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Clinical Methodology

PREPARED AND PRESENTED BY

DR. ABDINASIR ALI

Respiratory Examination
For most patients, start the examination on the right of the bed/couch
with the patient semirecumbent (approximately 45°). Do not dent the
confidence of an already anxious patient with heart failure or
peritonitis by moving him unnecessarily from the position he finds
most comfortable. From the right-hand side of the patient, it is
easier to examine the jugular veins, apex beat and abdominal
viscera, although left-handed students will take longer to master
this approach.
 Common Respiratory
presenting symptoms
 Breathlessness
 Wheeze
 Cough
 Sputum ( Color, Volume, Consistency)
 Hemoptysis
 Stridor
 Chest pain
 Fevers/rigors/night sweats
 Weight loss
 Sleepiness
Past medical History of Respiratory diseases
Respiratory Surface Anatomy
The physical examination

The patient should be reclining on an

examination couch or bed at about
45 degrees, with the thorax exposed
and the head supported by a pillow.
 Inspection
• Much can be learned about the respiratory system by careful
inspection from the end of the bed.
• Thenormal shape and respiratory movements of the chest wall are
significantly altered by the hyperinflation that accompanies
chronic airflow obstruction (Fig. 5.5). Such obstruction also
causes prolonged expiration relative to inspiration, and sometimes
‘pursed-lip’ breathing on expiration.
• Forceful inspiration at these very high lung volumes may cause
indrawing of the intercostal spaces during mid-inspiration and
also the recruitment of muscles not normally involved in
breathing (‘accessory muscles’). These include the
sternocleidomastoid muscles lifting the sternum, and
trapezius and the scalenes lifting the shoulder girdle.
• Patientssometimes sit forwards and brace their arms on a table,
allowing them to use pectoralis major to pull the ribs outwards during
inspiration.
• Incontrast to the hyperinflation of obstructive disease, interstitial
disease causes small, stiff lungs, diminishes thoracic volume and raises
resting respiratory rate.
• Chest deformity (Fig. 5.6) may be congenital, as in pectus excavatum,
or acquired, as in pectus carinatum. The latter is an inward displacement
of the lower ribs with a prominent sternum, caused by severe airflow
obstruction in early childhood, when the rib cage is developing.
Asymmetry of the chest may be secondary to scoliosis, shrinkage of
scarred lung following tuberculous infection, or prior surgical resection
of lung and/or ribs.
 Examination sequence
••Note the presence of nebulisers or inhalers (indicating
obstructive lung disease), oxygen therapy and cyanosis; check
sputum pots.
•• Look for asymmetry of the chest movement, deformities,
operative scars and chest drains, remembering that thoracotomy
scars may be visible only on the lateral and posterior aspects of
the chest, Type of Respiration, Visible dilated veins,
•• Quietly observe and time respiratory rate (for example, breaths
in 15 seconds × 4) without drawing the patient’s attention to it, as
this may cause it to change. Feeling the radial pulse, while timing
breathing, is a common solution to this problem.
•• Inspect the remaining skin for relevant abnormalities. At rest the
rate is normally 12–15 breaths per minute; anxious patients may
breathe at 15–20 breaths per minute but a rate of over 20 breaths
per minute is abnormal for an adult.
• Inhealthy adults at altitude, elderly people and patients with heart
failure, a distinctive pattern of alternating periods of deep and
shallow breathing may be seen. This is known as Cheyne–Stokes
respiration and is thought to represent abnormal feedback from
the carotid chemoreceptors to the respiratory centre.
 Hands and arms
• Finger clubbing is due to overgrowth of soft tissue in the terminal phalanx, which increases
the lateral and longitudinal curvature of the nail (see Fig. 3.8), raising the nail bed off the
underlying bone. It is palpable as a boggy fluctuation of the nail when pressure is applied
just proximal to the nail (see Fig. 3.9C).
• The most common respiratory causes of clubbing are chronic suppurative lung disease
(such as bronchiectasis), lung cancer and pulmonary fibrosis (see Box 3.4).
• An additional rare complication of lung cancer is hypertrophic pulmonary osteoarthropathy,
in which painful, tender swelling of the wrists and ankles accompanies pronounced finger
clubbing.
• X-rays of the distal forearm and lower legs show subperiosteal new bone formation
overlying the cortex of the long bones.
• Other important signs of respiratory disease in the hands include: cyanosis • tar staining of
fingers from tobacco use (Fig. 5.8) • small-muscle wasting (see Fig. 13.22), which may
indicateT1 root damage by an apical lung tumour • rarely, yellow–brown discoloration of
nails in yellow nail syndrome .
• Examination sequence
• Examine the hands for finger clubbing (see Fig. 3.9), tar staining, nail
discoloration and cyanosis.
• • Ask the patient to hold their arms out straight with the wrists extended (Fig.
5.10).
• • Check the pulse while examining the hands.
• • Check for any tenderness in the distal forearm. Fine tremor of the
outstretched hands is common in respiratory patients and usually due to the
direct effect of high-dose beta-agonist bronchodilators on skeletal muscle. A
coarse flapping tremor of the outstretched hands is seen in patients with
CO2 retention.
 Face
• Respiratory disease can cause important signs in the face.
• Superior vena cava obstruction causes dusky, generalised
swelling of the head, neck and face (Fig. 5.11) with
subconjunctival oedema (looking like a tear inside the lower lid,
but not mobile); this usually indicates tumour invasion of the
upper mediastinum. Tumour at the root of the neck may disrupt
the sympathetic nerves to the eye, which run from the upper
thoracic spinal segments via ganglia in the neck to join the carotid
artery sheath. This causes unilateral ptosis and pupillary
constriction (Horner’s syndrome).
 Examination sequence
•• Check the conjunctiva of one eye for anaemia, and the colour of
the tongue for central cyanosis (Fig. 5.12).
•• Check for ptosis and pupil asymmetry.
• Remember that cyanosis becomes visible only when a sufficient
quantity of deoxyhaemoglobin is circulating, making it hard to
detect in anaemia but obvious in polycythaemic patients with only
a mild percentage of desaturation.
 Neck
• Jugular venous pressure (JVP) is raised in many patients with
pulmonary hypertension, and may be acutely raised in those with
tension pneumothorax or large pulmonary embolism.
• In superior vena cava obstruction the JVP may be raised above
the angle of the jaw, making pulsatility invisible. In those who are
using the sternocleidomastoids as accessory muscles (see earlier),
it is frequently impossible to see the JVP, as the internal jugular
vein lies deep to the active muscle.
• Examination sequence
• • Support the patient’s head with a pillow before examining the neck, to
facilitate relaxation of the sternocleidomastoid muscles.
• • Examine the JVP (p. 52).
• • Check for tracheal deviation by gently advancing a single finger resting in
the sternal notch in the midline (Fig. 5.13).
• If the fingertip meets the centre of the trachea, it is not deviated.
• • Check the cricosternal distance (the vertical distance between the sternal
notch and the cricoid cartilage, the first prominent ridge felt above the
tracheal rings). In health, three average fingers fit between the sternal notch
and the cricoid.
• • Examine the cervical lymph nodes from behind with the patient sitting
forward. Tracheal deviation away from the affected side is seen acutely in
tension pneumothorax.
• Chronic tracheal deviation towards the affected side occurs with
loss of lung volume in upper lobe fibrosis or collapse, and following
lobectomy or pneumonectomy. Reduction in cricosternal distance is
a sign of hyperinflation and reflects upward displacement of the
sternum (see Fig. 5.5B).
• Upward movement of the sternum and downward movement of the
trachea on inspiration are normal, but may become more obvious
with forceful inspiratory efforts in respiratory disease. Rarely,
systolic downward movement of the trachea is felt in patients with
aortic aneurysm (sometimes called ‘tracheal tug’). Cervical lymph
nodes are frequently involved in lung neoplasms spreading via the
mediastinum.
 Thorax
• Firstinspect the chest closely again, in case abnormalities have
been missed from the end of the bed. In patients with a thin chest
wall and increased respiratory drive (as in exacerbation of asthma
or COPD), forced, rapid inspiration often causes visible indrawing
of the skin in the intercostal spaces during inspiration, seen more
easily with tangential light (see Fig. 5.6A).
 • Palpation
• Examination sequence
• • Locate the apex beat, the most inferior and lateral place where the finger is lifted by
the twisting systolic movement of the cardiac apex. This is normally in the fifth
intercostal space in the mid-clavicular line; count down the intercostal spaces from the
second, which is just below the sternal angle.
• The apex beat is displaced laterally by dilatation of the ventricles or leftward
displacement of the mediastinum.
• Hyperinflation in obstructive lung disease causes the lingula of the left upper lobe to
come between the heart and the chest wall, making the apex beat impalpable and the
heart sounds inaudible (see Fig. 5.5B; in this situation the heart sounds are best heard
in the epigastrium).
• In pulmonary hypertension the lower sternum is lifted by the cardiac cycle (right
ventricular heave). Next assess thoracic expansion in both the upper and lower anterior
chest wall.
• • Chest Movement: Cup your hands, with fingers spread, round the patient’s
upper anterior chest wall, pressing the fingertips firmly in the mid-axillary
line. Pull your hands medially towards each other to tighten any loose skin,
and use your thumbs (off the skin) as pointers to judge how much each hand
moves outwards when the patient is instructed to take a full breath in (Fig.
5.14). In a healthy thorax, the ribs move out and up with inspiration.
• • Check for any asymmetry. This is more important than the absolute degree
of expansion, which will vary between individuals.
• • Repeat the process in the lower anterior chest wall.
• In COPD with hyperinflation the normal outward movement of the lower
ribs on inspiration is replaced by paradoxical inward movement, caused by
contraction of the abnormally low flat diaphragm (see Fig. 5.5).
• Thisstriking sign (paradoxical rib cage movement or ‘Hoover’s sign’)
may be missed if expansion is assessed only in the upper chest or from
behind. Palpation of the chest wall may rarely reveal surgical
emphysema, indicating air trapped in the subcutaneous tissues (Fig.
5.15). This most commonly complicates pneumothorax with chest
drainage or rib fracture, and feels like a palpable crackling under the
skin of the upper thorax and neck.
• Expansion of the chest by measuring of tape below the nipple while
patient is taking deep inspiration and expiration.
• Vocal Fremitus: say one, one, one while you comparing both lungs
• Look for added sounds if you can feel it.
Vocal Fremitus
 Percussion
• Correctly performed, percussion can distinguish areas of the chest
wall over air-filled lung from those overlying consolidated lung or
fluid. It generates a hollow, ringing sound accompanied by a
palpable resonance over air-filled lung, but a dull thud lacking
resonance over consolidation or fluid.
• Theabsolute quality and volume of the percussed sound vary
widely between individuals with differing chest wall thickness,
muscularity and subcutaneous fat, and is of little value.
• Thevalue of percussion lies in detecting asymmetry of resonance
between mirror image positions on the right and left sides.
 Examination sequence
• • To percuss the chest, apply the middle finger of your non-dominant hand firmly to an
intercostal space, parallel to the ribs, and drum the middle phalanx with the flexed tip of
your dominant index or middle finger (Fig. 5.16A).
• • Percuss in sequence, comparing areas on the right with corresponding areas on the left
before moving to the next level (Fig. 5.16B).
• • Posteriorly, the scapular and spinal muscles obstruct percussion, so position the
patient sitting forwards with their arms folded in front to move the scapulae laterally.
• Percuss a few centimetres lateral to the spinal muscles, taking care to compare positions
the same distance from the midline on right and left (Fig. 5.16C).
• In healthy people, anterior chest percussion is symmetrical except for the area
immediately lateral to the lower left sternal edge, where the right ventricle causes
dullness; this ‘cardiac dullness’ is lost in hyperinflated patients in whom the lingula
overlies the heart (see Fig. 5.5). Clear resonance is the usual finding over a
pneumothorax, although the difference between normal lung and pneumothorax may be
quite subtle because normal lung is almost all air. Resonance on percussion together
with unilateral absent breath sounds indicates pneumothorax.
 Auscultation
• To understand chest auscultation it is necessary to understand the origin of
breath sounds. The tracheobronchial tree branches 23 times between the
trachea and the alveoli.
• This results in an exponential rise in the number of airways and their combined
cross-sectional area moving towards the alveoli. During a maximal breath in
and out, the same vital capacity (about 5 L of air in healthy adults) passes
through each generation of airway.
• In the larynx and trachea, this volume must all pass through a cross-sectional
area of only a few square centimetres and therefore flow rate is fast, causing
turbulence with vibration of the airway wall and generating sound. In the distal
airway, the very large total cross-sectional area of the multitude of bronchioles
means that 5 L can easily pass at slow flow rates, so flow is normally virtually
silent. The harsh ‘bronchial’ sound generated by the major airways can be
appreciated by listening with the diaphragm of the stethoscope applied to
the larynx (try this on yourself).
• Most of the sound heard when auscultating the chest wall
originates in the large central airways but is muffled and deadened
by passage through overlying air-filled alveolar tissue; this,
together with a small contribution from medium-sized airways,
results in ‘normal’ breath sounds at the chest wall, sometimes
termed ‘vesicular’.
• When healthy, air-filled lung becomes consolidated by pneumonia
or thickened and stiffened by fibrosis, sound conduction is
improved, and the centrally generated ‘bronchial’ breath sounds
appear clearly and loudly on the overlying chest wall. In the same
way, with soft speech (‘say one, one, one’), the laryngeal sounds
are muffled by healthy lung but heard clearly and loudly at the
chest wall overlying consolidation and fibrosis, due to improved
conduction of major airway sounds through diseased lung.
When there is lobar collapse caused by a proximal bronchial
obstruction, the signs are different from those in simple
consolidation. The usual findings are diminished expansion,
sometimes with chest asymmetry due to loss of volume,
dullness to percussion over the collapsed lobe, and reduced
breath sounds and vocal resonance. When the lung tissue is
physically separated from the chest wall by intervening air
(pneumothorax) or fluid (pleural effusion), sound conduction
is greatly impaired and the breath sounds are usually absent.
These two causes of absent sounds are readily distinguished by
percussion, which will be resonant with pneumothorax and
completely dull over pleural fluid.
• Use of the stethoscope
• Remember to wear the stethoscope with the ear pieces facing
forwards to align them with your auditory canal. Normal breath
sounds are relatively quiet, so the greater area of contact offered
by the diaphragm is usually well adapted to chest auscultation.
• The two common exceptions are in patients with:
••A cachectic chest wall with sunken intercostal spaces, where it
may be impossible to achieve flat skin contact with the
diaphragm.
•• A hairy chest wall, where movement of chest hairs against the
diaphragm are easily mistaken for lung crackles. In these
situations, use the stethoscope bell instead to listen to the breath
sounds.
• Breath sounds
• As with percussion, the absolute volume and character of breath sounds in
individuals are greatly affected by the thickness, muscularity and fat content of
the chest wall. The symmetry of sounds is therefore the key feature.
• Added sounds
• There are three common added sounds: wheezes, crackles and rubs. Wheeze is a
musical whistling sound accompanying airflow and usually originates in
narrowed small airways. It is most commonly expiratory, due to dynamic airway
narrowing on expiration, but can also occur on inspiration. Usually, multiple
wheezing sounds are heard together (polyphonic wheeze); this sign is common
in asthma, bronchitis and exacerbation of COPD.
• A solitary wheeze that is present consistently with each breath and does not
clear with coughing suggests a possible fixed bronchial obstruction and can be
an important sign of underlying cancer.
• Crackles accompanying deep breathing are thought to represent the sudden opening of small
airways but sometimes may indicate secretions in the airways or underlying lung fibrosis.
• In healthy people, gravitational compression of the dependent lung bases often causes a few
crackles on the first few deep breaths; these are of no pathological significance. Crackles that
persist after several breaths and do not clear with a deliberate cough are pathological. They
are graded as ‘fine’, meaning soft, multiple crackles, to ‘coarse’, indicating loud, scanty
crackles that tend to change with each breath. Showers of fine crackles during inspiration,
resembling the sound made by peeling a Velcro fastener, are characteristic of interstitial
pulmonary fibrosis, and are most commonly heard at the lung bases posteriorly and laterally.
• Fine crackles also occur in pulmonary oedema and some viral pneumonias. Coarse crackles
are generally heard in patients with significant purulent airway secretions such as those with
bronchopneumonia or bronchiectasis. Inspiratory crackles are also often heard over the areas
of incompletely inflated lung immediately above a pleural effusion.
• Pleural rub is a rasping, grating sound occurring with each breath and sounding superficial,
just under the stethoscope, like two sheets of sandpaper rubbing together.
• It indicates pleural inflammation, usually due to infection, and is often accompanied by
pleuritic chest pain.
 Vocal resonance
• Breath sounds normally reveal the presence of consolidation or fibrosis
(bronchial breath sounds) or pleural air or fluid (absent breath sounds). These
signs can be confirmed by asking the patient to generate laryngeal sounds
deliberately (‘Please say “one, one, one” each time I move my stethoscope on
the skin’) and listening on the chest wall in the same sequence of sites used
for breath sounds.
• The spoken sound is muffled and deadened over healthy lung, but the spoken
sound is heard loudly and clearly through the stethoscope over consolidation
or fibrotic lung scarring. Consistent with absent breath sounds, vocal
resonance is absent or greatly diminished over pneumothorax and pleural
effusion.
• ‘Whispering pectoriloquy’ may be used to confirm the same changes in sound
conduction. Whispered speech is muffled to silence by normal lung but may
be heard over consolidated or scarred lung.
 Any Questions

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