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)

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

Regional (frontal, parietal, occipital, cortical, and basal ganglia) cerebral blood flow (rCBF) was examined at 1.5 and 3.5 MAC inspired isoflurane/O2 anesthesia in the rat using the radioactive microsphere technique to determine the effects of controlled hypotension with deep isoflurane anesthesia on rCBF and the response of rCBF to changes in PaCO2 when mean blood pressure (BP) was decreased to levels below the lower limit of the autoregulatory threshold. Four groups of six rats were studied with rCBF 1 determined at 1.5 MAC (mean BP 80-90 mm Hg) followed by two rCBF determinations at 3.5 MAC (mean BP 46-48 mm Hg). For CBF 1 the regional CO2 response was a 3.1-3.9% increase in rCBF/mm Hg increase in CO2. Regional cerebral blood flow (ml/g/min) ranged from 0.64 +/- 0.05-0.83 +/- 0.15 at PaCO2 of 19 mm Hg to 1.34 +/- 0.11-1.80 +/- 0.33 at PaCO2 of 41 mm Hg to 2.61 +/- 0.26-3.72 +/- 0.37 at PaCO2 of 59 mm Hg (mean +/- SEM). With controlled hypotension (CBF 2) rCBF was unchanged during normocarbia, increased 100% during hypocarbia, P less than 0.01 vs CBF 1 and decreased 30% during hypercarbia, P less than 0.01 vs CBF 1. For rCBF 3 measurements, the BP and inspired concentration of isoflurane were kept constant, while PaCO2 was increased in two and decreased in two of the four groups. Within-group comparisons between rCBF 2 and rCBF 3 results demonstrated loss of CO2 responsiveness of the rat cerebrovasculature in every region during controlled hypotension to below the autoregulatory threshold at 3.5 MAC isoflurane/O2 anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral blood flow and response to carbon dioxide during controlled hypotension with isoflurane anesthesia in the rat. 312 43

To study the effects of anesthesia on respiratory function of the neonate, the authors investigated the effect of breathing 100% oxygen and of breathing oxygen plus 0.75 MAC halothane on functional residual capacity, lung and airway resistance, expired minute volume, work of breathing, lung compliance, and blood gases and pH in nine 5-8-day-old, 4.6-7.7-kg lambs. Breathing 100% oxygen increased PaO2 but had no effect on PaCO2, minute ventilation, or lung mechanics. Three-fourths MAC halothane depressed minute ventilation 34% +/- 13% (P less than 0.05) and increased PaCO2 50% +/- 5% (P less than 0.05). Lung and airway resistance increased 59% +/- 26% (P less than 0.05); work of breathing decreased (P less than 0.05); and lung compliance was unchanged. Functional residual capacity was reduced 32% +/- 6% (P less than 0.05), which may be due to loss of diaphragm and intercostal muscle function and to an inability to take deep breaths. The authors conclude that 0.75 MAC halothane significantly impairs the pulmonary function of lambs who breathe spontaneously. Similar changes in human infants could account for the hypoxemia and hypercarbia that often are seen during anesthesia.
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PMID:Halothane anesthesia reduces pulmonary function in the newborn lamb. 399 22

To assess the effects of isoflurane on chemical regulation of ventilation, we studied the ventilatory responses to (1) hyperoxic hypercarbia, (2) isocapnic hypoxaemia, and (3) a single half vital capacity breath of carbon dioxide 20 per cent in oxygen in 12 human subjects, awake and sedated or anaesthetized with isoflurane, 0.1 or 1.1 MAC. Sedation did not alter ventilation nor the ventilatory response to hypercarbia but reduced the responses to hypoxaemia and to the half vital capacity breath of CO2. Anaesthesia reduced ventilation and the response to hypercarbia and nearly abolished the responses to hypoxaemia and to the breath of CO2. The results indicate that isoflurane reduces ventilatory responses to several chemical drives and that it selectively impairs those responses mediated by peripheral chemoreceptors. In these respects, isoflurane is similar to halothane and enflurane.
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PMID:Chemical regulation of ventilation during isoflurane sedation and anaesthesia in humans. 641 54

We compared the ventilatory response to isocapnic hypoxaemia with a standard response to hyperoxic hypercarbia in human subjects sedated with methoxyflurane, diethyl ether or nitrous oxide, or anaesthetized with methoxyflurane. Compared to the awake state, methoxyflurane 0.1 MAC sedation did not alter either response significantly; methoxyflurane 1.1 MAC anaesthesia depressed both, with a somewhat greater effect on the hypoxaemic response. Diethyl ether 0.1 MAC sedation reduced only the hypoxaemic response. Nitrous oxide 0.1 MAC reduced both hypoxaemic and carbon dioxide responses in parallel. The evidence suggests that all three agents - like thiopentone, halothane and enflurane - can impair the ventilatory response to isocapnic hypoxaemia in man, but that in relation to the carbon dioxide responses, the magnitude of this depressive effect varies. Halothane and enflurane are the most depressant, nitrous oxide and thiopentone the least, with methoxyflurane and diethyl ether appearing to be intermediate in effect.
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PMID:Variable effects of anaesthetics on the ventilatory response to hypoxaemia in man. 2447 1

To assess the impact of surgical stimulation on regulation of ventilation in anaesthetized man, we measured ventilation and the ventilatory responses to either hyperoxic hypercapnia or to isocapnic hypoxaemia in fifteen subjects anaesthetized with enflurane 1.1 MAC, just prior to and then during a surgical procedure. Anaesthesia alone reduced ventilation, increased PaCO2, decreased the response to carbon dioxide and virtually abolished the response to hypoxaemia. The addition of operation at the same level of anaesthesia augmented ventilation and reduced PaCO2, but did not improve the anaesthesia-induced impairment of the responses to hypercarbia and hypoxaemia. Over the range of PCO2 and PO2 values studied, the effects of surgery were constant and independent of chemical drive.
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PMID:Surgical stimulation does not enhance ventilatory chemoreflexes during enflurane anaesthesia in man. 735 87

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

The azeotropic mixture of halothane and diethyl-ether has been claimed to be a suitable anaesthetic agent for use during difficult conditions because of its negligible effect on circulation and ventilation. The purpose was to evaluate the effect of halothane-diethyl-ether azeotrope (HE) and isoflurane (ISO) on ventilation. 12 patients scheduled to undergo minor orthopaedic surgery and belonging to ASA 1, were randomly allocated to the HE group or the ISO group. Evaluation of resting ventilation and ventilation stimulated by hypercarbia and hypoxaemia was done on three occasions: (A) before anaesthesia, (B) after inhalational induction of anaesthesia and intubation without muscle relaxants when the level of anaesthesia was 1 MAC and (C) half an hour after operation and during recovery. Resting ventilation and the ventilatory response to hypercarbia during anaesthesia were maintained in the HE group but not in the ISO group, whereas the ventilatory response to hypoxaemia during anaesthesia was absent in both groups. The responses had returned to normal values in both groups during recovery. We conclude that halothane-diethyl-ether azeotrope is comparatively safe during anaesthesia with spontaneous breathing provided arterial oxygenation is adequate. This makes this azeotrope suitable for use by anaesthetists with limited experience and during difficult conditions such as civil disaster or war.
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PMID:Influence of halothane-diethyl-ether azeotrope and isoflurane on ventilation. Re-evaluation of an obsolete drug. 772 80

Ventilatory responses to hypoxia (HVR) were investigated using poikilocapnic conditions (i.e. end-tidal CO2's allowed to seek it's own level) in 15 cardio-pulmonary healthy patients who were first studied awake and then at 0.85 MAC isoflurane. The influence of hypercapnia (HyperCapnic Ventilatory Response, HCVR) was also elucidated. Pneumotachography, capnography and airway occlusion pressures at 0.1 s (P degree 0.1) were used before and during both mild hypoxia (end-tidal O2 tension 8.7 kPa) and hypercapnia achieved by an inspired CO2 concentration of 5%. HCVR was attenuated by 60% during anesthesia (P < 0.01). In the awake state, five of the 15 patients decreased HVR during hypoxia as compared with during normoxia. This resulted in a VE that on average increased by 0.6 l.min-1 (P < 0.05) whereas P degree 0.1 was unchanged. In the anesthetized state, no case of decreased HVR was seen and hypoxia induced a mean VE increase (+/- s.d.) by 1.0 +/- 0.2 l.min-1 (P < 0.001) and a P degree 0.1 that on average was improved by 0.63 +/- 0.27 cm H2O (P < 0.01). It is suggested that when the aim is to evaluate the influence of volatile anesthetic agents on HVR and to quantitate its clinical relevance during and immediately after anesthesia, a poikilocapnic technique should be used. It is concluded that the poikilocapnic HVR to PEO2's of 8.7 kPa was maintained during 0.85 MAC isoflurane.
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PMID:Poikilocapnic hypoxic ventilatory response in humans during 0.85 MAC isoflurane anesthesia. 817 50

The use of laparoscopy for the diagnosis or therapeutic management of abdominal disease in the horse has distinct advantages when it allows the horse to remain standing. However, distending the abdomen by insufflation of a biologically active gas in an anaesthetised horse may add to the physiological challenge of general anaesthesia and recumbency. The cardiopulmonary responses to abdominal insufflation with carbon dioxide (CO2) to 15 mmHg pressure were evaluated in 6 horses in dorsal recumbency anaesthetised with halothane in oxygen and subjected to laparoscopic colopexy. Vaporiser settings targeted a fractional expired halothane of 1.5 MAC and a clinically acceptable depth of anaesthesia. Pressure and rate controlled positive pressure ventilation was adjusted to an ETCO2 of 35 mmHg before abdominal insufflation and was not changed thereafter. Cardiopulmonary data were collected before, at 30 and 60 min during and 30 min after CO2 insufflation. ANOVA for repeated measures followed by Tukey's protected t test were used to determine differences. Partial pressure of oxygen and pH of arterial blood, tidal volume and systemic vascular resistance decreased during abdominal insufflation and laparoscopic surgery whereas mean arterial blood pressure, right atrial pressure, cardiac index, stroke index, partial pressure of CO2 in arterial blood and end tidal respiratory gases, and calculated physiological shunt increased significantly. Only systemic vascular resistance returned to the pre-insufflation level after desufflation. The hypercapnia, acidosis and apparent increase in cardiac work that accompany CO2 pneumoperitoneum for laparoscopic surgery could place the anaesthetised horse at additional risk of perioperative complications.
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PMID:Cardiopulmonary changes associated with abdominal insufflation of carbon dioxide in mechanically ventilated, dorsally recumbent, halothane anaesthetised horses. 953 71


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