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
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
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.
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
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.
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
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:
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
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
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.
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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:
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.
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.
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,
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;
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
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,
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.
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
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.
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
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
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
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.