Key result
Low strength nonsynchronized shocks during canine ventricular tachycardia caused more ventricular fibrillation or accelerated tachycardia than high strength shocks (60% vs 14.6%; OR 8.9, P<0.01).
Why the study?
Do low strength nonsynchronized shocks increase the induction of ventricular fibrillation or accelerated ventricular tachycardia compared to high strength shocks in a canine model of myocardial infarction?
Do low strength nonsynchronized shocks increase the induction of ventricular fibrillation or accelerated ventricular tachycardia compared to high strength shocks in a canine model of myocardial infarction?
In a canine model, low strength nonsynchronized shocks during ventricular tachycardia are significantly more likely to induce ventricular fibrillation or accelerate tachycardia than high strength shocks.
Answers are grounded in this paper and cite their sources.
Should not change defibrillation practice; hypothesis-generating for strength-dependent proarrhythmia in canine VT.
UNLABELLED: Cardioversion shocks given during ventricular tachycardia may cause ventricular fibrillation or acceleration of ventricular tachycardia, or arrest the tachycardia. A recently proposed theory may explain why the former two phenomena may occur. Briefly, this theory states that potential gradient shock fields of a critical strength delivered to tissue with a critical degree of refractoriness will cause circulating wave fronts of ventricular activation ("rotors") manifest as ventricular arrhythmia. We tested this theory by delivering nonsynchronized shocks 50% higher than defibrillation threshold or 50% lower than defibrillation threshold during 275 episodes of ventricular tachycardia in eight dogs with 5- to 7-day-old myocardial infarcts. Shocks stronger than the defibrillation threshold are likely to create shock fields in the ventricles everywhere stronger than this critical value, and therefore would not generate rotors. Shocks less strong than the defibrillation threshold may create shock fields within the ventricles that include the critical value, and therefore cause rotors if given when critically refractory tissue is present. Nonsynchronized shocks were used to increase the likelihood of encountering tissue with a critical degree of refractoriness. Ventricular fibrillation or acceleration of ventricular tachycardia occurred following 83 of 138 (60%) low strength shocks and following 20 of 137 (14.6%) high strength shocks. The pooled odds ratio for induction of ventricular fibrillation or accelerated ventricular tachycardia after low strength shocks as compared to high strength shocks was 8.9. CONCLUSION: when given during ventricular tachycardia, low strength shocks are much more likely to cause ventricular fibrillation or accelerated ventricular tachycardia than are high strength shocks (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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McClelland et al. (1992) studied Ventricular tachycardia (n=8). Low strength nonsynchronized shocks vs. High strength nonsynchronized shocks was evaluated on Ventricular fibrillation or acceleration of ventricular tachycardia (OR 8.9, p=<0.01). Low strength nonsynchronized shocks during canine ventricular tachycardia caused more ventricular fibrillation or accelerated tachycardia than high strength shocks (60% vs 14.6%; OR 8.9, P<0.01).
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