Introduction:
A high heart rate (HR) after return of spontaneous circulation (ROSC) due to increased sympathetic drive is a compensatory mechanism of postresuscitation myocardial dysfunction. However, it increases myocardial oxygen demand and impairs oxygen supply, and may increase the severity of myocardial ischemia.
Hypothesis:
Reduction of HR would improve postresuscitation myocardial dysfunction.
Methods:
Thirty-two male Sprague-Dawley rats weighing 450-550g were randomized into 2 groups: 1) Saline group: Ventricular fibrillation was induced and untreated for 6 min followed by 8 min of CPR. Rats received 0.9% NaCl solution administered from the femoral artery at 1h after return of spontaneous circulation (ROSC). 2) Drug group: Ventricular fibrillation was induced and untreated for 6 min followed by 8 min of CPR. Rats received Ivabradine (0.5ml/kg) solution administered from the femoral artery at 1h after ROSC. All catheters including the endotracheal tube were removed at PR 5h and animals were returned to their cages and closely monitored for the duration of survival.
Results:
For both groups, postresuscitation myocardial function as expressed by CO, EF, MPI was impaired compared to baseline values. However, the IVA group was significantly inferior to the SAL group with myocardial function index from PR 120’ to PR 300 (*p<0.01) (Figure 1).A significantly shortened duration of survival was observed in the IVA group compared to the SAL group (p<0.01) (Figure 2).
Conclusions:
Lowering HR significantly reduces myocardial function the duration of survival following successful resuscitation.
Some Possible Reasons on the Failure of Cardiopulmonary-cerebral Resuscitation——The Enlightenments of a Successful Resuscitation of a Sudden Ventricular Fibrillation Patient during Resection of Lower Lob of Left Lung
