Examination of the patient with suspected pulmonary disease includes inspection, palpation, percussion, and auscultation of the chest.

Inspection

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 approximately 2:3. Tachypnea is an increased rate of breathing and is commonly associated with a decrease in tidal volume. Respiratory 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 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 respiration, a rhythmic waxing and waning of both rate and tidal volumes that includes regular periods of apnea as seen in end-stage LV failure, neurologic disease, and 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 increased work of breathing and is a sign of pulmonary impairment. As the diaphragm contracts, it pushes the abdominal contents down. Hence, the chest and abdominal wall normally expand simultaneously. 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.

Palpation

The examiner may palpate the trachea at the suprasternal notch, to detect shifts in the mediastinum; the posterior chest wall, to gauge fremitus and the transmission through the lungs of vibrations of spoken words; and the anterior chest wall to assess the cardiac impulse.

Percussion

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 but high specificity, therefore it is not necessary in every patient. However, perfusion may serve as a confirmatory test in patients with high pretest probability, such as in suspected tension pneumothorax; the combination of tracheal shift and hyperresonance can be lifesaving, permitting immediate decompression.

Auscultation

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 described as vesicular (AUDIO 9-1). 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 sounds (AUDIO 9-2). 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.

AUDIO 09-01: Normal vesicular breath sounds.

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Heart and Lung Sounds

AUDIO 09-02: Normal bronchial breath sounds.

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Heart and Lung Sounds

Abnormal lung sounds (“adventitious” breath sounds) may be continuous (more than 80 ms in duration) or discontinuous (less than 20 ms). Continuous lung sounds are divided into wheezes (AUDIO 9-3), which are high-pitched, musical, and have a distinct whistling quality; and rhonchi (AUDIO 9-4), which are lower-pitched, sonorous, and may have a gurgling quality. Wheezes occur with small airway narrowing, in the setting of bronchospasm, mucosal edema, or excessive secretions. Rhonchi originate in the larger airways when excessive secretions and abnormal airway collapsibility cause repetitive rupture of fluid films. Rhonchi may clear after a cough.

AUDIO 09-03: Wheezes.

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Heart and Lung Sounds

AUDIO 09-04: Rhonchi (coarse crackles).

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Heart and Lung Sounds

Discontinuous lung sounds are called crackles—brief, discrete, nonmusical sounds with a popping quality. Fine crackles (AUDIO 9-5) are soft, high-pitched, and crisp (less than 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 (less than 20 ms) and probably result from gas bubbling through fluid; they are heard in pneumonia, obstructive lung disease, and late pulmonary edema.

AUDIO 09-05: Fine crackles.

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Heart and Lung Sounds

Extrapulmonary Signs of Pulmonary Disease

Extrapulmonary signs of intrinsic pulmonary disease include digital clubbing, cyanosis, elevation of CVPs, jugular venous distention, and lower extremity edema.

Digital clubbing (Figure 6-39) 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. Symmetric clubbing may be a normal variant but commonly is a sign of underlying disease, such as chronic infections of the lungs and pleura (lung abscess, empyema, bronchiectasis, cystic fibrosis), malignancies of the lungs and pleura, interstitial lung disease (idiopathic pulmonary fibrosis [IPF]), and arteriovenous malformations. It does not normally accompany asthma or COPD; when seen in the latter, concomitant lung cancer should be suspected. Clubbing is not specific to pulmonary disorders; it is also seen in cyanotic congenital heart disease, infective endocarditis, cirrhosis, and IBD. 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 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 (more than 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 of hemoglobin saturation.

Estimation of CVP, jugular venous distention, and assessment of lower extremity edema are indirect measures of a patient's volume status, which may be associated with impaired LV function, pulmonary hypertension, pericardial effusion or restriction, or valvular heart disease.