Cerebral electrical activity influences the effects of etomidate on cerebral perfusion pressure in traumatic coma.

The effects of 124 boluses of etomidate 0.2 mg kg-1 i.v. on intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) were studied in eight patients with severe head injury (Glasgow coma score less than 8). The data were divided into two groups based on the minimum voltage of the cerebral function monitor (CFM) recording before the bolus. In group A this was less than 5 microV (representing profound cortical electrical depression), while in group B the minimum voltage was greater than 5 microV. The mean decrease in ICP following etomidate was significantly greater in group B (mean +/- SEM: -8.6 +/- 0.7 mm Hg) than in group A (-3.8 +/- 0.6 mm Hg) (P less than 0.0001). The decrease in arterial pressure was similar in both groups. Consequently, there was a small mean increase in CPP in group B (2.2 +/- 0.9 mm Hg), whereas in group A CPP decreased (-4.7 +/- 1.5 mm Hg) (P less than 0.001). There was a strong correlation between the decreases in ICP and MAP in group A (r = 0.70, P less than 0.01), but not in group B (r = 0.05). Thus, when cortical electrical activity was already maximally suppressed, further administration of an i.v. anaesthetic agent produced only relatively small decreases in ICP, largely as a passive response to decreases in MAP. CPP was therefore usually reduced. Conversely, in the absence of such depression larger decreases in ICP, unrelated to hypotension, occurred and these were usually associated with increases in CPP. However, even under these circumstances, potentially dangerous decreases in CPP may be seen.