MARK E. JOSEPHSON, M.D.; JOHN A. KASTOR, M.D., F.A.C.P.
Grant support: in part by grants from the National Institutes of Health (HL 14807) and the American Heart Association, Southeastern Pennsylvania Affiliate.
▸Requests for reprints should be addressed to Mark E. Josephson, M.D.; 669 White Building, Hospital of the University of Pennsylvania, 3400 Spruce St.; Philadelphia, PA 19104.
JOSEPHSON ME, KASTOR JA. Supraventricular Tachycardia: Mechanisms and Management. Ann Intern Med. 1977;87:346-358. doi: 10.7326/0003-4819-87-3-346
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Published: Ann Intern Med. 1977;87(3):346-358.
The phrase paroxysmal supraventricular tachycardia describes a group of arrhythmias with similar electrocardiographic features but different mechanisms that have been clarified in recent years with specialized intracardiac recording and pacing techniques. Reentry accounts for most cases and has been localized to the A-V node and less frequently to the sinus node, the atria themselves, and A-V nodal bypass tracts (Wolff-Parkinson-White syndrome). These forms of supraventricular tachycardia are initiated by premature beats that dissociate conduction between two pathways and permit the establishment of circulating electrical activity that spreads to atrial and ventricular myocardium. Paroxysms cease when the conducting properties of the reentrant circuits are disturbed by changes in autonomic tone or the application of certain drugs, pacing, or cardioversion. Supraventricular tachycardia may also result from abnormal automaticity in atrial tissues. Such automatic atrial tachycardias are often associated with A-V block ("paroxysmal atrial tachycardia with block") and may be due to digitalis intoxication. This arrhythmia is treated by withdrawal of digitalis or administration of antiarrhythmic drugs that decrease automaticity.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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