Milrinone facilitates resuscitation from cardiac arrest and attenuates postresuscitation myocardial dysfunction

Article; Proceedings Paper

关键词: PROLONGED VENTRICULAR-FIBRILLATION;    CHRONIC HEART-FAILURE;    SURVIVORS;    DEFIBRILLATION;    DOBUTAMINE;    COUNTERSHOCK;    AMRINONE;   

DOI  :  10.1161/01.CIR.0000101925.37174.85

来源: SCIE

【 摘 要 】

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, n = 16) as a bolus and infusion or milrinone 50 mug/kg as a bolus and then 0.5 mug/kg per min for 60 minutes ( treatment group, n = 16). After 2 minutes of CPR ( total VF time, 7 minutes), countershocks were given. Coronary perfusion pressures during CPR were similar for the groups ( 24 +/- 2 versus 21 +/- 4 mm Hg). All animals were defibrillated; 6 of 16 control animals developed refractory postcountershock pulseless electrical activity compared with 0 of 16 treated animals ( P = 0.018). At 30 minutes after restoration of spontaneous circulation, stroke volume ( 16 +/- 3 versus 26 +/- 7 mL, P < 0.01) and LV dp/dt ( 793 +/- 197 versus 1108 +/- 316 mm Hg/s, P < 0.02) 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 facilitates resuscitation from prolonged VF and attenuates LV dysfunction after resuscitation without worsening major determinants of myocardial oxygen demand.

【 授权许可】

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