• H W Gervais, A L Depta, B K Hiller, S Tag, R Kentner, J Brachlow, B Eberle, W Grimm, F Latorre, and W Heinrichs.
• Klinik für Anästhesiologie, Johannes Gutenberg-Universität Mainz.
• Anaesthesist. 1996 Oct 1; 45 (10): 941-9.

UnlabelledBlood 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.MethodsAfter 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.ResultsIn 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.ConclusionHypoglycaemia 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.

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