Factors determining ventricular fibrillation after induced cardiac arrest.

Ventricular fibrillation following release of the aortic cross clamp is not uncommon. In 38 patients undergoing aortic valve replacement we investigated if this disturbance of rhythm is due to perioperative myocardial ischemia or due to deterioration of myocardial function prior to surgery. In all cases hypothermic cardioplegic arrest (Bretschneider) was used. The mean duration of ischemia was 49.39 +/- 10.46 minutes. After release of the aortic cross clamp in 17 of 38 patients ventricular fibrillation occurred. To find out which factors are responsible for the occurrence of ventricular fibrillation we performed a statistical analysis. Thereby we found out that the occurrence of ventricular fibrillation did not correlate with ischemia, the maximal level of myocardium-bound creatine kinase, the NYHA stage, or the left ventricular end diastolic pressure. The left-ventricular concentration of noradrenaline determined just before release of the aortic cross clamp showed a significant negative correlation with the occurrence of ventricular fibrillation. From our results we conclude that ischemic injury was not the determining factor for the occurrence of ventricular fibrillation in our study. We suggest that the significant correlation with reduced myocardial noradrenaline content demonstrates that myocardial deterioration prior to surgery is the determining factor for the occurrence of ventricular fibrillation.

[Effect of the duration of reperfusion on metabolic recovery during unloading of the hypertrophic heart following induced heart arrest]. / Einfluss der Reperfusionsdauer auf die metabolische Erholung während Entlastung des hypertrophen Herzens nach induziertem Herzstillstand.

The methods of cardioplegia used today are not always able to sufficiently protect the hypertrophied heart. The present study investigated if a recovery period of 30 min before the end of ECC improves metabolic recovery of the heart in comparison to a recovery period of 15 min before terminating extracorporeal circulation. A clinical study was performed of patients undergoing aortic valve replacement. In one group reperfusion was performed for 15 min and in the second group for 30 min before the conclusion of extracorporeal circulation. The concentration of high energy phosphates in the left ventricle was determined at the end of the ischemic period, after 15 min and after 30 min of reperfusion. The behavior of the myocardial metabolites of the two groups showed no differences. Creatinephosphate increased continuously in both groups, while adenosine triphosphate and the adenonucleotide pool did not change during the reperfusion period. From our results we conclude that under the conditions given in our study a recovery period of 15 min is sufficient for metabolic recovery and prolongation of reperfusion before termination of extracorporeal circulation do not improve metabolic recovery.