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

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

Hypocapnia and induced hypotension have been claimed by some to cause cerebral hypoxia because of insufficient perfusion. Regional cerebral blood flow (rCBF) and regional cerebral glucose utilization (rCMRglc) were measured simultaneously in the same animal subjected to hypocapnia or hypocapnia combined with induced arterial hypotension. The rCMRglc was measured with (3H) deoxyglucose and the rCBF with (14C) iodoantipyrine with the use of tissue biopsy methods and scintillation counting. Nineteen male Wistar rats were anesthetized with halothane and artificially ventilated. Anesthesia was maintained with nitrous oxide/oxygen (70:30) and succinylcholine. Six rats were maintained at normocapnia, six rats were ventilated to a PaCO2 of 20 mmHg, and seven animals were ventilated to PaCO2 20 mmHg combined with arterial hypotension of 50 mmHg (mean blood pressure) induced by infusion of adenosine. Although hypocapnia alone did not cause a statistically significant decrease of rCBF except in hippocampus, hypocapnia combined with hypotension resulted in a significant reduction of rCBF in four of seven regions when compared with hypocapnia alone; rCMRglc values were unchanged during hypocapnia. However, the addition of hypotension induced by adenosine led to a significant decline of glucose utilization in five of seven brain regions. In the present study the authors observed no increase of regional glucose utilization and hence no signs of cerebral ischemia during hypocapnia alone or combined with hypotension induced by adenosine.
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PMID:Regional cerebral blood flow and glucose utilization during hypocapnia and adenosine-induced hypotension in the rat. 249 11

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

The effect of isoflurane 1.0% and 1.5% with nitrous oxide on ventricular cerebrospinal fluid pressure was studied in 17 patients who underwent intracranial shunt procedures. Isoflurane at both concentrations caused significant increases in cerebrospinal fluid pressure during normocapnic ventilation, but these could be prevented by simultaneous hyperventilation or by the prior induction of hypocapnia. Decreases in mean arterial pressure occurred also, and resulted in a significant reduction in cerebral perfusion pressure in normocapnic patients.
Anaesthesia 1989 Jan
PMID:Isoflurane and cerebrospinal fluid pressure--a study in neurosurgical patients undergoing intracranial shunt procedures. 249 3

Cerebral blood flow (CBF) responsiveness to alterations in arterial CO2 tensions (PaCO2) during 1.4% and 2.8% isoflurane anesthesia was assessed. Dogs were initially anesthetized with thiopental (12 mg/kg, iv bolus), their tracheae intubated, after which anesthesia was maintained with 1.4% isoflurane. In eight animals three levels of PaCO2 (25, 40, and 60 mmHg) were studied during 1.4% and 2.8% isoflurane. Mean arterial blood pressure, sagittal sinus pressure, and cerebrospinal fluid pressure were measured and CBF was determined using radiolabeled microspheres. Cerebral perfusion pressure (CPP) was maintained constant at approximately 80 mmHg by inflation of a balloon in the midthoracic aorta. CBF during normocapnia was 70 +/- 14 and 118 +/- 18 ml.min-1.100 g-1 with 1.4% and 2.8% isoflurane, respectively. As PaCO2 was decreased and increased, CBF decreased and increased to 42 +/- 7% and 185 +/- 16% of control, respectively, during 1.4% isoflurane. During 2.8% isoflurane, hypocapnia decreased CBF to 39 +/- 6% of control, but CBF did not increase with hypercapnia. In a second group of animals (n = 8), the effects of changes in CPP during hypercapnia with 1.4% and 2.8% isoflurane were assessed. Increasing CPP approximately 25 mmHg with both 1.4% and 2.8% isoflurane increased CBF but did not change CVR from control. With 1.4% isoflurane, the cerebral vasculature constricts with hypocapnia and dilates with hypercapnia, whereas with 2.8% isoflurane, vasoconstriction to hypocapnia is retained but vasodilation to hypercapnia is absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebrovascular responsiveness to carbon dioxide in dogs with 1.4% and 2.8% isoflurane. 249 63

The aim of this study was to determine whether hypocapnia causes bronchoconstriction by releasing tachykinins (TKs) from C-afferent nerves in airways. Hypocapnia-induced bronchoconstriction (HIBC) was induced in anesthetized vagotomized guina pigs by ventilating lungs with a heated humidified hypocapnic gas mixture for 15 min after sudden circulatory arrest. The intensity of bronchoconstriction was assessed by calculating changes in dynamic compliance and by measuring the relaxation lung volume at the completion of experiments. Visualization of the airways by tantalum bronchography showed constriction of segmental bronchi with relative sparing of more proximal airways. Hypocapnia-induced bronchoconstriction was prevented by prior administration of salbutamol aerosol. Three experimental interventions were used to investigate the role of TKs in HIBC: 1) repeated capsaicin injections to deplete airway sensory nerves of TKs, 2) treatment with phosphoramidon, an inhibitor of enkephalinase, the main enzyme responsible for TK inactivation, and 3) topical airway anesthesia. Capsaicin pretreatment markedly attenuated the hypocapnia-induced changes in dynamic compliance (P less than 0.0005) and relaxation lung volume (P less than 0.0002), whereas phosphoramidon augmented these changes (P less than 0.02, P less than 0.03, respectively). Topical anesthesia of airways with lignocaine postponed the onset of bronchoconstriction, whereas the longer-acting, more lipid-soluble local anesthetic, bupivacaine, almost completely prevented HIBC. We conclude that, in the guinea pig lung, HIBC is mediated by TKs that are released after the activation of bronchial axonal reflexes.
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PMID:Tachykinins mediate hypocapnia-induced bronchoconstriction in guinea pigs. 251 77

1. In cats anaesthetized with Saffan, which does not block afferent activation of the brain stem defence areas, we have analysed the cardiovascular changes induced by 3 min periods of graded systemic hypoxia (fraction of O2 in inspirate, Fi,O2, 0.15, 0.12, 0.08, 0.06). 2. At light levels of Saffan anaesthesia, hypoxia (particularly Fi, O2 0.08 and 0.06) or selective stimulation of carotid chemoreceptors evoked the pattern of tachycardia, decrease in renal and mesenteric vascular conductance (RVC, MVC), but increase in femoral vascular conductance (FVC) which is characteristic of the alerting-defence response. This supports our view that activation of the defence areas is an integral part of the response to systemic hypoxia. 3. Hypoxia also induced an increase in frequency of augmented breaths which was graded with the level of hypoxia: 0.6 min-1 at Fi, O2 0.21 to 1.1 min-1 at Fi, O2 0.06; in some cats each of these was accompanied by a transient fall in arterial pressure (ABP) and increase in FVC. It is proposed that these responses were all part of a reflex elicited by lung irritant receptors and facilitated by peripheral chemoreceptors. However, their low rate of occurrence and the liability of the vasodilatation suggests they do not make major contributions to the overall response. 4. The above short-lasting responses were superimposed upon gradual changes whose magnitudes were graded with the level of hypoxia: hyperventilation, slight tachycardia, but bradycardia at Fi, O2 0.6, small increases in ABP, FVC and MVC allowing femoral and mesenteric blood flow to increase, but decreases in RVC which maintained renal blood flow constant. 5. Vagotomy had no significant effect on these changes. Further, hyperinflation of the lungs with pressures of 10 mmHg evoked the Breuer-Hering reflex but had no noticeable cardiovascular effect. It is proposed that, in the cat, reflex tachycardia and vasodilatation elicited by lung stretch receptors play no significant part in the response to hypoxia. 6. By contrast, after pneumothorax, with ventilation and thereby arterial PCO2 (Pa, CO2) maintained constant, graded hypoxia produced graded bradycardia, decrease in MVC and RVC and no change in FVC. Taken together, these results suggest that in the spontaneously breathing cat, the response to hypoxia is dominated by the effects of hypocapnia secondary to hyperventilation, which by inhibiting peripheral and central chemoreceptor activity effectively counteracts the primary bradycardia and peripheral vasoconstriction elicited by hypoxic stimulation of peripheral chemoreceptors. 7. These proposals are compared with those drawn for other species.
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PMID:Analysis of factors that contribute to cardiovascular changes induced in the cat by graded levels of systemic hypoxia. 260 Aug 40

Sixteen patients with supratentorial cerebral tumours were subjected to craniotomy under thiopentone, fentanyl, nitrous oxide, halothane anaesthesia during moderate hypocapnia (PaCO2 level 4.0 kPa). The arterio-venous oxygen content difference (AVDO2) was measured peroperatively, and repeatedly during the first three hours after extubation. Peroperatively the level of AVDO2 averaged 8.0 vol% during opening of the dura, and decreased to 7.0 vol% during closure of the dura (P less than 0.05). Immediately after extubation the AVDO2 decreased to 4.3 vol% (P less than 0.05), and during the next 3 hours a gradual increase to 5.8 vol% (P less than 0.05) was disclosed. In individual cases the postoperative changes in AVDO2 correlated fairly well with changes in mean arterial blood pressure (MABP), but other factors including duration of the operation, age of the patients, size of the tumour, level of PaCO2 and adaptation to prolonged hyperventilation during operation are supposed to be responsible for the low levels of AVDO2 observed in the postoperative period.
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PMID:Per- and postoperative changes in the arterio-venous oxygen content difference (AVDO2) in patients subjected to craniotomy for cerebral tumours. 260 75

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

A 34-year-old woman with a recent history of a influenza-like illness and signs of bronchopneumonia presented with many of the features of acute epiglottitis, a condition which still carries a high mortality in adults. Urgent laryngoscopy and bronchoscopy under inhalational anaesthesia were negative. The results of arterial blood gases, taken when stridor was at its worst, revealed marked hypocapnia and respiratory alkalosis. We conclude that the resultant acute reduction of serum ionised calcium produced stridor as a result of tetany of the vocal cords. Similar cases from the literature and the role of emotional factors in the aetiology are discussed.
Anaesthesia 1989 Mar
PMID:Stridor in an adult. An unusual presentation of functional origin. 265 May 74


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