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)

A 41-year old, 50 kg female was scheduled for laparoscopic cholecystectomy. Anesthesia was induced with thiopental 250 mg IV and endotracheal intubation was performed using succinylcholine 60 mg IV. Anesthesia was maintained with N2O (67%)-oxygen-sevoflurane (1.5-2%) and pancuronium was used for muscle relaxation. The lungs were mechanically ventilated with TV 500 ml and RR 12.min-1. Immediately after the start of incision, PECO2 was 30 mmHg. But about thirty minutes after introducing carbon dioxide pneumoperitoneum, subcutaneous emphysema and high PECO2 (60 mmHg) were noted and arterial blood gas analysis showed PaCO2 63.2 mmHg, PaO2 135.4 mmHg and pH 7.32. Generally in laparoscopic cholecystectomy, subcutaneous emphysema is more common than in gynecologic laparoscopy and especially with severe subcutaneous emphysema, there is a risk of hypercapnia. This is because carbon dioxide in subcutaneous tissue is more absorbable than that in peritoneal cavity. As carbon dioxide in subcutaneous tissue is absorbed continuously after the operation, the patient should be carefully observed postoperatively.
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PMID:[Severe subcutaneous emphysema and hypercapnia during laparoscopic cholecystectomy]. 831 2

The present study was performed to clarify the influences of anesthetic methods and insufflating gases on arterial blood gas and ventilation during laparoscopy. Forty five women undergoing laparoscopy for gynecological procedure were studied after dividing into four groups; general anesthesia with control ventilation or epidural anesthesia with spontaneous breathing, plus insufflation with carbon dioxide (CO2) or nitrous oxide (N2O). After CO2 insufflation, PaCO2 increased significantly in the patients who were mechanically ventilated, but not in the patients breathing spontaneously. After N2O insufflation, the decrease in tidal volume (VT) and the increase in VD/VT were significant, but minute ventilation was well maintained by the compensatory increase in respiratory frequency during spontaneous breathing. On the other hand, after CO2 insufflation VE and VD/VT increased significantly without any change in VT. PaO2 decreased significantly after both insufflation and Trendelenburg tilt in all groups, probably secondary to the decrease in functional residual capacity. These findings suggest that during laparoscopy, ventilation could be well maintained by spontaneous breathing, although the increase in VD/VT and costal breathing indicate the increase in respiratory work load. We recommend that ventilation and oxygenation should be closely monitored during laparoscopy to avoid hypercapnia and hypoxia.
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PMID:[The effects of anesthetic techniques and insufflating gases on ventilation during laparoscopy]. 832 Aug 4

Intracellular pH and ammonium ion concentration are potent modulators of cerebral amino acid metabolism. Furthermore, intracellular acidosis and hyperammonemia accompany conditions such as ischemic encephalopathy and seizures and may contribute to the pathological sequelae observed. In vivo NMR spectroscopy permits multiple, non-destructive measurements of important cerebral metabolic intermediates in the same animal. We describe here the use of 1H, and 31P NMR spectroscopy to investigate the effects of acute changes in intracellular pH and ammonium ions on cerebral glutamate, glutamine, and lactate levels in vivo. We then show how 1H NMR can be used to indirectly follow the flow of 13C label from [1-13C] glucose into the cerebral glutamate pool, allowing us to measure cerebral TCA activity in normal and chronically hyperammonemic rats. Male Sprague-Dawley rats (160-210 gm), fasted 24-hours, were tracheotomized, paralyzed and ventilated on 30% O2/70% N2O. NMR spectroscopy was performed at a field strength of 8.4 Tesla using a Bruker AM-360 wide bore spectrometer. An elliptical surface-coil (8 x 12 mm) was double-tuned to either the 1H and 31P or 1H and 13C frequencies. After retraction of extracranial tissues, the coil was positioned over the skull 2 mm posterior to the bregma. Tail arteries and veins were cannulated allowing periodic measurements of PO2, pCO2, pH and glucose in arterial blood and intravenous infusions. Respiratory acidosis was induced in rats by the addition of CO2 to the ventilation gas mixture. Arterial pCO2 increased within 5 min from a pre-hypercarbic value of 36.4 +/- 6.1 mm Hg to 200-220 mm Hg and was maintained at this level for over 1 hour. Hypercarbia led to rapid cerebral acidification. Intracellular pH decreased from 7.18 +/- 0.08 (pre-hypercarbic period) to 6.68 +/- 0.06 (n = 4) at 10 min and remained stable throughout the NMR observation period. Glutamate decreased to 53 +/- 4% of control after 60 min of hypercarbia, while glutamine increased to 126 +/- 7% of control. Acute hyperammonemia was produced by a programmed intravenous infusion of 250 mM ammonium acetate, which rapidly raised and maintained the concentration of ammonium ions in the blood at approximately 500 microM. Shortly after the start of the infusion (10-20 min), the levels of glutamine and lactate rose continuously throughout the experiment, reaching levels of 170 +/- 25% and 260 +/- 60% of control, respectively (n = 12) after 50 min. Glutamate decreased during the same time interval to 80 +/- 4% of control (n = 12).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebral metabolic studies in vivo by combined 1H/31P and 1H/13C NMR spectroscopic methods. 842 59

Spinal-sciatic evoked responses (ScER) have been used successfully to monitor the integrity of the anterior spinal cord during spinal surgery. To evaluate the effects of hypercarbia, hypocarbia, induced hypotension, and hypothermia on the ScER, ten swine anesthetized with ketamine were subjected to varying levels of PaCO2, hypothermia, and induced hypotension. During variation of one physiologic variable, the other variables were closely regulated. There were no significant changes associated with variations in PaCO2. Decreasing temperature provided a consistent increase in latency (r = -0.78, P < 0.001) with no significant alteration in amplitude. Graded hypotension caused little increase in latency (3.2% at 30 mm Hg). The amplitude decrease averaged 23% at 60 mm Hg with a maximal decrease of 50% at 30 mm Hg. To study inhaled anesthetics, 21 swine anesthetized with ketamine were subjected to nitrous oxide (50% and 70%). After termination of the nitrous oxide, one of the potent inhaled anesthetics (n = 7 each) was administered in 0.25 minimum alveolar concentration (MAC) increments. Nitrous oxide caused a significant decrease in amplitude (average 43% and 61% at 50% and 70%) with minimal changes in latency. There was a dose-dependent decrease in amplitude and increase in latency with all inhaled anesthetics. The ScER disappeared at 1.0 MAC with all anesthetics. There were no differences between effects of equipotent concentrations of inhaled anesthetics. These findings may be helpful in the interpretation of the ScER response during anesthesia and surgery.
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PMID:Physiologic and anesthetic alterations on spinal-sciatic evoked responses in swine. 842 1

Plasma potassium concentrations during anesthesia with N2O and enflurane in O2 were measured in 12 patients on chronic hemodialysis (HD) who underwent HD for about 2 hours just before anesthesia. Pre-HD and pre-anesthetic plasma potassium concentrations were 5.0 +/- 0.2 and 4.3 +/- 0.2 mEq.l-1, respectively. The potassium levels decreased slightly following induction of anesthesia, but increased significantly during and after surgery; and at the end of anesthesia the levels were similar to those measured just before HD. None of the patients developed acidosis, hypoxia or hypercapnia. Based on our results, we consider that plasma potassium levels should be measured frequently during surgery in patients who have high potassium levels just before HD and are subjected to HD just before anesthesia, because hyperkalemia may occur.
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PMID:[Plasma potassium concentrations during N2O-enflurane anesthesia in patients on chronic hemodialysis]. 846 84

Hemodynamics during laparoscopic cholecystectomy under general anesthesia (isoflurane in N2O/O2 (50%)) were investigated in 15 nonobese ASA Class I patients by using invasive hemodynamic monitoring including a flow-directed pulmonary artery catheter. During surgery, intraabdominal pressure was maintained automatically at 14 mm Hg by a CO2 insufflator, and minute ventilation was controlled and adjusted to avoid hypercapnia. Hemodynamics were measured before anesthesia, after the induction of anesthesia, after tilting into 10 degrees head-up position, 5 min, 15 min, and 30 min after peritoneal insufflation, and 30 min after exsufflation. Induction of anesthesia decreased significantly mean arterial pressure and cardiac index (CI). Tilting the patient to the head-up position reduced cardiac preload and caused further reduction of CI. Peritoneal insufflation resulted in a significant increase (+/- 35%) of mean arterial pressure, a significant reduction (+/- 20%) of CI, and a significant increase of systemic (+/- 65%) and pulmonary (+/- 90%) vascular resistances. The combined effect of anesthesia, head-up tilt, and peritoneal insufflation produced a 50% decrease in CI. Administration of increasing concentrations of isoflurane, via its vasodilatory activity, may have partially blunted these hemodynamic changes. These results demonstrate that laparoscopy for cholecystectomy in head-up position results in significant hemodynamic changes in healthy patients, particularly at the induction of pneumoperitoneum.
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PMID:Hemodynamic changes during laparoscopic cholecystectomy. 848 9

A patient with Prader-Willi syndrome developed bronchospasm during anesthesia. The patient was a 9-year-old boy and was scheduled for orchiopexy. His psychomotor development was delayed, and at 12 months of age he was diagnosed as Prader-Willi syndrome by chromosomal examination. The patient weighed 17 kg, was 111 cm tall, and had no symptom of upper respiratory infection preoperatively. Preoperative examinations were normal except supraventricular extrasystole in electrocardiogram. Following administration of scopolamine 0.15 mg intramuscularly as preanesthetic medication, anesthesia was induced smoothly by slow induction using N2O-O2-sevoflurane. However, right after endotracheal intubation with vecuronium 2 mg, remarkable stridor was noticed. Despite hyperventilation, the patient exhibited hypercapnia, and the diagnosis of bronchospasm was made. Aminophylline and steroid were administered intravenously and halothane was inhaled instead of sevoflurane. The bronchospasm was improved gradually and surgery was finished. Prader-Willi syndrome is an uncommon disease first reported by Prader in 1956 and characterized by hypotonia, hypomentia, hypogonadism and obesity. In the perioperative management for a patient with Prader-Willi syndrome, special attention must be paid to the abnormalities in the upper and lower respiratory systems.
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PMID:[Bronchospasm during anesthesia in a patient with Prader-Willi syndrome]. 858 65

Midazolam in combination with nitrous oxide (N2O) is a commonly used sedative approach for pediatric dental patients. Respiratory morbidity and mortality have been reported with midazolam administration, particularly when used in combination with other drugs in the absence of supplemental oxygen. Thus, the purpose of this investigation was to determine the effect of midazolam alone and in combination with N2O on respiration in laboratory rats by measuring arterial blood gas levels. Sixty-four Sprague-Dawley rats, weighing 250-320 g, were assigned to one of eight groups (eight per group). Groups were allocated based upon the dosage of midazolam administered (0, 1.0, 2.0 or 4.0 mg/kg i.p.) and exposure to N2O/02 (50%/50%) or room air. Arterial blood was obtained from a femoral artery catheter and pH, O2, CO2 (mm Hg), and oxygen saturation (%) were determined. Samples were analyzed using a System 1306 pH/Blood Gas Analyzer. Baseline arterial blood gasses were obtained for each animal and at 15-min intervals following midazolam administration throughout the 45-min experiment. Following midazolam administration, animals were placed into a sealed chamber through which flowed either N2O or room air. Group comparisons demonstrated that: 1) arterial CO2 levels increased in midazolam-exposed animals breathing room air, but not in those exposed to N2O (P < 0.05), and 2) as expected, N2O/O2-exposed animals showed an increase in arterial O2 and a %saturation that was not observed in room air groups (P < 0.01). This investigation demonstrated that coadministration of N2O/O to midazolam-exposed animals did not result in hypercarbia, an early indicator of respiratory depression.
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PMID:The influence of midazolam and nitrous oxide on respiratory depression in laboratory rats. 885 55

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 phencyclidine derivative ketamine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist with the thalamo-neocortical projection system as the primary site of action. Racemic ketamine consists of the enantiomers S(+)-ketamine and R(-)-ketamine. Racemic ketamine has never been considered an adequate anaesthetic agent in neurosurgical patients since it produces regionally specific stimulation of cerebral metabolism (CMRO2) and increases cerebral blood flow (CBF) and intracranial pressure (ICP). However, recent experiments suggest that both tracemic ketamine and S(+)-ketamine may reduce infarct size in animal models of incomplete cerebral ischaemia and brain injury. This experimental protective effect appears to be related to decreases in Ca++ influx and maintenance of brain tissue magnesium levels due to NMDA and quisqualate receptor blockade by ketamine. Studies in dogs have shown that racemic ketamine (2.0 mg/kg) increases CBF in the presence of the cerebral vasodilator N2O. In contrast, studies in rats without background anaesthesia showed increases in CBF after racemic ketamine (100 mg/kg i.p.). This suggests that the cerebrovascular effects of racemic ketamine are related to the pre-existing cerebrovascular tone induced by background anaesthetics. Cerebrovascular CO2 reactivity was maintained regardless of the baseline cerebrovascular resistance. There are several mechanisms by which racemic ketamine may increase CBF. It induces dose-dependent respiratory depression with consequent mild hypercapnia in spontaneously ventilating subjects. This produces vasodilation due to the intact cerebrovascular CO2 reactivity. Racemic ketamine also induces regional neuroexcitation, which leads to stimulation of cerebral glucose consumption in the limbic, extrapyramidal, auditory, and sensory-motor systems. This regional neuroexcitation with increased CMRO2 produces increases in CBF that can be blocked by infusion of barbiturates or benzodiazepines. However, increases in CBF with racemic ketamine (1 mg/kg) may also occur during normocapnia and without changes in CMRO2. This effect is related to some additional direct cerebral vasodilating potency of racemic ketamine based on a mechanism involving blockade of Ca++ channels. The effects of racemic ketamine on CBF autoregulation have not been investigated systematically. However, studies in rats have shown that CBF autoregulation was maintained with low- and high-dose S(+)-ketamine. Infusion of racemic ketamine alters intracranial volume and ICP. Studies in spontaneously ventilating pigs with and without intracranial hypertension have shown that racemic ketamine (0.5-5.0 mg/kg) produces increases in PaCO2 and ICP. In contrast, identical experiments with mechanical ventilation and controlled PaCO2 showed no changes in ICP following racemic ketamine infusion. This implies that increases in ICP are related to inadequate ventilation with consecutive hypercapnia and increases in intracranial blood volume. However, mechanical ventilation may not be sufficient to control ICP following racemic ketamine. Experiments in mechanically ventilated dogs indicate that racemic ketamine (2 mg/kg) increases cerebral blood volume and ICP even in the presence of normoventilation, a response that is reversible by hyperventilation or the administration of diazepam. Studies in patients have shown that racemic ketamine (2.0 mg/kg) reduces CBF in the presence of cerebral vasodilators like halothane or N2O. In contrast, studies in unanaesthetised humans showed increases in CBF after racemic ketamine (2-3 mg/kg). This observation is consistent with animal studies and suggests that the cerebrovascular effects of racemic ketamine are related to the pre-existing cerebrovascular tone induced by background anaesthetics. Studies in humans with and without intracranial pathology confirm the data from animal experiments. (ABSTRACT TRUNCATED)
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PMID:[Ketamine racemate and S-(+)-ketamine. Cerebrovascular effects and neuroprotection following focal ischemia]. 916 80


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