Myocardial dysfunction after successful resuscitation from cardiac arrest

Gazmuri, Raúl J.; Weil, Max Harry; Bisera, Joe; Tang, Wanchun; Fukui, Michihiko; McKee, D

doi:10.1097/00003246-199606000-00020

Cited by 170 publications

(33 citation statements)

References 51 publications

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“…13 Inotropes and vasopressors should be considered if hemodynamic goals are not achieved despite optimized preload. Myocardial dysfunction after ROSC is well described in both animal 101,102,156,157 and human 97,99,112 studies. Post-cardiac arrest global myocardial dysfunction is generally reversible and responsive to inotropes, but the severity and duration of the myocardial dysfunction may impact survival.…”

Section: Circulatory Supportmentioning

confidence: 99%

Post–Cardiac Arrest Syndrome

Neumar¹,

Nolan²,

Adrie³

et al. 2008

Circulation

1,233

398

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Section: Circulatory Supportmentioning

confidence: 99%

Post–Cardiac Arrest Syndrome

Neumar¹,

Nolan²,

Adrie³

et al. 2008

Circulation

1,233

398

View full text Add to dashboard Cite

“…[13][14][15] The CPP was digitally computed from the differences in time-coincident diastolic aortic and right atrial pressures. Cardiac output was measured by conventional thermodilution techniques after injection of 5 mL of saline maintained between 0°C and 5°C.…”

Section: Measurementsmentioning

confidence: 99%

Adverse Outcomes of Interrupted Precordial Compression During Automated Defibrillation

et al. 2002

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Background-Current versions of automated external defibrillators (AEDs) require frequent stopping of chest compression for rhythm analyses and capacity charging. The present study was undertaken to evaluate the effects of these interruptions during the operation of AEDs. Methods and Results-Ventricular fibrillation was electrically induced in 20 male domestic swine weighing between 37. 5 and 43 kg that were untreated for 7 minutes before CPR was started. Defibrillation was attempted with up to 3 sequential 150-J biphasic shocks, but each was preceded by 3-, 10-, 15-, or 20-second interruptions of chest compression. The interruptions corresponded to those that were mandated by commercially marketed AEDs for rhythm analyses and capacitor charge. The sequence of up to 3 electrical shocks and delays were repeated at 1-minute intervals until the animals were successfully resuscitated or for a total of 15 minutes. Spontaneous circulation was restored in each of 5 animals in which precordial compression was delayed for 3 seconds before the delivery of the first and subsequent shocks but in none of the animals in which the delay was Ͼ15 seconds before the delivery of the first and subsequent shocks. Longer intervals of CPR interventions were required, and there was correspondingly greater failure of resuscitation in close relationship to increasing delays. The durations of interruptions were inversely related to the durations of subthreshold levels of coronary perfusion pressure. Postresuscitation arterial pressure and left ventricular ejection fraction were more severely impaired with increasing delays. Key Words: cardiopulmonary resuscitation Ⅲ fibrillation Ⅲ defibrillation Ⅲ compression Ⅲ myocardium A utomated external defibrillators (AEDs) provide the single best option for improving the currently poor outcomes of out-of-hospital cardiopulmonary resuscitation (CPR) performed by bystanders. Fundamental to the operation of AEDs is the capability of automated ECG rhythm analyses, during which CPR is interrupted. Previous experimental studies had demonstrated both decreased resuscitability and greater impairment of postresuscitation myocardial function and survival when precordial compression was interrupted for 20 seconds in small animals. 1-3 Because current versions of AEDs prompt "hands-off" intervals of Ͼ10 seconds for rhythm analyses before advising the rescuer to deliver an electrical shock, as documented below, we hypothesized that such interruptions would adversely affect the outcomes of CPR. Conclusions-InterruptionsThreshold levels of coronary perfusion pressure (CPP) are identified as major determinants of successful cardiac resuscitation. 4 -7 Interruptions in precordial compression predictably result in declines in CPP and therefore delays in restoring threshold values of CPP. 5,6 We therefore anticipated that increasing the length of intervals of interrupted chest compression results in corresponding decreases in the success of CPR and greater severity of postresuscitation myocardial dysfunction.These co...

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“…Prior laboratory work by others suggests that indices of LV function reach a nadir at 30 to 60 minutes after ROSC, when VF duration is of 4-to 10-minute duration, remains relatively constant during the ensuing 4 to 6 hours, and returns to prearrest values 24 to 72 hours after resuscitation. 2,3,12,26,28 It is likely that the postresuscitation ventricular dysfunction observed in the present study would have resolved spontaneously and without treatment if the observation period had been longer. However, the decline in arterial pressure and cardiac output observed in the control group (Table 2 and Figure 2) during the first hour after restoration of circulation would prompt intervention if encountered in the clinical setting.…”

Section: Limitationsmentioning

confidence: 81%

“…[1][2][3][4][5][6] Postresuscitation ventricular dysfunction has been ascribed to stunning of the globally ischemic heart and is presumed to share the pathobiological mechanisms that characterize reperfusion contractile dysfunction described in other models of myocardial ischemia. 7,8 Complicating the understanding of postresuscitation ventricular dysfunction is the fact that electrical defibrillation is used to terminate ventricular fibrillation (VF) in animal models and patients who experience sudden cardiac death attributable to VF.…”

mentioning

confidence: 99%

Milrinone Facilitates Resuscitation From Cardiac Arrest and Attenuates Postresuscitation Myocardial Dysfunction

et al. 2003

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Background-Left ventricular (LV) dysfunction with a low cardiac index after successful CPR contributes to early death attributable to multiorgan failure, and an effective treatment has not been identified. The purpose of this study was to investigate the use of milrinone, a selective phosphodiesterase III inhibitor, as treatment for LV dysfunction after resuscitation. Methods and Results-Ventricular fibrillation (VF) was induced electrically in 32 swine. After 5 minutes of VF, CPR was initiated and animals were randomized to receive either saline (control group, nϭ16) as a bolus and infusion or milrinone 50 g/kg as a bolus and then 0.5 g/kg per min for 60 minutes (treatment group, nϭ16). After 2 minutes of CPR (total VF time, 7 minutes), countershocks were given. Coronary perfusion pressures during CPR were similar for the groups (24Ϯ2 versus 21Ϯ4 mm Hg). All animals were defibrillated; 6 of 16 control animals developed refractory postcountershock pulseless electrical activity compared with 0 of 16 treated animals (Pϭ0.018). At 30 minutes after restoration of spontaneous circulation, stroke volume (16Ϯ3 versus 26Ϯ7 mL, PϽ0.01) and LV dp/dt (793Ϯ197 versus 1108Ϯ316 mm Hg/s, PϽ0.02) were higher in the treatment group. Similar differences were observed 60 minutes after restoration of spontaneous circulation. Significant differences in heart rates between groups were not observed, and peripheral vascular resistance was significantly greater in the control group 30 and 60 minutes after resuscitation. Conclusions-Milrinone

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Myocardial dysfunction after successful resuscitation from cardiac arrest

Abstract: Postresuscitation myocardial dysfunction in this animal model was characterized by impaired contractile function, decreased work capability, and ventricular dilation.

Cited by 170 publications

References 51 publications

Post–Cardiac Arrest Syndrome

Post–Cardiac Arrest Syndrome

Adverse Outcomes of Interrupted Precordial Compression During Automated Defibrillation

Milrinone Facilitates Resuscitation From Cardiac Arrest and Attenuates Postresuscitation Myocardial Dysfunction

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