Michael J R, Guerci A D, Koehler R C, Shi A Y, Tsitlik J, Chandra N, Niedermeyer E, Rogers M C, Traystman R J, Weisfeldt M L
Circulation. 1984 Apr;69(4):822-35. doi: 10.1161/01.cir.69.4.822.
The goals of this study were to quantify the effects of epinephrine on myocardial and cerebral blood flow during conventional cardiopulmonary resuscitation (CPR) and CPR with simultaneous chest compression-ventilation and to test the hypothesis that epinephrine would improve myocardial and cerebral blood flow by preventing collapse of intrathoracic arteries and by vasoconstricting other vascular beds, thereby increasing perfusion pressures. Cerebral and myocardial blood flow were measured by the radiolabeled microsphere technique, which we have previously validated during CPR. We studied the effect of epinephrine on established arterial collapse during CPR with simultaneous chest compression-ventilation with the abdomen bound or unbound. Epinephrine reversed arterial collapse, thereby eliminating the systolic gradient between aortic and carotid pressures and increasing cerebral perfusion pressure and cerebral blood flow while decreasing blood flow to other cephalic tissues. Epinephrine produced higher cerebral and myocardial perfusion pressures during CPR with simultaneous chest compression-ventilation when the abdomen was unbound rather than bound because abdominal binding increased intracranial and venous pressures. In other experiments we compared the effect of epinephrine on blood flow during 1 hr of either conventional CPR or with simultaneous chest compression-ventilation with the abdomen unbound. Epinephrine infusion during conventional CPR produced an average cerebral blood flow of 15 ml/min . 100 g (41 +/- 15% of control) and an average myocardial blood flow of 18 ml/min . 100 g (15 +/- 8% of control). In our previous studies, cerebral and myocardial blood flow were less than 3 +/- 1% of control during conventional CPR without epinephrine. Although flows during CPR with simultaneous chest compression-ventilation without epinephrine were initially higher than those during conventional CPR, arterial collapse developed after 20 min, limiting cerebral and myocardial blood flow. The use of epinephrine throughout 50 min of CPR with simultaneous chest compression-ventilation maintained cerebral blood flow at 22 +/- 2 ml/min . 100 g (73 +/- 25% control) and left ventricular blood flow at 38 +/- 9 ml/min . 100 g (28 +/- 8% control). The improved blood flows with epinephrine correlated with improved electroencephalographic activity and restoration of spontaneous circulation.(ABSTRACT TRUNCATED AT 400 WORDS)
本研究的目的是量化肾上腺素在传统心肺复苏(CPR)以及同步胸外按压-通气的CPR过程中对心肌和脑血流的影响,并验证肾上腺素通过防止胸内动脉塌陷以及使其他血管床血管收缩,从而增加灌注压,进而改善心肌和脑血流这一假设。采用放射性微球技术测量脑和心肌血流,该技术我们之前已在CPR过程中验证过。我们研究了在腹部束缚或未束缚的情况下,同步胸外按压-通气的CPR过程中肾上腺素对已发生的动脉塌陷的影响。肾上腺素可逆转动脉塌陷,从而消除主动脉与颈动脉压力之间的收缩期梯度,增加脑灌注压和脑血流,同时减少流向其他头部组织的血流。当腹部未束缚而非束缚时,在同步胸外按压-通气的CPR过程中,肾上腺素可产生更高的脑和心肌灌注压,因为腹部束缚会增加颅内压和静脉压。在其他实验中,我们比较了肾上腺素在1小时传统CPR或腹部未束缚的同步胸外按压-通气过程中对血流的影响。传统CPR过程中输注肾上腺素产生的平均脑血流为15 ml/min·100 g(为对照的41±15%),平均心肌血流为18 ml/min·100 g(为对照的15±8%)。在我们之前的研究中,无肾上腺素的传统CPR过程中脑和心肌血流低于对照的3±1%。尽管无肾上腺素的同步胸外按压-通气的CPR过程中的血流最初高于传统CPR,但20分钟后出现动脉塌陷,限制了脑和心肌血流。在50分钟的同步胸外按压-通气的CPR过程中全程使用肾上腺素可使脑血流维持在22±2 ml/min·100 g(为对照的73±25%),左心室血流维持在38±9 ml/min·100 g(为对照的28±8%)。肾上腺素使血流改善与脑电图活动改善及自主循环恢复相关。(摘要截选至400词)