Epicardial antiarrhythmic drug administration was studied as a therapeutic approach for experimental ventricular tachycardia (VT) in an open-chest dog model. Lidocaine-polyurethane matrices (28%, w/w) were formulated as a model system. Matrices were placed on the left ventricular epicardium in each of 23 anesthetized open-chest dogs with ouabain-induced VT, to evaluate effectiveness in restoring sinus rhythm. Conversion occurred in all animals treated with matrices containing 300 mg or more of lidocaine after 1.5 to 7.0 min. The matrix lidocaine content correlated linearly with the time required for conversion to sinus rhythm (r = 0.75, P = 0.0002); irrespective of matrix size the myocardial/plasma lidocaine ratio was 20.1 ± 4.2 (mean ± SD) at the time of conversion. In a separate series of five dogs without ventricular tachycardia, systolic wall thickening measured with sonomicrometers after 5 min of controlled-release lidocaine administration (500- to 1000-mg matrix lidocaine content, 7.48 ± 3.49-mg/kg dose) was only minimally diminished (–14.1%) and this effect was observed only at the site of matrix placement on the anterior-apical epicardium. In contrast, intracoronary injection of 0.3 or 1.0 mg/kg of lidocaine-HCl resulted in complete elimination of wall thickening or replacement by systolic thinning. Thus epicardial administration of lidocaine from polyurethane matrices was an effective means of treating ouabain-induced ventricular tachycardia. Regional myocardial function in the vicinity of the matrices was modified to a very limited degree, supporting the view that the matrices can be used safely, without serious risk to ventricular contractile performance. 相似文献
Background: 2-chloroprocaine (2-CP) used for lumbar epidural anesthesia (LEA) reportedly decreases the efficacy of epidural morphine (EM) administered for post-cesarean section (CS) analgesia. The amount of supplemental i.v. morphine self-administered by the patient via the patient-controlled analgesia device (PCA) is used to study the interaction between EM and 2-CP. Methods: Forty-two patients scheduled for elective CS were randomly divided into 3 equal groups, and received 2-CP, 2-CP+epinephrine (Epi, 5 μg ml-1) or 2% lidocaine (Lido) with Epi for LEA. All patients received 5 mg EM and i.v. PCA morphine for postoperative pain. Cumulative amount of i.v. morphine used in the first 24 hours as well as the amount of the drug used during each 2-h period were noted. Nonparametric analysis of variance and Chi-squared analysis were used for statistical comparisons. Results: The mean cumulative 24-h i.v. PCA morphine requirement in the 2-CP, 2-CP+Epi and Lido+Epi groups respectively was 20.5±24, 33.1.5±27 and 4.07±6.3 (mean±SD). The Lido+Epi group used significantly less morphine ( P = 0.01) compared to either of the 2-CP groups with no significant difference between the 2-CP groups. The maximum i.v. PCA morphine use occurred in the first 4 hours following surgery in all three groups. Conclusion: Analgesic efficacy of EM is decreased when 2-CP is used for LEA compared to when Lido+Epi is used. 相似文献
Study Objective: To test the hypothesis that the magnitude of the acute hemodynamic response to electroconvulsive therapy (ECT) is related to the duration of the seizure activity in patients receiving different dosages of intravenous (IV) lidocaine.
Patients: 21 ASA physical status I, II, and III patients undergoing four consecutive maintenance ECT treatments for chronic depression.
Interventions: Patients received lidocaine 50 mg, 100 mg, 200 mg IV, or saline prior to induction of anesthesia via a standardized anesthetic technique.
Measurements and Main Results: Noninvasive blood pressure (BP) and heart rate (HR), as well as the duration of motor and electroencephalographic (EEG) seizure, were measured. The duration of motor and EEG seizures (means ± SD) were 37 ± 13 sec and 64 ± 21 sec, 25 ± 11 sec and 52 ± 43 sec, 17 ± 12 sec and 32 ± 17 sec, 1 ± 3 sec and 18 ± 10 sec in the saline, lidocaine 50 mg, 100 mg, 200 mg groups, respectively. Although the duration of seizure activity was decreased in a dose-related fashion after lidocaine pretreatment, the peak increases in BP and HR were similar in the lidocaine and saline treatment groups.
Conclusions: Despite producing dose-related decreases in the duration of both motor and EEG seizure activity, lidocaine failed to attenuate the acute hemodynamic response to ECT. Thus, the acute hemodynamic response to ECT is not related to the duration of seizure activity. 相似文献
Background: The purpose of the present study was to assess the effects of intravenous lidocaine on spatial changes of electroen-cephalographic power and on psychomotoric status in conscious volunteers. Methods: In 11 healthy volunteers lidocaine (2-min bolus, 100 mg; 15-min infusion, 40 μg kg-1 min-1) or placebo were given intravenously in a randomized, single-blinded, two-way crossover study. Haemodynamics and lidocaine plasma concentrations were measured at baseline and within a period of 30 min following bolus injection. Vigilance and emotional status were tested using visual analogue scales (VAS). Toxic CNS effects were evaluated by a questionnaire. The raw EEG (17 leads, reference Cz) and computed power spectra were continuously recorded. Results: The chosen lidocaine dosage led to nearly constant plasma concentrations (unbound lidocaine 2.5 min and 15 min after bolus 0.36±0.14 μg/ml and 0.30±0.06 μg/ml, respectively [mean±SD]). The placebo caused no symptoms, changes in VAS-scores or EEG-parameters. Lidocaine induced pronounced subjective symptoms and significant increases in delta activity for 15 min, most dominant at the frontotemporal and occipital leads (max. +219% O1). Frontal and occipital beta1 and beta2 power (max. +131% and +124% at O1, respectively) was immediately increased after the bolus injection. No EEG changes occurred at central region Cz, and no interhemispheric EEG differences were noted. Theta, alphal, and alpha2 power remained unchanged. Conclusion: The current data demonstrate simultaneous changes in psychomotoric status as well as delta and beta spectral power during lidocaine infusion. These data could be an indication that the pronounced frontotemporal and occipital EEG changes are the electroencephalographic expression of subjective sensations. 相似文献