KETAMINE DOES NOT INCREASE CEREBRAL BLOOD-FLOW VELOCITY OR INTRACRANIAL-PRESSURE DURING ISOFLURANE NITROUS-OXIDE ANESTHESIA IN PATIENTS UNDERGOING CRANIOTOMY

Ketamine's effect on cerebral hemodynamics is controversial. We hypothesized that ketamine would not increase intracranial pressure (ICP) and cerebral blood flow (CBF) velocity in anesthetized, ventilated patients. Twenty patients requiring craniotomy for brain tumor or cerebral aneurysm were studied. After induction with thiopental, anesthesia was maintained with isoflurane and nitrous oxide in oxygen. During controlled ventilation (Pace(2) 34 +/- 1 mm Hg); middle cerebral artery blood flow velocity (V-MCA), mean arterial blood pressure (MAP), bilateral frontooccipital processed electroencephalogram (EEG), and ICP were measured before and for 10 min after intravenous ketamine 1.0 mg/kg. Cerebral arteriovenous oxygen content difference (AVDo(2)) and cerebral perfusion pressure (CPP) were calculated. After ketamine, MAP, CPP, Pace(2), and AVDo(2) were unchanged. ICP decreased from 16 +/- 1 mm Hg to 14 +/- 1 mm Hg (mean +/- SE; P < 0.001) and V-MCA decreased from 44 +/- 4 cm/s to 39 +/- 4 cm/s (P < 0.001). Total EEG power decreased (P < 0.02). These results suggest that ketamine can be used in anesthetized, mechanically ventilated patients with mildly increased ICP without adversely altering cerebral hemodynamics.