Jugular Bulb Venous Oxygen Saturation Monitoring in Brain Surgery / 대한마취과학회지

BACKGROUND: During intracranial brain surgery, numerous factors may alter cerebral blood flow and the oxygen supply-demend balance. Continuous monitoring of the jugular bulb venous oxygen saturation (SjvO2) may help in the anesthetic management of such procedures. METHODS: Fiberoptic SjvO2 was continuously monitored and recorded 1, 3 and 5 min after the skin incision, skull bone craniotomy, dura open and dura closure in 20 patients. RESULTS: The SjvO2 was increased after the skin (scalp) incision at 1, 3 and 5 minutes and also after endotracheal suctioning for removal of secretions. CONCLUSIONS: Although the accuracy of Fibroptic SjvO2 determination is limited, it allows the detection of cerebral blood flow and oxygen supply-demend imbalance during brain surgery. The frequent occurance of SjvO2 elevations is suggestive of reactive hyperemia mechaniams.

The Cerebral Oxygen Extraction Ratio during Propofol and Isoflurane Anesthesia / 대한마취과학회지

BACKGROUND: The cerebral vascular response to CO2 has been reported to be preserved during isoflurane and propofol anesthesia. This study compared the cerebral oxygen extraction ratio during normoventilation versus hyperventilation in propofol anesthesia and isoflurane anesthesia. METHODS: 28 patients undergoing cerebral aneurysmal surgery were studied following informed consent. In the isoflurane group (n = 14), anesthesia was induced with thiopental 5 mg/kg, and maintained with isoflurane and nitrous oxide (N2O) in oxygen (FiO2 0.33). In the propofol group (n = 14), anesthesia was induced with propofol 2 mg/kg, and maintained by infusion of propofol and N2O-O2 (FiO2 0.33). Monitoring included measurement of mean arterial blood pressure, heart rate, body temperature, end-tidal CO2 (PetCO2), jugular bulb O2 saturation (SjO2) and arterial O2 saturation (SaO2). Mechanical ventilation was adjusted to achieve PetCO2 levels of 40 and 25 mmHg. Ten minutes of equilibration were allowed at each PetCO2 level. Blood was sampled from the jugular bulb and radial artery at each PetCO2 level (40 and 25 mmHg). The cerebral oxygen extraction ratio was calculated as (CaO2 CjO2) / CaO2 (CaO2; arterial oxygen content, CjO2; jugular bulb oxygen content). RESULTS: The cerebral oxygen extraction ratio was higher in hyperventilation (PetCO2 25 mmHg) compared to normoventilation (PetCO2 40 mmHg) in each group (P < 0.05) and higher in the propofol group compared to the isoflurane group (P < 0.05). CONCLUSIONS: The increased cerebral oxygen extraction ratio in hyperventilation during both isoflurane and propofol anesthesia showed that cerebral vascular CO2 reactivity was maintained during both isoflurane anesthesia and propofol anesthesia. The cerebral oxygen extraction ratio was higher during propofol anesthesia compared to isoflurane anesthesia in both normoventilation and hyperventilation, therefore this data showed that cerebral blood flow was lower during propofol anesthesia compared to isoflurane anesthesia.

Effects of 10% Pentastarch Infusion on the Cerebral Blood Flow and Cerebral Metabolic Rate for Oxygen in Canine Hemorrhagic Shock Model / 대한마취과학회지

BACKGREOUND: Cerebral damage caused by hemorrhagic shock presents an important challenge for critical care medicine. The type of fluid to resuscitate hemorrhagic shock is important for the outcome of such patients. Pentastarch is low-molecular-weight hydroxyethyl starch, which increases cerebral blood flow (CBF) by plasma volume expansion and compensatory vasodilation, and improves the microcirculation in the ischemic brain area by reducing the blood viscosity. METHODS: The authors continuously determined CBF and CMRO2 in 10 mongrel dogs weighing 20.1 +/- 0.8 kg with posterior sagittal sinus outflow method. Dogs were subjected to the 20 minute-period of hemorrhagic shock to a mean arterial pressure of 40 mmHg. The shock phase was followed by resuscitation with the same volume of 10% pentastarch as blood loss. The authors assessed the changes of CBF, CMRO2, and CBF/CMRO2 ratio immediately and 30, 60, 90, 120 minutes after pentastarch infusion. Brain water content was assessed by the wet-dry weight method. RESULTS: CBF was increased above the control level, immediately and 30 minutes after 10% pentastarch infusion (p<0.05), and approximated to the control level for the remaining time. CMRO2 was increased, immediately and 30, 60, 90 minutes after 10% pentastarch infusion (p<0.05), and approximated to the control level at 120 minutes. CBF/CMRO2 ratio was recovered to the control level after 10% pentastarch infusion. Brain water content was not significantly different from the normal value of dogs. CONCLUSION: 10% pentastarch may be used with safety to resuscitate hemorrhagic shock because it recovers the balance between the cerebral oxygen supply and demand, and does not cause cerebral edema.

Transcranial Doppler Study in Mean Blood Flow Velocity and Carbon Dioxide Reactivity of Middle Cerebral Artery during Isoflurane-N2O and Propofol-N2O Anesthesia / 대한마취과학회지

BACKGROUND: The reduction is cerebral blood flow (CBF) caused by hypocapnia is an important element of anesthetic techniques for neurosurgery as well as for nonneurologic surgery in patients with reduced intracranial compliance. Accordingly, the impact of anesthetic agents on the CO2 responsiveness of the cerebral circulation has important implications with regard to anesthetic selection. The purpose of this study was to investigate the effects of isoflurane-N2O and propofol-N2O anesthesia on the CBF response to changes in end-tidal CO2 in healthy patients. METHODS: 19 healthy patients with nonneurological operation were selected. In group 1, anesthesia was induced with thiopental sodium 4 mg/kg, fentanyl 1 g/kg, succinylcholine 1~1.5 mg/kg and was maintained with isoflurane 0.5~1.5 vol%. In group 2, anesthesia was induced with propofol 2~2.5 mg/kg, fentanyl 1 g/kg, succinylcholine 1~1.5 mg/kg and was maintained with a propofol infusion of 10 mg/kg/h for 10 min and then 8 mg/kg/h for 10 min and then was reduced 3~6 mg/kg/h of the remainder of the study. All patients were ventilated with N2O in O2 (FIO2 0.5) and measured end-tidal CO2 (PETCO2). Mean blood flow velocity of middle cerebral artery was measured using transcranial Doppler in PETCO2 45, 40, 35, 30, 25, 20 mmHg. RESULT: CO2 reactivity of MCA flow velocity during isoflurane-N2O and propofol-N2O anesthesia was 5.1 +/- 1.8 %/mmHg, 4.4 +/- 1.0 %/mmHg respectively. CONCLUSION: The cerebral vasculature in healthy patients remains responsive to changes in PETCO2 during isoflurane-N2O and propofol-N2O anesthesia.

Responsiveness of Cerebral Blood Flow to changes in Arterial Carbon Dioxide during Propofol Anesthesia in Dogs / 대한마취과학회지

BACKGROUND: Propofol is a relatively new intravenous anesthetic agent, and the cerebral blood flow (CBF) response to changes in PaCO2 during propofol anesthesia has not been extensively studied. The purpose of this study was to investigate the effects of propofol anesthesia on the CBF response to changes in PaCO2 in dogs. METHODS: In six dogs, after surgical preparation for posterior sagittal sinus outflow method, loading dose of propofol 5~6 mg/kg was injected and then anesthesia was maintained with a propofol infusion of 20 mg . kg-1 . hr-1 during study. Ventilation was controlled to hypocapnia(PaCO2 20~35 mmHg), normocapnia(PaCO2 35~45 mmHg) and hypercapnia(PaCO2 45~60 mmHg) by adjustment of minute ventilation. Posterior sagittal sinus blood flow was measured by metered syringe and then CBF was calculated. Cerebral metabolic rate for oxygen(CMRO2) was calculated with arterial and sagittal sinus blood analysis. RESULTS: CBF at normocapnia (PaCO2 41+/-5 mmHg) was 28.7+/-11.6 ml . 100 g-1 . min-1 which increased to 46.5+/-14.4 ml . 100 g-1 . min-1 and decreased to 22.1+/-8.9 ml . 100 g-1 . min-1 on increasing PaCO2 (63+/-18 mmHg) and decreasing PaCO2 (33+/-3 mmHg), respectively. The slope of CBF versus PaCO2 was 1.29 ml . 100 g-1 . min-1 . mmHg. Blood pressure, herat rate, PaO2, CMRO2 were not changed between groups. CONCLUSIONS: CBF response to changes in PaCO2 during propofol anesthesia is maintained and the slope of the CBF-CO2 response is similar to that found during anesthesia with other intravenous agents such as thiopental, midazolam, etomidate, opioids.

Effects of Phenylephrine Induced Hypertension on the Cerebral Hemodynamics in Dogs / 대한마취과학회지

BACKGROUND: Induced hypertension has long been considered a potential adjunct to the management of focal cerebral ischemia. Whether induced hypertension causes an increase in cerebral blood flow(CBF), dependent on cerebral perfusion and/or an intracerebral redistribution of CBF by a vasoconstrictive effect of vasoconstrictor is controversial. In this study, effect of phenylephrine induced hypertension on the cerebral hemodynamics and mechanism of reduced ischemic area were studied. METHODS: Six mongrel dogs weighing between 13 and 18 kg were anesthetized with halothane 0.5 vo1%-N2O 1 L/min-O2 1 L/min. Ventilation was controlled to maintain PaCO2 within 35~40 mmHg. Cerebral blood flow was measured and calculated by the posterior sagittal sinus outflow method. Cerebral metabolic rate for oxygen(CMRO2) was calculated. Intracranial pressure(ICP) was also measured. Phenylephrine was infused to increase mean arterial blood pressure(MAP) to a level 30% above baseline value and MAP was held constant for 20 minutes before CBF, ICP, CMRO2 determination. These parameters were measured at 10, 20 minutes after induced hypertension. RESULTS: Induced hypertension resulted in increased MAP and decreased heart rate. There were no differences between baseline, hypertension 10 min, and hypertension 20 min in terms of PaCO2, PaO2, hematocrit and temperature. CBF was not changed after induced hypertension(39.1+/-9.7 vs 40+/-10 vs 40.2+/-10.1 ml 100g(-1) min(-1) (meanv+/-SD) at baseline, hypertension 10 min, hypertension 20 min, respectively). Cerebral metabolic rate was not changed also after induced hypertension. ICP increased after induced hypertension significantly(20.5+/-12.5 vs 26+/-15.3 vs 29.8+/-17 mmHg at baseline, hypertension 10 min, 20 min, respectively). CONCLUSIONS: Phenylephrine is a cerebral vasoconstrictor and that causes redistribution of cerebral blood flow to ischemic brain area.