Answers are grounded in this paper and cite their sources.
Shows that acute thoracotomy significantly and transiently raises defibrillation thresholds in canine models, indicating temporary physiological resistance to electrical shock.
INTRODUCTION: Despite innovations in nonthoracotomy defibrillation systems, thoracotomies are still required in some clinical settings and are utilized in many animal-based research protocols. The effect of a thoracotomy on defibrillation energy, however, has not been well characterized. METHODS AND RESULTS: Ten dogs in the immediate testing group underwent defibrillation testing immediately following a thoracotomy; another ten dogs in the delayed testing group were given 48 to 72 hours of recovery before defibrillation testing. A right ventricular endocardial coil to cutaneous thoracic patch biphasic system was used. At the time of defibrillation testing, the immediate testing group had a faster mean heart rate (144.7 +/- 30.2 vs 105.8 +/- 17.5 beats/min, P < 0.01), higher mean pulmonary artery pressures (systolic: 18.14 +/- 9.48 vs 11.28 +/- 6.46 mmHg, P = 0.1; diastolic: 6.59 +/- 2.88 vs 3.89 +/- 1.75 mmHg, P < 0.05), and higher mean defibrillation shock impedance (89.0 +/- 11.6 vs 70.9 +/- 7.3 omega, P < 0.002) than the delayed group. The mean ED50 (energy with a 50% success rate) was significantly higher in the immediate group than in the delayed group (26.9 +/- 14.9 vs 14.2 +/- 6.9 J, P < 0.05), and the slopes of the dose-response curves were significantly different (P = 0.03). CONCLUSION: In a right ventricular endocardial to cutaneous patch system, thoracotomy significantly and transiently increased the defibrillation threshold and modified the defibrillation dose-response curve.
No takes yet. Share an insight, caveat, or question.
Friedman et al. (1997) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: