Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the depressive effect of sevoflurane on ventilation has been reported, its potency and mode of action on the neural respiratory activity is still unclear. Therefore, the effects of sevoflurane on the phrenic nerve discharge and the respiratory timing were compared with those of halothane. The efferent activity of the phrenic nerve was recorded from decerebrate, un-anesthetized and artificially ventilated cats, and its power spectrum was calculated. The inspiratory and expiratory periods were measured. Sevoflurane and halothane of the doses of 0.5-1.5 MAC were inhaled for 15 min. With 0.5 MAC, sevoflurane decreased the total power and two dominant spectral components of the high-frequency oscillation and medium-frequency oscillation in the power spectrum. With the same MAC dose, halothane had a greater depressive effect in a normocapnic condition with the vagus nerves being intact. In a state of hypercapnia or after vagotomy, the effect of halothane was considerably attenuated whereas that of sevoflurane remained unaltered. Halothane increased the neural respiratory rate much more than sevoflurane in both normocapnic and hypercapnic states. Vagotomy significantly weakened the effect of halothane to increase the respiratory rate but did not modify the effect of sevoflurane. With 1.0-1.5 MAC, both anesthetics severely decreased the phrenic power spectra and the potency difference became indistinct. The present findings demonstrate that sevoflurane has a weaker depressive effect on the respiratory nerve discharge and a smaller effect on the neural respiratory rate than halothane when the effects of 0.5 MAC were compared.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of sevoflurane on respiratory activities in the phrenic nerve of decerebrate cats. 748 33

Improved understanding of the structure/activity relationship of inhaled anaesthetics has resulted in the synthesis of fluorinated compounds which are more potent and less toxic than their unfluorinated antecedents. The toxic effects of inhaled anaesthetics on the liver and kidney are complex but, in general, are related to the extent to which individual inhaled agents are metabolised. Halothane hepatotoxicity is a rare, idiosyncratic reaction which typically occurs in obese women having more than one exposure to the drug within a short time interval. All currently available volatile anaesthetic drugs have depressant effects on the cardiovascular and respiratory systems; arrhythmias are more likely with halothane than with the fluorinated ethers. Cerebral blood flow tends to increase during inhalation anaesthesia, especially with halothane and in the presence of hypercarbia; isoflurane may be given sparingly during neurosurgical procedures whilst monitoring its end-tidal concentration. Although the volatile agents tend to cause uterine relaxation they may be given safely in low concentration to avoid awareness during Caesarean section. In general, young children require rather higher concentrations of volatile agents than adults and seem to be less susceptible to organ toxicity. Two relatively new volatile agents, sevoflurane and desflurane, offer some advantages over isoflurane but neither is an "ideal drug'. Sevoflurane interacts with soda-lime to produce a series of degradation products, the most important of which is compound A. Production is greatest during low-flow, closed circuit anaesthesia using high inspired concentrations of the drug. Compound A has nephrotoxic potential in rats but the clinical significance of the interaction between sevoflurane and soda-lime is unclear. Nitrous oxide when given for prolonged periods may cause irreversible bone marrow depression.
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PMID:Comparative tolerability profiles of the inhaled anaesthetics. 909 54

The cardiopulmonary effects of sevoflurane (mean, 2.6, 3.8-3.9 and 5.2 per cent) were compared with those of halothane (1.2, 1.8 and 2.4 per cent), enflurane (2.4, 3.6 and 4.8 per cent) and isoflurane (1.6, 2.4 and 3.2-3.3 per cent) at end-tidal concentrations equivalent to 1, 1.5 and 2 minimal alveolar concentrations (MACs) during spontaneous or controlled ventilation (SV or CV) in 57 cats. Cats were assigned to four groups of nine animals each in SV trial and four groups of five or six animals each in CV trial. During SV, respiration rate was decreased by sevoflurane and isoflurane at 2 MAC and by enflurane at each MAC multiple when compared with control values, whereas halothane increased respiration rate at 2 MAC. The degree of hypercapnia and acidosis induced by sevoflurane was not different from that induced by isoflurane and was less than that induced by halothane at 1 to 1.5 MAC or enflurane at 2 MAC. During SV and CV, four anaesthetics decreased heart rate at 2 MAC when compared with control values, but there was no significant difference between anaesthetics. Sevoflurane, like halothane and isoflurane, induced hypotension at 2 MAC when compared with 1 MAC.
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PMID:Cardiopulmonary effects of sevoflurane in cats: comparison with isoflurane, halothane, and enflurane. 949 44

We have determined the influence of 0.1 minimum alveolar concentration (MAC) of sevoflurane on ventilation, the acute ventilatory response to a step change in end-tidal carbon dioxide and the ventilatory response to sustained hypercapnia in 10 healthy adult volunteers. Subjects undertook a preliminary 10-min period of breathing air without sevoflurane to determine their normal ventilation and natural end-tidal PCO2. This 10-min period was repeated while breathing 0.1 MAC of sevoflurane. Subjects then undertook two procedures: end-tidal PO2 was maintained at 13.3 kPa and end-tidal PCO2 at 1.3 kPa above the subject's normal value for 30 min of data collection, first with and then without 0.1 MAC of sevoflurane. A dynamic end-tidal forcing system was used to generate these gas profiles. Sevoflurane did not significantly change ventilation: 10.1 (SEM 1.0) litre min-1 without sevoflurane, 9.6 (0.9) litre min-1 with sevoflurane. The response to acute hypercapnia was also unchanged: mean carbon dioxide response slopes were 20.2 (2.7) litre min-1 kPa-1 without sevoflurane and 18.8 (2.7) litre min-1 kPa-1 with sevoflurane. Sustained hypercapnia caused a significant gradual increase in ventilation and tidal volume over time and significant gradual reduction in inspiratory and expiratory times. Sevoflurane did not affect these trends during sustained hypercapnia. These results suggest that 0.1 MAC of sevoflurane does not significantly affect the acute ventilatory response to hypercapnia and does not modify the progressive changes in ventilation and pattern of breathing that occur with sustained hypercapnia.
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PMID:Effects of subanaesthetic sevoflurane on ventilation. 1: Response to acute and sustained hypercapnia in humans. 1061 28

A crossover study design was used to investigate the dose-related effects of sevoflurane at end-tidal concentrations of 2.2 to 4.4 per cent on the respiratory rate, blood gases, heart rate, arterial blood pressure and ocular signs of chickens during spontaneous and controlled ventilation. The mean (sd) carbon dioxide partial pressure (PaCO2) increased as the concentration of sevoflurane increased, and was 86 (29) mmHg at an end-tidal concentration of 4.4 per cent during spontaneous ventilation, but was maintained between 29 and 42 mmHg during controlled ventilation. The heart rate increased as the concentration of sevoflurane increased during spontaneous ventilation, but did not change during controlled ventilation. Sevoflurane decreased arterial blood pressure during both spontaneous and controlled ventilation, but a dose-dependent decrease in arterial blood pressure was observed only during controlled ventilation. The mean arterial blood pressure at an end-tidal concentration of 4.4 per cent was significantly higher during spontaneous ventilation than during controlled ventilation. Controlled ventilation prevented the increases in PaCO2 and heart rate that were observed during spontaneous ventilation. The decrease in arterial blood pressure during spontaneous ventilation was less than that during controlled ventilation, possibly owing to the effects of hypercapnia.
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PMID:Sevoflurane anaesthesia in chickens during spontaneous and controlled ventilation. 1255 80

Malignant hyperthermia (MH) is a rare condition consisting of increased temperature and rigidity with mild to fulminant manifestation during anesthesia. Sevoflurane was thought to be a less potent triggering agent of MH; however, in literature review, the onset of MH after exposure to sevoflurane may be associated with calcium release from the sarcoplasmic reticulum. We present here a case of rarely-seen delayed MH induced by an inhalation agent of low-inducing probability, sevoflurane, after the second exposure to which within a short period of time. The patient was a five years old boy who received sevoflurane anesthesia for repeat orthopedic surgery within two days. Gradual elevation in heart rate, abrupt hypercarbia and hyperthermia were observed 90 min after induction. Dantrolene was administrated immediately with effective therapeutic response. Eventually, the patient recovered without any complication as an aftermath. Gradually elevated heart rate during the second exposure to sevoflurane was the atypical sign in the episode of MH in this case. One plausible explanation for the development of delayed onset of MH is the latent effect of the volatile anesthetic on the skeletal muscles. Therefore, it is worth noting for the anesthesiologists to recognize the possibility of an atypical MH and be alert for the possible occurrence of MH during routine anesthetic practice.
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PMID:Delayed onset of sevoflurane-induced juvenile malignant hyperthermia after second exposure. 1797 24