Cerebral blood flow and cerebral oxygen consumption during nitroprusside-induced hypotension to less than 50 mmHg.

The authors determined the effect of profound induced hypotension (i.e., mean arterial blood pressure less than 50 mmHg) during craniotomy for cerebral aneurysm on cerebral blood flow and cerebral metabolic rate for oxygen before, during, and after (20 min and 40 min after) the hypotensive period. The study was performed on nine adults (mean age, 29.2 yr) who were awake and conscious without peripheral neurologic deficits at the time of surgery. The study was conducted with the dura open with the use of a radial artery cannula, a 7-Fr thermodilution flow-directed pulmonary artery catheter, and an internal jugular vein catheter. The 133xenon intraarterial injection technique was used to determine regional cerebral blood flow (rCBF) in the nonoperated hemisphere. rCBF remained unchanged (from 22.8 +/- 4.1 ml.100 g-1.min-1 to 23.8 +/- 4.6 ml.100 g-1.min-1) during the hypotensive period (MAP from 87.8 +/- 10.4 mmHg to 40.0 +/- 4.4 mmHg; P less than 0.001) despite an increase in cardiac index since cerebral perfusion pressure and cerebrovascular resistance decreased to a similar degree. No gross cerebral metabolic disturbances were observed. A period of decreased cerebrovascular resistance and increased rCBF followed induced hypotension. rCBF increased from 23.8 +/- 4.6 ml.100 g-1.min-1 to 30.0 +/- 5.8 ml.100 g-1.min-1 (P less than 0.001) 20 min after sodium nitroprusside (SNP) was stopped without rebound hypertension. These modifications disappeared 20 min later. Reduction of mean arterial blood pressure to 40 mmHg by SNP was apparently safe for the brain, although the possibility of low perfused regions and local brain and cerebrospinal fluid lactoacidosis, particularly in the retracted hemisphere, cannot be excluded.