The effects of air in the venous system on cardiovascular and pulmonary physiology are complex. The basic cardiovascular dysfunction in venous air embolism is obstruction to right ventricular ejection. This affects either the pulmonary artery when a large bolus is implicated, or the pulmonary arterioles when microbubbles are involved. The pathophysiological cascade of venous air embolism is shown in Fig 1
Macrobubble pathophysiology causes circulatory standstill, leading to complete cardiorespiratory arrest. The fatal dose of air embolism in adults has not been scientifically established, but estimates from animal studies are of the order of 500 ml.
Microbubbles in the pulmonary circulation cause histopathological changes. The bubbles obstruct blood flow, and subsequently platelets, neutrophils, erythrocytes, fibrin, and fat aggregate on the bubbles and local endothelial cells. Neutrophil-released mediators and platelet activating factor play important roles. Platelet activating factor may contribute to cardiac deterioration from air embolism through its effects on pulmonary arteriolar vascular tone. The superoxide anion, hydrogen peroxide, leukotrienes, and thromboxanes, which are neutrophil derived, are implicated in pulmonary injury.
Administration of superoxide dismutase, catalase, and methylprednisolone can negate superoxide anion, hydrogen peroxide, and mediators derived from arachidonic acid and ameliorate the deleterious effects of venous air embolism in dogs.
Disturbances of cardiopulmonary physiology due to venous air embolism confined to the right heart circulation are profound, but the consequences of arterial embolization are even more dramatic. Less than 1 ml of air in a coronary artery may cause a fatal myocardial infarction ( Fig:,,,,?,).
The pathology of arterial gas embolism is not limited to simple intravascular mechanical obstruction. The delayed presentation of the condition is a consequence of a wide range of pathophysiological changes. As with gas in the venous system, local accumulation of fat, fibrin, platelets, and blood cells exacerbates local ischemia and can activate complement and clotting cascades.
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