Ventricular fibrillation

Surawicz, Borys

doi:10.1016/0002-9149(71)90115-9

Cited by 120 publications

(10 citation statements)

References 131 publications

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“…2 (1979) Ventricular vulnerability is a complex phenomenon depending on many variables mainly investigated in animal experiments (1)(2)(3)(4)(5). 74, No.…”

Section: *) Supported By Deutsche Forsehungsgemeinschaft Sfb 109 204mentioning

confidence: 99%

Rate and rhythm dependent vulnerability of the human ventricular myocardium

Fleischmann¹,

Marschall²,

Bakker³

1979

Basic Res Cardiol

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“…2 (1979) Ventricular vulnerability is a complex phenomenon depending on many variables mainly investigated in animal experiments (1)(2)(3)(4)(5). 74, No.…”

Section: *) Supported By Deutsche Forsehungsgemeinschaft Sfb 109 204mentioning

confidence: 99%

Rate and rhythm dependent vulnerability of the human ventricular myocardium

Fleischmann¹,

Marschall²,

Bakker³

1979

Basic Res Cardiol

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“…Agents that shorten and lengthen ventricular muscle refractory periods are expected to promote and retard ventricular fibrillation, respectively (Surawicz 1971(Surawicz , 1884Zipes 1975). Isoproterenol shortened the ventricular muscle refractory period while phenylephrine reversed the effects of isoproterenol on the effective refractory period of the ventricular muscle.…”

Section: Ventricular Refiact~ry Periodmentioning

confidence: 99%

The effects of sympathetic denervation on spontaneous ventricular defibrillation in the rat

Waxman¹,

Sharma²,

Asta³

et al. 1992

Can. J. Physiol. Pharmacol.

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Ventricular tachycardia or ventricular fibrillation was electrically induced in 38 normal rats (group 1) and 24 sympathetically denervated rats (6-hydroxydopamine) (group 2). The time for spontaneous reversion to sinus rhythm was measured during (1) control, (2) isoproterenol, and (3) the combination of isoproterenol and phenylephrine. The time for spontaneous reversion was the same in both groups in the three states. The reversion time was prolonged threefold by isoproterenol, and restored to control values when phenylephrine was added to the infusion of isoproterenol. The tachycardia duration and the refractory period were inversely related: log10 (tachycardia duration) = 3.466-0.091 (refractory period). Ventricular tachycardia/fibrillation induction was examined as follows: (i) Ventricular tachycardia/fibrillation was induced in 100% of normal rats (group 1), but only 42% of the denervated rats (group 2, p less than 0.001); (ii) during isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of rats of both groups; and (iii) when phenylephrine was added to isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of group 1 rats versus 82% of group 2 rats, (p = NS). These observations suggest (1) the induction of ventricular tachycardia/fibrillation is highly dependent on intact sympathetic innervation, and (2) exogenous adrenergic agonists modulate the duration of ventricular fibrillation through their effects on ventricular refractory period, independent of sympathetic innervation.

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“…In the previous review,' I concluded that the mechanisms causing VF are difficult to identify because: (1) in most types of experimental fibrillation one cannot localize the fiber or the group of fibers in which the first wave of reentry or the disorganized activity begins; (2) in many types of experimental fibrillation the onset of disorganized activity is due to a combination of several factors rather than to any This study supported in part by the Herman C. Krannert Fund; by Grants HlrO63O8 and HbO7182 from the National Heart, Lung, and Blood Institute of the National Institutes of Health; by the American Heart Association, Indiana Affiliate; and by the Veterans Administration. one single factor; and (3) an exploration of all cardiac and extracardiac factors that might have contributed to the development of fibrillation rarely has been carried out in any single experiment.…”

Section: Initiation Of Ventricular Fibriliationmentioning

confidence: 99%

“…Two different mechanisms of the initiation of VF were discussed in the previous article:' (1) rapid formation of impulses arising either from a single focus or from multiple foci, and (2) repetitive excitation of cardiac tissue by reentry. The mapping studies suggest that either of the two mechanisms may operate and that sometimes they occur simultaneously or in succession.…”

Section: Initiation Of Ventricular Fibriliationmentioning

confidence: 99%

Ventricular Fibrillation II: Progress Report since 1971

Surawicz

1984

Clinical Progress in Pacing and Electrophysiology

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The purpose of this paper is to present a progress report on the subject of ventricular fibrillation (VF) and to review the experimental and clinical studies published since my earlier review of this subject in 1971.' The vast number of studies related to VF makes it virtually impossible to include more than a fraction of the information published during the past 13 years. By necessity, the choice of references is arbitrary and favors the aspects discussed in the earlier review.' My apology goes to the numerous investigators whose work is not included or is insufficiently emphasized in this review. The format of this article follows the order of subjects in the previous report but the previously listed references are not repeated.

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Ventricular fibrillation

Cited by 120 publications

References 131 publications

Rate and rhythm dependent vulnerability of the human ventricular myocardium

Rate and rhythm dependent vulnerability of the human ventricular myocardium

The effects of sympathetic denervation on spontaneous ventricular defibrillation in the rat

Ventricular Fibrillation II: Progress Report since 1971

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