IM Board Review

A young man with an unusual cause of palpitations

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A 23-year-old man presents to the emergency department with the sudden onset of palpitations, lightheadedness, and dyspnea, accompanied by weakness and nausea, which started earlier in the evening. He estimates that he has experienced 15 similar episodes, lasting minutes to hours, since the age of 16, with the last one 3 years ago. These episodes typically end by themselves or with self-induced vomiting and lying supine. The current episode did not resolve with these maneuvers.

He has never received medical attention for these symptoms. He has no chest pain, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, or syncope. He has had no recent illness, contacts with sick people, or travel.

The patient’s history includes a “childhood heart murmur,” which resolved, and also mild asthma. He is otherwise healthy but has not received regular medical care. He used to play competitive soccer but quit because playing made his symptoms of dyspnea on exertion and palpitations much worse.

He uses marijuana frequently and alcohol occasionally. He does not smoke tobacco or use other recreational drugs. Other than infrequent use of albuterol, he does not take any prescription or over-the-counter medications. He has no allergies. He knows of no family history of arrhythmia or sudden cardiac death.

Physical examination. On initial examination, his temperature is 36.4°C (97.5°F), heart rate 230 bpm, systolic blood pressure 60 mm Hg, respiratory rate 30 breaths per minute, oxygen saturation 100% while breathing room air, and body mass index 25 kg/m2.

The patient's initial electrocardiogram

Figure 1. The patient’s electrocardiogram on presentation demonstrates regular wide complex tachycardia with a heart rate of 260 bpm. Note the “buried” retrograde P waves, best seen in the continuous strip of lead II (circle). This is consistent with supraventricular tachycardia with aberrancy, where the atrial impulse is conducted down an accessory pathway, resulting in a regular wide complex QRS.

He is awake, anxious, and appears ill. He speaks only in short sentences. A focused cardiac examination reveals a regular tachycardia with no appreciable murmur or extra heart sounds; the apical impulse is not displaced. His lungs are clear. His abdomen is soft and nontender. He has 2+ pulses on a scale of 0 to 4+, with no peripheral edema.

His initial electrocardiogram (ECG) (Figure 1) shows a heart rate of 260 bpm and a regular wide complex tachycardia, defined as a rate greater than 100 bpm and a QRS complex wider than 0.12 seconds.


1. Which of the following is not in the differential diagnosis of regular wide complex tachycardia?

  • Monomorphic ventricular tachycardia
  • Orthodromic atrioventricular reentrant tachycardia
  • Antidromic atrioventricular reentrant tachycardia
  • Sinus tachycardia with bundle branch block

Orthodromic atrioventricular reentrant tachycardia is not in the differential diagnosis.

Wide complex tachycardia can occur when the impulse originates outside the normal conduction system or when there is abnormal ventricular activation through the atrioventricular (AV) node and His-Purkinje system.

The main distinction to make when diagnosing the cause of a wide complex tachycardia is between the following:

Monomorphic ventricular tachycardia, which originates from a single ventricular focus that depolarizes the adjacent myocardium in a stepwise fashion, causing a wide QRS complex that does not begin in the native conduction system, and

Sinus tachycardia with bundle branch block, ie, supraventricular tachycardia with aberrant conduction within the normal conduction system.

Electrical conduction in atrioventricular reentrant tachycardia

Figure 2.

Three different conduction patterns are seen with atrioventricular reentrant tachycardia (Figure 2):

Sinus depolarization (Figure 2), in which the atrial impulse travels down the AV node, and the accessory pathway can be hidden and not contribute to the surface ECG.

Orthodromic atrioventricular reentrant tachycardia (Figure2), in which the depolarizing impulse travels antegrade down the AV node, then propagates from the ventricle back to the atria via the accessory pathway, resulting in a narrow QRS.

Antidromic atrioventricular reentrant tachycardia (Figure 2), in which the depolarization travels antegrade down the accessory pathway then propagates from the ventricle back to the atria via the AV node, resulting in a wide complex QRS with a delta wave.

Important features of the patient’s electrocardiogram (Figure 1) are consistent with antidromic atrioventricular reentrant tachycardia:

  • “Buried” retrograde P waves, which are best seen in the continuous strip of lead II as a positive deflection notching in the negative nadir of the wave
  • The PR segment is short, suggesting retrograde atrial depolarization
  • The P wave is followed by a slow slurred upstroke (delta wave), best seen in lead I.

Treatment depends on diagnosis

Distinguishing supraventricular tachycardia from ventricular tachycardia is important, as the treatments differ. Supraventricular tachycardia is treated with adenosine, calcium channel blockers, and beta-blockers, which are not only ineffective for ventricular tachycardia, but rarely may precipitate hemodynamic deterioration.

Also important is distinguishing pre-excitation atrial fibrillation from other types of supraventricular tachycardia with aberrancy, because the nodal blockade used to treat other causes of the condition may worsen the tachycardia via the accessory pathway. If pre-excitation atrial fibrillation is suspected on the basis of an irregular wide complex tachycardia with delta waves on ECG, then procainamide—a sodium channel blocker that affects the cardiac action potential and prolongs the refractory period of the accessory pathway—can be used to help control the arrhythmia.1

Brugada criteria aid diagnosis

Adapted from Brugada P, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991; 83:1649–1659, with permission from Lippincott Williams & Wilkins.

Figure 3.

In 1991, Brugada et al2 devised an algorithm to differentiate ventricular tachycardia from supraventricular tachycardia with aberrancy in the setting of regular wide complex tachycardia (Figure 3). It has a sensitivity of 98.7% and a specificity of 96.5% for diagnosing ventricular tachycardia and 96.5% sensitivity and 98.7% specificity for diagnosing supraventricular tachycardia with aberrant conduction. Using the algorithm, only 11 (ie, 2%) of the 544 tachycardias in their study were misclassified.2–4

The Brugada algorithm consists of four criteria, with the presence of any leading to a diagnosis of ventricular tachycardia:

  • Absence of an RS complex in all precordial leads (the QRS complexes in precordial leads have all negative or all positive deflections).
  • An RS interval in at least one precordial lead of at least 100 ms (the interval is measured from the onset of R to the nadir of the S wave).
  • AV dissociation, as determined by the existence of P waves marching out independent of the QRS complexes, capture beats (narrow QRS complexes resulting from the rare occasion when an intrinsic P wave conducts down the native pathway), or fusion beats (combined capture beat and ventricular beat, resulting in a different morphology than most of the wide QRS complexes present).
  • Leads V1, V2, and V6 satisfying the classic morphologic criteria for ventricular tachycardia.

If none of these criteria are met, supraventricular tachycardia is diagnosed.

In our patient, we can further confirm the diagnosis of antidromic atrioventricular reentrant tachycardia by using Brugada criteria to exclude ventricular tachycardia (Figure 3): the ECG (Figure 1) shows an RS complex in multiple precordial leads, the maximum RS interval is less than 100 ms in the precordial leads, there is no evidence of AV dissociation (lead II in the continuous strip shows buried P waves associated with QRS), and morphologic criteria are not met for ventricular tachycardia in leads V1, V2, and V6.

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