Effect of hyperventilation, mannitol, and ventriculostomy drainage on cerebral blood flow after head injury.

Therapies to lower intracranial pressure (ICP) after traumatic brain injury (TBI) include hyperventilation (HV), intravenous mannitol (IM), and cerebrospinal fluid drainage from a ventriculostomy (DV). To determine the effects of these therapies on cerebral blood flow (CBF), fiberoptic oximetry was used to measure jugular venous O2 saturation (SjvO2) as an index of the CBF to cerebral metabolic rate for O2 (CMRO2) ratio after IM (25 g IV for more than 5 min), DV (3 min), or HV (increase respiratory rate by 4) therapy for elevated ICP. Assuming CMRO2 is constant, changes in SjvO2 reflect changes in CBF. Continuous measurements of SjvO2, ICP, blood pressure, arterial O2 saturation, and end-tidal CO2 were obtained in 22 patients with a Glasgow Coma Scale score of 5.3 +/- 0.4 (mean +/- SD) in the first 5 days after TBI. Therapy was initiated a total of 196 times when ICP was > 15 mm Hg for > 5 minutes, and measurements made at 20 minutes after treatment were compared with those made just before. After DV, ICP fell in 90% of the observations by 8.6 +/- 0.7 mm Hg (mean +/- SEM, n = 119); after IM, ICP fell in 90% of the observations by 7.4 +/- 0.7 mm Hg (n = 43); and after HV, ICP fell in 88% of the observations by 6.3 +/- 1.2 mm Hg (n = 14). In patients where ICP fell, SjvO2 increased by 2.49 +/- 0.7% saturation (from 68.0 +/- 1.3%) with IM, but only by 0.39 +/- 0.4% saturation (from 67.2 +/- 0.9%) with DV.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral blood flow and blood volume in response to O2 and CO2 changes in normal humans.

Changes in cerebral blood volume (CBV) after head injury may be an important determinant of intracranial pressure (ICP). To determine the normal response of CBV to hypoxemia, hypercapnia, and hypocapnia, eight normal subjects (5 males and 3 females; ages 25 to 43) were studied under these conditions. Cerebral blood volume was measured using an external collimated gamma detector to determine 99m-Tc-labeled red blood cell (RBC) activity in the intracranial vascular pool, and cerebral blood flow (CBF) was determined by internal carotid artery duplex scanning. Hypocapnia (Paco2 = 26.0 +/- 1.7 mm Hg, mean +/- SE) was achieved by hyperventilation, hypercapnia (Paco2 = 47.8 +/- 1.5 mm Hg) was achieved by inhalation of 6% CO2, and hypoxemia (Pao2 = 38.1 +/- 1.1 mm Hg, O2 saturation = 76.7 +/- 2.0%) was achieved by inhalation of 10% O2. Changes in CBF and CBV were determined by comparing the values in each condition to the immediately preceding period of normoxia and normocapnia. For conditions of hypocapnia, hypercapnia, and hypoxemia, the percentage of change in CBV was: -7.2 +/- 0.01, 12.8 +/- 0.01, and 5.2 +/- 0.03, respectively. The simultaneous percentage of change in CBF for the same conditions was -30.7 +/- 4.0, 29.5 +/- 9.2, and 18.4 +/- 6.9, respectively. For all conditions, changes in CBF were greater than changes in CBV; however, this was most pronounced during hypocapnia induced by hyperventilation. Because the change in CBV reflects the potential change in ICP in response to treatment, therapeutic hyperventilation may impair CBF to a greater degree than it reduces ICP.(ABSTRACT TRUNCATED AT 250 WORDS)