[The authors respond]

Letters

CJEM 2009;11(2):124-125

We thank Drs. Healey, Mensour and Marshall for their interest in our diagnostic challenge published in the November 2008 issue of CJEM.1 They summarize their comment on our article by stating, "The safest approach for the emergency physician is to treat all wide complex tachycardias as ventricular tachycardia (VT)." As we indicated,1 we essentially agree with this point of view, with one notable exception. We welcome the opportunity to further discuss this distinction.

The correspondents posit that "one can rarely be certain of the diagnosis and should routinely proceed with the treatment of wide complex tachycardia as VT" by sedating and shocking the patient. We contend that, in treating a stable patient, supraventricular tachycardia (SVT) with aberrant conduction can be distinguished from VT with sufficient frequency to warrant the effort. Although the default position in uncertain cases is to treat as VT, when the rhythm is SVT with aberrant conduction, the American Heart Association guidelines for emergency care2 recommend adenosine as first-line therapy.

Our diagnostic challenge included an electrocardiogram (ECG) showing a regular, wide QRS tachycardia with typical left bundle branch block (LBBB) morphology. The differential diagnosis in this case includes VT and SVT with LBBB. The latter includes sinus tachycardia, true atrial tachycardia, atrioventricular (AV) nodal re-entry and orthodromic reciprocating tachycardia in a patient with Wolff-Parkinson-White (WPW) syndrome (down the normal conduction pathway and up the accessory AV connection); each with LBBB. This tachycardia has less than a 10% chance of being VT,3 and when it is VT, it is often adenosine-sensitive right ventricular outflow tract VT.4

Dr. Healey and colleagues suggest that "one still ought to avoid adenosine in these instances." As quoted by the correspondents, adenosine may be dangerous in WPW syndrome patients with pre-excited atrial fibrillation by increasing the frequency of accessory connection conduction of atrial fibrillation, thereby predisposing the patient to the development of ventricular fibrillation (VF). In the cases cited by Dr. Healey and coworkers that converted to VF after receiving adenosine,5,6 all initially presented with pre-excited atrial fibrillation. By definition, such rhythms are grossly irregular with atypical aberrancy that should not be mistaken for a regular SVT. This is not meant to imply that adenosine for regular SVT is without risk. One rarely reported risk is conversion of a regular SVT to atrial fibrillation which, in the presence of manifest WPW syndrome, could be conducted at a rapid rate.6 Our patient did not have manifest WPW syndrome, as confirmed by history and by previous and follow-up ECGs. We could find only 1 report of VT degenerating into VF after adenosine was given,7and reports of VT degenerating into VF in the absence of adenosine are numerous.8 Indeed, adenosine has been recommended as a safe diagnostic aid that can be used to distinguish regular SVT with aberrant conduction from VT.9-11 Thus the probability of a serious complication from adenosine in the setting of a regular wide QRS tachycardia is remote12 and does not support the correspondents' statement that adenosine in this setting "has grave risks associated with its use." Furthermore, alternative treatments, such as intravenous procainamide and direct current cardioversion, have complications of their own, including ventricular proarrhythmia. Finally, in our patient, treatment with procainamide was not advised as the patient was already on sotalol. Combining 2 agents known to prolong the QT interval might elicit torsades de pointes.

The correspondents conclude by stating, "Let us put the safety of our patients first and the vanity of superior academic skills second." We agree with the first statement and consider the second to be an unfortunate choice of words. Rather than a routine "sedate and shock" approach, we offer an alternative: "think and link" the treatment of a tachydysrhythmia to its evident pathophysiology. Nevertheless, what is ultimately done will depend on local standards of care and the confidence of the clinician in decision-making in the emergency department.

Jason Mitchell, BSc
Medical Student, University of Calgary Health Region, Calgary, Alta.

Gerald Lazarenko, MD
Clinical Assistant Professor, University of Calgary, Calgary, Alta.

References

1. Mitchell J, Lazarenko G. Wide QRS complex tachycardia. CJEM 2008; 6: 572-3.
2. ECC Committee; Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2005;112: IV1-203.
3. Griffith MJ, Garratt CJ, Mounsey P, et al. Ventricular tachycardia as default diagnosis in broad complex tachycardia. Lancet 1994;343:386-8.
4. Kim RJ, Iwai S, Markowitz SM, et al. Clinical and electrophysiological spectrum of idiopathic ventricular outflow tract arrhythmias. J Am Coll Cardiol 2007; 49:2035-43.
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6. Exner DV, Muzyka T, Gillis AM. Proarrhythmia in patients with Wolff-Parkinson-White syndrome after standard doses of intravenous adenosine. Ann Intern Med 1995;122:351-2.
7. Parham WA, Mehdirad AA, Biermann KM, et al. Case report: adenosine induced ventricular fibrillation in a patient with stable ventricular tachycardia. J Interv Card Electrophysiol 2001;5:71-4.
8. Bayes de Luna A, Coumel P, Leclercq JF. Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmias on the basis of data from 157 cases. Am Heart J 1989;117:151-9.
9. Rankin AC, Oldroyd KG, Chong E, et al. Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. Br Heart J 1989;62:195-203.
10. Sharma AD, Klein GJ, Yee R. Intravenous adenosine triphosphate during wide QRS complex tachycardia: safety, therapeutic efficacy, and diagnostic utility. Am J Med 1990;88:337-43.
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