Oral premedication for paediatric ambulatory anaesthesia: a comparison of midazolam and ketamine

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - To compare the clinical characteristics of two oral premedicants, midazolam and ketamine, 40 healthy children, one to six...     

Prophylactic administration of histamine1 and histamine2 receptor blockers in the prevention of protamine-related haemodynamic effects

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - We studied the effects of the prophylactic administration of histamine1 and histamine2 receptor blockers on haemodynamic...     

Interpleural block: a new technique for regional anaesthesia during percutaneous nephrostomy and nephrolithotomy

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - Interpleural block was used in four patients undergoing percutaneous nephrostomy, one of whom also underwent percutaneous...     

Bain circuit occluded by foreign body

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - The purpose of this report is to describe a potentially hypoxic event which occurred during mask induction with the Bain...     

Haemodynamic consequences of warm cardiac irrigation during cardiac surgery

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - Following cardiopulmonary bypass (CPB) and prior to closing the chest, some surgeons irrigate the heart and pericardium with...     

A randomized comparison of midazolam and diazepam injectable emulsion in cataract surgery

The purpose of this study was to compare the psychomotor recovery of patients sedated with either midazolam or Diazemuls using the digit symbol substitution test and the Trieger test. Sixty patients were allocated in random double-blind fashion to receive either midazolam or diazepam in oil emulsion (Diazemuls) as intravenous sedation for cataract surgery. Both groups received fentanyl 0.5 μg· kg^?1 IV. Tests of cognition were performed by the patients prior to sedation and at half-hourly intervals for three hours after cataract surgery. In a dose ratio of 1:4, midazolam was found to produce better sedation but more prolonged recovery than Diazemuls. Anterograde amnesia was comparable in the two groups, while more patients in the Diazemuls group developed episodes of apnoea and venous irritation.     

Propofol or midazolam for short-term alterations in sedation

It is often necessary to adjust a patient’s sedation level while they are in the intensive care unit. The purpose of this study was to compare propofol with midazolam for controlling short-term alterations in sedation. Twenty-three patients undergoing an interactive procedure, physiotherapy, during mechanical ventilation of the lungs were studied. The patients were randomly assigned to receive infusions of propofol or midazolam for sedation. Sedation was assessed using the method of Ramsay, where 3 is drowsy responding only to commands; and 5 is asleep with a slow response to light glabellar tap. Prior to physiotherapy sedation was deepened from 3 to 5 by increasing the sedative infusion rate, and level 5 was maintained during physiotherapy by adjusting the infusion rate whenever necessary. After physiotherapy, the sedative dose was reduced until level 3 was again achieved. During physiotherapy, sedation level 5 was achieved for 53.9% of the time with propofol but for only 25.7% with midazolam (P < 0.01). After physiotherapy, those patients sedated with propofol re-awakened to level 3 faster (8.3 ± 2.3 min, mean ±SE) than those receiving midazolam (92.8 ± 35.0 min, P < 0.05). After physiotherapy, a further 1.8 ± 0.5 dose adjustments were required to the midazolam infusion while only 0.4 ± 0.2 adjustments were required to the propofol infusion (P < 0.05). During physiotherapy 3.0 ± 0.5 dose adjustments to the propofol dose were required compared with 3.6 ± 0.5 adjustments to the midazolam dose (NS). It is concluded that, during a standardized stimulus, physiotherapy, propofol infusion allowed a desired sedation score to be maintained for more of the time than did infusion of midazolam. Subsequently, when the infusion rates were reduced, less time was taken to re-awaken to baseline levels after physiotherapy, with fewer adjustments to the infusion rate, in those patients receiving propofol than midazolam.     

Intraocular pressure in anaesthetized dogs given flumazenil with and without prior administration of midazolam

This study examined the effect of flumazenil, a benzodiazepine antagonist, on aqueous humour pressure in dogs receiving either midazolam or no benzodiazepine. Twenty-four halothane-anaesthetized dogs were assigned to one of four groups. Group I (n = 6) received saline iv at 0, 45 and 90 min. Group 2 (n = 6) received saline at 0 min, flumazenil 0.0025 mg.kg-1 iv at 45 min and flumazenil 0.16 mg.kg-1 at 90 min. Group 3 (n = 6) received midazolam 1.6 mg.kg-1 at 0 min followed by continuous iv infusion (1.25 mg.kg-1.hr-1). Flumazenil was given at 45 and 90 min as in Group 2. In Group 4 (n = 6) aqueous humour pressure was elevated to about 35 mmHg then midazolam and flumazenil were given as in Group 3. Aqueous humour pressure was determined using a 30-gauge needle placed into the anterior chamber. Saline or flumazenil produced no change in aqueous humour pressure in Groups 1 and 2. In Groups 3 and 4, midazolam decreased aqueous humour pressure from 18 +/- 2 mmHg (mean +/- SD) to 14 +/- 3 mmHg (P less than 0.001) and from 34 +/- 5 mmHg to 31 +/- 3 mmHg (P less than 0.01) respectively. Flumazenil given during continuous infusion of midazolam produced increases of aqueous humour pressure of 2 +/- 1 (P less than 0.01) to 5 +/- 2 mmHg (P less than 0.01) that lasted less than or equal to 12 min. It is concluded that at both normal and elevated aqueous humour pressures flumazenil produces statistically significant but clinically unimportant increases of aqueous humour pressure in anaesthetized dogs receiving midazolam, but not in dogs given no benzodiazepine.     

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.     

The evolution of anaesthesia as a specialty in Canada

Since 1847 anaesthesia in Canada has evolved through six phases. In the first (1847-1898), it was a craft without an academic and professional base. The second (1899-1919) was marked by the first academic appointments and by Canadians' wartime experiences of anaesthesia. The third phase (1920-1929) evidenced the professional satisfaction of anaesthesia and included the founding of the Canadian Society of Anaesthetists. In the fourth phase (1930-1943) the growth of the Royal College of Physicians and Surgeons of Canada, the introduction of certification and the founding of the definitive professional society--the Canadian Anaesthetists' Society--fostered the evolution of what was now becoming a recognizable specialty. The fifth phase (1944-1971) was one of resolution of problems affecting the status of anaesthesia: the first autonomous department of anaesthesia in a Canadian university was founded (at McGill in 1945), the Royal College Fellowship was approved for anaesthesia (in 1951), the Canadian Anaesthetists' Society Journal was launched (in 1954) and a single standard for certification of specialists was finally established (in 1971). In the sixth (1972-1989), the main elements were the assumption of responsibility for residency training by the universities and by the renaming of the journal as the Canadian Journal of Anaesthesia. Through these years of increasing professionalism, it has, however, been the accomplishments of individual Canadian physicians, facing many challenges, that have made the specialty in Canada recognizably Canadian.     

Comparison of the direct effects of sevoflurane,isoflurane and halothane on isolated canine coronary arteries

We have demonstrated previously, using dog epicardial arteries of different sizes, that isoflurane, like adenosine, is preferentially a small coronary artery dilator, whereas halothane, like nitroglycerin, is a large artery dilator. The present study was designed to compare the direct effects of sevoflurane with those of isoflurane and halothane. Proximal large coronary arteries with an outer diameter (o.d.) of 2.5–3.2 mm and distal small arteries of 0.6–0.9 mm o.d. were isolated from dogs and then cut into vascular rings. They were precontracted with KCl (20 mM), and their relaxant responses to anaesthetics were compared relative to the maximal responses induced by papaverine. Sevoflurane, halothane and isoflurane (1–3 human MAC) induced dose-dependent relaxation of these arteries. The relaxant response to sevoflurane did not differ between large and small arteries. However, the relaxant response of the large arteries to halothane (1.5–2.3%) was greater than that of small arteries (P < 0.01) and the response of small arteries to isoflurane (3.5%) was greater than that of large arteries (P < 0.05). In large arteries, the potency of the relaxant effect at equivalent human MAC could be ranked as halothane ≥ sevoflurane > isoflurane, and, in small epicardial arteries as isoflurane > sevoflurane ≫ halothane. We conclude that, unlike isoflurane, sevoflurane is not a preferential dilator of small coronary arteries. Nous avons déjà démontré sur des artères canines épicardiques de différents calibres, que l’isoflurane, comme l’adénosine est un dilatateur préférentiel des petites artères coronaires, alors que l’halothane, comme la nitroglycérine, est un dilatateur des grosses artères. L’étude présente vise à comparer les effets directs du sévoflurane avec ceux de l’isoflurane et de l’halothane. Chez le chien, on isole et sectionne en anneaux de grosses artères coronaires d’un diamètre externe de 2,5 à 3,2 mm et des petites artères coronaires distales de 0,6 à 0,9 mm. Elles sont préalablement contractées avec du KCl (20 mM) et leurs propriétés relaxantes en présence d’anesthésiques sont comparées à la réponse maximale provoquée par la papavérine. Il n’y a pas de différence entre le sévoflurane, l’halothane et l’isoflurane (MAC 1–3 humain); ils provoquent tous une relaxation artérielle qui dépend de la dose. L’effet relaxant du sévoflurane est identique que ce soit sur les grosses ou les petites artères. Cependant, la relaxation des grosses artères en réponse à l’halothane (1,5–2,3%) est plus importante que celle des petites artères (P < 0,01) et la réponse des petites artères à l’isoflurane (3,5%) est plus marquée que celle des grosses artères (P < 0,05). Pour les grosses artères, la puissance de l’effet relaxant à un MAC humain équivalent pourrait être classifiée dans l’ordre: halothane ≥ sévoflurane > isoflurane; et sur les petites artères épicardiques ainsi: isoflurane > sévoflurane ≫ halothane. Nous concluons que contrairement à l’isoflurane, le sévoflurane n’est pas un dilatateur préférentiel des petites artères coronaires.     

Effects of benzodiazepines on mid-latency auditory evoked potentials

Midlatency auditory evoked potentials (MLAEP) reflect primary cortical processing of auditory stimuli. The effects of benzodiazepines on MLAEP have not yet been studied. We examined the effects of intravenous induction of general anaesthesia using the benzodiazepines midazolam, diazepam and flunitrazepam on MLAEP in 30 patients scheduled for minor gynaecological procedures. Anaesthesia was induced with midazolam (0.2–0.3 mg · kg⁻¹, Group I, n = 10), diazepam (0.3–0.4 mg · kg⁻¹, Group II, n = 10) or flunitrazepam (0.03–0.04 mg · kg⁻¹, Group III, n = 10). Auditory-evoked potentials were recorded before and five to ten minutes after induction of general anaesthesia. Latencies of the peak V, Na, Pa, Nb and P1 (ms) and amplitudes Na/Pa, Pa/Nb and Nb/ P1 (μV) were measured. In the awake state, MLAEP had high peak to peak amplitudes and a periodic waveform. After induction of anaesthesia there was no or only a small increase in latencies of the peaks Na, Pa, Nb and P1, which was significant only for P1 in the midazolam group. Amplitudes Na/ Pa, Pa/Nb and Nb/P1 decreased only slightly and which reached statistical significance only for Na/Pa in the flunitrazepam group. The MLAEPs do not change markedly in amplitude or latency during induction of general anaesthesia with benzodiazepines. Primary cortical processing of auditory stimuli seems to be preserved under benzodiazepines. This may be seen in connection with cases of intraoperative awareness and especially the perception of auditory stimuli during anaesthetic regimens where benzodiazepines are used to suppress consciousness. Les potentiels évoqués auditifs de latence médiane (MLAEP) reflètent le premier processus de traitement cortical du stimulus auditif. Nous avons étudiés les effets de l’induction de l’anes-thésie générale intraveineuse avec les benzodiazépines midazolam, diazepam et flunitrazépam sur les MLAEP chez 30 patientes programmées pour des interventions gynécologiques mineures. L’induction anesthésique est réalisée par le midazolam (0,2–0,3 mg · kg⁻¹, groupe I, n = 10), le diazépam (0,3–0,4 mg · kg⁻¹, group II, n = 10) ou le flunitrazepam (0,03–0,04 mg · kg⁻¹, groupe III, n = 10). Les potentiels auditifs sont enregistrés avant et cinq ou dix minutes après l’induction de l’anesthésie générale. La latence des pointes V, Na, Pa, Nb et P1 (ms) et l’amplitude Na/Pa, Pa/Nb et Nb/P1 (μv) sont mesurées. A l’état vigile, les MLAEP ont des amplitudes de pointe élevées et une forme d’onde périodique. Après l’induction anesthésique, il n’y a pas d’augmentation ou une légère augmentation des pointes Na, Pa, Nb et P1, qui est significative pour P1 seulement dans le groupe midazolam. L’amplitude de Na, Pa, Nb et P1 diminue légèrement. Cette diminution n’est significative que pour Na/Pa avec le groupe flunitrazépam. Les MLAEP ne présentent vraiement pas de variations en amplitude et en latence pendant l’induction de l’anesthésie générale avec les benzodiazépines. Ceci peut être en rapport avec un état de veille peropératoire et spécialement avec la perception de stimuli auditifs pendant les techniques anesthésiques qui font appel aux benzodiazépines pour produire l’inconscience.     

A comparison of the cerebral pressure-flow relationship for halothane and isoflurane at haemodynamically equivalent end-tidal concentrations in the rabbit

The cerebral pressure-flow relationship for halothane and isoflurance was studied at end-tidal concentrations which resulted in similar baseline mean arterial pressure (MAP). Two groups of New Zealand white rabbits (n = 8; each group) were studied with five regional blood flow determinations in each animal. Blood flow was determined by injecting radioactive microspheres during the following conditions: injection 1: after stable 2.05 per cent end-tidal isoflurane (1.0 MAC) Group I; or after stable 0.74 +/- 0.04 per cent end-tidal halothane (0.53 MAC) Group H. Injections 2-5: after MAP was increased 20, 40, 60, and 80 per cent respectively above baseline MAP by phenylephrine infusion. Baseline MAP was the same for both groups (64.3 +/- 3.1 vs 67.2 +/- 2.0 mmHg; mean +/- SEM; Group I and H respectively). Baseline total CBF (tCBF; 0.68 +/- 0.03 vs 0.86 +/- 0.05) and hemispheric CBF (hCBF; 0.64 +/- 0.03 vs 0.96 +/- 0.06) were significantly greater in Group H; no significant difference between groups was seen for baseline posterior fossa CBF (pCBF; 0.79 +/- 0.06 vs 0.75 +/- 0.04). For each experiment a pressure-flow curve was generated by curvilinear regression analysis. Significantly greater phenylephrine concentrations were required for injections 2-5 in Group H. Mean slopes and intercepts were derived for each group. Within each group comparison of the pressure-flow curves for hCBF vs MAP and pCBF vs MAP showed autoregulation was less impaired in posterior fossa structures (cerebellum and brain stem) for both anaesthetic agents (P less than or equal to 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Sepsis reduces isoflurane MAC in a normotensive animal model of sepsis

Patients with sepsis often require anaesthesia for surgical procedures. Anaesthesia can be unpredictable and the most haemodynamically stable agents are used. No data are available for the minimum alveolar concentration (MAC) requirements in such patients or in animal models of sepsis. We have characterized the effect of sepsis on the MAC of isoflurane in a normotensive rodent model of sepsis. The minimum inhibitory concentration (MIC) of isoflurane to an identical stimulus was determined for rodents subjected to caecal ligation and perforation (CLP n = 8), or sham laparotomy (n = 7). The calculated MAC of isoflurane was reduced in the septic animals compared with the sham animals (MAC of isoflurane, CLP = 0.8% sham = 1.4% P < 0.003). No statistical differences were found in the haemodynamic variables measured in either group. Isoflurane leads to haemodynamic stability during anaesthesia in this animal model of sepsis. However, the MAC requirement for isoflurane is reduced by sepsis. En cas de sepsis, il faut souvent recourir à la chirurgie. Les répercussions anesthésiques sont imprévisibles et il faut utiliser des agents qui assurent la meilleure stabilité hémodynamique possible. Nous ne possédons pas de données sur la concentration alvéolaire minimale (MAC) requise chez le patients septique ou sur un modèle animal. Nous avons déterminé l’influence du sepsis sur le MAC de l’isoflurane sur un modèle de rongeur normotensif. La concentration inhibitrice minimale (MIC) de l’isoflurane à un stimulus identique a été déterminée chez des rongeurs soumis à une ligature et une perforation du caecum (CLP n = 8), ou une laparotomie factice (n = 7). Le MAC calculé de l’isoflurane diminuait chez les animaux septiques comparativement au groupe factice (MAC de l’isoflurane, CLP = 0,8%, factice = 1,4% P< 0,003). Nous n’avons pas trouvé de différence statistique pour les variables hémodynamiques entrer le deux groupes. L’isoflurane procure la stabilité hémodynamique sur ce modèle animal de sepsis. Cependant le MAC de l’isoflurane est abaissé.     

The microcirculation during enflurane and isoflurane anaesthesia in dogs

The effects of enflurane and isoflurane of 0.75 and 1.5 MAC on capillary blood flow were studied by the microsphere (9 ± 1 μm in diameter) method in two groups of seven dogs. Simultaneously, changes in the arteriolo-venular shunt were studied by collection of venous blood at a rate of 4.8 ml · min^?1 for two minutes. Enflurane anaesthesia at 0.75 MAC decreased capillary blood flow in the thyroid glands (35% of control), left and right ventricular wall (59% and 50%), adrenal gland (59%), liver (63%), spleen (56%), pancreas (35%), omentum (20%), and small intestine (60%) and at 1.5 MAC it decreased further in the thyroid glands (15%), left and right ventricular wall (31% and 32%), adrenal gland (42%), liver (47%), spleen (31%), pancreas (23%), omentum (20%), stomach (45%), and small intestine (54%). No marked changes were noted in the brain, kidney, large intestine or skeletal muscle. The arteriolo-venular shunt was decreased in the kidney from an initial rate of 12.1 to 3.8% at 0.75 MAC and to 2.5% at 1.5 MAC enflurane. In contrast, during isoflurane anaesthesia, capillary blood flow remained unchanged, except for a decrease to the thyroid glands (43%) and right ventricular wall (74%) during 1.5 MAC anaesthesia. However, the arteriolo-venular shunt was increased in the brain from 12.0 to 29.7% and 33.0% during 0.75 and 1.5 MAC isoflurane anaesthesia, respectively. It also increased from 25.0 to 41.0% and 46.3% in the skeletal muscle, and from 8.9 to 19.9% and 17.4% in the whole systemic circulation. These data indicate that capillary blood flow is better preserved during isoflurane than during enflurane anaesthesia, but is associated with increased arteriolo-venular shunting.     

Midazolam coinduction does not delay discharge after very brief propofol anaesthesia

Previous reports have demonstrated synergism of midazolam and propofol for induction of anaesthesia in humans. We tested the hypothesis that in the presence of alfentanil, the combination of midazolam with propofol for a very brief operative procedure would not affect the recovery phase. During pre-oxygenation, 64 outpatients scheduled for dilatation and curettage received placebo, or low-dose midazolam (0.03 mg · kg^?1), or high-dose midazolam (0.06 mg · kg^?1) iv, in a randomized double-blind manner. They then received alfentanil 10 μg · kg^?1 iv, followed by titrated doses of propofol iv for induction and maintenance of anaesthesia. Ventilation with 70% N₂O in O₂ by mask was controlled to achieve a PETCO₂ 30–40 mmHg. Outcome measures were: propofol dose (induction and maintenance), time until eye-opening to command, and time to discharge-readiness. Propofol induction dose was decreased by increasing doses of midazolam (P = 0.00005). Midazolam delayed time to eye-opening (P = 0.02) but not time to discharge-readiness. This study had an 80% power to detect a 39 min difference in time to discharge-readiness. We conclude that midazolam propofol co-induction in the presence of alfentanil delays eye-opening, but does not delay discharge after anaesthesia.     

Mechanisms of inhibition of endothelium-dependent relaxation by halothane,isoflurane, and sevoflurane

Volatile anaesthetics inhibit endothelium-dependent relaxation, but the underlying mechanism(s) have not been clarified. In an attempt to elucidate the mechanism(s), we determined the effects of halothane, isoflurane and sevoflurane on relaxation induced by acetylcholine and sodium nitro-prusside (SNP) and the cGMP formation elicited by exogenous nitric oxide (NO) and SNP in rat aortas. Acetylcholine (10^?7?10^?5M) - induced relaxation was attenuated by halothane (2%), isoflurane (2%) and sevoflurane (4%). SNP (10^?8 M) - induced relaxation was reduced by halothane (2%), but not by isoflurane (2%) or sevoflurane (4%). The cGMP level of NO-stimulated aorta was reduced by halothane (2%) and sevoflurane (4%), but not by isoflurane (2%). The cGMP level of SNP (10^?7 M) - stimulated aorta was reduced by halothane (2%), but not by isoflurane (2%) and sevoflurane (4%). We conclude that the mechanisms responsible for the inhibition of endothelium-dependent relaxation differ among anaesthetics. Isoflurane inhibits the relaxation mainly by inhibiting the formation of NO in the endothelium. In contrast, the effect of halothane on endotheliumdependent relaxation may be largely due to the inhibition of action of NO in the vascular smooth muscle and the effect of sevoflurane may be to inactivate NO or to inhibit the action of NO.     

Visual evoked potentials during thiopentone-fentanylnitrous oxide anaesthesia in humans

Visual evoked potentials (VEP) during thiopentone-fentanylnitrous oxide anaesthesia were studied in 15 healthy patients undergoing non-neurosurgical procedures. The VEP was recorded before and at 1 and 2 min after induction of anaesthesia with 5–6 mg · kg⁻¹ of thiopentone. After recording the 1 and 2 min VEPs, anaesthesia was maintained with a fentanylnitrous oxideoxygen combination, and further recordings were made at 5, 10, 15 and 20 min after induction. The 1 and 2 min VEPs showed a marked decrease in the amplitudes. Latencies were increased. The amplitudes gradually returned to the control level at 15 min, while the latencies remained increased throughout the study period. In conclusion, thiopentone should be avoided during the critical period of VEP recording. Once it is given, at least 15 min should elapse before an appropriate interpretation of the VEP can be made. Thiopentonefentanylnitrous oxide anaesthesia slightly increases the latencies of the VEP. These effects should be considered in the interpretation of the VEP when thiopentone-fentanylnitrous oxide anaesthesia is used. Nous avons enregistré les potentiels évoqués visuels (PEV) de 15 patients anesthésiés au thiopental-fentanyl-protoxyde d’azote pendant une intervention non neurochirurgicale. Les mesures avaient lieu une et deux minutes après l’injection de 5–6 mg · kg⁻¹ de thiopental puis sous fentanyl et protoxyde d’azote 5, 10, 15 et 20 minutes après l’induction. A une et deux minutes, les PEV avaient une période de latence prolongée et une amplitude réduite. Cette dernière revint progressivement à la normale au bout de 15 minutes mais la période de latence demeura allongée jusqu’ à la fin de l’étude. Ainsi, le thiopental interfère avec l’interprétation des PEV et cet effet dure au moins 15 minutes. L’anesthésie au thiopental-fentanyl-protoxyde d’azote prolonge aussi légèrement la période de latence des PEV. On devra tenir compte de ces effets dans l’ interprétation des PEV.

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Presented in part at the American Electroencephalographic Society’s annual meeting, San Diego, CA, October 1988.     

Nimodipine decreases the minimum alveolar concentration of isoflurane in dogs

Nimodipine is a calcium antagonist that binds with high affinity to neuronal membranes. It is a potent cerebrovasodilator and has been demonstrated also to affect neurotransmitter synthesis and release. Because patients undergoing surgery for intracranial aneurysms are frequently receiving nimodipine, the authors determined the MAC of isoflurane in six dogs before and during three infusion doses of nimodipine (0.5, 1.0 and 2.0 micrograms.kg-1.min-1). MAC was also determined in five dogs before and during infusion of the drug vehicle (10 microliters.kg-1.min-1). Nimodipine produced a reduction in MAC from 1.47 +/- 0.33% to 1.19 +/- 0.18, 1.15 +/- 0.18 and 1.15 +/- 0.09% during infusions of nimodipine 0.5, 1.0 and 2.0 micrograms.kg-1.min-1, respectively (P less than 0.05). Infusion of drug vehicle alone produced no change in MAC (1.39 +/- 0.15%). This reduction in anaesthetic requirement by nimodipine may be due to its effect on neurotransmission. Adjustments in anaesthetic dosage may be necessary in patients receiving nimodipine.     

Optimizing sedation following major vascular surgery: a double-blind study of midazolam administered by continuous infusion

A randomized, double-blind study was undertaken to determine the dose requirements, recovery characteristics, and pharmacokinetic variables of midazolam given by continuous infusion for sedation in patients following abdominal aortic surgery. Thirty subjects, 50–75 yr, scheduled to undergo aortic reconstructive surgery, entered the study. Following a nitrous oxide-isoflurane-opioid anaesthetic technique, patients were randomly allocated to receive one of three loading doses (0.03, 0.06 or 0.1 mg · kg^?1) and initial infusion rates (0.5, 1.0 or 1.5 μg · kg^?1 · min^?1) of midazolam, corresponding to groups low (L), moderate (M) and high (H). The infusion of midazolam was adjusted to maintain sedation levels of “3, 4 or 5,“ which permitted eye opening in response to either verbal command or a light shoulder tap, using a seven-point scale ranging from “0” (awake, agitated) to “6” (asleep, non-responsive). Additionally, morphine was given in increments of 2.0 mg iv prn for analgesia. On the morning after surgery, midazolam was discontinued, and the tracheas were extubated when patients were awake. Blood samples were taken during, and at increasing intervals for 48 hr following discontinuation of the infusion, and analyzed by gas chromatography. The desired level of sedation was maintained during more than 94% of the infusion period in all three groups, with a maximum of three dose adjustments per patient, for treatment which lasted 16.3 ± 0.6 hr. There was, however, an increase in both the infusion rates and mean plasma concentrations from Group L to Group H (P < 0.05), which corresponded to an inverse relationship of morphine requirements during the period of sedation (P < 0.05, Group H vs Group L). Optimal midazolam infusion rates and resulting plasma concentrations at the times the infusions were discontinued (in parentheses) were as follows — Group L: 0.60 ± 0.18 μg · kg^?1 min^?1 (76 ± 32 ng · mL^?1), Group M: 0.90 ± 0.52 μg · kg^?1 · min^?1 (133 ± 71 ng · mL^?1), and Group H: 1.34 ± 0.69 μg · kg^?1 · min^?1 (206 ± 106 ng · mL^?1). Times to awakening were longer in Group H: 3.1 ± 3.4 hr, than in Group L: 1.1 ± 0.8 h, P < 0.05. Pharmacokinetic variables were found to be dose- independent over the range of infusion rates. Mean values were t_1/2β = 4.4 ± 1.5 hr, CL = 5.94 ± 1.69 mL · min^?1 · kg^?1, Vd = 3.13 ± 1.07 L · kg^?1. It is concluded that midazolam, infused between 0.6–0.9 μg · kg^?1 · min^?1, provides a stable level of sedation, when administered in conjunction with intermittent iv morphine following AAS. This sedation technique, which costs $1.65 ± 0.73 hr^?1 ($Can), is associated with rapid recovery and minimal side effects.