Pathophysiology of intravenous air embolism in dogs

Abstract

Despite increasing awareness of the clinical incidence of venous air embolism, the pathophysiology of the resultant cardiovascular collapse is still obscure. Since venous air emboli frequently result from aspiration of air into a vein opened surgically, slow infusion (0.01 to 2.00 mg/kg/min) was compared with injection of boluses (25-200 ml; 1.0 to 13.3 ml/kg) of air into the external jugular veins of 52 dogs during various forms of anesthesia. Cardiopulmonary variables measured included heart sounds, respirations, systemic blood pressure, pulmonary arterial and central venous pressures, heart rate, cardiac output, and peripheral resistance with slow infusions. On slow infusion a progressive increase in central venous pressure, an abrupt increase in pulmonary arterial pressure to a plateau, a progressive decrease in peripheral resistance, and a compensatory increase in cardiac output were demonstrated. Blood pressure decreased moderately until compensation was exceeded, at which point blood pressure decreased sharply. Electrocardiographic changes initially involved peaking of the P waves, but later depression of the S-T segment occurred. Changes in heart sounds occurred only when significant cardiovascular decompensation had already occurred. Changes in physiologic variables on injection of a bolus of air included increase in central venous pressure, a decrease in pulmonary arterial pressure, S-T segment depression, and shock. It is concluded that bolus injection might lead to an air lock in the heart, but slow infusion initially causes a reflex decrease in peripheral resistance, possibly mediated through receptors in the lung.