BACKGROUND: The elimination of anesthetic agents is a decisive factor in the emergence from general anesthesia. In this pilot study, we hypothesized that hypercapnia would decrease the emergence time from propofol anesthesia by increasing cardiac output and cerebral blood flow. METHODS: A total of 32 patients were randomly divided into two groups based on the end-tidal carbon dioxide values: 30 mmHg (the hypocapnia group) and 50 mmHg (the hypercapnia group). Propofol and remifentanil were infused to maintain a bispectral index of 40–50. Remifentanil infusion was stopped 10 min before the discontinuation of propofol. After cessation of propofol infusion, ventilation settings in the hypocapnia group were maintained constant; a rebreathing tube was connected to the respiratory circuit in the hypercapnia group. The time to spontaneous respiration, eye opening (primary endpoint), mouth opening, and tracheal extubation was recorded and analyzed. RESULTS: Time to eye opening was 9.7 (1.3) min in the hypocapnia group and 9.0 (1.0) min in the hypercapnia group. The difference in the mean times to eye opening between groups was −0.7 min (95% CI, −4.0 to 2.7, P = 0.688). On multiple regression analysis, there was a significant difference in the mean time to eye opening between males and females. Females recovered about 3.6 min faster than males (95% CI, −6.1 to −1.1, P = 0.009). CONCLUSIONS: We could not detect a beneficial effect of hypercapnia on propofol emergence time. Irrespective of hypercapnia, females seemed to recover faster than males.
Airway Extubation ; Anesthesia* ; Anesthesia, General ; Anesthetics ; Carbon Dioxide ; Cardiac Output ; Cerebrovascular Circulation ; Clinical Study* ; Female ; Humans ; Hypercapnia* ; Hypocapnia ; Male ; Mouth ; Pilot Projects ; Propofol* ; Respiration ; Ventilation

We present a woman with heterozygous carnitine palmitoyl transferase 2 (CPT-2) deficiency who in the last 6 months suffered from episodic dyspnea and choking. Symptoms could not be attributed to her muscular energy defect, since heterozygous CPT-2 deficiency is usually asymptomatic or causes only mild muscle fatigability. Myopathy is usually triggered by concurrent factors, either genetic (additional muscle enzymes defects) or acquired (metabolic stress). The patient was referred to our respiratory clinic for suspect bronchial asthma. Spirometry showed mild decrease in inspiratory flows. Methacholine challenge was negative. Dyspnea was triggered by hyperventilation-induced hypocapnia, which produced marked decrease in airflow rates, particularly in inspiratory flows, consistent with laryngospasm. Nutritional assessment of the patient showed low serum level of calcium and vitamin D, attributable to avoidance of milk and dairy products for lactose intolerance and to insufficient sunlight exposure. After calcium and vitamin D supplementation episodic laryngospasm disappeared and hypocapnic hyperventilation test induced very mild change in airflow rates. Calcium and vitamin D deficiency may favour laryngeal spasm mimicking asthma, particularly in subjects with underlying myopathy.
Airway Obstruction ; Asthma* ; Calcium ; Carnitine ; Dairy Products ; Dyspnea ; Female ; Humans ; Hyperventilation ; Hypocapnia ; Lactose Intolerance ; Laryngismus* ; Methacholine Chloride ; Milk ; Muscular Diseases ; Nutrition Assessment ; Spirometry ; Sunlight ; Transferases ; Vitamin D ; Vitamin D Deficiency*

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

A 6-year-old male patient who was suffering from a cold and a transient ischemic attack was scheduled to undergo encephalo-duro-arterio-synangiosis for treating his moyamoya disease. Acute brain edema occurred just after opening the dura mater. Head elevation, reduction of the head rotation and hyperventilation were done. The inhalational agents were discontinued and total intravenous anesthesia was started. The swelling was reduced after intravenously infusing mannitol. An abrupt return from hypocapnia to normocapnea during the induction of general anesthesia was thought to be the cause of the acute brain swelling. In conclusion, correction of hypocapnea needs to be performed gradually during the induction of anesthesia and when performing an operation for treating a patient with moyamoya disease.
Anesthesia ; Anesthesia, General ; Anesthesia, Intravenous ; Brain ; Brain Edema ; Cerebral Revascularization ; Child ; Cold Temperature ; Dura Mater ; Head ; Humans ; Hyperventilation ; Hypocapnia ; Ischemic Attack, Transient ; Male ; Mannitol ; Moyamoya Disease ; Stress, Psychological

BACKGROUND: It is known that sympathetic stimulation and increase in cerebral blood flow velocity can be induced by desflurane. Cerebral oxygen balance could be disturbed during desflurane induction. Aim of this study was to elucidate that cerebral oxygen imbalance induced by desflurane mask induction can be reduced by combination of remifentanil and hypocapnia. METHODS: Twenty ASA 1-2 subjects were allocated randomly into 5 groups divided by concentration of remifentanil (0.0, 0.5, 1.0, 1.5, and 2.0 ng/ml). After confirmation of attaining proposed concentration of remifentanil, propofol and vecuronium were administered and mechanical ventilation was done with 8% desflurane with facial mask. Subsequently, changes in regional cerebral oxygen saturation (DeltarSO2), arterial blood pressure, heart rate, cardiac index, estimated alveolar concentration of desflurane (PDESF), and end-tidal concentration of carbon dioxide (PETCO2) were recorded for the following 10 minutes. According to concentration of desflurane and remifentanil, DeltarSO2 and hemodynamic factors were checked. RESULTS: During desflurane induction, changes in cerebral oximetry reached up to +10% (6 [first quartile], 13 [third quartile]). Arterial blood pressure, heart rate, and cardiac index were changed within clinical ranges. The DeltarSO2 showed S-shaped increasing pattern according to increasing PDESF. Hypocapnia and concentration of remifentanil reduced the maximum DeltarSO2 (P = 0.0046, P = 0.0060). Hypocapnia also shifted the curve to left (P = 0.0001). CONCLUSIONS: During 8% desflurane induction, regional cerebral oxygen saturation (rSO2) increases maximum +25%. Hypocapnia and use of remifentanil can reduce the increase in regional cerebral oxygen saturation.
Arterial Pressure ; Blood Flow Velocity ; Carbon Dioxide ; Heart Rate ; Hemodynamics ; Hypocapnia ; Isoflurane ; Masks ; Oximetry ; Oxygen ; Piperidines ; Propofol ; Respiration, Artificial ; Vecuronium Bromide

The aim of this study was to develop a nonlinear mixed-effects model for the increase in cerebral oximetry (rSO2) during the rapid introduction of desflurane, and to determine the effect of hypocapnia and N2O on the model. Twelve American Society of Anesthesiologist physical status class 1 and 2 subjects were allocated randomly into an Air and N2O group. After inducing anesthesia, desflurane was then increased abruptly from 4.0 to 12.0%. The PET(CO2), PET(DESF) and rSO2 were recorded at 12 predetermined periods for the following 10 min. The maximum increase in rSO2 reached +24-25% during normocapnia. The increase in rSO2 could be fitted to a four parameter logistic equation as a function of the logarithm of PET(DESF). Hypocapnia reduced the maximum response of rSO2, shifted the EC50 to the right, and increased the slope in the Air group. N2O shifted the EC50 to the right, and reduced the slope leaving the maximum rSO2 unchanged. The N2O-effects disappeared during hypocapnia. The cerebrovascular reactivity of rSO2 to CO2 is still preserved during the rapid introduction of desflurane. N2O slows the response of rSO2. Hypocapnia overwhelms all the effects of N2O.
Adult ; Anesthetics, Inhalation/*pharmacology ; *Cerebral Cortex/blood supply/drug effects/physiology ; Cerebrovascular Circulation/*drug effects/physiology ; Female ; Hemodynamics ; Humans ; Hypocapnia/*metabolism ; Isoflurane/*analogs & derivatives/pharmacology ; Male ; Middle Aged ; Models, Theoretical ; Nitrous Oxide/*metabolism ; *Oximetry ; Random Allocation ; Regional Blood Flow/drug effects

Moyamoya disease is characterized by a narrowing or occlusion of both internal carotid arteries in the presence of an abnormal hemangiomatosis vascular network at the base of the brain. These patients increasingly present for surgical management to improve the cerebral circulation. However, surgery may be complicated by cerebral ischemia, and thus patients require particular care during the perioperative period. The risk factors of perioperative ischemic complications include the presence of a preoperative low density area by computed tomography, the occurrence of frequent preoperative transient ischemic attacks, or hypocapnia or hypotension. We describe one case of general anesthesia for superficial temporal artery to middle cerebral artery anastomosis (STA-MCA) with encephalomyosynangiosis (EMS) in a moyamoya disease patient. The patient expired because of a developing cerebral infarction on the fifth postoperative day.
Anesthesia, General ; Brain Infarction* ; Brain Ischemia ; Brain* ; Carotid Artery, Internal ; Cerebral Infarction ; Humans ; Hypocapnia ; Hypotension ; Ischemic Attack, Transient ; Middle Cerebral Artery ; Moyamoya Disease* ; Perioperative Period ; Risk Factors ; Temporal Arteries

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

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: 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