Gervais H W, Depta A L, Hiller B K, Tag S, Kentner R, Brachlow J, Eberle B, Grimm W, Latorre F, Heinrichs W
Klinik für Anästhesiologie, Johannes Gutenberg-Universität Mainz.
Anaesthesist. 1996 Oct;45(10):941-9. doi: 10.1007/s001010050328.
Blood glucose alterations prior to cerebral ischaemia are associated with poor neurologic outcome, possibly due to extensive lactic acidosis or energy failure. Cerebral effects of hyper- or hypoglycaemia during cardiopulmonary resuscitation (CPR) are less well known. In addition, little information is available concerning cardiac effects of blood glucose alterations. The aim of this study was to evaluate the effects of pre-cardiac-arrest hypo- or hyper-glycaemia compared to normoglycaemia upon haemodynamics, cerebral blood flow (CBF) and metabolism (CMRO2), and regional cardiac blood flow during CPR subsequent to 3 min of cardiac and respiratory arrest and after restoration of spontaneous circulation.
After approval by the State Animal Investigation Committee, 29 mechanically ventilated, anaesthetised pigs were instrumented for haemodynamic monitoring and blood flow determination by the radiolabeled microsphere technique. The animals were randomly assigned to one of three groups: in group 1 (n = 9) blood glucose was not manipulated; in group II (n = 10) blood glucose was increased by slow infusion of 40% glucose to 319 +/- 13 mg/dl; in group III (n = 10) blood glucose was lowered by careful titration with insulin to 34 +/- 2 mg/dl. After 3 min of untreated ventricular fibrillation and respiratory arrest, CPR (chest compressor/ventilator (Thumper) and epinephrine infusion) was commenced and continued for 8 min. Thereafter, defibrillation was attempted, and if successful, the animals were observed for another 240 min. Cerebral perfusion pressure (CPP), CBF, CMRO2, coronary perfusion pressure (CorPP), and regional cardiac blood flow were determined at control, after 3 min of CPR, and at 10.30, and 240 min post-CPR.
In group 1. 4/9 animals (44%) could be successfully resuscitated; in group II 4/10 (40%); and in group III 0/10 (0%). Prior to cardiac arrest, mean arterial pressure, CPP, and CorPP in group III were significantly lower compared to groups I and II. In group I. CPP during CPR was 26 +/- 6 mmHg; CBF 31 +/- 9 ml/ min/100g CMRO2 3.8 +/- 1.2 ml/ min/100 g; CorPP 18 +/- 5 mmHg; and left ventricular (LV) flow 35 +/- 15 ml/min/100 g. In group II; CPP = 21 +/- 5; CBF 21 +/- 7; CMRO2 1.8 +/- 0.8; CorPP 16 +/- 6; and LV flow 22 +/- 9; and in group III: CPP 15 +/- 3; CBF 11 +/- 8; CMRO2 1.5 +/- 1.1; CorPP 4 +/- 2; and LV flow 19 +/- 10. During the 240-min post-resuscitation period, there were no differences in CBF, CMRO2, or LV flow between groups I and II.
Hypoglycaemia prior to cardiac arrest appears to be predictive for a poor cardiac outcome, whereas hyperglycaemia does not impair resuscitability compared to normoglycaemia. In addition, hyperglycaemia did not affect LV flow, CBF, or CMRO2. However, it has to be kept in mind that haemodynamics and organ blood flow do not permit conclusions with respect to functional neurologic recovery or histopathologic damage to the brain, which is very likely to be associated with hyperglycaemia.
脑缺血前的血糖改变与不良神经学预后相关,可能是由于广泛的乳酸酸中毒或能量衰竭。心肺复苏(CPR)期间高血糖或低血糖对大脑的影响尚不太清楚。此外,关于血糖改变对心脏的影响的信息也很少。本研究的目的是评估心脏骤停前低血糖或高血糖与正常血糖相比,对血流动力学、脑血流量(CBF)和代谢(CMRO2)以及心脏和呼吸骤停3分钟后及自主循环恢复后CPR期间局部心脏血流量的影响。
经国家动物研究委员会批准,对29只机械通气、麻醉的猪进行仪器安装,以便通过放射性微球技术进行血流动力学监测和血流量测定。动物被随机分为三组之一:第1组(n = 9)未控制血糖;第II组(n = 10)通过缓慢输注40%葡萄糖使血糖升高至319±13mg/dl;第III组(n = 10)通过小心滴定胰岛素使血糖降低至34±2mg/dl。在3分钟未经治疗的心室颤动和呼吸骤停后,开始CPR(胸外按压/通气(Thumper)和肾上腺素输注)并持续8分钟。此后,尝试除颤,如果成功,对动物再观察240分钟。在对照时、CPR 3分钟后以及CPR后10.30和240分钟时测定脑灌注压(CPP)、CBF、CMRO2、冠状动脉灌注压(CorPP)和局部心脏血流量。
第1组,9只动物中有4只(44%)成功复苏;第II组,10只中有4只(40%);第III组,10只中0只(0%)。心脏骤停前,第III组的平均动脉压、CPP和CorPP显著低于第I组和第II组。在第1组,CPR期间CPP为26±6mmHg;CBF 31±9ml/min/100g,CMRO2 3.8±1.2ml/min/100g;CorPP 18±5mmHg;左心室(LV)血流量35±15ml/min/100g。在第II组,CPP = 21±5;CBF 21±7;CMRO2 1.8±0.8;CorPP 16±6;LV血流量22±9;在第III组:CPP 15±3;CBF 11±8;CMRO2 1.5±1.1;CorPP 4±2;LV血流量19±10。在复苏后240分钟期间,第I组和第II组之间的CBF、CMRO2或LV血流量没有差异。
心脏骤停前的低血糖似乎预示着心脏预后不良,而与正常血糖相比,高血糖并不损害复苏能力。此外,高血糖不影响LV血流量、CBF或CMRO2。然而,必须记住,血流动力学和器官血流量不能得出关于功能性神经恢复或大脑组织病理学损伤的结论,而这很可能与高血糖有关。