Respiratory Factors Affecting Pulmonary Arterial Blood Pressure and Flow Through the Lungs

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Abstract
Pulmonary arterial pressure rises during expiration and falls during inspiration. This study was made to determine whether respiratory fluctuaations in pulmonary arterial pressure were a reflection of changing intrathoracic pressure, or whether there was also a respiratory variation in effective pulmonary arterial pressure. Simultaneously recorded pulmonary arterial pressure, pneumotachygram and intraesophageal pressure were analyzed in four patients with rheumatic heart disease and in one with pulmonary sarcoidosis. In one case of rheumatic heart disease with mitral stenosis, and in the one case of sarcoidosis, effective pulmonary arterial end-diastolic pressure rose during inspiration and fell during expiration, while recorded pulmonary arterial end-diastolic pressure fell on inspiration and rose on expiration. In two cases of mitral stenosis complicated by tricuspid insufficiency, both recorded and effective end-diastolic pulmonary arterial pressures fell during inspiration and rose during expiration. Increased venous return to the right heart during inspiration is probably an important factor in the inspiratory rise of effective pulmonary diastolic pressure seen in some cases. Failure of this to occur in two cases of tricuspid insufficiency indicates a possible fall in stroke volume of right ventricle in inspiration associated with increase in regurgitation secondary to increased flow to right side of the heart. One patient with mitral stenosis had cardiac cycles of unusual length, permitting measurement of pulmonary artery pressure during diastolic periods lasting through both phases of the respiratory cycle. When deep inspiration occupied most of a diastolic period, effective diastolic pressure fell during early part of inspiration, reached an asymptote and rose again toward end of inspiration. This paradoxical rise in effective pulmonary end-diastolic pressure suggests that inspiration may be associated with an increase in pulmonary vascular resistance in man as well as in animals. Submitted on July 13, 1956