I was reviewing some data related to the accidental de-priming of the MPS Microplegia delivery system, when in the process, I came up upon this very good article relating to the evolution of the body of knowledge concerning accidental introduction of air to the patient during surgery. It is a fascinating read, and well worth your time 🙂
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Surgical (operative) Air
In 1914, the danger of air embolism during cardiac surgery was reported by Carrel (151), who wrote, “The opening of the ventricles or of the pulmonary artery and the aorta is always followed by entrance of air into the heart.” Support for his statement was the observation of ventricular fibrillation and death in animals after coronary artery air embolism.
Air embolism on the left side of the heart was well known to thoracic surgeons before the advent of open heart surgery. Reyer and Kohl (152) reported 10 cases of venous or arterial air embolism, 5 of which resulted in the patients’ deaths, during a variety of surgical or diagnostic procedures. Kent and Blades (153) further warned that the two major hazards of thoracic surgery were infection and embolic phenomena. In their animal experiments, air embolism was found to be well tolerated on the venous side, in the absence of a patent foramen ovale, but fatal with small injections of air into the pulmonary veins.
Geoghegan and Lam (154) reported that the mechanism of death due to air embolism in dogs (0.25 to 2.0 mL/kg) was either coronary (immediate death) or cerebral (severe brain damage). Benjamin et al. (155) further sought to define the mechanisms of air embolism by injecting varying amounts of air (0.5 to 8.0 mL/kg) into the left atrium, left ventricle, aortic root, common carotid, or descending aorta of dogs. Left atrial air embolism was fatal 100% of the time, whereas the same volumes of air injected into the left ventricle caused death in 83% of the animals. Aortic root and carotid air embolism were better tolerated, and large volumes of air (up to 10 mL/kg) were required to cause death when given into the descending aorta. They, like other investigators (156–164), noted the dangers of left heart air but concluded that small amounts of air in the systemic circulation were generally well tolerated during surgical procedures if appropriate resuscitative maneuvers were undertaken when required.
Many retrospective reviews of early clinical experience with CPB have been published. Callaghan et al. (165) analyzed 60 deaths in 250 CPB patients operated on between 1956 and 1961. A variety of causes described included seven cases of cerebral damage, four of which were from air embolism. Ehrenhaft et al. (166) reported 19 of 244 (7.7%) patients undergoing open heart surgery suffered cerebral damage. Systemic air embolism was the suspected etiology because many operations involved closure of septal defects. Like Carrel nearly 50 years earlier, they warned of air entrance to the left side of the heart or aorta with subsequent embolization when the normal circulation was restored. Allen (167) reported cerebral damage in 18 of 500 (3.6%) patients undergoing repair of valvular or congenital cardiac defects and warned of the propensity of air to collect in the left atrium near the right superior pulmonary vein. Sloan et al. (168) reported 78 of 600 (13%) patients died after CPB; air trapped in the left ventricle was identified as the source of the air and was believed responsible for 49 deaths. Nicks (169) reported systemic air embolism in 40 of 340 (11.7%) patients undergoing congenital or valvular procedures; 10 patients died. Fishman et al. (170) later confirmed the left atrium and pulmonary veins as locations of trapped air whenever the left heart was opened. Anderson et al. (171) and Lin (172) also warned of the risks of pulmonary hypertension due to right-sided air embolism.
The preference of cannulation of the ascending aorta for CPB, although much safer than the femoral artery site, increased the risk of cerebral air embolism. Gomes et al. (173) found that air embolism via the femoral artery was five times less likely to involve the cerebral vessels if the air originated from the CPB arterial line. Beckman et al. (174) determined the optimum method of placement of the ascending aortic cannula to lessen the risk of air entry. Direct insertion of the cannula without use of a side-biting clamp, which tended to trap a small amount of air, was found to be safest.
In the article by Mills and Ochsner (114) on mechanisms of air embolism, two additional surgical sources were described: unexpected resumption of the heart beat and inadequate steps to remove air after cardiotomy. Coronary air embolism with cardioplegia techniques was reported in 1981 (175) and 1986 (110). Although air embolism was generally thought not to occur during coronary bypass operations, Hughes (176) reported the possibility of intraventricular air with right superior pulmonary vein venting that could draw air in via coronary arteriotomy, especially when the left anterior descending coronary artery was opened. Robicsek and Duncan (177) and Lee (178) subsequently confirmed this mechanism. Air also can be drawn retrograde through an opened coronary artery if an aortic root vent is used and placed under significant negative pressure.
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