Pharmacology Of Antidysrhythmic And Vasoactive Medications

Teresa M. Carlin AntjdysrhythmicAflents

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Chapter, References

To understand antidysrhythmic therapy, one must be familiar with the cardiac cycle. The action potential is made up of four phases, with phase 4 representing diastole. During diastole, pacemaker cells slowly depolarize (automaticity) while all other myocytes are electrically quiescent. Once the pacemaker reaches threshold, through propagation of an action potential, myocardial cells rapidly depolarize in coordinated fashion because of influx of sodium through voltage-dependent sodium channels (phase 0). The efflux of potassium down its concentration gradient initiates repolarization (phase 1). The phase 2 plateau occurs when ion fluxes across membranes are in equilibrium—namely, calcium influx via slow calcium channels and potassium efflux. The influx of calcium allows the heart to contract. During phase 3, the calcium channels close and potassium permeability increases, which permits rapid repolarization. The beginning of phase 0 (rapid depolarization) until midway through phase 3 (rapid repolarization) represents the absolute refractory period. During the effective refractory period (ERP), a second action potential cannot be elicited. (Fig 25-1).

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FIG. 25-1. Ventricular myocardial cell transmembrane action potential.

The Vaughan Williams classification of antidysrhythmics groups drugs based on their ability to block sodium channels (class I), block calcium channels (class IV), block beta-adrenergic receptors (class II), or prolong the refractory period (class III) ( T§bIe„25,-1). Digoxin and adenosine do not fit into this scheme.

Class Antidysrhythmics

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