cardiovascular disorders
Overview of Arrhythmias
Pathophysiology of Arrhythmias
Rhythm disturbances result from abnormalities of impulse formation, impulse conduction, or both. Bradyarrhythmias result from decreased intrinsic pacemaker function or blocks in conduction, principally within the AV node or the His-Purkinje system. Most tachyarrhythmias are caused by reentry; some result from enhanced normal automaticity or from abnormal mechanisms of automaticity. Reentry is the circular propagation of an impulse around 2 interconnected pathways with different conduction characteristics and refractory periods (see figure Mechanism of typical reentry ). Atrioventricular nodal reentry is used here as an example. Two pathways connect the same points. Pathway A has slower conduction and a shorter refractory period. Pathway B conducts normally and has a longer refractory period. I. A normal impulse arriving at 1 goes down both A and B pathways. Conduction through pathway A is slower and finds tissue at 2 already depolarized and thus refractory. A normal sinus beat results. II. A premature impulse finds pathway B refractory and is blocked, but it can be conducted on pathway A because its refractory period is shorter. On arriving at 2, the impulse continues forward and retrograde up pathway B, where it is blocked by refractory tissue at 3. A premature supraventricular beat with an increased PR interval results. III. If conduction over pathway A is sufficiently slow, a premature impulse may continue retrograde all the way up pathway B, which is now past its refractory period. If pathway A is also past its refractory period, the impulse may reenter pathway A and continue to circle, sending an impulse each cycle to the ventricle (4) and retrograde to the atrium (5), producing a sustained reentrant tachycardia. There is an abnormal P wave (P′) and atrioventricular nodal delay (long P′R interval) before onset of the tachycardia. Under certain conditions, typically precipitated by a premature beat, reentry can cause continuous circulation of an activation wavefront, causing a tachyarrhythmia (see figure Initiation of an atrioventricular nodal reentry tachycardia ). Normally, reentry is prevented by tissue refractoriness following stimulation. However, 3 conditions favor reentry: Shortening of tissue refractoriness (eg, by sympathetic stimulation) Lengthening of the conduction pathway (eg, by hypertrophy or abnormal conduction pathways) Slowing of impulse conduction (eg, by ischemia) 