Venous air embolism (VAE) is the entry of air into the venous system, as a consequence of trauma or iatrogenic complications (notably surgical procedures where venous structures (veins or venous sinuses) are open to air or when catheters are inserted into veins as in central venous cannulation or pressure infusion of fluids and blood). It has been identified as a component of decompression injury as well. VAE causes the heart to malfunction and pulmonary injury. It is associated with significant morbidity and mortality. Symptomatic VAE following central venous catheterization has mortality as high as 30%.
VAE results when a pressure gradient develops between a source of air and the venous system, which favours ingress of air into the venous system. Small amounts of air do not produce symptoms as the air is removed from the circulation. Large boluses of air can cause acute right ventricular outflow obstruction and result in cardiogenic shock and circulatory arrest. Intermediate amounts of air end up in the pulmonary circulation and produce a pulmonary vascular injury. Symptoms, which develop immediately following embolization, are similar to pulmonary thromboembolism and include: dyspnea, chest pain, tachycardia and hypotension. The severity of the above symptoms is related to the degree of air entry. Severe cases will present in circulatory shock or sudden death.
The true incidence of venous air embolism is unknown. Subclinical air embolism in hospitalized patients is possibly quite common. The frequency of clinically recognized VAE following central venous cannulation is less than 2%.