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

The clinical value of noninvasive continuous monitoring of conjunctival oxygen tension for assessment of cerebral perfusion during carotid endarterectomy performed under general anaesthesia has been evaluated. The patients (n = 17; mean age 62.5 +/- 1.7 years) were monitored as follows: conjunctival oxygen tension (PcjO2); internal jugular venous oxygen tension at the skull base level (PcijvO2); arterial blood pressure; arterial and internal jugular venous blood gases; acid-base data and lactate, pyruvate levels; end-tidal CO2 concentration. The mean preanaesthetic PcjO2 level of 4.86 +/- 0.40 kPa was significantly lower than PaO2(PcjO2)/PaO2 ratio of 0.48). Following anaesthesia, a larger PcjO2-PaO2 gradient (ratio 0.32) was seen in spite of the hyperoxic situation (FiO2 = 0.40) due to vasoconstriction induced by slight hypocapnia (reduction of PaCO2 from 5.13 +/- 0.08 to 4.64 +/- 0.10 kPa). The carotid artery crossclamping resulted in a rapid and pronounced decrease of PcjO2, while PcijvO2 remained unchanged. No relationship between PcjO2 and stump pressure was found, while a significant correlation (P less than 0.02) between PcjO2 and lactate in effluent venous blood from the brain was demonstrable. It is concluded that PcjO2 monitoring seems a clinically useful trend indicator of cerebral perfusion in the individual patient. Due to large interindividual variations in basal PcjO2 readings and in PcjO2 changes during carotid artery clamping, however, transconjunctival oxygen tension monitoring does not seem to allow early and accurate recognition of impending cerebral ischaemia during carotid endarterectomy, and its routine use therefore seems of limited value.
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PMID:Continuous conjunctival oxygen tension (PcjO2) monitoring for assessment of cerebral oxygenation and metabolism during carotid artery surgery. 281 41

1. The effect of varying artificial respiratory volume (at a fixed rate of 54 min-1) on cardiac output, its distribution and tissue blood flows were determined with tracer microspheres in control pithed rats or during pressor responses to either the alpha 1-adrenoceptor agonist phenylephrine or the alpha 2-agonist xylazine. Phenylephrine was investigated in the presence of propranolol (3 mg kg-1). The rats were pithed under halothane anaesthesia. 2. A respiratory volume of 15 ml kg-1 produced modest hypercapnia (PaCO2 = 47 mmHg), hypoxia (PaO2 = 60 mmHg) and acidosis (pH = 7.35) relative to control animals respired at 20 ml kg-1 (PaCO2 = 32 mmHg; PaO2 = 77 mmHg; pH = 7.47). In rats respired at 15 ml kg-1, total peripheral resistance was lower, and cardiac output greater (due to increased stroke volume), than in the controls. Lowering respiratory volume reduced distribution of cardiac output to the kidneys, increased it to the large intestine and also increased blood flow through the gastrointestinal tract, skin and spleen. A respiratory volume of 30 ml kg-1 gave mild hypocapnia (PaCO2 = 19 mmHg), hyperoxia (PaO2 = 101 mmHg) and alkalosis (pH = 7.59) compared to 20 ml kg-1 but had no effect on cardiac output distribution or organ blood flow although heart rate was 29% greater at 30 ml kg-1. 3. Xylazine (500 micrograms bolus followed by 100 micrograms min-1 infusion) at all three respiratory volumes gave well-sustained mean pressor responses of 62-64 mmHg by increasing both total peripheral resistance and cardiac output (resulting from increased stroke volume). It increased the proportion of cardiac output passing to the liver, reduced that going to the spleen and gastrointestinal tract and increased cardiac, renal and hepatosplanchnic blood flows. 4. The secondary, relatively sustained, pressor effect of phenylephrine (5 micrograms bolus followed by 0.4 micrograms min-1 infusion, i.v.) varied at the 3 respiratory volumes with mean values from 32 to 53 mmHg. This response was due to both increased total peripheral resistance and cardiac output (resulting from greater stroke volumes and/or heart rates). Phenylephrine increased the proportion of cardiac output passing to the gastrointestinal tract, heart, kidneys and hepatosplanchnic bed and increased cardiac, hepatosplanchnic, renal and gastrointestinal blood flows. 5. Respiratory volume had no effect on the cardiovascular effects of xylazine. However, respiratory volume modified the effects of phenylephrine on heart rate and changed the relative contributions of stroke volume and heart rate to the increased cardiac output. It also influenced the effects of phenylephrine on cardiac output distribution to the liver, epididimides and hepatosplanchnic bed and on blood flow through skeletal muscle and the large intestine. 6. Changes in respiratory volume of air ventilated pithed rats thus influence cardiac output, its distribution and regional blood flows. Such changes can also differently influence the responses of various vascular beds to phenylephrine whilst having no effect on their responses to xylazine.
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PMID:Effect of artificial respiratory volume on the cardiovascular responses to an alpha 1- and an alpha 2-adrenoceptor agonist in the air-ventilated pithed rat. 289 57

Propofol like thiopental and etomidate, suppresses cortical electrical activity in a dose-related manner, which leads to a 36% decrease in cerebral oxygen uptake and a 51% decrease in cerebral blood flow after an induction dose of 2 mg/kg followed by a maintenance dose of 0.2 mg/kg per min. In this study, the effects of propofol and varying paCO2 values on cerebral energy and amino acid metabolism were examined. METHODS. Eleven male patients between 49 and 63 years of age who were about to undergo coronary artery bypass surgery were studied. Measurements were performed with the patient awake (I), during steady-state maintenance anesthesia after propofol 2 mg/kg as an induction dose with 0.2 mg/kg per min by infusion with normocapnia (paCO2 39.9 +/- 3.1 mm Hg) (II), during hypocapnia (paCO2 29.9 +/- 2.6 mmHg) (III), and during hypercapnia (paCO2 50.6 +/- 3.3 mmHg) (IV). Cerebral blood flow was measured using the argon wash-in technique. A catheter was advanced into the superior bulb of the right internal jugular vein for measurement of cerebral oxygen, glucose, lactate, and amino acid uptake and release, which were calculated by multiplying the arterial-cerebral venous oxygen and substrate difference by the cerebral blood flow. Lactate/glucose index was calculated from the equation. Formula: see text. where a-vD lactate and a-vD glucose represent the arterial-cerebral venous substrate differences in mmol/l. Cerebral electrical activity was recorded by Fourier analysis of the EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Energy and amino acid metabolism in the human brain under Disoprivan anesthesia with various paCO2 values]. 289 87

The effects on cerebral metabolism and the electroencephalogram (EEG) of combining hypocapnia with hypotension have been only incompletely examined. The present study examined the possibility that hypocapnia may worsen the cerebral metabolic and EEG disturbances caused by hypotension. Cerebral metabolism and the EEG were studied at three levels of hypotension during hypocapnia (PaCO2 = 20 mm Hg) in dogs under light halothane anesthesia. A sequential decrease of the mean arterial pressure (MAP) to 60, 50, and 40 mm Hg (30 minutes at each level) was achieved with sodium nitroprusside (SNP) (n = 12) or trimethaphan (TMP) (n = 12). With SNP-induced hypotension plus hypocapnia, the power of the alpha and beta 2 spectra of the EEG decreased at MAP less than or equal to 60 mm Hg. Cerebral metabolic values were unchanged at a MAP of 60 or 50 mm Hg. Brain tissue phosphocreatine and the cerebral energy charge decreased, and the lactate/pyruvate ratio increased at a MAP of 40 mm Hg. With TMP-induced hypotension plus hypocapnia, power decreased in the alpha and beta 2 spectra of the EEG at MAP less than or equal to 60 mm Hg. Cerebral metabolic values were unchanged at a MAP of 60 mm Hg. At MAP less than or equal to 50 mm Hg, power in the beta 1 spectrum, brain tissue phosphocreatine, and the cerebral energy charge all decreased. At a MAP of 40 mm Hg, the cerebral glucose value decreased and the lactate/pyruvate ratio increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral metabolism and the electroencephalogram during hypocapnia plus hypotension induced by sodium nitroprusside or trimethaphan in dogs. 308 Jun 92

Expired carbon dioxide measurements (PeCO2) were used (1) to assess the adequacy of initial alveolar ventilation, and (2) to document intraoperative airway events and metabolic trends. Three hundred and thirty-one children were studied. Thirty-five intraoperative events were diagnosed by continuous PeCO2 monitoring; 20 were potentially life-threatening problems (malignant hyperthermia, circuit disconnection or leak, equipment failure, accidental extubation, endobronchial intubation, or kinked tube); only two of these were also diagnosed clinically. The duration of anaesthesia may be a factor: 3.9 hours for cases with events vs. 2.5 hours for cases without events (p less than 0.002). There was a higher incidence of hypercarbia (peak expired PeCO2 greater than or equal to 50) in children who were not intubated (29 per cent) compared to those who had an endotracheal tube in place (12 per cent) (p = 0.0001). Hypocarbia (peak expired PeCO2 less than or equal to 30) was more frequent in intubated cases (11 per cent) than in unintubated cases (three per cent) (p = 0.03). There was a high incidence of hypocarbia in infants less than one year of age (p = 0.02). We conclude: (1) life-threatening airway problems are common during anaesthesia in paediatric patients; (2) quantitative measurement of PeCO2 provides an early warning of potentially catastrophic anaesthetic mishaps; (3) the incidence of events increases with duration of anaesthesia.
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PMID:Intraoperative events diagnosed by expired carbon dioxide monitoring in children. 308 6

In 14 patients with supratentorial cerebral tumours with midline shift less than or equal to 10 mm, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice on the contralateral side of the craniotomy, using a modification of the Kety & Schmidt method. For induction of anaesthesia, thiopental, fentanyl and pancuronium were used. The anaesthesia was maintained with enflurane 1% in nitrous oxide 67%. Moderate hypocapnia to a level averaging 4.3 kPa was achieved. The patients were divided into two groups. In Group 1 (n = 7), 1% enflurane was used throughout the anaesthesia, and CBF and CMRO2 measured about 70 min after induction averaged 30.1 ml 100 g-1 min-1 and 1.98 ml O2 100 g-1 min-1, respectively. During the second CBF study 1 h later, CBF and CMRO2 were unchanged (P greater than 0.05). In Group 2 (n = 7), the inspiratory enflurane concentration was increased from 1 to 2% after the first CBF measurement. In this group a significant decrease in CMRO2 was observed, while CBF was unchanged. In six patients EEG was recorded simultaneously with the CBF measurements. In patients subjected to increasing enflurane concentration (Group 2), a suppression in the EEG activity was observed without spike waves. It is concluded that enflurane induces a dose-related decrease in CMRO2 and suppression in the EEG activity, whereas CBF was unchanged.
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PMID:CBF and CMRO2 during craniotomy for small supratentorial cerebral tumours in enflurane anaesthesia. A dose-response study. 310 85

This study examined the effect of prolonged hypocapnia on the rate of cerebrospinal fluid (CSF) production (Vf) and on other CSF dynamics in dogs. Determination of CSF values began 2 h after the onset of hypocapnia and continued for an additional 3 h. Two separate methods were used to determine Vf: modified open ventriculocisternal perfusion and closed ventriculocisternal perfusion. Dogs were examined both during hypocapnia plus anesthesia with halothane (0.8%) and nitrous oxide (66%), and during hypocapnia plus sedation with nitrous oxide (66%) and halothane (0.15%) combined with bupivacaine (0.75%) infiltration of wound edges. There were no differences in Vf measured by the two methods. At the first measurable time period, mean Vf values during hypocapnia and halothane anesthesia, 32 +/- 9 and 35 +/- 10 microliters/min (mean +/- SD), were lower than mean Vf values during hypocapnia and nitrous oxide sedation, 48 +/- 11 and 49 +/- 8 microliters/min. Vf did not change significantly during 3 h of hypocapnia. For both halothane anesthesia and nitrous oxide sedation, mean Vf values during hypocapnia were not significantly different from Vf values previously reported during normocapnia, 31 +/- 12 and 33 +/- 12 microliters/min and 44 +/- 13 and 47 +/- 14 microliters/min, respectively. The results indicate that prolonged hypocapnia does not decrease Vf, and, therefore, reduction of Vf is probably not one of the causes for reduction of elevated CSF pressure by prolonged hypocapnia. Regarding the other data on CSF dynamics, CSF pressure at hypocapnia was similar to that at normocapnia, suggesting that hypocapnia did not affect resistance to reabsorption of CSF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolonged hypocapnia does not alter the rate of CSF production in dogs during halothane anesthesia or sedation with nitrous oxide. 311 7

1. The effects of hypercapnia and hypocapnia on brain intracellular pH (pHi) and metabolism were investigated in new-born lambs under barbiturate anaesthesia. 2. 31P nuclear magnetic resonance (n.m.r.) spectroscopy was used to determine brain pHi and the relative concentrations of compounds containing mobile phosphorus nuclei including phosphocreatine (PCr), nucleoside triphosphates (NTP) and inorganic phosphate (Pi). Simultaneous measurements were made of the molar ratio of glucose to oxygen uptake by the brain. 3. During normocapnia (arterial partial pressure of CO2 Pa, CO2, 39 +/- 1 mmHg mean +/- S.E. of mean, n = 9) brain pHi was 7.13 +/- 0.02. Hypercapnia (Pa, CO2, 98 +/- 3 mmHg) was associated with a fall in brain pHi to 6.94 +/- 0.03 (n = 19, P less than 0.001), whereas no significant change in brain pHi occurred during hypocapnia (Pa, CO2, 16 +/- 1 mmHg; brain pHi 7.15 +/- 0.01). 4. During hypercapnia there was an increase in the ratio of Pi to NTP from 1.09 +/- 0.08 to 1.47 +/- 0.06 (P less than 0.001) and a decrease in the ratio PCr/Pi from 1.60 +/- 0.08 to 0.93 +/- 0.04 (P less than 0.001). There was a linear correlation between Pi/NTP and brain pHi. 5. Alterations in arterial PCO2 had no significant effect on the molar ratio of glucose to oxygen uptake by the brain, which remained close to unity. 6. The change in brain pHi observed during hypercapnia can be accounted for by the known physico-chemical buffering capacity of brain tissue. Homoeostasis of brain pHi during hypocapnia provides further evidence that additional regulatory mechanisms operate in these circumstances. 7. The observed changes in PCr and Pi can be accounted for in part by the [H+] dependence of the creatine kinase reaction.
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PMID:Brain intracellular pH and metabolism during hypercapnia and hypocapnia in the new-born lamb. 311 75

Effects of halothane/N2O anesthesia and in situ freezing of the brain on mean arterial blood pressure (MABP), pH, pCO2 and pO2 were evaluated in rabbits with either Streptococcus pneumoniae or Escherichia coli meningitis. Prior to anesthesia infected rabbits had, compared to controls, significantly lower values for MABP and pCO2, either with a compensated (S. pneumoniae group) or decompensated (E. coli group) metabolic acidosis. In most animals a slight additional decrease in MABP was observed during anesthesia. With maintained pre-anesthetic hypocapnia no further disturbance in acid-base balance occurred during anesthesia. After one minute of freezing MABP increased towards preanesthetic levels. We conclude that the technique for in situ freezing of the brain under halothane/N2O anesthesia may be applied for studies of cerebral metabolism in rabbit with experimental meningitis.
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PMID:Experimental meningitis in the rabbit. I. Arterial blood pressure and acid-base balance during halothane anesthesia and in situ freezing of the brain. 311 54

The intracranial pressure (ICP) responses to administration of either halothane or isoflurane were compared in New Zealand white rabbits following a standardized cryogenic brain injury. Animals were tracheally intubated and paralyzed, and background anesthesia was maintained with morphine sulfate and nitrous oxide. Following injury and attainment of an elevated and stable ICP, animals were divided into four groups. Animals in groups I and III were maintained normocapnic throughout the experiment and administered 1 MAC halothane or isoflurane, respectively. Group II and IV animals were made hypocapnic (PaCO2 = 20 mmHg) prior to the administration of either 1 MAC halothane or isoflurane, respectively. Monitored variables were mean arterial blood pressure, ICP (ventriculostomy), end-tidal (ET) CO2, ET volatile anesthetic, the electroencephalogram, temperature, and arterial blood gases. Prior to producing the lesion, ICP was approximately 5 mmHg in all animals with no differences among groups. Sixty to ninety minutes after injury, ICP increased significantly to approximately 20 mmHg in all animals. Introduction of either halothane or isoflurane was associated with significant increases in ICP in all groups to approximately 30 mmHg. These data suggest that further significant increases in ICP may occur following introduction of either halothane or isoflurane in the presence of acute brain injury and elevated ICP. Furthermore, these ICP increases may not be altered by the prior establishment of hypocapnia.
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PMID:The intracranial pressure effects of isoflurane and halothane administered following cryogenic brain injury in rabbits. 311 88


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