Prehospital Ventricular Defibrillation

Liberthson, Richard R.; Nagel, Eugene L.; Hirschman, Jim C.; Nussenfeld, Sidney R.

doi:10.1056/nejm197408152910701

Cited by 446 publications

(43 citation statements)

References 19 publications

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“…5 This recommendation is based on 2 older studies. In the 1970s, Liberthson et al 6 reported on the prognosis of 42 resuscitated patients who survived to discharge. Only 35% of these patients had an MI, which, in this era, was not treated by any form of reperfusion therapy.…”

Section: Discussionmentioning

confidence: 99%

Prognosis among survivors of primary ventricular fibrillation in the percutaneous coronary intervention era

Jong

Marsman

Henriques

et al. 2009

American Heart Journal

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Section: Discussionmentioning

confidence: 99%

Prognosis among survivors of primary ventricular fibrillation in the percutaneous coronary intervention era

Jong

Marsman

Henriques

et al. 2009

American Heart Journal

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“…15, 17 (3) The atrioventricular nodal artery that originates from the right coronary artery in 90% of patients and from the left circumflex artery in 10% of patients and supplies the atrioventricular node and also the left atrium directly and/or by anastomoses with other left atrial branches. [5][6][7][8][9][10][11][12][13][14][15][16][17][18] Early atrial fibrillation. Only seven of the 214 patients (3%) developed atrial fibrillation within 3 hr of the onset of chest pain.…”

Section: Methodsmentioning

confidence: 99%

Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion.

Hod¹,

Lew²,

Keltai³

et al. 1987

Circulation

106

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Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second-or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery. Our data indicate that early atrial fibrillation in acute myocardial infarction occurs when there is coexistent occlusion of the left circumflex artery proximal to the origin of its left atrial circumflex branch and impaired perfusion of the atrioventricular nodal artery. Since these two arteries both contribute to left atrial perfusion, our data suggest that acute left atrial ischemia is the pathophysiologic mechanism of early atrial fibrillation.Circulation 75, No. 1, 146-150, 1987. ATRIAL FIBRILLATION complicates acute myocardial infarction in about 20% of patients. It usually occurs later than 24 hr after the onset of infarction as a consequence of either pericarditis or heart failure.1 In contrast, atrial fibrillation during the early hours of myocardial infarction is rare`and its pathogenesis is poorly understood. The purpose of this study was to investigate the pathogenesis of atrial fibrillation in the early hours of an acute myocardial infarction in a population of patients who were admitted within 3 hr of the

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“…Between 10% and 40% of people who survive out of hospital circulatory arrest experience significant neurological damage [1]. Some of the damage caused by ischemic anoxia occurs after reperfusion and is amenable to therapy [2].…”

Section: Introductionmentioning

confidence: 99%

An experimental circulatory arrest model in the rat to evaluate calcium antagonists in cerebral resuscitation

Garavilla

Babbs

Tacker

1984

The American Journal of Emergency Medicine

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A circulatory arrest model in the rat was developed for use in cerebral and cardiac resuscitation studies. Whole-body ischemia was produced for 8 to 18 minutes by arresting the heart with a cold potassium chloride cardioplegic solution. Following cardiopulmonary resuscitation, minimal, standardized intensive care was provided. As the duration of ischemia was increased from 8 to 18 minutes, survival immediately following resuscitation decreased from 100% to 25%, and survival at 48 hours after ischemia decreased from 80% to 0%. Thirty per cent of the rats recovering from 11 minutes of ischemia suffered motor seizures. Survival and the incidence of motor seizures appear to be good measures of outcome following ischemic circulatory arrest. These measures can be used to test the possible anti-ischemic actions of calcium antagonists or other drugs.

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Prehospital Ventricular Defibrillation

Cited by 446 publications

References 19 publications

Prognosis among survivors of primary ventricular fibrillation in the percutaneous coronary intervention era

Prognosis among survivors of primary ventricular fibrillation in the percutaneous coronary intervention era

Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion.

An experimental circulatory arrest model in the rat to evaluate calcium antagonists in cerebral resuscitation

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