The effects of biphasic waveform design on post-resuscitation myocardial function

Tang, Wanchun; Weil, Max Harry; Sun, Shijie; Jorgenson, Dawn; Morgan, Carl; Klouche, Kada; Snyder, David

doi:10.1016/j.jacc.2003.10.055

Cited by 70 publications

(28 citation statements)

References 16 publications

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“…This injury is more evident when defibrillation is administered in the second and third phases of cardiac arrest that the heart is exposed to severe ischemic or acidic conditions [64]. The electrical shocks increase intramyocardial temperature leading to myocardial damage [65], potentiate excitationcontraction uncoupling, and are linked with dose-dependent release of free radicals and waveform-specific effects on mitochondrial function [66]. Biphasic waveforms are associated with less injurious effects on myocardial oxidative metabolism and hemodynamic performance [66].…”

Section: Pathophysiological Disturbances and Hemodynamics During Cardmentioning

confidence: 99%

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

2011

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The prognosis for cardiac arrest victims remains dismal, as only 17% survives to hospital discharge. Post-resuscitation myocardial stunning is the mechanical dysfunction that persists after the restoration of spontaneous circulation. Our knowledge regarding myocardial stunning has grown dramatically over the years, and several hypotheses have been proposed in order to explain its pathophysiology; however, the interrelationships among various mechanisms remain unclear. This review deals primarily with the basic aspects of the pathophysiology of post-resuscitation myocardial stunning. Given the large number of relevant studies and the fragmented information, an effort was made to summarize current knowledge in order to present a comprehensive pathophysiological mechanism. In this review, the pathophysiological disturbances occurring from the onset of cardiac arrest until the restoration of spontaneous circulation are addressed. Then, the pathophysiology of myocardial stunning during the post-resuscitation period is critically reviewed in 4 parts, the immediate, the early, the intermediate, and the recovery post-arrest phase. This article covers a huge gap in the existing literature regarding the pathophysiology of post-resuscitation period and provides a better understanding of the pathophysiology and pathogenesis of post-resuscitation myocardial stunning.

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Section: Pathophysiological Disturbances and Hemodynamics During Cardmentioning

confidence: 99%

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

2011

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“…33 We observed that biphasic compared with monophasic waveform defibrillation shortened the time from first shock to sustained ROSC by nearly 3 minutes. That this difference was not statistically significant could be because the study was underpowered or because a waveform effect, if present, was attenuated by the severity of cardiac dysfunction that accompanies protracted VF.…”

Section: Shock Energymentioning

confidence: 71%

Transthoracic Incremental Monophasic Versus Biphasic Defibrillation by Emergency Responders (TIMBER)

et al. 2006

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Background-Although biphasic, as compared with monophasic, waveform defibrillation for cardiac arrest is increasing in use and popularity, whether it is truly a more lifesaving waveform is unproven. Methods and Results-Consecutive adults with nontraumatic out-of-hospital ventricular fibrillation cardiac arrest were randomly allocated to defibrillation according to the waveform from automated external defibrillators administered by prehospital medical providers. The primary event of interest was admission alive to the hospital. Secondary events included return of rhythm and circulation, survival, and neurological outcome. Providers were blinded to automated defibrillator waveform. Of 168 randomized patients, 80 (48%) and 68 (40%) consistently received only monophasic or biphasic waveform shocks, respectively, throughout resuscitation. The prevalence of ventricular fibrillation, asystole, or organized rhythms at 5, 10, or 20 seconds after each shock did not differ significantly between treatment groups. The proportion of patients admitted alive to the hospital was relatively high: 73% in monophasic and 76% in biphasic treatment groups (Pϭ0.58). Several favorable trends were consistently associated with receipt of biphasic waveform shock, none of which reached statistical significance. Notably, 27 of 80 monophasic shock recipients (34%), compared with 28 of 68 biphasic shock recipients (41%), survived (Pϭ0.35). Neurological outcome was similar in both treatment groups (Pϭ0.4). Earlier administration of shock did not significantly alter the performance of one waveform relative to the other, nor did shock waveform predict any clinical outcome after multivariate adjustment. Conclusions-No statistically significant differences in outcome could be ascribed to use of one waveform over another when out-of-hospital ventricular fibrillation was treated.

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“…New approaches are being developed to optimize the effectiveness of electrical defibrillation by identifying the proper timing for shock delivery and by using safer and more effective defibrillation waveforms. (24,25) …”

Section: Decreased Left Ventricular Compliancementioning

confidence: 99%

Myocardial effects of cardiac arrest and resuscitation with especial reference to mitochondrial injury

Gazmuri

Ayoub

Radhakrishnan

2008

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The underlying mechanism of cell injury during ischemia and reperfusion is complex and timesesnsitive. Some processess develop coincidentally with the onset of ischemia and during reperfusion leading to abnormalities in energy metabolism, acid base status, and intracellular ion homeostasis. Other processes develop later and encompass activation of various SIGNA VITAE 2008; 3(1): 7 -12 Key words: cardiac arrest, mitochondrial injury, cardiopulmonary resuscitation, apoptosisThe working heart is a highly metabolically active organ that consumes close to 10% of the total body oxygen consumption. It extracts nearly 70% of the oxygen supplied by the coronary circuit but has little capability for extracting additional oxygen. Accordingly, increased metabolic demands are met through coronary vasodilation resulting in increased blood flow and oxygen delivery. (1,2) As a result, a severe energy imbalance develops during cardiac arrest shortly after coronary blood flow ceases. The severity of the energy deficit is contingent on the metabolic requirements and is particularly high when ventricular fibrillation (VF) is present; because the energy needs of the fibrillating heart are the same or more than the normally beating heart. (3) A lesser energy requirement occurs when cardiac arrest occurs in the quiescent or minimally active heart (i.e., asystole or pulseless electrical activity as a result of asphyxia or exsanguinations). (4) However, most experimental studies have examined the myocardial manifestations of cardiac arrest and resuscitation in animal models of VF. After cessation of coronary blood flow and oxygen delivery, the mitochondrial capability for ATP regenerating through oxidative phosphorylation stops prompting anaerobic regeneration of limited amount of ATP at the substrate level from breakdown of creatine phosphate and oxidation of pyruvate to lactate. (5-7) This leads to rapid depletion of creatine phosphate, marked elevation in lactate, and a relatively slow depletion of ATP. (6) We observed in a rat model of VF, that 10 minutes of untreated VF were accompanied by decreases in myocardial creatine phosphate and ATP to levels corresponding to 7% and 19% of baseline, respectively, whereas the lactate content increased by more than 50-fold. (8) Along with the energy deficit, ischemia is accompanied by accumulation of CO 2 and H + yielding profound myocardial acidosis. (9) Acidosis, however, is believed to be protective. Several studies have shown that hypoxic cells and tissues are preserved better in an acidic environment. (10-12) Conventional closed-chest resuscitation is hemodynamically limited failing to generate a coronary blood flow greater than 20% of normal. (13) Such low flow fails to reverse myocardial ischemia but is sufficient to activate multiple pathogenic mechanisms triggering what is known as reperfusion injury. Accordingly, resuscitation typically proceeds during and in spite of severe myocardial ischemia and in the midst of reperfusion injury compounded by specific resuscitation in...

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The effects of biphasic waveform design on post-resuscitation myocardial function

Abstract: Maximum survival and minimum myocardial dysfunction were observed with the low-capacitance 150-J waveform, which delivered higher peak current while minimizing energy and average current.

Cited by 70 publications

References 16 publications

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

Transthoracic Incremental Monophasic Versus Biphasic Defibrillation by Emergency Responders (TIMBER)

Myocardial effects of cardiac arrest and resuscitation with especial reference to mitochondrial injury

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