ABSTRACT
BACKGROUND: There are situations in anesthesia in which it may be desirable to achieve rapid tracheal intubation. Rapid tracheal intubation with rocuronium has been studied using a probability-based approach. But these studies used intravenous anesthetics for anesthetic induction. Therefore, we aimed to predict doses of rocuronium giving 90% and 95% probabilities of intubation within 60 seconds and to estimate their action durations using sevoflurane for anesthetic induction. METHODS: Anesthesia was induced in sixty patients with sevoflurane. Patients received randomly rocuronium, 0.0, 0.3, 0.6, 0.9 or 1.2 mg/kg (n = 12/dose). Laryngoscopy began 40 seconds later, aiming for intubation at 60 seconds, and conditions were graded as either perfect, acceptable or unacceptable, with the first two conditions being taken as successful intubation. Duration of action was accepted as time until a twitch height recovery of 15%. The dose versus the fraction of patients showing successful intubation was analyzed by logistic regression. Doses giving 90% and 95% (D90 and D95) probabilities of successful intubation were calculated. RESULTS: Of the 12 patients in each group (0.0, 0.3, 0.6, 0.9 or 1.2 mg/kg), intubation was successful in 4, 10, 12, 12 and 12 patients, respectively. The D90 and D95 doses were determined to be 0.34 and 0.43 mg/kg, respectively. CONCLUSIONS: After induction with sevoflurane, rocuronium at 0.43 mg/kg, gives a 95% probability of successful intubaton at 60 seconds.
Subject(s)
Humans , Anesthesia , Anesthetics, Intravenous , Intubation , Laryngoscopy , Logistic ModelsABSTRACT
BACKGROUND: Naloxone,an opioidant agonist, has been s hown t o have a c ar di ovascular pressor effect in states of hemorrhagic and endotoxic shock.We determined the direct inotropic effect of naloxone using guinea pig right ventricular papillary muscles. METHODS: With institutional approval,isometric contractile force was measured in normal and 26mM K+ Tyrode's solution at various stimulation rates.Normal and slow action potentials (APs) were measured with conventional microelectrode technique.The effects of naloxone on sarcoplasmic recticulum function were evaluated by measuring rapid cooling contractures (RCCs)in normal Tyrode 's solution and rested-state (RS)contraction in low Na+ (25 mM)Tyrode's solution.Patch clamp study was performed to examine the direct effect on Ca2+ current in myocytes. RESULTS: Naloxone (50,100,200 micro M)caused dose-dependent depression of peak force and maximal rate of peak force (dF/dt-max)by 30,50 and 70%,respectively.Modest depression was shown in RS contraction in low Na+ Tyrode's solution.In 26 mM K+ Tyrode's solution,100 micro M naloxone markedly depressed late force development.100 micro M naloxone depressed RCCs by 20%. While 100 micro M naloxone did not alter amplitude or dV/dt-max in normal and slow APs at 0.25 Hz, AP duration was prolonged significantly.In patch clamp study,50 micro M naloxone depressed Ca2+ current by 50%. CONCLUSIONS: Naloxone depresses contractile force.Myocardial depressant effect partly seems to be caused by depressed Ca2+ influx through cardiac membrane.Rapid release of Ca2+ from the sarcoplasmic reticulum by depolarization and release by rapid cooling seems to be minimally affected.