Pulmonary Physiology during Pulmonary Embolism

Abstract

In summary, acute pulmonary embolism causes major pulmonary physiologic derangements. Understanding these alterations may guide therapy. Increased pulmonary vascular resistance results from obstruction of the pulmonary arteries, and may result in acute right ventricular failure, hypotension, and death. This most important pathophysiologic derangement may be partially reversed by second-generation thrombolytic agents within hours of their administration. Arterial hypoxemia results from mismatching of ventilation and blood flow or from shunting of mixed venous blood. When hypoxemia is refractory to high inspired oxygen fractions (shunt), differentiation between intrapulmonary and intracardiac shunting may direct therapy. Intrapulmonary shunt is reversed by CPAP, whereas CPAP may adversely affect intracardiac shunt. Relief of pulmonary artery obstruction by thrombolysis may correct hypoxemia resulting from intracardiac shunts.