Recent insights into paroxysmal supraventricular tachycardia--an integrated approach to diagnosis and therapy.
Paroxysmal supraventricular tachycardia may result from re-entrance in the AV node, the normal A-V pathway with an accessory AV connection, in the sino-atrial node, in the atria, or else reflect ectopic impulse formation in a spontaneously automatic supraventricular focus. Electrocardiographic criteria which are helpful in differentiating these mechanisms involve an analysis of cycle length, changes in cycle length with intermittent bundle branch block, P wave morphology and the relationship of P wave to QRS complex, P-R interval, the presence of A-V block during tachycardia and the influence of autonomic tone on the tachycardia. Electrophysiologic studies further elucidate mechanism by demonstrating the mode of induction and termination of the tachycardia, the characteristics of antegrade and retrograde A-V conduction curves and refractory periods, atrial activation sequence of echo beats and the influence of premature beats introduced during tachycardia. These features are summarised in Table 1. Therapy can be accurately planned according to the results of experimental administration of antiarrhythmic agents and of pacing sequences upon induction and termination of tachycardia in the catheterisation laboratory.
D000328:Adult; D000818:Animals; D001283:Atrioventricular Node; D004071:Digitalis Glycosides / Q000627:therapeutic use; D004285:Dogs; D004562:Electrocardiography; D006325:Heart Atria; D006801:Humans; D011433:Propranolol / Q000627:therapeutic use; D011817:Rabbits; D012849:Sinoatrial Node; D013614:Tachycardia, Paroxysmal / Q000175:diagnosis* / Q000188:drug therapy
D004071:Digitalis Glycosides; D011433:Propranolol