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Supraventricular tachycardia may be defined as tachycardia in which the atrium or atrioventricular (AV) junction is the source or a vital link of the arrhythmia mechanism. Specific tachycardia entities have been traditionally cataloged descriptively using criteria such as atrial rate, P-wave contour, regularity of ventricular response, response to vagal stimulation, and mechanism.1 We have proposed a simple and clinically useful working classification that divides the supraventricular tachycardias into the “atrial” and “junctional” tachycardias (Table 6-1). The atrial tachycardias originate in the atria and are not affected by conduction over the AV node (“AV node-independent”) (Figure 6-1).
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Junctional tachycardias (Figure 6-2) require the AV node as a critical component of the tachycardia mechanism (“AV node-dependent”). The distinction can often be made clinically using vagal maneuvers or adenosine, observing the effect of AV node slowing or temporary block on the tachycardia. Adenosine may terminate some atrial tachycardias, possibly due to triggered activity, but termination may be preceded by a brief period of AV block in these cases. The AV reentrant tachycardias are considered in detail in Chapter 7.
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Sinus tachycardia is associated with a variety of physiologic and pathologic states resulting in increased sympathetic and decreased vagal stimulation of the sinus node. These are numerous and include exercise, anxiety, hypovolemia, hypoxia, fever, hyperthyroidism, and anemia. Agents such as alcohol and nicotine and many drugs with atropine-like or sympathomimetic effects cause sinus tachycardia. The heart rate is greater than 100/min (by definition) and can be 200/min or greater, although the maximal rate decreases with age. Sinus tachycardia is “non paroxysmal,” with a graduated onset and offset. It may be slowed transiently by carotid massage or other vagotonic manoeuvres. A shift in the site of the dominant pacemaker within the sinus node may cause ...