[Show abstract][Hide abstract]ABSTRACT: The sensory blockade induced by a lidocaine-bupivacaine mixture combines the faster onset of lidocaine and the longer duration of bupivacaine. The current study compared the effects of large doses lidocaine (16 mg/kg), bupivacaine (4 mg/kg), and a mixture of 16 mg/kg lidocaine-4 mg/kg bupivacaine on hemodynamic and cardiac electrophysiologic parameters in anesthetized and ventilated piglets.
After carotid artery cannulation, a double micromanometer measured mean aortic pressure, left ventricular end diastolic pressure, and the first derivative of left ventricular pressure. Electrocardiogram recording and a bipolar electrode catheter measured RR, PQ, QRS, QT C, JT C, AH, and HV intervals. Lidocaine, bupivacaine, or the mixture was administered intravenously over 30 s, and studied parameters were measured throughout 30 min.
Mean aortic pressure decreased in all groups ( P < 0.05). The first derivative of left ventricular pressure was decreased in all groups ( P < 0.001) but to a greater extent with the mixture compared with lidocaine ( P < 0.04). RR, QT C, and JT C intervals were similarly increased in all groups ( P < 0.05). In all groups, PQ, AH, HV, and QRS intervals were widened ( P < 0.001). The lengthening of PQ was greater with bupivacaine ( P < 0.02). The lengthening of AH was greater and delayed with bupivacaine compared with lidocaine ( P < 0.03). The lengthening of HV and the widening of QRS were greater and delayed with bupivacaine ( P < 0.01). The widening of QRS was greater with the mixture than with lidocaine ( P < 0.01).
The alterations of ventricular conduction parameters are greater with 4 mg/kg bupivacaine than with a mixture of 16 mg/kg lidocaine-4 mg/kg bupivacaine, whereas the hemodynamic parameters are similarly altered.
[Show abstract][Hide abstract]ABSTRACT: The study of induced circulatory changes requires simultaneous assessment of multiple regional circulations because of interactions and compensatory mechanisms. Positive end expiratory pressure mechanical ventilation (PEEP) is known to cause marked, and potentially deleterious, cardiovascular changes. Our aim was to use a comprehensive approach to assess PEEP-induced circulatory changes in open vs closed abdomen animals.
In the anesthetized rabbit, we used implantable Doppler micro-probes to measure blood flow simultaneously in the ascending aorta, inferior vena cava, portal vein, hepatic artery, common carotid artery, and renal artery. We studied spontaneously breathing animals (Group A), and open (Group B) and closed abdomen (Group C) animals mechanically ventilated at 0 (ZEEP) and 12 cm H(2)O PEEP.
In Group A, all biological and hemodynamic variables remained unchanged for three hours at the end of the surgical procedure. In Groups B and C, ZEEP produced no significant hemodynamic change. PEEP induced a decrease in carotid, hepatic, and renal artery blood flow in Groups B and C, a decrease in heart rate and mean arterial blood pressure in Group B, and a decrease in aorta blood flow in Group C.
These experimental results demonstrate the usefulness of the comprehensive approach of circulatory changes, and confirm that PEEP may have deleterious effects on regional blood flow, even without significant change in cardiac output, especially when the abdomen is open.
Full-text Article · Apr 2002 · Canadian Journal of Anaesthesia
[Show abstract][Hide abstract]ABSTRACT: Unlabelled:
Ropivacaine is less potent and less toxic than bupivacaine. We administered these two local anesthetics in a cardiac electrophysiologic model of sodium thiopental-anesthetized and ventilated piglets. After assessing the stability of the model, bupivacaine (4 mg/kg) and ropivacaine (6 mg/kg) were given IV in two groups (n = 7) of piglets. No alteration in biological variables was reported throughout the study. Bupivacaine and ropivacaine similarly decreased mean aortic pressure from 99 +/- 22 to 49 +/- 31 mm Hg and from 87 +/- 17 to 58 +/- 28 mm Hg, respectively, and decreased the peak of the first derivative of left ventricular pressure from 1979 +/- 95 to 689 +/- 482 mm Hg/s and from 1963 +/- 92 to 744 +/- 403 mm Hg/s, respectively. Left ventricular end-diastolic pressure was similarly increased from 6 +/- 5 to 9 +/- 5 mm Hg and from 6 +/- 4 to 12 +/- 4 mm Hg, respectively. Bupivacaine and ropivacaine similarly lengthened the cardiac cycle length (R-R; from 479 +/- 139 to 706 +/- 228 ms and from 451 +/- 87 to 666 +/- 194 ms, respectively), atria His (from 71 +/- 15 to 113 +/- 53 ms and from 64 +/- 6 to 86 +/- 10 ms, respectively), and QTc (QTc = QT x R-R(-0.5), Bazett formula; from 380 +/- 71 to 502 +/- 86 ms and from 361 +/- 33 to 440 +/- 56 ms, respectively) intervals. Bupivacaine altered to a greater extent the PQ (the onset of the P wave to the Q wave of the QRS complex) (from 97 +/- 20 to 211 +/- 60 ms versus from 91 +/- 8 to 145 +/- 38 ms, P < 0.05), QRS (from 58 +/- 3 to 149 +/- 34 ms versus from 60 +/- 5 to 101 +/- 17 ms, P < 0.05), and His ventricle interval (from 25 +/- 4 to 105 +/- 30 ms vs from 25 +/- 4 to 60 +/- 30 ms, P < 0.05) than ropivacaine. A 6 mg/kg ropivacaine dose induced similar hemodynamic alterations as 4 mg/kg bupivacaine. However, bupivacaine altered the variables of ventricular conduction (QRS and His ventricle) to a greater extent.
A 6 mg/kg ropivacaine dose induced similar hemodynamic alterations as 4 mg/kg bupivacaine. However, bupivacaine altered the variables of ventricular conduction (QRS and His ventricle) to a greater extent.
[Show abstract][Hide abstract]ABSTRACT: Measurement of the time elapsed from the decision to use a pulmonary artery catheter to the onset of the adapted treatment.
Critical care unit of a university hospital.
A total of 104 critically ill patients.
The time elapsed from the decision to use a pulmonary artery catheter to the onset of the adapted treatment. Five time intervals (availability, preparation, catheterization, data collection, and therapeutic intervals) were individualized according to the times of decision of pulmonary artery catheter insertion, operator's hand washing, venipuncture, postoperative dressing, data collection, and the effective onset of subsequent therapy.
Among 120 used pulmonary artery catheters, seven could not be inserted. The time to use the pulmonary artery catheter was never shorter than 45 mins (median value = 120 mins). For availability, preparation, catheterization, data collection, and therapeutic intervals, the median values were 30, 20, 20, 20, and 10 mins, respectively. The availability and data collection intervals were shortened during the night period and the fourth quarter of the study, respectively.
The pulmonary artery catheter use is time consuming. However, the availability and data collection intervals could be shortened.
[Show abstract][Hide abstract]ABSTRACT: Catheterization of the subclavian vein may lead to severe complications. The current randomized study compared a technique of pulsed Doppler ultrasonography guidance and the standard method for subclavian vein catheterization.
Standard and Doppler ultrasonography guidance methods were performed by the same physician in 286 patients, 143 in each group. Primary end points were immediate complications (arterial puncture, pneumothorax, wrong position of catheter tip), failures, the number of subclavian vein catheterizations with immediate complication or failure, the number of skin punctures per catheterization, and the time to placement of the guide wire. The secondary end points were the determination of predicting factors of successful cannulation in each group.
Both groups were similar according to morphologic parameters of the patients. A greater number of subclavian vein catheterizations were performed on the right side using Doppler guidance (105 vs. 73, P < 0.01). Doppler guidance decreased complications (5.6% vs. 16.8%, P < 0.01), largely because of a smaller number of catheters for which the tip was defined to be in incorrect position (0.7% vs. 7.7%, P < 0.01). The time to catheterization was longer with Doppler guidance (300 vs. 27 s, P < 0.001). Failures, catheterizations of the subclavian vein with immediate complications or failure, and the total number of skin punctures per catheterization were similar in both groups. Using Doppler guidance, the presence of a good Doppler signal (124 of 143) was predictive of successful catheterization (123 successful cannulations, P < 0.001).
Doppler guidance reduces the incidence of inappropriately positioned subclavian catheters.
[Show abstract][Hide abstract]ABSTRACT: Background: The aims of the study were to verify the effects of ketamine on ventricular conduction velocity and on the ventricular effective refractory period, to determine its effects on anisotropy and on homogeneity of refractoriness, and to use wavelength to determine whether ketamine has antiarrhythmic or arrhythmogenic properties, Methods: A high-resolution epicardial mapping system was used to study the effects of 50, 100, 150, and 200 mu M racemic ketamine in 15 isolated, Langendorff-perfused rabbit hearts, Five hearts were kept intact to study the effects of ketamine on spontaneous sinus cycle length (RR) interval and its putative arrhythmogenic effects, In 10 other hearts, a thin epicardial layer was obtained by an endocardial cryoprocedure (frozen hearts) to study ventricular conduction velocity, ventricular effective refractory periods (five sites), and ventricular wavelength, Results: Ketamine induced a concentration-dependent lengthening of the RR interval, Ketamine slowed longitudinal and transverse ventricular-conduction velocity with no anisotropic change, and it prolonged the ventricular effective refractory period with no significant increase in dispersion, Ventricular longitudinal and transverse wavelengths tend to increase, but this was not statistically significant, Finally, no arrhythmia could be induced regardless of the ketamine concentration, Conclusion: Ketamine slowed ventricular conduction and prolonged refractoriness without changing anisotropy or increasing dispersion of refractoriness. Although these effects should result in significant antiarrhythmic effects of ketamine, this should not be construed to suggest a protective effect in ischemic or other abnormal myocardium.
[Show abstract][Hide abstract]ABSTRACT: Background:: The aims of the study were to verify the effects of ketamine on ventricular conduction velocity and on the ventricular effective refractory period, to determine its effects on anisotropy and on homogeneity of refractoriness, and to use wavelength to determine whether ketamine has antiarrhythmic or arrhythmogenic properties.
[Show abstract][Hide abstract]ABSTRACT: This study was designed (a) to test and (b) to compare proarrhythmic effects of levcromakalim and nicorandil; and (c) determine the mechanism of arrhythmia initiation by using high-resolution ventricular epicardial mapping on 44 Langendorff-perfused rabbit hearts. Eighteen hearts were kept intact and received incremental doses (1-500 microM) of levcromakalim, nicorandil, and isosorbide dinitrate. In 26 hearts, a thin layer of epicardium was obtained after endocardial cryotechnique (frozen hearts). In intact hearts, isosorbide dinitrate did not produce any arrhythmia. In contrast, levcromakalim induced spontaneous ventricular fibrillation (VF) in all hearts at 50 microM, whereas only one VF occurred at 500 microM nicorandil. These three drugs produced a dose-dependent bradycardia in intact hearts. In frozen hearts, arrhythmias were induced by 5 microM levcromakalim and 50 microM nicorandil. Isosorbide dinitrate had no proarrhythmogenic effect. Epicardial mapping showed that most of induced ventricular tachycardias were based on reentry around an arc of functional conduction block. Ventricular conduction velocities did not change, but levcromakalim and nicorandil shortened ventricular effective refractory period. We conclude that (a) levcromakalim and nicorandil, used in toxic concentrations, have direct proarrhythmic effects; (b) nicorandil proarrhythmogenic effects are 10 times less marked than those of levcromakalim (arrhythmia is solely the result of the potassium channel opener property of nicorandil); and (c) most of ventricular tachycardias induced are based on reentry.
Article · Feb 1997 · Journal of Cardiovascular Pharmacology
[Show abstract][Hide abstract]ABSTRACT: Large and equipotent doses of several local anesthetics were administered in a cardiac electrophysiologic model on closed-chest dogs. Five groups of pentobarbital-anesthetized dogs were each given intravenously 16 mg/kg lidocaine, 12 mg/kg mepivacaine, 4 mg/kg or 8 mg/kg etidocaine, and 4 mg/kg bupivacaine. Lidocaine induced bradycardia, slowing of atrioventricular node conduction (AH), and marked hemodynamic depression, represented by a decrease in mean aortic pressure (MAoP), in the peak of first derivative of left ventricular pressure (LVdP/dt(max)) and by an increase in left ventricular end-diastolic pressure (LVEDP). Atrial pacing at pacing cycle length (PCL) of 298 ms did not enhance the alteration of variables of ventricular conduction (His ventricle [HV] interval and QRS duration). Mepivacaine induced slight alteration of electrophysiologic variables. Atrial pacing at PCL of 312 ms did not enhance the alteration of HV and QRS duration. Mepivacaine induced transient hemodynamic depression. Etidocaine (4 mg/kg) induced electrophysiologic and hemodynamic alterations similar to mepivacaine but artrial pacing at PCL of 330 ms enhanced HV lengthening and QRS widening (P < 0.05). Etidocaine (8 mg/kg) induced marked impairment of PR, HV, QRS, and QT, and dramatic hemodynamic depression represented by a decrease in MAoP from 123.5 +/- 16.2 at baseline to 36.5 +/- 8.3 mm Hg at 1 min (P < 0.001) and of LVdP/dtmax) from 1446 +/- 379 to 333 +/- 93 mm Hg/s (P < 0.001). Bupivacaine induced dramatic impairment of electrophysiologic variables. Bupivacaine also decreased LVDP/dtmax (from 1333 +/- 347 to 617 +/- 299,P < 0.001) and increased LVEDP. We conclude that mepivacaine induced moderate cardiotoxicity. In contrast, lidocaine induced dramatic hemodynamic depression while etidocaine and bupivacaine markedly impaired both electrophysiologic and hemodynamic variables. This double impairment could explain the great difficulty in resuscitating patients who have had cardiotoxic accidents induced by etidocaine or bupivacaine.
[Show abstract][Hide abstract]ABSTRACT: The purpose of the study was to compare cardiac output (CO) measurement by continuous (CTD) with that by conventional thermodilution (TD) in critically ill patients. In 19 of 20 critically ill patients requiring a pulmonary artery catheterism, 105 paired CO measurements were performed by both CTD and TD. Regression analysis showed that: CTD CO = 1.18 TD CO - 0.47. Correlation coefficient was 0.96. Bias and limit of agreement were -0.8 and 2.4 L.min-1, respectively. When a Bland and Altman diagram was constructed according to cardiac index ranges, biases were -0.2 and -0.3 and -0.8 L.min-1.m-2 and limits of agreement were 0.3, 0.7 and 1.6 L.min-1.m-2 for low (< 2.5 L.min-1.m-2), normal (between 2.5 and 4.5 L.min-1.m-2) and high (> 4.5 L.min-1.m-2) cardiac indexes, respectively. It is concluded that CTD, compared with TD, is a reliable method of measuring CO, especially when cardiac index is < or = 4.5 L.min-1.m-2.
Article · Nov 1995 · Canadian Journal of Anaesthesia
[Show abstract][Hide abstract]ABSTRACT: Possible mechanisms of the ability of clonidine to correct bupivacaine-induced ventricular electrophysiologic impairment were evaluated in an electrophysiologic model on closed-chest dogs. Nine groups (n = 6) of pentobarbital-anesthetized dogs were given atropine, 0.2 mg/kg intravenously (i.v.), and bupivacaine, 4 mg/kg i.v., over a 10-s period. Group 1 was then given only saline solution. Group 2 was given clonidine, 0.01 mg/kg i.v., over a 1-min period. Group 3 was given clonidine followed by i.v. administration of yohimbine, 1 mg/kg, an alpha 2-antagonist. Group 4 was given carbachol, 1 mg/kg i.v., a long-lasting cholinergic agonist, over a 1-min period. Group 5 was given electrical stimulation of the left vagus nerve. Group 6 was given physostigmine, 0.1 mg/kg i.v., known to inhibit cholinesterase degradation, 5 min before bupivacaine administration, and Group 7 received a combination of physostigmine pretreatment and electrical vagal stimulation. Group 8 was given physostigmine, 0.1 mg/kg i.v., and pancuronium bromide, 1 mg/kg i.v., known to inhibit nicotinic receptors, 5 min before bupivacaine administration. Then electrical stimulation of the left vagus nerve was performed. Group 9 was given nicotine, 0.1 mg/kg i.v., 1 min after bupivacaine injection over 1 min. Bupivacaine induced bradycardia, markedly increased the His-Purkinje conduction time (HV interval) and QRS duration. Bupivacaine decreased the peak of first derivative of left ventricle pressure (LVdP/dtmax) and increased left ventricular end-diastolic pressure (LVEDP). Clonidine improved QRS duration and HV interval. Yohimbine did not modify the effects of clonidine. QRS duration and HV interval were significantly improved in Groups 4-7. In Group 8, pancuronium pretreatment inhibited the beneficial effects of the combination of physostigmine pretreatment and electrical vagal stimulation. In contrast, in Group 9, like clonidine, nicotine improved QRS duration and HV interval. Three other groups of anesthetized dogs (n = 6) were then studied. All dogs were given hexamethonium, 10 mg/kg i.v. Then, Group 10 was given only saline solution; Group 11 was given bupivacaine, 4 mg/kg, and Group 12 was given bupivacaine and nicotine as in Group 9. In Group 11, bupivacaine induced its usual alterations. In contrast, nicotine did not modify the cardiotoxic profile of bupivacaine after hexamethonium pretreatment. We conclude that the beneficial effect of clonidine on the variables of ventricular conduction altered by bupivacaine 1) is not mediated by central alpha 2-activation, 2) is mediated by the activation of parasympathetic pathways, and 3) is indirect and not mediated by acetylcholine release but is mediated by the activation of parasympathetic ganglionic nicotinic receptors.(ABSTRACT TRUNCATED AT 400 WORDS)
[Show abstract][Hide abstract]ABSTRACT: Some reports suggest that activation of the autonomic nervous system by bupivacaine could participate in its cardiotoxicity. This is based in part on the fact that hexamethonium suppresses cardiac disturbances in anesthetized rabbits given small intracerebroventricular doses of bupivacaine. The aims of the current study were to determine, in anesthetized dogs, (1) whether the activation of the autonomic nervous system is deleterious after a large intravenous dose of bupivacaine and (2) whether the parasympathetic or sympathetic system is implicated in the bupivacaine-induced deleterious activation of the autonomic nervous system.
We used an electrophysiologic model in closed-chest dogs anesthetized with sodium pentobarbital. In group 1 (n = 6), dogs were given 4 mg/kg intravenous bupivacaine over 10 s. In group 2 (n = 6), dogs were given the same dose of bupivacaine 5 min after having received 0.2 mg/kg intravenous atropine sulfate. In group 3 (n = 9), dogs were pretreated with 10 mg/kg intravenous hexamethonium and then given bupivacaine 4 mg/kg. In addition, in group 3, the right atrium was paced at a basic cycle length of 400 ms to obtain a heart rate similar to that of group 1.
Bupivacaine in group 1 induced significant bradycardia; lengthening of PR, atria-His, His-ventricle, and QTc intervals; and QRS widening. The first derivative of left ventricular pressure was significantly decreased, whereas left ventricular end-diastolic pressure was increased. Atropine pretreatment did not modify cardiac disturbances induced by bupivacaine. Hexamethonium pretreatment induced significantly less QRS widening and QTc lengthening than was seen in group 1 but worsened the bupivacaine effects on bradycardia, atria-His and PR intervals, mean aortic pressure, and first derivative of left ventricular pressure. Moreover, atrial pacing in group 3 induced alterations of QRS similar to those in group 1.
Considering that marked slowing of ventricular conduction velocity (i.e., QRS widening) is known to facilitate reentrant ventricular arrhythmias, we conclude that (1) the activation of the autonomic nervous system by bupivacaine is not as deleterious as previously suggested; (2) the parasympathetic system is not markedly implicated in the worsening of direct bupivacaine cardiotoxicity; and (3) the sympathetic nervous system acts only by inducing a less marked bradycardia, which slows ventricular conduction velocity in a use-dependent manner, facilitating reentrant arrhythmias.
[Show abstract][Hide abstract]ABSTRACT: Although potassium channel openers have been demonstrated to induce arterial vasodilation and shortening of the QT interval, the complete in vivo hemodynamic and electrophysiologic profile of these drugs has not been fully established. We evaluated the effects of BRL 38227, the active enantiomer of cromakalim, on the electrophysiologic and hemodynamic parameters in anesthetized dogs. Four intravenous (i.v.) doses (0.01, 0.03, 0.1, and 0.3 mg/kg) of BRL 38227 (lemakalim) were given to four different groups of 6 anesthetized and mechanically ventilated dogs. Electrophysiologic and hemodynamic parameters were measured with bipolar catheters positioned in the right atria and the right ventricle and double micromanometers placed in the left ventricle and the aorta. Nine dogs died of ventricular fibrillation (VF; 6 of 6 after 0.3 mg/kg, 2 of 8 dogs after 0.1 mg/kg, and 1 of 7 dogs after 0.03 mg/kg BRL 38227). Three dogs had atrial tachycardia (1 had atrial flutter and 1 had atrial fibrillation after 0.03 mg/kg, and 1 had atrial fibrillation after 0.01 mg/kg BRL 38227). BRL 38227 did not modify heart rate (HR), corrected sinus recovery time (CSRT), and atrial or atrio-ventricular (A-V) conduction times. In contrast, PR interval, Luciani-Wenckebach cycle length (LW), HV interval, QRS duration, ventricular effective refractory period (VERP), QT interval, and monophasic action potential (AP) were significantly shortened in a dose-dependent manner. Left ventricular end-diastolic pressure (LVEDP) was not modified, whereas LVdP/dtmax decreased significantly at 0.1 mg/kg BRL 38227. Finally, there was a significant dose-dependent decrease in systolic, diastolic, and mean aortic blood pressure (SBP, DBP, MAP). We conclude that BRL 38227 shortens the ventricular parameters of conduction velocity and of repolarization and decreases BP, both in a dose-dependent manner. All doses were arrhythmogenic, suggesting that BRL 38227 has a low safety margin.
Article · Dec 1993 · Journal of Cardiovascular Pharmacology
[Show abstract][Hide abstract]ABSTRACT: Bupivacaine is more cardiodepressant than lidocaine. Nevertheless, the marked depression of contractility induced by bupivacaine cannot be completely explained by its electrophysiologic properties alone. Biophysical differences such as the greater lipid solubility of bupivacaine versus lidocaine must be taken into consideration. Perhaps more bupivacaine enters the cardiac cells and interacts with contractile processes. To test this hypothesis, the entry of lidocaine into the cells was facilitated by a membrane-permeant lipophilic anion, tetraphenylboron. We compared the spontaneous atrial rate and the contractile force of rabbit right atria bathing in solutions containing either 0.5 microgram/mL lidocaine or bupivacaine. Group 1 (n = 8) served to test the stability of the preparation. In group 2 (n = 6), tetraphenylboron (17 micrograms/mL) was added to Tyrode's solution; atrial rate was decreased by 8% and contractile force by 1.7%. In group 3 (n = 6), bupivacaine (0.5 microgram/mL) was added; bupivacaine decreased atrial rate by 11.3% and markedly depressed contractile force by 68.3%. In group 4 (n = 6), lidocaine (0.5 microgram/mL) was added; lidocaine did not change atrial rate but decreased contractile force by 6.0%. In group 5 (n = 6), both lidocaine and tetraphenylboron were added; atrial rate was decreased by 15.5% and contractile force was markedly depressed by 81.1%. In group 6 (n = 6), 0.2 mM adenosine triphosphate, tetraphenylboron, and then lidocaine were added; the addition of adenosine triphosphate partially counteracted the cardiodepressant effects of the combination of lidocaine and tetraphenylboron. Atrial rate was decreased by 10.4% and contractile force was depressed by 13.6%.(ABSTRACT TRUNCATED AT 250 WORDS)
[Show abstract][Hide abstract]ABSTRACT: The ability of clonidine and dobutamine to correct bupivacaine-induced cardiac electrophysiologic and hemodynamic impairment was evaluated in an experimental electrophysiologic model on closed-chest dogs. Five groups (n = 6) of pentobarbital-anesthetized dogs were given atropine (0.2 mg/kg IV). Group 1 was given a saline solution; all other dogs were given bupivacaine (4 mg/kg IV) over a 10-s period. Group 2 was given only bupivacaine. Group 3 was given clonidine (0.01 mg/kg IV) over a 1-min period. Group 4 was given a dobutamine infusion at 5 micrograms.kg-1.min-1. Group 5 was given the combination of clonidine and dobutamine. Bupivacaine induced bradycardia, prolonged atrioventricular conduction time (PR interval), atrioventricular node conduction time (AH interval), His-Purkinje conduction time (HV interval), and QRS duration. Bupivacaine decreased left ventricular (LV) dP/dt max and increased LV end-diastolic pressure (LVEDP). Clonidine improved QRS duration and HV interval but enhanced AH interval, bradycardia, and hemodynamic depression induced by bupivacaine. Dobutamine infusion improved LV dP/dt max but did not modify bupivacaine-induced ventricular electrophysiologic impairment. The combination of clonidine and dobutamine corrected not only the electrophysiologic impairment induced by bupivacaine but also the hemodynamic depression. As the HV interval and the QRS duration could be correlated with ventricular conduction velocities, we conclude that (a) clonidine reversed the slowing of ventricular conduction velocities induced by bupivacaine, and (b) the combination of clonidine and dobutamine was able to correct the cardiac disturbances induced by bupivacaine in anesthetized dogs.
[Show abstract][Hide abstract]ABSTRACT: The intravascular injection of a large dose of bupivacaine induces electrophysiological cardiac impairment, mainly by slowing ventricular conduction velocity, and haemodynamic depression, by a decrease in myocardial contractility. When cardiotoxicity occurs, succinylcholine rapidly stops convulsions. However, the possible interactions between bupivacaine and succinylcholine on cardiac electrophysiology and haemodynamic status have never been investigated. Thus, we used an experimental electrophysiological model involving closed-chest dogs. Three groups (n = 6) of pentobarbital-anaesthetized dogs were given 0.2 mg.kg-1 atropine iv. Dogs in Group 1 were given saline. The others received 4 mg.kg-1 bupivacaine iv over ten seconds. Dogs in Group 2 were then given saline and those in Group 3 were then given 2 mg.kg-1 succinylcholine iv from one to two minutes after the administration of bupivacaine. The following electrophysiological variables were measured: heart rate represented by RR interval (RR), PR, atria-His (AH), and His-ventricle (HV) intervals, QRS duration, and QT interval corrected for heart rate (QTc). The following haemodynamic variables were measured: mean aortic pressure (MAoP), the peak of the first derivative of left ventricular pressure (LV dP/dt max), and LV end diastolic pressure (LVEDP). Comparison between Groups 1 and 2 showed that bupivacaine induced more than 100% HV interval lengthening and QRS widening (P less than 0.01), prolonged QTc interval by more than 25% (P less than 0.01), and decreased LV dP/dt max by more than 50% (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Article · Mar 1992 · Canadian Journal of Anaesthesia
[Show abstract][Hide abstract]ABSTRACT: A common property of all Class I antiarrhythmic agents is the inhibition of the fast inward current INa. Consequently, ventricular conduction velocities are impaired and reentrant phenomena are counteracted. Unfortunately, these conductive pathway disturbances may also induce proarrhythmic effects and reduce cardiac contractility. Recent evidence indicates that a cholinergic agonist, carbachol, is able to correct in vitro both the duration of the action potential and the partial depolarization induced by lidocaine and quinidine in rabbit atria. In the present study, we demonstrated that i.v. carbachol is also a powerful agent in vivo for correcting conductive disturbances previously induced by four different Class I antiarrhythmic agents. The electrophysiological and hemodynamic parameters of ten groups of atropinized-anesthetized dogs, including six animals per group, were investigated. QRS duration, HV and V-St intervals were selected as in vivo indexes of ventricular conduction. Quinidine, procainamide, cibenzoline and flecainide were selected as representative agents of Class Ia and Ic antiarrhythmic drugs. In all treated groups, carbachol (1 mg/kg) was able to correct the indexes of ventricular conduction previously impaired by the antiarrhythmic drug used.