Effects of ventricular fibrillation on coronary blood flow and myocardial metabolism

Grover, Frederick L.; Fewel, John G.; Ghidoni, John J.; Norton, J.B.; Arom, Kit V.; Trinkle, J. Kent

doi:10.1016/s0022-5223(19)39903-9

Cited by 38 publications

(1 citation statement)

References 13 publications

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“…As a result of the early defibrillation shock delivery, deterioration of the DFT due to ventricular dilatation with an increasing intraventricular volume, global ischemia, and sympathetic discharge might not yet have been fully developed. [8][9][10][11][12] Clinical Relevance ICDs terminate VT and VF with a high efficacy and reduce the rate of sudden cardiac death in patients with otherwise fatal arrhythmias. [13][14][15] To increase the efficacy of ICD therapy, nonthoracotomy defibrillation leads, biphasic shock waveforms, and pectoral implantation of defibrillators with "active can" systems were developed.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ventricular Fibrillation Duration on the Defibrillation Threshold in Humans

Gradaus

Bode-Schnurbus

Weber

et al. 2002

Pacing Clinical Electrophis

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Early during ventricular fibrillation, the defibrillation threshold may be low, as ventricular fibrillation most probably arises from a localized area with only a few wavefronts and the effects of global ischemia, ventricular dilatation, and sympathetic discharge have not yet fully developed. The purpose of this study was to explore the effect of the timing of shock delivery in humans. During implantation of an ICD in 26 patients (24 men, 60 +/- 11 years, 19 coronary artery disease, NYHA 2.2 +/- 0.4, left ventricular ejection fraction 0.42 +/- 0.16), the defibrillation threshold was determined after approximately 10 and 2 seconds of ventricular fibrillation. Ventricular fibrillation was induced by T wave shocks. Mean defibrillation threshold was 9.9 +/- 3.6 J after 10.3 +/- 1.0 seconds. Within 2 seconds, 20 of 26 patients could be successfully defibrillated with < or = 8 J. In these patients, the mean defibrillation threshold was 4.0 +/- 2.1 J after 1.4 +/- 0.3 seconds compared to 9.5 +/- 3.1 J after 10.2 +/- 1.1 seconds (P < 0.001). There were no clinical differences between patients who could be successfully defibrillated within 2 seconds and those patients without successful defibrillation within 2 seconds. In the majority of patients, the defibrillation threshold was significantly lower within the first few cycles of ventricular fibrillation than after 10 seconds of ventricular fibrillation. These results should lead to exploration of earlier shock delivery in implantable devices. This could possibly reduce the incidence of syncope in patients with rapid ventricular tachyarrhythmias and ICDs.

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Section: Discussionmentioning

confidence: 99%

Effect of Ventricular Fibrillation Duration on the Defibrillation Threshold in Humans

Gradaus

Bode-Schnurbus

Weber

et al. 2002

Pacing Clinical Electrophis

View full text Add to dashboard Cite

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Aortocoronary Bypass Procedures Without Cross-Clamping the Aorta

Satter¹,

Eckel²,

Khuri³

et al. 1987

Coronary Artery Surgery in the Nineties

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Myocardial damage by ventricular fibrillation in isolated perfused rat hearts, and its underlying mechanisms

Heuer

Bernauer

1986

Basic Res Cardiol

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In isolated perfused rat hearts ventricular fibrillation (VF), elicited electrically and persisting further spontaneously, led to an extensive release of creatine kinase (CK). Coronary flow volume and oxygen consumption were increased. In contrast, the CK release was only very small in hearts which were stimulated permanently with rhythmic impulses of 10 Hz, whereas the increase in coronary flow and oxygen consumption was significantly greater. When a relative ischemia was induced by perfusion at a low pressure, the CK release from fibrillating hearts was not greater, but less than at a higher perfusion pressure. It appeared unlikely, therefore, that the CK release from fibrillating hearts was simply due to an oxygen deficiency, although a decrease of ATP and glycogen, and an increase of glucose-6-phosphate and lactate in the myocardium were found. When VF was interrupted by lidocaine, the enzyme leakage was reduced only in the experiments with the higher perfusion pressure. A partial restoration of the myocardial metabolites after 1 h was observed. Findings in maximally ischemic hearts further supported the idea that the enzyme release in fibrillating hearts was not merely due to a lack of oxygen. Complete interruption of the coronary perfusion led to the release of only small CK activities during subsequent coronary reperfusion, whereas the metabolic alterations were more distinct than in fibrillating hearts. Mechanisms responsible for the enzyme release during fibrillation, besides a moderate oxygen deficiency, are discussed.

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Effects of ventricular fibrillation on coronary blood flow and myocardial metabolism

Cited by 38 publications

References 13 publications

Effect of Ventricular Fibrillation Duration on the Defibrillation Threshold in Humans

Effect of Ventricular Fibrillation Duration on the Defibrillation Threshold in Humans

Aortocoronary Bypass Procedures Without Cross-Clamping the Aorta

Myocardial damage by ventricular fibrillation in isolated perfused rat hearts, and its underlying mechanisms

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