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Evaluation of the Pulmonary Patient
Key components in the evaluation of patients with pulmonary symptoms are the history, physical examination, and, in most cases, a chest x-ray. These components establish the need for subsequent testing, which may include pulmonary function testing and ABG analysis (see Overview of Tests of Pulmonary Function), CT or other imaging tests (see Chest Imaging), and bronchoscopy (see Bronchoscopy).
The history can often establish whether symptoms of dyspnea, chest pain, wheezing, stridor, hemoptysis, and cough are likely to be pulmonary in origin. When more than one symptom occurs concurrently, the history should focus on which symptom is primary and whether constitutional symptoms, such as fever, weight loss, and night sweats, are also present. Other important information includes
Physical examination starts with assessment of general appearance. Discomfort and anxiety, body habitus, and the effect of talking or movement on symptoms (eg, inability to speak full sentences without pausing to breathe) all can be assessed while greeting the patient and taking a history and may provide useful information relevant to pulmonary status. Next, inspection, auscultation, and chest percussion and palpation are done.
Inspection should focus on
Signs of respiratory difficulty and hypoxemia (eg, restlessness, tachypnea, cyanosis, accessory muscle use)
Signs of possible chronic pulmonary disease (eg, clubbing, pedal edema)
Chest wall deformities
Abnormal breathing patterns (eg, Cheyne-Stokes respiration, Kussmal respirations)
Jugular venous distention
Signs of hypoxemia include cyanosis (bluish discoloration of the lips, face, or nail beds), which signifies low arterial O2 saturation (< 85%); the absence of cyanosis does not exclude the presence of hypoxemia.
Signs of respiratory difficulty include tachypnea and use of accessory respiratory muscles (sternocleidomastoids, intercostals, scalenes) to breathe. Patients with COPD sometimes brace their arms against their legs or the examination table while seated (ie, tripod position) in a subconscious effort to provide more leverage to accessory muscles and thereby enhance respiration. Intercostal retractions (inward movement of the rib interspaces) are common among infants and older patients with severe airflow limitation; paradoxical breathing (inward motion of the abdomen during inspiration) signifies respiratory muscle fatigue or weakness.
Signs of possible chronic pulmonary disease include clubbing, barrel chest (the increased anterior-posterior diameter of the chest present in some patients with emphysema), and pursed lip breathing. Clubbing is enlargement of the fingertips (or toes) due to proliferation of connective tissue between the fingernail and the bone. Diagnosis is based on an increase in the profile angle of the nail as it exits the finger (to > 176°) or on an increase in the phalangeal depth ratio (to > 1—see Figure: Measuring finger clubbing.). “Sponginess” of the nail bed beneath the cuticle also suggests clubbing. Clubbing is most commonly observed in patients with lung cancer but is an important sign of chronic pulmonary disease, such as cystic fibrosis and idiopathic pulmonary fibrosis; it also occurs (but less commonly) in cyanotic heart disease, chronic infection (eg, infective endocarditis), stroke, inflammatory bowel disease, and cirrhosis. Clubbing occasionally occurs with osteoarthropathy and periostitis (primary or hereditary hypertrophic osteoarthropathy); in this instance, clubbing may be accompanied by skin changes, such as hypertrophied skin on the dorsa of the hands (pachydermoperiostosis), seborrhea, and coarse facial features. Digital clubbing can also occur as a benign hereditary abnormality that can be distinguished from pathologic clubbing by the absence of pulmonary symptoms or disease and by the presence of clubbing from an early age (by patient report).
Measuring finger clubbing.
Chest wall deformities , such as pectus excavatum (a sternal depression usually beginning over the midportion of the manubrium and progressing inward through the xiphoid process) and kyphoscoliosis, may restrict respirations and exacerbate symptoms of preexisting pulmonary disease. These abnormalities can usually be observed during careful examination after the patient's shirt is removed.
Abnormal breathing patterns cause fluctuations in respiratory rate so respiratory rate should be assessed and counted for 1 min.
Cheyne-Stokes respiration (periodic breathing) is a cyclic fluctuation of respiratory rate and depth. From periods of brief apnea, patients breathe progressively faster and deeper (hyperpnea), then slower and shallower until they become apneic and repeat the cycle. Cheyne-Stokes respiration is most often caused by heart failure, a neurologic disorder (eg, stroke, advanced dementia), or drugs. The pattern in heart failure has been attributed to delays in cerebral circulation; respiratory centers lag in recognition of systemic acidosis/hypoxia (causing hyperpnea) or alkalosis/hypocapnia (causing apnea).
Biot respiration is an uncommon variant of Cheyne-Stokes respiration in which irregular periods of apnea alternate with periods in which 4 or 5 deep, equal breaths are taken. It differs from Cheyne-Stokes respiration in that it is characterized by abrupt starts and stops and lacks periodicity. It results from injury to the CNS and occurs in such disorders as meningitis.
Kussmaul respirations are deep, regular respirations caused by metabolic acidosis.
Jugular venous distention, sometimes observed during inspection, indicates an increase in right atrial and right ventricular pressure. The elevated pressure is usually caused by left ventricular dysfunction, but it may also be due to a pulmonary disorder causing pulmonary hypertension (see Cardiovascular Examination : Neck veins). The presence of jugular venous distension should prompt a search for other signs of cardiac disorder (eg, 3rd heart sound [S3] gallop, dependent edema).
Auscultation is arguably the most important component of the physical examination. All fields of the chest should be listened to, including the flanks and the anterior chest, to detect abnormalities associated with each lobe of the lung. Features to listen for include
Cardiac auscultation (see Pulmonary Hypertension), conducted simultaneously with pulmonary auscultation, may reveal signs of pulmonary hypertension, such as a loud pulmonic 2nd heart sound (P2), and of right heart failure, such as a right ventricular 4th heart sound (S4) and tricuspid regurgitation.
The character and volume of breath sounds are useful in identifying pulmonary disorders. Vesicular breath sounds are the normal sounds heard over most lung fields. Bronchial breath sounds are slightly louder, harsher, and higher pitched; they normally can be heard over the trachea and over areas of lung consolidation, such as occur with pneumonia
Adventitious sounds are abnormal sounds, such as crackles, rhonchi, wheezes, and stridor.
Crackles (previously called rales) are discontinuous adventitious breath sounds. Fine crackles are short high-pitched sounds; coarse crackles are longer-lasting low-pitched sounds. Crackles have been compared to the sound of crinkling plastic wrap and can be simulated by rubbing strands of hair together between 2 fingers near one’s ear. They occur most commonly with atelectasis, alveolar filling processes (eg, pulmonary edema), and interstitial lung disease (eg, pulmonary fibrosis); they signify opening of collapsed alveoli.
Rhonchi are low-pitched respiratory sounds that can be heard during inspiration or expiration. They occur in various conditions, including chronic bronchitis. The mechanism may relate to variations in obstruction as airways distend with inhalation and narrow with exhalation.
Wheezes are whistling, musical breath sounds that are worse during expiration than inspiration. Wheezing can be a physical finding or a symptom and is usually associated with dyspnea.
Stridor is a high-pitched, predominantly inspiratory sound formed by extrathoracic upper airway obstruction. It usually can be heard without a stethoscope. Stridor is usually louder than wheezing, is predominantly inspiratory, and is heard loudly over the larynx. It should trigger a concern for life-threatening upper airway obstruction.
Decreased breath sounds signify poor air movement in airways, as occurs with asthma and COPD where bronchospasm or other mechanisms limit airflow. Breath sounds may also be decreased in the presence of a pleural effusion, pneumothorax, or obstructing endobronchial lesion.
Vocal sounds involve auscultation while patients vocalize.
Bronchophony and whispered pectoriloquy occur when the patient’s spoken or whispered voice is clearly transmitted through the chest wall. Voice transmission results from alveolar consolidation, as occurs with pneumonia.
Egophony (E to A change) is said to occur when, during auscultation, a patient says the letter “E” and the examiner hears the letter “A,” again as occurs with pneumonia.
Friction rubs are grating or creaking sounds that fluctuate with the respiratory cycle and sound like skin rubbing against wet leather. They are a sign of pleural inflammation and are heard in patients with pleuritis or empyema and after thoracotomy.
I:E ratio is normally 1:2 but is prolonged to ≥ 1:3 when airflow is limited, such as in asthma and COPD, even in the absence of wheezing.
Percussion is the primary physical maneuver used to detect the presence and level of pleural effusion. Finding areas of dullness during percussion signifies underlying fluid or, less commonly, consolidation.
Palpation includes tactile fremitus (vibration of the chest wall felt while a patient is speaking); it is decreased in pleural effusion and pneumothorax and increased in pulmonary consolidation (eg, lobar pneumonias). Point tenderness on palpation may signal underlying rib fracture or pleural inflammation.
In cor pulmonale (see Cor Pulmonale), a right ventricular impulse at the left lower sternal border may become evident and may be increased in amplitude and duration (right ventricular heave).
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