Abstract
Thoracotomized dogs with a reservoir and mechanical pump substitution of the right heart were subjected to pulmonary embolization by repeated injection of glass microspheres (80-120 뀅) or autologous clots (2-3 mm). Airway pressure was controlled by means of a Starling resistor connected to the expiratory line of the respirator. Following embolization with microspheres, the initial abrupt rise in pulmonary arterial pressure was followed by a more gradual increase, interpreted as due to delayed constriction of pulmonary vascular bed. Following emboli injection, systemic arterial oxygen saturation decreased to 82%, venous admixture rose to 30%. When the end-expiratory pressure was increased from 5 to 20 cm of water, the arterial oxygen saturation rose and venous admixture decreased to values not significantly different from pre-embolic levels. These findings suggest that pulmonary hypertension in pulmonary embolism is due not only to a mechanical obstruction of pulmonary vessels, but that some degree of pulmonary vasoconstriction also occurs when small-sized emboli are used. Arterial hypoxemia associated with pulmonary embolism appears to be due to perfusion of non- or poorly ventilated areas of the lung and not to significant blood flow through arteriovenous anastomoses. blood tensions; pulmonary edema; pulmonary venoarterial shunts Submitted on May 4, 1964