EFFECTS OF PREISCHEMIC BLOOD-GLUCOSE CONC ENTRATIONS ON HEMODYNAMICS AND REGIONAL ORGAN PERFUSION DURING AND AFTER CARDIOPULMONARY-RESUSCITATION (CPR) IN PIGS

Blood glucose alterations prior to cerebral ischaemia are associated w ith 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 g lucose alterations. The aim of this study was to evaluate the effects of pre-cardiac-arrest hypo- or hyperglycaemia compared to normoglycaem ia upon haemodynamics, cerebral blood flow (CBF) and metabolism (CMRO( 2)), and regional cardiac blood flow during CPR subsequent to 3 min of cardiac and respiratory arrest and after restoration of spontaneous c irculation. Methods. After approval by the State Animal Investigation Committee, 29 mechanically ventilated, anaesthetised pigs were instrum ented for haemodynamic monitoring and blood flow determination by the radiolabeled microsphere technique. The animals were randomly assigned to one of three groups: in group I (n=9) blood glucose was not manipu lated; 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. Afte r 3 min of untreated ventricular fibrillation and respiratory arrest, CPR (chest compressor/ventilator (Thumper(R)) and epinephrine infusion ) was commenced for 8 min. and continued Thereafter, defibrillation wa s attempted, and if successful, the animals were observed for another 240 min. Cerebral perfusion pressure (CPP), CBF, CMRO(2), coronary per fusion pressure (CorPP), and regional cardiac blood flow were determin ed at control, after 3 min of CPR, and at 10, 30, and 240 min post-CPR . Results. In group I, 4/9 animals (44%) could be successfully resusci tated; in group II 4/10 (40%); and in group III 0/10 (0%). Prior to ca rdiac arrest, mean arterial pressure, CPP, and CorPP in group III were significantly lower compared to groups I and II. In group I, CPP duri ng CPR was 26 +/- 6 mmHg; CBF 31 +/- 9 ml/min/100 g CMRO(2) 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; CMRO(2) 1.8 +/- 0.8; CorPP 16 +/- 6; and LV flow 22 +/- 9; and in group III: CPP 15 +/- 3; CBF 11 +/- 8; CMRO(2) 1.5 +/- 1.1; CorPP 4 +/- 2: and LV flow 19 +/- 10. During the 240-min post-resuscitation period, there w ere no differences in CBF, CMRO(2), or LV flow between groups I and II . Conclusion. Hypoglycaemia prior to cardiac arrest appears to be pred ictive for a poor cardiac outcome, whereas hyperglycaemia does not imp air resuscitability compared to normoglycaemia. In addition, hyperglyc aemia did not affect LV flow, CBF, or CMRO(2). However, it has to be k ept in mind that haemodynamics and organ blood flow do not permit conc lusions with respect to functional neurologic recovery or histopatholo gic damage to the brain, which is very likely to be associated with hy perglycaemia.