Pulmonary arterial pressures in congestive failure and emphysema

Abstract

Many phenomena seen in diseases of the heart and lungs are commonly ascribed to elevation of pressure in the lesser circulation. Until recently, there have been few opportunities for determination of this pressure in man. The technic of intracardiac catheterization permits measurement of pressures within the pulmonary artery and simultaneous determination of the cardiac output by the Fick method. This technic has been applied to the study of the pulmonary circulation in patients with pulmonary emphysema, congestive heart failure, and mitral stenosis, conditions which have been thought to bring about an elevation of pressure in the lesser circulation. Pulmonary arterial pressure and cardiac output were determined while subjects were at rest and while they were carrying out exercise sufficient approximately to double the resting oxygen consumption. In normal subjects the mean pulmonary arterial pressure at rest is of the order of 10 to 15 mm. of mercury and is substantially unchanged by increases in cardiac output up to nearly twice the resting level. Subjects with emphysema who have an elevated pulmonary pressure at ,rest show a further large increase in pressure when the cardiac output is raised by exercise. Subjects with congestive failure on the basis of hypertension or aortic regurgitation usually have a high resting pulmonary pressure. During exercise, the pulmonary pressure undergoes an additional large elevation, but the cardiac output is increased little or not at all. The results in subjects .with advanced mitral stenosis resembled those seen in left ventricular failure. The data indicate that the normal pulmonary vascular bed can accommodate considerable increase in blood flow over the resting level without a significant increase in pulmonary arterial pressure. The results in emphysema suggest a rigid vascular bed which responds with a sharp elevation of arterial pressure to an increase in cardiac output. The mechanism by which the pulmonary pressure becomes elevated in cases of left ventricular failure is uncertain. It might possibly result from elevation of the left atria1 pressure, constriction of pulmonary arterioles or development of edema within the lung. In mitral stenosis the failure of the cardiac output to rise in correspondence with the elevation of pulmonary pressure during exercise was unexpected.