Pulmonary hemodynamics and arterial oxygen saturation in pulmonary embolism

¹ Department of Physiology, National Jewish Hospital, Denver, Colorado

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 µ) 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.

Submitted on May 4, 1964

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