The cerebral arterio-venous oxygen content differences (AVDo2) during halothane and neurolept anaesthesia in patients subjected to craniotomy

In 20 patients subjected to craniotomy for supratentorial cerebral tumours, the haemodynamic changes during halothane and neurolept anaesthesia were evaluated by measuring mean arterial blood pressure (MABP) and cerebral arterio-venous oxygen content differences (AVDO2) repeatedly during the operation. Ten patients were given 0.5% halothane anaesthesia and ten patients neurolept anaesthesia. MABP, AVDO2 and PaCO2 were measured after induction of anaesthesia, before and after incision, after opening and closure of the dura, at the time of extubation and 1 h later. Concerning MABP and PaCO2, no significant difference between the two groups was found. In both groups an increase in MABP was observed after incision (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group) and in the neurolept group after extubation (P less than 0.01). In both groups a decrease in AVDO2 was observed after incision (P less than 0.01) and after extubation (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group). During the operation AVDO2 values were significantly higher in the neurolept group (P less than 0.05). The results indicate that even a moderate increase in MABP after incision during neuroanaesthesia affects AVDO2 values, suggesting an increase in cerebral blood flow. The study suggests that autoregulation of cerebral blood flow might be better preserved during neurolept anaesthesia. A state of hyperperfusion of the brain after extubation was unveiled in both groups.     

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2-reactivity during craniotomy for supratentorial cerebral tumours in halothane anaesthesia. A dose-response study

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anaesthesia was induced with thiopental 4-6 mg kg-1, fentanyl and pancuronium, and maintained with an inspiratory halothane concentration of 0.45% in nitrous oxide 67% at a moderate hypocapnic level. In one group of patients (n = 7) the inspiratory halothane concentration was maintained at 0.45% throughout anaesthesia. About 1 h after induction of anaesthesia CBF and CMRO2 averaged 35 +/- 2 ml 100 g-1 min-1 and 2.7 +/- 0.3 ml O2 100 g-1 min-1 (mean +/- s.c. mean), respectively. During repeat studies 1 h later CBF and CMRO2 did not change. In another group of patients (n = 7) an increase in halothane concentration from 0.45% to 0.90% was associated with a significant decrease in CMRO2 from 2.3 +/- 0.1 to 2.0 +/- 0.1 ml O2 100 g-1 min-1. The CO2-reactivity measured after the second flow measurement was preserved. It is concluded that halothane in this study induces a dose-dependent decrease in cerebral metabolism, an increase in CBF while CO2-reactivity is maintained.     

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2 reactivity during neurolept anaesthesia in patients subjected to craniotomy for supratentorial cerebral tumours

In 10 patients subjected to craniotomy for supratentorial cerebral tumours in neurolept anaesthesia, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice peroperatively by a modification of the Kety & Schmidt technique, using 133Xe. The relative CO2 reactivity was assessed indirectly as the % change of the arteriovenous oxygen difference (AVDO2) per mm change in PaCO2. The patients were premedicated with diazepam 10-15 mg perorally. For induction, thiopentone 4-6 mg/kg, droperidol 0.2 mg/kg and fentanyl 5 micrograms/kg were used, and for maintenance N2O 67% and fentanyl 4 micrograms/kg/h. During the first flow measurement the median and range of CBF was 30 ml/100 g/min (range 17-45), of AVDO2 8.0 vol % (range 4.1-9.5), and of CMRO2 2.28 ml O2/100 g/min (range 1.57-2.84). During the second CBF study, AVDO2 increased to 9.3 vol % (range 3.4-11) (P less than 0.05), and CMRO2 increased to 2.51 ml O2/100 g/min (range 1.88-3.00) P less than 0.05, while CBF was unchanged. The CO2 reactivity was present in all studies, median 1.8%/mmHg (range 0.5-15.1). The correlation coefficients between jugular venous oxygen tension/saturation, respectively, and CBF were high at tensions/saturations exceeding 4.0 kPa and 55%, indicating that hyperperfusion is easily unveiled by venous samples from the jugular vein during this anaesthesia.     

Per- and postoperative changes in the arterio-venous oxygen content difference (AVDO2) in patients subjected to craniotomy for cerebral tumours

Summary Sixteen patients with supratentorial cerebral tumours were subjected to craniotomy under thiopentone, fentanyl, nitrous oxide, halothane anaesthesia during moderate hypocapnia (PaCO₂ level 4.0 kPa). The arterio-venous oxygen content difference (AVDO₂) was measured peroperatively, and repeatedly during the first three hours after extubation.Peroperatively the level of AVDO₂ averaged 8.0 vol% during opening of the dura, and decreased to 7.0 vol% during closure of the dura (P<0.05). Immediately after extubation the AVDO₂ decreased to 4.3 vol% (P<0.05), and during the next 3 hours a gradual increase to 5.8 vol% (P<0.05) was disclosed. In individual cases the postoperative changes in AVDO₂ correlated fairly well with changes in mean arterial blood pressure (MABP), but other factors including duration of the operation, age of the patients, size of the tumour, level of PaCO₂ and adaptation to prolonged hyperventilation during operation are supposed to be responsible for the low levels of AVDO₂ observed in the postoperative period.     

The effect of metoprolol upon blood pressure, cerebral blood flow and oxygen consumption in patients subjected to craniotomy for cerebral tumours

Hypertension and cerebral hyperperfusion are often seen in the immediate postoperative period after craniotomy for supratentorial tumours. Metoprolol is known to attenuate the postoperative hypertensive response after hypotensive anaesthesia and this study was carried out to evaluate the effect of metoprolol on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRo₂) before extubation and cerebral arteriovenous oxygen content difference (AVDo₂), mean arterial blood pressure (MABP), Pao₂ and Paco₂ in a 180–min period after extubation. Twenty patients anaesthetized with thiopentone, fentanyl, nitrous oxide 67%, and halothane 0.5% were randomized to receive intravenous metoprolol or placebo at the end of the peroperative period. There were no significant differences in CBF– and CMRo₂ values between the two groups. In the period between closure of the dura and 5 min after extubation, an increase in MABP was observed in the control group ( P < 0.05), but not in the metoprolol group. During the same period a decrease in AVDo₂ was observed in both groups ( P < 0.05); during the next 10 min an increase was observed, but with no difference in AVDo₂ values between the groups. A higher level of Pao₂ in the metoprolol group was observed in the postoperative period. These findings suggest that peroperative treatment with metoprolol reduces postoperative MABP but does not influence the cerebral blood flow and metabolism.     

The effect of ketanserin upon postoperative blood pressure, cerebral blood flow and oxygen metabolism in patients subjected to craniotomy for cerebral tumours

Hypertension and cerebral hyperperfusion are often seen in the immediate postoperative period after craniotomy for supratentorial tunours. This study was performed to evaluate the effect of ketanserin, given at the end of the peroperative period, upon cerebral blood flow (CBF), and cerebral metabolic rate of oxygen (CMRO₂) before extubation. Mean arterial blood pressure (MABP), cerebral arterio-venous oxygen content difference (AVDO₂), PaO₂, and PaCO₂ were repeatedly measured during the operation, and 180 minutes after extubation. Ten patients were included in this study. The results were compared to those from a recent study in which ten patients served as control. All patients were anaesthetized with thiopentone, fentanyl, nitrous oxide 67%, halo-thane 0.5% anesthesia. Ten patients were given ketanserin 10–20 mg (mean 18,5 mg) before extubation. There was no significant difference in CBF- and CMRO₂ values between the two groups. During the period between closure of the dura and 5 minutes after extubation, an increase in MABP was observed in the control group ( P <0.05) but not in the ketanserin group. During the same period, a decrease in AVDO₂ was observed in both groups ( P <0.05) and during the next 10 minutes an increase was observed. However, no difference in AVDO₂ values between the two groups was found.
These findings suggest that peroperative treatment with ketanserin reduces postoperative hypertension without influencing the cerebral blood flow or metabolism.     

Changes in CMRO2, EEG and concentration of etomidate in serum and brain tissue during craniotomy with continuous etomidate supplemented with N2O and fentanyl

Fourteen patients with supratentorial cerebral tumours were anaesthetized with continuous etomidate infusion (30 or 60 μg kg^-1 min^-1) supplemented with N₂O 67% and fentanyl. Peroperatively cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMR_O2) were measured twice by the Kety and Schmidt method. Simultaneously with the CBF measurements, blood for serum etomidate was sampled and EEG was recorded in 2-min periods in 12 patients. In 10 patients a brain biopsy for etomidate was taken peroperatively and correlated with the other data. The results indicate a dose-dependant increase in scrum etomidate and brain tissue etomidate, a decrease in CMR_o2 and suppression of EEG activity. In individual studies an increase in serum etomidate or a decrease in CMR_o2 correlated to a suppression of the EEG activity, and vice versa . However, the wide variations in these relationships within and between patients make any conclusion regarding CMR_o2 impossible from the EEG recording, infusion rate of etomidate or scrum concentration of etomidate.     

Continuous conjunctival oxygen tension (Pcjo2) monitoring for assessment of cerebral oxygenation and metabolism during carotid artery surgery

The clinical value of noninvasive continuous monitoring of conjunctival oxygen tension for assessment of cerebral perfusion during carotid endarterectomy performed under general anaesthesia has been evaluated. The patients (n = 17; mean age 62.5 +/- 1.7 years) were monitored as follows: conjunctival oxygen tension (PcjO2); internal jugular venous oxygen tension at the skull base level (PcijvO2); arterial blood pressure; arterial and internal jugular venous blood gases; acid-base data and lactate, pyruvate levels; end-tidal CO2 concentration. The mean preanaesthetic PcjO2 level of 4.86 +/- 0.40 kPa was significantly lower than PaO2(PcjO2)/PaO2 ratio of 0.48). Following anaesthesia, a larger PcjO2-PaO2 gradient (ratio 0.32) was seen in spite of the hyperoxic situation (FiO2 = 0.40) due to vasoconstriction induced by slight hypocapnia (reduction of PaCO2 from 5.13 +/- 0.08 to 4.64 +/- 0.10 kPa). The carotid artery crossclamping resulted in a rapid and pronounced decrease of PcjO2, while PcijvO2 remained unchanged. No relationship between PcjO2 and stump pressure was found, while a significant correlation (P less than 0.02) between PcjO2 and lactate in effluent venous blood from the brain was demonstrable. It is concluded that PcjO2 monitoring seems a clinically useful trend indicator of cerebral perfusion in the individual patient. Due to large interindividual variations in basal PcjO2 readings and in PcjO2 changes during carotid artery clamping, however, transconjunctival oxygen tension monitoring does not seem to allow early and accurate recognition of impending cerebral ischaemia during carotid endarterectomy, and its routine use therefore seems of limited value.     

Brain tissue PO2, PCO2, and pH during cerebral vasospasm

BACKGROUND

The purpose of the present study was to assess brain tissue monitoring for detection of ischemia due to vasospasm in aneurysmal subarachnoid hemorrhage (SAH) patients.

METHODS

After obtaining informed consent, a burr hole was made in 10 patients and a Neurotrend 7 probe was inserted ipsilateral to the region of SAH. In eight patients the probe was inserted during surgery for clipping the aneurysm and in two patients the probe was inserted in the neurosurgery ICU. Brain tissue gases and pH were collected over 6-hour periods for 7 to 10 days until the termination of monitoring. The onset of vasospasm was confirmed by angiography and xenon computed tomography (Xe/CT) cerebral blood flow studies.

RESULTS

Seven patients did not develop vasospasm during monitoring and were considered as controls. In this group, brain tissue oxygen pressure (PO₂) remained above 20 mmHg, carbon dioxide pressure (PCO₂) stabilized at 40 mmHg and pH remained between 7.1 and 7.2. In three patients who developed vasospasm during monitoring, PO₂ was not different from the control group. However, PCO₂ increased to 60 mmHg and pH decreased to 6.7 (p < 0.001).

CONCLUSION

In this study, patients with SAH who developed vasospasm had significantly lower brain tissue pH and higher PCO₂ compared to controls. However, there was no significant change in PO₂ levels associated with vasospasm. Brain tissue monitoring can provide an indication of ischemia during vasospasm.     

Effects of sevoflurane on intracranial pressure, cerebral blood flow and cerebral metabolism: A dose-response study in patients subjected to craniotomy for cerebral tumours

Background: Studies concerning the cerebrovascular effects of sevoflurane in patients with space-occupying lesions are few. This study was carried out as a dose-response study comparing the effects of increasing sevoflurane concentration (1.5% (0.7 MAC) to 2.5% (1.3 MAC)) on cerebral blood flow (CBF), intracranial pressure (ICP), cerebrovascular resistance (CVR), metabolic rate of oxygen (CMRO₂) and CO₂-reactivity in patients subjected to craniotomy for supratentorial brain tumours.
Methods: Anaesthesia was induced with propofol/fentanyl/atracurium and maintained with 1.5% sevoflurane in air/oxygen at normocapnia. Blood pressure was maintained constant by ephedrine. In group 1 (n=10), the patients received continuously 1.5% sevoflurane. Subdural ICP, CBF and CMRO₂ were measured twice at 30-min intervals. In group 2 (n=10), sevoflurane concentration was increased from 1.5% to 2.5% after CBF₁. CBF₂ was measured after 20 min during 2.5% sevoflurane. Finally, CO₂-reactivity was studied in both groups.
Results: In group 1, no time-dependent alterations in CBF, CVR, ICP and CMRO₂ were found. In group 2, an increase in sevoflurane from 1.5% to 2.5% resulted in an increase in CBF from 29 ± 10 to 34±12 ml 100g⁻¹ min⁻¹ and a decrease in CVR from 2.7±0.9 to 2.3±1.2 mmHg ml⁻¹ min 100g ( P <0.05), while ICP and CMRO₂ were unchanged. CO₂-reactivity was maintained at 1.5% and 2.5% sevoflurane.
Conclusion: Sevoflurane is a cerebral vasodilator in patients with cerebral tumours. Sevoflurane increases CBF and decreases CVR in a dose-dependent manner. CO₂-reactivity is preserved during 1.5% and 2.5% sevoflurane.     

Effects of increases in the inspired oxygen fraction on brain surface oxygen pressure fields in pig and man

In six patients undergoing neurosurgical operation, brain surface oxygen pressure was studied during an increase of the inspired oxygen fraction (FiO2). The eight-channel oxygen surface electrode (MDO-electrode) was placed directly on the brain cortex. FiO2 was increased to four levels, from baseline level 0.21 to 0.3, 0.5, 0.7 and 1.0, respectively. During these four stages and FiO2 0.21, brain surface oxygen pressure (PtO2) was measured. The physiological variables such as blood pressure, PaCO2, pH and temperature were stable throughout the study. The results are presented as mean values +/- s.d. and a PtO2 histogram for each FiO2-level. Already at an FiO2 of 0.3 (at a PaO2 of 16.3 +/- 3.4 kPa) scattered histograms were seen in five of six patients. A scattered histogram indicates disturbed microcirculation. At the FiO2 levels of 0.5, 0.7 and 1.0, all histograms were scattered. The PtO2 values did not increase proportionally to PaO2 at FiO2 levels 0.3, 0.5 or 0.7. But at FiO2 1.0 four patients had normal mean PtO2 values and two patients very high mean PtO2 values. It is possible that the four patients with normal PtO2 values succeeded in regulating the cerebral microcirculation as a response to the high FiO2 leading to a high PaO2 (60.1 +/- 6.4 kPa). The same study was initially done on six pigs in which the regional cerebral blood flow (rCBF) was also measured. MDO-electrode measurements at different FiO2-levels gave the same results as in the patients. rCBF decreased when FiO2 was increased.     

Correlation of continuously monitored regional cerebral blood flow and brain tissue oxygen

Summary Background. The purpose of this study was to investigate the relationship between continuously monitored regional cerebral blood flow (CBF) and brain tissue oxygen (P_tiO₂).Methods. Continuous advanced multimodal neuromonitoring including monitoring of P_tiO₂ (Licox, GMS) and CBF (QFlow, Hemedex) was performed in eight patients after severe subarachnoid haemorrhage (n=5) and traumatic brain injury (n=3) for an average of 9.6 days. Parameters were measured using a flexible polarographic P_tiO₂-probe and a thermal diffusion CBF-microprobe.Findings. Regarding the whole monitoring period in all patients, the data indicated a significant correlation between CBF and P_tiO₂ (r=0.36). In 72% of 400 analysed intervals of 30 minutes duration with P_tiO₂ changes larger than 5mmHg, a strong correlation between CBF and P_tiO₂ existed (r>0.6). In 19% of intervals a still statistically significant correlation was observed (0.3<r<0.6). During the remaining 9% no correlation was found (r<0.3). Regarding the clinical stability of the monitoring devices, the CBF monitoring system allowed monitoring of CBF in 64% of the time when P_tiO₂ monitoring was possible only. Phases of non-monitoring were mostly due to fever of the patient, when the system does not allow monitoring to avoid overheating of the cerebral tissue.Conclusions. This study suggests a correlation between CBF and P_tiO₂. The level of P_tiO₂ seems to be predominately determined by regional CBF, since changes in P_tiO₂ were correlated in 90% of episodes to simultaneous changes of CBF.     

The effects of midazolam on cerebral blood flow and oxygen consumption Interaction with nitrous oxide in patients undergoing craniotomy for supratentorial cerebral tumours

Cerebral blood flow and the cerebral metabolic rate of oxygen were measured in 30 patients during craniotomy for supratentorial cerebral tumours by a modification of the Kety-Schmidt technique using Xenon 133 intravenously. Anaesthesia was induced with midazolam 0.3 mg/kg, fentanyl and pancuronium, and maintained with midazolam as a continuous infusion, fentanyl, pancuronium and nitrous oxide in oxygen or oxygen in air. The concentration of midazolam in the blood of 10 patients was about 300 ng/litre during two measurements; the patients' lungs were ventilated with N2O in oxygen. The concentration of midazolam in the blood of another 10 patients was doubled to about 600 ng/litre during the second flow measurement; the patients' lungs were ventilated with N2O/O2. The concentration of midazolam in the blood of the third group of 10 patients was doubled to 600 ng/litre during the second flow measurement; the patients' lungs were ventilated with oxygen in air. No relationship was found between the dose of midazolam and cerebral blood flow or oxygen consumption. Nitrous oxide in combination with midazolam also had no effect on these variables.     

Effects of iso- and hypervolemic hemodilution on regional cerebral blood flow and oxygen delivery for patients with vasospasm after aneurysmal subarachnoid hemorrhage

Summary. Summary.   Background: Arterial vasospasm after subarachnoid hemorrhage may cause cerebral ischemia. Treatment with hemodilution, reducing blood viscosity, and hypervolemia, increasing cardiac performance and distending the vasospastic artery, are clinically established methods to improve blood flow through the vasospastic arterial bed.   Method: Eight patients with transcranial Doppler verified vasospasm after subarachnoid hemorrhage were investigated with global (two-dimensional ¹³³Xenon) and regional (three-dimensional ^{99 m}Tc-HMPAO) cerebral blood flow (CBF) measurements, before and after 1/iso- and 2/hypervolemic hemodilution. Hematocrit was reduced to 0.28 from 0.36. Hypervolemia was achieved by increasing blood volume by 1100 ml.   Findings: Isovolemic hemodilution increased global cerebral blood flow from 52.25±10.12 to 58.56±11.73 ml * 100 g⁻¹ * min⁻¹ (p<0.05), but after hypervolemic hemodilution CBF returned to 51.38±11.34 ml * 100 g⁻¹ * min⁻¹. Global cerebral delivery rate of oxygen (CDRO₂) decreased from 7.94±1.92 to 6.98±1.66 ml * 100 g⁻¹ * min⁻¹ (p<0.001) during isovolemic hemodilution and remained reduced, 6.77±1.60 ml * 100 g⁻¹ * min⁻¹ (p<0.001), after the hypervolemic hemodilution. As a test of the hemodilution effect on regional CDRO₂ an ischemic threshold was defined as the maximal amount of oxygen transported by a CBF of 10 ml * 100 g⁻¹ * min⁻¹ at a Hb 140 g/l which corresponds to a CDRO₂ of 1.83 ml * 100 g⁻¹ * min⁻¹. The brain volume with a CDRO₂ exceeding the ichemic threshold was 1300±236 ml before intervention. After isovolemic hemodilution the non-ischemic brain volume was reduced to 1206±341 (p<0,003). After hypervolemic hemodilution the non-ischemic brain volume remained reduced at 1228±347 ml (p<0.05).   Interpretation: The present study of controlled isovolemic hemodilution demonstrated increased global CBF, but there was a pronounced reduction in oxygen delivery capacity. Both CBF and CDRO₂ remained decreased during further hypervolemic hemodilution. We conclude that hemodilution to hematocrit 0.28 is not beneficial for patients with cerebral vasospasm after SAH. Published online July 18, 2002     

The acute effect of nimodipine on cerebral blood flow,its CO2 reactivity,and cerebral oxygen metabolism in human volunteers

Summary The present study was undertaken in 8 healthy volunteers to examine the effect of a clinically relevant dose of nimodipine (NIM) (15 and 30 microgram/kg/h) on CBF, its CO₂ reactivity, and CMRO₂. Mean arterial blood pressure (MABP) was measured intra-arterially. Regional CBF was measured by SPECT of inhaled Xenon-133. During the CO₂ reactivity tests changes in CBF were estimated by the arterio-venous-oxygen-difference method. Median CBF was 52 ml/ 100 g/min (48–53) with a normal regional distribution, and median baseline MABP was 96 mmHg (92–99). MABP was slightly reduced, by 8 mmHg (7–9), and 9 mmHg (4–11) after infusion of NIM for 2 and 4 hours, respectively. CBF, however, remained constant, although correction for changes in PaCO₂, revealed a slight increase after 4 hours (p=0.08). CMRO2 was 3.5 ml/100 g/min (3.2–3.5) and was not changed by the infusion of NIM. At arterial CO₂ tensions ranging from 4.0 to 6.5 Kpa the CO₂ reactivity was 3.0% CBF/ 0.1 kPa (2.6–3.7) and decreased significantly to 2.6% CBF/0.1 kPa (1.8–3.2) after the infusion of NIM for 3 hours (p=0.02). The median slope of the LnCBFsat/PaCO₂ relationship was 1.5 at baseline compared to 1.3 after NIM (p<0.01). No side effects were observed.The present study shows a decreased CO₂ of the cerebral vessels and a maintained coupling of CBF and CMRO₂ during the infusion of nimodipine.     

Brain energy metabolism and blood flow during sevoflurane and halo thane anesthesia: effects of hypocapnia and blood pressure fluctuations

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood How (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (³¹P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a Paco₂ of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a Paco₂ of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50%) of the control value when Paco₂ was ≤2.7 kPa with 2 MAC of sevoflurane and ≤4.0 kPa with 2 MAC of halothane. Abnormal brian energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnie) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a Paco₂ of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane. The hypocapnia-induced abnormality during exposure to 2 MAC of either agent was due to decreased CBF associated with low perfusion pressure, indicating that there was no direct effect of these anesthetics on cerebral energy metabolism.     

CBF and CMRO2 during Continuous Etomidate Infusion Supplemented with N2O and Fentanyl in Patients with Supratentorial Cerebral Tumour. A Dose-Response Study

In 14 patients with supratentorial cerebral tumours with midline shift below 10 mm, CBF and CMRO2 were measured (Kety & Schmidt) during craniotomy. The anaesthesia was continuous etomidate infusion supplemented with nitrous oxide and fentanyl. The patients were divided into two groups. In Group 1 etomidate infusion of 30 micrograms kg-1 min-1 was used throughout the anaesthesia, and CBF and CMRO2 were measured twice. In this group CMRO2 (means +/- s.d.) averaged 2.31 +/- 0.43 ml O2 100 g-1 min-1 70 min after induction and 2.21 +/- 0.38 ml O2 100 g-1 min-1 130 min after induction. In Group 2 the etomidate infusion was increased from 30 to 60 micrograms kg-1 min-1 after the first study and a significant fall in CMRO2 from 2.52 +/- 0.56 to 1.76 +/- 0.40 ml O2 100 g-1 min-1 was found. Simultaneously, a significant fall in CBF was observed. The CO2 reactivity was preserved during anaesthesia.     

Measurement of transcutaneous P±o2, Pco2 and skin blood flow at different probe temperatures using mass spectrometry

Transcutaneously measured partial pressures of oxygen and carbon dioxide (PtcO2, PtcCO2) approximate the corresponding arterial values at a probe temperature of 44 degrees C. The temperature-dependent increase of PtcO2 and PtcCO2 is caused by an increased skin perfusion, a decrease in the mean diffusion path, a change of skin metabolism, a decrease of tissue solubility of oxygen and carbon dioxide and a right shift of the oxygen and carbon dioxide binding curves of blood. Seven healthy volunteer test subjects participated in the study. A transcutaneous probe connected to a mass spectrometer was placed on the earlobe of the test subject. Four measurements of the transcutaneous PO2, PCO2 and skin blood flow (from the washout kinetics of argon) were determined on each test subject. The first measurement was made with a transcutaneous probe temperature of 37 degrees C. The probe temperature was then increased to 44 degrees C before the next determination. Finally, two determinations were made at 37 degrees C, separated by a time interval of 1 h. The PtcO2 and skin blood flow increased when the probe temperature increased from 37 degrees C to 44 degrees C. However, when the probe temperature was decreased again from 44 degrees C to 37 degrees C, the estimated skin blood flow returned to the initial value while the PtcO2 remained unchanged. It required a further 1 h before the PtcO2 returned to the initial value at 37 degrees C. The most likely explanation of the experimental results is that heating of the skin to 44 degrees C causes a reversible decrease in the skin metabolism.     

A positron emission tomography study of cerebral blood flow and oxygen metabolism in healthy male volunteers anaesthetized with eltanolone

Background: The effects of eltanolone anaesthesia in humans on regional cerebral blood flow, regional cerebral metabolic rate of oxygen and oxygen extraction ratio were to be evaluated using positron emission tomography (PET).
Methods: Six healthy male volunteers were studied. Series of PET-measurements with ¹⁵O and H₂¹⁵O were carried out in the awake state (baseline) (n=6), during eltanolone anaesthesia (n= 5) and during early recovery (n=5), when the subjects were oriented with respect to person, place and time. Eltanolone was given as a programmed infusion.
Results: Cerebral blood flow (rCBF) was reduced in almost all cortex regions studied by 31216% (meanSD, P < 0.01). During recovery KBF increased to 10926% of pre-anaesthetic baseline levels ( P < 0.01). Eltanolone in the doses administered lowered oxygen metabolism (rCMRO₂) by 528% ( P < 0.01) in cortex regions. During recovery rCMRO₂ increased to 9013% of baseline ( P < 0.01). The oxygen extraction (OER) in cortical regions decreased by 32223% ( P < 0.01) during anaesthesia and returned to 82210% of baseline ( P < 0.01) during recovery. Less reduction in cortical blood flow during eltanolone anaesthesia was seen in the uncus ( P < 0.01), though no differences in the depression of oxygen metabolism were seen. Oxygen extraction remained homogeneous throughout the brain.
Conclusion: Eltanolone anaesthesia was shown to reduce cerebral oxygen metabolism and cerebral blood flow in healthy volunteers. There were no signs of ischaemic effects.     

Improvement of cerebral blood flow and/or CO2 reactivity after superficial temporal artery-middle cerebral artery bypass in patients with transient ischemic attacks and watershed-zone infarctions

The effect of extracranial-intracranial bypass anastomosis on cerebral blood flow and CO₂ reactivity during hypocapnia was investigated in ten patients with transient ischemic attacks or watershed infarctions due to carotid occlusive diseases. Six patients had occlusion and four had stenosis (>50%) of the internal carotid artery. Those with infarctions had increased cerebral blood flow and CO₂ reactivity postoperatively, and improved clinically. Those with transient ischemic attacks due to stenosis (>50%) of the internal carotid artery had increased CO₂ reactivity postoperatively but constant normal regional blood flow. Cerebral blood flow improved in those with poorer flow, CO₂ reactivity increased in those with better reactivity, and better CO₂ reactivity preoperatively brought about a greater flow increase. The pre- and postoperative evaluation of cerebral blood flow and CO₂ reactivity is believed to be useful in evaluating the effectiveness of bypass anastomosis. Preoperative evaluation might be informative in selecting candidates for bypass.