Clinical Methods1

The regular production of purulent sputum in large amounts is characteristic of bronchiectasis and chronic bronchitis; when it happens as a sudden event on a single occasion, the rupture of a lung abscess or rupture of empyema into the bronchial tree is the most likely cause. The continuous expectoration of a great quantity of thin watery sputum, sometimes with a salty taste, is an occasional symptom of rare alveolar cell carcinoma. The profuse expectoration of pink frothy sputum in an acutely breathless patient suggests pulmonary edema.

The colour of the sputum is also of diagnostic value. A green colour imparted by the pigment verdeperoxidase, indicates pus usually arising from a bacterial infection. Yellow sputum may also be due to pus or the presence of eosinophils in allergic states such as asthma. A brown coloured sputum may result from altered blood or from fungal infections and may rarely be seen when an amebic liver abscess ruptures into the lung. A greenish yellow tinge suggests a bronchobiliary fistula. The sputum of coalminers may be black due to breaking down and expectoration of a pneumoconiotic nodule. The presence of blood in sputum is considered separately (see below).

The consistency of sputum has great therapeutic significance. Thick, viscid, tenacious sputum is the most typical and dangerous feature of acute severe asthma; it is difficult to expel and the patient may asphyxiate from plugging of the smaller airways. The thin frothy sputum of acute pulmonary edema may drown the patient in his own secretions.

The shape and general appearance of any solid expectorated material should be noted. Viscid secretions sometimes assume the shape of the airway from which they are expectorated. These bronchial casts may appear as string-like strands or short elliptical plugs; they are a characteristic feature of bronchopulmonary aspergillosis in which they are often golden-brown in colour. Other solid matter which may be recognized in the sputum includes blood clot, necrotic tumour, inhaled foreign material and parasitic worms.

An offensive odor or taste suggests infection by anaerobic organisms as encountered in some cases of bronchiectasis, lung abscess and empyema.

A rough assessment of the amount of lost blood should be made. Whether this consists streaks or clots in the sputum, or a more diffuse staining or pure blood. Massive hemoptysis is defined as a loss greater than 600-800 ml of the blood, is also important, because the presence of blood in a single sample is much less likely to result from serious organic disease than staining of successive samples. Presence of any accompanying symptoms, notably dyspnea and pleuritic pain should be recorded.

The patient with hemoptysis tends to keep the bleeding side dependent. He may also be able to give history of a burning or deep pain which may localize the side of bleeding. In many cases, no serious cause for hemoptysis may be found other than an acute exacerbation of chronic bronchitis but a focal organic source for the bleeding must always be excluded. The most important of these are bronchial carcinoma, carcinoid, tuberculosis, bronchiectasis, mitral valve disease and pulmonary infarction; pneumonia can also produce hemoptysis in the form of rusty sputum, while acute left ventricular failure results in pink frothy sputum. Hemoptysis may be the sole presenting symptom of bronchial carcinoma, carcinoid tumour and tuberculosis but it is usually associated with purulent sputum in bronchiectasis, with dyspnea in mitral valve disease and with sudden dyspnea or pleuritic pain in pulmonary infarction. Rare causes for hemoptysis are mycetoma, vascular malformations, hemorrhagic disorders and Good pasture's syndrome. A recent history of blunt trauma to chest suggests a lung contusion. Hemoptysis is rare in metastatic carcinoma to the lung.

Pleuritic pain: It is typically sharp, stabbing and related to inspiration. Inflammation of the upper part of the parietal pleura causes pain localized to the chest itself. The lower portion including the outer segment of the diaphragmatic pleura, is innervated by the lower six intercostal nerves which also supply the abdominal wall; pleuritis at this site may give rise to pain in the upper abdomen or loin. The central part of the diaphragmatic pleura is innervated by the phrenic nerve (C3 and C₄); so that pain from this site is felt in the neck and tip of the shoulder. Pleural pain associated with pneumonia causes rapid, shallow, grunting respiration. When pleural effusion forms, the pain of pleurisy abates to a dull discomfort. The most important causes of pleuritic pain are pneumonia, cancer, tuberculosis, 14pulmonary infarction, and pneumothorax and, less commonly, autoimmune disorders such as systemic lupus erythematosus.

Chest wall pain: It results from respiratory diseases as well as from primary musculoskeletal disorders. Patients with chronic cough and dyspnea from any cause often complain of chest pain. This may vary from the vague discomfort or feeling of tightness commonly among asthmatic subjects, to the acute pain of rib fracture, torn muscle or disc injury induced by violent coughing. A local traumatic lesion in the chest wall causes pain very similar to pleuritic pain. The main distinguishing features of the former are the sudden onset following violent cough or other trauma and the presence of tenderness localized to the site of pain. The invasion of the chest wall by an intrathoracic neoplasm, metastasis of lung or malignant mesothelioma of pleura causes dull, aching or boring pain which is unrelated to respiratory or other movements. It tends gradually to become more persistent and disturb the patient's sleep. The Pancoast's tumor may infiltrate the brachial plexus and causes pain which radiates to the arm. The lung tumor usually causes deep seated vague chest pain due to involvement of bronchial nerve plexus.

Tracheobronchial pain: Pain of tracheobronchial origin may accompany acute inflammation due to infections or from inhalation of irritant fumes. It is usually described as a raw retrosternal discomfort and is distinguished from esophageal and cardiac pain by its relationship to cough rather than to meals or exertion.

Non-respiratory pain: Many chest pains are of non-respiratory origin. The retrosternal burning pain of acid reflux into the esophagus occurs after meals or on stooping or lying down. The retrosternal gripping pain of angina which occurs typically on effort may radiate to the neck, jaw, arm or back. The pain of pericarditis is usually retrosternal but can sometimes be pleuritic in character. Neuromusculoskeletal chest discomfort can be caused by cervical disc disease (because of compression of nerve roots) by arthritis of the shoulder or spine or by costochondritis, which is an inflammation of costochondral junctions. Intercostal muscle cramps may occur throughout the chest.

The body temperature is most often measured at one of the three sites; mouth, axilla or rectum. Rectal temperature most accurately reflects the actual body-core temperature. Oral temperature measurement is the most acceptable for an awake, adult patient, but this method cannot be used with infants, comatose patients, or orally intubated patients. After the patient has ingested hot or cold drink or has been smoking, a 10-15 minute waiting period is necessary. Before inserting the thermometer, it should invariably be washed in an antiseptic or cold water, and further ensured that mercury is well shaken down. The axillary temperatures may be taken safely in case of infants and small children who do not tolerate rectal thermometers.

The oral temperature is not affected significantly by simple oxygen administration via nasal cannula or mask. Therefore it is not necessary to remove oxygen or take rectal temperature of patients receiving simple oxygen therapy. But the oral temperature may not be a valid measure in patients breathing heated or cooled aerosol via face masks. There is tendency for oral temperature to be increased slightly with the application of heated aerosol and decreased slightly with cool aerosol inhalation. In these cases, if absolute accuracy is essential, the rectal route should be employed.

Three classical types of fever are described—continuous, remittent and intermittent. When fever fluctuates within 1°F to 2°F during 24 hours, but at no time touches the normal, it is termed as continuous. When the daily fluctuations exceed 2°F, it is called remittent, and when fever is present only for several hours during the day it is called intermittent. When a paroxysm of intermittent fever occurs daily, the type is quotidian; when on alternate days, tertian; when two days intervene between consecutive attacks, quartan. Pel-Elbstein fever is described as one lasting for a few days alternating with a number of afebrile days (cyclical fever) and often occurs in patients of lymphoma.

The most common site for evaluation of the pulse is the radial artery. The examiner's second and third finger pads are used in assessment of the radial pulse. Ideally the pulse rate should be counted for one minute. The following characteristics of the pulse should be noted and documented; rate—is it normal, high, or low; rhythm— is it regular, consistently irregular, or irregularly irregular; amplitude— are there any changes in the amplitude of the pulse in relation to ventilation or are these changes from one beat to another; the presence of thrills or bruits. If the patient's wrist is held too far above the level of his heart, the pulse may be difficult to obtain. When the patient's pulse strength decreases with spontaneous inhalation, it is referred to as pulsus paradoxus.

Other common sites for assessment of pulse include the carotid, brachial, femoral, temporal, popliteal, posterior tibial and dorsalis pedis arteries. When the blood pressure is abnormally low, the more centrally located pulses such as carotid and femoral pulses are identified more easily than the peripheral pulse. If the carotid site is used, great care must be taken to avoid the carotid sinus area, as mechanical stimulation of the latter can evoke a strong parasympathetic response and may cause bradycardia or even asystole.

The most common technique for measuring arterial blood pressure is the auscultatory method, which uses a blood pressure cuff (sphygmomanometer) and a stethoscope. When the cuff is applied to the upper arm and pressurised to exceed the systolic blood pressure, the brachial blood flow is stopped. As the pressure in the cuff is released slowly to a point just below systolic pressure, blood intermittently overcomes the obstruction. Partial obstruction of the arterial blood flow creates a turbulent flow, producing the vibrations called Korotkoff sounds. Korotkoff sounds can be heard over the artery distal to the obstruction with the aid of a stethoscope. To measure the blood pressure, a deflated cuff is wrapped snugly around the upper arm with its lower edge 2.5 cm above the antecubital fossa. The brachial pulse is palpated, and the cuff is inflated to a pressure 30 mm Hg higher than the point at which the pulse is obliterated. The bell of the stethoscope is placed over the site of brachial artery. Then the cuff is deflated at a rate of 2 to 3 mm Hg per second while observing the manometer. The systolic pressure is recorded at the point at which the initial Korotkoff sounds are heard. The point at which the sounds become muffled is recorded as the diastolic pressure. This muffling sound is the final change in the Korotkoff sounds just before they disappear. At this point, the cuff pressure is equal to the diastolic pressure, and no turbulent sounds are created. The examiner must be careful to perform the procedure rapidly, since the pressurized cuff impairs circulation to the forearm and hand. Common mistakes that can result in erroneously high measurements include too narrow a cuff, cuff applied too tightly or loosely, and excessive pressure in the cuff during measurement, inflation pressure held too long in the cuff, and incomplete deflation of cuff between measurements.

The systolic pressure usually decreases with normal inhalation. This decrease in systolic pressure is more significant during a forced maximal inhalation. If the drop is more than 6-8 mm Hg during inhalation at rest, a definite abnormality exists, termed as paradoxical pulse or pulsus paradoxus. The mechanism responsible for this fluctuation in blood pressure centers on the negative intrathoracic pressure created by the respiratory muscles during inhalation. The paradoxical pulse can be identified most accurately with a sphygmomanometer. However if the pulse can be felt to wane with inspiration in several accessible arteries, paradoxical pulse is present. To confirm and quantify its presence, the blood pressure cuff is inflated until no sounds are heard with the stethoscope bell over the brachial artery, and then it 20is gradually deflated until sounds are heard on exhalation only. The cuff pressure then is released even more slowly until sounds are heard throughout the respiratory cycle. The difference between these two pressure readings indicates the degree of paradoxical pulse. A reading in excess of 6 to 8 mm Hg is significant. A paradoxical pulse may occur with acute airway obstruction such as asthma or constrictive pericarditis.

Normally capillary blood has about 2.5 gm/100 ml reduced hemoglobin (Hb). For cyanosis to be detected, the capillaries in general must contain at least 5 gm/100 ml Hb of reduced. This occurs when oxygen saturation (SaO₂) drops below 80%, and corresponds to a PaO₂ of about 45 mm Hg. In anemia, there may not be enough unsaturated hemoglobin to produce central cyanosis until the arterial saturation drops well below 80%. Conversely in polycythemia or erythrocytosis, the amount of reduced hemoglobin may be sufficient to produce central cyanosis even when there is adequate oxygen delivery to tissues.

The evaluation of the presence and degree of cyanosis depends upon the examiner's perception and is modified by factors such as the ambient lighting, the colour of the skin, and the presence of abnormal blood pigments (e.g. methemoglobin or sulfhemoglobin).

In adults, approximately 75% to 85% of all clubbing is associated with respiratory diseases, such as lung tumours, bronchiectasis, pulmonary fibrosis, empyema and cystic fibrosis. Only 10% to 15% have an underlying disease and remaining 5% are associated with miscellaneous conditions.

Clubbing may be associated with a more generalised condition that affects the bones and joints and is known as hypertrophic pulmonary osteoarthropathy (HPOA see chapter 42). HPOA is a chronic inflammatory process that results in thickening of the periosteum, as evidenced on X-ray examination. Joints may also be swollen and inflamed. In a well-developed case, there may be pain and disabling limitations of motion. Clubbing may occur early in the development of HPOA.

Think anatomically. The right IJ runs between the two heads (sternal and clavicular) of the sternocleidomastoid muscle (Fig. 1.12) and up in front of the ear. This muscle can be identified by asking the patient to turn their head to the left and into your hand while you provide resistance to the movement. The two heads form the sides of a small triangle, with the clavicle making up the bottom edge. You should be able to feel a shallow fossa formed by the borders of these landmarks. Note, you are trying to identify impulses originating from the IJ and transmitted to the overlying skin in this area. You can not actually see the IJ.

The External Jugular (EJ) runs in an oblique direction across the sternocleidomastoid and, in contrast to the IJ, can usually be directly visualized (Fig. 1.12). If the EJ is not readily apparent, have the patient look to the left and attempt valsalva manouvre. This usually makes it quite obvious. EJ distention is not always a reliable indicator of elevated CVP as valves, designed to prevent the retrograde flow of blood, can exist within this vessel causing it to appear engorged even when CVP is normal. It also makes several turns prior to connecting with the central venous system and is thus not in a direct line with the right atrium.

Take your time. Look at the area in question for several minutes while the patient's head is turned to the left. The carotid artery is adjacent to the IJ, lying just medial to it. If you are unsure whether a pulsation is caused by the carotid or the IJ, place your hand on the patient's radial artery and use this as a reference. The carotid impulse coincides with the palpated radial artery pulsation and is characterized by a single upstroke timed with systole. The venous impulse (at least when the patient is in sinus rhythm and there is no tricuspid regurgitation) has three components, each associated with the aforementioned a, c and v waves. When these are transmitted to the skin, they create a series of flickers that are visible diffusely within the overlying skin. In contrast, the carotid causes a single up and down pulsation. Furthermore, the carotid is palpable. The IJ is not and can, in fact, be obliterated by applying pressure in the area where it emerges above the clavicle.

Search along the entire projected course of the IJ as the top of the pressure wave (which is the point that you are trying to identify) may be higher than where you are looking. In fact, if the patient's CVP is markedly elevated, you may not be able to identify the top of the wave unless they are positioned with their trunk elevated at 45° or more (else there will be no identifiable “top” of the column as the entire IJ will be engorged). After you have found the top of the wave, see what effect sitting straight up and lying down flat have on the height of the column. Sitting should cause it to appear at a lower point in the neck, while lying has the opposite effect. Realise that these maneuvers do not change the actual value of the central venous pressure. They simply alter the position 24of the top of the pulsations in relation to other structures in the neck and chest.

Shine a light tangentially across the neck. This sometimes helps to accentuate the pulsations. If you are still uncertain, apply gentle pressure to the right upper quadrant of the abdomen for 5 to 10 seconds. This elicits Hepato-Jugular Reflux which, in pathologic states, will cause blood that has pooled in the liver to flow in a retrograde fashion and fill out the IJ, making the transmitted pulsations more apparent. Make sure that you are looking in the right area when you push as the best time to detect any change in the height of this column of blood is immediately after you apply hepatic pressure.

Once you identify JVD, try to estimate how high in centimeters the top of the column is above the Angle of Louis. The angle is the site of the joint which connects the manubrium with the rest of the sternum. First identify the suprasternal notch, a concavity at the top of the manubrium. Then walk your fingers downward until you detect a subtle change in the angle of the bone, which is approximately 4 to 5 cm below the notch. This is roughly at the level of the 2nd intercostal space. The vertical distance from the top of the column to this angle is added to 5 cm, the rough vertical distance from the angle to the right atrium with the patient lying at a 45° angle. The sum is an estimate of the CVP. However, if you can simply determine with some accuracy whether JVD is present or not, you will be way ahead of the game. Normal JVD is 7-9 cm.

The level of jugular venous distension may vary with breathing. During inhalation the level of the blood column may descend towards the thorax; and return to the previous position with exhalation. For this reason, JVP should always be estimated at the end of exhalation.

The examination of the waves of jugular vein should be carried out while the patient is in sitting position, with light thrown tangentially on the neck; the examiner should sit by the side of the patient, to palpate the carotid artery of opposite side simultaneously to time and recognise the waves. The a wave precedes and v wave follows the artery pulse.

Neck veins are distended with absent pulsations in superior vena cava syndrome. In the absence of distended neck veins, the earliest sign of superior vena cava obstruction is the flushing of face and dizziness when the patient stoops to touch his feet.

How many are palpable?

What is their approximate diameter in centimeters?

What is the consistency?

Are these discrete or confluent (matted)?

Are these mobile or fixed?

Is the skin in the vicinity of nodes abnormal?

Scoliosis: Scoliosis is the most important of all chest deformities, because of its potential effect on the cardiorespiratory function. This lateral curvature of the spine is almost invariably accompanied by the rotation of the spine and only rarely by significant kyphosis, so that the popular term ‘kyphoscoliosis’ is often inappropriate. It is the rotation of the spine which causes a posterior hump comprising ribs and the scapula on one side (simulating a kyphosis) and an anterior hump on the other. The rotation is also largely responsible for the reduction in lung volume and impaired mechanical function, which in severe cases, leads to respiratory and then 28cardiac failure even in early middle life. This complication is more likely to occur if scoliosis affects the upper part of the spine. Postural scoliosis can be differentiated from pathological scoliosis, by asking the patient to stoop forward. In case of former, the lateral curvature is rectified while in latter case, it persists.

Kyphosis: Kyphosis is the most common cause of barrel chest which is therefore not a specific sign of emphysema alone. It is a deformity in which the spine has an abnormal anteroposterior diameter. Kyphosis unaccompanied by scoliosis does not cause any significant impairment of lung function except in extreme cases.

Pectus carinatum: Pectus carinatum is pigeon chest, with a sternal protrusion anteriorly. There is prominence of the sternum and/or anterior ends of the ribs. Pigeon chest may be congenital or a consequence of airflow obstruction in childhood as in Harrison's sulcus; but it does not by itself cause any respiratory dysfunction.

Pectus excavatum: Pectus excavatum is also known as funnel sternum. It is a congenital saucer shaped depression of the sternum and is only of cosmetic significance.

Rib deformity: Abnormalities of the ribs altering the configuration of the chest include those associated with scoliosis, local flattening of the chest resulting from surgical excision of ribs for tuberculosis (thoracoplasty) or empyema and the phenomenon of Harrison's sulcus. The latter consists of a bilateral groove in the rib cage, which has been attributed to the effect of diaphragmatic contraction in patients with airways obstruction (from adenoids or asthma) during early childhood when the bones are still malleable. It is particularly common among rachitic children in whom enlargement of the rib epiphyses may also be seen (‘rickety rosary’).

Soft tissue deformity: Asymmetry of the chest with either prominence or flattening may result from abnormalities of soft tissues, such as a diffuse lipoma, congenital absence of the pectoralis major or wasting of the scapular muscles. Pleural or pulmonary fibrosis can lead to flattening, contraction and impaired expansion of one hemithorax.

At rest, the normal adult has a consistent rate and rhythm of ventilation. Breathing effort is minimal on inhalation and exhalation is passive. Men typically breathe using their diaphragm, causing the abdomen to move slightly outward during inhalation. Women tend to use the combination of intercostal muscles and diaphragm, thus producing comparatively more chest wall movement than men.

A healthy subject breathes at a rate of 12-20 respirations per minute at rest. Rapid, shallow breathing suggests pulmonary consolidation, edema, diffuse fibrosis or other conditions associated with reduced compliance; but it may also occur when inspiration is painful. Abnormal slowing of respiration is invariably central in origin. Psychogenic causes account for most instances of 29irregular breathing, especially when this is punctuated by deep sigh breaths.

Individuals with disorders characterised by an increased elastic work of breathing, such as pulmonary fibrosis, tend to assume a rapid and shallow breathing pattern. For these patients, such a pattern results in the minimum mechanical work necessary to effectively ventilate the lungs. On the other hand, patients with obstructive lung disorders tend to assume the pattern best able to reduce the frictional work of breathing, and the breathing tends to be slow and deep. Table 1.3 describes the abnormal patterns of breathing.

The symmetry of movement of either side of the chest is observed from the foot end of bed of the supine patient. Of greater significance is the inequality of movement, as this may occur with any predominantly unilateral disease of the underlying pleura or lung. Inspiratory indrawing of intercostal spaces is commonly seen in children with respiratory distress from any cause. The distorted action of a depressed and flattened diaphragm in patients with chronic airflow obstruction, especially emphysema is probably responsible for the indrawing motion of lower ribs during inspiration and this paradoxical costal margin movement is known as Hoover's sign. The movements of the mouth are characteristic of severe airflow obstruction, especially in patients with emphysema.

In patients with airways obstruction, ‘Match test’ is applied at bed side. The subject is directed to blow out a lit-match held 15 cm from the open mouth. Inability to perform this test indicates severe airway obstruction with FEV1 less than 1.6 liters. The ‘20 deep breath test’ is conveniently performed in patients of hyperventilation syndrome (HVS). The subject is asked to take 20 deep breaths continuously; positive test produces the symptoms of dizziness and paraethesiae in the extremities and around the mouth, and is not only diagnostic of HVS but also therapeutic. Patients with HVS are more sensitive to the effects of hypocapnia.

Gasps: These are the noises of sudden, rapid, deep inspirations. These are physiological response to fright; and pathological response to severe expiratory airflow obstruction, where rapid deep inspiration compensates for slow prolonged expiration. Infrequent, irregular, gasping inspirations are also seen as a terminal event when the respiratory center is deranged.

Pants: These are noises of rapid shallow breathing, with inspiration and expiration being equal in duration and intensity of sound is also equal during both phases. These are the normal physiological response to exercise and a pathological response to decreased compliance of lungs in conditions such as interstitial pulmonary fibrosis, edema and consolidation.

Sighs and yawns: Both these consist of a slow deep inspiration to vital capacity, followed by an expiration which may be prolonged and intensified in sound because of apposition of the vocal cords. There is frequently a large psychogenic and voluntary component in proportion to the loudness of the sound. To prevent alveolar collapse from surface tension forces, even in healthy persons, the occasional deep breaths of sighs or yawns are required.

Hisses: Hissing or Kussmaul's breathing is the noise resulting from hyperventilation through apposed teeth and is characteristic of acidosis in patients of uremia, diabetic ketoacidosis and salicylate poisoning. These patients, in the absence of lung disease, hyperventilate without dyspnea and therefore without reflex opening of the mouth.

Sniffles: It is a noise from a sniffly nose either due to nasal obstruction, or discharge due to chronic sinus infection commonly accompanied by bronchiectasis, hay fever or nasal granulomas.

Snores: Snoring is mainly an inspiratory noise arising from vibrations of the soft tissues of the pharynx, tongue, palate and cheeks during sleep. It is quite a common condition; but in severe cases, may lead to obstructive sleep apnea syndrome.

Whistles and grunts: These are expiratory noises heard in patients with emphysema and especially important as these may be the only sounds heard in such patients, even with a stethoscope. There are several reasons for breathing being otherwise silent in emphysema; firstly, airway sounds are filtered out by the overinflated lung; secondly, expiratory airflow may be too slow to generate a wheeze; and thirdly, unlike asthma, emphysema is not associated with intrinsic airway narrowing. The wheeze of emphysema, which is often heard only on forced expiration, is due to passive collapse of proximal airways induced by the positive pressure needed to expel air from the inelastic lungs. Passive airway collapse can be reduced if the intrabronchial pressure is raised by expiratory apposition (pursing) of lips or larynx. Lip pursing gives rise to the characteristic expiratory whistle of emphysema. 31Laryngeal pursing is less common and consists of intermittent cogwheel like grunts during expiration, often thought to be attention-seeking device.

Whoops, wheezes and stridor: The inspiratory component of an asthmatic wheeze can be difficult to distinguish from ‘whoop’ or stridor of main airway narrowing. Stridor is of a higher pitch than the inspiratory wheeze of asthma and unlike wheeze may seem to continue even after airflow at the mouth has stopped. Stridor is a crowing sound due to obstruction in the larynx or trachea. When the diameter at site of lesion in either larynx or trachea is reduced to 5 mm, then inspiratory obstruction as well as stridor results at rest. Laryngeal stridor is high pitched while tracheal stridor is lower in pitch. Breathlessness is always associated with tracheal stridor; latter tends to be biphasic and is increased on coughing.

Rattles: This is the sound of air passing through fluid, or of mucus being set into vibrations in the main airways both during inspiration and expiration. It is usually a sign of failed cough reflex either because of decreased efficacy or excessive demand. The reflex may be impaired as a result of narcotics or extreme weakness, or it may be overwhelmed by a massive transudate into the airways in acute pneumonia or by aspiration of swallowed or regurgitated fluid.

Crackles: The early inspiratory crackles of chronic airways obstruction can sometimes be heard at the mouth.

The trachea should be palpated with the patient's head fully extended and the chin in mid-line (Fig. 1.15). A finger is gently slid deep into the suprasternal notch, where in a normal person it should meet the center of the trachea; or the observer should attempt gently to slide the tip of index finger between the trachea and the lower part of the belly of sternocleidomastoid muscle and feel for the resistance; the side to which the resistance felt is more, the trachea is considered shifted to the same side.

The site of apex beat is a less useful indicator of the position of the mediastinum, not only because it may be displaced by cardiac enlargement but also because it is more difficult to locate than the cervical trachea. It is mainly of value in detecting the lower lobe collapse where it shifts, while trachea remains central; and also for picking up the occasional case of dextrocardia in patients with bronchiectasis (Kartagener's syndrome).

The chest expansion or movement should be examined during tidal breathing as well. If the reduced movement of hemithorax seen during tidal inspiration improves on deep and maximal inhalation, it is indicative of partial obstruction of the whole lung or its part.

This is due to the fact that incomplete bronchial obstruction causes partial collapse and reduced air entry. The latter improves on deep inhalation, thereby improving the expansion of hemithorax.

A unilateral reduction in chest movement occurs with respiratory diseases that reduce the expansion of the lung or a major part of one lung. This may occur with lobar consolidation, atelectasis, pleural effusion and pneumothorax. Diseases that affect expansion of both lungs cause bilateral reduction in chest expansion, commonly seen with neuromuscular diseases and chronic obstructive pulmonary disease.

The overall expansion of the chest should be measured with a tape at the level of the nipples (or beneath the breasts in women). The circumference of chest should increase by 6 to 9 cm from full expiration to full inspiration. This measurement, though still required for job fitness, is of little clinical value except to demonstrate fusion of costovertebral joints in patients with ankylosing spondylitis.

The vibrations of tactile fremitus felt may be increased, decreased, or absent. Increased fremitus results from the transmission of vibrations through a more solid medium. The normal lung structure is a combination of solid and air-filled tissue. Any condition that tends to increase the density of the lung, such as consolidation, results in an increased intensity of fremitus. If the area of consolidation is not in connection with a patent bronchus, fremitus will not be increased; in fact it may be decreased. A reduced tactile fremitus is often present in patients who are obese or overly muscular. Also, when the pleural space lining the lung gets filled with air (pneumothorax) or fluid (pleural effusion), the vocal fremitus is reduced significantly or may even be absent.

In patients with emphysema, the lungs become hyperinflated with a significant reduction in the density of lung tissue. In this situation, the vibrations transmit poorly through the lung tissue, resulting in a bilateral reduction in tactile fremitus.

This bilateral reduction in tactile fremitus is more difficult to detect than the unilateral decrease or increase in fremitus.

The passage of air through airway(s) containing thick secretions may produce palpable vibrations referred to as rhonchial fremitus. Rhonchial fremitus is often identified during inhalation as well as exhalation and may clear if the patient produces an effective cough.

Percussion over lung fields: Percussion of the lung fields should be done systematically, consecutively testing comparable areas on both sides of the chest. Percussion over the bony structures and breasts of the female is not of value and should be avoided. Percussion over clavicle is performed with the striking finger directly, after stretching the overlying skin. Asking the patient to raise arms above shoulders will help to move the scapula laterally and minimise their interference during percussion of the posterior chest wall. The sounds generated during percussion of the chest are evaluated for intensity (loudness) and pitch. Percussion over normal lung fields produces a sound moderately low in pitch that can be heard easily. This sound is best described as normal resonance. When the percussion note is louder and lower in pitch than normal, the resonance is said to be increased or hyperresonant. Percussion may produce a sound with characteristics just the opposite of resonance, referred to as dull or flat. This sound is high pitched, brief and not loud.

Clinical implications: Percussion of the chest, by itself is of little value in making a diagnosis. When the percussion note is considered along with history and other physical findings, it may contribute significantly.

Any abnormality that tends to increase the density of lung tissue, such as consolidation of pneumonia, lung tumours, or alveolar collapse (atelectasis) results in a loss of resonance and a dull percussion note over the affected area. Percussion over pleural spaces filled with fluid, such as blood or water, also results in a dull or flat percussion note. An increase in resonance is detected in patients with hyperinflated lungs, which can occur as a result of acute bronchial obstruction (asthma), or emphysema, or when the pleural space contains air (pneumothorax).

Unilateral abnormalities are easier to be detected than bilateral ones because the normal side provides an immediate comparison. The dullness heard during percussion over consolidation is a distinct sound that is easier to detect than the subtle increase in resonance associated with hyperinflation or pneumothorax.

Limitations of percussion: Percussion of the chest has limitations that are often clinically important. Abnormalities that are small or more than 5 cm below the surface are likely to be missed (see auscultatory percussion below).

Diaphragmatic excursion (tidal percussion): The range of diaphragmatic movement may be estimated by percussion and is conducted best on the posterior chest wall. To estimate diaphragmatic movement, the patient is instructed to take first a deep, full breath and hold it. Then the examiner determines the lowest margin of resonance by percussion over the basal lung area and moving downward in small increments until a definite change in percussion note is detected. The patient is then instructed to exhale maximally, holding this position, while the percussion procedure is repeated. The examiner should work rapidly to prevent the patient from becoming short of breath. The normal diaphragmatic excursion during a deep breath is about 5 to 7 cm but it is reduced in patients with certain neuromuscular diseases or severe pulmonary hyperinflation.

Percussion of mediastinum: Over sternum and mediastinum, it is accomplished by light percussion if patient lying down and heavy percussion if patient sit up. The mediastinum is usually percussed to detect its widening by eliciting dullness on either side of the sternum.

Shifting dullness: The shifting dullness is elicited in hydropneumothorax, pyopneumothorax and moderate pleural effusion, because a shift or change in position of the fluid occurs on changing the posture of the patient. While patient sitting up, the upper border of dullness is delineated by percussion over anterior chest, the pleximeter finger is then kept at the same upper border of dull area and ask the patient to lie supine for 10-15 seconds (during this period the fluid flows to the dependent area) and dull area will become resonant on repercussion. Fluid can not shift in loculated or interlobar pleural effusions thus shifting dullness is absent. In case, the patient is not able to sit upright, shifting dullness may be demonstrated by rolling the patient to keep the dull area uppermost and repeating percussion after 10-15 seconds.

Shifting dullness in case of infrapulmonary effusion can be elicited by repeating the percussion over dull area with patient bent forward. The dull area at the base then changes to less dull or even normal resonant.

Stethoscope: A stethoscope possesses four basic parts: a bell, a diaphragm, tubing and earpieces.

Hair on chest wall can also alter the sounds; therefore if present these should be made wet to avoid the distortion of sounds. Also, the tubing should not rub against any object, since this may produce extraneous sounds. Auscultation should be systematic, and include all lobes and areas on the anterior, lateral and posterior chest (See Table 1.2). It is recommended that the examiner should start auscultating at the lung base, because certain abnormal lung sounds (e.g. fine end-inspiratory crackles) that primarily occur in the dependent lung areas may be altered by several deep breaths. At least one full ventilatory cycle should be evaluated at each stethoscope position. Television or radio should be turned off and the room should be calm and quiet. If alert, the patient should be asked to sit up; a comatose patient should be rolled onto side to auscultate posterior chest.

Four characteristics of breath sounds should be specifically looked for by the examiner; the pitch (vibration frequency), the amplitude or intensity (loudness), the distinctive characteristics (vesicular, bronchovesicular, bronchial) and finally the duration of inspiratory sound are compared with those of expiration sound. The acoustic characteristics of breath sounds can be illustrated in a breath sound diagram. The characteristics of normal breath sounds are described in Table 1. 4. The examiner must first be familiar with the characteristics of normal breath sounds before he can expect to identify the subtle changes that signify respiratory disease. Also, one should be familiar with the added (adventitious) sounds.

Measurements of the inspiratory breath sounds through the chest wall demonstrated regional difference between the apex and the base of the lung. Comparison of regional ventilation measured with ¹³³Xenon and the loudness of the breath sounds over the corresponding areas of the chest wall showed that the sounds are faint where ventilation is impaired.

Transmission of breath sounds: Sound transmits in air within large tubes like the trachea and main bronchi to reach the mouth almost un-attenuated.

The small bronchi offer greater resistance to the oscillations of air at acoustic frequencies, so that beyond segmental bronchi, the breath sounds travel mainly across the lung. The unattenuated breath sounds at the mouth contain a wide range of evenly distributed frequencies between 200 and 2000 Hz, while those recorded from the chest wall are at a relatively narrow range of low frequencies, with a steep fall in amplitude above 200 Hz, as chest wall acts like a low pass filter. When the examiner auscultates over the lung parenchyma of a healthy individual, soft and muffled sounds are heard. These sounds are referred to as vesicular or normal breath sounds, and is lower in pitch and intensity (loudness) than bronchial breath sounds. Vesicular sounds are most difficult to hear, and are heard primarily during inhalation with only a minimal exhalation component. The breath sounds transmitted through the chest fade out during expiration. This is due to the fact that during inspiration the turbulence generated is carried further towards periphery, while during expiration, flow rate falls and direction of flow is reversed.

Cavernous (low pitched) bronchial breathing can be normally heard over the occipital region of the skull. It has its peculiar hollow character. When it is heard over lung fields, it is suggestive of cavity of the lung, an open pneumothorax or when trachea shifted to one or other side by fibrosis or collapse of the lung (pulled trachea syndrome). The pulled trachea syndrome may thus lead to an erroneous diagnosis of cavitation of the lung apices. Tubular (high pitched) bronchial breathing, with its characteristic tubular quality is suggestive of consolidation of lung. Latter results from inflammation as in lobar pneumonia, engorgement of blood in pulmonary infarction or collapse of alveoli in atelectasis in presence of partial open bronchi. In certain cases of massive pleural effusion, breath sounds instead of being diminished or absent, paradoxically become high pitched bronchial breathing. It is due to the fact that collapsed lung under large pleural effusion transmits the sound from some large bronchus or bronchi to the fluid 40collected. Amphoric breathing is a special variety of high pitched bronchial breathing with a distinctive echo like or metallic quality that can be imitated artificially by blowing intensely across the mouth of a bottle. It is usually suggestive of large smooth walled cavity of the lung or bronchopleural fistula. This is due to the amplification of certain vibrations or high pitched overtones in the original bronchial sound. The d'Espine's sign is high pitched tubular bronchial breathing heard over the fourth or lower thoracic vertebrae. This is due to the transmission of tracheal breath sounds through a mass in the middle or posterior mediastinum between the trachea and the stethoscope. Similarly, tubular breath sounds can be transmitted from the trachea to anterior chest wall when there is a large mass in the anterior mediastinum.

Bronchial breath sounds, to be present on any part of lung, generally, need a partial or fully patent bronchus supplying it. Bronchial breathing may be heard over an airless upper lobe, irrespective of whether the lobar bronchus is patent or not; this is due to the fact that the mediastinal surface of the upper lobes is in direct contact with the trachea, and the sound from trachea is transmitted to solid lung directly. There is no such direct path of transmission to the lower lobes and thus sounds do not reach them unless the intervening bronchi are patent. Bronchial breathing is usually absent when the lower lobe is both consolidated and atelectatic as a result of bronchial obstruction.

Bronchophony: Voice sounds heard through the normal lung and chest wall are attenuated and filtered. The low 41frequencies upto 200 Hz are well transmitted while those above 200 Hz are attenuated. Due to this selective filtration, most of the vowel formants are lost and speech heard through the stethoscope over normal lung becomes a meaningless, low pitched rumble. When the lung between the trachea and point of auscultation is airless, the higher frequencies, including the formants of vowels are transmitted and speech becomes intelligible, known as bronchophony. The acoustic basis of bronchophony and bronchial sounds is identical, both being signs of unfiltered sound transmission through solid lung. Therefore bronchophony is an increase in intensity and clarity of vocal resonance resulting from enhanced transmission of vocal vibrations. It indicates an increase in lung tissue density, and can occur in the consolidation phase of pneumonia. This sign is easier to detect when unilateral and is often accompanied with bronchial breath sounds.

Whispering Pectoriloquy: During whispering, the vocal cords get abducted and do not oscillate and voice sounds are generated only by turbulent flow of air through the trachea, glottis and pharynx. This white noise is inaudible over the normal air-containing lung because it lacks the powerful low frequency component (fundamental note) which is selectively transmitted through the normal chest. On the other hand the high frequency component of this white noise of the turbulence and the formants of the vowels are transmitted through airless lung, with the result the whispered speech becomes intelligible. This sign known as whispering pectoriloquy occurs in the same conditions in which bronchial breathing and bronchophony are present; and thus completes the triad of auscultatory signs of consolidation. The patient is instructed to whisper ek do teen or one two three, while the examiner listens over the chest with a stethoscope, comparing both the sides. Through normal lung, muffled and low pitched sounds are heard. The high pitched sounds heard over the consolidated lung are clear and comprehensible.

Egophony: Like breath sounds, the voice sounds are reflected by fluid or air in the pleural cavity, so that in pleural effusion and pneumothorax, speech is inaudible over the chest wall. When the consolidated lung is separated from the chest wall only by a thin layer of fluid, the attenuation at the interfaces between fluid and the two layers of the pleura is selective. Low frequency sounds below 1000 Hz are lost, so that only the high frequency formants of the vowels survive. Thus speech remains intelligible, but the removal of the lower frequencies of vowel explains the nasal bleating quality of egophony. It is identified most easily when the patient says ‘e-e-e’. If egophony is present, the ‘e-e-e’ will be heard over the chest wall with the stethoscope as ‘a-a-a’. Egophony is usually detected only over an area of upper area of pleural effusion (where fluid layer is thin) and underlying consolidation.

Vocal resonance: If inspection, palpation, percussion and auscultation of the patients' chest suggest any respiratory abnormality, vocal resonance is assessed. It is produced by the same mechanism as that of vocal fremitus described earlier. The vibrations created by the vocal cords during phonation travel down the tracheobronchial tree and 42through the peripheral lung units to the chest wall. The patient is instructed to repeat the words ‘ek do teen’ or ‘one two three’ while the examiner listens over the chest wall with a stethoscope, comparing the sides. The normal, air filled lung tissue filters the voice sounds significantly, reducing intensity as well as clarity. Pathological abnormalities in lung tissue alter the transmission of voice sounds, resulting in either increased or decreased vocal resonance. Vocal resonance is reduced in same lung abnormalities as those resulting in reduced breath sounds and decreased vocal fremitus. Hyperinflation of lung parenchyma, pneumothorax, bronchial obstruction, and pleural effusion all reduce the vocal resonance through the lung or chest wall. An increase in intensity and clarity of vocal resonance resulting from enhanced transmission of vocal vibrations is referred to as bronchophony, and often present in the consolidation phase of pneumonia.

The mechanism for producing wheezes in the intrathoracic airways appears to involve the airway walls interacting with the air moving through them. As the airway is narrowed, the air flow velocity through it increases to cause fall in lateral pressure due to the venturi effect, which results in further narrowing or closing of airway. As soon as the airway is closed, the venturi effect ceases and the lumen of the airway reopens, and thus setting the cycle into operation again. This sequence of self perpetuating pressure changes results in rapid oscillations of the airway wall, to generate a musical sound (wheezing).

A fall in lateral pressure during inspiration can produce stridor in stenosis of cervical portion of trachea where the outside pressure is atmospheric.

In the presence of hyperinflated lungs, high pitched wheezes may be heard more easily over the trachea than lung. Tracheal auscultation has therefore been advocated as part of the routine clinical assessment in asthma.

Patients with chronic airflow obstruction who do not wheeze, are not likely to show significant improvement in expiratory flow rates, whereas those who wheeze are more likely to show a significant improvement after bronchodilators.

A single musical note of constant pitch is a characteristic sign of incomplete occlusion of a main or lobar bronchus is termed as fixed monophonic wheeze. In widespread airflow obstruction especially in bronchial asthma monophonic wheezes arise from airways narrowed to the point of closure by swelling of the mucosa. When there is more than one wheeze, they occur at random, vary in duration and often overlap in time, are called as random monophonic wheezes. A characteristic feature of polyphonic wheezing is that all its component notes begin at the same time and continue together to the end of expiration. Polyphonic wheezing at rest is a reliable sign of widespread airflow obstruction.

One, crackles may be due to the sudden opening of a succession of small airways, with rapid equalisation of pressure between the collapsed airways below and patent ones above, thus causing a sequence of implosive sound waves; the other mechanism could be the bubbling of air through secretions. The first of these is the likely mechanism for crackles heard in patients with interstitial lung disease and congestive heart failure.

Crackles are categorised into fine and coarse based on waveform analysis of tracings of time expanded crackles (Fig. 1.19). The fine crackles have been defined as those having an initial deflection width (IDW) of less than 0.9 ms and a two cycle duration (2CD) shorter than 6.0 ms. And those with IDW more than 0.9 ms and 2 CD longer than 6.0 ms are termed as coarse.

Pleural rub: The striking feature in pleuritis is the pleural rub or pleural crackles. The smooth well lubricated layers of the normal pleura move silently over one another. When the surface is roughened by fibrin deposits or infiltrated by inflammatory or malignant cells, the sliding motion is momentarily interrupted due to frictional resistance. The lung then acts on the chest wall like the bow of a string instrument. If a large area of the chest wall is set into resonant oscillation, the resulting sound is musical. More commonly, the jerky sliding movement of the lung produces a series of non-musical sounds which are usually longer lasting and of a lower pitch than crackles arising from the lung; and these non-musical sounds are termed as pleural rub. Sound of pleural rub heard during inspiration often recurs in reversed sequence during expiration giving a mirror image effect. Pleural friction rub often sounds similar to coarse crackles but is not affected by coughing. The intensity of pleural rub may increase with deep breathing and on pressing the chest wall with the chest piece of the stethoscope, while there is no effect on intensity of coarse crackles.

Chronic bronchitis: Crackles during expiration and at the beginning of inspiration are common in widespread airflow obstruction (Table 1.6). These sounds are low pitched, scanty, and loud and widely conducted through the lower lobes, transmitted through the large airways, and are often audible as a series of clicks through the stethoscope held near the patient's mouth. Crackles of chronic bronchitis are even-spaced and correspond to the passage of a bolus of gas through lightly closed central airways, which open intermittently when the upstream gas pressure rises above a critical level. The cause of intermittent obstruction is uncertain and could be due to the sputum lying in the large bronchi.

Emphysema: Patients of emphysema were studied both for production as well as transmission of sounds and compared with normal subjects. It was concluded that transmission of sounds varies from breath to breath. The study revealed areas of normal, decreased and increased sound transmission comprising areas of relatively normal lung parenchyma, areas of hyperinflation with airway obstruction and less ventilation, and areas of focal atelectasis or consolidation respectively. Sound heard through stethoscope at mouth has been reported to be decreased in emphysema whereas it is increased in bronchitis and asthma.

Bronchial asthma: The most prominent feature on auscultation of bronchial asthma patient is a high-pitched continuous sound. In mild cases, wheezing may be heard over the central airways only during expiration and becomes evident over the entire chest during both phases of respiration as asthma becomes more severe. The absence of wheezing in acute severe asthma is regarded as an ominous sign, because wheezes are not generated due to resulted low flow. Wheezing may occur in apparently normal persons during maneuver of forced expiration. With improvement in flow rate after bronchodilators or spontaneously, the frequency of wheezing also decreases.

Bronchiectasis: The dominant auscultatory feature of bronchiectasis is crackles. The crackles in patients of bronchiectasis can be distinguished from those of chronic bronchitis and interstitial fibrosis (Table 1.6). In bronchiectasis, inspiratory crackles start early in inspiration, continue to mid inspiration and fade by the end of it. Expiratory crackles are also present. Therefore the crackles of bronchiectasis are present in both phases of the respiratory cycle and may be made less abundant after coughing.

Interstitial fibrosis: The most striking feature in patients with interstitial fibrosis is the presence of fine crackles. These have been described as close to the ear cellophane or velcro crackles. In mild forms of the disease, these are usually confined to end-inspiration and are gravity dependent. These are best heard at the lung bases when the patient is upright, and their distribution can vary with the change in position (Table 1.6). They may disappear or reduce from lung bases as the patient bends forward. In advanced stages of illness, these crackles persist despite positional changes and are heard at higher levels above the base of lungs.

1. Fine crackles in interstitial fibrosis may become pan-inspiratory, often with an end-inspiratory accentuation as the disease progresses. Expiratory crackles can also be heard in this disease and their mechanism is explained as follows: the airways initially patent at the end of inspiration, close early in expiration, and then reopen with the building of pressure due to the air trapped within them; when pressure exceeds that of the adjacent airways during expiratory phase, it results in crackles.
2. In pulmonary fibrosis caused by asbestos exposure, crackles are end-inspiratory, present first at the inferior axillary area in the midaxillary lines, and tend to spread posteriorly at the bases of lungs. Some believe it to be an early sign of asbestosis.

Pneumothorax: The breath sounds are absent when there is a pneumothorax of either side. If left sided, a loud crackling sound may be heard; it is generated either by a sudden displacement of the small collection of air trapped in the mediastinal pleural space or by direct impact of the heart on the mediastinal surface of the lung. Shallow pneumothorax is associated with clicking, as the heart and lungs are separated only by a narrow air space. The clicking disappears when the lung reexpands or when the pneumothorax deepens.