Cardiopulmonary consequences of acute pulmonary embolic disease

Abstract

Observations of the cardiopulmonary alterations in 44 patients with acute pulmonary embolic disease were presented.o1.Hyperventilation was almost uniformly present. Most patients showed some degree of pulmonary restriction, bronchoconstriction and diminution of the pulmonary diffusing capacity.2.Arterial blood gas studies showed hypoxemia and hypocapnia in the great majority of patients. Factors responsible for this hypoxemia include venous admixture, diffusion and ventilation-perfusion defects.3.Cardiac decompensation manifested by elevation of the right ventricular end-diastolic pressure, low cardiac index and increased arteriovenous oxygen extraction was present in two-thirds of the patients.4.Pulmonary artery hypertension was present in 71 per cent of the patients: 48 per cent had mild-moderate, and 23 per cent had severe pulmonary hypertension. All patients with mean pulmonary artery pressures greater than 30 mm. Hg had cardiac decompensation. Following inhalation of oxygen for 20 minutes, there was a small but significant drop in the average mean pulmonary artery pressure. Similar results were obtained during an infusion of acetylcholine. These studies suggest that the underlying mechanisms for pulmonary hypertension include both a mechanical and vasoconstrictive factor. Much of the patient data in this study are in agreement with those from experimental studies. Exceptions are noted and discussed. Hyperventilation was almost uniformly present. Most patients showed some degree of pulmonary restriction, bronchoconstriction and diminution of the pulmonary diffusing capacity. Arterial blood gas studies showed hypoxemia and hypocapnia in the great majority of patients. Factors responsible for this hypoxemia include venous admixture, diffusion and ventilation-perfusion defects. Cardiac decompensation manifested by elevation of the right ventricular end-diastolic pressure, low cardiac index and increased arteriovenous oxygen extraction was present in two-thirds of the patients. Pulmonary artery hypertension was present in 71 per cent of the patients: 48 per cent had mild-moderate, and 23 per cent had severe pulmonary hypertension. All patients with mean pulmonary artery pressures greater than 30 mm. Hg had cardiac decompensation. Following inhalation of oxygen for 20 minutes, there was a small but significant drop in the average mean pulmonary artery pressure. Similar results were obtained during an infusion of acetylcholine. These studies suggest that the underlying mechanisms for pulmonary hypertension include both a mechanical and vasoconstrictive factor. Much of the patient data in this study are in agreement with those from experimental studies. Exceptions are noted and discussed.