The arrhythmogenic mechanisms are the basis for the genesis of a wide variety of complex dysrhythmias that can arise in both pacemaker and nonpacemaker cells. Automaticity, or the ability to rhythmically and spontaneously depolarize cardiac cells, is normally the domain of the sinus node. Altered automaticity takes place when conduction is enhanced or abnormal. A second mechanism, reentry, refers to a phenomenon that occurs when an impulse is delayed within a pathway of slow conduction and then reenters surrounding tissue and produces another impulse. One-way conduction is necessary to produce a return route for the reentrant circuit. Lastly, late potentials are fragmented, low-amplitude electrical currents that occur at the terminal portion of the QRS complex or during the ST segment. Supraventricular and ventricular beats and tachydysrhythmias are the consequences of these mechanisms. Common contributing factors include but are not limited to hypoxia, hypercapnia, electrolyte disturbance, catecholamines, and pharmacotherapy

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