Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

EEG, end-tidal CO2, neck muscle EMG, eye movements, and ECG were recorded in 17 children undergoing enflurane anesthesia combined with N2O and O2. All subjects were classified in the lowest risk group and had normal pre-anesthetic EEG recordings. Eleven subjects were breathing spontaneously and six were under controlled ventilation. Thirteen subjects were hyperventilated for short periods. As previously reported for adults, various signs of increased central nervous excitability appeared. At the enflurane concentration of 4% all three cases with PaCO2 below 32 mmHg showed generalized high voltage epileptic activity of grand mal type followed by several minutes of postictal slowing. One of these subjects also showed motor manifestations of the electrographic seizure activity. At 3% enflurane, three out of eight subjects showed electrographic seizure activity of poly-spike-suppression type. One of these children also had motor manifestations during this type of seizure activity at a PaCO2 of 31 mmHg. The results indicate that electrographic seizure activity is common among children with moderate hypocapnia at enflurane concentrations of 3% or more.
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PMID:Electroencephalographic activity in children under enflurane anesthesia. 121 Oct 75

The cerebrovascular response to CO2 has been reported to be preserved during propofol anesthesia, but no comparison with awake control values has been made, and the additional influence of N2O has not been investigated. Using the noninvasive technique of transcranial Doppler ultrasonography, this study investigated the cerebrovascular response to varying levels of PaCO2 while awake and during anesthesia with propofol and propofol/N2O. Seven adults without systemic diseases undergoing nonneurologic surgery were studied. A pulsed-wave Doppler monitor was used to measure the mean middle cerebral artery flow velocity (Vmca) during varying levels of PaCO2 (25-55 mmHg) under the following conditions: 1) awake; 2) propofol 2.5 mg.kg-1 bolus followed by continuous infusion of 150 micrograms.kg-1.min-1; and 3) propofol as in the condition above plus 70% N2O. During the awake study condition, hypocapnia was induced by voluntary hyperventilation, and hypercapnia was induced with rebreathing of 7% CO2 in a closed circuit. During the anesthetized study conditions, hypocapnia and hypercapnia were induced by adjustment of minute ventilation. A minimum of five to six simultaneous Vmca and PaCO2 measurements were obtained under each of the study conditions. Systemic blood pressure was monitored via a radial arterial catheter, and phenylephrine was administered if mean arterial blood pressure decreased below 60 mmHg (phenylephrine was used in three of five patients in the propofol-N2O group). Linear regression and analysis of covariance were used for statistical analysis of Vmca-PaCO2 relationships.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of propofol with and without nitrous oxide on cerebral blood flow velocity and CO2 reactivity in humans. 144 39

Desflurane causes dose-dependent decreases in cerebrovascular resistance and cerebral metabolic rate of oxygen consumption (CMRO2), suggesting that desflurane is a cerebral arteriolar dilator with global flow-metabolism coupling similar to halothane and isoflurane. Desflurane is also similar to isoflurane in that cerebrovascular responsivity to carbon dioxide appears to be maintained. In the dog, arterial hypotension to 40 mm Hg induced with 2.4 MAC desflurane resulted in global decreases in cerebral blood flow of 60% and CMRO2 of 20%. Concentrations of cerebral metabolites of high-energy phosphates were not significantly deranged. The intracranial pressure data from humans are controversial. Desflurane and oxygen at 1 MAC caused sustained increases in cerebrospinal fluid pressure (maximum of 19 +/- 6 mm Hg) in patients undergoing craniotomy for mass lesion, despite prior establishment of hypocapnia. In a more recent study, the same investigators reported similar cerebrospinal fluid pressures before and after 0.5 MAC of either isoflurane or desflurane in 50% N2O. The electroencephalographic effects of desflurane are similar to those of isoflurane in humans, and burst suppression is easily achieved. There are no data available concerning possible interactions between desflurane and the outcome of a cerebral ischemic event. Similar to other potent volatile agents, desflurane can cause cerebral vasodilation and may result in intracranial pressure changes in vulnerable patients, but if adequate hyperventilation and depth of anesthesia are maintained, it is probably safe to use desflurane in a manner similar to isoflurane in patients with decreased intracranial compliance.
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PMID:Effects of desflurane on the central nervous system. 152 38

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

The effects of variation of arterial CO2 tension (PaCO2) on the electroencephalogram (EEG) and posterior tibial nerve somatosensory cortical evoked potentials (PTN-SCEP) during opioid/N2O anesthesia have not been well documented. We studied the effects of hypocapnia (PaCO2 approximately 23 mmHg) and hypercapnia (PaCO2 approximately 50 mmHg) during steady-state alfentanil/N2O anesthesia in 16 patients. EEG and PTN-SCEP were recorded continuously, while PaCO2 was altered in 15-min intervals by varying the inspired CO2 concentration. Hypocapnia caused significant increases in power in the delta, theta, and beta bands (P less than 0.01), with the greatest increase observed in the alpha band. Relative power increased in the alpha band but remained unchanged in the delta, theta, and beta bands. Median frequency and 95% spectral edge frequency were unaltered during hypocapnia. In contrast, hypercapnia caused a significant decrease of power in the alpha and beta bands, whereas delta and theta power remained unchanged. This was reflected in a significant decrease of the 95% spectral edge frequency, from 8.9 (6.7-11.6) to 7.0 (5.6-8.6) Hz. All EEG parameters returned to normal upon restoration of normocapnia. There was a significant negative correlation between power in the alpha band and end-tidal CO2 in all patients (r = 0.47 to -0.89). PTN-SCEP latencies and amplitudes were not significantly different from control values during hypocapnia and hypercapnia. It is concluded that variations in PaCO2 within the limits 20-50 mmHg produce substantial changes in the EEG power spectrum, especially in the alpha band (8-12 Hz), but do not alter PTN-SCEP.
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PMID:Influence of changes in arterial carbon dioxide tension on the electroencephalogram and posterior tibial nerve somatosensory cortical evoked potentials during alfentanil/nitrous oxide anesthesia. 190 85

The effect of hypocapnia on arterial oxygenation was investigated in unilaterally thoracotomized patients (N = 11) and dogs (N = 9) anesthetized with N2O-O2-enflurane. In patients, a change in PaCO2 from 39.7 +/- 1.4 to 28.2 +/- 1.7 mmHg produced a significant fall in PaO2 from 146 +/- 32 to 126 +/- 27 mmHg. In dogs, the change in PaCO2 from 38.7 +/- 0.8 mmHg (normocapnia) to 22.4 +/- 0.9 mmHg (hypocapnia) produced a significant decrease in PaO2 from 94 +/- 6 to 77 +/- 5 mmHg and a significant increase in pulmonary shunt (Qs/Qt) from 13.5 +/- 1.6 to 19.4 +/- 1.7%. Hypocapnia induced significant decreases in cardiac output and pulmonary arterial pressure; from 3.6 +/- 0.4 to 3.1 +/- 0.3 l.min-1, and from 20.8 +/- 1.3 to 17.5 +/- 1.0 mmHg, respectively. After the thoracotomy, the end-expiratory volume of the lung of the thoracotomized side became smaller. Therefore, a large fraction of low VA/Q regions might have existed in the lung of the studied patients and animals. Since hypocapnia induces an attenuation of hypoxic pulmonary vasoconstriction (HPV), an attenuation of HPV by hypocapnia might have occurred in the present study, which in turn produced a disproportionate increase in perfusion to low VA/Q regions, leading to the increase in Qs/Qt as observed in the present study.
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PMID:[The effect of hypocapnia on arterial oxygenation in thoracotomized dogs]. 212 45

Apnea and desaturation following nitrous oxide inhalation were studied in seven adult volunteers breathing spontaneously. Arterial oxygen saturation (SpO2), end-tidal CO2 concentration in the nasal cavity and respiratory patterns were measured in volunteers breathing air after N2O (50% or 67%) + O2. SpO2 was measured with Biox 3700 and end-tidal CO2 concentration was measured with Normocap, and respiratory patterns were recorded with RESPIGRAPH. After breathing N2O, two volunteers had frequent apnea (greater than 20 sec) accompanied by desaturation (SpO2 less than 90%). The lowest value of SpO2 was 82%. When the apnea occurred, the airway seemed to be open and end-tidal CO2 concentration values were lower than those before N2O inhalation. The authors considered that this kind of apnea was due to several factors, such as hypocapnia caused by hyperventilation during N2O anesthesia, dilution of alveolar O2 and CO2 during N2O excretion, loss of consciousness by N2O, and depression of CO2 ventilatory response by N2O. Inhalation of O2 at high concentrations for five minutes could improve the hypocapnia and prevent the apnea.
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PMID:[Apnea and oxygen desaturation following nitrous oxide inhalation]. 223 28

The effect of hypocapnia on regional cerebral glucose utilization (L-CMRg) was studied in 14 Sprague Dawley rats. After cannulation of femoral vessels, halothane was discontinued and anesthesia was maintained with 70% N2O in oxygen. The animals' lungs were mechanically ventilated to achieve normocapnia (PaCO2 = 40 +/- 2 mmHg) in group A or hypocapnia (PaCO2 = 25 +/- 2 mmHg) in group B. L-CMRg was measured by the 14C-2-deoxyglucose autoradiographic method. Twenty-six anatomically discrete structures representing cortical, subcortical, limbic, and brainstem areas were studied. In hypocapnic animals, mean values for L-CMRg were higher in 25 out of 26 structures studied. The increase in L-CMRg was heterogenous. The structures that had higher L-CMRg during normocapnia showed the greatest increase in L-CMRg. When the two groups were compared using a profile analysis, in six regions (lateral and ventral thalamus, inferior colliculus, lateral habenulla, medial geniculate body, and auditory cortex), a value of P less than 0.05 was obtained.
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PMID:Effect of hypocapnia on local cerebral glucose utilization in rats. 249 55

To determine the effect of inhalation anaesthetics on the plasma concentration of laudanosine necessary to produce CNS excitation, we administered laudanosine 0.5 mg kg-1 min-1 i.v. to 40 rabbits under eight study conditions: 1.0 or 0.7% halothane, 1.6% isoflurane, 2.0% enflurane, during normocapnia and hypocapnia; 70% nitrous oxide, alone and with 1.0% halothane, and room air (control). At the onset of purposeless, unco-ordinated movements of the entire body, blood samples were obtained to determine the CNS excitation-threshold plasma concentration (ETPC) of laudanosine. During normocapnia, 1.0% halothane, 1.6% isoflurane and 2.0% enflurane increased ETPC (mean (SD) 11.8 (2.5), 11.3 (2.8) and 9.1 (1.4) micrograms ml-1, respectively) from control (5.0 (0.9) microgram ml-1). ETPC during enflurane anaesthesia did not change significantly with hypocapnia. Nitrous oxide, alone or in combination with halothane, did not change ETPC. The combination of nitrous oxide with 1.0% halothane significantly decreased ETPC to less than that for halothane alone (6.7 (1.2) v. 11.8 (2.5) micrograms ml-1, respectively).
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PMID:Modification of central nervous system effects of laudanosine by inhalation anaesthetics. 260 78

The effects of halothane and isoflurane on regional cerebral blood flow (CBF) were studied in 18 New Zealand White rabbits anesthetized with nitrous oxide (N2O) and morphine sulfate (MS) at three different levels of PaCO2. CBF was measured using the hydrogen clearance technique. Monitored variables were intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, electroencephalogram, arterial blood gases, end-tidal (ET) volatile anesthetic, and ET CO2. Addition of 1 MAC halothane to the N2O/MS background anesthetic caused flow to increase significantly in all three regions studied (cortex, dorsal hippocampus, white matter) at all three levels of PaCO2 (low: 20-25 mmHg; normal: 35-40 mmHg; high: 50-55 mmHg). Addition of 1 MAC isoflurane to the background anesthetic caused CBF to decrease significantly in all regions during hypocapnia. During normocapnia, CBF was unchanged with the addition of 1 MAC isoflurane in all regions and during hypercapnia, CBF increased significantly only in the dorsal hippocampus following addition of 1 MAC isoflurane to the MS/N2O background anesthetic. Volatile anesthetic administration was associated with significant, although small, increases in ICP at all PaCO2 levels. We conclude that 1 MAC concentrations of halothane and isoflurane have opposite effects on CBF when added to a N2O/MS anesthetic during hypocapnia and that the effects of isoflurane on regional CBF are dependent on PaCO2 in rabbits under the anesthetic conditions of this experiment.
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PMID:Isoflurane, halothane, and regional cerebral blood flow at various levels of PaCO2 in rabbits. 308 28


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