Continuous measurement of jugular venous oxygen saturation in response to transient elevations of blood pressure in head-injured patients

Abstract

✓ Following traumatic brain injury, continuous jugular venous oxygen saturation (SjvO2) measurements have been made and used to assess cerebral oxygenation. Transients of SjvO2 may reflect cerebral blood flow (CBF) changes if measurements are made over a short period of time during which cerebral metabolic rate for oxygen is assumed unchanged. In response to alterations in perfusion pressure, transients of SjvO2 may indicate the extent to which autoregulation has been preserved after injury. The effect of arterial pressure changes on SjvO2 was measured in 14 severely head-injured patients (Glasgow Coma Scale score < 8) within 36 hours of injury. Mean arterial blood pressure (MABP), arterial oxygen saturation, and intracranial pressure (ICP) data were also continuously recorded by a computer at the patients' bedside. The reliability of the SjvO2 oximetry measurements varied among patients, and an average 38% of SjvO2 measurements were off by more than 6% saturation, necessitating recalibration. During periods of satisfactory catheter performance, 120 instances were found in which MABP was elevated more than 8 torr (mean ± standard deviation: 32 ± 13 torr) due to endotracheal suctioning. In 94 of these measurements, there was an associated increase in the ICP of 5 torr or more, averaging 16.6 ± 10.2 torr. The SjvO2 was 0.62 ± 0.10 before the increase in MABP and rose to a peak of 0.77 ± 0.10 during the maximum MABP elevation, suggesting increased CBF during the transient hypertension. In 34 of 37 instances of persistent blood pressure elevations lasting for more than 10 minutes (mean 16.0 ± 8.0 minutes), the SjvO2 elevation persisted (average duration 15.0 ± 12.4 minutes), suggesting impaired or lost autoregulatory vasoconstriction. The presence or absence of hyperemia was unrelated to the extent of the autoregulation response. Results indicate that SjvO2 rises with increasing perfusion pressure during and after endotracheal suctioning, suggesting a feeble or absent autoregulatory response following traumatic brain injury.