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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two hundred ninety patients undergoing carotid endarterectomy were reviewed. From 1968 to 1972, 188 patients had carotid endarterectomy under general anesthesia with use of a shunt and hypercarbia. Stump pressures were not recorded in this group. There were three deaths, three postoperative hemiplegias and two complications of transient limb weakness. From 1973 to 1975, 102 patients were operated on under local anesthesia with systemic Innovar and Sublimaze, normocarbia and intra-operative assessment of stump pressure. In this group there was one death, no hemiplegia, and no complications of transient limb weakness. Twenty of the 102 were shunted either on the basis of stump pressure or the loss of motor ability or consciousness on carotid clamping. Those shunted had stump pressures ranging from 10 to 70 mm Hg with a mean of 20 while those not shunted had stump pressures ranging from 20 to 85 mm Hg with a mean of 53 mm Hg. Five patients lapsed into unconsciousness despite internal carotid stump pressures of 30, 30, 34, 36 and 70 mm Hg respectively, thus requiring intraoperative shunting. This experience seriously questions the reliability of carotid stump pressure as the sole determinant to identify those patients who require intraoperative shunting. We have come full circle, back to operation under local anesthesia, since intraoperative assessment of the patient's motor ability and consciousness alone provide the only absolute criteria for assessing the need for intraoperative shunting. Since the operation can be performed with greater technical efficiency without a shunt and without the potential complications of shunting itself, it behooves the surgeon to have a reliable method of knowing when it is not required.
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PMID:Improved results with carotid endarterectomy. 88 76

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in six dogs each with a tracheostomy, awake and during anaesthesia with halothane, enflurane and isoflurane (1-2.5 MAC). Isocapnic hypoxic ventilatory response (HVR) was expressed as the parameter A, such that the greater the value of A, the greater the hypoxic response. In the anaesthetized dogs HVR (A) was reduced significantly from the awake value of 2010 +/- 172 (mean + SEM) to 630 +/- 173 by 1 MAC halothane, 495 +/- 105 by 1 MAC enflurane and 952 +/- 157 by 1 MAC isoflurane (PL0.05). All three anaesthetic agents produced significant depression of HUR at 1 MAC, but enflurane was more depressant than isoflurane. At 1.5 MAC all three anaesthetics produced equal and significant depression of HVR at equianalgesic concentrations. Further increases in anaesthetic concentration caused no increase in depression. Hypercapnic drive, as measured by the slope of the VE/PACO2 response curve, was reduced significantly from 9.75 litre min-1 kPa-1 +/- 2.4 in awake dogs to 0.83 +/- 0.56 after 1 MAC halothane, 0.68 +/- 0.53 after 1 MAC enflurane and 1.58 +/- 0.75 after 1 MAC isoflurane. In addition, hypercapnia-induced augmentation of the hypoxic drive was abolished by 1 MAC halothane or enflurane and diminished markedly by 1 MAC isoflurane. It may be clinically significant that hypoxia and hypercapnia during anaesthesia with these agents did not produce optimal stimulation of ventilation.
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PMID:Depression of hypoxic ventilatory response by halothane, enflurane and isoflurane in dogs. 92 74

The effects of halothane and enflurane anesthesia under conditions of normo-, hyper-, and hypocarbia on the autoregulation of cerebral blood flow (CBF) in the goat were evaluated. The goat was selected because of its unique arterial blood supply to the head and the development of a method by which CBF may be continuously measured. The study revealed that 1 MAC of halothane or enflurane anesthesia at normocarbia abolished cerebral autoregulation, CBF increasing or decreasing with increasing or decreasing peripheral blood pressure. Reduction of anesthesia to 0.5 MAC partially restored cerebral autoregulatory capability. The effect of 1 MAC and 0.5 MAC anesthesia on cerebral autoregulation of blood flow was potentiated by hypercarbia and antagonized by hypocarbia, indicating that the vascular response to blood CO2 fluctuations remained intact.
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PMID:Absence of autoregulation of cerebral blood flow during halothane and enflurane anesthesia. 94 20

The breathing patterns during hypoxia and hypercapnia are similar in anesthetized cats but are qualitatively different in awake cats. The differences seen in the awake animals can be explained by either the central depressive effect of hypoxia or by a specific effect of hypercapnia on supra-pontine structures. The Breuer-Hering reflex sensitivity, i.e. the VT-TI relationship, appears, in the awake cat, quite similar to that recently described in man. The inspiratory activity is shown to be controlled by mechanisms dependent on the nature of the respiratory stimulation. The recent model proposed for the control of inspiration during anesthesia must be modified to account for the results observed in awake animal.
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PMID:Pattern of breathing during hypoxia or hypercapnia of the awake or anesthetized cat. 95 76

One hundred consecutive patients were randomly given hypocarbic (PaCO2 less than 25 torr) or hypercarbic (PaCO2 greater than 60 torr) general anesthesia during carotid endarterectomy to test the effect of the two regimens upon the incidence of postoperative neurological deficit. An indwelling shunt was not used. One patient died, two have permanent neurological deficits and two have temporary neurological deficits. Although hypocarbic patients had fewer neurological complications than hypercarbic patients, the difference was not statistically significant (p less than 0.13). Hypercarbia significantly increased the incidence of intraoperative arrhythmia. Also, no relationship was found between the incidence of postoperative stroke and the internal carotid back pressure or the time of carotid occlusion.
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PMID:An evaluation of hypocarbia and hypercarbia during carotid endarterectomy. 96 Jan 66

The pressures generated by the inspiratory muscles as they contract isometrically during airway occlusion seem to be a measure of respiratory neuron efferent activity. The ventilatory and occlusion pressure responses to increasing levels of CO2 were studied in goats, awake and anesthetized, with and without inspiratory flow resistance. Hypercapnia was produced by rebreathing. Randomly, during rebreathing, inspiratory airflow was prevented on single breaths. Ventilation and pressures developed during the first 100, 200, 300 and 400 milliseconds of an inspiratory effort against a complete occlusion increased linearly with CO2 in both awake and anesthetized animals. Anesthesia reduced both the ventilatory and occlusion pressure responses to CO2. Inspiratory resistance increased occlusion pressure responses in awake goats but not in the same animals when anesthetized. Inspiratory airflow resistance seems to augment respiratory efferent activity as reflected in the pressure responses only in conscious goats. Thus the response to an inspiratory resistance seems to depend on the state of consciousness.
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PMID:Airway occlusion pressures in awake and anesthetized goats. 96 4

In the dog, FFA (free fatty acid) and cortisol levels in arterial blood plasma are lowered by anesthesia. Induced hypercapnia does not alter the cortisol levels but increases FFA levels. Hypoxia tends to raise the FFA levels. Possible causes of modifications in the FFA and cortisol levels are briefly discussed.
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PMID:Effects of hypoxia and hypercapnia on non-esterified free fatty acid and cortisol levels. 98 77

Changes in the uterine and umbilical circulations during induced hypercapnia were studied in nine unanesthetized near-term pregnant sheep. Blood flows were measured with electromagnetic flow transducers and arterial pressures with vascular catheters implanted under anesthesia 2-16 days prior to experiments. Hypercapnia was induced in the fetus alone by giving acetazolamide iv to the fetus, 100-200 mg/kg. Mean fetal arterial Pco2 increased from 49.5 to 63.4 mmHg but no significant changes in umbilical blood flow occurred. Stepwise increases in both maternal and fetal arterial Pco2 were induced by increasing maternal inspired CO2 concentration to a maximum of 12%. No dignificant changes occurred in uterine or umbilical circulations until hypercapnia was severe (maternal arterial Pco2 greater than 60 mmHg, fetal arterial Pco2 greater than 70 mmHg). With severe hypercapnia uterine vascular resistance increased significantly and uterine blood flow decreased despite an increase in maternal arterial pressure; fetal arterial pressure and umbilical blood flow increased significantly, but umbilical vascular resistance did not. We conclude that hypercapnia in conscious pregnant sheep is associated with significant changes in uterine and umbilical circulations, but only when hypercapnia is severe. Carbon dioxide is unlikely to be a factor in normal physiological regulation of the uteroplacental circulation in this species.
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PMID:Effects of hypercapnia on uterine and umbilical circulations in conscious pregnant sheep. 99 46

The bile acid-base parameters are analyzed in 42 male Wistar rats under pentobarbital anaesthesia, in normal conditions of blood acid-base equilibrium. The reproducibility of the results is emphasized. In acute hypercapnia (FICO2 : 0.12 for 15 min) without hypoxia, and for the same increase in PCO2, and pH variation is lesser in bile than in blood, thus showing an high buffer capacity. In vitro and in vivo comparative studies show that bile buffer capacity is about five times higher in vivo, independently of a possible increase in choleresis. Comparative studies of bile-acid-base equilibrium are effected during perfusions of dehydrocholate, sodium taurocholate, secretin and acetazolamide. Sodium and chlorine remain stable during hypercapnia both in blood and in bile ; potassium concentration is increased in the two media. To explain these results, the role of the liver is still to specify.
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PMID:[Acute hypercapnia and bile. Experimental studies in the rat (author's transl)]. 101 82

Autoregulation of the cerebral blood flow is a wellknown fact. In normal man the arterial pressure can vary from 80 mm Hg to 150 mm Hg without a change in the normal cerebral blood flow of 50 ml/100 g/min. The mechanism which is responsible for this autoregulation is not clearly understood. Several theories were proposed to explain this phenomenon. 1. The tissue pressure increases with an increase of the arterial pressure. A mechanical process should neutralize an increase of the cerebral blood flow. 2. The metabolic theory says that a decrease of the blood pressure, without a change of metabolism, involves an increase of the PaCO2, and a decrease of the PaO2. Those two factors provoke a decrease of the vascular tone. 3. The myogenic theory explains autoregulation by the fact that a change of the transmural pressure in the small vessels, involves a change in the activity of the smooth muscles of the vessels. 4. The exact mechanism of the autonomic nervous system in the autoregulation of the cerebral blood flow is still obscure. In some pathological conditions autoregulation is completely lost or is functioning not optimal: hypoxia, hypercapnia and brain contusion. We have measured the cerebral blood flow before and after an intravenous injection of 5 mg thiopental (Pentothal) on occasion of a carotid angiography in man. We noticed a decrease of the cerebral blood flow and at the same moment a decrease of the arterial pressure. We thought that maybe barbiturates could influence autoregulation. Our results could not prove this hypothesis. For ethical reasons we could not make the necessary measurements to prove or to reject this hypothesis (i.e. intracranial pressure, deep controlled hypotension). In the literature there are arguments which support this hypothesis although most workers found an intact autoregulation after a barbiturate anesthesia. Some workers saw that the increase of the cerebral blood flow by increasing the PaCO2 was depressed by barbiturates and exhausted by halothane and cyclopropane. As autoregulation is a more vulnerable mechanism than CO2 reactivity as seen in clinical situations, it could be true that anesthetics do influence autoregulation.
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PMID:Influence of anesthesia on autoregulation of the cerebral blood flow. 102 Jun 37


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