Partial Pressure Of Brain Tissue Oxygen Research Articles

Prone position in subarachnoid hemorrhage patients with acute respiratory distress syndrome: effects on cerebral tissue oxygenation and intracranial pressure.

To analyze the effect of prone position on cerebral perfusion pressure and brain tissue oxygen partial pressure in subarachnoid hemorrhage patients with acute respiratory distress syndrome (ARDS). Clinical study with retrospective data analysis. Neurosurgical intensive care unit of a primary level university hospital. Sixteen patients treated for intracranial aneurysm rupture with initial Hunt and Hess grade III or worse who developed ARDS within 2 wks after the bleeding. Routine neurosurgical intensive care treatment for subarachnoid hemorrhage and posthemorrhagic vasospasm including cerebral monitoring with continuous intracranial pressure and brain tissue oxygen partial pressure recordings. Hemodynamics, arterial oxygenation, ventilatory setting, intracranial pressure, cerebral perfusion pressure, and brain tissue oxygen partial pressure in the supine as well as in the prone position were analyzed and compared. A significant increase in Pao(2) from 97.3 +/- 20.7 torr (mean +/- sd) in the supine position to 126.6 +/- 31.7 torr in the prone position was joined by a significant increase in brain tissue oxygen partial pressure from 26.8 +/- 10.9 torr to 31.6 +/- 12.2 torr (both p <.0001), whereas intracranial pressure increased from 9.3 +/- 5.2 mm Hg to 14.8 +/- 6.7 mm Hg and cerebral perfusion pressure decreased from 73.0 +/- 10.5 mm Hg to 67.7 +/- 10.7 mm Hg (both p <.0001). The beneficial effect of prone positioning on cerebral tissue oxygenation by increasing arterial oxygenation appears to outweigh the expected adverse effect of prone positioning on cerebral tissue oxygenation by decreasing cerebral perfusion pressure in ARDS patients.

Cerebral Venous and Tissue Gases and Arteriovenous Shunting in the Dog

Cerebral venous blood gas values have been used to indicate brain tissue oxygenation. However, it is not clear how cerebral tissue and venous measures may vary under physiologic conditions caused by arteriovenous shunt. The purpose of this study was to measure brain tissue and local cerebral venous oxygen (PO2) and carbon dioxide (PCO2) partial pressure during changes in ventilation and to calculate shunt fraction. Eight dogs were anesthetized with isoflurane. After a craniotomy, a Neurotrend probe (Diametrics Inc., St. Paul, MN) that measures PO2, PCO2, pH, and temperature was inserted into brain tissue, and a small vein that drained the same tissue was catheterized. Arterial, cerebral venous, and brain tissue PO2 and PCO2 were measured during random changes in ventilation to produce five different levels of inspired oxygen (room air, 40%, 60%, 80%, 95%) at each of three different end-tidal PCO2 (20 mm Hg, 40 mm Hg, 60 mm Hg). Arteriovenous shunt was calculated from oxygen and CO2 content in artery, vein, and tissue, representing capillary. Tissue PCO2 was 8 mm Hg greater than vein PCO2 during hypocapnia and this difference increased to 20 mm Hg during hypercapnia. Vein PO2 was 8 mm Hg higher than tissue PO2 during hypocapnia, and this difference increased to 40 mm Hg during hypercapnia. Shunt fraction increased from 10%–20% during hypocapnia to 50%–60% during hypercapnia. These results show that brain vein and tissue PO2 and PCO2 differ because of arteriovenous shunting and this difference is increased as end-tidal PCO2 increases. Implications We found, in dogs, that the gradient between brain venous and tissue PO2 and PCO2 is increased with increased arterial PCO2. The divergence between tissue and venous gases can be described by arterial to venous shunting.

The Effects of Exogenous Epinephrine on a Convulsive Dose of Lidocaine: Relationship with Cerebral Circulation

In order to understand why exogenous epinephrine decreases the convulsive dose of lidocaine, the authors investigated cerebral circulation and plasma lidocaine concentrations in Wistar rats under general anesthesia. In the first experiment, baseline evaluations of each rat's electroencephalogram (EEG), mean arterial pressure (MAP), regional cerebral blood flow (r-CBF), cerebrospinal fluid (CSF) pressure, and cerebral perfusion pressure (CPP) were made. The rats were then assigned to one of three groups: Group L (n=6) received intravenous lidocaine (5 mg/kg/min); Group LE (n=6) received intravenous lidocaine (5 mg/kg/min) and epinephrine (2.5 kg/kg/min); and Group E (n=5) received intravenous epinephrine (2.5 microg/kg/min). Cumulative doses of lidocaine at the onset of EEG spike activity in Groups L and LE were compared. Blood-brain barrier (BBB) permeability was evaluated by observing extravasation of Evans blue (EB) dye. In the second experiment, additional rats were allocated to two treatment groups: Group L' (n=6) received intravenous lidocaine (5 mg/kg/min); Group LE' (n=6) received intravenous lidocaine (5 mg/kg/min) and epinephrine (2.5 microg/kg/min). Brain tissue oxygen partial pressure (PtO2) was monitored during infusion, and arterial and sagittal sinus blood samples were obtained immediately after the onset of EEG spike activity to determine plasma lidocaine concentration. The convulsive dose of lidocaine was significantly decreased when lidocaine was administered with epinephrine (Group L: 61.5+/-5.3 mg/kg (mean+/-SD); Group LE: 30.1+/-4.0 mg/kg) (p < 0.05), but there were no significant differences in plasma lidocaine concentration among these groups. R-CBF, CSF pressure, and CPP immediately before EEG spike activity were higher in Group LE than in Group L. Neither decreased PtO2 nor extravasation of EB was observed in rats treated with epinephrine and lidocaine, excluding cerebral ischemia and BBB breakdown from possible mechanisms by which epinephrine decreased the convulsive dose of lidocaine. None of the rats in Group E exhibited EEG findings suggestive of a preconvulsive state, ruling out a convulsive effect of epinephrine itself. The results suggest that an increase in lidocaine supply to the brain caused by increased CBF causes the low cumulative dose of lidocaine at the onset of convulsion in rats given lidocaine plus epinephrine.

Measuring Brain Tissue Oxygenation Compared with Jugular Venous Oxygen Saturation for Monitoring Cerebral Oxygenation After Traumatic Brain Injury

Jugular bulb oximetry is the most widely used method of monitoring cerebral oxygenation.More recently, measurement of brain tissue oxygenation has been reported in head-injured patients. We compared the changes in brain tissue oxygen partial pressure (PbO2) with changes in jugular venous oxygen saturation (SjVO2) in response to hyperventilation in areas of brain with and without focal pathology. Thirteen patients with severe head injuries were studied. A multiparameter sensor was inserted into areas of brain with focal pathology in five patients and outside areas of focal pathology in eight patients. A fiberoptic catheter was inserted into the right jugular bulb. Patients were hyperventilated in a stepwise manner from a PaCO2 of approximately 35 mm Hg to a PaCO2 of 22 mm Hg. There was no significant change in cerebral perfusion pressure or arterial partial pressure of oxygen with hyperventilation. In areas without focal pathology, there was a good correlation between changes in SjVO2 and PbO2 (Delta SjVO2 and Delta PbO2; r2 = 0.69, P < 0.0001). In areas with focal pathology, there was no correlation between Delta SjVO2 and Delta PbO2 (r2 = 0.07, P = 0.23). In this study, we demonstrated that measurement of local tissue oxygenation can highlight focal differences in regional cerebral oxygenation that are disguised when measuring SjVO2. Thus, monitoring of PbO2 is a useful addition to multimodal monitoring of patients with traumatic head injury. Implications: Brain oxygenation is currently monitored by using jugular bulb oximetry, which attracts a number of potential artifacts and may not reflect regional changes in oxygenation. We compared this method with measurement of brain tissue oxygenation using a multiparameter sensor inserted into brain tissue. The brain tissue monitor seemed to reflect regional brain oxygenation better than jugular bulb oximetry. (Anesth Analg 1999;88:549-53)

Clinical experience with 118 brain tissue oxygen partial pressure catheter probes.

We assessed the technical and diagnostic reliability of partial pressure of oxygen (PO2) of brain tissue (P(ti)O2) monitoring. The monitoring system and the catheter probes were tested in vitro, and clinical experiences obtained with 118 brain P(ti)O2 catheter probes, used in 101 patients, are reported. The polarographic (LICOX; Medical Systems Corp., Greenvale, NY) P(ti)O2 catheter probe lies 22 to 27 mm below the dura level; its PO2-sensitive surface is 7.1 mm2. For 10 patients, the adaptation time (with initially unreliable signals after insertion) was determined. For 27 patients, the probe was removed in a stepwise fashion (three increments of 5 mm) and the heterogeneity of brain P(ti)O2 levels was investigated. After removal of the catheter probes, their PO2 and zero display error values were determined and compared with probe performance data obtained in vitro with unused PO2 catheter probes. Small iatrogenic hematomas were observed for two patients (1.7%). No infection occurred after 6.7 +/- 3.9 days (mean +/- standard deviation) of monitoring. The technical complication (dislocation or defect) rate was 13.6%. The mean adaptation time was 79.0 +/- 51.7 min. A flow chart is presented, which helps to rule out artifacts. The mean P(ti)O2 measured at 22 to 27 mm below the dura was 23.8 +/- 8.1 mm Hg, at 17 to 22 mm was 25.7 +/- 8.3 mm Hg, at 12 to 17 mm was 33.0 +/- 13.3 mm Hg (P < 0.01, compared with the initial value), and at 7 to 12 mm was 33.3 +/- 13.3 mm Hg (P < 0.01). Recent catheter probe versions exhibited a PO2 display error of -1.2 +/- 5.1% (mean +/- standard deviation, n = 38) and a mean zero display error of 1.1 +/- 0.9 mm Hg (n = 34). The greatest PO2 display errors were measured during the first 4 days of continuous monitoring. In the in vitro test (of 12 unused catheter probes), the maximal probe display error was 1.07 +/- 2.14%, tested at temperatures between 22 degrees C and 37 degrees C and tested at oxygen pressures of 0, 44, and 150 mm Hg. In vitro, the zero display error was -0.21 +/- 0.25 mm Hg. Brain P(ti)O2 monitoring, reflecting an area 17 to 27 mm below the dura, is a safe and reliable technique for monitoring cerebral oxygenation. Excluding the first 1 hour after insertion, data are reliable, with almost 100% good data quality.