal findings: obvious abdominal bulge (marked protuberance of
the abdomen), no distention of abdominal wall veins, soft, no pain, shifting
dullness(+), normal active intestinal sound, moderate edema of the lower limbs,
NS(-).
CLINICAL THINKING (Questions and Answers)
(1) According to the patient’s symptoms, physical signs and the findings of the
abdominal ultrasonography, we confirmed the diagnosis of ascites.
(2) Among the causes of ascites, liver cirrhosis accounts for 80% while other
causes such as cancer, heart failure, tuberculosis, renal disease and pancreatic
disease account for 20%. Because the patient had the history of hepatitis B
infection and the abdominal ultrasonography also suggested liver cirrhosis, the
cause for this patient’s ascites was most likely secondary to liver cirrhosis.
(3) To ascertain the cause of ascites is very important for the diagnosis and
treatment of ascites. Before we start the treatment, diagnostic paracentesis is
necessary. According to the analysis of ascites, including routine tests,
biochemical tests, and etiological tests, we could further verify the cause of ascites
and make differential diagnosis of simple ascites of liver cirrhosis and ascites of
cirrhosis.
CLINICAL COURSE
Blood
test
showed
WBC
2.3×109/L,
RBC
3.5×1012/L,Hb95g/L,
BPL45×109/L. Liver function test showed TB/CB 21/37μmol/L, A/G 32/49g/L,
ALT 75U/L, AST 94U/L. Serologic tests for hepatitis B showed HBsAg(+),
anti-HBe(+), anti- HBc(+), others(-). A diagnostic paracentesis was performed on
the day of admission and the analysis of the ascitic fluid was as follows.
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Routine tests showed the fluid was clear in appearance, an absolute RBC count
of 10/μL and a WBC count of 25/μL. Biochemical tests of the fluid showed
protein concentration of 5g/L，albumin concentration of 2g/L and specific gravity
of 1.010. Culture for bacteria showed negative result. Cytology study of the fluid
was also negative.
CLINICAL THINKING (Questions and Answers)
(4) The patient’s blood test showed that the blood counts were low. This is
consistent with the diagnosis of liver cirrhosis and hypersplenism. The patient’s
liver function test showed a reversed ratio of albumin to globulin, mild
hyperbilinemia and elevated transaminases. This is also consistent with the
decompensated stage of liver cirrhosis. Serologic tests in hepatitis B suggested
that the cause of liver cirrhosis was chronic hepatitis B infection. All the
laboratory tests further confirmed the diagnosis of liver cirrhosis.
(5) For this patient with ascites, the most valuable examination is paracentesis.
Let’s go over the standard in the differential diagnosis of ascites. According to the
traditional standard, ascitic fluid can be divided into exudate or transudate.
Transudate is characterized by clear appearance, protein concentration <25g/L,
gravity <1.018, cell count <100/μL and negative bacteria culture, whereas exudate
is
characterized
by
cloudy
appearance,
protein
concentration
>25g/L,
gravity >1.018, cell count >500/μL and often with positive bacterial culture.
Transudate is often caused by liver cirrhosis, heart failure and renal disease.
Exudate is more often caused by tumor, tuberculosis and pancreatic disease. The
transudate ascitic fluid could become exudate when spontaneous bacterial
peritonitis occurs. It is obvious that the analysis of this patient’s ascitic fluid
confirms its classification as transudate.
(6) Serum ascites albumin gradient [(SAAG) = (32-2)g/L =30g/L(>11g/L)] in this
patient indicated that the ascites was due to portal hypertension. Therefore, the
diagnosis of liver cirrhosis with ascites could be confirmed.
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Chapter 6
Genitalia, Anus, and Rectum
Inspection of the genitalia, anus, and rectum is one of the important parts of the
systemic physical examination, which should not be ignored. The correct inspection
can result in a high degree of accuracy in the diagnosis of abnormalities. However,
because of wide variation in the appearance of normal genitalia, the examiner must
rely on a careful history, inspection, and palpation to distinguish healthy, normal
structures from those that are malformed of diseased.
Male Genitalia
The male genitalia include penis, scrotum, epididymis and seminal vesicle. The
scrotum contains testes, epididymide, and spermatic cords. Inspection of the external
genitalia (penis and scrotum) is followed by inspection of the internal genitalia
(epididymis and seminal vesicle).
1.Penis
The normal size of penis in adult is about 7-10 cm, being conformed with 3 corpora
cavernosa. The engorgement of the corpora, producing elongation and rigidity, is
called erection. Various conditions that may alter this normal state of erection can be
detected by careful inspection and palpation of even a flaccid organ.
1).Pretuce
The normal foreskin should be soft and pliable without breaks in continuity. If it is
uncircumcised, it will be retracted and the urethral meatus can be found. At times
retraction of the foreskin is difficult, and this condition, called phimosis, may require
and incision to enable exposure of the glans penis. The causes of phimosis usually are
adhesions of the prepuce to the underlying glans penis, inflammation, and congenital
factors. When the foreskin is too long, but not infecting the exposure of the urethral
meatus, it is termed prepuce redundant. The latter and Phimosis may be the
pathogenic factors of penis infection or even cancer.
2).Glans penis and neck of penis
The glans penis and the neck of penis should be inspected throughly for its cdour,
engorgement, excreta, edema, and nodular lesion. Finding a raised, firm, single, at
times ulcerated lesion in the neck of penis may indicate chancre, which is important to
the diagnosis of primary syphilis.
3). Urethral meatus
Swelling, excreta, and ulceration in urethral meatus opening may be the
manifestation of urethritis infected by diplococcus gonorrhoeae or other organisms.
The stricture of urethral meatus may be due to inflammatory adhesion or congenital
deformation. Hypospadias can result in the ventral position of urethral meatus
opening.
4).Size and conformation of penis
The size and conformation of penis may reflect the function of gonades. Too small
in adult seen in patients with hypogonadism and too large in child seen in patients
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with proeotia are all abnormalities.
2.Scrotum
The scrotum is a musculocutaneous pouch that contains the testes, epididymides,
and spermatic cords. It functions as a thermal regulator, keeping the testes one to two
degrees cooler than normal body temperature. Its external appearance varies under
different circumstances. The scrotum and its contents can be palpated with the
patients in a standing or recumbent position.
1) Spermatic cord
Spermatic cord is a flaccid structure with strip form. It contains vasa deferent,
cremasteric muscle, arteries, veins, nerves of spermatic cord, and lymphatic vessels.
Two spermatic cords are seen in left and right scrotal sac, respectively. Tenderness and
swelling are seen in acute scrotitis, and beaded swelling in tuberculosis of spermatic
cord. Infection, acute, subacute, or chronic, may involve the spermatic cord
(funiculitis). Spermatocele and epididymal cysts are nontender, round masses palpable
along the epididymis or cord.
2) testis
Testis usually lies in the scrotum with its long axis in a vertical position. The
normal testis may vary in size, shape, and consistency. These parameters should be
examined carefully. Inflammation of the testis (orchitis) is rarely encountered in the
absence of epididymal infection. Enlargement of the cord, epididymis, and testis may
result from trauma. A tumor of the testis may appear as a painless, asymmetrically
enlarged, firm, heavy, and sometimes nodular scrotal mass. Edema and redness
seldom appear except as corollaries to inflammation and trauma.
3) Epididymides
Along the posterior border of the testis is a ridge of tissue, called the epididymis,
which is usually adherent and has about the same consistency as the testis itself.
Nodularity of either the upper or lower pole indicates the presence of chronic
infection or fibrosis. Epididymitis is the most common of all intrascrotal,
inflammatory lesions in the adult male. Acute infection of the eididymis produces a
firm, exquisitely tender enlargement of the entire epididymal body, swollen and
reddened scrotal wall. Gonorrheal infections should be considered when there is an
associated urethritis. In tuberculous epididymitis fistula may develop and the prostate,
seminal vesicles, and vasa deferent are usually beaded or nodular.
Other abnormalities of scrotum are described as follows:
(1) edema of scrotum: may be the result of systemic or localized diseases. It can
accompany chronic congestive heart failure, cirrhosis of the liver, and chronic
nephritis.
(2) scrotium elephantiasis: massive scrotal swelling (elephantiasis) caused by
lymphatic blockage with microfilaria occurs in tropical climates.
(3) Scrotal hernia: usually the condition of indirect inquinal hernia. The
manifestation is often the enlargement of unilateral or bilateral scrotums, and
descent to its normal scrotal position by cough or pushing.
(4) Effusion of tunica vaginalis: a common finding occurring in about 7.5% of all
males. Diagnosis is usually simple because the scrotum is thin, smooth, and elastic
and the cystic character of the hydrocele is easily appreciated on palpation. Light is
readily transilluminated through a hydrocele, which can differentiate the hydrocele
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of tunica vaginalis from hernia and tumor.
(5) Scroti eczema: the characteristic presentation is great exudates, thickening of
scrotal skin, small squama, erosion, and intractable itch.
3. prostate
A careful evaluation of the prostate is an essential part of any physical examination
in the male. The normal prostate in the adult is about the size and shape of a chestnut,
and the location of the prostate gland is such that its posterior surface comes into
close proximity with the rectum, so that it can be examined by touch when a finger is
introduced into the rectum. Digital examination can be made with the patient standing
beside the bed or examining table, leaning forward with hands on knees or lying on
the bed in a knee-chest position. The gloved examining finger should be well
lubricated and introduced gently into the anal orifice. Much more information can be
obtained by performing this examination gently and tactfully. The first part of the
urinary passage where it leaves the bladder channels directly through this gland in
such a way that the lining of the urethra at this point is comprised of the exposed inner
surface of the gland. This arrangement explains why enlargements of the prostate
gland tend to encroach upon the urethral channel and cause obstruction to normal flow
of urine. Enlargement of the prostate gland, and resulting interference with urination,
occurs in about one third of elderly men. But the enlargement may not by directly
proportional to degree of obstruction. The consistency of the prostatic tissue is usually
firm and rubbery but may vary from a very soft, fluctuant texture that suggests
prostatic abscess, soft carcinoma, or congestive prostatitis, to a stony hard nodularity
that may involve small areas or the entire gland, usually suggesting granulomatous
prostatitis, prostatic calculi, prostatic infarction, tuberculosis, or localized carcinoma.
If any secretions are produced by prostatic palpation or massage, a specimen should
be placed on a glass slide for microscopic examination to determine the presence of
bacteria as well as cellular elements.
4. seminal vesicle
The seminal vesicles extend up laterally from the prostatic base beneath the bladder
and usually are not palpable unless they are diseased. The abnomalities of the seminal
vesicles are usually produced secondarily from the prostate diseases.
Female genitalia
An abnormality in any one pelvic organ may easily produce signs, symptoms, or
abnormal findings in another. But it must be remembered that abnormalities of pelvic
organs, some of which are very serious, may be absolutely asymptomatic, so during
the pelvic examination the physician should take advantage of the opportunity to
incorporate any additional important details of the history. The patient should not
douche for at least 24 hours prior to the pelvic examination, and it is essential that the
patients bladder be emptied immediately prior to the pelvic examination. The
dorsolithotomy position is the most practical position, and the knee-chest position
may be used when the urethra or the anterior vaginal wall must be carefully inspected.
1.external genitalia
1) mons veneris
The mons veneris structure is part of vulva ahead of the public tubercle, richly
133
containing lipid tissue.
2) labia majora
The labia majora are usually plump and well formed, in elderly patients the skin of
the vulva is atrophic and in some instances, if this condition is exaggerated, it results
in shrinking and fibrosis. White, slightly raised plaques are seen commonly in this age
group.
3) labia minora
In the nonpapous individual, the labia minora lie together in the midline. If there is
relaxation or laceration of the perineal muscles, they gape and fall to either side.
4) clitoris
The size and development of the clitoris normally may be quite variable. True
enlargement of the organ is obvious and represents some type of masculinization.
Inflammatory conditions of the clitoris or its prepuce are uncommon but may appear
as cellulitis or abscesses.
5) vaginal vestibule
The tissue of the vestibule between the inner surfaces of the labia minora, of which
the clitoris forms the anterior boundary, is the most common site of the granulomatous
and ulcerative venereal lesions in younger women and of malignant changes in the
elderly. Within the vestibule, the skin is soft and much more delicate than that of the
labia majora. It is devoid of hair follicles but does contain sweat and sebaceous glands
that may become inflamed or cystic. The lesser vestibular glands and the periurethral
glands secrete mucus. These are often involved in acute and chronic gonorrhea, at
times they are infected by nonvenereal organisms.
2. internal genitalia
1) vagina
The vagina is a passage between internal and external genitalia. The hymen or
hymeneal remnants appear just inside the introitus. In the virgin this structure is quite
variable, both in its thickness and in its restriction of the opening of the vagina. It
normally will admit one finger. As the fingers are introduced into the vagina, any
firmness, induration, or tumefaction of the vaginal walls is noted.
2) uterus
The position, mobility, size, shape, and consistency of the uterus is palpated
bimanually. The vagenal fingers should first survey the anterior vaginal fornix. The
uterus in its usual position of anteflexion is palpable here. It is normally firm, and
softens and become easily compressible in early pregnancy. Irregular enlargement of
the uterine body is suggestive of fibroid tumors (leiomyomata). In approximately 20%
of women the uterus is normally retrodisplaced. The normal size of uterus in
nonpregnant adults is 7.54.52.5cm.
3) oviduct (tube)
Palpation of the tube, generally referred to as the uterine adnexa, is the most
difficult part of the pelvic examination. It should be stated that the normal tube is not
palpable. Acute tubal infection invariably involves the ovary.
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4) ovary
Palpation of the ovary is also very difficult. The ovary is about 431cm, in size
and normally is sensitive to pressure. It is best palpated by the vaginal fingers. It lies
deep in the pelvis above the lateral fornix of the vagina. Ovarian tumors may be cystic,
solid, or mixtures of both elements. Marked tenderness is a characteristic finding in
acute inflammatory change cause by tubo-ovarian infection.
Anus and rectum
The terminal gut is formed by rectum, anal canal and anus. Rectum is
approximately 12 to 15 cm in length and extends from the sigmoid colon to the anal
canal. The anal canal is approximately 2.5 to 4 cm long and the outlet of anal canal is
the anus. The anal verge is the junction between anal and perianal skin. The dentate
line is a true mucocutaneous junction located 1 to 1.5 cm above the anal verge. A 6- to
12-mm transitional zone exists above the dentate line, in which the squamous
epithelium of the anoderm becomes cuboidal and then columnar epithelium. The
columns of Morgagni are 8 to 14 mucosal folds located just above the dentate line that
are surrounded by anal crypts. The anorectal ring is 1 to 1.5 cm above the dentate line
and is the palpable upper border of the anal sphincter complex. The rectum is behind
the prostate in male and behind the uterus and vagina in female.
Most disorders affecting the anorectum can be diagnosed by history and physical
examination. Data shows the rectal carcinoma within 7 cm to anus accounts for 42.2%,
so examination of anus and rectum is essential to the diagnosis of early rectal
carcinoma. Doctors should explain the necessity of the examination to the patients
because the patients always feel uncomfortable or nervous during the examination.
1. Position
(1) the inverted knee-chest position.
This position can be used while examming the prostate.
(2) the left lateral lying position.
Patients can be examined while lying on their left side and it is always used in older
patients and female.
(3) the squatting position.
This position is always used to examine hemorrhoids and rectum polyp.
2. Inspection
The rectal examination begins with inspection of the perianal area for skin lesions.
Pay attention to the skin lesion, ulceration, abscess and so on. The inspection should
be made carefully for several abnormalities as follows:
 Atresia and stricture of anus: usually seen in congenital deformity.
 Trauma and infection of anus: usually causing scar and abscess.
 Anal fissure: representing denuded epithelium of the anal canal overlying the
internal sphincter. The characteristic presentation is pain and tenderness
because of the position below the mucocutaneous juncture.
135
 Hemorrhoids: The term hemorrhoids refers to a condition in which the veins
around the anus or lower rectum are swollen and inflamed. Hemorrhoids may
result from straining to move stool. Other contributing factors include
pregnancy, aging, chronic constipation or diarrhea, and anal intercourse.
Hemorrhoids are either inside the anus (internal) or under the skin around the
anus (external) or both of them (mixed). ①Internal hemorrhoids are a plexus of
superior hemorrhoidal veins above the mucocutaneous junction which are
covered by mucosa. ②External hemorrhoids occur below the mucocutaneous
junction in the tissues beneath the anal epithelium of the anal canal and the
skin of the perianal region. ③The mixed hemorrhoids have characters both of
internal and external hemorrhoids. Rectal bleeding, protrusion, mucoid
discharge may be found in hemorrhoids.
 Anorectal fistula: The concept of anorectal fistula is that the two openings
of perianal skin and rectum are connected by a hollow tract, usually due to
pyogenic infection or, less commonly, to granulomatous disease of the
intestine, to tuberculosis or to Crohn’s disease.
 Proctoptosis: also named hedrocele, with partial or whole extrophia of
rectal wall out of the anus.
3. Palpation
Digital rectal and anal examination is easy to carry out, and is important to
diagnosis. In addition to palpating for masses or conditions of the anal canal and
lower rectal segment, other structures such as the prostate, cervix, coccyx, and the
pubococygeus muscle may be felt. Sphincter tone, stenosis of the anal canal, and the
presence of blood on the examining finger should be noted. Using a well-lubricated
gloved finger, the examiner places the finger on the anus and, while applying gentle
pressure, asks that the patient bear down as if having a bowel movement. This
maneuver facilitates entry of the finger into the rectum. A normal rectal response
includes tightening of the anal sphincter around the finger. The examiner should
palpate circumferentially around the length of the fully inserted finger for masses.
Common abnormal changes
extensive tenderness: seen in anal fissure anal infection;
 tenderness with cystic feeling: seen in abscess:
 soft, smooth, elastic tumor: seen in proctopolypus;
 truly firm tumor: seen in rectal cancer;
 mucus or blood stain on examining finger: seen in inflammation or invasive
disease.
4. endoscopy
Endoscopic examination is usually anoscopic examination and proctosimoidoscopy.
Size, shape, position, bleeding, ulceration and other characters of lesions must be
inspected and noted carefully.
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Chapter 7
Spine and Extremities
SPINE
Diseases of spine often present with pain abnormalities of posture or configuration,
and limited activity.
Curvature of Spine
Physiologic curvature
Four curvatures including cervical, thoracic, lumbar and sacral vertebrae can be
seen in human when observe laterally, characterized as shape “S”. Lateral curvature
may not be inspected in normal people.
Pathological deformity
1. Kpphosis or gibbus
This condition usually occurs in thoraoispine. The causes as follows are common:
(1) rachitis:It is seen more in children.
(2) tuberculosis
(3) Rheumatoid spondylitis
(4) Osseous retrogrde degeneration
(5) Others: trauma, dysplasia, or spondylous osteochondritis.
2.
scoliosis
It is divided into three types as scoliosis of thoracic, lumber, and thoracolumbar
segment, based on the developing site; or it can be divided into posture and organic
scoliosis, based on the nature of the disease.
(1) posture scoliosis: The bending of this type is not fixed, especially on early stage.
It will be corrected by changing posture. The common causes are: (a) false posture
in maturity of child hood; (b) the unilateral lower extremity is much shorter than
the other side; (c) prolapse of intervertebral cartilages; (d) poliomyelitic sequelae.
(2) Organic scoliosis: The character of this condition is that it can not be corrected
by changing posture.
Activity of spine
Normal activity: The normal active ranges of cervical and lumbar vertebrae are as
follows:
Cervical vertebrae
Lumbar vertebrae
antexion
extension
45
45
45
35
left and right
lateral curvature
45,ana
30,ana
rotation
60
45
limited activity
The common causes of limited activity of cervical vertebrae are: (1)
cervicomuscular strain; (2)proliferative arthritis; (3) tuberculosis or cancer; (4)
fracture or trauma of cervical vertebrae.
The common causes of limited activity of lumbar vertebrae are: (1) strain of lumbar
muscles; (2) proliferative arthritis; (3) tuberculosis or cancer; (4) fracture or trauma of
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lumbar vertebrae; (5) prolapse of intervertebral cartilages.
Pressing and Percussive Pain
Pressing pain
The common causes are tuberculosis of spine, prolapse of intervertebral cartilages,
fracture, or trauma
Percussive pain
The inspecting methods include direct and indirect percussion. Positive of this sign
will indicate some diseases of spine as tuberculosis, fracture, or prolapse of
intervertebral cartilages. The percussive pain site usually hints the disease site.
Extremities and articulus
Examination of the extremities is conducted primarily by inspection and palpation.
The two methods will be considered together. Normally any two comparable
extremities are nearly symmetric. Asymmetry, when present, may be attributed to
atrophy, congenital defects, or traumatic deformities.
Extremities
Paramorphia
1. koilonychia: an abnormality seen in malnutrition, such as iron deficiency anemia.
2. Acropachy: In this condition the tips of the fingers are bulbous, resembling the ends
of drumsticks, and there is excessive curvature of the nails in all directions. The
presence of this clubbing finding should prompt a diligent search for disease, such
as:
(1) pulmonary diseases: lung cancer, lung abscess, bronchiectasis, and hypertrophic
pulmonary osteoasthropathy.
(2) Heart disease: congenital heart diseases, and myocarditis.
(3) Malnutrition: kwashiorkor, ulcerative colitis, liver cirrhosis, Crohn disease.
(4) Subclavicular: aneurism.
3. acromegaly: In acromegaly, the hands are large, the fingers broad, and the palms
wide. This is termed a spade hand.
4. Genua varus and valgus: The two conditions may be common in Glissons disease
and Kaschin-Becks disease.
5. Pes varus and pes valgus: commonly seen in congenital defects and central myelitis
sequela.
6. Fracture and abarticulation: These conditions can cause limited movements,
tenderness, and redden area.
7. Pes planus or flatfoot: It is a common deformity and is classified as first-, second-,
or third-degree, depending on the amount of relaxation in the plantar arch.
8. Muscle atrophy: Muscle atrophy may be unilateral or bilateral. Atrophy usually
follows lower motor neuron paralysis but may be caused by disuse resulting from
previous injury disease.
9. Varicose veins of lower extremities: Tortuous, dilated, and elongated superficial
veins are commonly encountered in adult patients, especially women. They are
referred to as varicose veins and may be accompanied, by varicose ulcers and
bronze pigmentation termed stasis dermatitis.
10. Edema: Edema is one of the most common causes of enlargement of the legs.
When edema is present, the tissues will pit (indent) if the examiner presses them
with his thumb. Edema may be limited to the feet or ankles or may extend to the
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knees or even the thighs. Bilateral edema in the lower extremities may result from
congestive heart failure, portal cirrhosis, nephritis, and pressure on the inferior vena
cava caused by ascites or an intra-abdominal tumor mass. Unilateral edema in the
lower extremities may result from varicose veins, thrombophlebitis (inflammation
of veins), lymphangitis, and enlargement of the regional lymph nodes compressing
the femoral veins. Patients who have a hemiplegia often develop edema of the
paralyzed leg as the result of stasis cause by disuse.
Unusual Movements and Abnormalities
unusual movements of the upper and lower extremities are in most instances
manifest by disturbances of gait, movement tremor, rest tremor, liver flap, and so on
(details in Chapter 9).
Articulus
Normally all the articuli will remain their special conformation and function well
unless they are disease. Any joint deformity should be described with regard to its
location, general appearance, range of movement, swelling, redness, warmth,
tenderness, and crepitation.
Paramorphia
1. wrist joints
Abnomalities of wrist joints are commonly seen in diseases as follows:
(1) tendovaginal synovitis: Soft and nodular changes with tenderness are present in
perijoint area. Usually this condition is caused by rheumatoid arthritis or
tuberculosis.
(2) Ganglion cyst: more common in dorsal or radialis lateral of the wrist joints. It is
often present as nonpainful apophysis.
(3) Tendovaginal fibrolipoma: more common in dorsal surface of the wrist joint. The
characteristic presentation is round, nonpainful, soft, movable masses.
(4) Others: parenchyma, fractures, or trauma in or near the wrist joint area, resulting
in deformity of the joints.
2. phalangeal joints
(1) fusiform joints: The fusiform deformity is a symmetrical change with redness, pain
in primary stage, and deformation, unusual movements in advanced stage. It is
often seen in rheumatoid arthritis.
(2) Claw hand: clawlike configuration of hands is often present in patients with
paralysis of ulnar and median nerves. This deformity is characterized by
hyperflexion of the phalangeal joints and metacarpal joints.
(3) Others: Senile arthritis is characterized by firm nodules in distant phalangeal
joints.
3. articulationes genu
Asymmmetry of the articulationes genu with redness, swelling, fever, tenderness,
and unusual movements are often due to inflammation by acute rhenmatic arthritis.
Effusion of cavum articulare can be diagnosed by palpation characteristically as
floating patella phenomenon.
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4. others
Rigdity, hypertrophia, or deformity of joints, and nodular tophi due to irregular
bony erosions caused by hyperuricaemia are present in gout. The most commonly
involved joints are the great toe, ankle, tarsus, and knee. In 40% it involves more than
one joint.
Movement Function
Movement range and tenderness should be detected during the active and passive
movement of each joint.
Normal Movement Range
(1) articulationes humeri: Flexion of this joint is about 90 with extension 45 ,
abduction 90, extorsion 30, and intorsion 80.
(2) Articulationes cubiti: The only movement forms are flexion and extension.
(3) Wrist joints: Extension of this joint is about 40, with flexion about 50-60,
abduction 15, and endoduction 30.
(4) Phalangeal joints: Every phalangeal joint can be extended straightly.
(5) Articulationes coxae: Regiones femoris anterior will cling to abdominal wall
when this joint is flexed. Otherwise, extension is about 30, with abduction 60,
endoduction 25, both extorsion and intorsion 45.
(6) Articulationes genu: Regiones femoris posterior will cling to gastrocnemius when
this joint is flexed. Extension movement can be made at 180.
(7) Articulationes talocruralis: Dorsiflexion of this joint is about 35, with
downflexion 45, and both extorsion and intorsion 35.
Unusual Movements
Pain, spasm of muscles, inflammation, adhesion, and diminished movement of
involved joints can be caused by diseases of joints, such as infection, gout, fracture,
trauma, or dislocation.
Training Manual For The Neurological Examination
The examination of the neurological system includes five main sections: General
Examination, Cranial Nerve Examination, Motor System Examination, Sensory
System Examination and Reflex Examination.
1.General Examination
It mainly checks the state of consciousness(see the detail in the chapter on
unconciousness)
2.Cranial Nerve Examination
It checks 12 cranial nerves in sequence.
2.1. Olfactory Nerve(Ⅰ)
In testing olfactory sense,one nostril is occluded while the patient sniffs an
unknown substance. Readily available and nonpungent materials such as soap,tabacco,
and coffee are used.
2.2 Optic Nerve(Ⅱ)
2.2.1 Cranial Nerve Ⅱ is the optic nerve. There are three main aspects to this nerve:
visual acuity, visual fields, and fundi opticus.
2.2.2 Check the visual acuity
When we check visual acuity,we are really checking the vision of the macula
lutea(the yellow spot).Usually we use the nearsighted test in neurology(each eye
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separately).The distance of the patient’s eye from the printed material should be about
30 cm.
 Decrease in vision
 The number of fingers
 The movement of the fingers
 The reaction to the light(if he can not ,the patient is considered to be
blind(total loss of vision)
2.2.3 Check the visual fields
A visial field is the maxium scope of vision when the patient is looking
straight ahead. In clinics we usually use gross testing to see if the patient’s visual
fields are within normal parameters. Normal visual fields are about 90 temporallly,60
nasally, 60 superiorly, and 70 inferiorly.
2.2.4 Check the optic fundi
The optic fundi should be examined with an ophthalmoscope.
 The presence of a sharp disc outline (abnormal: Swelling, edema of the optic
disc,optic atrophy)
 The presence of spontaneous pulsation of the veins on the disc.
2.3 Oculomotor Nerve(Ⅲ), Trochlear Nerve (Ⅳ) and Abaucens Nerve(Ⅵ)
2.3.1 Eye movements
Cranial Nerves Ⅲ,Ⅳ and Ⅵ supply the muscles of eye movement and are
tested as a unit. Eye movements are tested by having the patient’s eyes follow the
finger of the examiner while keeping his head stationary. Move the finger laterally
from side to side, vertically up and down, left up and down, right up and down when
lateral gaze is reached. Inspect for nystagmus and limitation in eye movement. Ask if
the patient has double vision.
Loss of function of Cranial Nerve Ⅲ results in:
 a dilated pupil
 external deviation of the eyeball
 ptosis of the upper lid
 double vision
 loss of light reflex and accommodation reflex
 limitation of the eye’s upward and downward movement
Loss of function of Cranial Nerve Ⅳ results in:
 weakness of internal rotation , gaze downward and inward
 double vision.
Loss of function of Cranial Nerve Ⅵ results in:
 the eye’s deviation inward ( lateral rectus muscle weakness)
 double vision
 The lateral movement of eyeball is decreased.
2.3.2 Pupillary size and reaction to light
The size of the pupils is compared with each other.The reaction to light is
tested by swinging the light beam from the patient’s side onto the pupil and watching
for pupillary constriction in the eye being tested(direct light reflex) and in the other
eye(consensual light reflex). Normally the pupils constrict quicklly both directly and
consensually.
2.3.3 Pupillary reaction to convergence and accommodation reflex
Ask the patient to look at your finger and bring your finger in from a distance
of 1 meter to within a few centimeters of he patient’s nose.The eyes should converge
and the pupils constrict in a normal person.
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2.4. Trigeminal Nerve(Ⅴ)
2.4.1 Trigeminal nerve is divided into three divisions:
 The first division, ophthalmic nerve, conducts sensation from the forehead and
eye.
 The second division, maxillary nerve, conducts sensation from the middle portion
of the face and nostrils.
 The third division, mandibular nerve, carries sensation from the lower jaw.
2.4.2 Check the sensation of touch and pain ,temperature in the face
Test each area supplied by the three divisions for sensitivity to light touch
(cotton), pain (pinprick) , cold and hot water ,comparing bilaterally.
2.4.3 Corneal reflex
The corneal reflex ,which is mediated through the ophthalmic division, is tested
by touching the cornea lightly with cotton twisted into a point.The cotton should be
introduced away from the direction of gaze to minimize blinking.Prompt patial or
completed closure of the eyelids bilaterally is the normal response.
2.4.4 Check muscle strength of masseter (motor fibers of trigeminal)
Masseter and temporalis muscle are tested by having the patient close his jaw
against resistance of the examiner’s hand placed against the chin with the patient
clenching his jaw or chewing. The Pterygoid muscles move the jaw forward and to the
contralateral side. In testing these muscles ,the patient moves his jaw to the
contralateral side and resists the examiner’s attempt to push it to the opposite side. In
pterygoid weakness, the opened jaw tends to deviate to the side of the weak muscles.
2.5 Facial Nerve(Ⅶ)
2.5.1 Check the movement of facial nerve
The moter portion of the seventh cranial nerve innervates all the facial muscles,
the platysma,and the stylohyoid. During the initial interview, the patient’s facial
movements have been observed and gross weakness such as inability to smile or close
the eyelids will be apparent.The frontalis muscle is tested by asking the patient to look
upward and to wrinkle his forehead.To test the orbicularis oculi, the patient closes his
eyes tightly and resists the attempt to try them open. The lower facial muscles are
tested by having the patient show his teeth, purse his lips, and blow the cheeks
out .The platysma is seen to contract when the patient makes a vigorous effort to show
his teeth.
Lesions of the corticobulbar tracts at any point above the facial nucleus will
produce contralateral lower facial weakness with sparing of the forehead movement
because of bilateral cortical representation of upper facial muscles.
In nuclear or peripheral seventh nerve lesions, the entire facial musculature on
the same side is weak.
2.5.2 Check the sense of taste
The sensory portion mediates taste from the anterior two-thirds of the tongue.The
sensation of taste is tested with sodium chloride(salty),sugar(sweet),quinine(bitter)
and vinegar (sour).The patient protrudes his tongue, which must be moist,and with a
wet applicator one of these substances is gently rubbed on one side of the tongue.The
patient is instructed not to withdraw the tongue until he identifies the substance as
sweet,sour, bitter, or salty.
2.6 Vestibulocochlear Nerve(Ⅷ)
Auditory acuity can be tested crudely by rubbing thumb and forefinger together
about 2 inches from each ear. If there are complaints of deafness or if the patient
cannot hear the finger rub, proceed to the following tests.
2.6.1 Rinne Test
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Hold the base of a lightly vibrating high-pitched (512Hz)tuning fork on the
mastoid process until the sound is no longer perceived, then bring the still vibrating
fork up close to the ear. Normally—or if the hearing loss is sensorineural—air
conduction is greater than bone conduction and the patient will again hear the tone. If
there is significant conductive loss, the patient will not be able to hear the
air-conducted tone longer than the bone-conducted tone.
2.6.2 Weber Test
Lightly strike a high-pitched(512Hz)tuning fork and place the handle on the
midline of the forehead.If there is conductive loss, the tone will sound louder in the
affected ear;if the loss is sensorineural, the tone will be louder in the unaffected ear.
2.6.3 Vestibular Funtion
Vestibular funtion needs to be tested only if there are complaints of dizziness or
vertigo or evidence of nystagmus.
2.7 Glossopharyngeal Nerve(Ⅸ), Vagus Nerve(Ⅹ)
Some useful tests for detectiion of deficiencies in motor funcuion of the
palate,pharynx, and larynx are described below.Sensory function needs to be checked
if one suspects cranial neuropathy or a brain stem lesion.
2.7.1 Palatal Elevation
Ask the patient to say "ah." Look for full and symmetric palatal elevation.If one
side is weak, it will fail to elevate and will be pulled toward the strong side.
2.7.2 Gag reflex (afferent Ⅸ,efferent Ⅹ)
Gently touch each side of the posterior pharyngeal wall with a cotton swab and
compare the vigor of the gag.
2.7.3 Sensory funtion
Lightly touch each side of the soft palate with the tip of a cotton swab.
2.7.4 Voice Quality
Listen for hoarseness or "breathness", suggesting laryngeal weakness.
2.8 Accessory Nerve(Ⅺ)
2.8.1 Sternocleicomastoied
Press a hand against the patient's jaw and have the patient rotate the head
against resistance. Pressing against the right jaw tests the left sternocleicomastoid and
vice versa.
2.8.2 Trapezius
Have the patient shrug shoulders against resistance and assess weakness.
2.9 Hypoglossal Nerve(Ⅻ)
The hypoglossal nerve supplies extrinsic and intrinsic muscles of the tongue.
Atrophy of one side of the tongue,fasciculations, and deviation of the protruded
tongue toward the atrophied side indicate a lesion of the hypoglossal nucleus or nerve.
Strength of the tongue
is estimated by the amount of force exerted as the tongue is
pressed laterally against a wooden blade.
3. Motor System Examination
This includes 6 aspects; myotrophy, involuntary movement, muscle tone, muscle
strength, coordination, gesture and gait.
3.1 Myotrophy
Observe the patient’s muscle size(atrophy or hypertrophy). If atrophy is present or
suspected, the circumference of limbs should be measured bilaterally; record the point
at which the measurement is taken.
3.2 Involuntary movement
Observe if there is any involuntary movement.
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


Resting tremor(4-6 per second)
Intention tremor
Choreic movements----irregular, spontaneous movements usually involving more
than one joint.
3.3 Muscle tone
Tone is defined as resistance of muscle to passive movement at a joint.Tone can be
decreased, normal, or increased. The hardest part of evaluating tone is getting the
patient to relax.Check muscle resistance to passive movement of the upper limbs and
the lower limbs by flexion and extention at the elbows,wrists, and shouldrs or at knees
and ankles.Palpate muscle tone.
3.4 Muscle Strength
Strength is measured by the ability to contract the muscle against force or gravity.
The classic grading system scores as follows:
 5,full strength;
 4,movement against gravity and resietance;
 3, movement against gravity only;
 2, movement only if gravity is elliminated;
 1, palpable contraction but little visible movement;
 0, no contraction.
Ask the patient to perform flexion and extension of every joint against resistance
given by examiner. Pay particular attention to the relative strength of the sides and the
differences between proximal and distal groups. Special attention shoud be paid to
any area that strength of dorsiflexion and plantar or the feet, extension and flexion of
the wrist and forearm, and abduction of the shoulders.
 Musculus triangularis strength
 Biceps strength
 Triceps strength
 Flexor carpi muscle and extensor carpi muscles strength
 Strength of the flexor muscle of the fingers
 Strength of the palmar intercoatales musculi
 Strength of the dorsal intercostales musculi
 Strength of the musculus iliopsoas
 Strength of the musculus quadriceps
 Strength of the musclus femoris posterior
 Strength of the musclus tibialis anterior
 Strength of the musclus gastrocnemius
 Strength of the musclus extensor hallux
 Strength of the musclus flexor hallux
3.5 Coordination
This examine cerebella function.
 Finger-to-nose test
 Rapid and repeated movement
 Alternating movement
 Heel-to-knee-to-shin
 Rebound test
 Romberg test
 Tandem gait test
3.6 Gait
Every patient must be observed standing and walking.Standing, starting to walk,
stopping, and turning should each be assessed and the associated movements of the
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limbs noted with each maneuver.
 Steppage Gait
 Cerebellar Gait
 Sensory-Ataxic Gait
 Hemiplegic Gait
 Paraplegic Gait
 Dystrophic Gait
 Parkinsonian Gait
 Apraxic Gait
 Antalgic Gait
 Choreic Gait
4. Sensory System
This can be divided into examination of superficial sensation, deep sensation and
combined sensation.Sensory testing is usually done with patient’s eyes closed.
Compare the sensation of the two sides and the differences between proximal and
distal areas.
4.1 Superficial sensation
 Examine pain sensation
The skin is usually touched in an irregular fashion either with the sharp end of the
pin or the dull head, and the patient responds with “sharp” or “dull.”
 Examine temperature sensation
For temperature testing, one test tube is filled with cold water ane another with
warm water.The patient responds with either “cold” or “warm”
 Examine sensation of touch
Light touch is tested by gently touching the skin with a wisp of cotton;the patient
responds with “Yes” or “No” whenever he feels the stimulus.
4.2 Deep Sensation
 Examine motion sensation
The patient’s ability to detect small passive movements is tested by holding a
finger or toe between the examiner’s fingers.The digit is moved up or down
irregularly and the patient responds with “up”,”down”,or “I don’t know”.
 Examine position sensation
 Examine vibration sensation
Placeing a tuning fork over bone mechanically intensifies the stimulus.Usually
the vibrating fork is placed over the sternum,elbows,fingers, iliac crest,knees, ankles,
and toes and determine whether the patient can feel the vibration.
4.3 Combined Sensation
 Two point distinction (discrimination):A pair of calipers or a compass with dull
points is used to test two-point discrimination.
 One point sensation of two opposite stimuli (Bilateral simultaneous stimulation)
 Stereognosis
5. Reflex System
Reflexes are graded as follows;
(-)
absence of the reflex
(+)
hypoactive without movement of the joint; may be normal or abnormal
(++)
physiological or normal
(+++) hyperactive without clonus, may be normal or abnormal
(++++) hyperactive with transient clonus
(+++++) markedly hyperactive with sustained clonus; it is pathological
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e.g. ankle clonus and patellar clonus
5.1. Deep Reflex
 Biceps reflex
C5,6
Musculocutaneous nerve
 Brachioradialis reflex
C5,6
Radial nerve
 Triceps reflex
C7,8
Radial nerve
 Quadriceps(Patellar reflex,knee jerk)
L3,4
Femoral nerve
 Achilles tendon reflex (ankle jerk)
S1,2
5.2. Superficial reflex
 Abdominal reflex
Upper abdomen
T8,9,10
Lower abdomen
T11,12
 Cremasteric reflex
L1,2
 Anal reflex
S3,4
5.3. Pathologic Reflex
 Hoffman reflex
 Babinski reflex
 Chaddock sign
 Gordon sign
5.4. Meningeal Stimulation Sign
 Neck rigidity
 Kernig sign
 Brudzinski sign
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PART IV
Laboratory Examination
Chapter 1
Electrocardiography
1.Basic Principles and Patterns
DEFINITION
An electrocardiogram (ECG) records cardiac electrical currents (voltages, potentials)
by means of metal electrodes placed on the surface of the body. These metal
electrodes are placed on the arms, legs, and chest wall (precordium).
BASIC CARDIAC ELECTROPHYSIOLOGY
Before discussing the basic ECG patterns, we will review some elementary aspects of
cardiac electrophysiology. Fortunately, only certain simple principles are required for
clinical interpretation of ECGs. In addition, it is worth mentioning now that no special
knowledge of electronics or electrophysiology is necessary despite the connotations of
the term “electrocardiography.”
In simplest terms the function of the heart is to contract and pump blood to the
lungs for oxygenation and then to pump this oxygenated blood into the general
(systemic) circulation, the signal for cardiac contraction is the spread of electrical
currents through the heart muscle. These currents are produced both by specialized
nervous conducting tissue within the heart and by the heart muscle itself. The ECG
records the currents produced by the heart muscle.
ELECTRICAL STIMULATION OF THE HEART
Normally the signal for cardiac electrical stimulation starts in the sinus node (also
called the sinoatrial or SA node). The sinus node is located in the right atrium near the
opening of the superior vena cava. It is a small collection of specialized cells capable
of spontaneously generating electrical stimuli (signals). From the sinus node, this
electrical stimulus spreads first through the right atrium and then into the left atrium.
In this way the sinus node functions as the normal pacemaker of the heart.
The first phase of cardiac activation consists of the electrical stimulation of the
right and left atria, electrical stimulation, in turn, signals the atria to contract and to
pomp blood simultaneously through the tricuspid and mitral valves into the right and
left ventricles respectively. The electrical stimulus then spreads to specialized
conduction tissues in the atrioventricular (AV) junction (which includes the AV node
and bundle of His) and then into the left and right bundle branches, which carry the
stimulus to the ventricular muscle cells.
The AV junction, which functions as an electrical “bridge” connecting the atria and
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ventricles, is located at the base of the interatrial septum and extends into the
ventricular septum. It has two subdivisions; the upper (proximal) part is the AV node.
(in older texts the terms “AV node” and “AV junction” are used synonymously.) the
lower (distal) segment of the AV junction is called the bundle of His, after the
physiologist who described it. The bundle of His then divides into two main branches;
the right bundle branch, which brings the electrical stimulus to the right ventricle, and
the left bundle branch, which brings the electrical stimulus to the left ventricle.
The electrical stimulus spreads simultaneously down the left and right bundle
branches into the ventricular muscle itself (ventricular myocardium). The stimulus
spreads itself into the ventricular myocardium by way of specialized conducting cells,
called Purkinje fibers, located in the ventricular muscle.
Under normal circumstances, when the sinus node is pacing the heart (normal sinus
rhythm), the AV junction appears to function primarily as a shuttle, directing the
electrical stimulus into the ventricles. However, under some circumstances (described
later) the AV junction can also function as an independent pacemaker of the heart. For
example, if the sinus node fails to function properly, the AV junction may act as an
escape pacemaker. In such cases an AV junctional rhythm (and not sinus rhythm) is
present. This produces a distinct ECG pattern Just as the spread of electrical stimuli
through the atria leads to atrial contraction, so the spread of the electrical stimuli
through the ventricles leads to ventricular contraction with pumping of blood to the
lungs and into the general circulation.
In summary, the electrical stimulation of the heart normally follows a repetitive
sequence of five steps:
1. Production of a stimulus from pacemaker cells in the sinus node (in the right
atrium)
2. stimulation of the tight and left atria
3. spread of the stimulus to the AV junction AV node and bundle of His)
4. spread of the stimulus simultaneously through the left and right bundle branches
5. stimulation of the left and right ventricular myocardium
CARDIAC CONDUCTIVITY AND AUTOMATICITY
The speed with which the electrical impulses are conducted through different parts of
the heart varies. For example, conduction speed or slowest through the AV node and
fastest through the Purkinje fibers. The relatively slow conduction speed through the
AV node is of functional importance because it allows the ventricles time to fill with
blood before the signal for cardiac contraction arrives.
In addition to conductivity the other major electrical feature of the heart is
automaticity. Automaticity refers to the capacity of certain myocardial cells to
function as pacemakers, to spontaneously generate electrical impulses that spread
throughout the heart. Normally, as mentioned earlier, the sinus node is the pacemaker
of the heart because of its inherent automaticity. Under special conditions other cells
outside the sinus node (in the atria, the AV junction. Or the ventricles) can also act as
independent pacemakers. For example, as mentioned before, if the automaticity of the
sinus node id depressed, the AV junction may function as an escape pacemaker. In
other conditions the automaticity of pacemakers outside the sinus node may become
abnormally increased, and these ectopic (non-sinus) pacemakers may compete with
the sinus node for control of the heartbeat. Ectopy is discussed in detail in Part II of
this book (in the section on cardiac arrhythmias).
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If you understand the normal physiologic stimulation of the heart, you have the
basis for understanding the abnormalities of heart rhythm (arrhythmias) and
conduction that produce distinctive ECG patterns. For example, failure of the sinus
node to stimulate the heart properly may result in various rhythm disturbances, such
as sinoatrial block (SA block)... Similarly, blockage of the spread of the stimulus
through the AV junction produces various degrees of AV heart block. Disease of the
bundle branches may produce left or right bundle branch block .. Finally, any disease
process that involves the ventricular muscle itself (for example, destruction) also
produces marked changes in the normal ECG patterns.
11.Basic ECG Waves
DEPOLARIZATION AND REPOLARIZATION
We have. used the general term “electrical stimulation” to refer to the spread of
electrical stimuli through the atria and ventricles. The technical term for this cardiac
electrical stimulation is depolarization. The return of heart muscle cells to their resting
state following stimulation (depolarization) is called repolarization. These terms are
derived from the fact that the normal myocardial cells (atrial and ventricular) are
polarized; that is, they carry electrical charges on their surface. The resting polarized
state of a normal heart muscle cell. Notice that the outside of the resting cell is
positive and the inside of the resting cell is positive and the inside of the cell is
negative (about –90mV).
When a heart muscle cell is stimulated, it depolarizes. As a result, the outside of the
cell, in the area where the stimulation has occurred, becomes negative, while the
inside of the cell becomes positive. This produces a difference in electrical voltage on
the outside of the cell between the stimulated depolarized area and the unstimulated
polarized area. As a result, a small electrical current is formed. This electrical current
spreads along the length of the cell as stimulation and depolarized. The path of
depolarization can be represented by an arrow. Ffor individual myocardial cells (fibers)
depolarization and repolarization proceed in the same direction. However, for the
entire myocardium depolarization proceeds from innermost layer (endocardium) to
outermost layer (epicardium) while repolarization proceeds in the opposite direction.
The mechanism of this difference is mot well understood.
This depolarizing electrical current is recorded by the ECG as a P wave (when the
atria are stimulated and depolarize) and as a QRS complex (when the ventricles are
stimulated and depolarize).
After a period of time, the fully stimulated and depolarized cell begins to return to
the resting state. This is known as repolarization. A small area on the outside of the
cell becomes positive again. The repolarization spreads along the length of the cell
until the entire cell is once again fully repolarized. Ventricular repolarizarion is
recorded by the ECG as the ST segment, T wave, and U wave. (Atrial repolarization is
usually obscured by ventricular potentials)
The ECG records the electrical activity of a large mass of atrial and ventricular
cells, not just the electrical activity of a single cell. Since cardiac depolarization and
repolarization normally occur in a synchronized fashion, the ECG is able to record
these electrical currents as specific waves (P wave, QRS complex, ST segment, T
wave, and U wave).
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To summarize, regardless of whether the ECG is normal or abnormal, it merely
records two basic events: (1) depolarization, the spread of a stimulus through the heart
muscle, and (2) repolarization, the return of the stimulated heart muscle to the resting
state.
BASIC ECG COMLOEXES: P, QRS, ST, T, AND U WAVES
This spread of a stimulus through the atria and ventricles and the return of the
stimulated atrial and ventricular muscle to the resting state produce, as noted
previously, the electrical currents recorded on the ECG. Furthermore each phase of
cardiac electrical activity produces a specific wave or complex. These basic ECG
waves are labeled alphabetically and begin with the P wave.
P wave: atrial depolarization (stimulation)
QRS complex: ventricular depolarization (stimulation)
ST segment
T wave
ventricular repolarization (recovery)
U wave
The P wave represents the spread of a stimulus through the atria (atrial
depolarization). The QRS complex represents the spread of a stimulus through the
ventricles (ventricular depolarization). The ST segment and T wave represent return
of the stimulated ventricular muscle to the resting state (ventricular repolarization).
The U wave is a small deflection sometimes seen just after the T wave. It represents
the final phase of ventricular repolarization, although its exact significance is not
known.
You are probably wondering why there is no wave or complex representing the
return of the stimulated atria to the resting state. The atrial ST segment (STa) and
atrial T wave (Ts) are generally not observed on the normal ECG because of their low
amplitudes. Similarly the routine ECG is not sensitive enough to record any electrical
activity during the spread of the stimulus through the AV junction (AV node and
bundle of His). The spread of the electrical stimulus through the AV junction occurs
between the beginning of the P wave and the beginning of the QRS complex. This
interval, which is known as the PR interval, is a measure of the time it takes for the
stimulus to spread through the atria and pass through the AV junction.
To summarize, the P-QRS-ST-T-U sequence represents the repetitive cycle of the
electrical activity in the heart, beginning with the spread of a stimulus through the
atria (P wave) and ending with the return of the stimulated ventricular muscle to the
resting state (ST-T-U sequence). This cardiac cycle repeats itself again and again.
ECG PAPER
The P-QRS-T sequence is recorded on special ECG paper. This paper is divided into
gridlike boxes. Each of the small boxes is 1 millimeter square (1 mm2). The paper
usually moves out of the electrocardiograph at a speed of 25 mm/sec. Therefore,
horizontally, each millimeter of the ECG paper is equal to 0.04 second (25 mm/sec x
0.04 sec = 1 mm). Notice also that between every five boxes there are heavier lines,
so each of the 5 mm units horizontally corresponds to 0.2 second (5 x 0.04 = 0.2).
The ECG can therefore be regarded as a moving graph, which horizontally
corresponds to time, with 0.04 and 0.2 second divisions. Vertically, the ECG graph
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measures the voltage, or amplitudes, of the ECG waves or deflections. The exact
voltage can be measured because the electrocardiograph is so standardized that 1
millivolt (1mV) produces a deflection of 10 mm amplitude (1 mV = 10 mm). (in most
electrocardiographs, the standardization can also be set at one-half or two times
normal sensitivity.)
BASIC ECG MEASUREMENTS AND SOME NORMAL VALUES
Standardization Mark
As just noted, the electrocardiograph must be properly standardized so a 1 mV signal
produces a 10 mm deflection. Therefore every electrocardiograph has a special
standardization button that produces a 1 mV wave. The standardization mark (St)
produce when the machine is correctly calibrated is a square wave 10 mm tall. If the
machine is not standardized correctly, the 1 mV signal will produce a deflection either
more or less than 10 mm, and the amplitudes of the P, QRS, and T deflection will be
larger or smaller than they should. The standardization deflection is also important
because the standardization can be varied in the newer electrocardiographs. When
very large deflections are present (as occurs, for example, in some patients who have
an electronic pacemaker that produces very large spikes), it may be advisable to take
the ECG at half standardization to avoid damaging the stylus and to get the entire
tracing on the paper. If the ECG complexes are very small, it may be advisable to
double the standardization (for example, to study a small Q wave more thoroughly).
The standardization need be set only once on an ECG—just before the first lead is
recorded.
Because the ECG is standardized, we can describe any part of the P, QRS, and T
deflections in two ways. We can measure the amplitude (voltage) of any of the
deflections, and we can also measure the width (duration) of any of the deflections.
We can therefore measure the amplitude and width of the QRS complex, the
amplitude of the ST segment deviation (if present), and the amplitude of the T wave.
For clinical purposes, if the standardization is set at 1 mV = 10 mm, the height of a
wave is usually recorded in millimeters and not in millivolts. For example, the P wave
is 1 mm in amplitude, the QRS complex is 8 mm, and the T wave is about 3.5 mm.
In describing the amplitude of any wave or deflection, it is also necessary to specify
if it is positive or negative, by convention, an upward deflection or wave is called
positive. A downward deflection or wave is called negative. A deflection or wave that
rests on the baseline is said to be isoelectric. A deflection that is partly positive and
partly negative is called biphasic. For example, the P wave is positive, the QRS
complex is biphasic (initially positive, then negative), the ST segment is isoelectric
(flat on the baseline), and the T wave is negative.
In this chapter we shall describe the P, QRS, ST, T, and U waves in a general way
and the measurement of the heart rate, the PR interval, the QRS width, the QT interval,
and their normal values in detail.
P wave
The P wave, which represents atrial depolarization, is a small deflection before the
QRS complex. The normal values for P wave amplitude and width are described in
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PR Interval
The PR interval is measured from the beginning of the P wave to the beginning
of the QRS complex. The PR interval may vary slightly in different leads, and the
shortest PR interval should be noted. The PR interval represents the time it takes for
the stimulus to spread through the atria and to pass through the AV junction. (This
physiologic delay allows the ventricles to fill fully with blood before ventricular
depolarization occurs.) in adults the normal PR interval is between 0.12 and 0.2
second (three to five small boxes). When conduction through the AV junction is
impaired, the PR interval may become prolonged. Prolongation of the PR interval
above 0.2 second is called first-degree heart block.
QRS Nomenclature
One of the most confusing aspects of electrocardiography for the beginning student is
the nomenclature of the QRS complex. The QRS complex, as noted previously,
represents the spread of a stimulus through the ventricles. However, not every QRS
complex contains a Q wave, an R wave, and an S wave; hence the confusion. This
bothersome but unavoidable nomenclature becomes understandable if you remember
the following: if the initial deflection of the QRS complex is negative (below the
baseline), it is called a Q wave. The first positive deflection in the QS complex is
called an R wave. A negative deflection following the R wave is called an S wave.
Thus this QRS complex contains a Q wave, an R wave, and an S wave. If the entire
QRS complex is positive, it is simply called an R wave. However, if the entire
complex is negative, it is termed a QS wave (not just a Q wave as you might expect).
Occasionally the QRS complex will contain more than two or three deflections, and in
such cases the extra waves are called R’ (R prime) waves if they are negative. Shows
the various possible QRS complexes and the nomenclature of the respective waves.
Note that the capital letters (QRS) are used to designate waves of relatively large
amplitude while small letters (qrs) are used to label relatively small waves.
This nomenclature is confusing at first, but it allows you to describe any QRS
complex over the phone and to evoke in the mind of the trained listener an exact
mental picture of the complex named. For example, in describing an ECG you might
say that lead V1 showed an rS complex (“small r, capital S”) while lead aV F showed a
QS wave.
QRS Width (Interval)
The QRS width represents the time required for a stimulus to spread through the
ventricles (ventricular depolarization) and is normally 0.1 second or less. If the spread
of stimulus through the ventricles is slowed, for example, by a block in one of the
bundle branches, the QRS width will be prolonged.
ST Segment
The ST segment is the portion of the ECG cycle from the end of the QRS complex to
the beginning of the T wave. It represents the beginning of ventricular repolarization.
The normal ST segment is usually isoelectric (that is, flat on the baseline, neither
positive nor negative), but it may be slightly elevated or depressed normally (usually
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by less than 1 mm). Some pathologic conditions, such as myocardial infarction,
produce characteristic abnormal deviations of the ST segment. The very beginning of
the ST segment (actually the junction between the end of the QRS complex and the
beginning of the ST segment) is sometimes called the J point.
T Wave
The T wave represents part of ventricular repolarization. A normal T wave has an
asymmetric shape; that is, its peak is closer to the end of the wave than to the
beginning. When the T wave is positive, it normally rises slowly and then abruptly
returns to the baseline. When the T wave is negative, it descends slowly and abruptly
rises to the baseline. The asymmetry of the normal T wave contrasts with the
symmetry of T waves in certain abnormal conditions, such as myocardial infarction ,
and high serum potassium (hyperkalemia).
QT Interval
The QT interval is measured from the beginning of the QRS complex to the end of the
T wave. The QT interval primarily represents the return of the stimulated ventricles to
their resting state (ventricular repolarization). The normal values for the QT interval
depend on the heart rate. As the heart rate increases (RR interval shortens), the QT
interval normally shortens; as the heart rate decreases (RR interval lengthens), the QT
interval lengthens.
You should measure several QT intervals and use the average value. The QT
interval is often difficult to measure when it is long because the end of the T wave
may merge imperceptibly with the U wave. As a result you may be measuring the QU
interval rather than the QT interval.
Because of this problem, another index of the QT has been devised. It is the
rate-corrected QT is obtained by dividing the QT that you actually measure by the
square root of the RR interval: QR / RR . Normally the QTc is less than 0.44 sec.
There are a number of factors that can abnormally prolong the QT interval. For
example, certain drugs, such as quinidine and procainamide (Pronestyl, procan SR),
and electrolyte disturbances, such as a low serum potassium (hypocalcemia), can
prolong the QT interval. The QT interval may also be prolonged with myocardial
ischemia and infarction and with subarachnoid hemorrhage. QT prolongation may
predispose patients to potentially lethal ventricular arrhythmias.
The QT interval may also be shortened, for example, by digitalis in therapeutic
doses or by hypercalcemia (high serum calcium concentration). The lower limits of
normal for the QT interval have not been well defined.
U wave
The U wave is a small rounded deflection sometimes seen after the T wave. As noted
previously, the exact significance of the U wave is not known. Functionally U waves
represent the last phase of ventricular repolarization. Prominent U waves are
characteristic of hypokalemia (low serum potassium). Very prominent U waves may
also be seen in other settings, for example, in patients taking drugs such as quinidine
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or one of the phenothiazine, or sometimes after cerebrovascular accidents. The
appearance of very prominent U waves in such settings, with or without actual QT
prolongation, may also predispose patients to ventricular arrhythmias.
Normally the direction of the U wave is the same as the direction of the T wave.
Negative U waves sometimes appear with positive T waves. This is abnormal and has
been noted in left ventricular hypertrophy and myocardial ischemia.
Calculation of the Heart Rate
There are two simple methods for measuring the heart rate (number of heartbeats per
minute) from the ECG.
1. the easier way, when the heart rate is regular, is to count the number of large
(0.2 sec) boxes between two successive QRS complexes and divide the constant
(300) by this. (the number of large time boxes is divided into 300, because 300
x 0.2 = 60 and we are calculating the heart rate in beats per minute or 60
seconds.)
For example, the heart rate is 100 beats/min, since there are three large time
boxes between two successive R waves (300 ÷ 3 =100). Similarly, if there
are two large time boxes between two successive R waves, the heart rate is 150
beats/min. if there are five intervening large time boxes, the heart rate is 60
beats/min.
2. If the heart rate is irregular, the first method will not be accurate since the
intervals between QRS complexes will vary from beat to beat. In such cases an
average rate can be determined simply by counting the number of cardiac cycles
every 6 seconds and multiplying this number by 10. (A cardiac cycles is the
interval between two successive R waves.) Counting the number of cardiac
cycles every 6 seconds can be easily done because the top of the ECG paper is
generally scored with vertical marks every 3 seconds.
By definition, a heart rate exceeding 100 beats/min is termed “tachycardia”
(tachys, Greek, swift) while one slower than 60 beats/min is called
“bradycardia” (bradys, slow). Thus, during exercise you probably develop a
sinus tachycardia but during sleep or relaxation your pulse rate may drop into
the 50s, or even lower, indication a sinus bradycardia.
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111. ECG Leads
The heart produces electrical currents similar to the familiar dry cell battery. The
strength or voltage of these currents and the way they are distributed throughout the
body can be measured by a suitable recording instrument, such as an
electrocardiograph.
The body acts as a conductor of electricity, therefore, recording electrodes placed at
some distance from the heart, such as on the arms, legs, or chest wall, are able to
detect the voltages of the cardiac currents conducted to these locations. The usual way
of recording these voltages from the heart is with the 12 standard ECG leads. The
leads actually show the differences in voltage (potential) between electrodes placed on
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the surface of the body.
Taking an ECG is like drawing a picture or taking a photograph of a person. If we
want to know what a person’s face really looks like, for example, we have to draw it
or take photographs from the front, side, and back.. One view is not enough. Similarly,
it is necessary to record multiple ECG leads to be able to describe the electrical
activity of the heart adequately. Notice that each lead presents a different pattern.
The 12 leads can be subdivided into two groups: the six extremity (limb) leads and
the six chest (precordial) leads.
The six extremity leads--I, II, III, aVR, aVL, and aVF—show voltage differences by
means of electrodes placed on thd limbs. They can be further divided into two
subgroups: the bipolar extremity leads (I, II, and III) and the unipolar extremity leads
(aVR, aVL, and aVF).
The six chest leads—V1, V2, V3, V4, V5, and V6—present voltage differences by
means of electrodes placed at various positions on the chest wall.
positions on the chest wall.
The 12 ECG leads can also be viewed as 12 “channels.” However, in contrast to
television channels (which can be turned to different events), the 12 ECG channels
(leads) are all tuned to the same event (the P-QRS-T cycle), with each lead viewing
the event from a different angle.
EXTREMITY (LIMB) LEADS
Bipolar Leads (I, II, and III)
We will begin with the extremity leads, since they are recorded first. In connecting a
patient to an electrocardiograph, first place metal electrodes on the arms and legs. The
right leg electrode functions solely as an electrical ground, so you need concern
yourself with it no further. Attach the arm electrodes just above the wrist and the leg
electrodes above the ankles.
The electrical voltages of the heart are conducted through the torso to the
extremities. Therefore an electrode placed on the right wrist will detect electrical
voltages equivalent to those detect below the right shoulder. Similarly, the voltages
detected at the left wrist or anywhere else on the left arm will be equivalent to those
detected below the left shoulder. Finally, voltages detected by the left leg electrode
will be comparable to those at the left thigh or near the groin. In clinical practice the
electrodes are attached to the wrists and ankles simply for convenience.
As mentioned, the extremity leads consist of two groups: the bipolar (I, II, and III)
and the unipolar (aVR, aVL, and aVF) leads. The bipolar leads are so named because
two extremities are recorded by them.
From lead I, for example, the difference in voltage is recorded between the left arm
(LA) and the right arm (RA). Lead I = LA – RA
From lead II the difference is recorded between the left leg (LL) and the right arm
(RA).
Lead II = LL- RA
From lead III the difference is recorded between the left leg (LL) and the left arm
(LA).
Lead III = LL – LA
Consider then what happens when you turn on the electrocardiograph to lead I. The
LA electrode detects the electrical voltages of the heart transmitted to the left arm, the
RA electrode detects the voltages transmitted to the right arm. Inside the
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electrocardiograph the RA voltages are subtracted from the LA voltages and the
difference appears at lead I. When lead II is recorded, a similar situation occurs
between the voltages of LL and RA. When lead III is recorded, the same occurs
between the voltages of LL and LA.
Leads I, II, and III can be represented schematically in terms of a triangle, called
Einthoven’s triangle (after the Dutch physician who invented the electrocardiograph).
At first the ECG consisted only of recordings from leads I, II, and III. Einthoven’s
triangle shows the spatial orientation of the three bipolar extremity leads (I, II, and III).
As you can see, lead I points horizontally. Its left pole (LA) is positive and its right
pole (RA) is negative. Therefore lead I = LA – RA. Lead II points diagonally
downward. Its lower pole (LL) is positive and its upper pole (RA) is negative.
Therefore lead II = LL – RA. Lead III also points diagonally downward. Its lower
pole (LL) is positive and its upper pole (LA) is negative. Therefore lead III = LL –LA.
Einthoven, of course, could have hooked the leads up differently; but because of the
way he arranged them, the bipolar leads are related by the following simple equation:
lead I + lead III = lead II. In other words, add the voltage in lead I to that in lead III
and you get the voltage in lead II. You can test this equation by looking at the ECG.
Add the voltage of the R wave in lead I to the voltage of the R wave in lead III and
you get the voltage of the R wave in lead II. You can do the same with the voltages of
the P waves and T waves.
It is a good custom to scan leads I, II, and III rapidly when you first look at a
mounted ECG. If the R wave in lead II does not seem to be the sum of the waves in
leads I and III, this may be a clue that the leads have been either recorded incorrectly
or mounted improperly.
Unipolar Extremity Leads (aVR, aVL, aVF)
Following the invention of the three bipolar extremity leads nine additional leads
were added. In the 1930s Dr. frank N. Wilson and his colleagues at the University of
Michigan invented the unipolar limb leads and introduced the six unipolar chest leads,
V1 through V6. shortly after this, one of the authors of this text (E.G.) invented the
three augmented unipolar extremity leads, aVR, aVL, aVF. The abbreviation a refers to
augmented; V, voltage R, L, and F, right arm, left arm, and left foot (leg) respectively.
So, today, 12 leads are routinely employed.
A unipolar lead records the electrical voltages at one location relative to zero
potential, rather than relative to the voltages at another extremity, as in the case of the
bipolar extremity leads. The zero potential is obtained inside the electrocardiograph
by joining the three extremity leads to a central terminal. Since the sum of the
voltages of RA, LA, and LL equals zero, the central terminal has a zero voltage. The
aVR, aVL, and aVF leads are derived in a slightly different way, because the voltages
recorded by the electrocardiograph have been augmented 50% over the actual
voltages detected at each extremity. This augmentation is also done electronically
inside the electrocardiograph.
Just as we used Einthoven’s triangle to represent the spatial orientation of the three
bipolar extremity leads. Note that each of the unipolar leads can be represented by a
line (axis) with a positive and a negative pole. Since the diagram has three axes, it is
also called a triaxial diagram.
The positive pole of lead aVR, the right arm lead, point upward and to the patient’s
right arm as you would expect. The positive pole of lead aVL points upward and to the
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patient’s left arm. The position pole of lead aVF points downward toward the patient’s
left foot.
Furthermore, just as leads I, II, and III are related by Einthoven’s equation, so leads
aVR, aVL, and aVF likewise are related: aVR + aVL + aVF = 0. In other words, when
the three unipolar extremity leads are recorded, they should total zero. Thus the sum
of the P wave voltages is zero, the sum of the QRS voltages is zero, and the same
holds for the T wave voltages. You can test equation by adding the sum of the QRS
voltages in the three unipolar extremity leads, aVR, aVL, and aVF.
It is also a good custom to scan leads aVR, aVL, and aVF rapidly when you first
look at a mounted ECG. If the sum of the waves in these three leads does not equal
zero, this may also be a clue that these leads have either been recorded incorrectly or
mounted improperly.
The ECG leads, both bipolar and unipolar, have two major features, which we have
already described, they have axis of lead I is oriented horizontally while the axis of
lead aVR point diagonally downward. The orientation of the bipolar leads is shown in
Einthoven’s triangle.
The second major feature of the ECG leads, their polarity, can be represented by a
line (axis) with a positive and a negative pole, as shown before. The polarity and
spatial orientation of the leads are discussed further in Chapters 4 and 5 (when we
describe the normal ECG patterns seen in each of the leads and the concept of
electrical axis).
Do not be confused by the difference in meaning between ECG electrodes and ECG
leads. And electrode is simply the metal plate used to detect the electrical currents of
the heart in any location. An ECG lead, as we have been discussing, shows the
differences in voltage detected by these electrodes. (For example, lead I presents the
differences in voltage detected by the left and right arm electrodes.) Therefore, a lead
is simply a means of recording the differences in cardiac voltages obtained by
different electrodes.
Relationship Between Unipolar and Bipolar Extremity leads
The Einthoven triangle shows the relationship of the three bipolar extremity leads (I,
II, and III). Similarly the triaxial shows the relationship of the three unipolar
extremity leads (aVR, aVL, and aVF). For convenience, we can combine these six
extremity leads intersect at a common point. The result is the hexaxial lead. The
hexaxial shows the spatial orientation of the six extremity leads (I, II, III, aVR, aVL,
and aVF).
The exact relationships among the three unipolar extremity leads can also be
describved mathematically. However, for present purposes, the following simple
guidelines allow you to get an overall impression of the similarities between these two
sets of leads.
As you might expect by looking at the hexaxial diagram, the pattern in lead aV L
uusually resembles that in lead I. Lead aVR and lead II, on the other hand, point in
opposite directions. Therefore, the P-QRS-T pattern recorded by lead II. (For example,
when lead II shoes a qR pattern lead aVR usually shows an rS pattern.) Finally, the
pattern shown by lead aVF usually but not always resemble that shown by lead III.
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CHEST (PRECORDIAL) LEADS
The chest leads (V1 to V6) show the electrical currents of the heart detected by
electrodes placed at different positions on the chest wall. The chest leads used today
are also unipolar leads in that they measure the voltage in any one location relative to
zero potential. By convention the six leads are placed as follows:
Lead V1 is recorded with the electrode in the fourth intercostal space just to the
right of the
sternum.
Lead V2 is recorded with the electrode in the fourth intercostal space just
to the lest of the
sternum.
Lead V3 is recorded on a line midway between leads V2 and V4.
Lead V4 is recorded in the midclavicular line in the fifth interspace.
Lead V5 is recorded in the anterior axillary line at the same level as lead V4.
Lead V6 is recorded in the midaxillary line at the same level as lead V4.
The chest leads are recorded simply by means of electrodes (usually attached to
suction cups to hold them in place on the chest) at six designated locations on the
chest wall .
TAKING AN ECG
Now you are ready to take an ECG. The extremity electrodes are attached toe the
patient. First, the machine is standardized. Then the dial in the electrocardiograph is
turned to lead 1. Several P-QRS-T cycles are run. Nest, the dial is advanced to lead II
and the ECG records a few more cycles. This is repeated for leads III, aVR, aVL, and
aVF. Next the dial is turned to the V position for the chest leads. The suction cup is
placed in the V1 position, and so on until the six V leads have been recorded. The
result is a long ECG strip showing the 12 leads recorded sequentially.
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THE 12-LEAD ECG: FRONTAL AND HORIZONTAL PLANE LEADS
You may now be wondering why we use 12 leads in clinical electrocardiograph; why
not 12 or 22? The reason for exactly 12 leads is partly historical, a matter of the way
the ECG had evolved over the years since Einthoven’s original three bipolar extremity
leads. There is nothing sacred about the electrocardiographer’s dozen. In some cases,
for example, we do record additional leads by placing the chest electrode at different
positions on the chest wall. There are good reasons for using multiple leads. The heart,
after all, is a three-dimensional structure, and its electrical currents spread out in all
directions across the body. Recall that we described the ECG leads as being like
photographs by which we can see the electrical activity of the heart from different
locations. To a certain extent, the more points we record from the more accurate will
be our representation of the heart’s electrical activity.
The importance of multiple leads is illustrated in the diagnosis of myocardial
infarction (MI). An MI typically affects one localized portion of the left ventricle. The
ECG changes produced by an anterior MI are usually best shown by the chest leads,
which are close to and face the injured anterior surface of the heart, while the changes
seen with an inferior MI usually appear only in leads such as II, III and aV F, which
face the injured inferior surface of the heart. The 12 leads therefore provide a
three-dimensional view of the electrical activity of the heart.
Specifically, the six extremity leads (I, II, III, aVR, aVL, aVF) will show electrical
voltages transmitted onto the frontal plane of the body. For example, if you walk up to
and face a large window, the window will be parallel to the frontal plane of your body.
Similarly heart voltages directed upward and downward and to the right and left will
be presented by the frontal plane leads.
The chest leads (V1 through V6) present heart voltages from a different viewpoint,
on the horizontal plane of the body. The horizontal plane cuts your body into an upper
and a lower half. Similarly the chest leads present heart voltages directed anteriorly
(front), posteriorly (back), and to the right and left.
We therefore have two sets of ECG leads six extremity leads (three unipolar and
three bipolar), which record voltages on the frontal plane of the body, and six chest
(precordial) leads, which record voltages on the horizontal plane. Together these 12
leads provide a three-dimensional picture of atrial and ventricular depolarization and
repolarization.
IV. The Normal ECG
THE NORMAL P WAVE
Let us begin our description of the normal ECG with the first waveform seen in any
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cycle, the P wave, which represents atrial depolarization. Atrial depolarization is
initiated by the sinus node, in the right atrium. The atrial depolarization path therefore
spreads from right to left and downward toward the AV junction. Therefore we can
represent the spread of atrial depolarization by an arrow that points downward and to
the patient’s left.
Notice that the positive pole of lead aVR points upward in the direction of the right
shoulder. The normal path of atrial depolarization, as described, spreads downward
toward the left leg (away from the positive pole of lead aVR). Therefore, with normal
sinus rhythm, lead aVR will always show a negative P wave. Conversely, lead II is
oriented with its positive pole pointing downward in the direction of the left leg.
Therefore the normal atrial depolarization path will be directed toward the positive
pole of lead II. When normal sinus rhythm is present, lead II will always record a
positive (upward) P wave.
When the AV junction is pacing the heart atrial depolarization will have to spread
up the atria in a retrograde direction, just the opposite of what happens in normal
sinus rhythm. Therefore an arrow representing the spread of atrial depolarization in
AV junctional rhythm will point upward and to the right, just the opposite of normal
sinus rhythm. Spread of atrial depolarization upward and to the right will result in a
positive P wave in lead aVR, since the stimulus is spreading toward the positive pole
of lead aVR. Conversely, lead II will show a negative P wave . we will discuss AV
junctional rhythms in detail in Part II. The topic was introduced here simply to show
how the polarity of the P wave in lead aVR and lead II depends on the direction of the
atrial depolarization and how the patterns can be predicted using simple basic
principles.
.
THE NORMAL QRS COMPLEX
The QRS, which represents ventricular depolarization, is somewhat more complex
than the P wave, but the same basic ECG rules apply to both.
Predict what the QRS will look like in the different leads, you must first know the
direction of ventricular depolarization. Although the direction of atrial depolarization
can be represented by a single arrow, the spread of ventricular depolarization consists
of two major sequential phases:
The first phase is of relatively brief duration (shorter than 0.04 sec) and small
amplitude; it results from the spread of stimulus through the ventricular septum. The
ventricular septum is the first part of the ventricles to be stimulated. Furthermore, the
left side of the septum is stimulated first (by a branch of the left bundle of His); thus
the depolarization spreads from the left ventricle to the right across the septum. Phase
one of ventricular depolarization, the phase of septal stimulation, can therefore be
represented by a small arrow pointing from the left septal wall the right.
The second phase of verntricular depolarization involves the simultaneous
stimulation of the main mass of both the left and right ventricles from the inside
(endocardium) to the outside (epicardium) of the heart muscle. In the normal heart the
left ventricle is electrically predominant. In other words, it electrically overbalances
the right ventricle. Therefore an arrow representing phase two of ventricular
stimulation will point toward the left ventricle.
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Chest Leads
Lead V1 shows voltages detected by an electrode placed on the right side of the
sternum (fourth intercostal space). Lead V6, a left chest lead, shows voltages detected
in left midaxillary line . What will the QRS complex look like in these leads?
The first phase of ventricular stimulation, septal stimulation, will produce a small
positive r wave in lead V1, reflecting the left-to-right spread of stimulus through the
septum. The arrow representing septal stimulation will point toward lead V1. what will
lead V6 show? The left-to-right spread of septal stimulation will produce a small
negative deflection (q wave) in lead V6. thus the same electrical event, septal
stimulation, will produce a small positive deflection (or r wave) in lead V1 and a small
negative deflection (q wave) in a left precordial lead like V6. (This situation is
analogous to the one described for the P wave, which is normally positive in lead II
but always negative in lead aVR.)
The second phase of ventricular stimulation is represented by an arrow pointing in
the direction of the left ventricle. The spread of stimulation to the left during the
second phase will result in a negative deflection in the right precordial leads and a
positive deflection in the left precordial leads. Lead V1 will therefore show a deep
negative (S) wave while lead V6 shows a tall positive (R) wave.
Let us summarize what we have learned about the normal QRS pattern in leads V1
and V6. normally lead V1 will show an rS type of complex. The small initial r wave
reprewents the left-to-right spread of septal stimulation. This wave is sometimes
referred to as the septal r wave because it reflects septal stimulation. The negative (S)
wave reflects the spread of ventricular stimulation forces during phase two, away
from the right and toward the dominant left ventricle. Conversely, the same electrical
events, septal and ventricular stimulation, viewed from an electrode in the V6 position
will produce a qR pattern. The q wave is a septal q wave, reflecting the left-to-right
spread of the stimulus through the septum away from lead V6. the positive ( R) wave
reflects the leftward spread of ventricular stimulation voltages toward the left
ventricle.
Once again, we reemphasize, the same electrical event, whether depolarization of
the atria or depolarization of the ventricles, will produce very different-looking
waveforms in different leads because the spatial orientation of the leads in different.
We have described the patterns normally seen in leads V1and V6. What happens
between these leads? The answer is that as you move across the chest (in the direction
of the electrically predominant left ventricle) the R wave tends to become relatively
larger and the S wave becomes relatively smaller. This increase in height of the R
wave, which usually reaches a maximum around lead V4 or V5, is called normal R
wave progression.
At some point, generally around the V3 or V4 position, the R/S ratio becomes 1.
This point, where the amplitude of the R wave equals that of the S wave, is called the
transition zone. In some normal people the transition may be seen as early as lead V2.
This is called early transition. In other cases the transition zone may be delayed to leas
V5 and V6, and is called a delayed transition.
Examine the set of normal chest leads. Note the rS complex in lead V1 and qR
complex in lead V6. The R wave tends to get gradually larger here as you move
toward the left chest leads. The transition zone, where the R wave and S wave are
about equal, is in lead V4. In normal chest leads the R wave voltage need not get
literally larger as you go from leads V1 to V6. However, the overall trend should show
a relative increase. For example, notice that in this example there is not much
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difference between the complexes in leads V2 and V3, and that the R wave in lead V5
is taller than the R wave in lead V6.
Extremity Leads
The positive pole of lead aVR is oriented upward and toward the right shoulder. The
ventricular stimulation forces are oriented primarily toward the left ventricle.
Therefore, lead aVR normally shows a predominantly negative QRS complex. You
may see any of the QRS-T complexes shown in lead aVR. In all cases, the QRS is
predominantly negative. The T wave in lead aVR is also normally negative.
The QRS patterns in the other five extremity leads are somewhat more complicated.
The reason is that there is considerable normal variation in the QRS patterns seen in
the extremity leads. For example, some normal people have an ECG that shows one
pattern in the extremity leads. In this case, leads I and aVL show qR-type complexes
while leads III and aVF show rS-type complexes. In other normal people the extremity
leads may show just the reverse picture. Here, leads II, III, and aV F show qR
complexes while lead aVL and sometimes lead I show RS complexes.
The extremity leads in normal people can show a variable QRS pattern. Lead aVR
normally always shows a predominantly negative QRS complex (Qr, QS, or rS). The
QRS patterns in the other extremity leads will vary depending on the “electrical
position” (QRS axis ) of the heart, with an electrically vertical axis, leads I and aV L
show qR waves. Therefore, there is no single normal ECG pattern; rather, there is a
normal variability. Students and clinicians must familiarize themselves with the
normal variants we have described both in the chest leads and in the extremity leads.
THE NORMAL ST SEGMENT
As noted in Chapter 2, the normal ST segment, representing the early phase of
ventricular repolarization, is usually isoelectric (flat on the baseline). Slight deviations
of the ST segment (usually less than 1 mm) may be seen normally. As described in
Chapter 10, certain normal subjects will show more marked ST segment elevations
as a normal variant (early repolarization pattern). Finally, examine the ST segments in
the right chest leads (V1 to V3). Notice that in these examples the ST segment is short
and the T wave appears to take off almost from the J point (junction of QRS complex
and ST segment). This pattern of an early takeoff of the T wave in the right chest leads
is mot an uncommon finding in normal subjects.
THE NORMAL T WAVE
Up to this point, we have deferred discussion of ventricular repolarization-the return
of stimulated muscle to the resting state, which produces the ST segment, T wave, and
U wave. Deciding whether the T wave in any lead is normal or not is generally
straightforward. As a rule, the T wave follows the direction of the main QRS
deflection. Thus, when the main QRS deflection id positive (up-right), the T wave is
normally positive. We can also make some more specific rules about the direction of
the normal T wave.
The normal T wave in lead aVR is always negative, while in lead II it is always
positive. Left-sided chest leads, such as V4 to V6, normally always show a positive T
wave.
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The T wave in the other leads may be variable. In the chest leads the T wave may
be normally negative, isoelectric, or positive in leads V1 and V2. in most normal adults,
the T wave becomes positive by lead V3. Furthermore, if the T wave is positive in any
chest lead, it must remain positive in all chest leads to the left of that lead. Otherwise,
it is abnormal. For example, if the T wave is negative in chest leads V1 and V2 and
becomes positive in lead V4, it should normally remaim positive in leads V4 to V6.
The polarity of the T wave in the extremity leads depends on the electrical position
of the heart. With a horizontal heart, the main QRS deflection is positive in leads I and
aVL, and the T wave is also positive in these leads. However, in some normal ECG
with a vertical axis, the T wave may be negative in lead III.
v.Electrical Axis and Axis Deviation
MEAN QRS AXIS
The depolarization stimulus spreads through the ventricles in different directions from
instant to instant, for example, the depolarization wave may be directed toward lead I
at one moment and toward lead III at the next . we can also talk about the mean
direction of the QRS complex or mean QRS electrical axis. If you could draw an
arrow to represent the general, or, mean, direction in which the QRS is pointed in the
frontal plane of the body, you would be drawing the electrical axis of the QRS
complex.
The term “mean QRS axis,” therefore, describes the general direction in the frontal
plane toward which the QRS complex is predominantly pointed.
Since we are defining the QRS axis in the frontal plane, we are describing the QRS
only in reference to the six extremity leads (the six frontal plane leads). Therefore the
scale of reference used to measure the mean QRS axis is the diagram of the frontal
plane leads . We also know the Einthoven triangle and how the triangle can easily by
simply having the three axes (leads I, II, and III) radiate from a central point.
Similarly we showed how the axes of the three unipolar extremity leads (aVR, aVL,
and aVF) also form a triaxial lead diagrams were combined to produce a hexaxial lead
diagram. This is the lead diagram we shall use in determining the mean QRS axis and
in describing axis deviation.
Each of the leads has a positive and a negative pole. As a wave of depolarization
spreads toward the positive pole, an upward (positive) deflection occurs. As a wave of
depolarization spreads toward the negative pole, a downward (negative) deflection is
inscribed.
Finally, in order to determine or calculate the mean QRS axis, we need a scale. By
convention, the positive pole of lead I is said to be at 00; all point below the lead I axis
are negative. Thus, as we move toward lead aVL (-300), the scale becomes more
positive-lead II at +600, lead aVF at +900, lead III at +1200.
The completed hexaxial diagram used to measure the QRS axis. By convention
again, we can say that an electrical axis that points toward lead aVL is leftward or
horizontal. An axis that points toward leads II, III, and aVF is rightward or vertical.
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Calculation
In calculating the mean QRS axis you are answering the question: in what general
direction or toward which lead axis is the QRS complex predominantly oriented? For
example, notice that there are tall R waves in leads II, III, and aVF, indication that the
heart is electrically vertical (vertical electrical axis). Furthermore, the T wave is
equally tall in leads II and III. Therefore, by simple inspection, the mean electrical
QRS axis can be seen to be directed between leads II and III and toward lead aVF.
Lead aVF on the hexaxial diagram is at +900.
As a general rule the mean QRS axis will point midway between any two leads that
show tall R waves of equal height.
In the preceding example the mean electrical axis could have been calculated a
second way. Recall from Chapter 3 that if a wave of depolarization is oriented at right
angles to any lead axis a biphasic complex (RS or QR) will be recorded in that lead.
Reasoning in a reverse manner, if you find a biphasic complex in any of the extremity
leads, then the mean QRS axis must be directed at 900 to that lead. Are there any
biphasic and shows an RS pattern. Therefore, the mean electrical axis must be
directed at right angles to lead I. Since lead I on the hexaxial lead scale is at oo, the
mean electrical axis must be at right angles to 00 or at either –900 or + 900. if the axis
were –900, then the depolarization forces would be oriented away from the positive
pole of lead aVF and lead aVF would show a negative complex. In this case lead aVF
shows a positive complex (tall R wave), so the axis must be + 900.
Another example. In this case, by inspection, the mean QRS axis is obviously
horizontal since leads I and aVL are positive and leads II, III, and aVF are
predominantly negative. The precise electrical axis can be calculated by looking at
lead II, which shows a biphasic RS complex. Therefore, using the same logic as
before, we can say that the axis must be at right angles to lead II. Since lead II is at +
600 on the hexaxial scale, the axis must be either –300 or + 1500. if the axis were +
1500, then leads II, III, and aVF would be positive. Clearly in this case the axis is –300.
Another example is presented the QRS complex is positive in leads II, III, and aVF.
Therefore we can say that the axis is relatively vertical. Since the R waves are of
equal magnitude in leads I and III, the mean QRS axis must be oriented between these
two leads, or at + 600.
Alternatively, we could have calculated the axis by looking at lead aVL (in Fig. 5-5),
which shows a biphasic RS-type complex. The axis must be at right angles to lead
aVL (-300), that is either –1200 or +600. Obviously, in this case, the answer is + 600.
The electrical axis must be oriented toward lead II, which shows a tall R wave.
We now describe a second general rule: the mean QRS axis will be oriented at right
angles to any lead showing a biphasic complex. In such cases the mean QRS axis will
point in the direction of leads showing tall R waves.
Still another case is, by inspection, the electrical axis can be seen to be oriented
away from leads II, III, and aVF and toward leads aVR and aVL, which show positive
complexes. Since the R waves ate of equal magnitude in leads aVR and aVL, the axis
must be oriented precisely between these leads, or at –900. Alternatively, look at lead I,
which shows a biphasic RS complex. In this case the axis must be directed at right
angles to lead I (00); that is, it must be either –900. lf +900, since the axis is oriented
away from the positive pole of lead aVF and toward the negative pole of lead aVF, it
must be –900.
Still another case can be noted. There are two ways of approaching the calculation
of the mean QRS axis in this case. Since lead aVR shows a biphasic RS-type complex,
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the electrical axis must be right angles to the axis of lead aVR. Since the axis of lead
aVR is at –1500, the electrical axis in this case must be either –600 or +1200. clearly it
must be –600 in this caser since lead aVL is positive and lead III shows a negative
complex.
These basic examples should establish the ground rules for estimating the mean
QRS axis. It is worth emphasizing that such calculations are generally only an
estimate or a near approximation. And error of 100 or 150 is not significant. Therefore,
it is perfectly acceptable to calculate the axis from leads in which the QRS is nearly
biphasic or from two leads where the R (or S) waves are approximately equal in
amplitude.
AXIS DEVIATION
The mean QRS axis is a basic measurement that should be made in every ECG you
read. In most normal individuals the mean QRS axis will lie between –300 and +1000.
and axis of –300 or more negative is described as left axis deviation (LAD). The term
right axis deviation (RAD) refers to an axis of +1000 or more positive. In other words,
left axis deviation is an abnormal extension of the mean QRS axis found in persons
with an electrically horizontal heart; right axis deviation is an abnormal extension of
the QRS axis found in persons with an electrically vertical heart.
The mean QRS axis is determined by two major factors: (1) the anatomic position
of the heart and (2) the direction of ventricular depolarization (the direction in which
the stimulus spreads through the ventricles).
The influence of cardiac anatomic position on the electrical axis can be illustrated
by the effects of respiration. With inspiration, the diaphragm descends and the heart
becomes more vertical in the chest cavity. This change in cardiac position generally
shifts the electrical axis vertically (to the right). (Patients with emphysema and
chronically hyperinflated lungs also have anatomically vertical hearts and electrically
vertical QRS axes.) Conversely, with complete expiration, the diaphragm ascends and
the heart assumes a more transverse or horizontal position in the chest. With
expiration, the electrical axis generally shifts horizontally (to the left).
The second major determinant, the direction of depolarization through the
ventricles, can be illustrated by left anterior hemiblock (Chapter 7), where there is a
delay in the spread of stimuli through the left ventricle and the mean QRS axis is
shifted to the left. On the other hand, right ventricular hypertrophy shifts the QRS axis
to the right.
Recognition of right and left axis deviations is easy.
RAD, as stated before, is defined as a QRS axis more positive than +1000. Recall
that if leads II and III show tall R waves of equal height then the axis must be +900. as
an approximate rule, if leads II and III show tall R waves and the R wave in lead III
exceeds that in lead II, then right axis deviation is present. In addition, lead I will
show an RS pattern, with an S wave that is deeper than the R wave is tall.
The cutoff for LAD is –300. Notice that lead II shows a biphasic complex (RS
complex). Remember that the location of lead II is at +600 and a biphasic complex
indicates that the electrical axis must be at right angles to lead II or at –300 (or at
+1500). Thus, with an axis of –300, lead II will show an RS complex where the R
wave equals the S wave in amplitude. If the electrical axis is more negative than –300
(left axis deviation) then lead II will show an RS complex where the S wave is deeper
than the R wave is tall.
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VI. Atrial and Ventricular Enlargement
The basics of the normal ECG have been described in the first five chapters. From this
point on, will be concerned primarily with abnormal ECG patterns, beginning in this
chapter with a consideration of the effects on the ECG of enlargement of the four
cardiac chambers.
Several basic terms must first be defined. “Cardiac enlargement” refers to either
dilation of a heart chamber or hypertrophy of the heart muscle. In dilation of a
chamber the heart muscle is stretched and the chamber becomes enlarged. In cardiac
hypertrophy the heart muscle fibers actually increase in size, with resulting
enlargement of the chamber. When cardiac hypertrophy occurs, the total number of
the heart muscle fibers does not increase; rather, each individual fiber becomes large.
One obvious ECG effect of cardiac hypertrophy will be an increase in voltage of the P
wave or QRS complex. Not uncommonly hypertrophy and dilation occur together.
Both dilation and hypertrophy usually result from some type of chronic pressure or
volume load on the heart muscle. We will proceed with a discussion of the ECG
patterns seen with enlargement of each of the four cardiac chambers, beginning with
the right atrium.
RIGHT ATRIAL ENLARGEMENT (RAE)
Enlargement of the right atrium (either dilation or actual hypertrophy) may increase
the voltage of the P wave. To recognize a large P wave, you must know the dimension
of the normal P wave.
When the P wave is positive (upward), its amplitude is measured in millimeters
from the upper level of the baseline, where the P wave begins, to the peak of the P
wave. A negative (downward) P wave is measured from the lower level of the baseline
to the lowest point of the P wave.
Normally the P wave in every lead is less than or equal to 2.5 mm (0.025 mV) in
amplitude and less than 0.12 second (three small boxes) in width. A P wave exceeding
either of these dimensions in any lead is abnormal.
Enlargement of the right atrium may produce an abnormally tall P wave (greater
than 2.5 mm). However, because pure RAE does not generally increase the total
duration of atrial depolarization, the width of the P wave in RAE is sometimes
referred to as P pulmonale because the atrial enlargement is often seen with severe
pulmonary disease. Fig. 6-2 shows an actual example of RAE with a P pulmonale
pattern.
The tall narrow P waves characteristic of RAE can usually best be seen in leads II,
III, aVF, and sometimes V1. The ECG diagnosis of P pulmonale can e made by
finding a P wave exceeding 2.5 mm in any of these leads. Recent echocardiographic
evidence, however, suggests that the finding of a tall peaked P wave does not always
correlate with RAE. On the other hand, patients may have RAE and not tall P waves.
LEFT ATRIAL ENLARGEMENT (LAE); LEFT ATRIAL ABNORMALITY (LAA)
Enlargement of the left atrium (either by dilation or by actual hypertrophy) also
produces distinct changes in the P wave. Normally the left atrium depolarizes after the
right atrium. Therefore, enlargement of the left atrium should prolong the total
duration o atrial depolarization, indicated by an abnormally wide P wave. LAE
characteristically produces a wide P wave of 0.12 second (three small boxes) or more
duration. The amplitude (height) of the P wave in LAE may be either normal or
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increased.
The characteristic P wave changes seen in LAE. Sometimes, as shown, the P wave
will have a distinctive “humped” or “notched” appearance. The second hump
corresponds to the delayed depolarization of the left atrium. These humped P waves
are usually best seen in one or more of the extremity leads. The term “P mitrale” is
sometimes used to describe these wide P waves seen with LAE because they were
first described in patients with rheumatic mitral valve disease.
In cases of LAE, lead V1 sometimes shows a distinctive biphasic P wave. This
biphasic P wave has a small initial positive deflection and a prominent wide negative
deflection. The negative component will be of > 0.04 second duration or >1 mm depth.
The prominent negative deflection corresponds to the delayed stimulation of the
enlarged left atrium.
Some patients particularly those with coronary artery disease, may show broad P
waves without actual LAE. The abnormal P waves in these cases probably represent
an atrial conduction delay. Therefore, the more general term “left atrial abnormality”
is used by some authors in preference to left atrial “enlargement” to describe
abnormally broad P waves.
RIGHT VENTRICULAR HYPERTROPHY (RVH)
Although atrial enlargement (dilation or hypertrophy) produces characteristic changes
in the P wave, the QRS complex will be modified primarily by ventricular
hypertrophy. The ECG changes that will be described indicate actual hypertrophy of
the ventricular muscle and not simply ventricular dilation.
The ECG changes produced by both right and left ventricular hypertrophy can be
predicted on the basis of what you already know about the normal QRS patterns.
Normally the left and right ventricles depolarize simultaneously and the left ventricle
is electrically predominant because it is normally the larger chamber. As a result, leads
placed over the right side of the chest, such as lead V1, record rS-type complexes, in
which the deep negative S wave indicates the spread of depolarization voltages away
from the right side and toward the left side. Conversely, a lead placed over the left
chest, such as V5 or V6, records a qR-type complex, in which the tall positive R wave
indicates the predominant depolarization voltages that point to the left generated by
the left ventricle.
Now, if the right ventricle becomes sufficiently hypertrophied, this normal
electrical predominance of the left ventricle can be overcome. In such case of RVH,
what type of QRS complex might you expect to see in the right chest leads? With
RVH, the right chest leads will show tall R waves, indicating the spread of positive
voltages from the hypertrophied right ventricle toward the right. Instead of the rS
complex normally seen in lead V1, we now see a tall positive (R) wave, indicating
marked hypertrophy the right ventricle.
How tall an R wave in lead V1 do you have to see to make a diagnosis of RVH? As
a general rule, the normal r wave in lead V1 in adults is usually smaller than the S
wave in that lead. An R wave exceeding the S wave in lead V1 is suggestive, but not
diagnostic, of RVH. Sometimes, a small q wave precedes the tall R wave in lead V1 in
cases of RVH.
Although with tall right chest R waves, RVH also often produces two additional
ECG signs: right axis deviation and right ventricular strain T wave inversions.
The normal mean QRS axis in adult lies approximately between –300 and +1000. A
mean QRS axis of +1000 or more in called right axis deviation. One of the most
common causes of right axis deviation is RVH. Therefore whenever you see an ECG
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with right axis deviation, you should search carefully for other confirmatory evidence
of RVH.
RVH not only produces depolarization (QRS) changes but also affects
repolarization (the ST-T complex). Hypertrophy of the heart muscle alters the normal
sequence of repolarization. In RVH the characteristic repolarization change is the
appearance of inverted T wave in the right and middle chest leads. These right chest T
wave inversions are referred to as a right ventricular strain pattern. (Strain is a
descriptive term. The exact mechanism for the strain pattern is not understood)
To summarize, ECG criteria of RVH
1. Right axis deviation > 1100 in frontal plane.
2. RV1 >10mm, RaVR >0.5mV.
3. RV1 + S V5 >1.2mV.
4. RV1 R/S > 1
5. ST segment depression, T wave inversion seen in right ventricular leads.
LEFT VENTRICULAR HYPERTROPHY (LVH)
The ECG changes produced by LVH, like as noted, the left ventricle is electrically
predominant over the right ventricle and produces prominent S waves in the right
chest leads and tall R waves in the left chest leads. When LVH is present, the balance
of electrical forces is tipped even further to the left. Thus, when LVH is present, the
chest leads will show abnormally tall R waves (left chest leads) and abnormally deep
S waves (right chest leads).
The following criteria and guidelines have been established to help in the ECG
diagnosis of LVH:
1. If the depth of the S wave in lead V1 (SV1) added to the height of the R wave in
either lead
V5 or V6 (RV5 or RV6) exceeds 35 mm (3.5 mV), then
suspect LVH.
2. You should also realize that high voltage in the chest leads in commonly seen as a
normal finding, particularly in young adults with thin chest walls. Consequently,
high voltage in the chest leads (SV1 + R V5 or RV6 > 35 mm) is not a specific
indicator of LVH.
3. In some cases LVH will produce tall R waves in lead aVL. And R wave of 13 mm
or more in lead aVL is another sign of LVH. Occasionally a tall R wave in lead
aVL may be the only ECG sign of LVH and the voltage in chest leads may be
normal. In other cases the chest voltages may be abnormally high, with a normal
R wave in lead aVL.
4. Furthermore, just as RVH is associated with a right ventricular strain pattern, so
left ventricular strain ST-T changes are often seen in LVH. Notice that the ST-T
complex has a distinctive asymmetric appearance, with slight ST-T segment
depression followed by a broadly inverted T wave. In some cases these left
ventricular strain T wave inversions may be very deep. The left ventricular strain
pattern is seen in leads with tall R waves.
5. With LVH the electrical axis usually horizontal. Actual left axis deviation (axis
–300 or more negative) may also be seen. In addition, the QRS complex may
become wider. Not uncommonly patients with LVH will eventually develop
complete left bundle branch block.
6. Finally, ECG signs of LAE (broad notched P waves in the extremity leads or wide
biphasic P waves in lead V1) are often seen in patients with ECG evidence of
LVH. Most conditions that lead to LVH ultimately produce LAE as well
A variety of clinical conditions are associated with LVH. In adults, three of the most
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common are (1) valvular heart disease, such as aortic stenosis, aortic regurgitation, or
mitral regurgitation, (2) hypertension, and (3) cardiomyopathies.
VII. Ventricular Conduction Disturbances
Bundle Branch Blocks
The normal process of ventricular stimulation was outlined in Chapter 4. The
electrical stimulus reaches the ventricles from the atria by way of the AV junction. As
mentioned, the first part of the ventricles normally stimulated (depolarized) is the left
side of the ventricular septum. Soon after, the depolarization spreads to the main mass
of the left and right ventricles by way of the left and right bundle branches. Normally
the entire process of ventricular depolarization is completed within 0.1 second.
Therefore, the normal width of the QRS complex is less than or equal to 0.1 second
(two and a half small boxes on the ECG graph paper). Any process that interferes with
the normal stimulation of the ventricles may prolong the QRS width. In this chapter
we will be concerned primarily with the effects of blocks within the bundle branch
system on the QRS complex.
RIGHT BUNDLE BRANCH BLOCK (RBBB)
Consider, first, the effect of cutting the right bundle branch. Obviously this will delay
right ventricular stimulation and widen the QRS complex. Furthermore, the shape of
the QRS complex with a right bundle branch block (RBBB) can be predicted on the
basis of some familiar principles.
Normally, as noted above, the first part of the ventricles to be depolarized is the
interventricular septum. The left side of the interventricular septum is stimulated first
(by a branch of the left bundle). This septal depolarization produces the small septal q
wave in lead V6 seen on the normal ECG. Clearly, RBBB should not affect this first
septal phase of ventricular stimulation, since the septum is stimulated by a part of the
left bundle.
The second phase of ventricular stimulation is the simultaneous depolarization of
the left and right ventricles. RBBB should not effect this phase either, since the left
ventricle is normally electrically predominant, producing deep S waves in the right
chest leads and tall R waves in the left chest leads.
The change in the QRS complex produced by RBBB is a result of the delay in the
total time needed for stimulation of the right ventricle. This means that following the
completion of left ventricular depolarization, the right ventricle continues to
depolarize. This delayed right ventricular depolarization produces a third phase of
ventricular stimulation. The electrical voltages in the third phase are directed to the
right, reflection the delayed depolarization and slow spread of the depolarization wave
outward through the right ventricle. Therefore a lead placed over the right side of the
chest will record this third phase if ventricular stimulation as a positive wide
deflection (R’wave). The same delayed and slow right ventricular depolarization
voltages spreading to the right will produce a wide negative (S wave) deflection in the
left chest leads. T wave inversions in the right chest leads are a characteristic finding
in RBBB. These T wave inversions are referred to as secondary changes because they
are related to the abnormal process of ventricular stimulation.
ECG criteria in RBBB
1. V1 rSR’.
2. I, V5, V6 qRS, (slurred and wide S waves.)
3. QRS > or = 0.12”
4. ST segment slight depression, T waves inversion.
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Complete vs Incomplete RBBB
RBBB can be further divided into complete and incomplete forms depending on the
width of the QRS complex. Complete RBBB is defined by a QRS complex (rSR’ in
lead V1 and qRS in V6) of 0.12 second or more width. Incomplete RBBB shows the
QRS shape described in the preceding section but the QRS duration is between 0.1
and 0,12 second.
Clinical Significance
RBBB may be caused by a number of factors. First, some normal people will show an
RBBB pattern without any underlying heart disease; therefore, RBBB per se is not
necessarily abnormal. In many persons, however, RBBB is associated with organic
heart disease. RBBB may be caused by any conditions that affect the right side of the
heart. In some cases, individuals (particularly older people) develop RBBB because of
chronic degenerative changes in the conduction system. RBBB may also occur with
myocardial ischemia and infarction. Pulmonary embolism, which produces acute
right-sided heart strain, may also produce RBBB.
The conduction disturbance does not, in itself, require any specific treatment.
LEFT BUNDLE BRANCH BLOCK (LBBB)
Left bundle branch block (LBBB) also produces a pattern with a widened QRS
complex. However, the shape of the QRS complex with LBBB is very different from
that with RBBB. The reason for this difference is that RBBB affects mainly the
terminal phase of ventricular activation. LBBB, on the other hand, affects the early
phase of ventricular depolarization as well.
Recall that the first phase of ventricular stimulation-depolarization of the left side
of the septum-is started by a part of the left bundle branch. LBBB, therefore, will
block this normal pattern of septal depolarization. When LBBB is present, the septum
depolarizes from right to left and not from left to right. Thus the first major change on
the ECG produced by LBBB will be a loss of the normal septal r wave in lead V1 and
the normal septal q wave in lead V6. Furthermore, the total time for left ventricular
depolarization will be prolonged with LBBB, resulting in an abnormally wide QRS
complex. Lead V6 will show a wide entirely positive (R) wave. The right chest leads
record a negative QRS (QS) complex because the left ventricle is still electrically
predominant with LBBB and produces greater voltages than the right ventricle. The
major change is that the total time for completion of left ventricular depolarization is
delayed. Therefore, with LBBB, the entire process of ventricular stimulation is
oriented toward the left chest leads-the septum depolarizing from right to left, with
stimulation of the electrically predominant left ventricle prolonged.
Just as there are secondary T wave inversions with RBBB, so there are also
secondary T wave inversions with LBBB. The T wave in the leads with tall R waves
is inverted. This T wave inversion is characteristic of LBBB. However, T wave
inversions in the right precordial leads cannot be explained solely on the basis of
LBBB and, if present, reflect some primary abnormality, such as ischemia.
Occationally an ECG will show wide QRS complexes that are not typical of an RBBB
or LBBB pattern. In such cases, the general term intraventricular delay is used.
ECG criteria in LBBB
1. V1 QS or rS with a wide S wave
2. I, V5, V6 a notched, wide tall R wave without a preceding q wave.
3. QRS > or = 0.12”
4. ST segment depression, T waves inversion in leads with a predominant R wave.
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Complete vs incomplete LBBB
As with RBBB, there are complete and incomplete forms of LBBB. With complete
LBBB, the QRS complex has the characteristic appearance described previously, and
the QRS complex is 0.12 second or wider. With incomplete LBBB, the QQRS
complex is between 0.1 and 0.12 second.
Clinical Significance
Unlike, RBBB, which is occasionally seen n normal people, LBBB is usually a sign
of organic heart disease. LBBB is often seen in elderly patients with chronic
degenerative changes in their myocardial conduction system. LBBB may develop in
patients with long-standing hypertensive heart disease, with valvular lesions or the
different types of cardiomyopathy. LBBB is also seen in patients with coronary artery
disease. Most patients with LBBB have underlying left ventricular hypertrophy. When
LBBB occurs with an acute myocardial infarction it is often a forerunner of complete
heart block. In rare instances some otherwise normal individuals will show an LBBB
pattern.
HEMIBLOCKS
We will conclude this chapter on ventricular conduction disturbances by introducing a
slightly more complex but important topic, the hemiblocks. Up to now we have
discussed the left bundle branch system as if it were a single pathway. Actually it has
been known for many years that the left bundle subdivides into major two branches,
or fascicles (fasciculus, latin, small bundle). The left bundle subdivides into an
anterior fascicle and a posterior fascicle. The right bundle branch, on the other hand,
is a single pathway and consists of just one main fascicle or bundle.
A block in either fascicle of the left bundle branch system is called a hemiblock.
Recognition of hemiblocks on the ECG is intimately related to the subject of axis
deviation, presented in chapter 5. Somewhat surprisingly, a hemiblock (unlike a full
left or right bundle branch block) does not widen the QRS complex markedly. It has
been found experimentally that the main effect of cutting these fascicles is to
markedly change the QRS axis. Specifically, left anterior hemiblock results in a
marked left axis deviation (- 450 or more); left posterior hemiblock produces a right
axis deviation (+ 1200 or more).
Left anterior hemiblock. Left anterior hemiblock is diagnosed by finding a mean
QRS axis of – 450 or more and a QRS width of less than 0.12 second. A mean QRS
axis of – 450 or more negative can be easily recognized because left axis deviation is
present and the S wave in lead aVF equals or exceeds the R wave in lead 1. rS wave in
leads II, III, and aVF, S III > S II.
Left posterior hemiblock. Left posterior hemiblock is diagnosed by finding a mean
QRS axis of + 1200 or more, with a QRS width of less than 0.12 second. However, the
diagnosis of left posterior hemiblock can be considered only if other, more common,
causes of right axis deviation (right ventricular hypertrophy, normal variant,
emphysema, lateral wall infarction, and pulmonary embolism) are first excluded.
Left anterior hemiblock is relatively common, while isolated left posterior
hemiblock is rare. We will discuss the clinical importance of the hemiblocks and
bifascicular and trifascicular blocks further in the section on complete heart block. In
general, the finding of isolated left anterior or left posterior hemiblock is not of much
clinical significance.
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VIII Myocardial Ischemia and Infarction-1
Transmural Infarct Patterns
MYOCARDIAL ISCHEMIA
Myocardial cells require oxygen and other nutrients to function. Oxygenated blood is
supplied by the coronary arteries. If blood flow becomes inadequate due to severe
narrowing or complete blockage of a coronary artery, ischemia of the heart muscle
will develop. The term “ischemia” means literally “to hold back blood.” Myocardial
ischemia may occur transiently. For example,. patients who experience angina
pectoris with exercise are having transient myocardial ischemia. If the ischemia is
more severe, actual necrosis (depth) of a portion of heart muscle may occur. The term
“myocardial infarction” (MI) refers to myocardial necrosis caused by severe ischemia.
TRANSMURAL AND SUBENDOCARDIAL ISCHEMIA
The left ventricle can be subdivided into an outer layer, the epicardium, and an inner
layer, the subendocardium. This distinction is important because myocardial ischemia
or infarction is sometimes limited to just the inner layer (subendocardial ischemia and
infarction) and sometimes affects the entire thickness of the ventricular wall
(transmural ischemia and infarction).
TRANXMURAL MI
Transmural infarction, as mentioned, is characterized by ischemia and ultimately, by
necrosis of a portion of the entire thickness of the left ventricular wall. Not
surprisingly, transmural infarction produces changes in both myocardial
depolarization (QRS complex) and myocardial repolarization (ST-T complex.)
The earliest changes seen with an acute transmural infarction occur in the ST-T
complex. There are two sequential phases to these ST-T changes seen with MI: the
acute phase and the evolving phase. The acute phase is marked by the appearance of
ST segment elevations and sometimes tall positive (hyperacute). T waves in certain
leads. The evolving phase (occurring after hours or days) is characterized by the
appearance of deep T wave inversions in those leads that previously showed ST
elevations.
Transmural MI can also be described in terms of the location of the infarct: anterior
means involving the anterior and/or lateral wall of the left ventricles (chest leads V1 to
V6, limb leads 1 and aVL): inferior means involving the inferior (diaphragmatic) wall
of the left ventricle.(leads II, III and aVF). For example, with an acute anterior wall
MI the ST segment elevations and tall hyperacute T waves appear in one or more of
the anterior leads.
One of the most important characteristics of the ST-T changes seen in MI is their
reciprocity. The anterior and inferior leads tend to show inverse patterns. Thus in an
anterior infarction with ST segment elevations in leads V1 to V6, 1, and aVL, leads II,
III and aVF will characteristically show ST segment depression.
The ST segment elevation seen in acute MI is called a “current of injury” and
indicates the acute injury to the epicardial layer of the heart, which occurs with
transmural infarction. The ST segment elevations (and reciprocal ST depressions) are
the earliest ECG signs of infarction and are generally seen within minutes of the
infarct. As mentioned previously, tall positive (hyperacute) T waves may also have the
same significance as the ST elevations. In some cases hyperacute T waves actually
precede the appearance of ST elevation.
After a variable time lag of hours to days, the ST segment elevations start to return
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to the baseline. At the same time the T waves begin to be inverted in leads that
previously showed ST segment elevations. This phase of T wave inversions is called
the evolving phase of the infarct. Thus, with an anterior wall infarction the T waves
become inverted in one or more of the anterior leads (V1 to V6, I, aVL). With an
inferior wall infarction the T waves become inverted in one or more of the inferior
leads (II, III, aVF).
QRS Changes: Q Waves of Transmural Infarction
Transmural infarction also produces distinctive changes in the QRS (depolarization)
complex. The characteristic sign of a transmural infarct is the appearance of new Q
waves. A Q wave in any lead simply indicates that the electrical voltages are directed
away from that particular lead. When transmural infarction occurs, there is necrosis of
heart muscle in a localized area of the ventricle; therefore the electrical voltages
produced by this portion of the myocardium will disappear. Instead of positive (R )
waves over the infarcted area. Q waves will be recorded (either a QR or a QS
complex).
LOCALIZATION OF INFARCTS
As mentioned, MIs are generally localized to a specific portion of the left ventricle,
affecting either the anterior or the inferior wall. Anterior infarcts are sometimes
considered as anteroseptal, strictly anterior, or anterolateral depending on the leads
that show signs of the infarct.
Anterior wall Infarcts
The characteristic feature of anterior wall infarcts is a loss of the normal R wave
progression in the chest leads. Normally there is a progressive increase in the height
of the R wave as you move from the right to the left chest leads. An anterior infarct
interrupts this normal R wave progression, resulting in pathologic Q waves in one or
more of the chest leads.
Anteroseptal infarcts. Normally, as mentioned earlier, the ventricelar septum is
depolarized from left to right. So leads V1 and V2 show small positive r waves (septal
r waves), consider the effect of damaging the septum. Clearly, you would expect to
see a loss of septal depolarization voltages; thus, in leads V1 and V2 the normal septal
r waves will be lost and an entirely negative QS complex will appear.
The septum is supplied with blood by the left anterior descending coronary artery,
and septal infarction generally suggests that there has been an occlusion of this artery
or one of its branches.
Strictly anterior infarcts. Normally leads V3 and V4 show RS- or Rs-type complexes.
If the anterior wall of the left ventricle is infarcted, then the positive R waves that
reflect the voltages produced by this muscle area will be lost. Instead, Q wave, as part
of QS or QR complexes, Q waves, as part of QS or QR complexes will be seen in
leads V3 and V4. Strictly anterior infarcts generally also result from occlusion of the
left anterior descending coronary artery.
Anterolateral infarcts. Infarction of the lateral wall of the left ventricle produces
changes in the more laterally situated chest leads, for example, leads V5 and V6. With
lateral wall infarction, abnormal Q waves, as part of QS or QR complexes, appear in
leads V5 and V6. Lateral wall infarction is often caused by an occlusion of the left
circumflex coronary artery but may also result from occlusion of the left anterior
descending coronary artery or a branch of the right coronary artery.
Differentiating anterior wall infarctions. The above classification of anterior
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infarcts – as anteroseptal, strictly anterior, and anterolateral – is not absolute. Often
there is overlap. You can simply describe Mis by calling any infarct that shows ECG
changes in one or more of leads I, aVL, and V1 to V6 as “anterior” and then specifying
which leads show Q waves and ST-T changes.
Inferior wall infarcts
Infarction of the inferior (diaphragmatic) portion of the left ventricle is indicated by
changes in leads II, III, and aVF. These three leads, as shown in the frontal plane axis
diagram, are oriented downward or inferiorly. Thus these leads will record voltages
from the inferior portion of the ventricle. An inferior wall infarct will produce
abnormal Q waves in leads II, III, and aVF.
Inferior wall infarction is generally caused by occlusion of the right coronary artery
and, less commonly, by a left circumflex coronary obstruction.
“Posterior” Infarcts
The posterior (back) surface of the left ventricle can also be infarcted. This may be
difficult to diagnose because characteristic abnormal ST elevations may not appear in
any of the 12 conventional leads. Instead, a tall R wave and ST segment depression
may occur in chest leads V1 and V2 (reciprocal to the Q wave and ST segment
elevations that would be recorded at the back of the heart). During the evolving phase
if such infarcts, when deep T wave inversions appear in the posterior leads, the
anterior chest leads will show reciprocally tall positive T waves.
In most cases of posterior MI the infarct extends either to the lateral wall of the left
ventricle, producing characteristic changes in lead V6, or to the inferior wall of the left
ventricle, producing characteristic changes in leads II, III, and aVF. Because of the
overlap between inferior and posterior infarcts the more general term
“inferoposterior” can be used when the ECG shows changes consistent with either
inferior or posterior infarction.
Right Ventricular (RV) Infarcts
A related topic is right ventricular (RV) infarction. Recent studies show that a high
percentage of patients with an inferoposterior infarct have associated RV involvement.
In one autopsy study RV infarction was noted in about one of four cases of
inferoposterior MI but not in cases of anterior MI. Clinically patients with an RV
infarct may have elevated central venous pressure (distended neck veins) because of
the abnormally high diastolic filling pressures in the right side of the heart. If the RV
damage is severe, hypotension and even cardiogenic shock may result. AV conduction
disturbances are not uncommon in this setting. The presence of jugular venous
distension in a patient with an acute inferoposterior MI should always suggest this
diagnosis. In addition, many of these patients will show ST segment elevations in
leads reflecting the right ventricle, such as V1 to V3 and V3R to V5R.
Recognition of RV infarction is of major clinical importance. Volume expansion
may be critical in patients who are hypotensive and have a low or normal pulmonary
capillary wedge pressure despite elevated systemic venous pressure. Patients with an
acute RV infarct may also be at increased risk for the development of ventricular
fibrillation during placement of a temporary pacemaker.
Subendocardial Ischemia and Infarct Patterns
Transmural myocardial infarction (MI) may be associated with abnormal Q waves and
typical progression of ST-T changes described in Chapter 8. In other cases (described
in this Chapter), however, myocardial ischemia with or without actual infarction may
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be limited to the subendocardial layer of the ventricle.
SUBENDOCARDIAL ISCHEMIA
The most common ECG change with subcardial ischemia is ST segment depression.
The ST segment depression caused by subendocardial ischemia nay be limited to the
anterior leads or to the inferior leads, or may be seen more diffusely in both groups of
leads. The ST segment depression seen with subendocardial ischemia has a
characteristic squared-off shape. (ST segment elevations may be seen in lead aVR.)
ECG Changes with Angina pectoris
The term “angina pectoris” refers to transient attacks of chest pain caused by
myocardial ischemia. Angina is a symptom of coronary artery disease. The classic
attack of angina is experienced as a dull, burning, or boring substernal pressure or
pain. angina is typically precipitated by exertion, stress, exposure to cold, and so on,
and is relieved by rest and nitroglycerin.
Many patients with classic angina will show an ECG pattern of subendocardial
ischemia, with ST segment depressions during an attack. When the pain disappears,
the ST depressions generally return to the baseline. Not all patients with angina will
show ST depressions during chest pain. The presence of a normal ECG does not rule
out underlying coronary artery disease. However, the appearance of transient ST
segment depression with chest pain is a strong indicator of myocardial ischemia.
Similar ST segment depressions may develop during exercise (with or without
chest pain) in people with ischemic heart disease. Recording the ECG during exercise
(stress electrocardiography) is a method of determining the presence of ischemic heart
disease. ST segment depression of 1 mm or more, lasting 0.08 second or more, is
generally considered a positive (abnormal) response. However, false-negative (normal)
results can occur in patients with ischemic heart disease and false-positive results can
occur in normal people.
SUBENDOCARDIAL INFARCTION
If the ischemia to the subecdocardial region is severe enough, actual subendocardial
infarction may occur. In such cases the ECG may show persistent ST segment
depression instead of the transient ST depressions seen with reversible subendocardial
ischemia.
Do Q waves appear with pure subendocardial infarction? The answer is that if only
the subendocardium is infarcted abnormal Q waves are seen only with transmural
infarction. Subendicardial infarction generally affects ventricular repolarization (ST-T
complex) and not depolarization (QRS complex). However, exceptions may occur.
Another pattern sometimes seen in cases of nontransmural (non-Q wave) infarctions
is T wave inversion with or without ST segment depressions.
ECG Changes Associated with Noninfarctional Ischemia
Prinzmetal’s angina occurs in patients who develop transient ST segment elevations,
suggestive of epicardial or transmural ischemia, during attacks of angina. These
patients have atypical chest pain, which occurs at rest or at night, in contrast to classic
angina, which is typically exertional and is associated with ST segment depressions.
Prinzmetal’s (variant) angina pattern is generally a marker of coronary artery spasm
with or without underlying coronary obstructions.
The ST segment elevations of acute transmural MI can be simulated by the ST
segment elevations of Prinzmeral’s angina as well as by the normal variant ST
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segment elevations seen in some healthy people (“early repolarization pattern”) and
by the ST segment elevations of acute pericarditis.
The abnormal ST segment depressions of subendocardial ischemia or infarction can
be simulated by the pattern of left ventricular strain, digitalis effect, or hypokalemia.
T wave inversions may be a sign of ischemia or infarction but may also occur in a
variety of other settings, including normal variants, ventricular strain, pericarditis,
subarachnoid hemorrhage, secondary ST-T changes due to bundle branch block, and
so on.
x. Miscellaneous ECG Patterns
WOLFF-PARKINSON-WHITE SYNDROME (WPW)
The Wolff-Parkinson-White (WPW) syndrome is an unusual and distinctive ECG
abnormality caused by pre-excitation of the ventricles. Normally the electrical
stimulus passes to ventricles from the atria via the AV junction. The physiologic lag of
conduction through the AV junction results in the normal PR interval of 0.12 to 0.2
second. Imagine the consequences of having an accessory conduction pathway
between the AV junction and pre-excite the ventricles. This is exactly what occurs in
the WPW syndrome: an accessory conduction fiber (the bundle of Kent) connects the
atria and ventricles, bypassing the AV junction.
Pre-excitation of the ventricles in the WPW syndrome produces the following three
characteristic changes on the ECG:
1. The PR interval is shortened (often but not always <0.12 sec) because of
ventricular pre-excitation.
2. The QRS complex is widened, giving the superficial appearance of a bundle
branch block pattern. The wide QRS in the WPW syndrome is caused not by a
delay in ventricular depolarization but by early stimulation of the ventricles. The
QRS complex will be widened to the degree that the PR interval is shortened.
3. There is slurring, or notching, of the upstroke of the QRS complex. This is called
a delta wave.
The significance of the WPW syndrome is twofold. First, patients with this pattern
are prone to atrial arrhythmias, especially paroxysmal atrial tachycardia and atrial
fibrillation. Second, the ECG of these patients is often mistaken as indicating a bundle
branch block or myocardial infarction.
The WPW syndrome predisposes to paroxysmal atrial tachycardia in particular
because of the accessory conduction pathway. For example, an impulse traveling
down the AV junction may recycle up the bundle of Kent and then back down the AV
junction, and so on. This type of reentry mechanism (circus movement) may also
account for other types of tachycardias.
Another type of pre-1excitation variant, the Lown-Ganong-Levine (LGL) pattern, is
caused by a bypass tract (James fiber) that connects the atria and AV junction.
Bypassing the AV node results in a short PR interval (less than 0.12 sec). However,
the QRS width will not be prolonged because ventricular activation occurs normally.
Therefore, the LGL pattern consists of a short PR interval with a normal-width QRS
and no delta wave; the WPW syndrome consists of a short PR interval with a wide
QRS and delta wave. Patients with the LGL pattern may also have “reentrant”
paroxysmal atrial tachycardia (PAT).
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I.Arrhythmia
NORMAL SINUS RHYTHM (NSR)
The diagnosis of normal, or regular, sinus rhythm (NSY) was already described in
Chapter 3. When the sinus (SA) node is pacing the heart, atrial depolarization spreads
from right to left and downward toward the AV junction. An arrow representing this
atrial depolarization wave will point downward and toward the left. Therefore, as
described earlier, with NSR, the P wave is negative in lead aVR and reciprocally
positive in lead II.
By convention, NSR is defined as sinus rhythm with a heart rate between 60 and
100 beat/min. Sinus rhythm with a heart rate of less than 60 beat/min is called sinus
bradycardia; one with a heart rate greater than 100 beat/min is called sinus
tachycardia.
REGULATION OF THE HEART RATE
The heart, like the other organs, has a special nerve supply from the autonomic
nervous system, which controls involuntary muscle action. The autonomic nerve
supply to the heart consists of two opposing groups of never fibers: the sympathetic
nerves and the parasympathetic nerves. The sympathetic fibers supply the sinus node,
the atria, the AV junction, and the ventricles. Sympathetic stimulation produces an
increased heart rate and also increases the strength of myocardial contraction. The
parasympathetic nervous supply to the heart is from the vagus nerve, which supplies
the sinus node, atria, and AV junction. Vagal stimulation produces a slowing of the
heart rate as well as a slowing of conduction through the AV junction. In this way, the
autonomic nervous system exerts a counterbalancing control of heart rate. The
sympathetic nervous system acts as a cardiac accelerator, while the parasympathetic
(vagal) fibers produce a braking effect. For example, when you become excited or
upset, increased sympathetic stimuli (and diminished parasympathetic tone) result in
an increased heart rate and increased contractility, producing the familiar sensation of
a pounding heart (palpitations).
SINUS TACHYCARDIA
Sinus tachycardia is simply sinus rhythm with a heart rate exceeding 100 beats/min.
Generally in adults the heart rate with sinus tachycardia is between 100 and 180
beats/min. in sinus tachycardia, each QRS complex is preceded by a P wave. Note that
the P waves are positive in lead II. With sinus tachycardia at very fast rates, the P
waves may merge with the preceding T wave and become difficult to distinguish.
The following conditions are commonly associated with sinus tachycardia:
1. Anxiety, emotion, and exertion
2. Drugs such as epinephrine, ephedrine, and isoproterenol (isoprel) that increase
sympathetic
tone
3. Drugs such as atropine that block vagal tone
4. Fever
5. Congestive heart failure (Sinus tachycardia caused by increased sympathetic tone
is generally seen with pulmonary edema.)
6. Pulmonary embolism (Sinus tachycardia ia the most common arrhythmia seen
with acute pulmonary embolism)
7. Acute myocardial infarction, which may produce virtually any arrhythmia (Sinus
tachycardia persisting after an acute infarct is generally a bad prognostic sign and
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implies extensive heart damage.)
8. Hyperthyroidism (Sinus tachycardia occurring at rest is a common finding.)
9. Hypotension and shock associated with myocardial infarction, sepsis, or blood
loss
SINUS BRADYCARDIA
With sinus bradycardia, sinus rhythm is present and the heart rate is less than 60
beats/min. It is commonly occurs in the following conditions:
1. as a normal variant (Many normal people have a resting pulse rate of less than 60
beats/min, and trained athletes may have a pulse rate as low as 35 beats/min.)
2. Drugs that increase vagal tone, such as digitalis or edrophonium (Tensilon), or
that decrease sympathetic tone, such as propranolol (Inderal) or reserpine (In
addition, calcium channel-blocking drugs such as diltiazem hydrochloride and
verapamil may cause marked sinus bradycardia.)
3. Hypothyroidism (This is generally associated with a sinus bradycardia, just as
hyperthyroidism produces a resting sinus tachycardia.)
4. “sick sinus syndrome” (Some patients, particularly among the elderly, will have
marked sinus bradycardia without obvious cause, probably from degenerative
disease of the sinus node.
5. Sleep apnea syndrome
6. Carotid sinus syndrome
SINUS ARRHYTHMIA
Even in healthy persons the sinus node does not pace the heart at a perfectly regular
rate. Actually, there is normally a slight beat-to-beat variation in sinus rate. Sometimes,
when this beat-to-beat variability in sinus rate is more accentuated, the term “sinus
arrhythmia” is used. Sinus arrhythmia, therefore, is sinus rhythm with an irregular rate.
The variation of the P-P interval is grater than 0.12 seconds.
The most common cause of sinus arrhythmia is respiration. With inspiration the
heart rate normally increases slightly; with expiration it slows slightly. This
respiratory, or phasic, sinus arrhythmia is caused by slight changes in vagal tone
occurring during the different phases of respiration.
Occasionally a nonphasic sinus arrhythmia occurs, and the heart rate varies from
beat to beat without relation to the respiratory cycle.
Phasic sinus arrhythmia is a normal finding. Particularly in children. A nonphasic
sinus arrhythmia, while not strictly normal, does not have any special pathologic or
therapeutic significance.
SINUS ARREST AND ESCAPE BEATS
Suppose for some reason the sinus node fails to function for one or more beats. Such
failure of the sinus node to pace is called sinoatrial block (SA block). SA block may
occur intermittently, where there is simply a missing beat (no P wave or QRS complex)
at occasional intervals, or it may be more extreme. Sinus pause or arrest is the sinus
node fails to function altogether for a prolonged period. This type of block will lead to
cardiac arrest with asystole unless the sinus node regains function or some other
pacemaker (escape pacemaker) takes over. Fortunately, as mentioned earlier, other
parts of the cardiac conduction system are capable of producing electrical stimuli and
functioning as an escape pacemaker in these circumstances. Escape beats may come
from the atria, the AV junction, or the ventricles.
SA block and sinus arrest can be caused by numerous factors, including hypoxia,
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myocardial ischemia, hyperkalemia, digitalis toxicity, and toxic reactions to other
drugs such as the beta-blockers and calcium-channel blockers. In elderly people the
sinus node may undergo degenerative changes and fail to function effectively. The
term “sick sinus syndrome” is used to refer to this type of sinus node dysfunction.
SICK SINUS SYNDROME AND THE BRADY-TACHY SYNDROME
The term “ sick sinus syndrome” has been coined to describe patients who develop
sinus node dysfunction that causes marked sinus bradycardia, sinus arrest, or
junctional escape rhythms, which may lead to symptoms of light-headedness and even
syncope.
In some patients with the sick sinus syndrome, these bradycardic episodes alternate
with periods of tachycardia (for example, paroxysmal atrial tachycardia, atrial
fibrillation, or even ventricular tachycardia). Sometimes the bradycardia will occur
immediately after spontaneous termination of the tachycardia. The term “brady-tachy
syndrome” has been used to describe this subset of patients with sick sinus syndrome
who have tachyarrhythmias as well as bradyarrhythmia.
2. Supraventricular Arrhythmias – 1
Premature Atrial Contractions, Paroxysmal Atrial Tachycardia, AV junctional
Rhythms
The normal pacemaker of the heart is the sinus node, and normally it initiates each
heartbeat. However, pacemaker stimuli can arise from other parts of the heart-the atria,
the AV junction, or the ventricles. The terms “ectopy,” “ectopic pacemaker,” and
“ectopic beat” are used to describe these nonsinus beats. Ectopic beats are often
premature; that is, they come before the next sinus beat is due. Thus we may find
premature atrial contractions (PACs), premature AV junctional contractions (PJCs),
and premature ventricular contractions (PVCs). Ectopic beats can also come after a
pause in the normal rhythm, as in the case of AV junctional or ventricular escape beats.
Ectopic beats originating in the AV junction or atria are referred to as supraventricular
(that is, coming from above the ventricles).
PREMATURE ATRIAL CONTRACTIONS (PACs)
Premature atrial contractions (PACs) are ectopic beats arising from somewhere in
either the left or the right atrium but not in the sinus node. The atria, therefore, are
depolarized from an ectopic site. Following atrial stimulation, the stimulus will spread
normally through the AV junction into the ventricles. For this reason, ventricular
depolarization (QRS) is generally not affected by PACs.
PACs have the following major features:
1. The beat is premature, occurring before the next normal beat is due. This is in
contrast to escape beat, which come after a pause in the normal rhythm.
2. The PAC is often, but not always, preceded by a visible P wave. This P wave
usually has a slightly different shape and/or slightly different PR interval from the
P wave seen with the normal sinus beats. The PR interval of the PAC may be
either longer or shorter than the PR interval of the normal beats.
3. Following the PAC there is generally a slight pause before the normal sinus beat
resumes.(incomplete compensatory pause)
4. Occasionally, no clear P wave will be seen preceding the PAC. In such cases the P
wave may be “buried” in the T wave of the preceding beat.
5. The QRS complex of the PAC is usually identical or very similar to the QRS
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6.
7.
complex of the preceding beats. Remember that with PACs the atrial pacemaker
is in an ectopic location, but the ventricles are depolarized in a normal way. This
contrasts with premature ventricular contractions where the QRS complex is
abnormally wide because of abnormal depolarization of the ventricles.
Occasionally, PACs will result in aberrant ventricular conduction so the QRS is
wider than normal. Differentiation of such PACs “with aberration” from
premature ventricular contractions may be difficult.
Sometimes, when the PAC is very premature, the stimulus will reach the AV
junction shortly after it has already been stimulated by the preceding normal beat.
Because the AV junction, like all other conduction tissue, requires time to recover
its capacity to conduct impulses, this premature atrial stimulus may reach the
junction when it is still refractory. In such cases the PAC may not be conducted to
the ventricles and no QRS complex will appear. This situation will result in a
blocked PAC. The ECG will show a premature P wave not followed by a QRS
complex. Following the blocked P wave, there is a slight pause before the next
normal beat resumes. The blocked PAC, therefore, produces a slight irregularity
of the heartbeat. If you do not search carefully for these blocked PACs you will
overlook them.
PACs may occur frequently (for example, five or more times/min) or sporadically.
Two PACs occurring consecutively are referred to as “paired PACs.” Sometimes,
each sinus beat is followed by a PAC. This pattern is referred to as atrial
bigeminy.
Clinical Significance
PACs are very common. They may occur both in persons with normal hearts and in
persons with organic heart disease. Finding PACs, therefore, does not imply that the
person has cardiac disease. In normal subjects PACs may be seen with emotional
stress, with excessive coffee drinking, or as a result of sympathomimetic drugs. PACs
may produce palpitations-the patient may complain of feeling a skipped beat or an
irregular pulse. PACs, as noted, may also be seen with any type of heart disease.
Frequent PACs are sometimes the forerunner of atrial fibrillation or paroxysmal atrial
tachycardia.
PAROXYSMAL ATRIAL TACHYCARDIA (PAT)
Paroxysmal atrial tachycardia (PAT) is the second tachyarrhythmia we shall discuss.
The first was sinus tachycardia. PAT is simply a run of three or more consecutive
PACs.
In some cases, the run of PAT may be brief and self-limited. In other cases, it may
be sustained for hours, days, or even weeks.
PAT has the following characteristics:
1. The heart rate with PAT is generally between 140 and 250 beats/min. Recall that
with sinus tachycardia the heart rate in adults did not generally exceed 160 to 180
beats/min.
2. PAT is usually extremely regular. Each beat falls exactly on time, and the RR
intervals between beats do not generally show any variability. This also contrasts
with sinus tachycardia, in which there is generally some slight but discernible
beat-to-beat variability.
3. P waves may or may not be visible. When seen, they are generally different from
the P waves in a patient with normal sinus rhythm. The PR interval may be the
same as, greater than, or less than the patient’s usual PR interval.
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4. The QRS complexes are usually of normal width, since intraventricular
conduction is generally normal with PAT. (A wide QRS complex will be seen if
the patient has an underlying bundle branch block or if the PAT induces a
“rate-related” bundle branch block.)
Clinical Significance
PAT may be seen both in normal persons and in those with organic heart disease. It ,
therefore, does not necessarily imply that the patient has any significant heart disease.
PAT may also occur with heart disease of any type. Occasionally, a run of PAT in a
patient with limited cardiac reserve may precipitate angina pectoris or congestive
heart failure.
AV JUNCTIONAL RHYTHMS
With PACs and PAT the ectopic pacemaker is located somewhere in the atria outside
the sinus node. Under certain circumstances, the AV junction may also function as an
ectopic pacemaker, producing an AV junctional rhythm.
AV junctional rhythm shows the following features:
1. The P, when seen, is negative (downward) in lead II and positive (upward ) in
lead
aVR, just the reverse of the pattern seen with normal sinus rhythm.
These are called retrograde P wave.
2. These retrograde P waves may precede or follow the QRS complex.
3. In some cases, retrograde P waves may be buried within the QRS complex. If this
occurs, then the baseline between the QRS complexes remains completely flat.
AV junctional rhythms can be considered in two general classes-slow escape
rhythms and tachycardias-depending on the rate. The slow junctionl escape rhythms
are less than 60 beats/min. The junctional tachycardias have rates between 100 and
250 beats/min.
AV Junctional Escape Rhythms
AV junctional escape beats were mentioned previously in the section on sinus arrest.
An AV junctional escape beat is simply a beat comes after a pause because the normal
sinus pacemaker fails to function. The AV junctional escape beat, therefore, is a
“safety beat.” Following this escape beat, the normal sinus pacemaker may resume
function. However, if this does not occur, a slow AV junctional escape rhythm may
continue. An AV junctional escape rhythm is simply a consecutive run of AV
junctional beats. The heart rate is usually slow, between 30 and 60 beats/min.
AV junctional escape rhythms can be seen in a number of clinical setting – digitalis
toxicity, toxic reactions to betablockers or calcium-channel blockers, acute myocardial
infarction, hypoxemia, hyperkalemia,
AV Junctional tachycardias
The AV junction can also be the site of ectopic stimuli producing premature AV
junctional contractions (PJCs) and junctional tachycardia.
PJCs are simply premature beats formed in the AV junction. They resemble
premature atrial contractions (PACs), except that the P waves, when seen, will be
retrograde with a PJC. If no P wave is seen before the premature beat, then there is no
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way of telling if it is a PAC (with P wave lost in the preceding T wave) or a PJC (with
the P wave buried in the QRS complex). The distinction is purely academic. PACs and
PJCs have the same clinical significance, and treatment is the same.
An AV junctional tachycardia, analogous to PAT, is simply a run of three or more
consecutive PJCs. AV junctional tachycardia and PAT can be considered clinically as a
single entity. They have the same clinical significance and treatment.
3.Supraventricular Arrhythmias-II
Atrial flutter and Atrial Fibrillation
Atrial flutter and atrial fibrillation are two distinct but related arrhythmias. Like PAT,
atrial flutter and atrial fibrillation are ectopic atrial rhythms. With all three
arrhythmias, the atria are not stimulated from the sinus node but from an ectopic site.
In PAT the atria are stimulated at a rate generally between 140 and 250 beats/min. In
atrial fullter, the atrial rate is even faster, generally between 250 and 350 beats/min.
Finally, with atrial fibrillation, the atrial depolarization rate is between 400 and 600
beats/min. You can consider these three ectopic atrial tachyarrhythmias on a
continuum from PAT to atrial flutter to atrial fibrillation, with the atrial rate becoming
progressively more rapid in each case.
ATRIAL FLUTTER
Atrial flutter shows the following;
1. Characteristic sawtooth flutter waves occur instead of P waves.
2. The ventricular rate may vary. For example, QRS complexes may occur with
every fourth flutter wave. This is called 4:1 flutter. With 2:1 flutter, there is one
QRS complex for every two flutter waves, and the ventricular rate is half the
atrial rate. A 1:1 atrial flutter with a ventricular rate about 300 beats/min is rare.
Atrial flutter rarely, if ever, occurs in normal hearts and is most
often seen in patients with valvular heart disease, ischemic heart
disease, lung disease, cardiomyopathy, pulmonary emboli, and after
cardiac surgery.
ATRIAL FIBRILLATION
Atrial fibrillation shows the following:
1. Rapid irregular undulations of the baseline (fibrillatory wave) occur instead of P
waves.
2. A ventricular rate that is usually grossly irregular is seen. When the patient is
given digitalis, the ventricular rate will slow.
In some cases, atrial fibrillation occurs chronically. In other cases,
it is paroxysmal. Atrial fibrillation occasionally occurs in normal
people. Common cause of atrial fibrillation are coronary artery
disease, hypertensive heart disease, and rheumatic valvular heart
disease. Atrial fibrillation may also occur with hyperthyroidism,
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cardiomyopathy, cardiac surgery,
pericarditis, and other conditions.
pulmonary
emboli,
chronic
4 Ventricular Arrhythmias
PREMATURE VENTRICULAR CONTRACTIONS (PVCs)
Premature ventricular contractions (PVCs) are premature beat arises in either the right
or the left rntricle. Therefore, the ventricles will not be stimulated simultaneously, and
the stimulus will spread through the ventricles in an aberrant direction. Thus the QRS
complex will be wide with PVCs just as it is with a bundle branch block pattern.
PVCs have two major characteristics:
1. They are premature and occur before the next normal beat is expected.
2. They are aberrant in appearance. The QRS complex is abnormally wide (usually
0.12 sec or more). The T wave and the QRS complex usually point in opposite
directions.
3. A fully compensatory pause.
Features
There are several features of PVCs that are of clinical importance.
PVCs may occur with varying frequency. Two in a row are called a couplet. Three
in a row are ventricular tachycardia. When a PVCs occurs regularly after each normal
beat. This is called ventricular bigeminy. When the rhythm is two normal beats
followed by a PVC, this is ventricular trigeminy.
The term coupling interval is refers to the interval between the PVC and the
preceding normal beat. There are two types of coupling interval. one is fixed coupling
interval. Another is variably coupling interval.
A PVC is often followed by a fully compensatory pause before the next beat. A full
compensatory pause indicates that the interval between the normal QRS complexes
immediataly before and immediately after the PVC is exactly twice the basic RR
interval. A full compensatory pause is more characteristic of PVCs than of PACs.
Sometimes a PVC will fall almost exactly between two normal beats, and in such
cases the PVC is said to be interpolated.
Uniform PVCs have the same shape in a single lead. Multiform PVCs have
different shapes in the same lead.
When a PVC occurs simultaneously with the apex of the T wave of the preceding
beat, this is called an R on T phenomenon. It may be the forerunner of ventricular
tachycardia or ventricular fibrillation.
Clinical Significance
PVCs are among the most commonly seen arrhythmias. They may occur both in
normal people and also in those with serious organic heart disease. They may be a
stable and benign finding. Or they may be precursors of cardiac arrest and sudden
death from ventricular fibrillation.
PVCs may cause by anxiety or excessive caffeine. Certain drugs, such as
epinephrine, isoproterenol, and aminophylline. PVCs are very common in cardiac
disease, such as valvular heart disease, hypertensiove heart disease, ischemic heart
disease with or without myocardial infarction, hypoxemia, congestive heart failure,
digitalis toxicity or toxicity due to other drugs, hypokalemia, hypomagnesemia and so
on.
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VENTRICULAR TACHYCARDIA
Ventricular tachycardia is a run of three or more PVCs. Ventricular tachycardia may
occur as a single isolated burst, may recur paroxysmally, or may persist for a long run.
The heart rate is generally between 100 and 200 beats/min. Very rapid ventricular
tachycardia with a sine-wave appearance is sometimes referred to as ventricular flutter
and usually leads to ventricular fibrillation.
Sustained ventricular tachycardia is a life-threatening arrhythmia for tow major
reasons. First, most patients are not able to maintain an adequate blood presure with
this rapid a heart rate and quickly become hypotensive. Second, sustained ventricular
tachycardia may degenerate into ventricular fibrillation, producing cardiac arrest.
The etiologic factors of ventricular tachycardia are the same as those discussed
earlier with PVCs. The same list of reversible cause of PVCs also applies in
evaluating patients with ventricular tachycardia.
VENTRICULAR FIBRILLATION
In ventricular fibrillation, the ventricles do not beat in any coordinated fashion but
instead fibrillate or twitch asynchronously and ineffectively. There is no cardiac
output, and the patient becomes unconscious immediately. Ventricular fibrillation is
one of the three major ECG patterns seen with cardiac arrest. The other two are
asystole and electromechanical dissociation.
The ECG in ventricular fibrillation shows characteristic fibrillatory waves with an
irregular pattern that may be either coarse or fine.
Ventricular fibrillation may occur in patients with heart disease of any type. It may
be preceded by warning arrhythmias, such as PVCs or ventricular tachycardia, or it
may occur spontaneously. Ventricular fibrillation may also occur in normal hearts,
owing to the toxic effects of drugs such as epinephrine, during anesthesia, with
lightning stroke, and so on.
ACCELERATED IDIOVENTRICULAR RHYTHM (AIVR)
AIVR is a ventricular arrhythmia that resembles a slow ventricular tachycardia with a
rate between 50 and 100 to 110 beats/min. The ECG with AIVR shows wide QRS
complexes without P waves. It is commonly seen with myocardial infarction and is
usually self-limited.
TORSADES DE
TACHYCARDI
POINTES:
A
SPECIAL
FORM
OF
VENTRICULAR
Torsades de pointes is the name of a recently described form of ventricular
tachycardia in which the QRS complexes appears to rotate cyclically, pointing
downward for several beats and then twisting and pointing upward in same lead.
This arrhythmia classically occurs in the setting of delayed ventricular
repolarization, evidenced by prolongation of the QT interval or the presence of
prominent U wave. Reported causes include
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1. Drug toxicity, particularly that due to quinidine and related antiarrhythmic agents
2. Electrolyte imbalance, including hypokalemia, hypomagnesemia, and
hypocalcemia, which prolong repolarization
3. Miscellaneous factors such as complete heart block, hereditary QT prolongation
syndrome, liquid protein diets, and myocardial ischemia
5 AV Heart Block
Heart block is the general term for atrio-ventricular (AV) conduction disturbances.
Normally, the AV junction acts like an apparent bridge between the atria and the
ventricles. The PR interval is between 0.12 and 0.2 second. Heart block occurs when
there is impaired condition through the AV junction, either transiently or permanently.
The mildest form of heart block is called first-degree heart block. The second-degree
heart block is an intermediate grade of AV conduction disturbance. The most extreme
form of heart block is called third-degree or complete heart block. Here the AV
junction does not conduct any stimuli between the atria and ventricles.
ECG criteria:
1. First-degree AV block- the RP interval is uniformly prolonged beyond 0.2 second.
2. Second-degree AV block- there are two subtypes:
a) Wenckebach (mobitz type 1) AV block – increasing prolongation of the PR
interval occurs until a P wave is blocked and not followed by a QRS complex.
This produces a distinctive clustering of QRS complexes separated by a pause
resulting from the dropped beat. The QRS clustering is known as group beating.
b) Mobitz type II AV block – a series of P waves occurs without QRS complexes,
followed by a P wave and a QRS complex; for example, with 3:1 block, every
third P wave is conducted and followed by a QRS complex. The conduced P
waves have the same PR interval.
3. Third-degree (complete) AV block – this shows the following:
a) The atria and ventricle beat independently because stimuli cannot pass
through the AV junction.
b) The atrial rate is faster than the ventricular rate.
c) The PR interval constantly changes.
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Chapter 2
Ultrasonic Examination
All diagnostic ultrasound applications are based on the detection and display of
acoustic energy reflected from interfaces within the body. These interactions provide
the information needed to generate high-resolution, gray-scale images of the body as
well as display information related to blood flow. The unique imaging attributes of
ultrasound have made it an important and versatile medical imaging tool.
In the past 50 years, along with the development of acoustic theory, computer
technology, the diagnostic ultrasound, which developed from the earliest A-mode
and M-mode one-dimensional ultrasound imaging, B-mode two-dimensional imaging
to the dynamic real-time three-dimensional imaging, from grey-scale ultrasound to
color Doppler flow imaging, has experienced unprecedented advancement.
Since diagnostic ultrasound now is used not only to observe appearance, but also
detect human organ function and blood flow, it plays an important role in clinical
diagnosis and treatment. Ultrasonic diagnostics has now become a mature subject and
an important branch in the medical imaging.
Physics of Ultrasound
I． Physical characteristic
1. Ultrasound:
In nature, acoustic frequencies span a range from less than 1 Hz to more than
100,000 Hz(100 kHz). Human hearing is limited to the lower part of this range,
extending from 20 to 20,000 Hz. Ultrasound differs from audible sound only in its
frequency, and is more than 20,000 Hz.
Sound frequencies used for diagnostic applications typically range from 2.5 to 10
MHz.
In tissue and fluids, ultrasound propagation is along the direction of particle
movement(longitudinal waves). The propagation velocity of sound, c, is related to
frequency and wavelength by the following simple equation:
c=fλ
The velocity at which the wave moves through tissue varies greatly and is
affected by the physical properties of the tissue. Propagation velocity is largely
determined by the resistance of the medium to compression. This, in turn, is
influenced by the density of the medium and its stiffness or elasticity. Propagation
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velocity is increased by increasing stiffness and reduced by increasing density. In the
body, propagation velocity may be regarded as constant for a given tissue and is not
affected by the frequency or wavelength of the sound. In the body, the propagation
velocity of sound is assumed to be 1540 m/sec. This value is the average of
measurements obtained from normal tissue. Although this is a value representation of
most soft tissues, some tissues, such as aerated lung and fat, have propagation
velocities significantly less than 1540 m/sec, and others, such as bone, have greater
velocities.
2. Acoustic Impedance:
Acoustic impedance, Z, is determined by product of the density, ρ, of the medium
propagating the sound and the propagation velocity, c, of sound in that medium(Z=ρ
c). At the junction of tissues or materials with different acoustic impedance, acoustic
interfaces are present.
3. Reflection
When ultrasound strikes an acoustic interface, the direction of propagation will
change, which produces reflection, refraction and scatter.
Figure 1
Incidence, reflection and refraction
4. Absorption and Attenuation
Contributing to the attenuation of sound are the transfer of energy to tissue
resulting in heating (absorption), and the removal of energy by reflection and
scattering. Attenuation depends on the insonating frequency as well as the nature of
the attenuating medium. High frequencies are attenuated more rapidly than lower
frequencies, and transducer frequency is a major determinant of the useful depth from
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which information can be obtained with ultrasound. Attenuation determines the
efficiency with which ultrasound penetrates a specific tissue and varies considerably
in normal tissues.
5. Doppler effect
When high-frequency sound impinges on a stationary interface, the reflected
ultrasound has essentially the same frequency or wavelength as the transmitted sound.
If, however, the reflecting interface is moving with respect to the sound beam emitted
from the transducer, there is a change in the frequency of the sound scattered by the
moving object. This change in frequency is directly proportional to the velocity of the
reflecting interface relative to the transducer and is a result of the Doppler effect. The
relationship of the returning ultrasound frequency to the velocity of the reflector is
described by the Doppler equation:
ΔF=(FR-FT)=(2FT-v/c)cosθ
ΔF is the Doppler frequency shift; FR is the frequency of sound reflected from the
moving target; FT is the frequency of sound emitted from the transducer; v is the
velocity of the target toward the transducer; and c is the velocity of sound in the
medium; θ is the angle between the axis of flow and the incident
ultrasound beam.
II．
Production of ultrasound
A transducer is any device that converts one form of energy to another. In the
case of ultrasound, the transducer converts electric energy to mechanical energy and
vice versa. In diagnostic ultrasound systems, the transducer servers two functions. It
converts the electric energy provided by the transmitter to the acoustic pulses directed
into the patient. The transducer also serves as the receiver of reflected echoes,
converting weak pressure changes into electric signals for processing. Ultrasound
transducers use piezoelectricity. Piezoelectric materials have the unique ability to
respond to the action of an electric field by changing shape. They also have the
property of generating electric potentials when compressed. Changing the polarity of
a voltage applied to the transducer changes the thickness of the transducer, which
expands and contracts as the polarity changes. This results in the generation of
mechanical pressure waves that can be transmitted into the body. The piezoelectric
effect also results in the generation of small potential across the transducer when the
transducer is struck by returning echoes. Positive pressures cause a small polarity to
develop across the transducer; negative pressure during the rarefaction portion of the
acoustic wave produces the opposite polarity across the transducer. These tiny polarity
changes and the voltages associated with them are the source or all of the information
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processed to generate an ultrasound image or Doppler display.
Figure 2 Piezoelectric effect
(1)Positive pressure
(2) negative pressure
III．
Mode and properties of ultrasonography
1. A-mode ultrasound
A-mode devices displayed the voltage produced across the transducer by the
backscattered echo as a vertical deflection on the face of an oscilloscope. The
horizontal sweep of the oscilloscope was calibrated to indicate the distance from the
transducer to the reflecting surface. In this form of display, the strength or amplitude
of the reflected sound is indicated by the height of the vertical deflection displayed on
the oscilloscope. With A-mode ultrasound, only the position and strength of a
reflecting structure are recorded. At present, it is used for diagnosis of intracranial
diseases.
2. M-mode ultrasound
M-mode ultrasound, displays echo amplitude and shows the position of moving
reflectors. M-mode imaging uses the brightness of the display to indicate the intensity
of the reflected signal. The time base of the display can be adjusted to allow for
varying degrees of temporal resolution, as dictated by clinical application. M-mode
ultrasound is interpreted by assessing motion patterns of specific reflectors and
determining anatomic relationships from characteristics patterns of motion. Today, the
major application of M-mode display is in the evaluation of the rapid motion of
cardiac valves and of cardiac chamber and vessel walls, which is called M-mode
echocardiography.
3. B-mode ultrasound
The mainstay of imaging with ultrasound is provided by real-time, gray-scale,
B-mode display in which variations in display intensity or brightness are used to
indicate reflected signals of differing amplitude. To generate a two-dimensional (2-D)
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image, multiple ultrasound pulses are sent down a series of successive scan lines,
building a 2-D representation of echoes arising from the object being scanned. When
an ultrasound image is displayed on a black background, signals of greatest intensity
appear as white; absence of signal is shown as black; and signals of intermediate
intensity appear as shades of gray.
Real-time ultrasound produces the impression of motion by generating a series of
individual 2-D images at rates from 24 to 30 frames per second. Real-time, 2-D,
B-mode ultrasound is now the major method for ultrasound imaging throughout the
body and is the most common form of B-mode display.
4. Doppler ultrasound
In contrast to A-mode, M-mode, and B-mode gray-scale ultrasonography, which
display the information from tissue interfaces, Doppler ultrasound instruments
according to the Doppler effect are optimized to display flow information regarding
the direction and velocity of blood. More commonly, the Doppler shift data are
displayed in graphic form as a time-varying plot of the frequency spectrum of the
returning signal.
The most common form of Doppler ultrasound to be used for radiology
applications is color Doppler flow imaging. In color flow imaging systems, flow
information determined from Doppler measurements is displayed as a feature of the
image itself. Signal phase provides information about the presence and direction of
motion, and changes in echo signal frequency relate to the velocity of the target.
Backscattered signals from red blood cells are displayed in color as a function of their
motion toward or away from the transducer, and the degree of the saturation of the
color is used to indicate the relative velocity of the moving red cells.
IV． The principles of diagnostic ultrasound
Four echogenicity of human organs:
1. anecho: urine, bile, blood, pleural fluid, ascites, pericardial effusion
2. Low echo: liver, myocardium
3. High echo: endocardium, epicardium, heart valve,
4. strong echo: calcification, stone, bone, lung
Clinical application of the diagnostic ultrasound
I． Echocardiography
1. M-mode Echocardiography
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(1) Position 1: ventricular echo pattern at the level of the apex of the heart
(2)
(3)
(4)
(5)
(6)
Position 2a: ventricular echo pattern at the level of the chordae
Position 2b and 3: mitral valve echo pattern
Position 4: heart base echo pattern
Position 5: tricuspid valve echo pattern
Position 6: pulmonary valve echo pattern
Figure 3 M-mode echocardiography
CW: chest wall; ARVW: anterior right ventricular wall; RVOT: right ventricular
outflow tract; RV: right ventricle; PA: pulmonary artery; PV: pulmonary valve; RA:
right atrium; LA: left atrium; LAW: left anterior wall; LVOT: left ventricular outflow
tract; LV: left ventricle; IVS: interventricular septum; AO: aorta; AOV: aortic valve;
AMVL: anterior mitral valve leaflet; PMVL: posterior mitral valve leaflet; ATVL:
anterior tricuspid valve leaflet; Ch: chorda tendineae; PPM: posterior papillary muscle;
En: endocardium; EP: epicardium; L: lung; APS: atriopulmonic sulcus
2. Cross sectional echocardiography
(1) Long-axis view: transecting the heart parallel to the long axis of the heart. We can
see right ventricle, left ventricle, left atrium, interventricular septum, aorta, aorta
valve and mitral valve in this view.
(2) Short-axis view at the level of the base of the heart: transecting the heart
perpendicular to the long axis of the heart. Aorta, aorta valve, left atrium, right
atrium, tricuspid valve, right ventricle, right ventricular outflow tract, pulmonary
valve, left coronary artery can be seen in this view.
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(3) Short-axis view at the level of mitral valve: left ventricle, right ventricle,
interventricular septum and mitral orifice can be seen in this view.
(4) Subcostal four-chamber view: with the transducer in the subcostal position. Left
and right atrium, left and right ventricle, interatrial septum and interventricular
septum is visualized in this view.
(5) four-chamber and five-chamber view over the cardiac apex: left and right atrium,
left and right ventricle, interatrial septum, interventricular septum, mitral valve,
tricuspid valve, aortic root and left ventricular outflow tract.
3. Abnormal echocardiography
(1) Mitral stenosis
① Clinical manifestation
Classic mitral stenosis accounts for 40% of rheumatic heart diseases. The main
pathological change is the orifice stenosis caused by the thickness and adhesion of the
valve leaflets.
② USG
 2-D ultrasound provides a spatial image of the valve and allows direct
mearsurement of the valve orifice.
 M-mode: Great Wall-like picture
Anterior and posterior leaflets of the mitral valve move in the same
direction


EF decreased
Color Doppler flow imaging: turbulent flow at the mitral orifice during diastole
Pulsed Doppler: the peak velocities are increased
Figure 4
M-mode ECG of mitral stenosis
Increased thickness of MV; no A wave; decreased EF; Great Wall-like picture (arrow);
anterior and posterior move in the same direction
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(2) Atrial septal defect
① Clinical manifestation
Atrial septal defect is the most common disease in the congenitive
cardiomyopathy. It is classified into the ostium secundum type and the primum type
defect according to the involved region of the atrial septum.
② USG
 2-D ultrasound: direct sign is the presence of an atrial septal defect; indirect sign is
the
enlargement of right atrium and ventricle, and the widened pulmonary
artery.
 M-mode: dialated right ventricle and abnormal septal motion
 Pulsed-Doppler: diastolic turbulent flow with upward spectrum
 Color Doppler flow imaging: red-encoded blood passing from the left atrium to the
right atrium through the defect.
Figure 5
B-mode echocardiography of atrial septal defect
The defect of atrial septum and enlarged RA and RV is shown in the four-chamber
view
Abdominal Sonography
I． The Liver
1. USG of normal liver
 Size: the upper border of the liver lies at the level of the fifth intercostal space at
the midclavicular line. The lower border extends to or slightly below the costal
margin.
The longitudinal diameter of the liver in the midclavicular line <13cm
The mean anteroposterior diameter of the left lobe at the left costal border <5cm
 Echotexture: homogeneous, contains fine-level echoes, and is either minimally
hyperechoic or isoechoic compared to the normal renal cortex. The liver is
hypoechoic or isoechoic compared to the spleen.
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 Portal vein: an echogenic wall
travels along to the liver long axis, like “工” in the left lobe of liver.
 Hepatic vein: right, middle and left hepatic veins which all drain into the inferior
vena cava
right hepatic vein runs in the intersegments of the the right lobe,
divides of anterior and posterior segments of the right lobe
middle hepatic vein courses in the main lobe fissure, separating right
and left lobe
left hepatic vein runs in the intersegments of the left lobe, divides of
medial and lateral segments of the left lobe
MHV
LH
RHV
V
HH
HH
Figure 6 Hepatic venous anatomy
The three hepatic veins－right (RHV), middle (MHV), and left (LHV), are interlobar
and intersegmental, separating the lobes and segments. Three hepatic venous
confluence with the inferior vena cava
2. USG of common diseases of liver
(1) Liver cirrhosis
① Clinical manifestation:
There are three major pathologic mechanisms which, in combination, create
cirrhosis: cell death, fibrosis, and regeneration. Hepatitis B is the main cause in China.
The main clinical manifestations are liver dysfunction, portal hypertension and
ascites.
② USG:
 In the early stages, the liver may be enlarged, whereas in the advanced states, the
liver is often small, with relative enlargement of the caudate, left lobe, or both, in
comparison with the right lobe.
 Nodular surface
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 Coarse echotexture, regeneration nodules
 Decreased amplitude of phasic oscillations with loss of reversed flow, and a
flattened waveform.
 Luminal narrowing of the hepatic veins
 Wide PV
 Splenomegaly
 Ascites
③Differential diagnoses:
The liver cirrhosis tubercle need to identify with the small liver cancer, CT can clear
diagnosis.
As
GB
RL
PV
Figure7
Liver cirrhosis
Small end-stage right liver(RL) with surface nodularity, best appreciated with
ascites(As), hydropic wall of gallbladder(GB), Wide portal vein(PV)
(2) Liver cyst
① Clinical manifestation:
Liver cysts have a ductal origin, although their precise cause is unclear. Occasionally,
the patient may develop pain and fever secondary to cyst hemorrhage or infection.
② USG:
 Anechoic lumen




Well-demarcated thin wall
Posterior acoustic enhancement
Sidewall echo loses
When the cyst complicated with hemorrhage or infection, it may contain internal
echoes and septations, a thickened wall, or may appear solid.
③ Differential diagnoses:
Identify with cystic metastases and the liver abscess at the liquefaction period,
according to the wall thickness, thickness uneven and the margin.
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Figure 8 Liver cyst
Anechoic cyst with a clear and thin wall, posterior acoustic enhancement, sidewall
echo loses
(3) Liver abscess
① Clinical manifestation:
The most common presenting features of liver abscess are fever, malaise, anorexia,
and right upper quadrant pain. It is usually cased by pyogenic bacteria infection or
amoebic parasite, and can often be find in right lobe.
② USG:
 The abscess appears cystic, with the fluid ranging from echofree to highly
echogenic.





Rough wall
A round or oval-shaped lesion
Clear sidewall
Posterior acoustic enhancement
Occasionally gas-producing organisms give rise to echogenic foci with a posterior
reverberation artifact.
③ Differentiaion:
the differential diagnaosis of liver abscess includes amebaic or echinococcal
infection, simple cyst with hemorrhage, hematoma, and necrotic or cystic neoplasm.
(4) Liver hemangioma
① Clinical manifestation:
Four types: angiocavemoma, sclerosing hemangioma, hemangioendothelioma and
capillary hemangioma.
② USG:




Hyperechoic or homogeneous
Clear margin
Uniformly granular or lacelike in character
Echogenic border, either a thin rim or a thick rind
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 A tendency to scalloping of the margin
 Extremely slow blood flow
③ Differential diagnoses:
Identify with liver cancer, according to the wall thickness, acoustic halo
surround.
liver
Figure 9
Liver hemangioma
An echoic mass with clear margin in the liver
RL
(5) Primary liver carcinoma
① Clinical manifestation:
More than 90% is HCC. Generally it has no symptom at early, but later shows liver
pain, fatigue and abdominal mass. Most patients has AFP positive.
② USG:
 The mass may be hypoechoic, complex, or echogenic






Solid mass
Multiple nodules
Diffuse infiltration
A thin, peripheral hypoechoic halo
“Hump sign”
Small tumors may appear diffusely hyperechoic, secondary to fatty metamorphosis
or sinusoidal dilation
 Doppler: high-velocity signals
③ Differential diagnoses:
Identify with liver hemangioma, liver cirrhosis tubercle and focal hyperplasia
nodular.
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Figure 10
Primary Bliver carcinoma
A
H
H
H lobe
H A, A large hyperechoic mass in the right liver
B, Color Doppler shows a disorganized flow pattern
(6) Metastatic liver disease
① Clinical manifestation:
It is usually origin the cancer of esophagus, stomach, gallbladder, pancreas and
other digestive organs.
② USG:
 Multiple masses: echogenic, hypoechoic, target, calcified, cystic and diffuse
 Bull's-eye configuration or target pattern is characterized by a peripheral
hypoechoic halo
 Calcified metastases are distincitive by virtue of their marked echogenicity and
distal acoustic shadowing. Adenocarcinoma of the colon is most frequently
associated with calcified mestases.
 Carcinoma of pancreas is associated with multiple hypoechoic metastases with no
posterior acoustic enhancement.
③ Differential diagnoses:
Identify with hepatic abscess, echinococcosis of liver, hepatic phthisis and other
liver disease with multiple nodules.
II． Gallbladder
1. USG of normal gallbladder
 Location: inferior to interlobar fissure between left and right lobe;
 Size: <3cm transverse, <9cm longitudinal;
 Wall: clear wall, <3mm in thickness;
 Lumen: anechoic
2. USG of common diseases of gallbladder
(1) Cholelithiasis
① Clinical manifestation:
More common in adult females, pain in the right upper quadrant, fever, nausea or
vomiting
② USG:
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 Typical gallstone:
Hyperechoic, clear acoustic shadow, mobility (when the patient position changed)
 Stone-filled gallbladder:
Echo shadowing structure in the right upper quadrant, WES (wall-echo-shadow)
complex: three arc-shaped lines followed by a shadow
 Multiple dependent gallstones:
Multiple dependent stones arrange along the dependent gallbladder wall, acoustic
shadow, and mobile.
 Intramural cholesterol crystals:
Multiple bright reflectors in the gallbladder lumen, short comet tail artifact, lack of
acoustic shadow non-mobile
③ Differential diagnoses:
According to the echo, shadow and mobility. Mobility is a key feature of stones,
allowing differentiation from polyps or other entities.
RL
GB
S
Figure 11 Typical gallstone
Image show a stone (arrow) in the gallbladder (GB) appearing as hyperechoic stone
with acoustic shadow(S)
(2) Acute cholecystitis
① Clinical manifestation:
Usually have pain in the right upper quadrant, fever, disgusting or vomiting. It is
caused by Stone obstruction, bacterial infections and pancreatic reflux.
② USG:






Gallbladder enlargement
Gallbladder wall thickening>3 mm
Hyperemia of the gallbladder wall
Biliary sludge in the gallbladder lumen
Gallbladder distention
Choledocholithiasis
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 Hepatic abscesses
③ Differential diagnoses:
Generally according to the clinical symptom, physical sign and laboratory
examination can make diagnoses.
GB
Figure 12 Acute cholecystitis
Classic appearance with hyperemia and thickening wall and biliary sludge
(3) GB polyp
① Clinical manifestation:
It contains cholesterol polyp, inflammatory polyps, adenomatoid polyps and
adenomyomatosis of gallbladder.
② USG:
 Multiple, oval lesions attached to the gallbladder wall
 High-level echo
 Non-shadowing
 Non-mobile
 Larger lesions may contain a fine pattern of echogenic foci within them
③ Differential diagnoses:
According to the echo, shadow and mobility.
III． Pancreas
1. USG of normal pancreas




Size: head<3cm, body<2cm, tail 1~3cm
Pancreatic duct:<2mm
Echogenicity: isoechoic or hyperechoic compared with liver
Texture echo: homogeneous
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SP
Figure 13
Normal pancreas
Splenic vein(SPV), superior mesenteric artery (SMA), aorta(AA), inferior vena
cava(IVC), common bile duct(CBD), duodenum(DUO), spine(SP), left renal
vein(LKV); Liver and stomach is anterior to the pancreas.
2. USG of common diseases of pancreas
(1) Acute pancreatitis
① Clinical manifestation:
Mainly have intense abdominal pain suddenly, nausea and vomiting, hypotension
and shock, muscular tension, tenderness. Amylase in blood and urinary is high. It has
two styles: dropsy and hemorrhage necrosis.
② USG:
 Pancreas enlargement
 Pancreatic echogenicity: decreased
 Echotexture: inhomogeneous
 Inflammatory mass
 Hemorrhage
 Intrapancreatic and extrapancreatic fluid collections
 Pseudocyst formation
 Ascites
③ Differential diagnoses:
The diagnosis of acute pancreatitis is usually based on clinical and laboratory
findings.
(2) Pancreatic carcinoma
① Clinical manifestation:
It is easy to see in middle-aged person and old person, and generally has no
symptom at early, but later shows stomachache, jaundice, body weight decreased
significantly, besides has anorexia, nausea, vomiting and diarrhea.
② USG:
 Poorly defined, homogeneous or inhomogeneous, hypoechoic mass
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 Obstruction of the pancreatic and biliary duct: double-duct sign (combined dilation
of the pancreatic and common bile duct) and enlarged gallbladder
 Lesional vascularity is uncommonly shown with conventional Doppler imaging
③ Differential diagnoses:
It needs identify with chronic pancreatitis, which has pancreatic atrophy and
calcify, thickening perirenal fascia, and string-of-beads pancreatic duct.
IV． Spleen
1. USG of normal spleen
 Size: length 10-12cm, Spleen port thick 3-4cm
 Echo: <liver
 Texture echo: homogeneous
2. USG of common diseases of spleen
(1) Spleen trauma
① Clinical manifestation:
Spleen is the most vulnerable organ in abdomen. It has three styles: central
rupture (breakage in deep parenchyma), capsule rupture (breakage in the surrounding
parenchyma) and true rupture (breakage involved capsule)
② USG:
Spleen sub-capsular hematoma
 Size: normal
 Anechoic area between spleen surface contour and spleen capsule
 Move with breath
 Internal distribution of scattered small weak echo
Spleen parenchyma hematoma
 Size: enlarge
 Contour: smooth
 Anechoic area in parenchyma
V． Kidney
1. USG of normal kidney
 Size: length 10-12cm, thick 3-4cm
 Renal sinus echo: high level echo
 Renal parenchyma thick: 1.5-2.5cm
2. USG of common diseases of kidney
(1) Kidney stone
Strong echo in the renal sinus with acoustic shadow, if it has Secondary
hydronephrosis, the renal calices and pelvis showed irregular anechoic area.
(2) Hydronephrosis
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① Clinical manifestation:
It can be caused by stone, tumor, infection and so on. The patients can have renal
colic, hematuresis and fever.
② USG:
 dilated renal sinus ≥1cm
 collecting system: anechoic space
 moderate and marked hydronephrosis: kidney enlarge
 marked hydronephrosis: renal parenchyma atrophia
 hydroureter
③ Differential diagnoses:
Drink too much water, filling of bladder, pregnancy or drugs can cause
physiological renal sinus dilated, but it usually <8mm. With polycystic kidney
disease or multiple renal cysts identification: the anechoic area of hydronephrosis is
communicating with each other, while the renal cysts are not.
Small parts Sonography
I． Thyroid
1. USG of normal thyroid
 Shape: lobus lateralis sinister and dexter, isthmus at front.
 Clear contour, regular borderline,
 Echo: medium intensity or a litter low level echo
 Texture echo: homogeneous
2. USG of common diseases of thyroid
(1) Thyroid nodule
 Solid nodules: including cancer, adenomas and cystic nodules.
 Admixture nodules: including adenomas cystic degeneration or adenoma
hemorrhage.
(2) Thyroid diffuse lesions
 Including simple goiter, nodular goiter, hyperthyroidism, and thyroiditis and so on.
 By glandular echo and color flow distribution can make discrimination.
II． Breast
1. USG of normal breast
Three type:
 Diffuse homogeneous type: breast tissue was uniformity detailed echo
 Micro-vesicles: 1~ 2mm vesicle area opaca in breast diffusely
 Mixed type
2. USG of common diseases of breast
(1) Cyclomastopathy
 Bilateral breast: symmetry increase mildly
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 Glandular organ structure: disorder
 Echo: diffuse increased
 Texture echo: uneven
 Hypoechoic nodules or cysts in breast
(2) Fibroadenoma of breast
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


Round or oval, lobulated when large
Smooth boundary, has peplos
Low level echo, homogeneous
CDFI: no or a litter blood flow
(3) Breast cancer
 Mass: heterogeneous hypoechoic, irregular form, no peplos, angular margin,
crab-foot extension.
 CDFI: multiple vessles demonstrated
A
B
Figure 14 Breast tumor
A, Benign fibroadenoma: elliptical, wider than tall and completely encompressed by a
thin, echogenic capsule.
B, Malignant nodule: hypoechoic mass with angular margin and spiculation surround
it.
Gynecologic and Obstetric Ultrasound
I． Uterus
1. USG of normal uterus
 Position: The uterus lies in the true pelvis between the urinary bladder and the
rectosigmoid colon posterioly.
 Size: the adult uterus is 7~8 cm in length, 4~5 cm in width and 2~3 cm in
anteroposterior diameter.
 Shape: inverse pear-shaped appearance.
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 Sonography:
The normal endometrial cavity is seen as a thin echogenic line. The
sonographic appearance of the endometrium varies during the menstrual cycle. The
endometrium is composed of a superficial functional layer and a deep basal layer.
The functional layer thickens throughout the menstrual cycle and is shed with
menses. The menstrual phase endometrium consists of a thin echogenic line.
During the proliferative phase, the endometrium thickens, reaching 2 to 4 mm. The
endometrium in secretory phase measures 7 to 10mm.
2. USG of common diseases of uterus
(1) Leiomyoma
① Clinical manifestation:
Leiomyomas (fibroids) are the most common neoplasm of the uterus. Women
with leiomyomas can experience pain and uterine bleeding. Leiomyomas may be
classified as intramural, submucosal and subserosal.
② USG:
 the uterus may be enlarged
 distorted and irregular external contour of the uterus
 localized leiomyomas are most commonly hypoechoic or heterogeneous in
echotexture
 leiomyomas impinge on the endometrium, distorting the cavity
Fig 15 Uterus leiomyoma
A hypoechoic nodus (arrow) in the anterior wall of uterus; BL:bladder
③ Differential diagnoses:
 adenomyosis: diffuse uterine enlargement with a normal contour, normal
endometrial texture
thickening of the posterior myometrium, with the involved area being
slightly more anechoic than normal myometrium
 Endometrial carcinoma: The most common clinical presentation is uterine bleeding.
Sonographically, a thickened endometrium, which has a heterogeneous echotexure
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with irregular or poorly defined margins.
II． Ovary
1. Normal Ultrasonography of Ovary
 Position: Uterine location influences the position of the ovaries. The normal
ovaries are usually identified laterally or posterolaterally to the anteflexed midline
uterus. Their craniocaudad axes are paralleling the internal iliac vessels, which lie
posteriorly and serve as a helpful reference.
 Size: the adult ovary is 4×3×1cm
 Shape: the ovaries are ellipsoid in shape
 Sonography: the normal ovary has a relatively homogenous echotexure with a
central, more echogenic medulla. Well-defined, small anechoic or cystic follicles
may be seen peripherally in the cortex. The appearance of the ovary changes with
age and with the phase of the menstrual cycle.
2. USG of common diseases of ovary
(1) Ovarian cystadenoma
① Clinical manifestation:
Ovarian cystadenomas are the most common, comprising 45% of all benign
ovarian neoplasms. The peak incidence of cystadenoma is in third to fifth decades
women. Ovarian cystadenomas are classified into serous and mucinous cystadenomas.
Approximately 20% of serous cystadenomas are bilateral. Their sizes vary greatly, but
in general, they are smaller than mucinous tumors. Mucinous cystadenomas are often
huge and less frequently bilateral.
② USG:
 Serous cystadenomas are usually large, thin-walled, unilocular cystic masses that
may contain thin septations. Papillary projections are occasionally seen.
 Mucinous cystadenomas can be huge multiloculated cystic masses, measuring up
to 15 to 30 cm. Mutiple thick septae are present and low-level echoes caused by the
mucoid material may be seen in the dependent portions of the masse. Papillary
projections are less frequently seen than in the serous cystadenomas.
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Fig 16 Ovarian mucinous cystadenoma
A huge multiloculated cystic mass with multiple septae of ovary
3. Normal early pregnancy
The whole gestational period is 40 weeks (menstrual age). Early pregnancy or
the first trimester of pregnancy is the first 12 weeks. Ultrasound is a readily available,
noninvasive, and safe means of evaluating fetal health, determining gestational age,
and assessing the intrauterine environment.
(1) USG of normal early pregnancy
 uterus enlargement
 gestational sac: a round or oval shape intradecidual sac which can be detected at 5
weeks of gestational age(GA) using transvaginal sonography(TVS)
 embryo: visualized from 6 to 7 weeks of GA using TVS, clear crown-rump length
(CRL) is shown from 8 weeks of GA.
 fetal heart: heart tube beating can be seen as early as 6 weeks of GA, clear
embryonic cardiac cavity can be seen at 12 weeks of GA.
 fetal movement: happen from 9 weeks of GA, and active fetal movement can be
seen from 12 weeks of GA.
 placenta: can be seen at 8 to 9 weeks of GA, hyperechoic compared with uterus
 yolk sac: the first structure to be seen normally within the gestational sac and can
be seen till 11 weeks of GA
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1
Fig 17
2
4
3
Early pregnancy (TVS)
1. exocoelom and amnion(arrow) 2.yolk sac 3.embryo 4. amniotic sac
(2) Ectopic pregnancy
① Clinical manifestation: Pain, abnormal vaginal bleeding, and a palpable adnexal
mass ,amenorrhea, adnexal tenderness, and cervical excitation tenderness
② USG:
 Enlarged uterus without gestational sac in the cavity
 Adnexal mass
 Free fluid in the recto-uterine fossa
New technique
1. Harmonic imaging：
Variation of the propagation velocity of sound in fat and other tissues near the
transducer results in phase aberration that distorts the ultrasound image. Tissue
harmonic imaging provides an approach for reducing the effects of phase aberrations,
reducing the noise and clutter. Because harmonic beam do not interact with superficial
structures and are narrower than the originally transmitted beam, spatial resolution is
improved and clutter and side lobes are reduced.
2. 3-D ultraousnd
Dedicated 3-D scanners used for fetal, gynecologic and cardiac scanning may
employ hardware-based image registration, high density 2-D array, or software
registration of scan planes as a tissue volume is acquired. 3-D ultrasound permits
collection and review of data obtained from a volume of tissue in multiple imaging
planes as well as rendering of surface features.
3. Contrast enhanced ultrasound
The principle requirements for an ultrasound contrast agent are that it should be
easily introducible into the vascular system, be stable for the duration of the
diagnostic examination, have low toxity, and modify one or more acoustic properties
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of tissues which determine the ultrasound imaging process. The new generation of
ultrasound contrast agents has extend their capabilities, redefining the role of
ultrasound in resolving the vascular questions that were until now left to CT and MRI.
Contrast agents as blood pool agents can help delineate vascular structures and
enhance Doppler signals from small volumes of blood. More excitingly, contrast
agents make it possible for ultrasound to achieve entirely new objectives, the most
striking of which is the ability for the first time to image organ and lesion perfusion in
real time.
4. Interventional ultrasound
(1) ultrasound-guided biopsy
Ultrasound-guided needle biopsy is an important diagnostic technique in
radiology practices throughout the world. It has become an accurate, safe, and widely
accepted technique for confirmation of suspected malignant masses and
characteristics of many benign lesions in various intra-abdominal locations. It also
decreases patient’s costs by obviating the need for an operation, decreasing the
duration of hospital stay, and decreasing the number of examination necessary during
a diagnostic evaluation.
Traditionally, ultrasound-guided needle biopsy has been used for the biopsy of
large, superficial, and cystic masses. Currently, however, because of improvements in
instrumentation and biopsy techniques, small, deeply located, and solid masses can
also undergo accurate biopsy.
Indications: Suspected malignancy before nonsurgical treatment, such as
chemotherapy and radiation therapy.
Contraindications: Relative contraindications to needle biopsy include uncorrectable
coagulopathy, lack of a safe biopsy route, and an uncooperative patient.
(2) Ultrasound-guided drainage
Percutaneous aspiration and drainage procedures have gained wide acceptance in
clinical practice because of their safety, simplicity, and effectiveness. Modalities such
as ultrasound and CT allow for precise needle placement for superficial and deep
abdominal fluid collections or abscesses.
Indications:
① Percutaneous catheter drainage of pyogenic abscesss and cysts
② Percutaneous cholecystostomy
③ Percutaneous transhepatic cholangiography and drainage
Contraindications:
Contraindications to image-guided percutaneous catheter drainage include lack of safe
route, bleeding diathesis and uncooperative patient.
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5. Intraoperative sonography
Intraoperative sonography (IOS) is a dynamic and growing imaging technique
providing important real-time diagnostic information to the radiologist and the
surgeon. It identifies and characterizes lesions seen on preoperative imaging and
discovers new lesions not detected by preoperative imaging or surgical inspection and
palpation. The ultimate goal is to correlate preoperative images, surgical inspection
and palpation, and IOS findings to determine the most appropriate surgical procedure.
Indications and applications: detection of occult masses; determinination of
relationships and vascular abnormalities; characterization of masses; guidance for
intervention
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