Halothane inhibits hypoxic pulmonary vasoconstriction in the presence of cyclooxygenase blockade

Using an isolated lung the effects of halothane on hypoxic pulmonary vasoconstriction (HPV) were studied in the presence of cyclooxygenase blockade. The pulmonary vasculature can be divided into arterial, middle and venous segment resistances. Analysis of the vascular pressure-flow relationship further separates resistance into a flow dependent resistance (1/slope) and a zero-flow pressure intercept (PCRIT). We ventilated six lobes with control (35 per cent O2) and hypoxic (three per cent O2) gas mixtures with the addition of either 0, 0.5, 1.0, or 2.0 per cent halothane. We found that after addition of indomethacin (5 mg.kg-1), ventilation with three per cent O2 increased total resistance by 87 per cent over baseline with the increase primarily in the middle vascular segment. During normoxic ventilation PCRIT was 7.9 cm H2O and this increased significantly with hypoxia to 11.5 cm H2O). Only 2.0 per cent halothane blocked the increases in middle segment resistance and in PCRIT. We conclude that following cyclooxygenase blockade, halothane inhibits HPV by acting on middle segment vessels.     

Epidural morphine reduces halothane MAC in the dog

Morphine, 0.1 mg.kg-1 was administered epidurally on two different occasions to ten dogs to determine the effect of two different volumes of saline dilution, 0.13 and 0.26 ml.kg-1, on the minimum alveolar concentration (MAC) of halothane as determined by subcutaneous electrical current applied to the fore and hind limbs in a random order. Following MAC determination with halothane alone, epidural morphine was administered and MAC was redetermined. Epidural morphine significantly reduced, P less than 0.001, the MAC of halothane for fore and hind legs in both volume groups; from 1.04 +/- 0.038 to 0.68 +/- 0.034 and 0.60 +/- 0.017 for for and hind limbs, respectively, in the large volume group, and from 0.96 +/- 0.038 to 0.66 +/- 0.088 and 0.60 +/- 0.030 for fore and hind limbs, respectively, in the small volume group. The reduction in MAC was significantly greater, P less than 0.025, in the hind limb. This study indicates that epidural morphine reduces the halothane requirements in the dog in a segmental manner. The volume of administration was not shown to be critical. Epidural morphine, 0.1 mg.kg-1, diluted in 0.13 to 0.26 ml.kg-1 saline produces significant analgesia in the dog as far forward as the fore limb and will reduce the halothane requirement to permit surgery.     

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.     

Interpleural analgesia improves pulmonary function after cholecystectomy

The purpose of this study was to examine the effects of interpleural bupivacaine on analgesia and ventilatory capacity after cholecystectomy. Forty-two patients undergoing elective cholecystectomy were randomly assigned to two groups: one to receive interpleural administration of bupivacaine-adrenaline mixture (Group 1 = 22 patients) and the other standard administration of intramuscular meperidine (Group 2 = 20 patients) for postoperative pain relief. The intensity of pain was evaluated by a visual analogue scale (VAS) preoperatively as well as at 2, 8, 24 and 48 hr postoperatively. At the same time, FVC and FEV1.0 measurements were obtained for all patients. The group given interpleural bupivacaine had better pain relief with mean VAS of 0.6 +/- 0.9 (mean +/- SD) 1.1 +/- 1.4, 0.6 +/- 0.9 and 0.8 +/- 1.2 compared with 5.2 +/- 2.2, 5.8 +/- 2.7, 5.5 +/- 2.2 and 4.5 +/- 1.8 for patients receiving meperidine (P less than 0.001). The patients in Group 1 also had larger FVC and FEV than those in Group 2: FVC 22 +/- 14.5 per cent vs 32 +/- 15.2 per cent (P less than 0.005), FEV1.0 25 +/- 15.5 vs 38 +/- 14.8 per cent (P less than 0.001) (mean +/- SD). We conclude that the interpleural analgesia can achieve better pain relief with greater ventilatory capacity than a standard analgesic regimen in the first two days after cholecystectomy.     

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.     

Malignant hyperthermia and the clean machine

Following use with halothane, ten anaesthestic machines were sampled using infrared analysis for halothane contamination. Baseline measurements of halothane were made in the room and at the machine's common gas outlet. Five per cent halothane with four litres per minute oxygen flow was delivered for ten minutes into a scavenged breathing circuit. Halothane was then discontinued, an oxygen flow rate of 12 litres per minute was begun, and continuous measurements were made until the halothane concentration became undetectable. Baseline measurements of the rooms and anaesthestic machines ranged from 0 to 0.8 parts per million. Following the oxygen flow, the halothane concentration decreased to undetectable levels within six minutes in all ten machines.     

Comparison of haemodynamic changes induced by sevoflurane and halothane in paediatric patients

The purpose of this study is to investigate the haemodynamic effects of 1 MAC and 2 MAC of sevoflurane in children in comparison with halothane. Thirty-eight children (aged from one to six years, average age; 3.6± 0.2 yr) were randomly assigned to four groups, depending on the dose and agent (1 and 2 MAC of sevoflurance: SI and S2; 1 and 2 MAC of halothane: H1 and H2, respectively). After collecting control data during 0.2 MAC of either anaesthetic, end-expired anaesthetics were kept at 1 MAC or 2 MAC for 15 min. Mean blood pressure (mBP) and stroke volume index (SV1), measured by impedance cardiometry, decreased in all groups without differences between groups. Heart rate (HR) increased in groups S1, S2 and H2 but not in group H1. The HR in S2 was higher than that in H2. The cardiac index (CI), a product of SVI and HR, tended to decrease but not significantly in all groups. These results suggested that the haemodynamic depressant effects of sevoflurane in children were similar to those of equipotent halothane concentration except for HR.     

Haemodynamic and cerebral blood flow alterations after reduction of increased cerebrospinal fluid pressure in dogs

To clarify some of the mechanisms for the hypotension that may occur after cranial decompression, the authors examined alterations in cerebral blood flow (CBF) and systemic and pulmonary haemodynamic variables when cerebrospinal fluid (CSF) pressure was increased and then suddenly reduced in eight anaesthetized dogs. After CSF pressure was elevated to 50-85 mmHg for two hours, CBF decreased from 46.3 +/- 4.4 to 31.6 +/- 8.5 ml.100 g-1.min-1 (mean +/- SD, P less than 0.01). Mean systemic arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and systemic vascular resistance index (SVRI) increased by 20 +/- 11 mmHg, 3.9 +/- 2.5 mmHg, 5.2 +/- 3.3 mmHg, and 1448 +/- 1377 dynes.sec.cm-5.m2 from baseline values, respectively (P less than 0.01). Rapid reduction of increased CSF pressure caused CBF to increase to 61.5 +/- 19.1 ml.100 g-1.min-1, whereas MAP, MPAP, PAWP, and SVRI decreased by 22 +/- 11 mmHg, 2.4 +/- 0.9 mmHg, 2.3 +/- 2.0 mmHg, and 1289 +/- 1237 dynes.sec.cm-5.m2 from previous values (P less than 0.01) at 30 min following the decompression. However, cardiac index and pulmonary vascular resistance index remained unchanged during the study period. The present animal data indicate that the decrease in MAP after decompression is mainly a result of a reduction in systemic vascular resistance.     

Postoperative neuromuscular block following atracurium or alcuronium in children

Postoperative neuromuscular block (NMB) was evaluated in 60 children who received randomly either atracurium or alcuronium to induce and maintain an 85-95 per cent NMB during balanced anaesthesia. The EMG-monitor was turned away from the anaesthetist 10-15 min before the end of surgery. The average NMB was comparable between the groups at the time of reversal with neostigmine 50 micrograms.kg-1 (84 +/- 9 per cent, mean +/- SD) as were the NMB and the train-of-four ratio when the tracheas were extubated on a clinical basis (32 +/- 20 per cent and 50 +/- 18 per cent, respectively). Patients who had been paralyzed with atracurium arrived at the recovery room earlier and on arrival had greater train-of-four ratios than the patients paralyzed with alcuronium (P less than 0.01). Time to a train-of-four ratio of greater than 90 per cent was significantly shorter in the atracurium group (10 +/- 5 min vs 26 +/- 15 min, P less than 0.001). Thus, an intermediate-acting muscle relaxant offers a safer recovery profile of the NMB than a long-acting muscle relaxant in paediatric patients.     

Safety and efficacy of alfentanil and halothane in paediatric surgical patients

Alfentanil, a congener of the opioid fentanyl, possesses properties that make it an attractive choice for use during short operative procedures. Since the phannacodynamic aspects of alfentanil have not been well documented in children, this study was undertaken to evaluate the safety, efficacy, and dose requirements of alfentanil when used with nitrous oxide or halothane in paediatric patients. Eighty unpremedicated patients, ASA physical status I or II and aged 2–12 yr were studied. Patients were randomly assigned to one of four groups. After induction of anaesthesia with nitrous oxide, oxygen, and halothane, the groups were treated as follows. In Group I (n = 19), after halothane was discontinued, alfentanil 50 μg · kg^?1 was infused over 30 sec. In Group 2 (n = 20), the end-tidal halothane was maintained at 0.5% and alfentanil 25 μg · kg^?1 was infused. In Group 3 (n = 20), the end-tidal halothane concentration was maintained at 1% and alfentanil 12.5 μg · kg^?1 was infused. In Group4(n = 21), the end-tidal halothane concentration was maintained at 1.5% and no alfentanil was administered. Patients in Groups 1, 2, and 3 received bolus doses of alfentanil 12.5 μg · kg^?1 as needed to maintain haemodynamic stability. After alfentanil administration, there were transient decreases in systolic blood pressure in Groups 1 and 2, and in heart rate in Group 2. With surgical stimulation, haemodynamic stability was well maintained except in patients in Group 1, who had an increase in systolic blood pressure. Children Group 1 were alert sooner and their tracheas were extubated earlier than those in Groups 2, 3, and 4. The four groups were similar in postoperative narcotic analgesic administration and incidence of vomiting. In summary, alfentanil (12.5–50.0 μg · kg^?1) was a safe anaesthetic, whether combined with nitrous oxide alone or with nitrous oxide and halothane.     

Epidural epinephrine and the systemic circulation during peripheral vascular surgery

This study was designed to determine the haemodynamic effects of epidural epinephrine, 5 micrograms.ml-1, added to bupivacaine, 0.75 per cent, in elderly patients with cardiac disease undergoing peripheral vascular surgery (PVS). The effect of epidural epinephrine on the plasma concentration of bupivacaine was also measured. Twenty patients with a history and/or ECG evidence of myocardial ischaemia requiring PVS were randomly assigned to two groups. The patients were monitored with a modified V5 ECG, oscillometric BP monitor and a PA catheter. After control haemodynamic measurements, 12 ml of bupivacaine, 0.75 per cent, +/- epinephrine, 5 micrograms.ml-1, was injected over five minutes into the epidural space at L3-4. Supine haemodynamic measurements were repeated at 15 and 45 min after injection. At 15 min after epidural injection, compared with control values, patients receiving epidural epinephrine showed a significantly greater decrease in mean blood pressure and systemic vascular resistance, and a significantly greater increase in cardiac output than patients receiving plain epidural bupivacaine (79.3 +/- 11.6 per cent vs 94.6 +/- 16.8 per cent, 61.6 +/- 9.0 vs 91.6 +/- 19.2 per cent, 130.8 +/- 23 vs 105 +/- 20.8 per cent, respectively). These differences were not present at 45 min after epidural injection. Heart rate was not significantly different between groups at either time. The presence of epidural epinephrine reduced the peak plasma concentration of bupivacaine from 0.86 +/- 0.20 to 0.64 +/- 0.33 micrograms.ml-1 and increased the time to achieve this concentration from 16.1 +/- 11.2 to 33.7 +/- 20.1 min.     

Neuromuscular and cardiovascular effects of mivacurium chloride in surgical patients receiving nitrous oxide-narcotic or nitrous oxide-isoflurane anaesthesia

The neuromuscular and cardiovascular effects of mivacurium chloride were studied during nitrous oxide-oxygen narcotic (fentanyl) (n = 90) and nitrous oxide-oxygen isoflurane (ISO) anaesthesia (n = 45). In addition, a separate group (n = 9) received succinylcholine during fentanyl anaesthesia to compare its neuromuscular effects with mivacurium. Mivacurium was initially administered as a single bolus in doses from 0.03 mg.kg-1 to 0.25 mg.kg-1 to study the dose-response relationships, as well as the cardiovascular effects of mivacurium. Neuromuscular block (NMB) was measured by recording the twitch response of the adductor pollicis muscle following ulnar nerve stimulation (0.15 Hz, 0.2 ms supramaximal voltage). The ED95 values for mivacurium were estimated to be 0.073 mg.kg-1 and 0.053 mg.kg-1 in the fentanyl and ISO groups respectively. The duration of block (time from injection to 95 per cent recovery) for a dose of 0.05 mg.kg-1 mivacurium was 15.3 +/- 1.0 min and 21.5 +/- 1.3 min for fentanyl and ISO anaesthesia, respectively. The recovery index (25-75 per cent) between initial bolus dose (6.1 +/- 0.5 min), repeat bolus doses (7.6 +/- 0.6 min), mivacurium infusion (6.7 +/- 0.7 min) and succinylcholine infusion (6.8 +/- 1.8 min) were not significantly different. There was minimal change in mean arterial pressure (MAP) or heart rate (HR) following bolus doses of mivacurium up to 0.15 mg.kg-1. Bolus administration of 0.20 mg.kg-1 or 0.25 mg.kg-1 of mivacurium decreased MAP from 78.2 +/- 2.5 to 64.0 +/- 3.2 mmHg (range 12-59 per cent of control) (P less than 0.05). The same doses when administered slowly over 30 sec produced minimal change in MAP or HR.     

Denitrogenation in pregnancy

This study measured nitrogen washout in ten pregnant and nine non-pregnant women to understand better how pregnancy effects denitrogenation. Nitrogen concentration was monitored continuously while the women breathed 100 per cent O2 for three minutes and took four deep breaths of 100 per cent O2 using a circle anaesthesia system and 8 L.min-1 fresh gas flow. Parturients achieved 95 per cent denitrogenation significantly (P less than 0.0005) faster than non-pregnant women (54.5 +/- 17.8 vs 110.8 +/- 35.7 sec). In parturients, denitrogenation for three minutes lowered expired N2 concentration to 1.0 +/- 0.2 per cent while four deep breaths lowered it to 5.1 +/- 1.7 per cent (P less than 0.0001). This difference, while statistically significant, is predicted to supply only 10-15 sec of extra protection against hypoxaemia, and thus is probably not clinically significant. The authors conclude that either two minutes of tidal breathing or four deep breaths of 100 per cent O2 provide adequate denitrogenation and similar protection against apnoeic hypoxaemia in normal parturients.     

Factors influencing the R-R interval during central venous injection in newborn swine

Seven Yorkshire swine, ages 7-11 days and weighing 1.4-2.8 kg were studied to determine the effects of temperature and volume of injectate, depth of anaesthesia, position of the central venous catheter tip and vagotomy on the R-R interval after central venous injection of saline. The swine were anaesthetized with halothane in 100 per cent oxygen and their lungs ventilated to normocapnia. The length of the R-R varied inversely with the temperature of the injectate between 0 and 20 degrees C reaching a maximum prolongation of 152 per cent above control values with 0 degrees C saline. Injecting saline at 37 degrees C did not affect the R-R interval. The length of the R-R interval varied directly with the volume of injectate between 1.5 and 4.5 ml.kg-1 (P less than 0.05). The R-R interval response also varied directly with the depth of anaesthesia: the post-injection R-R interval increased from 185 per cent to 341 per cent as the end-tidal halothane concentration increased from 0.45 to 1.20 per cent. The position of the tip of the central venous catheter that produced the maximum increase in the R-R interval, as determined radiographically, was at the junction of the superior vena cava and the right atrium. Neither bilateral vagotomy nor atropine (50 micrograms.kg-1) affected the R-R interval after injecting 3 ml.kg-1 saline 0 degrees C. We conclude that the increases in R-R interval after injection of fluid into the right atrium are due to direct effects on the nerve conduction system of the heart, possibly on the sino-atrial node.     

A defasciculating dose of d-tubocurarine causes resistance to succinylcholine

Forty-four patients, ASA physical status I or II, undergoing thiamylal, fentanyl, N2O/O2 anaesthesia were studied to determine the dose-response to succinylcholine (Sch) without prior defasciculation (24 pt - Group 1), or three minutes following d-tubocurarine (dTC), 0.043 mg.kg-1 (20 pt - Group 2). The individual log dose-logit response curve for each patient was determined using a cumulative dose plus infusion technique and integrated EMG monitoring of the first dorsal interosseous muscle. The mean (+/- SEM) ED50, ED90 and ED95 values for Sch in Group 1 were 0.13 +/- 0.01, 0.19 +/- 0.01 and 0.22 +- 0.01 mg.kg-1, and in Group 2 were 0.16 +/- 0.01, 0.25 +/- 0.01 and 0.29 +/- 0.02 mg.kg-1, respectively. The mean ED values in Group 2 were significantly greater than the equivalent values in Group 1 (P less than 0.05). Compared with values in Group 1, ED values in Group 2 represented mean increases of 23, 32, and 32 per cent, respectively. These pharmacodynamic data indicate that the dose of Sch needs to be increased by 32 per cent following a defasciculating dose of dTC 3 mg.70 kg-1 (0.043 mg.kg-1).     

Preservation of renal blood flow during hypotension induced with fenoldopam in dogs

The introduction of drugs that could induce hypotension with different pharmacological actions would be advantageous because side effects unique to a specific drug could be minimized by selecting appropriate therapy. Specific dopamine-1, (DA1) and dopamine-2 (DA2) receptor agonists are now under clinical investigation. Fenoldopam mesylate is a specific DA1 receptor agonist that lowers blood pressure by vasodilatation. The hypothesis that fenoldopam could be used to induce hypotension and preserve blood flow to the kidney was tested. Systemic aortic blood pressure and renal blood flow were measured continuously with a carotid arterial catheter and an electromagnetic flow probe respectively, in order to compare the cardiovascular and renal vascular effects of fenoldopam and sodium nitroprusside in ten dogs under halothane general anaesthesia. Mean arterial pressure was decreased 30 +/- 8 per cent from control with infusion of fenoldopam (3.4 +/- 2.0 micrograms.kg-1.min-1) and 34 +/- 4 per cent with infusion of sodium nitroprusside (5.9 micrograms.kg-1.min-1) (NS). Renal blood flow (RBF) increased during fenoldopam-induced hypotension 11 +/- 7 per cent and decreased 21 +/- 8 per cent during sodium nitroprusside-induced hypotension (P less than 0.01). Sodium nitroprusside is a non-selective arteriolar and venous vasodilator that can produce redistribution of blood flow away from the kidney during induced hypotension. Fenoldopam is a selective dopamine-1 (DA1) receptor agonist that causes vasodilatation to the kidney and other organs with DA1 receptors and preserves blood flow to the kidney during induced hypotension.     

Effects of halothane on arrhythmias induced by myocardial ischaemia

The effect of halothane on arrhythmias induced by ischaemia was investigated in rats, isolated perfused rat hearts, and pigs. Responses to the occlusion of the left anterior descending coronary artery were determined in groups (n = 9) of chronically prepared rats treated with no halothane, 0.5, or 1.0 per cent halothane immediately after occlusion; in isolated rat hearts (n = 10) treated with no halothane, 0.5, 1.0, 2.0, or 4.0 per cent halothane for 15 min before and after occlusion; and 20–25 kg pigs (n = 11) anaesthetised with halothane or pentobarbital. The ECG, arrhythmias, blood pressure (BP), heart rate (HR) and extent of infarction were determined in each model. In pigs, left ventricular pressure, dp/dt_max and cardiac output were also measured. In chronically prepared rats, halothane anaesthesia started after occlusion was antiarrhythmic and decreased the incidence of ventricular fibrillation and resulting mortality. In isolated rat hearts, 0.5 or 1.0 per cent halothane had little effect on occlusion-induced arrhythmias. The highest concentration of halothane increased the incidence of ventricular fibrillation both before and after occlusion. Halothane decreased developed ventricular pressure in a dose-dependent manner. In acutely prepared pigs, halothane pre-treatment had no appreciable effect upon occlusion-induced arrhythmias when compared with pentobarbital anaesthesia. Thus, halothane is antiarrhythmic when treatment is initiated after occlusion in the rat but this action is not seen in isolated hearts or intact pigs. The antiarrhythmic action of halothane is, therefore, species and model dependent.     

Comparison of end-tidal carbon dioxide,oxygen saturation and clinical signs for the detection of oesophageal intubation

The reliability of various methods for detecting oesophageal intubation was assessed by means of a single blind study in rats. Both oesophagus and trachea were simultaneously intubated. The presence or absence of various clinical signs was noted during tracheal or oesophageal ventilation and arterial blood gases and end-tidal CO2 were measured. Oesophageal ventilation for one minute was associated with significant decreases (P less than 0.001) in pH, PaO2 and SaO2 and a significant (P less than 0.001) increase in PaCO2. Although mean PaO2 decreased by 70 per cent and mean SaO2 decreased by 31 per cent, 43 percent of rats failed to demonstrate a decrease in SaO2 below 85 per cent. Oxygen saturation was the least reliable method for detecting oesophageal intubation (sensitivity = 0.5, specificity = 0.9, positive predictive value (PPV) = 0.8). Chest movement was the most reliable clinical sign for detecting oesophageal intubation (sensitivity = 0.9, specificity = 1.0, PPV = 1.0). Oesophageal rattle was the second most reliable clinical sign (PPV = 0.9). Moisture condensation in the tracheal tube (PPV = 1.0) and abdominal distension (PPV = 0.9) were judged to be the least reliable because each had a high false negative rate of 0.3. The most reliable method for the early detection of oesophageal intubation in rats was end-tidal, CO2 (sensitivity 1.0, specificity = 1.0, PPV = 1.0). In addition, end-tidal CO2 when used in conjunction with the four clinical signs improved the reliability of these signs.     

Side effects of nalbuphine while reversing opioid-induced respiratory depression: report of four cases

Nalbuphine hydrochloride, an agonist-antagonist opioid, is reported to reverse the respiratory depression of moderate doses of fentanyl (20 micrograms.kg-1) and still provide good analgesia. We report four patients having abdominal aortic aneurysm repair in which we attempted to reverse the respiratory depression of large doses of fentanyl (50-75 micrograms.kg-1) with nalbuphine (0.3 mg.kg-1, 0.1 mg.kg-1 or 0.05 mg.kg-1). Nalbuphine reversed respiratory depression in all four patients and the respiratory rate increased from 10 to 23 breaths per minute, end-tidal CO2 decreased from 7.0 +/- 0.3 per cent to 5.6 +/- 0.7 per cent, and peak inspiratory pressure after 0.1 seconds increased from 4 +/- 1.4 to 13 +/- 2.6 mmHg. However, hypertension, increased heart rate, and significant increase in analogue pain scores accompanied reversal of respiratory depression. Agitation, nausea, vomiting, and cardiac dysrhythmias also were observed frequently. We do not recommend the use of nalbuphine to facilitate early extubation of the trachea after large doses of fentanyl for abdominal aortic surgery.     

Haemodynamic instability and myocardial ischaemia during carotid endarterectomy: A comparison of propofol and isoflurane

The purpose of this study was to compare two anaesthetic protocols for haemodynamic instability (heart rate (HR) or mean arterial pressure (MAP) <80 or > 120% of ward baseline values) measured at one-minute intervals during carotid endarterectomy (CEA). One group received propofol/alfentanil (Group Prop; n = 14) and the other isoflurane I alfentanil (Group Iso; n = 13). Periods of haemodynamic instability were correlated to episodes of myocardial ischaemia as assessed by Holler monitoring (begun the evening before surgery and ceasing the morning of the first postoperative day). In Group Prop, anaesthesia was induced with alfentanil 30 μg · kg^?1 rv, propofol up to 1.5 mg · kg^?1 and vecuronium 0.15 mg · kg^?1, and maintained with infusions of propofol at 3–12 mg · kg^?1· hr^?1 and alfentanil at 30 μg · kg^?1 · hr^?1. In Group Iso, anaesthesia was induced with alfentanil and vecuronium as above, thiopentone up to 4 mg · kg^?1 and maintained with isoflurane and alfentanil infusion. Phenylephrine was infused to support MAP at 110 ± 10% of ward values during cross-clamp of the internal carotid artery (ICA) in both groups. Emergence hypertension and/or tachycardia was treated with labetalol, diazoxide or propranolol. Myocardial ischaemia was defined as ST-segment depression of >-1 mm (60 msec past the J-point) persisting for >-one minute. For the entire anaesthetic course (induction to post-emergence), there was no difference between groups for either duration or magnitude outside the <80 or >120% range for HR or MAP. However, when the period of emergence from anaesthesia (reversal of neuromuscular blockade to post-extubation) was assessed, more patients were hypertensive (P = 0.004) and required vasodilator therapy in Group Iso (10/ 13 vs 5/14; P = 0.038 Fisher’s Exact Test). The mean dose of labetalol was greater in Group Iso (P = 0.035). No patient demonstrated myocardial ischaemia during ICA cross-clamp. On emergence, 6/13 patients in Group Iso demonstrated myocardial ischaemia compared with 1/14 in Group Prop (P = 0.029). Therefore, supporting the blood pressure with phenylephrine, during the period of ICA cross-clamping, appears to be safe as we did not observe any myocardial ischaemia at this time. During emergence from anaesthesia, haemodynamic instability was associated with myocardial ischaemia. Under these specific experimental conditions, with emergence, hypertension and myocardial ischaemia were more prevalent with more frequent pharmacological interventions in patients receiving isoflurane.