TopBackground
Knowing the physiology of the heart is important to understand how VAE occurs, and what may be done to prevent the problems associated to this event.
Both volume and rate of air accumulation are dependent on the size of the vascular lumen as well as the pressure gradient determining the morbidity and mortality of any episode of VAE (Mirski, 2007). For these reasons surgeries in the head or the brain have a high risk of VAE episodes (negative pressure gradient).
Pathophysiologic pathways are highly dependent on the volume of air accumulated within the right ventricle. If the rate of embolism is high (approximately 5 ml/kg), the probability of air bubble accumulation in the heart is higher. As consequence, the normal blood flow is interrupted. This outflow obstruction may be the result from the inability to decompress the tension of ventricular wall, which leads to heart failure and cardiovascular collapse. When the volumes of VAE are moderate, a decrease in cardiac output, hypotension, myocardial and cerebral ischemia, and even death may occur (Sigel, 1998). At the pulmonary level, an entrainment of air may lead to vasoconstriction, release of inflammatory mediators and bronchoconstriction. Not only negative pressure gradients but also positive pressure insufflation of gas may present a serious VAE hazard (Sigel, 1998).
Main symptoms of VAE include chest pain, dyspnea, coughing (Gan, 1997), tachycardia, cyanosis (Sigel, 1998) and sense of impending death (Avidan, 2008); however such symptoms may only be referred by conscious patients, while VAE occurs mostly during surgery under general anesthesia.
Relating the incidence of VAE with the positioning of the patient, neurosurgical procedures performed in the sitting position have the highest rate of VAE (80% for seated posterior fossa surgery) (Eikaas, 2009).