Saturday, April 11, 2009

Examination of the patient with suspected pulmonary disease includes inspection, palpation, percussion, and auscultation of the chest. An efficient approach begins with observing the pattern of breathing, auscultation of the chest, and inspection for extrapulmonary signs of pulmonary disease. More detailed examination follows from initial findings.
The pattern of breathing refers to the respiratory rate and rhythm, the depth of breathing or tidal volume, and the relative amount of time spent in inspiration and expiration. Normal values are a rate of 12–14 breaths per minute, tidal volumes of 5 mL/kg, and a ratio of inspiratory to expiratory time of 2:3. Tachypnea is an increased rate of breathing and is commonly associated with a decrease in tidal volume. The rhythm is normally regular, with a sigh (1.5–2 times normal tidal volume) every 90 breaths or so to prevent collapse of alveoli and atelectasis. Alterations in the rhythm of breathing include rapid, shallow breathing, seen in restrictive lung disease and as a precursor to respiratory failure; Kussmaul breathing, rapid large-volume breathing indicating intense stimulation of the respiratory center, seen in metabolic acidosis; and Cheyne-Stokes respirations, a rhythmic waxing and waning of both rate and tidal volumes that includes regular periods of apnea. This pattern is seen in patients with end-stage left ventricular failure or neurologic disease and in many normal subjects at high altitude, especially during sleep.
During normal quiet breathing, the primary muscle of respiration is the diaphragm. Movement of the chest wall is minimal. The use of accessory muscles of respiration, the intercostal and sternocleidomastoid muscles, indicates high work of breathing. At rest, the use of accessory muscles is a sign of significant pulmonary impairment. As the diaphragm contracts, it pushes the abdominal contents down. Hence, the chest and abdominal wall normally expand simultaneously. Expansion of the chest but collapse of the abdomen on inspiration indicates weakness of the diaphragm. The chest normally expands symmetrically. Asymmetric expansion suggests unilateral volume loss, as in atelectasis or pleural effusion, unilateral airway obstruction, asymmetric pulmonary or pleural fibrosis, or splinting from chest pain.
The examiner may palpate as follows: the trachea at the suprasternal notch, to detect shifts in the mediastinum; on the posterior chest wall, to gauge fremitus and the transmission through the lungs of vibrations of spoken words; and on the anterior chest wall to assess the cardiac impulse. All these maneuvers are characterized by low interobserver agreement.
Chest percussion identifies dull areas that correspond to lung consolidation or pleural effusion or hyperresonant areas suggesting emphysema or pneumothorax. Percussion has a low sensitivity (10–20% in several studies) compared with chest radiographs to detect abnormalities. Specificity is high (85–99%). Since an insensitive test is a poor screening examination, percussion and palpation are not necessary in every patient. These techniques do serve as important confirmatory tests in specific patients when the prior probability of a finding is increased. For example, in a patient with a suspected tension pneumothorax, the finding of tracheal shift and hyperresonance can be lifesaving, permitting immediate decompression of the affected side.
Auscultation of the chest depends on a reliable and consistent classification of auditory findings. Normal lung sounds heard over the periphery of the lung are called vesicular. They have a gentle, rustling quality heard throughout inspiration that fades during expiration. Normal sounds heard over the suprasternal notch are called tracheal or bronchial lung sounds. They are louder, higher-pitched, and have a hollow quality that tends to be louder on expiration. Bronchial lung sounds heard over the periphery of the lung are abnormal and imply consolidation. Globally diminished lung sounds are an important finding predictive of significant airflow obstruction.
Abnormal lung sounds (“adventitious” breath sounds) may be continuous (> 80 ms in duration) or discontinuous (< 20 ms). Continuous lung sounds are divided into wheezes, which are high-pitched, musical, and have a distinct whistling quality; and rhonchi, which are lower-pitched, sonorous, and may have a gurgling quality. Wheezes occur in the setting of bronchospasm, mucosal edema, or excessive secretions. In each, the airway is narrowed to the point where adjacent airway walls flutter as airflow is limited. Rhonchi originate in the larger airways when excessive secretions and abnormal airway collapsibility cause repetitive rupture of fluid films. Rhonchi frequently clear after cough.
Discontinuous lung sounds are called crackles— brief, discrete, nonmusical sounds with a popping quality. Fine crackles are soft, high-pitched, and crisp (< 10 ms in duration). They are formed by the explosive opening of small airways previously held closed by surface forces and are heard in interstitial diseases or early pulmonary edema. Coarse crackles are louder, lower-pitched, and slightly longer in duration (< 20 ms) and probably result from gas bubbling through fluid. Coarse crackles are heard in pneumonia, obstructive lung disease, and late pulmonary edema.
Interobserver agreement regarding auscultatory findings is good. The clinical usefulness of these findings is also well established. The presence of wheezes on physical examination is a powerful predictor of obstructive lung disease. The absence of wheezes is not helpful since patients may have significant airflow limitation without wheezing. Such patients will have globally diminished lung sounds as the clinical clue to their obstructive lung disease. Normal lung sounds exclude significant airway obstruction. The timing and character of crackles can reliably distinguish different pulmonary disorders. Fine, late inspiratory crackles suggest pulmonary fibrosis, while early coarse crackles suggest pneumonia or heart failure.
Extrapulmonary signs of intrinsic pulmonary disease include digital clubbing, cyanosis, elevation of central venous pressures, and lower extremity edema.
Digital clubbing refers to structural changes at the base of the nails that include softening of the nail bed and loss of the normal 150-degree angle between the nail and the cuticle. The distal phalanx is convex and enlarged: its thickness is equal to or greater than the thickness of the distal interphalangeal joint. Symmetric clubbing may be a normal variant but more commonly is a sign of underlying disease. Clubbing is seen in patients with chronic infections of the lungs and pleura (lung abscess, empyema, bronchiectasis, cystic fibrosis), malignancies of the lungs and pleura, chronic interstitial lung disease (idiopathic pulmonary fibrosis), and arteriovenous malformations. It does not normally accompany asthma or COPD; when seen in the latter, one should suspect concomitant lung cancer. It is observed less often in small-cell cancer than in other histologic types. Clubbing is not specific to pulmonary disorders; it is also seen in cyanotic congenital heart disease, infective endocarditis, cirrhosis, and inflammatory bowel disease. Hypertrophic pulmonary osteoarthropathy is a syndrome of digital clubbing, chronic proliferative periostitis of the long bones, and synovitis. It is seen in the same conditions as digital clubbing but is particularly common in bronchogenic carcinoma. The cause of clubbing and hypertrophic osteoarthropathy is not known with certainty, but the disorder may reflect platelet clumping and local release of platelet-derived growth factor at the nail bed. Both clubbing and osteoarthropathy may resolve with appropriate treatment of the underlying disease.
Cyanosis is a blue or bluish-gray discoloration of the skin and mucous membranes caused by increased amounts (> 5 g/dL) of unsaturated hemoglobin in capillary blood. Since the oxygen saturation at which cyanosis becomes clinically apparent is a function of hemoglobin concentration, anemia may prevent cyanosis from appearing while polycythemia may lead to cyanosis in the setting of mild hypoxemia. Cyanosis is therefore not a reliable indicator of hypoxemia but should prompt direct measurement of arterial PO2 or oxyhemoglobin saturation.
Estimation of central venous pressure (CVP) and assessment of lower extremity edema are indirect measures of pulmonary hypertension, the major cardiovascular complication of chronic lung disease. Estimation of CVP can be done with precision. Elevated CVP is a pathologic finding associated with impaired ventricular function, pericardial effusion or restriction, valvular heart disease, and chronic obstructive or restrictive lung disease. Peripheral edema is a nonspecific finding that, in the setting of chronic lung disease, suggests right ventricular failure.


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