[Resuscitation in a toxic cardiac accident involving bupivacaine. Experimental study].
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Animals↗
Biomedical subjects
B Bassoul
Publications and source records attributed to B Bassoul.
[Nalbuphine versus pentazocine in the period following surgery of the digestive system in patients with cardiovascular disease].
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Aged↗
[Mechanisms of the cardiac toxicity of bupivacaine].
Of all the amide local anaesthetics, bupivacaine is said to be the most cardiotoxic. This toxicity is seen mostly when there is a sudden increase in the plasma concentration of bupivacaine. It involves both, or either, electrical and mechanical structures within the heart. The main site of action on cardiac conduction tissue is the Vmax of phase 0 of the action potential of fast-reacting structures (INa current). Bupivacaine, like lidocaine and the other class I antiarrhythmic drugs, blocks the sodium channels, this block being more slowly reversible. The disturbance of sodium channels throughout the heart leads to a decreased conduction speed throughout the conduction system, thus explaining possible acute conduction disturbances originating below the bundle of His. The ventricular dysrhythmias described are due to a re-entry circuit secondary to a slowing in conduction speed. However, the sinus bradycardias and junctional disturbances seen in toxic accidents are probably due to an inhibition of the slow current of the atrial and atrio-ventricular nodes (Isi current). The experimental observation of an increase in the atrial monophase potential and the corrected QT interval suggests that repolarization currents are also involved (IK current ?). It would therefore seem that modifications in membrane permeabilities are the cause of the seriousness of the clinical picture. Bupivacaine, at toxic levels, has a direct effect on contractility. The negative inotropic effects seem to be due to a fall in the intracytoplasmic calcium concentration on which depends the excitation-contraction couple, as well as disturbed cellular energetic events dependent on the contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
Action Potentials↗
Reduction by carbachol of ventricular conduction impairments induced by various class I antiarrhythmic drugs in anesthetized dogs.
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.
Anesthesia↗