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The basic scientist is able to explore mechanisms experimentally in a controlled and rigorous fashion that can never be duplicated by the clinical electrophysiologist. On the other hand, the clinician is dealing with the actual pathologic entity and does not have to be concerned with the clinical relevance of the model. Basic and clinical information are complementary to the student of arrhythmias. The following will attempt to summarize basic tachycardia mechanisms, emphasizing highlights of interest to clinicians.


Tachycardia mechanisms have been traditionally classified as due to disorders of impulse formation, impulse conduction, or combinations of the two (Table 5-1).1

TABLE 5-1Mechanisms of tachycardia.

Abnormal Impulse Formation

Normal automaticity

All impulse formation results from localized changes in ionic currents that traverse cell membranes2,3. The natural pacemaker cells exhibit a phasic, spontaneous depolarization during diastole (phase 4), which results in an action potential when threshold potential is reached (Figure 5-1). These cells are found in the sinus node, parts of the atria, the atrioventricular (AV) junctional region, and the His-Purkinje system. In the normal heart, the sinus node is the dominant pacemaker, because it depolarizes most rapidly and remains dominant due to “overdrive suppression” of the subsidiary pacemakers.4 Subsidiary pacemakers may become dominant under certain conditions, such as sympathetic stimulation or ischemia. Digitalis may enhance the automaticity of subsidiary pacemakers by inhibiting extracellular Na+ transport that promotes Ca2+ entry into cells. By definition, automaticity can neither be initiated nor terminated by pacing techniques.


Action potentials from typical ventricular (Panel A), sinoatrial node (Panel B), and atrial (Panel C) cells. Cells with intrinsic automaticity show clear spontaneous depolarization during phase 4, typical of the SA node. Panel D is a representation of the major mechanisms responsible for changes in frequency of depolarization of a fiber with normal automaticity. A decrease in the slope of phase 4 (a to b) in the upper trace reduces frequency. A lowering (less negative) of threshold potential, TP-1 to TP-2, in the lower trace also prolongs cycle length, as does an increase in resting potential from a to d. (Reproduced with permission from Hoffman BF, Cranefield PF. Electrophysiology of the Heart. Mount Kisco, New York: Futura; 1976.)

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