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Harrison’s Manual of Medicine




An abnormally uncomfortable awareness of breathing; intensity can be quantified by establishing the amount of physical exertion necessary to produce the sensation, but the pt’s general physical condition should be considered.
HEART DISEASE   Dyspnea is due to
pulmonary capillary pressure, left atrial hypertension, and sometimes fatigue of respiratory muscles. Vital capacity and lung compliance are ¯ and airway resistance
. Begins as exertional breathlessness ® orthopnea ® paroxysmal nocturnal dyspnea and dyspnea at rest. Diagnosis depends on recognition of heart disease, e.g., Hx of MI, presence of S3, S4, murmurs, cardiomegaly, jugular vein distention, hepatomegaly, and peripheral edema (Chap. 116). Objective quantification of ventricular function (echocardiography, radionuclide ventriculography) is often helpful.
OBSTRUCTIVE DISEASE OF THE AIRWAYS   May occur with obstruction anywhere from extrathoracic airways to lung periphery. Acute dyspnea with difficulty inhaling suggests upper airway obstruction. Physical exam may reveal inspiratory stridor and retraction of supraclavicular fossae. Acute intermittent dyspnea with expiratory wheezing suggests reversible intrathoracic obstruction due to asthma. Chronic, slowly progressive exertional dyspnea characterizes emphysema and CHF. Chronic cough with expectoration is typical of chronic bronchitis and bronchiectasis.
DIFFUSE PARENCHYMAL LUNG DISEASES   Many parenchymal lung diseases, ranging from sarcoidosis to the pneumoconioses, may cause dyspnea. Dyspnea is usually related to exertion early in the course of the illness. Physical exam typically reveals tachypnea and late inspiratory rales.
PULMONARY EMBOLISM (See Chap. 132)   Dyspnea is the most common symptom of pulmonary embolus. Repeated discrete episodes of dyspnea may occur with recurrent pulmonary emboli, but others describe slowly progressive dyspnea without abrupt worsening; tachypnea is frequent. Finding of deep venous thrombosis usually absent in chronic pulmonary embolism
DISEASE OF THE CHEST WALL OR RESPIRATORY MUSCLES   Severe kyphoscoliosis may produce chronic dyspnea, often with chronic cor pulmonale. The spinal deformity must be severe before respiratory function is compromised. Pts with bilateral diaphragmatic paralysis appear normal while standing, but complain of severe orthopnea and display paradoxical abnormal respiratory movement when supine.

Approach to the Patient

Elicit a description of the amount of physical exertion necessary to produce the sensation and whether it varies under different conditions.

If acute upper airway obstruction is suspected, lateral neck films or a fiberoptic exam of upper airway may be helpful. Pt should be accompanied by a physician adept in all aspects of airway management during the evaluation. With chronic upper airway obstruction the respiratory flow-volume curve may show inspiratory cutoff of flow, suggesting variable extrathoracic obstruction.

Dyspnea due to emphysema is reflected in a reduction in expiratory flow rates (FEV1), and often by a reduction in the diffusing capacity for carbon monoxide (DLCO).

Pts with intermittent dyspnea due to asthma may have normal pulmonary function if tested when asymptomatic. In severe acute asthma the intensity of dyspnea may fail to reflect the degree of compromise evident on pulmonary function testing.

Cardiac dyspnea usually begins as breathlessness on strenuous exertion with gradual (months-to-years) progression to dyspnea at rest.

Pts with dyspnea due to both cardiac and pulmonary diseases may report orthopnea. Paroxysmal nocturnal dyspnea occurring after awakening from sleep is characteristic of CHF.

Dyspnea of chronic obstructive lung disease tends to develop more gradually than that of heart disease.

PFTs should be performed when etiology is not clear. When the diagnosis remains obscure a pulmonary stress test is often useful.

Management depends on elucidating etiology.

Differentiation between cardiac and pulmonary dyspnea is summarized in Table 14-1.

Table 14-1 Differentiation between Cardiac and Pulmonary Dyspnea


For a more detailed discussion, see Ingram RH Jr., Braunwald E: Dyspnea and Pulmonary Edema, Chap. 32, p. 199, HPIM-15.


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