Clinical medicine – Chest
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CHEST
Anatomy
N.B.: to find a certain rib:
 Find angle of Lewis  2nd rib.
 Find last rib from the back  12th rib.
 Find apex of scapula  7th rib.

N.B.: the rib is followed by its space downwards.

N.B.: Vertical lines:
 Midline (ML).
 Parasternal line (PSL).
 Midclavicular line (MCL).



Anterior axillary line (AAL): passes through
anterior axillary fold.
Midaxillary line (MAL) ‫خط خياطة القميص‬
Posterior axillary line (PAL): passes through
posterior axillary fold.
Scapular line (SL): passes through apex of
scapula.
Paravertebral line (PVL): midway between ML
and SL.
 Surface anatomy of right lung:
Match between the following points:
4 cms above midclavicular point sternoclavicular junction angle of Lewis
midline at 6th rib  PSL at 6th rib MCL at 6th rib AAL at 7th rib MAL at 8th rib
 PAL at 9th rib SL at 10th rib  PVL at 10th back to 1st point again.
 Surface anatomy of left lung:
As right lung but in ML till 4th rib.
 Surface anatomy of pleura:
As lungs, but add 2 ribs to the points of lower border.
NB: right lung  3 lobes and 2 fissures.
Left lung  2 lobes and 1 fissure.

Oblique fissure:
o Starts from T2
o Move parallel to medial border of scapula (while patient rising his arms
up) till MAL at 5th rib.
o Move forwards and medially till MCL at 6th rib.
NB:
o T2: below T1 below C 7 to get its process tell the patient to flex his
neck; it will be the most prominent.
o When the examiner asks you to examine lower lobe  examine back.
o Lateral view of right lung is the best to see the 3 lobes.

Transverse Fissure: right lung only
o From right MAL at 5th rib.
o To ML at 4th rib
NB: Upper and middle lobes are examined from front.
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
Kronigs Isthmus:
o Apex  apex of lung
o Base 4 pints:
1. Sterno-clavicular junction.
2. Spine of C 7.
3. Junction between lateral 1/3 and medial 2/3 of clavicle.
4. Junction between lateral 2/3 and medial 1/3 of spine of scapula.

Traub’s Area: of left lung (5, 8, 9, 11)
o 5th space MCL
o 8th rib PSL




o 9th rib MAL
o 11th rib MAL
Upper border by lower border of left lung
Lower border by costal margin
Right border by lower border of left lobe of liver
Left border by anterior border of spleen
NB: Trachial bifurcation:
From front: angle of Lewis
From back: spine of T4
NB:
Upper lobe:
Middle lobe:
Lower lobe:

Right lung
Apical
Anterior
Posterior
Medial
Lateral
Apical basal
Anterior basal
Posterior basal
Lateral basal
Left lung
Apical
Anterior
Posterior
Superior lingular
Inferior lingular
No middle lobe
Apical basal
Anterior basal
Posterior basal
Lateral basal
Mediastinum:
o Upper: presented by trachea, affected by lesions to upper ½ of lung.
o Lower: presented by cardiac apex, affected by lesions to lower ½ of
lung.
Histology
o Trachea  main bronchus  lobar bronchus  bronchioles  respiratory
bronchioles  alveoli.
o Elsatin around alveoli is responsible for recoil tendency of lungs.
o Pleura:
 Visceral layer.
 Parietal layer: lining chest wall, mediastinum and diaphragm. In
between, there is monomolecular layer of serous fluid. The 2 layers can
Clinical medicine – Chest
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slide over each other but cannot be separated. In inspiration, diaphragm
descends pulling parietal pleura  pulling visceral pleura  pulling
lungs.
Monomolecular layer is responsible for sliding and adhesion between the 2 pleural
layers.
For you: Capacity of thoracic cage is 5 liters while capacity of lungs is 1 liter. In
spite of that, there are impressions for ribs on lung surface. This is explained as
follow:
At birth capacities are equal.
During life, hard tissue grows faster than soft tissue. Monomolecular layer of pleura
pulls thoracic cage inwards and lungs out wards making both of them stretched and
making capacity of both 2.5 liters.
After death, when we dissect  they have their real capacities.
Physiology
 Respiration is controlled by:
1) Chemical control:
a) Inspiration  ↑ O2  -- R.C.  Expiration.
b) Expiration  ↑ CO2  ++ R.C.  Inspiration.
R.C. is inhibited by: ↑ O2, ↓ CO2, severe hypoxia.
R.C is stimulated by: ↑ CO2, H2, hypoxia
2) Neural control: (Herring-Brever Reflex)
R.C. discharges continuous impulses to diaphragm and intercostals muscles  active
inspiration + inflation of lungs  inflation of alveoli  stimulation of stretch receptors
on alveoli  reflex inhibition of R.C  relaxation of diaphragm and intercostals
muscles  passive expiration.

Inspiratory
Expiratory
Active
Need muscle contraction
Homogenous air flow
 Bronchial Diseases:
o Bronchitis
o B.A.
o Bronchiectasis
 Pulmonary diseases:
o Consolidation
o Emphysema
o Cavitations
Passive
Depends on recoil tendency
80% of air in 1st 1/3 time
20% of air in last 2/3 time
Pathology
o Bronchogenic
carcinoma+bronchial edema
o Bronchopneumonia
o Lung fibrosis
o Lung collapse
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 Pleural diseases:
o Pleurisy
o Pleural effusion
o pneumothorax
Bronchitis:
 Inflammation of bronchial mucosa: edema+ hypersecretion  generalized
narrowing in proximal bronchi.
 It is chronic if occurs for 3 months in 2 successive years.
 Chronic bronchitis is usually associated with emphysema  together called
COPD (chronic obstructive pulmonary disease) or COLD (chronic obstructive
lung disease) or COAD (chronic obstructive airway disease).
 May be associated with B.A or bronchiectasis.
N.B:
-
Cilia spill mucous and distribute it.
Ciliary dysfunction  mucus accumulation  COPD, and predisposes
to infection  destruction of bronchial wall  become thin:
o Dilatation (bilateral and basal [anaerobic infection])
o Surrounded by consolidation, fibrosis and collapse.
o Filled with pus ( suppurative lung syndrome) and blood (
bronchiectasis sicca hemorrhagica)
Bronchial Asthma:
 On 1st exposure to antigen  formation of IgE without Ag-Ab reaction.
 On 2nd exposure  Ag-Ab  component fixation  degradation of mast cells
 liberation of chemical mediators  distal bronchi: bronchospasm, edema
in mucosa and hypersecretion  generalized narrowing of peripheral
airways.
N.B: Generalized narrowing in B.A. is more severe than in bronchitis due to
broncho-spasm and distal bronchi have been already narrower.

Course:
o During attack: severe dyspnea, wheezy chest
o In between attacks: complete free.
Chronic bronchitis
B.A.
N.B: Sometimes B.A. comes on top of chronic bronchitis  Asthmatic Bronchitis.
Bronchogenic carcinoma and bronchial edema:
 Produce localized narrowing of airway.
 Bronchogenic carcinoma in apex of lung called Superior Sulcus Syndrome
may affect:
o Trachea
o Pharynx
o Chest wall
o Sympathetic chain  pancoast tumor.
Clinical medicine – Chest
Bronchopneumonia:
Terminal bronchitis +patchy pneumonitis.
Consolidation:
 Alveoli are filled with fluid, cellular exudates and fibrin.
 Causes:
o Pneumonia (broncho-, lobar-)
o Bronchiectasis
o Around lung abscess.
Emphysema:
 Compensatory
 Localized due to partial obstruction
 As part of COPD
 Mechanism:
Inhaled micro-organisms contain lipase to digest fat, amylase to digest CHO,
protease (α1 trypsin) to digest proteins, but α1 trypsin of micro-organism is
inhibited by α1 anti-trypsin. Smoking  decreased synthesis of α1 antitrypsin, and accumulation of monocytes containing α1 trypsin leading to loss
of recoil tendency  hyperinflation (emphysema).
NB: smokers suffer from emphysema and chronic bronchitis.
COPD:
 Type A:
o Emphysema > chronic bronchitis.
o Pink puffer ‫المريض أحمر وينافخ‬
o Inflation  rupture of interalveolar septa  decreased surface of gas
exchange 
 Decreased O2, increased CO2  stimulation of R.C.  wash
CO2, increased O2  pinkish.
 Tachycardia  puffer.
 Type B:
o Bronchiectasis > emphysema.
o Blue bloater ‫المريض منفوخ وأزرق‬
o Breathing is difficult due to bronchitis  cyanosis  blue.
o Acidosis due to increased H2CO3  increased H+ acidic urine +
increased Na+ reabsorption together with its iso-osmotic water 
bloater.
Cavitations:
 Filled:
o Cyst
o Abscess:
 Pyogenic
 T.B.
 Amebic
 Empty:  old abscess.
Lung fibrosis: narrowing.
Lung collapse:
 Compressive:
o Pleural effusion
o Pneumothorax
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Clinical medicine – Chest

Obstructive:
o With obstructive main bronchus:
 Tumor
 F.B.
 Fibrosis
o With patent main bronchus:
 Hypersection.
Pleurisy: edema and roughness of parietal and visceral pleura.
Pleural effusion: accumulation of fluid in pleural sac:
- Serous fluid  hydrothorax
- Blood  hemothorax
- Lymph  chylothorax
- Pus  pyothorax
- Fibrosis of pleura  fibrothorax.
 Pyothorax + broncho-pleural fistula  coughing pus 
suppurative lung syndrome.
NB: Suppurative lung disease:
 Lung abscess
 Bronchiectasis
 Pyothorax + broncho-pleural fistula.
Pneumothorax:
A. Closed: forced cough  rupture of alveoli into cavity. If
emphysematous  rupture of emphysematous bullae  more serious
condition.
B. Open:
 Trauma:
 Stab wound
 Iatrogenic by needle in drainage of pleural pleural
effusion.
 Bronchopleural fistula.
In this case there is direct connection with atmosphere and so air inside pleura ↔
with inspiration and expiration and not accumulated.
C. Tension pneumothorax:
 Cause: stab wound at angle, where the 2 holes not opposing
each other.
 In inspiration: air enters inside pleural cavity.
 In expiration: air is trapped as 2 holes not opposing each other
 +ve pressure.
NB: Closed  regressive course: air is absorbed.
Open  stationary course: air ↔
Tension  progressive course: treatment by making open
pneumothorax.
D. Hydropneumothorax.
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Local Examination
1) Inspection:
a) Skin:
i) Dilated veins:
(1) SVO, commonest, due to tumor, thrombus.
(2) IVO.
ii) Scar: right and left thoracotomy: in lobectomy or pleurectomy.
b) Chest Wall:
i) Shape:
NB: For inspecting shape, look from foot side while patient lying on flat bed
and watch carefully right and left antero-posterior length.
(1) Symmetrical:
(a) Elliptical: antero-posterior: Transverse =5:7 (normal shape).
(b) Barrel shaped= permanent inspiratory position:
 Antero-posterior≥Transverse ≈ 1:1
 Wide subcostal angle.
 Horizontal ribs.
 Wide intercostal spaces.
Cause: hyperinflated chest (clinical term), e.g.: Emphyema which
is pathological term.
(c) Pigeon chest=Pecten Cranium:
Causes:
 Hard tissue: Rickets, osteomalacia.
 Soft tissue: severe precordial bulge (RVE), hyperinflation as
COPD since childhood.
Rickets: delayed bone growth and inability for ossification  soft
tissue grows and bulges at cartilaginous parts.
NB: to say: this is a ricketic chest, must be there one of two signs:
Harrison sulcus + rosary beads.
-
-
Harrison Sulcus:
In healed rickets
Diaphragm originates from lower ribs. In inspiration, diaphragm
pulls cartilaginous parts inwards forming a sulcus at costal margin,
even in healed rickets.
Rosary beads:
Normally costal cartilage proliferates from adjacent to bone then
ossifies.
Here, growth of cartilage without ossification  masses in vertical
lines.
When patient recovers  atrophy of them.
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(d) Pectus Excavatum=Funnel shaped:
Causes:
- Congenital 95%
- Acquired 5%: in Shoemakers as pressure atrophy on chest 
indentation of lower 1/3 of sternum.
If severe:
 Disturbs anatomy of:
 Heart  H.F.
 Lung  R.F.
 Press on the R.V.  picture of constrictive pericarditis.
(e) Flat (alar) chest: For examination: only mentioned with pulmonary
T.B.
(f) Kyphosis: if severe, it disturbs anatomy of heartH.F., Lung
R.F.
(2) Asymmetrical Chest:
1. Unilateral bulge
Pleural effusion
Pneumothorax
Fluid, air disturb
mononuclear layer of
pleural cavity  outward
expansion of thoracic
cage.
NB: Compressive collapse  bulge
Obstructive collapse  retraction
NB: Both bulge and retraction cause
limitation of movement.
2. Unilateral retraction
Lung
fibrosis
Lung
collapse
3. Scoliosis
Retractile tissue pulls
visceral + parietal
pleura which pull
thoracic cage
Q. Is this side bulged or the other is
retracted?
A. If limitation from the bigger side,
it's
a
bulge
and
vice
versa.
ii) Movement:
(1) Type:
In males, diaphragm is dominant  abdominothoracic breathing.
In females, intercostals muscles are dominant  thoracoabdominal
breathing.
For you: In pregnancy, there is limitation of diaphragmatic movement
(‫)الحمد هلل‬
o Thoracoabdominal breathing in males:
- Tense ascites
- Peritonitis
- Diaphragmatic paralysis
o Abdominothoracic breathing in females:
- Intercostal muscle paralysis
- Marked pleural effusion
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- Pleurisy, pneumothorax
- Severe COPD
(2) Rate:
o H.R. is involuntary while R.R. is both voluntary and involuntary.
o During sleep, respiration is controlled by chemical and neuronal
control.
o Voluntary control of respiration indicates mood, so to examine rate,
you have to draw patient's attention away from breathing, not to be
under voluntary control, so pretend that you are measuring pulse
while you are LOOKING to patient's chest.
o R.R.:
- 14-20  normal
- >20  Tachypnea
- <14 bradypnea
Bradypnea
Pontine hemorrhage
Increased intracranial
pressure
Barbiturate toxicity
Morphine
Severe hypoxia
Tachypnea
as CO2 cannot
cross BBB
CO2 + H2O  H2CO3
HCO3-+H+
Acidosis and
stimulation of R.C.
H+
↓R.C.
↑R.C.
Acidosis:
- Metabolic  hyperventilation (rapid+deep)
In:
 Diabetic ketoacidosis
 Uremia
 Excessive acid intake (salycylate poisoning)
- Respiratory: in respiratory failure  tachypnea (rapid + shallow):
 > 40  decompensated R.F.
 <40  compensated R.F.
(3) Inspiratory retraction:
- Caused by:
o Diaphragm
o –ve intrathoracic pressure
Both pull lower inercostals. If exaggerated it's called Litting's Sign.
- Exaggerated in R.F. as COPD.
- Lost in:
o Diaphragmatic paralysis
o Pleural effusion+pneumothorax
o obesity
(4) Expansion:
o Type test:
- Using meter tape around patient's chest at level of nipple or below
breast in female (4th rib in both sexes).
- Let him take deep inspiration and measure inspiration and expiration
difference: 3-5 cm normal, <3 cm limited movement.
Clinical medicine – Chest
c) Pulsations:
-
Examine pulsation of heart (see inspection in cardiology).
Invisible apex: emphysema/pleural effusion/pleural thickening.
Extracardiac causes of apex displacement:(lesion affecting lower 1/2 of
lung)
 Ipsilateral pulling  coolapse, fibrosis.
 Contralateral pushing  tumor, pneumothorax, pleural effusion.
- Signs of RVE:
 Apex is shifted outwards
 Systolic retraction
 Diffuse apex
 LPS pulsation
 Epigastric pulsation
- Significance of RVE  diagnoses Cor-pulmonale (=RVE with or without failure
due to lung disease)
- The most important pulse to examine is Epigastric because if patient is
emphysematous it will be the only seen pulse.
N.B.: Normal HR is 60
Normal RR is 15
So Normal C/P ratio is 4:1
If heart problem  tachycardia  >4:1
If lung problem  tachypnea  <4:1
Exercise, Stress, thyrotoxicosis  affect both unchanged ratio.
2) Palpation:(TPE‫)طبي‬
a) Trachea:





Normally cenral
Causes of shifted ttrachea: lesion affecting upper 1/2 of lung:
o Ipsilateral pulling  coolapse, fibrosis.
o Contralateral pushing  tumor, pneumothorax, pleural effusion.
How to examine?
Left hand on the patient head to fix it making him looking forwards.
Index of right hand with the nail laterally in suprasternal notch, then
move to feel distance between trachea and sternomastoid muscle inboth
sides:
o Equal  central.
o Wider  shifted to the other side.
b) Tenderness:


Palpate by pressure, looking to patient face noticing facial
expressions. ‫التسأله‬
Causes of tenderness: from in to out:
o Pleurisy: especially lower axillary+beneath breast.
o Bone:
 Traumatic: fracture rib
 Inflammation: osteomylitis=Teid's Syndrome.
 Neoplastic: leukemia, 1ry, 2ry bone tumor.
o Muscle: myositis.
o Veins of breast: thrombophlebitis (Monder's disease)
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Clinical medicine – Chest
o Skin: Herpes Zoster.
N.B.: In herpes zoster, in the first 24 hours no signs, only severe pain, so patient go
to internist doctor not to dermatologist.
N.B.: In ischemic heart diseases (Angina, myocardial infarction) there is pain
without tenderness.
c) TVF=tactile Vocal Fremitus:
o Rules:
- Comparative
- By the same hand
- Tips of fingers directed laterally
- Sites:
 Supramamary, mammary, inframammary
 Upper, middle, lower axillary.
 Supra-, inrascapular on both sides, interscapular.
- Each time tall patient to say ‫أربعة أربعة‬
o ↑↑ TVF:
- Consolidation:
o Pneumonia
o Bronchiectasis
o Around lung abscess
- Lung cavity: large, superficial, empty, connected to a bronchus.
- Obstructive collapse with patent main bronchus.
o ↓↓ TVF:
 obstruction:
 F.B.
 Tumor
 Fibrosis
 Barrier:
 Pleural effusion
 Pleural thickening
 Pneumothorax
 Emphysema
 Obesity
d) Palpable Rhonchi:
o Rules: as TVF but ask patient to take deep breath.
o Causes:
o Bronchitis
o B.A.
o Fibrosis
o F.B.
o Tumor
o Secretions (air way obstruction).
e) Pulsation: see inspection + cardiology.
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Clinical medicine – Chest
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f) Expansion:
i) Apical ‫يامنيّل‬
ii) Basal:
(1) Anterior (infrasternal).
(2) Posterior (interscapular).
Method:
o Take skin fold medially.
o Ask patient to breath.
o Notice widening.
3) Percussion:
o Rules:
 Comparative
 From up downwards
 Horizontal pleximeter in intercostal spaces, nut horizontal or vertical
in paravertebral.
 Light percussion except the back heavy.
o Sites:
 Lungs:
 Apex:
o Vertical pleximeter from behind patient.
o Normally resonant.
o Causes of dullness:
- apical fibrosis
- apical collapse
- apical tumor (Pancoast tumor)
- apical abscess (T.B.)
- apical consolidation (Freidlander's)
- apical pleural effusion (massive or encysted by
adhesion)
- pleural thickening
 Clavicle: direct percussion as clavicle acts as pleximeter,
infraclavicular.
 Main mass of lung:
o
 Heart:
 Tidal percussion
 Right border
 Bare area.
 Traube's area‫بالطلب‬
o
4) Auscultation