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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the antagonistic effect of naloxone on fentanyl-induced respiratory depression, 55 patients (randomly divided into various study and control groups were studied during nitrous-oxide-oxygen-halothane anaesthesia. Respiratory depression after 0.1 mg of fentanyl was totally reversed by 10 microgram/kg of naloxone, measured as 100% restoration of spontaneous respiration, normal minute volume and end-tidal CO2, while 15 microgram/kg of naloxone was needed to antagonize 0.2 mg of fentanyl. The respective control groups remained apnoeic. If no fentanyl had previously been administered, there was no difference in the respiratory behaviour of naloxone-treated and control patients, which indicates that no unspecific analeptic effect of naloxone could be demonstrated. The circulatory changes after fentanyl were nearly reversed by naloxone, as has been found earlier with other narcotics. Recovery from anaesthesia was scored from 0 to 10 (using a modification of Apgar scores for newborns), and somewhat higher mean scores were obtained with the naloxone-treated patients than with their controls. However, higher postoperative pain scores were recorded in these patients as well as a higher incidence of nausea and vomiting. The study demonstrates the dose-relationships of fetanyl and naloxone for estimation of total antagonism; however, the use of naloxone for partial antagonism at the termination of anaesthesia cannot be based on these findings.
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PMID:Antagonism of fentanyl with naloxone during N2O+O2+ halothane anaesthesia. 60 61

Different modes of naloxone administration were studied in 100 patients following N2O-O2-relaxant anaesthesia, where fentanyl was administered for analgesia according to a standardized dose schedule (mean 4.3 microgram/kg/h). After reversal of muscular relaxation, the patients were randomly given naloxone--either 1.0 or 2.5 microgram/kg i.v. or 2.5 or 5.0 microgram/kg i.m., or none (control). Each group consisted of 20 patients. Awakening was fastest after 2.5 microgram/kg i.v. of naloxone (1.8 +/- 0.1 min), the time being significantly shorter (P less than 0.025) than in the control group (2.7 +/- 0.4 min). After 15 min, the minute volume and frequency of respiration were significantly higher (P less than 0.05) in all naloxone groups than in the control group. However, the arterialized venous PCO2 did not show significant differences during the recovery. It is therefore suggested that naloxone reversal may cause an increase in CO2 production. The immediate postoperative pain (score 0-3) was mildest in the control group (1.0 mean) and severest after 2.5 microgram/kg i.v. of naloxone (1.8 mean); the difference was statistically significant (P less than 0.05). The groups receiving 1.0 microgram/kg i.v. and 2.5 microgram/kg i.m. did not differ from each other (1.2 mean). Nausea and vomiting were reported more often after 5.0 microgram/kg im. of naloxone than in other groups. After moderate doses of fentanyl during balanced anaesthesia, routine use of naloxone does not seem to be necessary, but if rapid recovery is essential, 1.0 microgram/kg i.v. or 2.5 microgram/kg i.m. of naloxone may be recommended and these doses do not cause a higher incidence of side effects.
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PMID:Naloxone as narcotic antagonist after balanced anaesthesia. 60 62

The hemodynamic interaction of acute hypovolemia and halothane anesthesia in dogs with increased intra-abdominal pressure caused by intraperitoneal instillation of N2, N2O and CO2 was studied. During normovolemia and just basal pentobarbital anesthesia, the response to increase of intra-abdominal pressure to 40 torr consisted of a 35 per cent decrease in cardiac output, which was equal to the decrease in magnitude of inferior vena caval blood flow. During basal pentobarbital anesthesia, the addition of halothane anesthesia (1 MAC) in combination with hypovolemia (15 per cent blood volume loss) depressed the pre-inflation cardiac output more than addition of halothane anesthesia alone or induction of hypovolemia alone. During each of these conditions, superimposition of increased intra-abdominal pressure to 40 torr caused a further 26-43 per cent decrease in cardiac output compared with the pre-inflation value. Therefore, the greatest cardiovascular depression occurred when the animals were both hypovolemic and anesthetized with halothane. There was no difference in the responses to increased intra-abdominal pressure with the different inflating gases at any time. These findings indicate that in the presence of halothane anesthesia or hypovolemia, induction of pneumoperitoneum may cause severe cardiovascular depression.
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PMID:Hemodynamics of increased intra-abdominal pressure: Interaction with hypovolemia and halothane anesthesia. 61 5

Cerebral cortical blood flow was measured in rabbits with the hydrogen clearance technique. The reactivity to CO2, tested by changing the end tidal CO2 (ETCO2) in steps from 2 to 6 volumes %, was highly dependent on the kind of anesthesia, being greatest under halothane and least under nitrous oxide. Reactivity to CO2 in halothane-anesthetized animals also depended on arterial blood pressure, being greatest when pressure was below 70 mm Hg. Intravenous atropine blocked the increase in reactivity in halothane-anesthetized animals at low blood pressures. Conversely, intravenous eserine (physostigmine) greatly increased the reactivity to CO2 in nitrous oxide-anesthetized animals. Precollicular decerebration considerably decreased CO2 reactivity of halothane-anesthetized rabbits, while partial brain stem lesions that spared midline structures had no effect on CO2 reactivity. It is concluded that a central neurogenic mechanism with a cholinergic link may be responsible, at least in part, for the cerebrovascular effect of CO2. Moreover, the cerebrovascular effects of halothane may result from stimulation of the same system.
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PMID:Cerebrovascular CO2 reactivity: role of a cholinergic mechanism modulated by anesthesia. 64 10

A new CO2-Analyzer for continuous measurement of CO2 content during artificial respiration is described. Based on infra red absorption, this device may be used for measuring the carbon dioxide content of expiration in anaesthesia and intensive care. Carbon dioxide infrared absorption is affected by nitrous oxide. This side effect can be compensated by a single switch, if the sample contans N2O.
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PMID:[A new CO2 analyzer for monitoring of artificial ventilation (author's transl)]. 64 90

The relationship between the plasma concentration of morphine and morphine-induced changes in ventilation and the ventilatory response to carbon dioxide was studied in 17 healthy adults undergoing elective surgery under general anaesthesia. Each subject was given morphine sulphate 0.15 mg kg-1 i.m.; ventilation (Ve), end-tidal PCO2(PE'CO2), mixed venous PCO2(PVCO2) and ventilatory response to carbon dioxide (delta Ve/deltaPCO2) were measured before and within 90 min after injection. Mixed venous PCO2 and deltaVe/deltaPCO2 were measured by standard rebreathing methods; plasma morphine concentration was measured by radioimmunoassay. Maximum plasma morphine ranged from 30 to 120 ng ml-1, between 4 and 60 min after injection. There was a significant increase in mixed venous PCO2 (P less than 0.001), and PE'CO2 (P less than 0.01) after morphine while Ve decreased insignificantly. Morphine displaced the carbon dioxide response curve to the right (P less than 0.01) and delta Ve/delta PCO2 decreased from 12.3 to 10.0 litre min-1 kPa-1 (P less than 0.05). The magnitude of changes in Ve and deltaVe/deltaPCO2 were not related to the peak plasma concentration of morphine or to the mean concentration immediately before and after the carbon dioxide response measurement. Plasma concentrations of morphine, under the conditions of the present study, are not an objective indicator of pharmacological activity between one patient and another.
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PMID:Ventilatory effects and plasma concentration of morphine in man. 67 62

Ventilation (Ve), end-tidal (Pe' CO2), mixed venous PCO2 (PVCO2) and the ventilatory response to carbon dioxide (deltaVE/deltaPCO2) were measured before and within 90 min after morphine 0.15 mg kg-1 i.m. given to 17 adult patients undergoing elective surgery under general anaesthesia. The hypothesis that patients with a low ventilatory response to carbon dioxide are more susceptible to the ventilatory depressant effects of morphine was tested. Morphine induced increases in PE'CO2 and PVCO2 were not correlated with either the slope or the position of hte preinjection response to carbon dioxide. Mean delta Ve/deltaPCO2 was depressed after morphine (P less than 0.05), but individual responses varied widely. Seven patients whose control delta Ve/PCO2 was 9.9 litre min-1 kPa-1 or less decreased delta Ve/deltaPCO2 after morphine. In four patients, delta Ve/deltaPCO2 increased after morphine; however, in each case, PE'CO2 and PVCO2 increased also. Morphine displaced the carbon dioxide response to the right (P less than 0.001) but no correlation was found betwen either the magnitude of the displacement or change in slope and control delta Ve/deltaPCO2. The results suggest that patients with a low value for delta Ve/deltaPCO2 are not more susceptible to the ventilatory depressant action of morphine.
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PMID:Low ventilatory response to carbon dioxide not associated with increased depression by morphine. 67 63

To elucidate the effects of halothane on chemical regulation of ventilation in man, the authors studied the ventilatory responses to isocapnic hypoxia and hyperoxic hypercapnia in 33 human subjects while fully conscious and during sedation or anesthesia with halothane, .1, 1.1, or 2 MAC. In each group, the ventilatory effect of intravenous administration of doxapram, .4 mg/kg, was also measured. Halothane, 1.1 and 2 MAC, totally abolished the hypoxic response and nearly abolished the response to doxapram, while leaving the response to CO2 relatively brisk. Halothane, .1 MAC, decreased the responses to hypoxia and doxapram to less than a third of control, but did not alter the response to CO2. It is concluded that halothane selectivity impairs two ventilatory responses mediated by peripheral chemoreceptors in man.
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PMID:Ventilatory responses to hypoxia and hypercapnia during halothane sedation and anesthesia in man. 69 78

Hysteroscopy has added a new dimension to the management of patients with common clinical problems, increasing the accuracy of diagnosis and serving as an adjunct in treatment of intrauterine conditions. This report summarizes the hysteroscopic experience with 320 selected patients, 104 in the reproductive age group with abnormal uterine bleeding, 91 who underwent hysteroscopy for location and retrieval of intrauterine contraceptive devices, 36 with primary or secondary infertility, 36 with postmenopausal bleeding, and 15 with uterine leiomyomas. Paracervical block anesthesia was used successfully in 214 patients. General anesthesia was used in the remainder because of planned additional surgical intervention. Uterine distention was achieved with D5W in 270 patients, with dextran 32% in 30 patients, and with CO2 gas insufflation in 20 patients. In 71.6 per cent of the patients,visually recognizable or pathologically suspicious intrauterine abnormalities were found. This study further demonstrated the utility of hysteroscopy in diagnosis of endometrial polyps, uterine submucous leiomyomas, uterine malformations, and intrauterine adhesions. Hysteroscopy was also helpful in taking directed biopsies of selected areas of the endometrium in patients with adenomatous hyperplasia and early adenocarcinoma of the endometrium and helpful in removal of intrauterine foreign bodies and evaluation of the recently pregnant uterus when there was a question of persistent pregnancy. Hysteroscopy is a safe ambulatory procedure that is appealing to both patient and gynecologist in its economy and simplicity.
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PMID:Hysteroscopy: a clinical experience with 320 patients. 83 33

Myocardial metabolism, blood flow distribution within the heart, and coronary and systemic circulations were observed during halothane anesthesia using 15 mongrel dogs. Pao2 and Paco2 were maintained near 100 and 40 torr respectively throughout the study. As arterial halothane content increased, most parameters of systemic circulation were depressed significantly. Coronary blood flow was reduced in parallel with myocardial oxygen consumption (MVo2) (r=+0.89, pless than0.001). Myocardial contractility decreased significantly as anesthesia deepened. MVo2 and myocardial CO2 production were reduced as arterial halothane concentration rose. Arterial-coronary venous difference in blood oxygen content remained unchanged even in deep stage. Lactate and pyruvate were continuously taken up by the myocardium, although the amounts of uptake were reduced as anesthesia progressed. Calculated excess lactate and redox potential did not show any signs of myocardial hypoxia even in deep halothane anesthesia. Among major hemodynamic parameters, left ventricular dp/dt max showed the closest correlation with MVo2. Microsphere injection method was used to observe blood flow distribution within the heart. Halothane did not influence the distribution significantly and I/O ratio of the left ventricular free wall remained near 1.0 during the study.
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PMID:Effects of halothane on coronary and systemic circulations, myocardial metabolism and blood flow distribution within the canine heart. 85 19


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