Cerebral circulatory and metabolic effects of hypotension produced by deep halothane anaesthesia

Abstract

SUMMARY 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.Controlled hypotension is used to diminish bleeding and to facilitate surgery. There is, however, a considerable disagreement about the safety of the technique; for example, Mayrhofer (1971) has written that: 'Induced hypotension, using ganglion-blocking drugs, should have been abandoned long ago as it is an unsafe and potentially dangerous technique', while Enderby (1972) has replied: 'We are today using this technique routinely and, moreover, have been doing so for more than 20 years'. When such divergent opinions are expressed, further investigation is indicated, and the present study was designed to elucidate the effect of controlled hypotension on cerebral blood flow, cerebral metabolism, and acid-base balance. Since it has been suggested (Nilsson and Siesjo, 1971) that hypotension with deep halothane anaesthesia may be safer than with other methods, because of the associated reduction in cerebral oxygen demand, it was decided to produce hypotension by this means in experimental animals. METHODSEleven baboons were premedicated with phencyclidine (0-8-1-0 mg/kg) and anaesthesia was induced and maintained with halothane, nitrous oxide, and 898 oxygen. After intramuscular injection of suxamethonium (50 mg) an endotracheal tube was inserted and the animals were artificially ventilated by a Palmer pump. Muscle relaxation was maintained by injecting pancuronium (I mg) intramuscularly at half-hourly intervals. End-tidal CO2 was monitored by an infrared gas analyser and ventilation was adjusted to maintain normocapnia. Endtidal halothane was measured intermittently by an ultraviolet halothane meter. The inspired oxygen was adjusted so that PaO2 remained above 100 mmHg. The temperature of the animal was kept at 370 C by automatically controlled heating lamps.Not all measurements were made on all animals and the animals were divided into three experimental groups as indicated in Table 1

Changes in CO2 responsiveness and in autoregulation of the cerebral circulation during and after halothane-induced hypotension.

“…Thus, in the two animals subjected to the most severe reduction in cerebral perfusion pressure (Expts 134 and 136) there was a total loss of autoregulation after hypotension, whereas in the animals subjected to lesser BP reduction (Expts 138 and 140) there was little change in autoregulation index. Furthermore, when these results are viewed together with those reported by Keaney et al (1973) it becomes clear that the critical cerebral perfusion pressure below which loss of autoregulation occurs in the post-hypotensive period lies between 30 and 40 mmHg. These results emphasize the value of a quantitative index of autoregulatory ability, rather than the use of a simple present or absent schema.…”

“…Changes in cerebrovascular control mechanisms during hypotension, such as have been demonstrated here, are usually ascribed to maximum vascular dilatation, produced either by the low intravascular pressure ('Bayliss' effect) or by tissue acidosis ('metabolic' effect); the latter mechanism appears very unlikely in view of our earlier finding (Keaney et al, 1973) that even more extreme halothane-induced hypotension produces no CSF acidosis over a two hour period. The tissue metabolite measurements of Eklof et al (1972) also support this conclusion.…”

“…After hypotension, the autoregulation index varied between -14 and + 700/, with a mean value of 30°4, whereas in the study of Keaney et al (1973) the mean value was 13%. The greater disturbance of autoregulation in the earlier study can be ascribed to the more severe hypotension employed-that is, mean BP 33 mmHg as compared with 44 mmHg in the present study.…”

Effects of decreasing arterial blood pressure on cerebral blood flow in the baboon. Influence of the sympathetic nervous system.

“…The probable reason for the observed increase in blood flow at normal blood pressures following hypotension and retransfusion is the cerebral hypoxia accompanying the first arterial blood pressure reduction. This posthypotensive loss of the usual pressure-flow relationship (and cerebral hyperemia at normotension) has been noted in both dogs (31) and primates (32), although in the primate study the duration of the hypotensive episode was more extreme. Other studies have confirmed this posthypoxic loss of the pressureflow relationship, which may persist for several hours following the insult in both stagnant and hypoxic hypoxia (33, 34).…”

Autoregulation of Cerebral Blood Flow in Experimental Focal Brain Ischemia

“…Halothane is a potent vasodilator that increases CBF in anesthetic concentrations in normal (Keaney et al, 1973;Anderson et al, 1980) as well as in ischemic (Smith et al, 1973) brain tissue. Morita et al (1977) demonstrated intact autoregula tion during 0.5% halothane anesthesia, which is in accordance with our results.…”