AIR EMBOLISM

Abstract

Air embolism is a subtle and ever-possible scourge during medical and surgical procedures and can result in severe morbidity and even mortality. Gravitational gradients as small as 5 cm may cause the entrainment of air from an open vein or sinus into the dependent heart. The adage out of sight, out of mind appears to be applicable to this problem because our perceptions are blinded, as anesthesiologists generally associate air embolism only with neurosurgical cases carried out in the sitting position. We are also blinded by our lack of a knowledge of history, because prior to the twentieth century, literally hundreds of cases of venous air embolism in nonneurosurgical procedures were described in the medical literature. The entrance of air into the venous circulation can start a process in which small volumes may coalesce in the right side of the heart owing to surface tension, break up because of the pumping action of the heart, and then vent through the lungs out of the body. When the entrained volume is large, an air lock may develop, impede venous return, and either pass through the pulmonary circulation and out through the lungs or, if there is a probe-patent foramen ovale, move into the left atrium and from there into the coronary sinuses, brain, and arterial circulation. Air may also move across the pulmonary bed into the left side of the heart when the filtering ability of the lungs is overwhelmed. Signs of VAE include, in the order of increasing severity, a change in the Doppler heart tones; a decrease in end tidal CO2; increases in central venous and pulmonary artery pressures; hypotension; tachycardia or bradycardia; alterations in peripheral resistance, cardiac output, and electrocardiograph; and the development of a mill-wheel murmur. This latter sign occurs last and indicates that a substantial quantity of air has entered the heart chambers. The key to the treatment of VAE lies in the ability to recognize it before hemodynamic problems occur; the precordial Doppler air bubble detector appears to have the greatest sensitivity, followed by end tidal CO2 monitoring. A multiorificed central venous catheter of which the tip is 1 cm past the superior vena cava-atrial junction provides the best opportunity to aspirate air and thus to prevent or break up an air lock. If VAE is suspected, N2O should be discontinued and the patient put on 100% O2. At an O2:N2O ratio of 1:1, the volume of the embolus doubles as N2O replaces the N2 in the air bubble. If a patient suspected of having had a VAE remains comatose after a surgical procedure or awakens with a neurologic dysfunction, the possibility of cerebral air embolism must be considered, resulting from either paradoxical embolus or passage of air through the pulmonary circulation to the left side of the heart. Under these circumstances, the CNS should be examined by computed tomography or magnetic resonance imaging for intra-axial brain or spinal cord air. The finding of intra-axial air may then necessitate treatment with hyperbaric oxygenation. The key thought in handling the problem of VAE can best be described in two Latin words Praemonitus, Praemunitus, forewarned is forearmed.