What is the pathophysiology of venous air embolism (VAE)?

Updated: Dec 30, 2017
  • Author: Brenda L Natal, MD, MPH; Chief Editor: Erik D Schraga, MD  more...
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The key factors determining the degree of morbidity and mortality in venous air emboli are related to the volume of gas entrainment, the rate of accumulation, and the patient’s position at the time of the event. [1, 6, 15]

Generally, small amounts of air are broken up in the capillary bed and absorbed from the circulation without producing symptoms. Traditionally, it has been estimated that more than 5 mL/kg of air displaced into the intravenous space is required for significant injury (shock or cardiac arrest) to occur. [1] However, complications have been reported with as little as 20 mL of air [7] (the length of an unprimed IV infusion tubing) that was injected intravenously.

Injection of 2 or 3 mL of air into the cerebral circulation can be fatal. [18] Furthermore, as little as 0.5 mL of air in the left anterior descending coronary artery has been shown to cause ventricular fibrillation. [11, 18] Basically, the closer the vein of entrainment is to the right heart, the smaller the lethal volume is. [1]

Rapid entry or large volumes of air entering the systemic venous circulation puts a substantial strain on the right ventricle, especially if this results in a significant rise in pulmonary artery (PA) pressures. This increase in PA pressure can lead to right ventricular outflow obstruction and further compromise pulmonary venous return to the left heart. The diminished pulmonary venous return will lead to decreased left ventricular preload with resultant decreased cardiac output and eventual systemic cardiovascular collapse. [1, 4, 6]

With VAE, resultant tachyarrhythmias are frequent, but bradyarrhythmias can also occur. [2, 4]

The rapid ingress of large volumes of air (>0.30 mL/kg/min) into the venous circulatory system can overwhelm the air-filtering capacity of the pulmonary vessels, resulting in a myriad of cellular changes. [3] The air embolism effects on the pulmonary vasculature can lead to serious inflammatory changes in the pulmonary vessels; these include direct endothelial damage and accumulation of platelets, fibrin, neutrophils, and lipid droplets. [1]

Secondary injury as a result of the activation of complement and the release of mediators and free radicals can lead to capillary leakage and eventual noncardiogenic pulmonary edema. [1, 3, 7]

Alteration in the resistance of the lung vessels and ventilation-perfusion mismatching can lead to intra-pulmonary right-to-left shunting and increased alveolar dead space with subsequent arterial hypoxia and hypercapnia. [1, 4, 15]

Arterial embolism as a complication of VAE can occur through direct passage of air into the arterial system via anomalous structures such as an atrial or ventricular septal defect, a patent foramen ovale, or pulmonary arteriovenous malformations. This can cause paradoxic embolization into the arterial tree. [1, 2, 3, 4, 11] The risk for a paradoxical embolus seems to be increased during procedures performed in the sitting position. [1, 5]

Air embolism has also been described as a potential cause of the systemic inflammatory response syndrome (case report), triggered by the release of endothelium-derived cytokines. [17]

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