Electrophysiology and Indications for Pacing in the ‘8O’s*

Bradycardias originate either from a dysfunction of impulse formation in the sinoatrial node or from a disturbed conduction of the impulse. Different pathogenetic mechanisms are discussed as causes of tachyarrhythmias; circus movement (re‐entry) is primarily due to pathological changes in conduction and refractoriness. Focal impulse formation results from local disturbances of depolarization and repolar‐ization of the cell membrane: increased automaticity, abnormai outomaticity, triggered activity. Symptomatic bradycardias still represent the standard indication for cardiac pacing particularly with implantable pacemakers. Based on clinical electrophysiology, various types of pacemakers are available at present: atrial triggered and atrial pacing pacemakers, AV‐sequential pacemakers, ventricuiar demand‐pacemakers, stand‐by pacemakers, and fixed rate pacemakers. The multiprogrammability of newer pacemaker devices is a very useful tool in avoiding secondary interventions. For antitachycardia pacemaker therapy there are essentially three methods in use: 1. overdrive pacing to prevent re‐entry phenomena and automaticity and also to suppress tachyarrhythmias based on increased or abnormai automaticity; 2. competitive stimulation for termination of tachycardias by means of single impulses; and 3. rapid atrial stimulation to convert atrial flutter into atrial fibrillation and consequently to normal sinus rhythm. In very rare cases rapid ventricular stimulation is mandatory. The positive results achieved with temporary stimulation methods have led to the development of permanent (impiantable) antitachycardia pacemakers for long‐term therapy, which have proven to be a low‐risk alternative in drug‐resistant tachyarrhythmias. (PACE, Vol. 5, July‐August, 1982)