The effects of propofol (emulsion formulation) on cardiovascular dynamics, myocardial blood flow and myocardial metabolism were studied in 12 patients scheduled for elective coronary artery bypass surgery. Measurements were performed with the patient awake, during steady-state maintenance anaesthesia with propofol 200 micrograms kg-1 min-1 at rest, and during sternotomy when the propofol was supplemented with fentanyl 10 micrograms kg-1. Propofol alone decreased mean arterial pressure and cardiac index; heart rate was increased. Myocardial blood flow and myocardial oxygen consumption were decreased by 26% and 31%, respectively. Myocardial lactate production was seen in one patient during this period. Surgical stimulation, under propofol-fentanyl anaesthesia, led to the return of arterial pressure and heart rate towards baseline; cardiac index decreased further. Myocardial blood flow and oxygen consumption increased such that they almost achieved their baseline values. Myocardial lactate production was seen in one patient. These results suggest that propofol may on occasions, lead to myocardial ischaemia in patients with coronary artery disease, but that it is able to block the sympathetic responses to surgical stimulation when combined with a suitable analgesic.
In order to compare the effects of blood-gas management on cerebral blood flow, metabolism and neurological outcome after hypothermic cardiopulmonary bypass (CPB) we have studied 65 patients undergoing aorto-coronary bypass surgery allocated randomly to either a pH-stat (temperature-corrected blood-gas management) or an alpha-stat (temperature-uncorrected blood-gas management) group. All patients were examined neurologically on the day before and the 7th day after operation. In 20 patients of the pH-stat group and in 15 patients of the alpha-stat group we measured cerebral blood flow (CBF), using the argon washin technique, and also cerebral oxygen (CMRO2) and glucose (CMRg) uptake. Measurements were performed in awake patients, after induction of anaesthesia with fentanyl, midazolam and pancuronium under normothermic conditions, during CPB at a venous blood temperature of 26 degrees C and at the end of surgery. Compared with postinduction values, hypothermia was associated with an 18% reduction in CBF and decreases in CMRO2 and CMRg of 61% and 60%, respectively, in the alpha-stat group. In the pH-stat group, CMRO2 and CMRg decreased also, by 58% and 74%, respectively, whereas CBF increased by 191%, indicating uncoupling of flow and metabolism. As there were no statistically significant differences between the metabolic variables in both groups, we conclude that acid-base management did not affect cerebral metabolism, despite its influence on blood flow. After rewarming, CBF and cerebral metabolism normalized independently of acid-base management during hypothermia. Nevertheless, neurological dysfunction occurred more often in the pH-stat group (P = 0.036).
We have undertaken a randomized study on 20 patients undergoing coronary artery bypass surgery in order to determine the influence of cardiopulmonary pump prime solutions on colloid osmotic pressure and extravascular lung water. Crystalloid priming with Ringer lactate was compared with an albumin solution of nearly physiological colloid osmotic composition (4%). Measurements of extravascular lung water were performed by a modified, highly sensitive thermal dye technique, with additional detection of tracer signals in the pulmonary artery. In the Ringer lactate group, a significantly greater decrease in colloid osmotic pressure occurred immediately after onset of cardiopulmonary bypass. The more pronounced decrease in colloid osmotic pressure and in transcapillary gradient (difference between colloid osmotic pressure and pulmonary capillary wedge pressure) in the Ringer lactate group was associated with a significant increase in extravascular lung water (by 60%) in the postoperative period; the human albumin group, however, showed only a slight tendency to increased lung water. There were no differences in haemodynamic or respiratory states after operation.
We investigated the cerebral haemodynamic effects of 1 MAC desflurane anaesthesia in nine male patients scheduled for elective coronary bypass grafting. For the measurement of cerebral blood flow (CBF) a modified Kety-Schmidt saturation technique with argon as inert tracer gas was used. Measurements of CBF were made before induction of anaesthesia and 30 min after induction under normocapnic, hypocapnic and hypercapnic conditions in sequence. Changes in mean arterial pressure after induction of anaesthesia and during the course of the study were minimized using norepinephrine infusion. In comparison with the awake state under normocapnic conditions, desflurane reduced mean cerebral metabolic rate of oxygen (CMRO2) by 51% and mean cerebral metabolic rate of glucose (CMRglc) by 35%. Concomitantly, CBF was significantly reduced by 22%; jugular venous oxygen saturation (SjvO2) increased from 58 to 74%. Hypo- and hypercapnia caused a 22% decrease and a 178% increase in CBF, respectively. These findings may be interpreted as the result of two opposing mechanisms: cerebral vasoconstriction induced by a reduction of cerebral metabolism and a direct vasodilator effect of desflurane. CBF alterations under variation of PaCO2 indicate that cerebrovascular carbon dioxide reactivity is not impaired by application of 1 MAC desflurane.
In order to clarify the relative contribution of the liver to the short term disposition of propofol, hepatic blood flow was measured during induction of anaesthesia with an i.v. bolus dose of propofol 2 mg kg-1. Total clearance of the drug was 2390 (SD 340) ml min-1, hepatic extraction 82% and hepatic clearance 1060 (260) ml min-1. During the 60-min period of observation, hepatic extraction of propofol increased from 79% to 92%. It is concluded that, within 1 h, only 44% of the administered dose is removed by the liver. Consequently, drug accumulation may occur with repeated dosing or infusion of propofol. The increase in extraction results presumably from slow release of propofol from the soy-bean emulsion.
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