Class I Drugs

Class I antiarrhythmic drugs are characterized by their ability to block the voltage-gated sodium channel. The class I agents may block the channel when it is in either the open or the inactivated state. Inhibition of the sodium channel results in a decrease in the rate of rise of phase 0 of the cardiac membrane action potential and a slowing of the conduction velocity. Additionally, class I drugs, through inhibition of the sodium channel, require that a more hyperpolarized membrane potential (more negative) be achieved before the membrane becomes excitable and can propagate an excitatory stimulus. As a result, the ERP of fast-response fibers is prolonged. Although many class I antiarrhythmic drugs possess local anesthetic actions and can depress myocardial contractile force, these effects are usually observed only at higher plasma concentrations.

The antiarrhythmic drugs in class I suppress both normal Purkinje fiber and His bundle automaticity in addition to abnormal automaticity resulting from myo-cardial damage. Suppression of abnormal automaticity permits the sinoatrial node again to assume the role of the dominant pacemaker.

The antiarrhythmic agents that belong to class I are divided into three subgroups (Table 16.1) with slightly different properties. Class IA drugs slow the rate of rise of phase 0 (Vmax>) of the action potential and prolong the ventricular ERP. Members of this class impair the function of the membrane sodium channel, thereby decreasing the number of channels available for membrane depolarization. Class IA drugs do not alter the resting membrane potential. Because they decrease Vmax>, class IA drugs slow conduction velocity. Members of this class directly decrease the slope of phase 4 depolarization in pacemaker cells, especially those that arise outside of the sinoatrial node.

Members of class IB have a minimal effect on the rate of depolarization and are characterized by their ability to decrease the duration of action potential and ERP of Purkinje fibers. Members of this class have a minimal effect on conduction velocity in ventricular myocardium and are without apparent effect on refractoriness.

The drugs in class IC produce a marked depression in the rate of rise of the membrane action potential and have minimal effects on the duration of membrane action potential and ERP of ventricular myocardial cells.

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