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

Anesthesia was induced with intravenous thiopental, fentanyl, and succinylcholine, and maintained with isoflurane, N2O-O2 and atracurium after denitrogenation in 20 adult patients. Inspired and end-tidal concentrations of O2, N2O, CO2, isoflurane and oxygen saturation of pulse oximeter (SpO2) were monitored. After intubation, N2O (750 ml/min) and O2 (250 ml/min) were administrated. When inspired N2O concentration (FiN2O) reached 60% the closed anesthesia was initiated by adjusting fresh gas flow rate in order to meet the oxygen demand of the patients. The N2O/O2 ratio was constantly kept at 0.7. The results revealed that during wash-in period, FiN2O increased, on average, to 30% at 3.83 min, 40% at 6.22 min, 50% at 14.13 min respectively. After 30 min of closed anesthesia, FiN2O decreased to 49.4%. It was 46.8% at 60 min. Thereafter it increased smoothly to 51.9% at 180 min. No hypoxia and hypercapnia occurred. Compared with commonly used high flow N2O-N2 inhalation, the technique of low flow wash-in and closed circuit maintenance with N2O-O2 may be less expensive and feasible and causes less pollution.
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PMID:Closed anesthesia with nitrous oxide. 927 7

In order to evaluate the effect of brain acidosis on neuronal functions as assessed by the in vivo studies, changes of cerebral blood flow (CBF), brain pH ([pH]o) and brain amino acid levels in the same brain region of the two different acidosis model rats were measured under isoflurane anesthesia. Three micro probes to measure CBF, [pH]o and amino acids, respectively, were implanted into the frontal cortex, and these parameters were recorded simultaneously. In the metabolic acidosis rats, the sustained decrease of [pH]o and amino acid levels, particularly Glu, were detected after the treatment with 10 min-i.v. infusion of 1 N HCl, although the significant changes of CBF did not appear because of the respiratory management. In the respiratory acidosis model, however, transient and significant increase of CBF and decrease of Glu and [pH]o were recorded after 10 min-exposure to about 30% CO2 (N2O:O2:CO2 = 2:5:3). The levels of Gly and Gln were reduced after acute exposure to hypercapnia, but these levels recovered to the control level in 20-30 min after hypercapnia exposure. In both animals, the amounts of Tau was gradually reduced after the treatment with 1 N HCl and hypercapnia, and these levels did not return to the control level when other amino acid levels had recovered. These differences of brain amino acid levels in the two different types of acidosis model rats may be related to the brain amino acid metabolic pathway. Thus, during brain acidosis induced by 1 N HCl and hypercapnia, the amount of extracellular Glu in the brain was reduced, and this reduction may contribute to the neuroprotective effects.
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PMID:[Acidosis and neuroprotection in two types of acidosis model rats under isoflurane anesthesia: evaluation of blood flow, pH and amino acid levels in the cortex]. 983 87

Global cerebral ischemia and subsequent reperfusion induce early impairment of the vasodilator responses to hypercapnia and vasoactive substances. Nitric oxide (NO) is involved in the regulation of cerebral blood flow (CBF) in both health and disease. The present study was designed to assess possible changes in the cerebrovascular reactivity to NO donors induced by cerebral ischemia-reperfusion in goats. Female goats (n = 9) were subjected to 20 min global cerebral ischemia under halothane/N2O anesthesia. Sixteen additional goats were sham-operated as a control group. One week later the effects of ischemia-reperfusion on relaxations to NO donors sodium nitroprusside (SNP), diethylamine/NO (DEA/NO), diethylenetriamine/NO (DETA/NO), and spermine/NO (SPER/NO) were studied in rings of middle cerebral artery (MCA) isolated in an organ bath for isometric tension recording. SNP, DEA/NO, DETA/NO, and SPER/NO induced concentration-dependent relaxations of MCA precontracted with KCl (DEA/NO > SPER/NO > SNP > DETA/NO) or with endothelin-1 (DEA/NO > SNP > SPER/NO > DETA/NO). Relaxations were always higher in endothelin-1-precontracted arteries. One week after cerebral ischemia concentration-response curves to SNP and DEA/NO were displaced to the right, indicating a reduction in relaxant potency of NO donors. The classical nitrovasodilator SNP and NONOates induce relaxation of isolated goat MCA which is partially inhibited by arterial depolarization. Global cerebral ischemia followed by reperfusion induces delayed impairment of the relaxant effects of NO on cerebrovascular smooth muscle, which results in reduced vasodilatory potency of NO donors in large cerebral arteries.
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PMID:Relaxant effects of sodium nitroprusside and NONOates in goat middle cerebral artery: delayed impairment by global ischemia-reperfusion. 1035 99

Videolaparoscopic techniques are an increasingly used modality for peritoneal dialysis catheter implant and rescue procedures. The greatest impediment for acceptance of the laparoscopic approach has been the necessity of general anesthesia because peritoneal insufflation of CO2 gas produces pain. In addition, complications of CO2 pneumoperitoneum include hypercarbia, acidosis, and cardiac arrhythmias. Renal failure patients commonly have severe coexisting medical conditions that make them an unacceptable risk for both general anesthesia and CO2 peritoneal insufflation. From December 1996 through November 1997, laparoscopy was performed utilizing nitrous oxide (N2O) as the insufflation gas. Since N2O produces neither pain nor metabolic effects, the laparoscopic procedure was safely performed under local anesthesia. Thirty-one patients have had laparoscopic implantation of peritoneal dialysis catheters under local anesthesia with 22 procedures performed on an ambulatory basis. The remaining cases were already hospitalized for complications of their renal failure. Four laparoscopic rescue procedures for catheter dysfunction were performed under local anesthesia with 3 cases as outpatients. Surgical laparoscopy under local anesthesia with N2O insufflation is a safe approach for both implantation procedures and salvaging of malfunctioning catheters. The procedure can be performed on an outpatient basis, frequently without delay in initiation or interruption of peritoneal dialysis.
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PMID:Videolaparoscopic peritoneal dialysis catheter implant and rescue procedures under local anesthesia with nitrous oxide pneumoperitoneum. 1064 98

A model of global hypoxia during Caesarean-section (C-section) birth has been widely used to study long-term effects of birth hypoxia on central nervous system (CNS) function. However, the actual degree of CNS and systemic hypoxia produced by the birth insult in this model has never been characterised. Additionally, the way in which the dam is anaesthetised during the C-section procedure may impinge on the degree of hypoxia experienced by the neonate. This study examined how a period of global birth anoxia and isoflurane/N2O anaesthesia interact to affect measures of CNS and systemic hypoxia in neonatal rats born by C-section compared with control, vaginally born animals. A 10-min period of global anoxia just before birth increased blood lactate, a metabolic indicator of systemic hypoxia, increased brain lactate and decreased brain ATP to a similar extent in pups born by C-section from either decapitated, unanaesthetised dams or dams anaesthetised with 2.5% isoflurane. Thus, this model does produce systemic and CNS hypoxia in the neonate. Pups born by C-section with a higher concentration of isoflurane (3.5%), in the absence of added global anoxia, also showed reductions in brain ATP at birth. In addition, 10 min of global anoxia produced greater increases in blood lactate in pups born from dams anaesthetised with the higher concentration of isoflurane. Thus, the concentration of anaesthetic used in this model may affect the degree of CNS or systemic hypoxia experienced by the neonate. Compared with vaginal birth, pups born by C-section with 2.5% or 3.5% isoflurane (and no added global anoxia) showed decreased PO2 and pH, and increased pCO2 in systemic blood taken <30 s after birth. Exposure to global anoxia during C-section birth actually increased systemic PO2 at <30 s after birth, presumably due to ventilatory responses to hypoxemia and hypercapnia; this effect of anoxia was reduced in anaesthetised compared with unanaesthetised pups. Thus, global anoxia acts as a stimulus for rapid recovery of systemic PO2 at birth, and this stimulus is dampened by isoflurane/N2O anaesthesia. These results should aid in understanding how CNS and systemic hypoxia at birth contribute to long-term changes in brain biochemistry and behaviour in this model.
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PMID:Interactive effects of anoxia and general anesthesia during birth on the degree of CNS and systemic hypoxia produced in neonatal rats. 1080 20

Malignant Hyperthermia (MH) has been a recognized complication of general anesthesia after the first case reports in the 1940's. Since then a great deal has been discovered about the genetics, pathophysiology and treatment of this once fatal syndrome. MH is the only clinical entity specifically related to and caused by anesthetic agents. MH once triggered during anesthesia results in a profound hyper metabolic state with rise in the core temperature, increased carbon dioxide production and oxygen consumption. Death will ensue if specific treatment is not started. The incidence of fulminant MH ranges from 1:62,000 to 1: 84,000 of general anesthesia cases if succinylcholine and inhalation agents are used. Massseter muscle spasm on induction of anesthesia, with an incidence of between 1:16,000 and 1:4,000, may be a predromal indication of the development of MH. Anesthetic agents, which may trigger MH in susceptible individuals, are the depolarizing muscle relaxant, succinyl choline and all the volatile anesthetic gasses. Nitrous oxide, intravenous induction agents, benzodiazepines, opioids, and the non-depolarizing relaxants do not trigger MH. MH susceptibility is associated with certain disorders, such as Duchene muscular dystrophy, and triggering agent should not be used in these patients. Inheritance is an autosomal dominant trait with variable penetrance. The pathogenesis of MH involves the loss of control of intracellular calcium ions in skeletal muscle with resultant protracted spasm and hyper metabolism. Clinically this will progress to hypercarbia, hypoxia, hyperthermia, hyperkalemia and death will result if specific treatment is not started. Management involves immediate discontinuation of the triggering anesthetics, hyperventilation with 100% oxygen and most importantly the definitive treatment with intravenous dantrolene.The importance of instigating the use of dantrolene in cases of MH cannot be overemphasized. MH is now treatable when once it would be fatal before the availability of dantrolene. Unless of an emergent nature, surgery should be canceled following the acute phase of MH. The patient should be admitted to intensive care for at least 24 hours and dantrolene continued as recurrence has been described. It is imperative that the patient and their family are counseled, Medalert bracelets provided and registration with the Malignant Hyperthermia Association of the United States (MHAUS), encouraged. The caffeine/halothane testing of muscle biopsies is currently the most definitive test for malignant hyperthermia susceptibility. The routine use in suspected cases or the immediate family of known cases remains a matter of contention.
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PMID:Malignant hyperthermia. 1450 52

Nitrous oxide is an inflammable gas that gives no smell or taste. It has a history of abuse as long as its clinical use, and deaths, although rare, have been reported. We describe two cases of accidental deaths related to voluntary inhalation of nitrous oxide, both found dead with a gas mask covering the face. In an attempt to find an explanation to why the victims did not react properly to oncoming hypoxia, we performed experiments where a test person was allowed to breath in a closed system, with or without nitrous oxide added. Vital signs and gas concentrations as well as subjective symptoms were recorded. The experiments indicated that the explanation to the fact that neither of the descendents had reacted to oncoming hypoxia and hypercapnia was due to the inhalation of nitrous oxide. This study raises the question whether nitrous oxide really should be easily, commercially available.
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PMID:Death from Nitrous Oxide. 2625 92

This study was designed to observe the haemodynamic changes, recovery status and cost effectiveness during anaesthesia in laparoscopic cholecystectomy with medical air in comparison to anaesthesia with nitrous oxide associated with maintain of adequate analgesia and was conducted in the department of Analgesia and Intensive Care Medicine, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh from January 2017 to June 2017. Nitrous oxide is popularly using as an analgesic in current balanced general anesthesia in addition carrier agent for anesthetic. Intraoperative pain intensity depends on many variables including, type of surgery, surgical stimulation and surgical incision. It is difficult to measure intraoperative pain properly under general anesthesia therefore anesthetist depends on the surrogate marker of inadequate analgesia like raised heart rate, blood pressure, sweating and lacrimation. However, unfortunately, these parameters may changes in same direction with light plane of anesthesia, hypercarbia and ongoing procedural status of the patient.
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PMID:Nitrous Oxide versus Medical Air Using in General Anaesthesia During Laparoscopic Cholecystectomy: A Comparative Study. 3191 49


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