The lethal dose of intravascular air in humans is unknown, but accidental injections of between 100 and 300 ml have been fatal. The mechanism of death from massive air embolus is circulatory obstruction and cardiovascular collapse resulting from air trapped in the right ventricular outflow tract.
VAE that does not cause immediate death can cause paradoxical embolization by acutely increasing right atrial pressure resulting in right to left shunt through a patent foramen ovale. Pulmonary microvascular occlusion can also occur; the air can produce increasing obstruction to blood flow, undergo resorption, or result in increased dead space.
Bronchoconstriction may result from release of endothelial mediators, complement production, and cytokine release. During spontaneous respiration, slow entrainment of air that causes obstruction of 10% of the pulmonary circulation causes a "gasp" reflex that results in chest pain and tachypnea. The resulting decrease in intrathoracic pressure and right atrial pressure can increase the rate of air entrainment.
Morbidity and mortality from air embolism are directly related to the size of the embolus and the rate of entry. Doses of air greater than 50 ml (1 ml/kg) cause hypotension and dysrhythmias. 300 ml of air entrained rapidly can be lethal. Bronchoconstriction results in increased airway pressure, and wheezing. Other manifestations of air embolism include hypoxemia, hypercapnia and decreased ETCO2 (due to increased functional dead space). Hypotension, cardiac dysrhythmias, and cardiovascular collapse occur as air entrainment continues.