Protection from coronary air embolism by a perfluorocarbon emulsion (FC-43)

The protective effects of a perfluorocarbon emulsion (FC-43) against the physiological sequelae of selective coronary air embolism (CAE) were examined in dogs. Animals were randomly assigned to two groups: group 1 received 20 mL/kg of 6% hetastarch in 0.9 normal saline solution with 280 mg/L of CaCl₂: group 2 received 20 mL/kg of FC-43 (Oxypherol, Alpha Therapeutic Corp. Los Angeles). Infusion time for both groups was 30 minutes. Following a ten-minute stabilization period, a 0.02-mL/kg bolus of air was injected into the left anterior descending coronary artery distal to the first branch. Surface and epicardial ECGs, systemic BP, pulmonary artery pressure, central venous pressure, left ventricular pressure, left ventricular end-diastolic pressure (LVEDP), dP/dt_max, and V_max were recorded continuously. Cardiac output (by thermodilution technique), myocardial creatine phosphokinase levels and the lactic acid concentration were measured. The study revealed a significantly lower systemic mean arterial pressure (MAP), LVEDP, left ventricular stroke work index (LVSWI), and right ventricular stroke work index (RVSWI) in the group receiving the FC-43 prior to receiving CAE. Possible causes of the differences are a species-specific direct vasodilating effect of FC-43 or histamine release. Following CAE, myocardial function as measured by dP/dt_max, V_max, and MAP was lower in group 1 during the first five minutes following CAE. ECG tracings showed all of the ten group 1 dogs had ST-T changes (>2 mm), and six of the ten had ventricular dysrhythmias or conduction defects. Only one of the group 2 dogs showed ST-T wave changes (P = .0006, Fisher's exact test), and none had dysrhythmias (P = .005, Fisher's exact test). Three animals expired within five minutes of CAE in group 1, whereas none was lost in group 2 (P = .005, Fisher's exact test). Thus, FC-43 pretreatment altered the sequelae of CAE in pentobarbital-anesthetized, oxygen-ventilated dogs.