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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven normoventilated and five hyperventilated healthy adults undergoing cholecystectomy and anaesthetized with methohexitone, fentanyl and pancuronium were studied with measurement of cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and quantified electroencephalography (EEG) under two sets of conditions: 1) 1.7% end-tidal concentration of isoflurane in air/oxygen; 2) 0.85% end-tidal concentration of isoflurane in nitrous oxide (N2O)/oxygen. The object was to study the effects of N2O during isoflurane anaesthesia on cerebral circulation, metabolism and neuroelectric activity. N2O in the anaesthetic gas mixture caused a 43% (P less than 0.05) increase in CBF during normocarbic conditions but no significant change during hypocapnia. CMRO2 was not significantly altered by N2O. EEG demonstrated an activated pattern with decreased low frequency activity and increased high frequency activity. The results confirm that N2O is a potent cerebral vasodilator in man, although the mechanisms underlying the effects on CBF are still unclear.
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PMID:Effects of nitrous oxide on cerebral haemodynamics and metabolism during isoflurane anaesthesia in man. 153 78

Energy metabolism of the cat brain was studied using phosphorous-31 nuclear magnetic resonance (31P-NMR) during sevoflurane/halothane anesthesia with normo- and hyperventilation. Under normocapnia, the findings associated with abnormal energy metabolism were not observed at concentration of sevoflurane/halothane up to 2 MAC. Meanwhile under hypocapnia by hyperventilation, the value of phosphocreatine began to decrease at and below 20 mmHg of PaCO2 (2 MAC sevoflurane) and 30 mmHg of PaCO2 (2 MAC halothane) respectively. These abnormal findings of brain metabolism were limited to the cases with cerebral blood flow (CBF) of less than a half of control state (nonanesthetized and normoventilated), and they were normalized with increased CBF by the vasoconstrictor, metaraminol. From the above data, it was concluded that the deteriorated energy metabolism by hyperventilation was due to decrease in CBF with hypotension and there was no direct effect on cerebral metabolism with less than 2MAC of both sevoflurane and halothane.
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PMID:[The effects of sevoflurane/halothane anesthesia during normo- and hyperventilation on the energy metabolism of the cat brain]. 154 5

We evaluated transcranial Doppler sonography (TCD) for the detection of cerebral ischaemia during carotid endarterectomy in 30 male and 14 female patients with ipsilateral focal cerebro-vascular symptoms. Surgery was performed during halothane-nitrous oxide anaesthesia with moderate hypocapnia. Eight patients had a temporary shunt owing to contralateral occlusion or a stump pressure below 40 mmHg, and/or EEG flattening. Transcranial Doppler sonography was followed intra-operatively together with electro-encephalography (EEG), internal carotid artery (ICA) pressures and cerebral blood flow (CBF). Middle cerebral artery mean flow velocity (Vmean) was 38 (22-96) cm s-1 (median and range) and decreased during cross-clamping to 28 (10-60) cm s-1 (p less than 0.0001). After removal of the clamp it increased to 42 (20-102) cm s-1 (p less than 0.0001). AVmean clamp of less than 30 cm s-1 together with a Vmean clamp: Vmean pre-clamp ratio of less than 0.6 showed an accuracy with respect to CBF below 20 ml 100 g-1 min-1 of 89%. AVmeanclamp:Vmean pre-clamp ratio below 0.4 detected all all patients with EEG flattening (n = 3) (accuracy 97%). The corresponding level of accuracy obtained with stump pressure was 80%. The results indicate that middle cerebral flow velocity enables an increase in the accuracy of detecting cerebral ischaemia during carotid endarterectomy.
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PMID:Transcranial Doppler for detection of cerebral ischaemia during carotid endarterectomy. 157 54

Although hyperventilation with hypocapnia is frequently used in the management of neurosurgical patients in whom sensory-evoked potentials may be monitored, the effects of hypocapnia on evoked potentials have not been described with precision. In the present experiment, the effects of randomized arterial carbon dioxide tensions of 20, 25, 30, and 35 mm Hg on spinal, subcortical, and cortical somatosensory-evoked potentials (SEPs) were measured in dogs anesthetized with 1.40% isoflurane. Other variables known to affect the SEP (temperature, blood pressure, and arterial oxygen tension) were stable throughout the experiment. Hypocapnia caused reductions in the latencies of the early peaks of the spinal and subcortical SEPs. These differences were small, consisting of a 2% shortening of latency at 20 mm Hg carbon dioxide tension when compared with 35 mm Hg. No changes were detected in the later subcortical and cortical latencies. SEP amplitudes were also unchanged. These results in a controlled animal study corroborate the direction and magnitude of changes due to hypocapnia observed by other investigators in surgical patients. The magnitude of the changes indicates that SEP monitoring sensitivity is not compromised by clinically useful levels of induced hypocapnia during isoflurane anesthesia. Because hypocapnia may produce small SEP changes, baseline recordings should be acquired prior to initiation of hyperventilation. It is not warranted, however, to impute a severe deterioration of the SEP to hypocapnia alone, and causes must be sought elsewhere in a patient's status and management.
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PMID:Effects of hypocapnia on canine spinal, subcortical, and cortical somatosensory-evoked potentials during isoflurane anesthesia. 158 48

An enclosed afferent reservoir breathing system (EAR) designed by Ohmeda was evaluated during anaesthesia with controlled ventilation in 104 healthy children. Carbon dioxide production and arterial carbon dioxide tension were measured in 12 children in order to determine the proportion of fresh gas (VF) involved in gas exchange. When the ratio of minute volume ventilation to fresh gas flow (VE:VF) exceeded 1.5, fractional utilization of fresh gas with the EAR was 0.92. This value and values of carbon dioxide production obtained from 43 children were used to derive a simple formula relating fresh gas flow requirements to body weight. The formula, VF = 0.6 x weight 0.5, was assessed in 49 children weighing 10-70 kg. The mean end-tidal partial pressure of carbon dioxide in these patients was 4.5 kPa (range 3.8-5.2 kPa). We conclude that the EAR has an efficiency of 92% in the use of fresh gas during controlled ventilation in healthy children, provided the VE:VF ratio is greater than 1.5. Under these conditions, normocapnia to mild hypocapnia was produced accurately using the formula VF = 0.6 x weight 0.5.
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PMID:Fresh gas requirements of an enclosed afferent reservoir breathing system during controlled ventilation in children. 832 78

The effect of hypocapnic alkalosis (HA) on nicardipine-induced cerebral vasodilatation was studied in 2 groups of patients undergoing stereotaxic brain biopsy under general anaesthesia. Arterial diameter (AD) was measured in 16 different locations on a carotid arteriogram (lateral view), and intracranial pressure (ICP) was recorded with an intraventricular catheter. At time T0, in normocapnia an arteriogram was performed in both groups. The first group (GI) was then studied in hypocapnia (T1) and following an injection of nicardipine (T2), while the second group (GII) was studied first after injection of nicardipine (T1) and then in hypocapnia (T2). Groups GI (n = 6; 44 y) and GII (n = 6; 46 y) were similar with regard to age, blood pressure, heart rate and PaO2 at all three phases of the study. HA caused a 9.5% decrease in AD (GI.T1) compared to baseline values, and a 15.2% decrease when preceded by injection of nicardipine (GII.T2). In the latter case the decrease was 3% in comparison with baseline. Nicardipine increased AD by 14.7% (GII.T1) and by 18.5% when preceded by HA (GI.T2), but the rise (7.3%) was not significant in comparison with the baselines value. The changes variations were similar whether the entire arterial trunk or only the supraclinoid region were studied. HA decreased ICP by 44% (GI.T1) and by 50% after nicardipine (GII.T2). Nicardipine did not cause an increase in ICP. Nicardipine and HA antagonise each others vasomotor effects, as previously shown in the baboon using nimodipine.
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PMID:Combined effects of nicardipine and hypocapnic alkalosis on cerebral vasomotor activity and intracranial pressure in man. 174 37

The main disadvantages of the to-and-fro system (the bulky canister and the progressive increase in apparatus deadspace) may be overcome by the use of a smaller canister. In this laboratory study, we have evaluated a 160 g canister in a low-flow to-and-fro system (fresh gas flow 1 litre/minute). Two carbon dioxide productions of 150 and 200 ml/minute were simulated. The mean times to exhaustion, defined here as a 0.5 kPa rise in end-tidal PCO2, were 112 and 79 minutes in the 150 and 200 ml/minute carbon dioxide groups respectively. Ventilation to normacapnia or hypocapnia did not affect the times to exhaustion. The soda lime absorbed 16 litres of carbon dioxide before exhaustion, and this was not affected by minute volume or carbon dioxide production. A small soda lime canister is suitable for carbon dioxide absorption in a low-flow to-and-fro system for ventilated adults.
Anaesthesia 1991 Nov
PMID:Evaluation of a small soda lime canister in a to-and-fro system. 175 May 99

Sufentanil, a synthetic opioid that is 5-10 times as potent as fentanyl, has been suggested for use during neurosurgical procedures because it maintains cardiovascular stability and produces hypnosis without the use of additional anesthetic agents. Doses as low as 2.5 micrograms.kg-1 are reported to create deep levels of anesthesia as demonstrated by EEG changes to high-amplitude delta-waves. However, there are no reports concerning the effects of sufentanil on blood flow and metabolism in the human brain. The present study was designed to investigate the influence of high-dose sufentanil-O2 anesthesia on the cerebral circulation, metabolism, and the cerebrovascular response to CO2 in man. METHODS. Nine male and 2 female patients between 41 and 60 years of age who were scheduled for coronary artery bypass surgery were studied. Premedication consisted of flunitrazepam 2 mg orally and piritramide 15 mg and promethazine 50 mg i.m. 1 h before arrival in the induction room. Measurements were performed with the patients awake (I), after sufentanil 10 micrograms.kg-1 as an induction dose followed by 0.15 micrograms.kg-1.min-1 as an infusion with normocapnia (pa CO2 42.1 +/- 2 mmHg) (II), during hypercapnia (pa CO2 53.7 +/- 3.5 mmHg) (III), and during hypocapnia (pa CO2 31.7 +/- 2 mmHg) (IV). Cerebral blood flow (CBF) was measured using the argon wash-in technique. Cerebral venous blood was obtained from a catheter in the superior bulb of the right internal jugular vein. Cerebral metabolic rates of oxygen (CMRO2) glucose (Mgluc) lactate (CMlac) were calculated by multiplying the arterial-cerebral venous oxygen and substrate differences by CBF. The Anaerobic Index was calculated from the equation avD lactate x 100/2 x avD glucose = ANI (%) Cerebral electrical activity was recorded by aperiodic analysis of the EEG (Lifescan). RESULTS AND DISCUSSION. In the EEG sufentanil anesthesia was characterized by a decrease in the number of high-frequency waves and an increase in the number and amplitude of delta-waves, a pattern that did not change throughout the study period. Concomitantly, under normocapnic conditions high-dose sufentanil led to the significant decrease in CBF by 29% accompanied by an 18% increase in cerebral vascular resistance (CVR). CMRO2 decreased by 22% while CMRgluc and CMRlac changed only insignificantly such that the ANI, which represents the percentage of anaerobically metabolized glucose, essentially remained unchanged. Mean perfusion pressure declined by 18% but stayed within the range of autoregulation. Hypoventilation (III) was followed by an 82% increase in CBF as a result of a 55% reduction in CVR, whereas cerebral metabolic parameters did not show important changes when compared to measurement II. Hyperventilation (IV), on the other hand, produced a distinct fall in CBF by 56% to a value that was 21% below the one obtained under normocapnia. This was due to an increase in CVR of the same magnitude. There was a 31% rise in CMRO2, resulting in a decrease in cerebral venous oxygen tension, but in no case did it fall below the critical value of 20 mmHg at which tissue hypoxia becomes severe. Although CMRlac increased and CMRgluc did not significantly change, the ANI remained essentially unchanged, which suggests a predominantly aerobic metabolism. The increase in metabolic activity with sufentanil during hypocapnia might be caused by an alkalosis-induced stimulation of glycolysis. It might also be related to a reduction in the depth of anesthesia, although neither the EEG nor the hemodynamic parameters indicated this. This study shows that the coupling between CBF and metabolism is well maintained and that the cerebrovascular response to CO2 is unimpaired during high-dose sufentanil anesthesia.
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PMID:[The effect of sufentanil on cerebral blood flow, cerebral metabolism and the CO2 reactivity of the cerebral vessels in man]. 182 62

In this study cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice during craniotomy for supratentorial cerebral tumors by the Kety and Schmidt technique. The anaesthetic procedures included halothane, enflurane isoflurane and continuous infusion with midazolam, etomidate, althesin and neurolept anaesthesia (dehydrobenzpyridol). Moderate hypocapnia was used and the anaesthesia was supplemented with nitrous oxide and fentanyl. In general, both CBF and CMRO2 were decreased. However, with inhalation anaesthetics an increase in concentration resulted in an increase in CBF (halothane) or unchanged CBF (isoflurane and enflurane) and a decrease in CMRO2. With the hypnotic agents a dose related decrease in CMRO2 was observed, while CBF either was unchanged (midazolam) or decreased (Althesin and etomidate).
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PMID:Measurement of cerebral blood flow (CBF) with the Kety and Schmidt technique during craniotomy. 184 39

Arterial CO2 tension (PaCO2) is an important factor controlling cerebral blood flow (CBF) and cerebral vascular resistance (CVR) in animals and humans. The normal responsiveness of the cerebral vasculature to PaCO2 is approximately 2 ml.min-1.100 g-1.mmHg-1. This study examined the effect of desflurane, a new volatile anesthetic, on the responsiveness of the cerebral vasculature to changes in PaCO2. Mean arterial pressure (MAP), CBF, CVR, intracranial pressure (ICP), and cerebral metabolic rate for O2 (CMRO2) were measured in five dogs anesthetized with desflurane (0.5-1.5 MAC) at normocapnia (PaCO2 = 40 mmHg) and at two levels of hypocapnia (PaCO2 = approximately 30 and approximately 20 mmHg). Under desflurane anesthesia, similar changes in CBF and CVR occurred with hyperventilation at all MAC levels of desflurane. At 0.5 MAC, CBF decreased significantly, from 81 +/- 6 to 40 +/- 3 ml.min-1.100 g-1 (P less than 0.05, mean +/- SE) when PaCO2 was decreased from 40 to 24 mmHg; i.e., the CBF decreased approximately 2.6 ml.min-1.100 g-1.mmHg-1. At 1.0 MAC desflurane, CBF decreased significantly, from 79 +/- 10 to 43 +/- 5 ml.min-1.100 g-1 with hyperventilation (2.0 ml.min-1.100 g-1.mmHg-1); at 1.5 MAC desflurane, CBF decreased from 65 +/- 6 to 38 +/- 2 ml.min-1.100 g-1 with hyperventilation (1.6 ml.min-1.100 g-1.mmHg-1). Despite the significant decreases in CBF with hyperventilation, there was no significant change in ICP. Dose-dependent decreases in MAP were observed with increasing concentrations of desflurane but were not significantly affected by ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The response of the canine cerebral circulation to hyperventilation during anesthesia with desflurane. 190 Mar 97


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