Halothane depresses baroreflex control of heart rate in man.

Baroreflex control of heart rate was determined during three awake control situations and during two depths of halothane anesthesia in man. Baroreflex function was quantiated by calculating the pressor test slope from the R-R interval change on the ECG produced by a pharmacologically induced pressor response. During the three awake control situations the subjects breathed room air or 100 per cent O2 spontaneously or 100 per cent O2 with ventilation controlled. Mean (+/- SD) slopes obtained were 15.1 +/- 4.5, 15.6 +/- 6.8 and 18.4 +/- 9.9, respectively. No significant difference in baroreflex function slope was observed. During light halothane anesthesia (0.7 per cent endtidal) baroreflex function was significantly depressed (mean slope = 2.5 +/- 1.5), and it was abolished at 1.1 per cent end-tidal halothane (mean slope = 0.03 +/- 0.04). It is concluded that halothane anesthesia produces depression of baroreflex control of heart rate in man.     

Comparison of metaproterenol, isoetharine and salbutamol in the relief of methacholine-induced bronchospasm in dogs

We evaluated cardiovascular effects and effectiveness of isoetharine, metaproterenol and salbutamol, when administered intratracheally to relieve methacholine-induced bronchospasm in dogs anaesthetized with 50 per cent nitrous oxide, oxygen, halothane and mechanically ventilated. Methacholine 2 micrograms X kg-1 X hour-1 was administrated first followed by halothane (1 MAC) for 30 minutes (control), then metaproterenol, isoetharine or salbutamol. Metaproterenol (15 mg) significantly decreased transpulmonary pressure to 20.1 +/- 0.5 (SE) from 22.5 +/- 1.15 cmH2O (p less than 0.025) after three min and to 15 +/- 0.5 cmH2O (p less than 0.005) after 90 min. Isoetharine (2.5 mg) decreased transpulmonary pressure after five min to 22.1 +/- 1 from 24.5 +/- 1.5 cmH2O (p less than 0.05), and to 21.75 +/- 0.55 mmH2O after 90 min. Salbutamol 25 micrograms X kg-1 decreased transpulmonary pressure to 20.7 +/- 0.75 from 24.25 +/- 1.28 after three min and to 16 +/- .5 after 90 min. The peak effects on airway pressure occurred at 15 min for metaproterenol, 25 min for salbutamol and 20 min for isoetharine. Pulmonary vascular resistance was not significantly changed during halothane anaesthesia alone but decreased significantly after metaproterenol and isoetharine infusion. Heart rate increased ten per cent after metaproterenol, three per cent after isoetharine, and five per cent after salbutamol. No arrhythmias occurred in any group. Cardiac output increased significantly to 3.25 +/- 0.2 from 1.5 +/- 0.17 L X min-1 (p less than 0.025) after metaproterenol to 3.2 +/- .025 from 1.45 +/- .009 after salbutamol and was unchanged after isoetharine. Metaproterenol and salbutamol in the presence of 1 MAC halothane anaesthesia relieved methacholine-induced bronchospasm more rapidly than did isoetharine. The onset of effect was 3 +/- 0.05 min for metaproterenol and salbutamol and 5 +/- 0.01 min for isoetharine. The effect lasted 210 +/- 10.5 min for metaproterenol, 170 +/- 12.5 min for salbutamol and 90 +/- 4.75 min for isoetharine.     

A low-pressure portable anaesthesia system for field use: clinical trials

This is a report of our experience with a portable anaesthesia system that was developed for use under field conditions, when compressed gas supplies are limited. We first assembled and bench-tested a low-pressure plenum system, based upon the Farman entrainer. The entrainer required a low flow of compressed gas, O2 at 1-2 L.min-1, and generated a low-pressure mixture of O2 and air which was directed through an Oxford miniature vaporizer, a non-return valve, and a widebore T-piece circuit. With this system we anaesthetized 24 patients with intermittent positive pressure ventilation (IPPV) and nine patients breathing spontaneously. During IPPV, the circuit resembled a T-piece and provided effective gas exchange with a FGF of 1.2 times minute ventilation. Inspiratory and expiratory valves were arranged so that the spontaneous mode was non-rebreathing, and FGF was adjusted to equal minute ventilation. The system was very economical, using 1-2 L.min-1 O2 and 20-25 ml.hr-1 liquid halothane to produce a FGF of 6-10 L.min-1, an FIO2 of 0.33, and FIhal of 1-1.5 per cent. We have demonstrated that this is a versatile, safe, and economical system, compatible with the practice of modern inhalational anaesthesia under field conditions. It can be readily assembled from commercially available components.     

Effect of halothane,enflurane and isoflurane on the end-systolic pressure-length relationship

Myocardial contractility was measured using the end-systolic pressure-length (ESPL) relationship in dogs subjected to increasing concentrations of halothane (0.5-2 per cent), enflurane (0.77-2.6 per cent) or isoflurane (0.70-2.13 per cent), combined with an infusion 7 micrograms X kg-1 X min-1 of fentanyl, after induction of anaesthesia with 15 mg X kg-1 thiopentone. The relationship between the concentrations of the different drugs and contractility (ESPL) can best be described by ESPL = a + b/(MAC fraction) where "a" is a constant and "b" is the slope of the curve relating ESPL to MAC. At 1.0 MAC values, the ESPL for halothane (69.04 +/- 25.83 mmHg X mm-1) did not differ from that of isoflurane (63.19 +/- 17.36 mmHg X mm-1). However, the myocardial contractility during 1.0 MAC halothane and isoflurane anaesthesia was better preserved than that of enflurane (38.66 +/- 9.73 mmHg X mm-1: p less than 0.01, p less than 0.05 respectively).     

Changes in myocardial oxygen consumption,efficiency and haemodynamics when systemic pressure is increased during morphine and added halothane anaesthesia in dogs

Depression of left ventricular function by the combination of halothane anaesthesia and increased ventricular afterload may undesirably reduce stroke volume and increase myocardial oxygen consumption by increasing ventricular wall stress. To investigate this possibility we studied six dogs instrumented to measure systemic and left ventricular pressures, ascending aortic and left anterior descending coronary artery flows and external left ventricular diameters. We sampled arterial and coronary sinus blood gases and oxygen contents. During morphine anaesthesia (4mg·kg^-1 intravenously with hourly supplements of 0.1 mg·kg^-1) and during added halothane anaesthesia (1.5 per cent end tidal) we measured systemic pressure, heart rate, stroke volume, stroke work, cardiac output, left ventricular end diastolic pressure and diameter and myocardial oxygen consumption. After infusing phenylephrine (0.02 mg/ml) to increase systolic pressure to 23.28 kPa (175 torr) we repeated measurements in both groups. We found that added halothane depressed systemic pressures (52 per cent), stroke volume (30 per cent), and myocardial oxygen consumption (46 per cent) compared to morphine alone. When afterload was increased with phenylephrine, stroke volume (20 per cent), cardiac output (25 per cent) and myocardial efficiency (47 per cent) were further depressed during added halothane anaesthesia compared to control halothane anaesthesia. Left ventricular end diastolic diameter (5 per cent) and pressure (320 per cent) were significantly increased by added afterload, compared to the control added halothane state. Conversely, increased afterload produced few changes during morphine anaesthesia alone. However, at comparable systemic pressures, myocardial oxygen consumption was similar during both anaesthetic states. We conclude that during added halothane anaesthesia increased afterload decreases stroke volume and myocardial efficiency. Cardiac output is reduced without increased myocardial oxygen consumption compared to morphine anaesthesia at comparable afterload states. In patients with already compromised cardiac output, further depression of stroke volume by increased ventricular afterload during halothane anaesthesia may be deleterious.     

Laryngo-pharyngeal complaints after use of the laryngeal mask airway

PURPOSE: To compare the incidence of dysphagia, dysphonia and sore throat following anesthesia, using the laryngeal mask airway (LMA), among patients receiving intermittent positive-pressure ventilation (IPPV) and those breathing spontaneously (SV) and with two different concentrations of nitrous oxide (N2O) in oxygen. METHODS: In a prospective trial, 120 patients (ASA I-III, 16-70 yr, > 60 kg) undergoing minor peripheral surgery were randomised into four groups with respect to type of ventilation and N2O concentration (50% or 66%) received. Cuff pressure measurements were monitored continuously. Twenty-four hours after surgery, patients were questioned for sore throat, dysphagia and dysphonia. RESULTS: At 30 min post-LMA insertion, increases in cuff pressure were 35.2+/-17.1 mmHg (22.8%) vs 50.1+/-16.3 mmHg (32.7%) in patients breathing 50 and 66% N2O, respectively (P < 0.01). There were no differences in cuff pressure increment between patients in the SV and IPPV groups. Cuff pressure values at the end of surgery depended on the duration of surgery and on the concentrations of N2O. The overall incidence of postoperative discomfort at 24 hr was dysphagia 11%, dysphonia 11% and sore throat 28.8%. Only two patients reported sore throat as more than mild. There was no relationship between cuff pressure and laryngo-pharyngeal complaints. The incidence of dysphonia in the groups receiving IPPV was higher than that in the groups with spontaneous ventilation (17.2 vs 5%, P < 0.05). CONCLUSION: Post-operative discomfort is related to the type of ventilation but not to variation in LMA cuff pressure.     

Comparison of the effects of succinylcholine and atracurium on intracranial pressure in monkeys with intracranial hypertension

The effects of succinylcholine (1.5 mg X kg-1 IV) administered five minutes after a defasciculating dose of curare (0.05 mg X kg-1 IV), were compared with the effects of atracurium (0.5 mg X kg-1 IV) on intracranial pressure (ICP) in 13 cynomolgus monkeys with intracranial hypertension (ICP approximately 25 mmHg). Neither succinylcholine nor atracurium increased ICP during general anaesthesia with 60 per cent N2O/O2, 0.5-1 per cent halothane. During a rapid sequence induction and intubation with thiopentone 5 mg X kg-1 IV, ICP increased equally with intubation following both atracurium (25 +/- 1 to 32 +/- 2 mmHg) and succinylcholine (25 +/- 1 to 31 +/- 2 mmHg) (p less than 0.05). Intubation was also associated with significant increases in PaCO2, CVP and MAP. We conclude that in this primate model of intracranial hypertension, neither atracurium nor succinylcholine (when given following a defasciculating dose of curare) elevates ICP. In terms of the elevation of ICP associated with intubation, atracurium was found to offer no advantage over succinylcholine.     

Arterial air embolism of venous origin in dogs: effect of nitrous oxide in combination with halothane and pentobarbitone

The effects of using nitrous oxide (N2O) with halothane or pentobarbitone anaesthesia on the filtration of venous air emboli (VAE) by the pulmonary circulation were studied in dogs. Dogs anaesthetized with either pentobarbitone, pentobarbitone/N2O, halothane, or halothane/N2O were embolized with venous air into the right atrium at 0.25 to 0.35 ml.kg-1.min-1 for 30 min. The animals were in a supine, head down position. A Doppler ultrasonic probe located over the suprarenal aorta detected arterial bubbles that escaped filtration by the lungs. No bubbles were detected at 0.25 ml.kg-1.min-1, but at 0.30 ml.kg-1.min-1 the incidence was 11 per cent (pentobarbitone), 0 per cent (pentobarbitone/N2O), 33 per cent (halothane), and 63 per cent (halothane/N2O) and at 0.35 ml.kg-1.min-1, 44 per cent (pentobarbitone), 14 per cent (pentobarbitone/N2O), and 56 per cent (halothane). Half of the dogs receiving VAE with halothane/N2O at 0.30 ml.kg-1.min-1 died within the first 10 min of the air infusion. Thus, no animals were studied at the next higher dose (0.35 ml.kg-1.min-1). The results suggest that the occurrence of VAE with nitrous oxide anaesthesia may result in greater haemodynamic consequence and increased likelihood for spillover of the venous bubbles into the arteries if used with halothane as compared to pentobarbitone.     

Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two0dimensional echocardiographic dimensions of the left ventricle and pulmonary artery bloodflow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg·kg⁻¹ IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in bothgroups, but decreases in EF (32 ± 5 percentvs18 ± 5 per cent) and increases in LVEDV (18 ± 7 per cent vs7 ± 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 ± 6 per cent), than during isoflurane anaesthesia (18 ± 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 ± 4 per cent) following atropine in both groups, and CO returned to control levels. Halothane decreased EF and increased LVEDV more than isoflurane at 1.5 MAC end— expired anaesthetic levels. Atropine did not diminish the myocardial depression produced by halothane or isoflurane. The increase in CO following atropine during halothane and isoflurane anaesthesia in infants and small children is the result of increases in HR alone. Nous avons utilisé un appareil à échocardiographie bi-dimensionnelle couplé à un Doppler pulsé chez des bébés et de jeunes enfants pour évaluer l’impact hémodynamique de l’halothane (n = 15) et de l’isoflurane (n = 16) et la modification possible de ces effets par l’atropine. Nous avons mesure la frequence cardiaque (FC), la pression artérielle moyenne (PAM), la dimension de la cavité ventriculaire gauche (par écho bi-dimensionnelle) et la vélocité du flot sanguin pulmonaire (par Doppler) et ce, en trois occasions soit avant l’induction, après l’instauration de 1.5 MAC d’halothane ou d’isoflurane et finalement, deux minutes après l’injection IV de 0.02 mg·kg⁻¹ d’atropine. On ne nota une baisse de la frequence cardiaque qu’avec l’halothane tandis que la PAM, le débit cardiaque (DC) et le volume d’éjection (VE) diminuaient autant avec l’un ou l’autre anesthésique. La diminution de la fraction d’éjection (FE) et l’augmentation du volume télédiastolique du ventricule gauche (VTDVG) significatives pour les deux groupes, étaienl plus marqué avec l’halothane qu’avec l’isoflurane: FE 32 ± 5 pour cent vs18 ±5 pour cent; VTDVG 18 ± 7 pour cent vs 7 ± 5 pour cent. Avec l’atropine, la FC monta plus dans le groupe halothane (31 ± 6 pour cent) que dans le groupe isoflurane (18 ± 5 pour cent), le DC augmentant dans les deux groupes, alors que le VE et la FE demeuraient inchangés. Comparée aux mesures pré-induction, l’atropine amenait une hausse significative de la FC, semblable dans les deux groupes (18 ± 4 pour cent) et restaurait le DC. Donc, chez les bebes et les jeunes enfants, a 1.5 MAC, l’halothane diminue la FE et augmente le VTDVG plus que ne le fait l’isoflurane. L’atropine ne modifie pas la depression myocardique et elle ne restaure le DC que par une hausse de la FC.

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Supported by PHS Grant No. 8507300 from the College of Medicine, University of Iowa Hospital, Iowa City, IA.     

The cardiovascular effects of anticholinergic agents administered during halothane anaesthesia in children

The cardiovascular effects of anticholinergic agents administered during halothane anaesthesia were studied in 31 children aged 1-12 years undergoing peripheral orthopaedic surgery. Either normal saline, glycopyrrolate (10 micrograms.kg-1) or atropine (20 micrograms.kg-1) was administered in randomized double-blind fashion during the induction of anaesthesia with halothane while the electrocardiogram was continuously recorded. After induction, the children were paralyzed with atracurium, intubated, and ventilated. Anaesthesia was maintained with N2O/O2 and halothane (up to 2.5% inspired). The concentrations of expired CO2 and halothane were measured continuously using mass spectrometry. Sixty-one percent (19/31) of the children developed one or more dysrhythmias. Junctional rhythm occurred in 74% (14/19) of the children with dysrhythmias, developed early during induction (mean +/- s.d. time = 2.29 +/- 2.0 min after commencement of induction), and usually resolved before the administration of the study drug (8/14). All dysrhythmias initially occurred before or during induction and none developed during intubation, during incision, during the maintenance of anaesthesia, or after the administration of anticholinergic agents. The data suggest that: 1) a combination of factors present during halothane induction is highly dysrhythmogenic especially for junctional rhythm; 2) junctional rhythm will resolve spontaneously; 3) the administration of an anticholinergic agent during halothane induction is safe but may be unnecessary in children greater than 1 year of age; and 4) the dysrhythmogenic factors present during induction are attenuated during the maintenance of halothane anaesthesia.     

The role of halothane and fentanyl in the production of balanced anaesthesia

The aim of the study was to quantitate the degree of respiratory depression when tolerance of superficial nociception and of an endotracheal tube was achieved by supplementing N2O + O2 anaesthesia either with halothane alone or with halothane in combination with fentanyl. Eighty-four patients, matched into seven groups, were studied after induction of anaesthesia with thiopental (4 mg/kg) and suxamethonium (3 mg/kg) using the following supplementation: 0.8, 0.6, 0.4% halothane alone or 0.4, 0.2, 0% halothane with 0.5-2 micrograms/kg fentanyl. After 10 min administration of the anaesthetic mixture using manual intermittent positive pressure ventilation (IPPV) (end-tidal CO2 c. 5.5%), IPPV was discontinued and spontaneous respiration allowed to return. When the end-tidal CO2 had stabilized, samples for blood gas analysis were taken and superficial antinociception was tested by pinching an inguinal skin fold. Supplementation of an N2O + O2 mixture with 0.8% halothane without fentanyl or with 0.4% halothane with 0.5 microgram/kg fentanyl seemed to come closest to the optimum in producing tolerance of an endotracheal tube and of superficial nociception (in about 85% of cases with an increase in PCO2 to only 7 kPa.     

Changes in arterial oxygen tension during and after enflurane or halothane anesthesia as well as epidural analgesia

Recovery from inhalation anesthesia is often marked by the occurrence of postoperative hypoxemia. In this study, we compared the effects of enflurane or halothane anesthesia and epidural analgesia on arterial oxygen tension during and after the operation in 60 ASA physical status 1-2 patients who underwent cholecystectomy. Anesthesia was induced with thiopental and maintained with 66% N2O and -enflurane (1.5%), -halothane (1%), or -epidural lidocaine (1% solution, 17.5 ml) in oxygen. Blood gas analysis was done before and 10, 30, 60 min after induction. PaO2 was measured on 1st and 3rd postoperative days in all patients breathing air spontaneously. PaO2 decreased during operation in all three groups of anesthesia. PaO2 values on first postoperative day were significantly lower than those before operation, and PaO2 value in enflurane group (PaO2 = 67 +/- 1 mmHg) was significantly lower than that in halothane group (PaO2 = 72 +/- 2 mmHg, P less than 0.05).     

Anticonvulsant therapy increases fentanyl requirements during anaesthesia for craniotomy

This study was designed to determine whether patients receiving chronic anticonvulsant therapy demonstrate an altered requirement for fentanyl during anaesthesia. Sixty-one patients undergoing craniotomy were studied; 20 controls (MED = 0) who had never received anticonvulsants and 41 epileptics in whom therapeutic plasma concentrations of either one (MED = 1), two (MED = 2), or three (MED = 3) different anticonvulsants were documented. During anaesthesia with 60-70 per cent N2O in O2 and 0.2 per cent isoflurane, a maintenance dose (MD) of fentanyl was administered using a continuous variable-rate IV fentanyl infusion, supplemented by intermittent 50 micrograms IV boluses. In order to define the minimal dosage of fentanyl required, the MD was titrated according to increases or decreases in the heart rate and/or mean arterial pressure exceeding 15 per cent of baseline ward values. A progressively higher fentanyl MD was required in the epileptic patients (MED = 1-4.3 +/- 0.5 microgram.kg-1.hr-1; MED = 2-5.4 +/- 0.6; MED = 3-7.6 +/- 0.6) compared with the control MD (MED = 0-2.6 +/- 0.5) (P less than 0.001). These findings indicate that there appears to be a dose-effect relationship between the number of anticonvulsants received and the maintenance dose of fentanyl required during balanced anaesthesia.     

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2-reactivity during craniotomy for supratentorial cerebral tumours in halothane anaesthesia. A dose-response study

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anaesthesia was induced with thiopental 4-6 mg kg-1, fentanyl and pancuronium, and maintained with an inspiratory halothane concentration of 0.45% in nitrous oxide 67% at a moderate hypocapnic level. In one group of patients (n = 7) the inspiratory halothane concentration was maintained at 0.45% throughout anaesthesia. About 1 h after induction of anaesthesia CBF and CMRO2 averaged 35 +/- 2 ml 100 g-1 min-1 and 2.7 +/- 0.3 ml O2 100 g-1 min-1 (mean +/- s.c. mean), respectively. During repeat studies 1 h later CBF and CMRO2 did not change. In another group of patients (n = 7) an increase in halothane concentration from 0.45% to 0.90% was associated with a significant decrease in CMRO2 from 2.3 +/- 0.1 to 2.0 +/- 0.1 ml O2 100 g-1 min-1. The CO2-reactivity measured after the second flow measurement was preserved. It is concluded that halothane in this study induces a dose-dependent decrease in cerebral metabolism, an increase in CBF while CO2-reactivity is maintained.     

Attenuation of contraction of isolated canine coronary arteries by enflurane and halothane

Contraction of vascular smooth muscle such as that existing in coronary arteries is regulated in part by Ca++ entry into cells via Ca++ channels. Volatile anaesthetics are known to attenuate agonist-induced coronary artery constriction. The purpose of this experiment was to determine if 1.5 MAC concentrations of halothane or enflurane attenuated contractions evoked by activation of one type of Ca++ channel--the potential operator channel. In the current experiment, potential operator channels were activated by depolarizing isolated canine coronary artery rings with high concentration of K+, causing Ca++ entry and vessel contraction. Rings without endothelium were suspended for isometric force measurement in organ chambers containing aerated Krebs-Ringer solution. Maximum response to Ca++ in rings depolarized with K+ was 120 +/- 5 per cent in untreated versus 101 +/- 3 per cent in rings treated with enflurane (P less than 0.01). The maximum response was 123 +/- 6 per cent in untreated versus 111 +/- 5 per cent during halothane administration (P less than 0.05). In contrast, nifedipine 10(-9) M depressed maximum contractions from 114 +/- 5 per cent to 37 +/- 4 per cent (P less than 0.01) and nifedipine 10(-8) M depressed contractions to 30 +/- 4 per cent (P less than 0.01). In a further series of experiments, sustained contractions were depressed by continued administration of the anaesthetics, indicating no loss of anaesthetic effect with time. The results indicate that 1.5 MAC halothane and enflurane attenuate contractions of canine coronary arteries evoked by depolarization and Ca++ entry through potential operated channels. However, neither halothane nor enflurane exhibited the marked depressant effect exerted by nifedipine.     

Local spinal cord glucose utilization in conscious and halo-thane-anaesthetized rats

The authors used the 2-[14C]deoxyglucose method to study local spinal and cerebral glucose utilization simultaneously during 1.2 per cent halothane anaesthesia in adult Sprague-Dawley rats. In conscious animals (n = 5) the rate of glucose utilization in lumbar spinal gray matter was about 50 per cent lower than that of cerebral cortex. Halothane anaesthesia (n = 6) reduced spinal cord and cerebral metabolic rate. Spinal glucose utilization was reduced 12-35 per cent, but this was less than the 45-70 per cent decrease halothane produced in 8 of 16 cerebral structures examined and was independent of the hypotension produced. These results indicate that halothane is a spinal metabolic depressant but that its effects on this tissue are substantially less than those it has on many cerebral structures.     

A COMPARISON OF THE EFFECT OF THREE ANAESTHETIC TECHNIQUES ON POSTOPERATIVE ARTERIAL OXYGENATION IN THE ELDERLY

Ninety patients (age range 49–99 yr) with a fracture ofthe neck of the femur were anaesthetized by a technique usinghalothane in oxygen in a closed circuit, halothane and 66% nitrousoxide in oxygen in a Magill circuit or artificial ventilationwith 66% nitrous oxide in oxygen ("IPPV group"). In all threegroups, there was a small decrease in Pa_O2 from an overall meanof 9.07 kPa before operation to 8.13 kPa at 60 min after anaesthesia.There was no significant difference between the groups in respectof the decrease; it was concluded that closed-circuit halothanein oxygen anaesthesia for this type of surgery was not accompaniedby a significant degree of absorption collapse.     

Cardiopulmonary effects of an anterior mediastinal mass in dogs anesthetized with halothane

The authors evaluated the cardiac effects of an anterior mediastinal mass to better understand the acute cardiovascular collapse that has been associated with anesthesia and positive-pressure ventilation. An 800-ml-capacity intravenous bag was placed within the anterior mediastinum of 12 dogs to simulate a mediastinal mass. After mediastinal mass inflation, the authors measured cardiac index (CI) during periods of spontaneous ventilation (SV), SV with added continuous positive airway pressure (CPAP), intermittent positive-pressure ventilation (IPPV), and continuous positive-pressure ventilation (CPPV). Similar mediastinal mass volumes resulted in similar decreases in CI during SV (169 +/- 51 to 105 +/- 10 ml.kg-1.min-1); CPAP (175 +/- 48 to 122 +/- 34 ml.kg-1.min-1); IPPV (151 +/- 15 to 93 +/- 24 ml.kg-1.min-1); and CPPV (183 +/- 56 to 117 +/- 46 ml.kg-1.min-1). The authors also found, by linear regression, that the relationship between CI and mass volume was similar during both SV and IPPV. In six dogs, transesophageal echocardiography (TEE) was used to measure ventricular short axis dimensions. The authors found that mass inflation caused left ventricular end-diastolic dimension to decrease significantly by 6 +/- 2 mm and 4 +/- 1 mm during SV or IPPV, respectively, and right ventricle dimensions to increase by 2 +/- 1 mm and 3 +/- 1 mm during SV or IPPV, respectively. The changes in chamber dimensions were similar with either SV or IPPV. These results suggest that the decrease in CI associated with a mediastinal mass results from an increase in right ventricular afterload, causing right ventricular enlargement. Subsequently, there is impingement on the left ventricle volume because of interventricular interdependence.     

Induction reflex actions with intravenous nalbuphine as an adjunct to isoflurane

Ninety unpremedicated patients undergoing mask anaesthesia were assigned to one of three groups according to the volatile anaesthetic and the acute intravenous premedication administered. Group I received saline placebo as premedication and halothane by inhalation. Group II received saline placebo and isoflurane by inhalation. Group III received nalbuphine 0.1 mg.kg-1 IV as premedication and isoflurance by inhalation. Mean time to loss of consciousness (71 sec) did not differ among groups. The dosage of thiopentone required to induce loss of consciousness was decreased by 15 per cent (from 3.9 to 3.3 mg.kg-1) by nalbuphine premedication (P less than 0.05), and time to induction of surgical anaesthesia using isoflurane was decreased by 15 per cent (P less than 0.05). The incidence of reflex actions (coughing, laryngospasm, breath holding, hiccoughs and movement) during induction was no different in the saline-premedicated halothane or isoflurane groups. Acute intravenous nalbuphine premedication decreased significantly the incidence of reflex actions during induction of isoflurane anaesthesia from 77 per cent to 37 per cent (P less than 0.02). Desaturation episodes (SaO2 less than 90 per cent) were more frequent with isoflurane inductions compared with halothane (55 per cent vs 17 per cent, P less than 0.01). Apnoeic episodes accounted for the majority of desaturations associated with nalbuphine premedication, while excitatory reflexes (coughing and laryngospasm) accounted for more desaturations with isoflurane alone.     

Serum gastrin and blood glucose levels during halothanenitrous oxide anaesthesia and strabismus surgery in children

The purpose of this study was to determine whether serum gastrin levels are increased by reflexogenic stimuli applied to the extrinsic muscles of the eye. Serum gastrin and blood glucose concentrations were measured in ten normal children aged between 5 and 12 yr during general anaesthesia with halothane and nitrous oxide and during strabismus surgery. Fasting basal concentrations of gastrin (33.6 +/- 14.8 pg.ml-1) and of glucose (4.43 +/- 0.72 mmol.L-1) were in the normal range of values for children. Intravenous atropine (0.01 mg.kg-1), general anaesthesia with halothane in nitrous oxide and oxygen by mask for three minutes, tracheal intubation, extraocular muscle stimulation and surgical stress did not cause any variation in the mean serum gastrin concentration. On the contrary, tracheal intubation and surgical stress increased blood glucose concentrations (P less than 0.05). There was no difference in the serum gastrin levels after extraocular muscle stimulation between children with positive or negative oculocardiac reflexes (44.5 +/- 16.7 pg.ml-1 vs 38 +/- 14.7 pg.ml-1, respectively). The incidence of vomiting predischarge was 60 per cent. Serum gastrin levels did not differ between children who vomited and children who did not (44.3 +/- 18.5 pg.ml-1 vs 47.1 +/- 16.9 pg.ml-1, respectively). Vomiting after strabismus surgery cannot be attributed to high gastrin serum levels. Consequently, it is unlikely that vomiting after strabismus surgery is linked to an "oculogastric reflex" with the vagus nerve as the efferent pathway.