Moreover, lidocaine possesses a dissociation constant (pKa) of 7.7 and is considered a weak base. Subsequently, in cardiac myocytes, lidocaine can potentially block or otherwise slow the rise of cardiac action potentials and their associated cardiac myocyte contractions, resulting in possible effects like hypotension, bradycardia, myocardial depression, cardiac arrhythmias, and perhaps cardiac arrest or circulatory collapse. In particular, such cardiac effects are likely associated with the principal effect that lidocaine elicits when it binds and blocks sodium channels, inhibiting the ionic fluxes required for the initiation and conduction of electrical action potential impulses necessary to facilitate muscle contraction. The net effect is normally a modest hypotension when the recommended dosages are not exceeded. With central neural blockade these changes may be attributable to the block of autonomic fibers, a direct depressant effect of the local anesthetic agent on various components of the cardiovascular system, and/or the beta-adrenergic receptor stimulating action of epinephrine when present. Duration of action potential and effective refractory period are also reduced.Įxcessive blood levels of lidocaine can cause changes in cardiac output, total peripheral resistance, and mean arterial pressure. In the heart, lidocaine reduces depolarisation of the ventricles during diastole and automaticity in the His-Purkinje system. It stabilises the neuronal membrane and inhibits Na ion movements, which are necessary for conduction of impulses. Depo-medrol With Lidocaine is an amide type local anaesth.
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