Electrical threshold for defibrillation of canine ventricles following myocardial infarction

Tacker, Willis A.; Geddes, L. A.; Cabler, P.; Moore, A. G.

doi:10.1016/0002-8703(74)90208-7

Cited by 48 publications

(11 citation statements)

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“…However, although the majority of the patients that undergo defibrillation typically suffer from some form of coronary disease, little is known about the effect of acute ischemia on defibrillation efficacy. Experimental studies provide conflicting evidence: some report an increase in defibrillation threshold (DFT) (3,29,38,43), whereas others find no change (5,20,22,32) or even a decrease (2) in DFT during acute ischemia.Numerous studies (5,7,18) have demonstrated that the DFT is strongly linked to the upper limit of vulnerability (ULV) of cardiac tissue to electric shocks. Much research has focused on investigating the mechanisms of cardiac vulnerability in an attempt to better understand how failed defibrillation shocks reinitiate cardiac arrhythmias.…”

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confidence: 99%

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Effect of acute global ischemia on the upper limit of vulnerability: a simulation study

Rodríguez

Tice²,

Eason³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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. Effect of acute global ischemia on the upper limit of vulnerability: a simulation study. Am J Physiol Heart Circ Physiol 286: H2078 -H2088, 2004. First published January 29, 2004 10.1152/ajpheart.01175.2003The goal of this modeling research is to provide mechanistic insight into the effect of altered membrane kinetics associated with 5-12 min of acute global ischemia on the upper limit of cardiac vulnerability (ULV) to electric shocks. We simulate electrical activity in a finiteelement bidomain model of a 4-mm-thick slice through the canine ventricles that incorporates realistic geometry and fiber architecture. Global acute ischemia is represented by changes in membrane dynamics due to hyperkalemia, acidosis, and hypoxia. Two stages of acute ischemia are simulated corresponding to 5-7 min (stage 1) and 10 -12 min (stage 2) after the onset of ischemia. Monophasic shocks are delivered in normoxia and ischemia over a range of coupling intervals, and their outcomes are examined to determine the highest shock strength that resulted in induction of reentrant arrhythmia. Our results demonstrate that acute ischemia stage 1 results in ULV reduction to 0.8A from its normoxic value of 1.4A. In contrast, no arrhythmia is induced regardless of shock strength in acute ischemia stage 2. An investigation of mechanisms underlying this behavior revealed that decreased postshock refractoriness resulting mainly from 1) ischemic electrophysiological substrate and 2) decrease in the extent of areas positively-polarized by the shock is responsible for the change in ULV during stage 1. In contrast, conduction failure is the main cause for the lack of vulnerability in acute ischemia stage 2. The insight provided by this study furthers our understanding of mechanisms by which acute ischemia-induced changes at the ionic level modulate cardiac vulnerability to electric shocks. ionic channels; computer simulations; arrhythmias ELECTRICAL DEFIBRILLATION is recognized as the most effective therapy against the malignant arrhythmias that lead to sudden cardiac death. However, although the majority of the patients that undergo defibrillation typically suffer from some form of coronary disease, little is known about the effect of acute ischemia on defibrillation efficacy. Experimental studies provide conflicting evidence: some report an increase in defibrillation threshold (DFT) (3,29,38,43), whereas others find no change (5,20,22,32) or even a decrease (2) in DFT during acute ischemia.Numerous studies (5,7,18) have demonstrated that the DFT is strongly linked to the upper limit of vulnerability (ULV) of cardiac tissue to electric shocks. Much research has focused on investigating the mechanisms of cardiac vulnerability in an attempt to better understand how failed defibrillation shocks reinitiate cardiac arrhythmias. During the past decade, experiments using optical mapping techniques (8,12,13,46) and computer simulation studies (25,30,37,41) have significantly improved the understanding of the mechanisms of shockinduced arrhythmogenesis, cul...

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confidence: 99%

Effect of acute global ischemia on the upper limit of vulnerability: a simulation study

Rodríguez

Tice²,

Eason³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…The degree of acidosis and thus the duration of ventricular fibrillation may affect the energy required.2' In dogs the energy required for defibrillation is related to the time after ligation of the coronary vessel. 21 Clinically many or all of these factors may operate, and it is therefore not surprising to find a lack of correlation of energy requiremcents with a single factor such as body weight.…”

Section: Discussionmentioning

confidence: 99%

Current required for ventricular defibrillation.

Patton¹,

Pantridge²

1979

BMJ

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513They had a higher success rate in the accident and emergency department where the defibrillator was kept.Two main reasons may account for our relatively high success rate. The availability of resuscitation ambulances encourages earlier admission after infarction3 and therefore leads to more primary fibrillation in hospital. Of the 68 survivors of circulatory arrest who were admitted in these ambulances, 22 were resuscitated within 30 minutes of arriving at the hospital. In more conventional circumstances most of these 22 patients might have developed ventricular fibrillation before admission. The second reason is immediate access to resuscitation equipment throughout the hospital and the ability of nurses on the open general wards to defibrillate promptly on their own initiative. We believe that the chances of ultimate success are inversely related to the duration of the circulatory arrest, which must be shorter when observation is close and suitably trained personnel are at hand.The role of coronary care units is being debated and it is becoming clear that some patients with an acute myocardial infarction can be managed at home,'2 13 particularly when complications are absent and diagnosis is made three or more hours after the onset of symptoms. We emphasise that our high success rate for defibrillation in general medical wards does not imply that a specialised unit is unnecessary. We believe that one of the principal functions of a coronary care unit is to train doctors and nurses from all areas of the hospital in resuscitation procedures. The influence of a successful unit should extend throughout the general wards and into other departments. We believe that our results underline the value of this philosophy. There is no real paradox in the statement that only a hospital with an efficient coronary care unit does not then need one.Defibrillators and monitoring equipment have been donated by the Brighton Rotary Club, Brighton Lions, Hove Lions, and Hove Round Table. Contributions have also been made by many private individuals. Our resuscitation system could not have functioned so effectively without this help. Many nurses have studied long hours in their own time in order to play a leading part in resuscitation procedures. ReferencesIArmstrong, A, et al, British Heart Journal, 1972, 34, 67. 2 Peatfield, R C, et al, Lancet, 1977, 1, 1223. 3Briggs, R S, et al, British Medical_Journal, 1976, 2, 1161 4Mackintosh, A F, et al, British Medical_Journal, 1978, 1, 1115. 5 Brown, J, Nursing Times, 1975, 71, 1572. 6 Pantridge, J F, et al, British Medical Journal, 1975 Dhurander, R W, MacMillan, R, and Brown, K W G, American Journal of Cardiology, 1971, 27, 347. 8 Wyman, M G, et al, Circulation, 1973 Conley, M J, et al, American Journal of Cardiology, 1977, 39, 7. 1°Reynell, P C, British Heart Journal, 1975, 37, 166. " Messert, B, and Quaglieri, C E, Lancet, 1976, 2, 410.1 Mather, H G, et al, British Medical_Journal, 1976, 1, 925. 13 Hill, J D, Hampton, J R, and Mitchell, J R A, Lancet, 1978, 1, 837. (...

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“…[1] The shock strength required for defibrillation of the ventricles depends upon body weight in animals and in man, [2][3][4][5] but also may be influenced by physiologic factors such as myocardial ischemia, electrolyte imbalance, drug action, and body temperature. [6][7][8] Knowledge of the factors which determine the shock strength necessary for defibrillation is important because a shock which is too weak may fail to defibrillate, and a shock which is too strong may damage the heart. [9][10] All controlled experimental studies of electrical ventricular defibrillation reported to date have used anesthetized animals as subjects--in most cases barbiturate anesthetized dogs.…”

Section: Introductionmentioning

confidence: 99%

Effect of pentobarbital anesthesia on ventricular defibrillation threshold in dogs

Babbs

1978

American Heart Journal

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The effect of pentobarbital anesthesia upon the minimal voltage and current required for electrical ventricular defibrillation (the defibrillation threshold) was investigated in dogs. Threshold current, energy, and charge in five dogs averaged 2 per cent, 13 per cent, and 6 per cent less under surgical levels of pentobarbital anesthesia than thresholds in the same animals in the awake, unanesthetized state. In dogs given sufficient pentobarbital to produce apnea and supported by mechanical ventilation, threshold current, energy, and charge averaged 3 per cent, 17 per cent, and 2 per cent less than comparable awake values. These differences were far from statistically significant. In a second study, five dogs were kept for 8 to 10 hours at a surgical level of anesthesia with pentobarbital sodium. Defibrillation threshold current, determined at hourly intervals, did not drift outside ± 10 per cent limits. Arterial blood gas measurements revealed a stable, compensated metabolic acidosis in all animals (pH 7.36 ± 0.06, pCO 2 33 ± 4 mm. Hg, pO 2 71 ± 9 mm. Hg). These data support the validity of defibrillation studies using animals anesthetized with pentobarbital and indicate the stability of the defibrillation threshold under controlled experimental conditions.

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Electrical threshold for defibrillation of canine ventricles following myocardial infarction

Cited by 48 publications

References 3 publications

Effect of acute global ischemia on the upper limit of vulnerability: a simulation study

Effect of acute global ischemia on the upper limit of vulnerability: a simulation study

Current required for ventricular defibrillation.

Effect of pentobarbital anesthesia on ventricular defibrillation threshold in dogs

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