The most common form of conduction disturbance affects the AV node, causing various degrees of heart block. The result can be a simple slowing of impulse propagation through the AV node, which is reflected by an increase in the PR interval of the ECG. At the extreme, the result can be complete heart block, where no impulses are conducted from the atria to the ventricles. In this situation, ventricular activity is generated by a latent pacemaker, such as a Purkinje cell. Because the AV node is typically under the tonic influence of the parasympathetic nervous system, which slows conduction, AV block can sometimes be relieved by antimuscarinic agents like atropine.
A serious form of conduction abnormality involves reentry (also known as “circus movement”). In this situation, one impulse reenters and excites areas of the heart more than once. The path of the reentering impulse may be confined to very small areas, such as within or near the AV node or where a Purkinje fiber makes contact with the ventricular wall (Figure 14–6), or it may involve large portions of the atria or ventricles. Some forms of reentry are strictly anatomically determined. For example, in Wolff-Parkinson-White syndrome, the reentry circuit consists of atrial tissue, the AV node, ventricular tissue, and an accessory AV connection (bundle of Kent, a bypass tract). Depending on how many round trips through the pathway a reentrant impulse makes before dying out, the arrhythmia may be manifest as one or a few extra beats or as a sustained tachycardia. Circulating impulses can also give off “daughter impulses” that can spread to the rest of the heart. In cases such as atrial or ventricular fibrillation, multiple reentry circuits may meander through the heart in apparently random paths, resulting in the loss of synchronized contraction.
An example of how reentry can occur is illustrated in Figure 14–6. In this scenario, there are three key elements: (1) First is an obstacle (anatomic or physiologic) to homogeneous impulse conduction, thus establishing a circuit around which the reentrant wave front can propagate. (2) The second element is unidirectional block at some point in the circuit. That is, something has occurred such that an impulse reaching the site initially encounters refractory tissue. This can occur under conditions such as ischemia,
TABLE 14–1 Molecular and genetic basis of some cardiac arrhythmias.
1Ankyrins are intracellular proteins that associate with a variety of transport proteins including Na+ channels, Na+/K+-ATPase, Na+, Ca2+ exchange, and Ca2+ release channels. 2Also known as Andersen syndrome. 3Also known as Timothy syndrome; multiple organ dysfunction, including autism. 4CPVT, catecholaminergic polymorphic ventricular tachycardia; mutations in intracellular ryanodine Ca2+ release channel or the Ca2+ buffer protein, calsequestrin, may result in enhanced sarcoplasmic reticulum Ca2+ leakage or enhanced Ca2+ release during adrenergic stimulation, causing triggered arrhythmogenesis. 5HCN4 encodes a pacemaker current in sinoatrial nodal cells; mutations in sodium channel gene (SCN5A) cause conduction defects. GF, gain of function; LF, loss of function; LQT, long QT syndrome; PCCD, progressive cardiac conduction disorder; SQT, short QT syndrome.
A. Normal conduction B. Unidirectional block