ANTIARRHYTHMIC DRUGS

A. Causes of arrhythmias.
Arrhythmias may be due to both improper impulse generation and
impulse conduction. These manifest as abnormalities of rate or regularity or as
disturbances
in the normal sequence of activation of atria and ventricles.
1. Altered automaticity. Altered automaticity can arise from the following:

a. Sinus node (sinus tachycardia and bradycardia). Increased vagal activity

can impair
nodal pacemaker cells by elevating K1 conductance, leading to hyperpolarization.
Increased sympathetic activity increases the rate of phase 4 depolarization. Intrinsic
disease can produce faulty pacemaker activity (sick sinus syndrome).
b. Ectopic foci are areas within the conduction system that may, in the diseased state,
develop high rates of intrinsic activity and function as pacemakers.
c. Triggered automaticity results from delayed after-polarizations that reach threshold
and are capable of initiating an impulse.

2. Abnormal impulse conduction in conduction pathways

a. Heart blocks may produce bradyarrhythmias.
b. Reentry circus conduction may produce tachyarrhythmias.
B. Goals of therapy (Table 4.2)

1. Therapy aims to restore normal pacemaker activity and modify impaired conduction

that leads to arrhythmias.

2. Therapeutic effects are achieved by sodium- or calcium-channel blockade, prolongation
of effective refractory period, or blockade of sympathetic effects on the heart. Many
antiarrhythmic
drugs affect depolarized tissue to a greater extent than they affect normally
polarized tissue