After 10 min of untreated ventricular fibrillation, mechanical chest compressions were provided for 60 min (100 CPM, 1.25" deep) in 26 domestic swine (30.5 ± 1.7 kg) with concurrent hypothermia induction using one of eight cooling methods.
After 3 min of untreated ventricular fibrillation, cardiopulmonary resuscitation (CPR) was started in all animals and continued until return of spontaneous circulation (ROSC); defibrillation was performed 3 minutes after the start of CPR.
In part II, 3 min after induction of ventricular fibrillation, CPR was started and 5 min later epinephrine (group A, 0.1 mg/kg; group B, 1.0 mg/kg) was administered.
Nevertheless, we chose 11 mins of a ventricular fibrillation model and the prolonged no-flow time of core organs could generate severe ischemic injury.
Precordial chest compression was initiated 4 min after the start of ventricular fibrillation, continued for 4 min, and followed by defibrillation.
Conclusions: In this porcine laboratory model, 90 s and 3 min of CPR improved ventricular fibrillation mean frequency, which correlated positively with coronary perfusion pressure, and mean arterial pressure.
There were 933 ICD-detected tachyarrhythmias (separated by at least 60 min), of which 798 (86%) were ventricular (63 ventricular fibrillation, 25 nonsustained ventricular fibrillation, 622 ventricular tachycardia, and 88 nonsustained ventricular tachycardia).
Out of the 25 randomized pigs, one assigned to the postconditioning group died at 1 h and 20 min of reperfusion due to ventricular fibrillation resistant to defibrillation and was excluded from further analysis.
