Optimal timing for electrical defibrillation after prolonged untreated ventricular fibrillation

Kolarova, Julieta D; Ayoub, Iyad M.; Yi, Zhong; Gazmuri, Raúl J.

doi:10.1097/01.ccm.0000070446.84095.f4

Cited by 59 publications

(44 citation statements)

References 31 publications

(50 reference statements)

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“…In a dog model, a brief CPR before defibrillation improved the resuscitation outcome from prolonged VF [15]. Kolarova et al [16] showed that the rate of restored spontaneous circulation increased in proportion to the duration of CPR before defibrillation. In this study, less than 2 minutes of CPR before defibrillation did not improve the rate of restored spontaneous circulation [16].…”

Section: Discussionmentioning

confidence: 99%

“…Several experimental studies reported that CPR before defibrillation had various benefits [14][15][16]. In swine with 8 minutes of untreated VF, CPR for 90 seconds followed by defibrillation shock resulted in physiological benefits and a superior response to initial defibrillation in comparison with immediate defibrillation [14].…”

Section: Discussionmentioning

confidence: 99%

“…Kolarova et al [16] showed that the rate of restored spontaneous circulation increased in proportion to the duration of CPR before defibrillation. In this study, less than 2 minutes of CPR before defibrillation did not improve the rate of restored spontaneous circulation [16]. This result also indicates that CPR may have to be performed for more than 3 minutes before defibrillation shock.…”

Section: Discussionmentioning

confidence: 99%

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Shortening of cardiopulmonary resuscitation time before the defibrillation worsens the outcome in out-of-hospital VF patients

Hayakawa

Gando

Okamoto

et al. 2009

The American Journal of Emergency Medicine

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Shortening of cardiopulmonary resuscitation time before the defibrillation worsens the outcome in out-of-hospital VF patients

Hayakawa

Gando

Okamoto

et al. 2009

The American Journal of Emergency Medicine

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“…This was also demonstrated by a study by Achleitner et al 21 in which VF mean frequency (CF correspondent) was shown to correlate significantly with the coronary perfusion pressure during compressions in pigs, whereas VF mean amplitude (ENRG correspondent) demonstrated no such correlation. Finally, Kolareva et al 22 recently concluded that improved outcome after prolonged untreated VF in rats may result from strategies that provide chest compressions before defibrillation and avoid early and repetitive defibrillation attempts. In their model, 6 minutes of CPR gave the best ROSC and survival results, and they found a progressive increase in a variant of AMSA and mean amplitude (ENRG correspondent) with a compression duration that correlated significantly with the chance of ROSC.…”

Section: Discussionmentioning

confidence: 99%

Effects of Cardiopulmonary Resuscitation on Predictors of Ventricular Fibrillation Defibrillation Success During Out-of-Hospital Cardiac Arrest

2004

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Background-Early defibrillation is considered the most important factor for restoring spontaneous circulation in cardiac arrest patients with ventricular fibrillation. Recent studies have shown that, after prolonged ventricular fibrillation, the rates of return of spontaneous circulation (ROSC) and survival are improved if defibrillation is delayed so that CPR can be given first. To examine whether CPR improves myocardial readiness for defibrillation, we analyzed whether CPR causes changes in predictors of defibrillation success calculated from the ventricular fibrillation waveform. Methods and Results-ECG recordings were retrieved for 105 patients from an original study of 200 patients receiving CPR or defibrillation first. Altogether, 267 CPR sequences from 77 patients were identified on which the effect of CPR could be evaluated. Five predictors of ROSC (spectral flatness measure, energy, centroid frequency, amplitude spectrum relationship, and estimated probability of ROSC) were determined from a spectral analysis of the ventricular fibrillation waveform immediately before and immediately after each of the 267 sequences. CPR increased spectral flatness measure, centroid frequency, and amplitude spectrum relationship (PϽ0. 05, PϽ0.001, PϽ0.01). In an analysis of the effect of the duration of CPR, the probability of ROSC and amplitude spectrum relationship showed a positive change for CPR sequences lasting Ͼ3 minutes (PϽ0.001, PϽ0.05). Conclusions-During

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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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Optimal timing for electrical defibrillation after prolonged untreated ventricular fibrillation

Cited by 59 publications

References 31 publications

Shortening of cardiopulmonary resuscitation time before the defibrillation worsens the outcome in out-of-hospital VF patients

Shortening of cardiopulmonary resuscitation time before the defibrillation worsens the outcome in out-of-hospital VF patients

Effects of Cardiopulmonary Resuscitation on Predictors of Ventricular Fibrillation Defibrillation Success During Out-of-Hospital Cardiac Arrest

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

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