Optimal timing for electrical defibrillation after prolonged untreated ventricular fibrillation.
OBJECTIVE
It currently is recommended that electrical shocks be delivered immediately on recognition of ventricular fibrillation. However, decreased effectiveness of this approach has been reported after prolonged intervals of untreated ventricular fibrillation. We investigated the optimal strategy for successful defibrillation after prolonged untreated ventricular fibrillation by using a rat model of ventricular fibrillation and closed-chest resuscitation.


METHODS
Controlled, randomized, laboratory study.


METHODS
Research laboratory at a VA hospital.


METHODS
Seventy pentobarbital anesthetized Sprague-Dawley rats.


METHODS
After 10 mins of untreated ventricular fibrillation, four groups of rats were randomized to receive electrical shocks (which we designated as "experimental shocks") immediately before or at 2, 4, or 6 mins of chest compression. Unsuccessfully defibrillated rats received additional shocks (which we designated as "rescue shocks") after 8 mins of chest compression.


RESULTS
The number of rats that restored spontaneous circulation after the experimental shocks increased with increasing duration of the predefibrillatory interval of chest compression (0 of 8, 0 of 8, 2 of 8, and 7 of 8, respectively, p <.005). Two additional groups then were randomized to receive repetitive experimental shocks at 2, 4, and 6 mins or a single attempt at 6 mins of chest compression. Although a comparable number of rats restored spontaneous circulation in each group, rats subjected to repetitive defibrillation attempts had more intense postresuscitation ectopic activity and worse survival. Two final groups were used to investigate whether inhibition of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) could facilitate return of spontaneous circulation during repetitive defibrillation attempts. Although spontaneous circulation was restored earlier in more rats subjected to NHE-1 inhibition, the differences were statistically insignificant. NHE-1 inhibition, however, replicated previously reported resuscitation and postresuscitation benefits. The optimal predefibrillation interval of chest compression was approximately 6 mins, and this coincided with partial return of the amplitude and frequency characteristics of the ventricular fibrillation waveform to those present immediately after induction of ventricular fibrillation.


CONCLUSIONS
Improved outcome after prolonged untreated ventricular fibrillation may result from strategies that provide chest compression before attempting defibrillation and avoid early and repetitive defibrillation attempts. The amplitude and frequency characteristics of the ventricular fibrillation waveform could help identify the optimal timing for attempting electrical defibrillation.
Kolarova
Julieta
J
CPR Research Laboratories, North Chicago VA Medical Center, IL, USA.
Ayoub
Iyad M
IM
Yi
Zhong
Z
Gazmuri
Raúl J
RJ
D000818:Animals; D016887:Cardiopulmonary Resuscitation; D004554:Electric Countershock; D004562:Electrocardiography; D006146:Guanidines / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors / Q000502:physiology; D013450:Sulfones / Q000494:pharmacology; D013997:Time Factors; D016896:Treatment Outcome; D014693:Ventricular Fibrillation / Q000503:physiopathology / Q000628:therapy*
D006146:Guanidines; D017923:Sodium-Hydrogen Exchangers; D013450:Sulfones; C069139:growth factor-activatable Na-H exchanger NHE-1; C093373:cariporide