Analysis of determinants of ventricular fibrillation induced by reperfusion: Dissociation between electrical instability and myocardial damage

Abstract

To assess the underlying mechanisms of ventricular fibrillation induced by myocardial reperfusion after cardioplegic arrest, 62 patients undergoing an open heart operation were divided into two groups based on the absence (group 1, n = 37) or the development (group 2, n = 25) of reperfusion-induced ventricular fibrillation. There was no close relationship between the incidence of reperfusion-induced ventricular fibrillation and aortic clamp time. On reperfusion, the time to onset of cardiac activity was similar in groups 1 (2.4 ± 1.8 minutes) and 2 (1.9 ± 1.1 minutes). At that time, there was no significant difference in values of arterial oxygen and bicarbonate contents, pH, or base excess between the two groups, but myocardial temperature was significantly higher in group 2 (25.6 ° ± 3.4 ° versus 27.6 ° ± 2.4 °C; p < 0.05). In addition, serum levels of sodium (123.9 ± 4.2 versus 126.1 ± 3.7 mmol/L; p < 0.05) and calcium (0.80 ± 0.07 versus 0.84 ± 0.05 mmol/L; p < 0.05) were significantly higher and serum potassium levels (3.98 ± 0.58 versus 3.55 ± 0.61 mmol/L; p < 0.02) and the serum potassium to calcium ratio (4.94 ± 0.90 versus 4.29 ± 0.72; p < 0.01) significantly lower in group 2. Postoperative serum levels of the myocardial-specific isoenzyme of creatine kinase and myoglobin were similar in both groups. By multivariate analysis, shorter ischemic time, higher myocardial temperature, higher serum sodium concentration, and lower serum potassium to calcium ratio were found to influence induction of reperfusion-induced ventricular fibrillation. We conclude that ion imbalance and myocardial temperature, rather than severity of ischemia-related and reperfusion-related myocardial damage, may be important for the genesis of reperfusion-induced ventricular fibrillation and that reperfusion injury, if reperfusion-induced ventricular fibrillation is a representative phenomenon of reperfusion injury, may not be a major cause of postoperative cardiac dysfunction.