This study shows that there is a 60% increase in Vmca above the awake value at extubation. This increase in Vmca did not depend on the anesthetic technique (IV or inhaled) and lasted 30 to 60 minutes after extubation. Vmca changes reflect changes in cerebral blood flow (CBF) if the angle of insonation between the probe and the vessel, and the vessel diameter, remain constant. Although the probe was hand-held, the two operators performing TCD measurements had more than five years’ experience with TCD and tried to limit as much as possible the variations in the angle of insonation. For a change in the angle of insonation from 0 to 10 degrees, the error in Vmca is 2%. For the MCA, the intraobserver variability for repeat measurements is <10%(5). This is far less than the magnitude of the changes measured in this study, and small changes in the angle of insonation would not significantly alter the results. The diameter of the MCA is not significantly affected by changes in blood pressure (6,7), Paco2(7,8), or moderate hemodilution (9–11). The validity of TCD as an index of changes in CBF is supported by a good correlation between Vmca and 133Xe-clearance CBF measurements of CO2 reactivity (12). However, the effect of sympathetic stimulation on human MCA diameter is still controversial. By using indirect measurements of MCA diameter, Pott et al. (13) found that sympathetic activation had no effect, whereas Giller et al. (14) estimated a 10% decrease in diameter. A simulated orthostatic stress induced by lower-body negative pressure did not change MCA diameter measured by magnetic resonance imaging (8). Thus, vasoconstriction of the MCA cannot be excluded in this study, but available data do not support this hypothesis as a main mechanism to explain our results.
Hemodilution increases Vmca. There was a 5% decrease in the hematocrit value during the operation in the 30 patients. There was a 2% change in Vmca for each 1% decrease in the hematocrit value (21). Thus, hemodilution was responsible for a 10% increase in Vmca. With hemodilution, CBF increases to maintain a constant oxygen delivery to the brain when the arterial oxygen content decreases. The balance between oxygen supply and demand is unchanged, and moderate hemodilution cannot explain changes in Sjvo2.
Impaired cerebral autoregulation caused by a residual effect of anesthetics is also unlikely to explain the results. There was no difference between patients anesthetized with isoflurane or propofol. With propofol doses used for clinical care, cerebral pressure autoregulation and CO2 reactivity remain intact (22). Furthermore, there was not any correlation between MAP and Vmca during recovery at any time. But CBF autoregulation is not an instantaneous process during blood pressure changes. It is possible that transient increases in MAP could induce transient increase in CBF and Vmca. Rapid increases in blood pressure may occur before extubation but are less likely to occur in neurosurgical patients after extubation, when the painful stimulus caused by the presence of the tracheal tube has been removed.
Hypercapnia or return to normocapnia after prolonged hyperventilation during anesthesia may increase Vmca. Compared with the preoperative value, the postoperative increase in Paco2 was not statistically significant. Furthermore, there was no correlation between Paco2 and Vmca at any time. Although Paco2 changes were not significant, the patients were mildly hyperventilated during anesthesia. Over a few hours, CBF adapts to the imposition of hyperventilation and returns to normal. With termination of hyperventilation, CBF increases above the control level measured before hyperventilation (23). In this study, Paco2 increased from 33 ± 3 mm Hg to 40 ± 5 mm Hg five minutes after extubation. Several investigators have reported Vmca changes from 2.5% to 4% per mm Hg change of Paco2(24). Assuming a 3% change in Vmca per mm Hg Paco2 in our patients, there would be a mean 21% increase in Vmca caused by relative hypercapnia. This value would be less in case of incomplete adaptation of CBF to hypocapnia during anesthesia.
Clinically, postoperative cerebral hyperemia may lead to adverse cerebral outcome. It may promote vasogenic edema, which may cause intracranial hypertension. In a retrospective study in 514 neurosurgical patients whose intracranial pressure was monitored after elective intracranial surgery, 89 had a sustained postoperative increase in intracranial pressure (32). Cerebral hyperperfusion may also lead to cerebral hemorrhage (33,34). There is an association between intraoperative or early postoperative systemic hypertension and the risk of intracranial hemorrhage (4). Although a causal relation could not be established, systemic hypertension was a plausible cause of intracranial hemorrhage. In our study, cerebral hyperperfusion was observed without a significant change in MAP. The incidence of systemic hypertension after neurosurgery is >50%(3,4). It is likely that severe hypertension occurring during extubation would aggravate this hyperperfusion state.
In conclusion, we found that Vmca increased 60% above the preoperative value at extubation. Sjvo2 measurements indicated cerebral hyperemia. Vmca then gradually returned toward the baseline value but remained significantly increased until 30 to 60 minutes after extubation. These changes in the cerebral circulation were not related to the anesthetic technique or to changes in MAP or Paco2. Cerebral hyperemia could be the result of CBF adaptation to hypocapnia during anesthesia, incomplete cerebral autoregulatory adaptation to transient changes in MAP, or stress-related changes in CBF. Further studies are needed to test these hypotheses.
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