ECG Review - SVT With An Answer by Ken Grauer, MD

Clinical Scenario: The 12-lead ECG in the Figure shown here was obtained from a young adult man with chest tightness. Might his symptoms be explained by the cardiac rhythm? What is the likely mechanism of this rhythm? (Hint: The probable answer lies with searching for atrial activity on this tracing!)

Interpretation: The rhythm is a regular supraventricular tachycardia (SVT) at a rate of just under 150 beats/minute. Atrial activity is not initially evident. For practical purposes, the differential diagnosis consists of three entities: 1) sinus tachycardia; 2) atrial flutter; and 3) paroxysmal supraventricular tachycardia (PSVT).

Definitive diagnosis of the etiology of this rhythm is not possible on the basis of this single 12-lead tracing. Nevertheless, several key presumptions can still be made. Of the three entities listed above, the one least likely to be present is atrial flutter. Despite the fact that the ventricular response in the Figure is very close to 150/minute (the most common ventricular rate seen with untreated atrial flutter)—there is not the slightest hint of flutter waves anywhere on the tracing. Atrial activity with a sawtooth pattern can usually be discerned if carefully looked for in at least one or more leads of a 12-lead tracing when flutter is present.

Sinus tachycardia is also unlikely to be the etiology of this arrhythmia. Admittedly, one can’t rule out the possibility that the small upright deflection at the midpoint of the R-R interval in lead II could be a P wave (or a combined P and T wave). However, in view of the rapid rate, we would usually expect a shorter PR interval than would be the case if this upright deflection in lead II was in fact concealing a P wave. Moreover, sinus P wave activity is also clearly lacking in lead V1 (the second best lead for detection of sinus conducted P waves).

By the process of elimination, PSVT is the most likely etiology of this arrhythmia. The mechanism of PSVT is most often reentry that typically involves at least a portion of the AV node. Confirmation that this mechanism is operative will sometimes be forthcoming from evidence of retrograde atrial activity during the tachycardia in several leads. Such activity is suggested here by the subtle slender negative deflections that occur at the end of the QRS complex in each inferior lead, as well as from the simulated r’ deflection in lead V1. Verification that these deflections truly represent reentry conduction during the tachycardia was established by their disappearance after the patient converted to sinus rhythm. This patient’s chest tightness also resolved with resumption of sinus rhythm.