FIGURE 14–6 Schematic diagram of a reentry circuit that might occur in small bifurcating branches of the Purkinje system where they enter the ventricular wall. A: Normally, electrical excitation branches around the circuit, is transmitted to the ventricular branches, and becomes extinguished at the other end of the circuit due to collision of impulses. B: An area of unidirectional block develops in one of the branches, preventing anterograde impulse transmission at the site of block, but the retrograde impulse may be propagated through the site of block if the impulse finds excitable tissue; that is, the refractory period is shorter than the conduction time. This impulse then reexcites tissue it had previously passed through, and a reentry arrhythmia is established.
which cause an increase in extracellular potassium that partially depolarizes the resting membrane potential, slowing sodium channel recovery from inactivation and prolonging the refractory period in the affected area. (3) Finally, conduction time around the circuit must be long enough so that by the time the impulse returns to the site after traveling around the obstacle, the tissue is no longer refractory. In other words, conduction time around the circuit must exceed the effective refractory period duration in the area of unidirectional block. Representative ECGs of important arrhythmias are shown in Figures 14–7 and 14–8.
Unidirectional block can be caused by prolongation of refractory period duration due to depression of sodium channel activity in atrial, ventricular, and Purkinje cells. In the AV node, it may also be a result of depressed calcium channel activity. Drugs that
Panel 1: Normal sinus rhythm
Panel 2: Atrial flutter
Panel 3:
Panel 4: Ventricular tachycardia (starting at arrow)
Panel 5: Ventricular fibrillation
FIGURE 14–7 Electrocardiograms of normal sinus rhythm and some common arrhythmias. Major deflections (P, Q, R, S, and T) are labeled in each electrocardiographic record except in panel 5, in which electrical activity is completely disorganized and none of these deflections is recognizable. (Adapted, with permission, from Goldman MJ: Principles of Clinical Electrocardiography, 11th ed. McGraw-Hill, 1982. Copyright © The McGraw-Hill Companies, Inc.) abolish reentry may do so by further reducing excitability by blocking sodium (Figure 14–4) or calcium channels, thus converting an area of unidirectional block to bidirectional block. Drugs that block repolarizing potassium currents may also be effective in converting a region of unidirectional block to bidirectional block by prolonging action potential duration, and thereby increasing the refractory period duration.
Mechanisms of Action
Arrhythmias are caused by abnormal pacemaker activity or abnormal impulse propagation. Thus, the aim of therapy of the arrhythmias is to reduce ectopic pacemaker activity and modify conduction or refractoriness in reentry circuits to disable circus movement. The major pharmacologic mechanisms currently available for accomplishing these goals are (1) sodium channel blockade, (2) blockade of sympathetic autonomic effects in the heart, (3) prolongation of the effective refractory period, and (4) calcium channel blockade.