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It’s now time to begin our discussion of arrhythmias, one of the most important aspects of clinical electrocardiography. In the last chapter, we reviewed the fate of the normal sinus depolarization, using either a simple or expanded laddergram to illustrate passage of the impulse through the AV node and the remainder of the specialized conduction system until activating the ventricles (Figure 13-1). A cardiac arrhythmia may be defined as any disruption or aberration of this normal electrical sequence from start to finish.

Figure 13-1.

Laddergram depicting the normal sequence of conduction during sinus rhythm.


There has been some debate regarding the proper term to describe abnormalities of the cardiac rhythm—arrhythmia or dysrhythmia. The ancient Greek meaning of rhythmos is “proportion, order, or symmetry.” Applying the prefix “a” indicates the absence of these characteristics. Therefore in the purest sense, the term arrhythmia means “no rhythm.” Using the prefix dys suggests ill, bad, or defective. One may then conclude that dysrhythmia should be the preferred choice to describe an abnormality of the cardiac rhythm. However, arrhythmia has the benefit of widespread usage and tradition. I consider the terms interchangeable, so you have my permission to use whichever term you prefer.


In Chapter 3 we reviewed in detail the components of the action potential and the two different types of cardiac cells, pacemaker and nonpacemaker. Let’s take another look to help us understand the mechanisms of arrhythmias.

In nonpacemaker cells the action potential is divided into five phases (0, 1, 2, 3, 4) (Figure 13-2a). Phase 0 represents rapid depolarization, which begins when an adjacent cell provides a stimulus that raises the membrane potential from a resting potential of −90 mV to the threshold potential of −60 mV to −70 mV. Phases 1, 2, and 3 represent repolarization and phase 4 is the resting phase between depolarizations. Nonpacemaker cells constitute the atrial and ventricular myocardium and cannot normally initiate spontaneous depolarization without an outside stimulus.

Figure 13-2.

Action potential of a nonpacemaker cell (a) and pacemaker cell (b). A nonpacemaker cell requires an outside stimulus (*) to raise the membrane potential from the resting potential (RP) to the threshold potential (TP), thereby initiating depolarization (phase 0). Pacemaker cells have the property of automaticity, which intrinsically increases the voltage from the maximum diastolic potential (MDP) until reaching the threshold potential.

In pacemaker cells the action potential has only three phases (0, 3, 4) (see Figure 13-2b). Pacemaker cells possess the property of automaticity, characterized by a phase 4 that slopes gradually upward from a maximum diastolic potential in the range of −60 mV until reaching ...

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