Journal article
Hemodynamic effects of ventricular defibrillation
The Journal of clinical investigation, Vol.49(2), pp.282-297
02/1970
DOI: 10.1172/JCI106238
PMCID: PMC322471
PMID: 4904240
Abstract
Hemodynamic responses to ventricular defibrillation were studied in anesthetized dogs. Observations were made on arterial, right atrial and left ventricular end-diastolic pressures, on cardiac output (dye dilution), heart rate, and right atrial electrocardiogram. Ventricular fibrillation was induced electrically with a bipolar electrode catheter placed in the right ventricle. Fibrillation was maintained for 15 or 30 sec and terminated with a 400 w sec capacitor discharge across the thoracic cage.\nResponses lasted 1-10 min after conversion and included a cholinergic and an adrenergic component. The cholinergic component was characterized by sinus bradycardia, periods of sinus arrest, atrioventricular block, and ventricular premature beats. The adrenergic component included increases in arterial pressure, in cardiac output, and in left ventricular stroke work at a time when left ventricular end-diastolic pressure was normal; there was no change in total peripheral resistance. The pH of arterial blood decreased slightly and pCO\n2\nincreased but pO\n2\nand the concentration of lactate were unchanged. Bilateral vagotomy and intravenous administration of atropine blocked the cholinergic component, unmasked a sinus tachycardia, and accentuated the adrenergic component of the response. The latter was blocked by intravenous administration of propranolol and phenoxybenzamine.\nThese responses were related primarily to conversion of ventricular fibrillation rather than to the electrical discharge of countershock because countershock without ventricular fibrillation caused more transient and smaller responses than those observed with defibrillation: furthermore, the hemodynamic effects of defibrillation were augmented by prolongation of the duration of fibrillation. The results suggest that the cholinergic component of the response may be detrimental in that it favors spontaneous recurrence of fibrillation; on the other hand, the adrenergic component may be essential for conversion since only one of six dogs depleted of endogenous catecholamines with reserpine survived ventricular defibrillation.
Details
- Title: Subtitle
- Hemodynamic effects of ventricular defibrillation
- Creators
- Donald G Pansegrau - Cardiovascular Research Laboratories, Department of Medicine, University of Iowa, College of Medicine, Iowa City, Iowa 52240François M Abboud - Cardiovascular Research Laboratories, Department of Medicine, University of Iowa, College of Medicine, Iowa City, Iowa 52240
- Resource Type
- Journal article
- Publication Details
- The Journal of clinical investigation, Vol.49(2), pp.282-297
- Publisher
- American Society for Clinical Investigation
- DOI
- 10.1172/JCI106238
- PMID
- 4904240
- PMCID
- PMC322471
- ISSN
- 0021-9738
- eISSN
- 1558-8238
- Language
- English
- Date published
- 02/1970
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
- Record Identifier
- 9984025351002771
Metrics
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