A closed-chest model for the study of electromechanical dissociation of the heart in dogs

Thijs, L. G.; Vincent, Jean‐Louis; Weil, Max Harry; Michaels, W S; Carlson, Richard W.

doi:10.1016/0300-9572(82)90005-3

Cited by 17 publications

(3 citation statements)

References 11 publications

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“…"1-'3 Of note, immediate countershock of prolonged ventricular fibrillation has been used as an animal study model for EMD. [14][15][16] The likelihood of successful restoration of spontaneous circulation after electrical countershock appears to be time dependent. The earlier that countershock can be performed, the greater the likelihood that defibrillation will be followed by a spontaneous perfusing rhythm and survival.…”

Section: Treatment Of Prolonged Ventricular Fibrillationmentioning

confidence: 99%

Treatment of prolonged ventricular fibrillation. Immediate countershock versus high-dose epinephrine and CPR preceding countershock.

et al. 1992

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Background. Early countershock of ventricular fibrillation has been shown to improve immediate and long-term outcome of cardiac arrest. However, a number of investigations in the laboratory and in the clinical population indicate that immediate countershock of prolonged ventricular fibrillation most commonly is followed by asystole or a nonperfusing spontaneous cardiac rhythm, neither of which rarely respond to current therapy. The use of epinephrine in doses greater than those currently recommended has recently been shown to improve both cerebral and myocardial perfusion during cardiopulmonary resuscitation (CPR). The purpose of this study was to compare cardiac resuscitation outcome between immediate countershock of prolonged ventricular fibrillation with high-dose epinephrine therapy and conventional CPR before countershock of prolonged ventricular fibrillation in a canine model.Methods and Results. After sedation, intubation, induction of anesthesia, and instrumentation, ventricular fibrillation was electrically induced in 28 dogs. After 7.5 minutes of ventricular fibrillation, animals were randomly allocated to two treatment groups: group 1, immediate countershock followed by recommended advanced cardiac life support (ACLS) interventions, or group 2, 0.08 mg/kg epinephrine and manual closed-chest CPR before countershock and ACLS. In both groups, ACLS was continued until a spontaneous perfusing rhythm was restored or for 20 minutes (total arrest time, 27.5 minutes). A spontaneous perfusing rhythm was restored in three of 14 group 1 animals and in nine of 14 group 2 animals (p=0.014 by sequential analysis method of Whitehead). Coronary perfusion pressure (aortic minus right atrial pressure during CPR diastole) before countershock was significantly greater in group 2 (21+7 mm Hg) when compared with mean circulatory pressure in group 1 (9+8, p<0.01).Conclusions. The findings of this study suggest that a brief period of myocardial perfusion before countershock improves cardiac resuscitation outcome from prolonged ventricular fibrillation. (Circulation 1992;85:281-287)

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Section: Treatment Of Prolonged Ventricular Fibrillationmentioning

confidence: 99%

Treatment of prolonged ventricular fibrillation. Immediate countershock versus high-dose epinephrine and CPR preceding countershock.

et al. 1992

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“…Both the shock itself (19) as well as the preceding VF (1,14) can contribute to depressed myocardial function following successful defibrillation. If VF continues long enough [ϳ120 s in dogs (18)], pulseless electrical activity can result and the subject will die if hemodynamic support is not started. The mechanism for this depressed myocardial function is not well understood.…”

mentioning

confidence: 99%

Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation

Walcott

Melnick

Killingsworth

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms pulses of various amplitudes delivered before the defibrillation shock can improve hemodynamics following the shock, and 2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1–10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After β-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without β-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after β-blockade. We conclude that a burst of 15–30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. β-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.

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“…The animal model used in our study was developed previously by Thijs and associates 12 and reproduced in studies by other investigators. 13,14 The model was designed to simulate clinical situations in which defibrillation occurs without adequate coronary perfusion, producing EMD.…”

Section: Experimental Protocolmentioning

confidence: 99%

Endotracheal versus intravenous epinephrine during electromechanical dissociation with CPR in dogs

Ralston

Tacker

Showen

et al. 1985

Annals of Emergency Medicine

127

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The dose-response curves of epinephrine given either IV or endotracheally (ET) were compared during resuscitation from electromechanical dissociation (EMD). Ten anesthetized dogs were subjected to a two-minute period of electrically induced ventricular fibrillation (VF) followed by defibrillation without CPR to produce EMD. Mechanical CPR was followed by injection of either ET or IV epinephrine. Successful response was defined as a return of pulsatile blood pressure within two minutes of drug administration. Using log-dose increments of epinephrine, experimental trials were repeated in each animal. The IV and ET median effective doses were 14 and 130 g/kg, respectively. When the trials were successful, the time between drug administration and either arterial blood pressure increases or return of spontaneous circulation did not differ significantly for the ET and IV groups. These results show that the dosage for epinephrine delivered ET must be higher than the IV dosage to achieve the same response during CPR.

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A closed-chest model for the study of electromechanical dissociation of the heart in dogs

Cited by 17 publications

References 11 publications

Treatment of prolonged ventricular fibrillation. Immediate countershock versus high-dose epinephrine and CPR preceding countershock.

Treatment of prolonged ventricular fibrillation. Immediate countershock versus high-dose epinephrine and CPR preceding countershock.

Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation

Endotracheal versus intravenous epinephrine during electromechanical dissociation with CPR in dogs

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