Deryck Duncalf

A Multicenter Evaluation of Total Intravenous Anesthesia with Remifentanil and Propofol for Elective Inpatient Surgery

Remifentanil is a mu-opioid receptor agonist with a context sensitive half-time of 3 min and an elimination half-life <or=to10 min. This study sought to evaluate the efficacy of remifentanil and propofol total intravenous anesthesia (TIVA) in 161 patients undergoing inpatient surgery. Remifentanil 1 micro gram/kg was given intravenously (IV) followed by one of two randomized infusion rates: small dose (0.5 micro gram centered dot kg-1 centered dot min-1) or large dose (1 micro gram centered dot kg-1 centered dot min-1). Propofol (0.5-1.0 mg/kg IV bolus and 75 micro gram centered dot kg-1 centered dot min-1 infusion) and vecuronium were also given. Remifentanil infusions were decreased by 50% after tracheal intubation. End points included responses (hypertension, tachycardia, and somatic responses) to tracheal intubation and surgery. More patients in the small-dose than in the large-dose group responded to tracheal intubation with hypertension and/or tachycardia (25% vs 6%; P = 0.003) but there were no other differences between groups in intraoperative responses. Recovery from anesthesia was within 3-7 min in both groups. The most frequent adverse events were hypotension (systolic blood pressure [BP] < 80 mm Hg or mean BP < 60 mm Hg) during anesthesia induction (10% small-dose versus 15% large-dose group; P = not significant [NS]) and hypotension (27% small-dose versus 30% large-dose group; P = NS), and bradycardia (7% small-dose versus 19% large-dose group; P = NS) during maintenance. In conclusion, when combined with propofol 75 micro gram centered dot kg-1 centered dot min-1, remifentanil 1 micro gram/kg IV as a bolus followed by an infusion of 1.0 micro gram centered dot kg-1 centered dot min-1 effectively controls responses to tracheal intubation. After tracheal intubation, remifentanil 0.25-4.0 micro gram centered dot kg-1 centered dot min-1 effectively controlled intraoperative responses while allowing for rapid emergence from anesthesia. (Anesth Analg 1996;83:279-85)

Comparison of Ondansetron Versus Placebo to Prevent Postoperative Nausea and Vomiting in Women Undergoing Ambulatory Gynecologic Surgery

BackgroundPostoperative nausea and emesis, especially in ambulatory surgical patients, remains a troublesome problem. This study was performed to compare the incidence of nausea and emesis during the 24-h postoperative period in ondan-setron-treated patients versus placebo-treated patients. MethodsUsing a randomized prospective double-blind study design, women between the ages of 18 and 70 yr undergoing gynecologic surgical procedures with general opioid anesthesia on an outpatient basis were enrolled. Ondansetron or placebo was administered prior to induction of anesthesia. Patients were stratified according to history of nausea and emesis during previous exposure to general anesthesia and randomized to dose received. ResultsData from the 544 women showed that all doses of intravenous ondansetron tested (1, 4, and 8 mg) were significantly more effective (62%, 76%, and 77%, respectively) than placebo (46%) in reducing the incidence of emesis following surgery until 24 h after recovery room entry. All these doses were more effective than placebo in patients with no prior history of emesis following surgery and the 4− and 8-mg doses were more effective than placebo in patients with a prior history of emesis following surgery. All doses of ondansetron tested were generally well tolerated with adverse events, clinical laboratory tests, and recovery room vital signs similar to those of placebo. Serum aspartate transaminase (AST) was increased in five patients (1 mg, 2 patients; 4 mg, 1 patient; 8 mg, 2 patients). In the three patients in whom subsequent analysis were performed, the serum AST had decreased to preoperative levels. ConclusionsOndansetron given intravenously to prevent postoperative nausea and emesis was highly effective in the 4− and 8-mg doses in women having ambulatory gynecologic surgery.

Common bile duct pressure changes after fentanyl, morphine, meperidine, butorphanol, and naloxone.

Five groups of 10 patients received thiamylal, enflurane, nitrous oxide-oxygen anesthesia for elective cholecystectomy. The common bile duct was intubated via the cystic duct with a 16-g plastic catheter, and the control intraductal pressure was measured. Patients then were given equianalgesic doses of fentanyl, morphine, meperidine, butorphanol, or placebo intravenously, and the common bile duct pressure was recorded for 20 min. Fentanyl, morphine, and meperidine significantly increased pressure in the common duct (P < 0.001). Butorphanol produced only insignificant changes. Naloxone given 20 min later significantly (P < 0.001) decreased pressure in patients given fentanyl, morphine, and meperidine. Naloxone given without narcotics caused an increase in pressure that, although statistically significant (P < 0.03), was clinically insignificant. In five additional patients anesthetized with thiamylal, nitrous oxide-oxygen and intermittent doses of fentanyl, common bile duct pressures were normal.

THE RESPIRATORY, CIRCULATORY, AND NARCOTIC ANTAGONISTIC EFFECTS OF NALORPHINE, LEVALLORPHAN, AND NALOXONE IN ANAESTHETIZED SUBJECTS

SummaryNalorphine (150 μg/kg) and levallorphan (20 μg/kg), when administered to lightly anaesthetized subjects who had not received a narcotic, caused significant depression of respiratory rate and minute volume. In contrast, 5 and 10 μg/kg naloxone caused no respiratory depression. These doses of nalorphine, levallorphan, and naloxone caused a moderate decrease of pulse rate and systolic blood pressure. Naloxone 5 and 10 μg/kg offered significantly greater protection against the respiratory depressant effects of 20 μg/kg oxymorphone administered five minutes later than 150 μg/kg nalorphine or 20 μg/kg levallorphan. None of the three narcotic antagonists affected the oxymorphone-induced decrease of pulse rate, and all had about the same protective effect against the fall of systolic blood pressure caused by this compound. Since doses of naloxone, which provide significantly better protection against narcotic-induced respiratory depression than the conventional doses of nalorphine and levallorphan, cause no respiratory depression in themselves, it should be considered the narcotic antagonist of choice for clinical use.FrRésuméLa nalorphine (150 μ/kg) et la levallorphan (20 μg/kg), administrés à des sujets sous anesthésie légère et qui n’avaient pas reçu de narcotique, ont produit une dépression marquée du rythme respiratoire et du volume minute. Par contre, 5 et 10 μg/kg de naloxone n’ont pas causé de dépression respiratoire. Ces doses de nalorphine, de levallorphan et de naloxone ont produit une diminution modérée de la fréquence cardiaque et de la pression sanguine systolique. Cinq et dix μg/kg de naloxone ont donné une bien meilleure protection contre la dépression respiratoire produite par 20 μg/kg d’oxymorphone, administrés cinq minutes après, que 150μg/kg de nalorphine ou 20 μg/kg de levallorphan. Aucun de ces trois antagonistes des narcotiques n’a modifié le ralentissement du pouls provoqué par l’oxymorphone et tous ont exercé a peu près le même effet protecteur contre la chute de pression systolique produite par ce médicament.Puisque des doses de naloxone, qui produisent une protection réellement meilleure contre la dépression respiratoire consécutive aux narcotiques que ne le font les doses ordinaires de nalorphine et de levallorphan, ne produisent par ellesmêmes aucune dépression respiratoire, il faudrait considérer ce produit (naloxone) comme 1’antagoniste de choix des narcotiques pour usage clinique.

the influence Of VENTILATION AND HYPERCAPNEA ON INTRAOCULAR PRESSURE during ANESTHESIA

ENERAL ANESTHESIA is indicated for G intraocular s u r g e r y in c e r t a i n groups of patients, such as children and apprehensive adults. Moreover, an increasing number of ophthalmic surgeons prefer general anesthesia for operation on the eye. When the eye is opened, in the course of operation on the anterior chamber, an i n c r e a s e in intraocular pressure (IOP) may result in extrusion of vitreous and loss of vision. For this reason IOP should be maintained within or below normal limits for this type of surgery.

Studies on the Specificity of Narcotic Antagonists

Experiments with five narcotics, (morphine 0.3 mg./kg., oxymorphone 20 μg./kg., levorphan 50 μg./kg., meperidine 1.5 μg./kg. and fentanyl 1.5 μ./kg.) and three narcotic antagonists (nalorphine 150 μg./kg., naloxone 5 μg./kg., and levallorphan 20 μg./kg. were designed, to investigate whether or not the various antagonists exhibit a more pronounced effect against the pharmacological actions of their parent compounds, than against those of structurally less closely related narcotics. No such specificity of action was found. Naloxone appeared more effective than nalorphine or Ieval-lorphan. With all three antagonists there was a direct relation between the degree of narcotic-induced respiratory depression and the efficacy of the antagonist.

A simple and sensitive method of acetylcholine identification and assay. Bioassay combined with minicolumn gel filtration or high-performance liquid chromatography

A modified technique of acetylcholine assay on the guinea pig ileum has been combined with either minivolume gel filtration or high-performance liquid chromatography separation of the samples. In addition, labeled acetylcholine (14C-ACh) was eluted with unlabeled acetylcholine or with the samples expected to contain acetylcholine, and their elution profiles were compared by bioassay plus radioassay of eluate fractions. When the elution of both biological activity and label occurred in the same eluates, it was concluded that the substance assayed on guinea pig ileum was acetylcholine. The method was sensitive to 0.5 ng (1.8 pmol) of acetylcholine and its reproducibility was within 5%. It thus represents a substantial improvement in chemical specificity over the previous bioassay method described by Paton and Vizi (1969).

Aspergillus pancarditis and cardiac arrest during anesthesia.

Endocarditis, which may progress to myocardial and pericardial involvement (pancarditis), may be a slow, insidious disease with few clinical signs and symptoms. It may also be seen with clinical features that mimic other disease states, including renal failure. Clinical features common to endocarditis and renal failure include lassitude, anemia, embolic phenomena, heart murmurs, fever, and elevated white cell counts. We present a case of Aspergillus pancarditis associated with end stage nephrosclerosis, first, because it illustrates the difficulty in establishing the antemortern diagnosis of this type of endocarditis, and second, because repeated general anesthetics were associated with severe cardiovascular instability, including cardiac arrest. A relationship between intraanesthetic cardiovascular instability and mycotic pancarditis has not been previously reported.

Naloxone Fails to Antagonize Thiopental Anesthesia

A study was undertaken to determine the effect in man of naloxone on the central nervous system depression produced by IV thiopental. Eight normal volunteers were given 5 mg/kg thiopental IV. On a separate occasion the same 8 volunteers were given 50 microgram/kg naloxone IV 5 minutes prior to 5 mg/kg thiopental. Naloxone had no significant effect on the rate of return of consciousness following administration of thiopental. Naloxone also had no significant effect on the responses of blood pressure, heart rate, or respiratory rate to thiopental.

Naloxone fails to antagonize halothane-induced depression of the longitudinal muscle of the guinea pig ileum.

The influence of halothane, or naloxone, or halothane followed by naloxone was investigated in the in vitro myenteric plexus longitudinal muscle preparation of the guinea pig ileum. Halothane alone in 1.5 to 2.0% (v/v) concentration caused about 50% depression of the twitch and decreased both spontaneous acetylcholine (ACh) release (p < 0.02) and volley output of ACh (p < 0.02). Very high concentrations (>1 μM) of naloxone caused a nonspecific, postsynaptic depression of the twitch. Higher than 100 nM concentrations of naloxone increased spontaneous ACh release, but had no effect on the volley output of ACh. Over a wide concentration range, from 15 nM to 3 μM, naloxone did not antagonize in the longitudinal muscle preparation the effects of halothane on any of the parameters investigated. These findings indicate that the sites of action of halothane and naloxone in this preparation are not identical.