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Separating

Thomas A. DYSPNEA
awareness

Cardiac From Pulmonary Dyspnea


are easily documented. The situation with respect to the restrictive lung diseases is more complex. The stiff lungs of cardiac disease usually result from increased extravascular water in the lung (pulmonary edema).3 This, in turn, arises from increases in pulmonary capillary pres sure as a result of abnormal hemodynamics. The stiff lungs in primary lung disease usually result from the pres ence of abnormal substances in the interstitial or intra-alveolar spaces of the lung (fibrosis, cellular infiltration, or increased extracellular H20). Despite the difference in proximal mechanisms, the remainder of the pathogenetic sequence is identical both in cardiac and in this form of pulmo nary dyspnea. Local stretch receptors and interstitial receptors (J receptors) seem to be involved in sensing the abnormal mechanics. The dyspnea appears to be at least partially mediated by vagal afferent nerve fibers. Rapid shallow breathing, roentgenographic evidence of similar chest abnormalities, and similar positional effects on dyspnea and identical pul monary functional abnormalities are found with both. Given these similarities, how can the physician distinguish between the two

Raffin, MD, James Theodore, MD

is an uncomfortable of the act of breathing, leading to a sensation most conveniently described as breathlessness. It may arise as a result of numerous mechanisms.1,2 However, in both cardiac and pulmonary disease, the most common cause is disordered lung

airways obstruction

dyspnea. Hyperinflated lungs, prolonged expiration, a small heart, and the bedside and laboratory evidence of

mechanics. The two major forms of disordered lung mechanics that result in pulmonary dyspnea are obstructive lung diseases, causing increased airway resistance, and restrictive lung diseases, causing increased lung stiffness. In patients with cardiac dyspnea, the major cause of dyspnea also is increased lung stiffness, leading to a type of restrictive lung disease. As a result, patients with dyspnea purely related to obstructive lung disease seldom pose a problem in the separation of cardiac and pulmonary

of restrictive lung disease? Aside from the obvious, namely that restrictive disease in the presence of heart disease usually means cardiac dyspnea and without heart disease means pulmonary disease, the most reliable approach is a therapeutic trial with diuretics. In cardiac dyspnea, the loss of excess lung water will often lead to a rapid resolution of the physiologic, roentgenographic, and clinical abnor malities. In pulmonary dyspnea, this
causes

This article is one of a series sponsored by the American Heart Association, edited by Richard L. Popp, MD. From the Stanford University School of Medicine and Medical Center, Stanford, Calif. Reprint requests to Stanford University School of Medicine and Medical Center, Stanford, CA 94305 (Dr Raffin).

There are a number of circumstances in which this simplistic approach is not adequate. Cardiac asthma (recurrent episodes of bronchoconstrietion asso ciated with pulmonary edema) can usually be distinguished from bron chial asthma by the existence of left ventricular disease, by the absence of eosinophilia, and by elimination of the bronchial constrictive episodes by ap propriate diuresis. Dyspnea with both cardiac and pulmonary components is often diffi cult or impossible to separate into component parts. Here again, the empirical use of diuretics may be help ful. Clinical abnormalities still present after adequate treatment of the cardiac component usually can be attributed to underlying pulmonary disease. In pa tients who are either undergoing

usually will not occur.

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cardiac catheterization or are critically ill in an intensive care unit, the finding of an elevated pulmonary capillary wedge pressure points toward a prob able cardiac component. However, as before, determining whether or not the cardiac component is playing an impor tant clinical role is based on a carefully controlled trial of diuretics. The dyspnea related to intrinsic pulmonary vascular disease is particu larly difficult to diagnose. Its patho genesis is not clear. It may be seen without mechanical abnormalities of the lung and in the absence of other abnormalities of pulmonary function (normal blood gas values). The second ary cardiac disturbances may be so subtle that they are difficult to detect early in the disease. Possibly, the best approach is to consider the possibility of primary pulmonary vascular disease in patients whose mechanical abnor malities of lung function and hemodynamic abnormalities are insufficient to explain the existence of continued and

disease produce similar abnormalities. The differences that are present involve a difference in pathogenetic mechanism and the fact that the functional abnormalities are usual ly more easily reversed in cardiac as compared to pulmonary dyspnea. Blood gas measurements are not useful in differential diagnosis because abnor malities of blood gases, such as hypoxemia, play little or no role in clinical dyspnea, and also because identical changes in blood gases occur in both forms of dyspnea. Occasionally, mea surements of pulmonary wedge pres sures may indicate the existence of subtle forms of heart disease causing increased pulmonary capillary pres sure. Measurements of pulmonary ar tery pressure may be useful in identify ing patients with dyspnea related to pulmonary vascular disease. Newer techniques for noninvasively estimat

primary lung

progressive dyspnea.

ing pulmonary capillary wedge pres sure and for total lung water are still in the developmental and testing
stage.
Conclusions

Since the abnormalities of lung function and the neurophysiological basis of dyspnea are identical, the separation is often difficult. The ability to rapidly reverse the physiologic abnormalities with diuretics in cardiac dyspnea is of major assistance. Pa tients with both lung and heart disease are particularly difficult to separate. Diuresis is particularly helpful in such patients. The dyspnea associated with primary pulmonary vascular disease is poorly understood. This possibility should be considered in patients with pulmonary mechanical abnormalities that do not seem adequate to explain the degree of dyspnea. Hemodynamic measurements may be useful in pa tients with subtle forms of heart disease or with pulmonary vascular dyspnea. Separating the two forms of dyspnea may be extraordinarily diffi cult in some patients. This investigation was supported in part by
eases.

grant HLO-5929 from the National Institutes of Health (T.A.R.). References


1. Richards DW Jr: The nature of cardiac and

What is the role of special measure ments in the differential diagnosis of cardiac vs pulmonary dyspnea?4 Mea surements of pulmonary function are helpful only to demonstrate the exis tence of obstructive lung disease. Given a restrictive mechanical defect, then both primary cardiac disease and

Dyspnea associated with chronic lung disease is usually easily distinguished from cardiac dysp nea. Stiff lungs are the usual cause of both cardiac dyspnea and the dyspnea associated with restrictive lung disobstructive

pulmonary dyspnea. Circulation 7:15-29, 1953. 2. Rapaport E: Dyspnea: Pathophysiology and differential diagnosis. Prog Cardiovasc Dis

function in patients with heart disease. Med Clin North Am 50:141-157,1966.

13:532-545, 1975. 3. Robin ED, Cross CE, Zelis R: Pulmonary edema. N Eng J Med 288:239-246, 292-304, 1973. 4. Kettel LJ, Moran F, Cugell DW: Pulmonary

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Requirement

for Authors

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