TABLE 5.

EXAMPLES OF CONDITIONS AND CAUSES OF DYSPNEA GROUPED BY PHYSIOLOGICAL MECHANISM^*

Increased respiratory drive—increased afferent input to respiratory centers

Stimulation of pulmonary receptors (irritant, mechanical, vascular)†

Interstitial lung disease

Pleural effusion (compressive atelectasis)

Pulmonary vascular disease (e.g., thromboembolism, idiopathic pulmonary hypertension)

Congestive heart failure

Simulation of chemoreceptors

Conditions leading to acute hypoxemia, hypercapnia, and/or acidemia

Impaired gas exchange, e.g., asthma, pulmonary embolism, pneumonia, heart failure‡

Environmental hypoxia, e.g., altitude, contained space with fire

Conditions leading to increased dead space and/or acute hypercapnia

Impaired gas exchange, e.g., acute, severe asthma, exacerbations of COPD, severe pulmonary edema

Impaired ventilatory pump (see below), e.g., muscle weakness, airflow obstruction

Metabolic acidosis

Renal disease (renal failure, renal tubular acidosis)

Decreased oxygen carrying capacity, e.g., anemia

Decreased release of oxygen to tissues, e.g., hemoglobinopathy

Decreased cardiac output

Pregnancy

Behavioral factors

Hyperventilation syndrome, anxiety disorders, panic attacks

Impaired ventilatory mechanics—reduced afferent feedback for a given efferent output (corollary discharge of motor command)

Airflow obstruction (includes increased resistive load from narrowing of airways and increased elastic load from hyperinflation)

Asthma, COPD, laryngospasm, aspiration of foreign body, bronchitis

Muscle weakness

Myasthenia gravis, Guillain-Barre, spinal cord injury, myopathy, post-poliomyelitis syndrome

Decreased compliance of the chest wall

Severe kyphoscoliosis, obesity, pleural effusion

This adapted table was published in Saunders, Mason RJ, Broaddus VC, Martin TR, King TE, Schraufnagel DE, Murray JF, Nadel JA, Murray and Nadel's Textbook of Respiratory Medicine, Copyright Elsevier 2012. This permission is granted for non-exclusive world rights in all languages. Reproduction of this material is granted for the purpose for which permission is hereby given.

^*In most cardiopulmonary disease states, a combination of increased respiratory drive and impaired mechanics will be present.

^†These conditions probably produce dyspnea by a combination of increased ventilatory drive and primary sensory input from the receptors.

^‡Heart failure includes both systolic and diastolic dysfunction. Systolic dysfunction may produce dyspnea at rest and with activity. Diastolic dysfunction typically leads to symptoms primarily with exercise. In addition to the mechanisms noted above, systolic heart failure may also produce dyspnea via metaboreceptors; these are receptors that are postulated to lie in muscles and that are stimulated by changes in the metabolic milieu of the tissue that result when oxygen delivery does not meet oxygen demand.