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

The influence of a anesthetic, ethyl-ether, on arterial plasma levels of glucose, insulin and lipids was studied in starved Wistar rats. Ethyl-ether increased significantly (P < 0.05) glucose plasma levels, as a result not only of stress and of the release of catecholamines and glucocorticoids, but also of the decrease in the use of glucose by the tissues. Ethyl-ether did not change significantly the level of triglycerides, cholesterol and phospholipids. Insulin concentration was not increased, even when hyperglycemia was established. Ketonuria, acidosis and hypercapnia were increased. In these rats the administration of insulin produced a diminution in glycemia. The findings suggest that, under anesthesia with ether, the endocrine pancreas is incapable of recognizing glucose as a specific stimulus to promote the release of insulin.
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PMID:Effects of inhalation of ethyl-ether on glycemia and on some variables of intermediate metabolism in rats. 128 85

This paper reviews the principal aspects of the immediate management of patients suffering from spinal injury. An understanding of the pathophysiology of primary and secondary spinal cord injury enables appropriate initial care to be provided, thereby avoiding exacerbation and/or progressive deterioration of the lesion. It includes protective measures, restoration of vital functions to maintain adequate tissue perfusion and oxygenation, as well as pharmacological prevention of secondary injury. Protective measures include proper immobilisation of the spine with a semi-rigid collar and tape on a long backboard, or on vacuum mattress, taking great care to avoid deleterious in-line compression forces on the spinal column. The combination of cervical spine instability, a full stomach, unopposed vagal reflexes, hypoxia and hypercarbia makes airway management of these patients difficult. Tracheal intubation under fibroscopic control, with insertion of the tube only after topical anaesthesia of the airways under titrated intravenous sedation, offers safety and comfort to the patient. However, in cases of severe deterioration of vital functions, intubation must be performed without any delay at the site of the accident or in the emergency room. Three options are available: blind naso-tracheal intubation with spontaneous breathing, modified rapid sequence induction with orotracheal intubation under double protection, and immediate surgical airway if these techniques fail. Patients with cervical spine injury may demonstrate severe hypotension requiring sympathomimetic agents and careful fluid loading to avoid pulmonary oedema. To prevent aggravation of the spinal cord injury by systemic factors, the goal of initial resuscitation is to restore an adequate perfusion pressure of at least 60 mmHg, a PaO2 > 100 mmHg, and to keep PaCO2 below 45 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia of patients with injury to the cervical spine]. 130 64

The purpose of the present study was to examine the dynamic aspects of the cerebrovascular events occurring during and up to 2 h following cortical spreading depression (CSD) in the rat, using the mass spectrometry technique which enables continuous measurements of the cortical tissue PO2 and PCO2 and repeated blood flow measurements (CoBF) by helium clearance. We mostly sought to determine whether cortical perforation by a stimulation electrode induced long-lasting perturbation of the cortical vasoreactivity to hypercapnia and basal forebrain electrical stimulation. Cortical perforation in the animal under alpha-chloralose anesthesia, chronically implanted with mass spectrometry probes, was associated with biphasic changes in tissue gases. PO2 first briefly decreased (-7.8%) and then strongly increased (+79%) while PCO2 changed in the opposite direction (+7%, -13%) in the ipsilateral frontal cortex. Qualitatively similar changes occurred in the ipsilateral parietal cortex. The CoBF measurements showed a marked vasodilation (131 and 108% in the frontal and parietal cortex, respectively) in parallel with the PO2 increase, followed by a prolonged (60 min), moderate hypoperfusion (maximum -17% at 20 min after CSD). There was a pronounced reduction of vascular reactivity to both hypercapnia (20.3% of the control response) and substantia innominata stimulation (1/6 of the response obtained 80 min later) at 10 min after CSD. Both reactivities progressively recovered in approximately 2 h. Since the issue of CSD in human has become a popular hypothesis for migraine, the reduced cerebrovascular reactivity could constitute the basis of a test for the involvement of CSD in migraine.
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PMID:Spreading depression induces prolonged reduction of cortical blood flow reactivity in the rat. 139 64

1. The effects of two anaesthetics, sodium pentobarbital and urethane, and the effects of anaesthesia-associated hypothermia on acid-base status and blood gases were studied in rats without assisted ventilation. 2. Manipulation of conscious rats produces a progressive increase in arterial lactate associated with slight hyperventilation. 3. Sodium pentobarbital anaesthesia produces mild respiratory acidosis accompanied by increase in lactate arterial values. Urethane anaesthesia leads to partially compensated metabolic acidosis. 4. Hypothermia reduces metabolic acidosis and hypercapnia induced by sodium pentobarbital anaesthesia. No difference between hypothermic and normothermic values was observed in urethane anaesthesia.
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PMID:Differential effects of hypothermia upon blood acid-base state and blood gases in sodium pentobarbital and urethane anaesthetised rats. 139 74

Until recently, only the racemic mixture of ketamine has been used in anaesthesia. Little is known of the central nervous effects of the pharmacologically more potent S(+)-isomer. Information in regard to the putative receptor site involved in the mediation of its anaesthetic/analgesic effect is particularly sparse. METHODS. In order to evaluate the anaesthetic and antinociceptive properties of S(+)-ketamine, a dose-response relationship of the compound on the EEG, somatosensory-evoked potentials (SEP), and respiration was established. Increasing doses (2, 5, 10, 20 mg/kg) were given to trained and awake dogs (n = 10) at 10-min intervals. In order to detect a possible opioid receptor-related interaction, an antagonist of the methoxymorphinane series (cyprodime 80 g/kg i.v.) with higher selectivity than naloxone for the mu-receptor was given at the end. RESULTS. Compared to controls, S(+)-ketamine induced a dose-related increase in output in the theta-(3-8 Hz) band and an increase in output in the alpha-domain (8-13 Hz) following 20 mg/kg. Both effects were reversed completely by the opioid antagonist. At low doses (2-5 mg/kg) there was an increase in output (P less than 0.05) in the beta-(13-30 Hz) and a concomitant decrease in output (P less than 0.05) in the delta-(0.5-3 Hz) band. These effects were reversed with increasing doses (5-10 mg/kg). After 20 mg/kg, however, output in the delta-domain increased while power in the beta band decreased significantly (P less than 0.005) when compared to controls. Both effects were reversed by the opioid antagonist. Compared to controls, the reversal resulted in a 12% increase in output in the beta- and a 49% decrease in output in the delta-domain. In SEP, S(+)-ketamine induced a dose-related increase in peak latency and depression of amplitude of more than 50% when compared to controls. While latency changes were completely reversed, amplitude height was only partly restored by the antagonist. Respiration was depressed in a dose-related fashion (PaO2 decreased, PaCO2 increased). Hypoxaemia was fully reversed by the antagonist; hypercapnia was only partly reversed. CONCLUSION. The results support the presumption that the S(+)-isomer of ketamine induces opioid mu-receptor-mediated central effects. Hypersynchronisation of the EEG suggests a deep plane of anaesthesia after S(+)-ketamine. The pronounced blockade of impulses in the sensory nervous pathways suggests an efficient analgesic effect that is partly mediated by the opioid-receptor. The respiratory depression may be of importance when S(+)-ketamine is used in high dosages in man.
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PMID:[Pharmacodynamic effects of S-(+)-ketamine on EEG, evoked potentials and respiration. A study in the awake dog]. 141 7

A 2-year-old Thoroughbred racehorse developed ventricular tachycardia after elective laryngoplasty and ventriculectomy were performed while anesthesia was maintained with halothane. During surgery, the horse became febrile and developed transient mild hypercarbia. The horse was treated with an IV infusion of quinidine gluconate. Continuous electrocardiographic monitoring was used to evaluate cardiac rhythm during treatment, and conversion was achieved after 12 hours of IV infusion. The inciting cause for the arrhythmia was not determined.
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PMID:Postsurgical ventricular tachycardia in a horse. 142 29

The ventilatory changes during the course of high spinal anesthesia and the effect of hypotension on ventilation during high spinal anesthesia were studied. Spinal anesthesia with hyperbaric tetracaine was applied to 30 patients scheduled for elective surgery. Patients breathed by mask for ten minutes at rest before and after receiving spinal anesthesia. Respiratory parameters were measured in supine position during (1) pre-anesthetic period under resting condition, (2) anesthetic period when analgesia with pin prick extended to T4 level and (3) anesthetic period when analgesia extended to T1 level. The patients were divided into two groups; those with and without hypotension. In hypotension group, tidal volume and minute ventilation decreased significantly for 30% compared with the control values after spinal anesthesia. PaO2 decreased and PaCO2 increased. In non-hypotension group, tidal volume and minute ventilation after spinal anesthesia increased for 10% compared with the control values. In conclusion, hyperventilation tended to occur in patients with high spinal anesthesia unless hypotension was severe enough. Once severe hypotension had occurred, obvious hypoventilation and respiratory irregularity were observed. Decrease of tidal volume and minute ventilation, hypoxia, hypercarbia and increase in VD/VT were significant during hypotension. The results suggest that during high spinal anesthesia severe hypotension causes hypoventilation and if not treated respiratory arrest ensues.
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PMID:[Ventilation under high spinal anesthesia--the effect of hypotension]. 143 30

Technical problems during anaesthesia are important causes of anaesthesia-related deaths and brain damage. During general endotracheal anaesthesia for ophthalmic surgery (41-year-old man, ASA 1) we observed an increase in inspiratory pressure without other clinical changes. Disconnection and ventilation with a resuscitation bag showed normal inspiratory pressures. Inspection demonstrated an obstruction due to an aneurysm of the inner layer of the inspiratory tubing. The classification of this rare blockage of ventilation differs in the literature (pressure, hypoventilation, hypercarbia). In addition, it demonstrates the principal problem of clinical decision-making during anaesthesia based on monitoring information. Strategies for responding to alarms indicating hazards of ventilation must be based on immediate restoration of sufficient ventilation, and not primarily on detecting the cause.
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PMID:[Obstructive respiration disorders. An aneurysm of the ventilator tubing during general anesthesia]. 144 14

The cerebrovascular response to CO2 has been reported to be preserved during propofol anesthesia, but no comparison with awake control values has been made, and the additional influence of N2O has not been investigated. Using the noninvasive technique of transcranial Doppler ultrasonography, this study investigated the cerebrovascular response to varying levels of PaCO2 while awake and during anesthesia with propofol and propofol/N2O. Seven adults without systemic diseases undergoing nonneurologic surgery were studied. A pulsed-wave Doppler monitor was used to measure the mean middle cerebral artery flow velocity (Vmca) during varying levels of PaCO2 (25-55 mmHg) under the following conditions: 1) awake; 2) propofol 2.5 mg.kg-1 bolus followed by continuous infusion of 150 micrograms.kg-1.min-1; and 3) propofol as in the condition above plus 70% N2O. During the awake study condition, hypocapnia was induced by voluntary hyperventilation, and hypercapnia was induced with rebreathing of 7% CO2 in a closed circuit. During the anesthetized study conditions, hypocapnia and hypercapnia were induced by adjustment of minute ventilation. A minimum of five to six simultaneous Vmca and PaCO2 measurements were obtained under each of the study conditions. Systemic blood pressure was monitored via a radial arterial catheter, and phenylephrine was administered if mean arterial blood pressure decreased below 60 mmHg (phenylephrine was used in three of five patients in the propofol-N2O group). Linear regression and analysis of covariance were used for statistical analysis of Vmca-PaCO2 relationships.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of propofol with and without nitrous oxide on cerebral blood flow velocity and CO2 reactivity in humans. 144 39

The combined use of midazolam and spinal anesthesia is common in clinical practice. Despite the known potential for each to alter ventilation, the effect of their interaction has not been examined. Nineteen healthy volunteers were studied to assess the impact of intravenous midazolam (0.05 or 0.075 mg/kg), spinal anesthesia (T3-T8; mean level, T6), and their combination on resting ventilation and ventilatory responses to progressive hyperoxic hypercapnia. Resting ventilatory pattern was altered significantly by each condition. Midazolam caused a 29% decrease in resting tidal volume and a 24% decrease in mean inspiratory flow rate, while respiratory frequency increased by 14% and minute ventilation remained unchanged. By contrast, spinal anesthesia alone caused a 32% increase in tidal volume, a 24% increase in mean inspiratory flow rate, and a 13% increase in minute ventilation accompanied by a 14% decrease in respiratory frequency. The combination of midazolam and spinal anesthesia caused a significant decrease in minute ventilation (19%), tidal volume (28%), and mean inspiratory flow rate (27%), all of which were significantly more than the predicted sum of the individual interventions. Midazolam and spinal anesthesia each produced a significant decrease in hypercapnic ventilatory response slope, whereas their combination provoked no net change in hypercapnic ventilatory response slope. Interpretation of the hypercapnic ventilatory response data was complicated by shifts in the position of the ventilatory response curve, particularly under the spinal anesthesia condition. It is concluded that intravenous midazolam depresses resting ventilation, spinal anesthesia stimulates resting ventilation, and their combination has a modest synergistic effect of depressing resting ventilation.
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PMID:Respiratory interaction after spinal anesthesia and sedation with midazolam. 144 45


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