The routine management of head injury includes hyperventilation to produce hypocapnis with arterial CO2 tension 25~30 torr. But a decrease in cerebral blood flow with hypocapnia may result in cerebral ischemia. Our study was to evaluate the change of cerebral blood flow during hyperventilation in halthane anesthesia. The jugular venous oxygen saturation(SjvO2), arterio-venous oxygen content difference(CaO2-CjvO2), and oxygen extraction ratio(O2ER) were used as criteria of cerebral ischemia with reduced cerebral blood flow. The results are as follows: 1) SjvO2 was lower in group 2(PaCO2=22.8torr) than group 1(PaCO2=30.3 torr). 2) CaO2-CjvO2 and O2ER were higher in Group 2 than group 1. 3) No more increased possibility of cerebral ischemia with reduced cerebral blood flow was observed Group 2 than group 1.
Anesthesia ; Brain Ischemia ; Craniocerebral Trauma ; Hyperventilation ; Hypocapnia ; Oxygen*

Seizure following percutaneous endoscopic lumbar discectomy (PELD) is extremely rare. We report that generalized seizure occurred in a patient with radiating right leg pain after PELD under sevoflurane anesthesia. Cerebrospinal fluid (CSF) was detected from a dura tear in the operative field. On emergence from anesthesia, generalized tonic-clonic activity continued for approximately 2 minutes and the level of consciousness was decreased to a stuporous state. Under sedation, a pneumocephalus which was thought to be caused by the dura tear was evaluated with a brain computed tomography (CT) and a continuous slow wave was found on electroencephalography (EEG) without any epileptiform discharges. Eight hours postoperatively, the decreased level of consciousness recovered, and after 2 weeks, the patient was discharged without any neurologic sequealae. Clinicians should recognize the epileptogenic potential of sevoflurane and limit the maximum dose with avoidance of hypocapnia by hyperventilation. If an intracerebral lesion is accompanied, it may increase the possibility of the occurrence of seizure.
Anesthesia ; Brain ; Consciousness ; Diskectomy ; Electroencephalography ; Humans ; Hyperventilation ; Hypocapnia ; Leg ; Methyl Ethers ; Pneumocephalus ; Seizures ; Stupor

PURPOSE: We are inclined to analyze the relationship between the intrapulmonary right-to-left shunt and the PaO2/PaCO2 after endotracheal single-dose surfactant instillation to premature neonates with respiratory distress syndrome within 6 hours after birth. METHODS: From Jan. 1993 to Jun. 1995, we have conducted a clinical trial of surfactant replacement therapy to the premature neonates with respiratory distress syndrome at the neonatal intensive care unit of InHa University Hospital. The surfactant group (n=17) was given Surfactant-TA and mechanical ventilator care, but the control group (n=22) was treated with only mechanical ventilator. We analyzed umbilical arterial blood gases and estimated respiratoy indexes before and after treatment. RESULTS: 1) The QSP/QT decreased initially in the surfactant group, but significantly increased 24 hours after treatment in the control group (40.6+/-4.7%, P<0.05). 2) The PaO2 significantly decreased 2 hours and 24 hours after treatment in the control group (60.8+/-10.1mmHg, 63.5+/-7.6mmHg, P<0.05 respectively). There were significant correlations between the QSP/QT and the PaO2 in both groups, and specifically in the conrol group 24 hours after treatment (r=-0.94, P<0.001). 3) The PaCO2 significantly increased 1 hour after treatment, but significantly decreased specifically in the control group 24 hours after treatment (32.5+/-1.8mmHg, P<0.01). However, there were no signifacnt correlations between the QSP/QT and the PaCO2 in both groups. CONCLUSIONS: Specifically in the control group 24 hours after treatment, with hypocapnia, significant increase in pulmonary blood flow to capillary shunt and low VA/Q units (VA/Q<0.1) at high FIO2 (>0.5) resulted in a decrease in PaO2 and also a significant relationship was found between the QSP/QT and the PaO2. However, there was no significant relationship between the QSP/QT and the PaCO2.
Capillaries ; Gases ; Humans ; Hypocapnia ; Infant, Newborn* ; Intensive Care, Neonatal ; Parturition ; Pulmonary Surfactants* ; Ventilators, Mechanical

Changes of brain stem blood flow(BBF) during physiologic stimulation, such as hypoxia, hypo-and hypercapnia, and hemorrhagic hypotension, were studied by hydrogen clearance technique through closed clival window in the brain stem of nerborn piglet. Induction of moderate hypercapnia(PaCO2=65.4+/-2.11mmHg) caused prominent increases in BBF(354+/-39%;p<0.0001). Conversely, in response to moderate hypocapnia(PaCO2=23.9+/-0.64mmHg), a significant decreases in BBF(-30.38+/-3.22%;p<0.0001) was observed. During severe hypoxia(PaO2=3.7+/-1.4mmHg)moderate increases in BBF(161+/-51.4%;p=0.005) occurred. Interestingly, in response to systemic hypotension(Mean Arterial Blood Pressure=34+/-0.7mmHg), a nonsignificant reduction of BBF was recorded(-14+/-10%;p=0.240). These findings suggest that CO2 reactivity of newborn piglet posterior circulation is high;however, hypoxic reactivity is relatively moderate, and BBF is autoregulated during systemic hypotension.
Anoxia* ; Brain Stem* ; Brain* ; Humans ; Hydrogen ; Hypercapnia* ; Hypocapnia* ; Hypotension* ; Infant, Newborn*

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.
Anesthesia* ; Anesthetics ; Blood Flow Velocity* ; Carbon Dioxide* ; Carbon* ; Compliance ; Fentanyl ; Humans ; Hypocapnia ; Isoflurane ; Middle Cerebral Artery* ; Neurosurgery ; Propofol ; Succinylcholine ; Thiopental

BACKGROUND: Near infrared spectroscopy (NIRS) to monitor regional cerebral oxygen saturation (rSO2) is a noninvasive and simple modal ity in clinical use. The ability of rSO2 as an index of cerebral oxygenation has been well demonstrated. However, the reliability of rSO2 to reflect the changes of cerebral vascular reactivity in the changes of arterial partial pressure of CO2 (PaCO2) has not been established. The aim of this study was to verify the reliability of rSO2 to measure the CO2 reactivity of cerebral vasculatures. METHODS: Twenty healthy adult patients undergoing general anesthesia were enrolled in this study. Anesthesia was induced with propofol and maintained with desflurane/N2O. Respiration was mechanically controlled. The radial artery and jugular bulb were cannulated. The sensor of the NIRS was attached to the ipsilateral forehead. During normocapnia (PaCO2 40 +/- 1.3 mmHg) and hypocapnia (PaCO2 30 +/- 2.4 mmHg), blood was obtained from the radial artery and jugular bulb and analyzed. rSO2 was compared with fSO2 (estimated field oxygen satuation), and the gold standard of tissue oxygen saturation. fSO2 was calculated from the following equation: fSO2 = 0.75 SjO2 + 0.25 SaO2. RESULTS: rSO2 significantly correlated with fSO2 (P = 0.000, r2 = 0.56). A bias of - 5.8% with a precision 12.94% was found. CONCLUSIONS: We concluded that rSO2 can be a reliable predictor to measure CO2 reactivity of cerebral vasculatures during normocapnia and hypocapnia.
Adult ; Anesthesia* ; Anesthesia, General ; Bias (Epidemiology) ; Forehead ; Humans ; Hypocapnia ; Oxygen ; Partial Pressure ; Propofol ; Radial Artery ; Respiration ; Spectrum Analysis

BACKGROUND: Mannitol is widely used in neurosurgical patients and may induce an increase in serum potassium concentration according to doses and administration rates with unknown mechanism. The treatment of hyperkalemia is aimed at eliminating the causes and includes calcium, sodium bicarbonate, glucose with insulin, loop diuretics and hyperventilation. This study was undertaken to observe the effects of hyperventilation on the serum potassium concentration following infusion of mannitol (2.0 gm/kg). METHODS: We studied 30 patients who were operated brain aneurysm clipping surgery and were divided into 3 groups (n=10). In control group, mild hypocapnia was maintained (PaCO2, 32 2 mmHg) before and after mannitol infusion. In group I, moderate hypocapnia was maintained (PaCO2, 27 2 mmHg) before and after mannitol infusion. In group II, mild hypocapnia (PaCO2, 32 2 mmHg) was maintained before 30 minutes of mannitol infusion and moderate hypocapnia (PaCO2, 27 2 mHg) after mannitol infusion. We started infusion of 20% mannitol with a dosage of 2.0 gm/kg, 15~20 min after cranium was opened. RESULTS: The changes of serum potassium were as follows (Mean SD mEq/l) (just before and 15min, 30min, 60min after mannitol infusion): 3.79 0.48, 4.66 0.60, 4.44 0.48, 4.13 0.40 (Control group), 3.62 0.18, 3.63 0.42, 4.14 0.51, 3.95 0.33 (Group I), 3.76 0.20, 3.91 0.15, 4.11 0.30, 4.04 0.23 (Group II). After 15 minutes of mannitol infusion, the serum potassium levels of group I and II were lower than that of control group (p<0.05) and there was no significant difference between group I and II. CONCLUSIONS: These results suggest that hyperventilation may blunt the increase in serum potassium concentration following rapid infusion of high dose mannitol.
Calcium ; Glucose ; Humans ; Hyperkalemia ; Hyperventilation* ; Hypocapnia ; Insulin ; Intracranial Aneurysm ; Mannitol* ; Potassium* ; Skull ; Sodium Bicarbonate ; Sodium Potassium Chloride Symporter Inhibitors

Hyperventilation is a common form of anesthetic management in neurosurgical patients with increased intracranial pressure. Acute hypocapnia through hyperventilation causes an increase in cerebrovascular resistance which decreases the cerebral blood flow within one minute. When the hyperventilation is sustained, the cerebral blood flow gradually rises toward normal. We performed this study for evaluation of the changes of acid-base balance in cerebrospinal fluid (CSF) according to duration of acute hyperventilation. We have studied 12 patients for elective surgery for cerebral aneurysm with a relatively clear mental state. The patients underwent induction of anesthesia with thiopental, fentanyl and vecuronium. After intubation, their ventilation was controlled and maintained at a PaCO2 of about 30 mmHg. Samples in arterial and lumbar CSF were obtained at hourly intervals for 6 hours after the onset of hyperventilation. The results were as follows: 1) The PaCO2 was low 30s mmHg and all arterial blood values were not changed throughout the period of observation. 2) The values of CSF were changed; the pH of CSF was increased for 3 hours and then gradually decreased after 4 hours, carbon dioxide tension was a steady state after an initial fall for 2 hours, HCO3-, was decreased from 2 hours and more significantly decreased after 5 hours, and the base excess was more significantly negative after 5 hours of hyperventilation. From the above data, we conclude that prolonged hyperventilation produces first a rise in CSF pH by decreased CSF PCO2 and then gradually a fall in CSF pH by decreasing CSF HCO3-, concentration, and measurable compensated acidosis in CSF was initiated within 5 hours after onset of hyperventilation.
Acid-Base Equilibrium ; Acidosis ; Anesthesia ; Carbon Dioxide ; Cerebrospinal Fluid ; Fentanyl ; Humans ; Hydrogen-Ion Concentration ; Hyperventilation* ; Hypocapnia ; Intracranial Aneurysm ; Intracranial Pressure ; Intubation ; Thiopental ; Vecuronium Bromide ; Ventilation

Glutamate (GLU) is a neurotransmitter. Massive release of GLU and glycine (GLY) into the brain's extracellular space may be triggered by ischemia, and may result in acute neuronal lysis or delayed neuronal death. The aim of this study was to evaluate the possible relationship between hyperventilation and the level of GLU and GLY during brain ischemia. Rabbits were anesthetized with halothane and oxygen. Group 1 was allowed to hyperventilate (PaCO2 25-35 mmHg). PaCO2 was maintained throughout the study. Group 2 was a normal control group that maintained normocapnia. Two global cerebral ischemic episodes were produced. Microdialysate was collected during the peri-ischemic and reperfusion periods from the dorsal hippocampus. GLU and GLY concentrations were determined using high-performance liquid chromatography. In the control group, GLU and GLY were significantly elevated during each episode of ischemia; these levels returned to baseline within 10 minutes after reperfusion. In contrast, in the hyperventilation group GLU and GLY concentrations increased during ischemia, but they were not statistically significant. We were able to demonstrate that hypocapnia during periischemic period lowered extracellular GLU and GLY concentrations. These results can explain a part of the protective action of hypocapnia during cerebral ischemia.
Animal ; Brain Ischemia/*metabolism ; Glutamic Acid/*analysis ; Glycine/*analysis ; Hippocampus/*chemistry ; Hyperventilation/metabolism ; Hypocapnia/*metabolism ; Potassium/metabolism ; Potassium Channels/physiology ; Rabbits ; Support, Non-U.S. Gov't

In the care of neonates, complications from the use of mechanical ventilation and other treatment of respiratory problems have important effects on cardiac output, cerebral blood flow, cerebral oxygenation and cerebral venous return that at times result in brain injury. Hypercapnia or hypocapnia following mechanical ventilation during the first few days of life may result in adverse effect on the CNS in perterm and term infants. Hypocapnia, particularly at PaCO2 levels less than 25 to 30 mmHg, has been associated with periventricular leukomalcia, cerebral palsy and poor neurologic outcomes in preterm infants. Use of smaller tidal volumes combined with permissive hypercapnia to reduce ventilator-induced lung injury may protect against hypocapnia-induced brain injury. Recent randomized clinical studies have demonstrated the safety of mild permissive hypercapnia, but found only small clinical benefits. Several studies have reported that the use of postnatal dexamethasone for severe RDS evolving into BPD have adverse effects on growth and neurodevelopmental outcomes. The results of large long-term follow-up studies strongly suggest an association between use of postnatal dexamethasone and poor neurodevelopmental outcome including cerebral palsy. Further studies including an evaluation of neurodevelopmental outcome as a primary endpoint must be needed for postnatal use of systemic or inhaled steroid.
Brain Injuries* ; Brain* ; Cardiac Output ; Cerebral Palsy ; Dexamethasone ; Follow-Up Studies ; Humans ; Hypercapnia ; Hypocapnia ; Infant ; Infant, Newborn ; Infant, Premature* ; Oxygen ; Respiration, Artificial* ; Tidal Volume ; Ventilator-Induced Lung Injury