Cerebral Circulatory and Metabolic Effects of Hypotension Produced by Deep Halothane Anaesthesia

Abstract

Hypotension to a mean blood pressure of 33 mmHg for periods of 70 to 187 minutes was induced by increasing the inspired halothane concentration in 11 baboons which were already anaesthetized with 0.500 halothane, nitrous oxide, and oxygen. During hypotension, cerebral blood flow, measured by Xenon clearance and by a carotid electromagnetic flowmeter, decreased by more than half, and sagittal sinus oxygen saturation was 46%. Cerebral oxygen uptake fell from 5*15 to 3-56 ml./100 g/min at this deeper level of halothane anaesthesia. Cerebral hyperaemia developed after hypotension in those animals which regained a mean blood pressure greater than 70 mmHg. Acidbase measurements on CSF from the cisterna magna revealed no metabolic acidosis during or after hypotension. In all four animals with intact autoregulation before hypotension, this was absent or impaired afterwards.

The Effect of Halothane Anaesthesia upon Cerebral Oxygen Consumption in the Rat

“…A comparable reduction in F* CMR,, of about 30% was subsequently reported in baboons subjected to profound halothane-induced hypotension ( KEANEY et al 1973). In these cases, comparison was made to values obtained in nitrous oxide anaesthesia (MCDOWALL 1967) or in light halothane anaesthesia (KEANEY et al 1973). , using a torcular outflow technique in the dog, found an average CMR,, reduction of 17% in light halothane anaesthesia, and no additional reduction was noted when the partial pressure of halothane in sagittal sinus blood was increased.…”

“…MCDOWALL (1967), using the method of LASSEN & INGVAR (1961) for measuring cerebral (cortical) blood flow (CBF), and the superior sagittal sinus (SSS) for sampling of cerebral venous blood, found that an inspired concentration of 0.5% halothane reduced CMR,, by 12% in dogs, whereas 2% halothane caused a 30% fall in metabolic rate. A comparable reduction in F* CMR,, of about 30% was subsequently reported in baboons subjected to profound halothane-induced hypotension ( KEANEY et al 1973). In these cases, comparison was made to values obtained in nitrous oxide anaesthesia (MCDOWALL 1967) or in light halothane anaesthesia (KEANEY et al 1973).…”

Vasodilator Drugs: Systemic and Regional Considerations

“…In conscious man however, using combination of trimetaphan and postural changes, Strandgaard et al found that the lower limit for autoregulation in their subjects was about 60 mm Hg mean arterial pressure, and this lower limit was shifted upwards in hypertensive subjects in proportion to the resting arterial pressure, reaching values of over 100 mm Hg.55 Another disturbing feature of loss of autoregulation is that this impairment may persist for some time after the return of arterial pressures to resting levels. 56 Recently, Turner et al studied changes in intracranial pressure (lCP) in neurosurgical patients in whom sodium nitroprusside was used to lower arterial pressure. 57 During the intravenous infusion of nitroprusside they found that ICP rose until mean arterial pressure was reduced to 70 per cent of resting level or less, when ICP began to fall.…”