Targeting tachycardia: Diagnostic tips and tools

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Applied Evidence

Targeting tachycardia: Diagnostic tips and tools

J Fam Pract. 2012 May;61(5):258-263

By

Dmitriy Kireyev, MD, FACC

Stanley F. Fernandez, MD

Vipul Gupta, MD, MPH

Mikhail V. Arkhipov, MD

Joseph A. Paris, MD, FACC

Many narrow QRS complex tachycardias are benign, but some require rapid intervention. The review, EKG strips, and algorithm you’ll find here will help you get to the source of the problem without delay.

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References

1. Yusuf S, Camm AJ. Deciphering the sinus tachycardias. Clin Cardiol. 2005;28:267-276.

2. Lee RJ, Shinbane JS. Inappropriate sinus tachycardia. Diagnosis and treatment. Cardiol Clin. 1997;15:599-605.

3. Morillo CA, Klein GJ, Thakur RK, et al. Mechanism of ‘inappropriate’ sinus tachycardia. Circulation. 1994;90:873-877.

4. Bauernfeind RA, Amat-y-Leon F, Dhingra RC, et al. Chronic nonparoxysmal sinus tachycardia in otherwise healthy persons. Ann Intern Med. 1979;91:702-710.

5. Low PA, Opfer-Gehrking TL, Textor SC, et al. Postural tachycardia syndrome (POTS). Neurology. 1995;45(suppl 5):S19-S25.

6. Raj SR. The postural tachycardia syndrome (POTS): pathophysiology, diagnosis & management. Indian Pacing Electrophysiol J. 2006;6:84-99.

7. Grubb BP, Kanjwal MY, Kosinski DJ. Review: the postural orthostatic tachycardia syndrome. J Interv Card Electrophysiol. 2001;5:9-16.

8. Kanjwal MY, Kosinski DJ, Grubb BP. Treatment of postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia. Curr Cardiol Rep. 2003;5:402-406.

9. Simmers TA, Sreeram N. Sinoatrial reentry tachycardia: a review. Indian Pacing Electrophysiol J. 2003;3:109-116.

10. Saoudi N, Cosío F, Waldo A, et al. Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases. Eur Heart J. 2001;22:1162-1182.

11. Teh AW, Kistler PM, Kalman JM. Using the 12-lead ECG to localize the origin of ventricular and atrial tachycardias: part 1.J Cardiovasc Electrophysiol. 2009;20:706-709.

12. Roberts-Thomson KC, Kistler PM, Kalman JM. Focal atrial tachycardia I: clinical features, diagnosis, mechanisms, and anatomic location. Pacing Clin Electrophysiol. 2006;29:643-652.

13. Rosso R, Kistler PM. Focal atrial tachycardia. Heart. 2010;96:181-185.

14. Schwartz M, Rodman D, Lowenstein SR. Recognition and treatment of multifocal atrial tachycardia: a critical review. J Emerg Med. 1994;12:353-360.

15. Kwaku KF, Josephson ME. Typical AVNRT-an update on mechanisms and therapy. Cardiol Electrophysiol Rev. 2002;6:414-421.

16. Nawata H, Yamamoto N, Hirao K, et al. Heterogeneity of anterograde fast-pathway and retrograde slow-pathway conduction patterns in patients with the fast-slow form of atrioventricular nodal reentrant tachycardia. J Am Coll Cardiol. 1998;32:1731-1740.

17. Fox DJ, Tischenko A, Krahn AD, et al. Supraventricular tachycardia. Mayo Clin Proc. 2008;83:1400-1411.

18. Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention. JAMA. 2001;285:2370-2375.

19. Falk RH. Atrial fibrillation. N Engl J Med. 2001;344:1067-1078.

20. Garson A, Gillette PC. Junctional ectopic tachycardia in children: electrocardiography, electrophysiology and pharmacologic response. Am J Cardiol. 1979;44:298-302.

21. Villain E, Vetter VL, Garcia JM, et al. Evolving concepts in the management of congenital junctional ectopic tachycardia. A multicenter study. Circulation. 1990;81:1544-1549.

22. Sarubbi B, Vergara P, D’Alto M, et al. Congenital junctional ectopic tachycardia: presentation and outcome. Indian Pacing Electrophysiol J. 2003;3:143-147.

23. Tada H, Nogami A, Naito S, et al. Simple electrocardiographic criteria for identifying the site of origin of focal right atrial tachycardia. Pacing Clin Electrophysiol. 2006;21:2431-2439.

24. Kistler PM, Roberts-Thomson KC, Haqqani HM, et al. P wave morphology in focal atrial tachycardia. J Am Coll Cardiol. 2006;48:1010-1017.

25. Divakara Menon SM, Healey JS, Nair GM, et al. A case of long-RP tachycardia. J Cardiovasc Electrophysiol. 2009;20:702-704.

26. Lerman BB, Greenberg M, Overholt ED, et al. Differential electrophysiologic properties of decremental retrograde pathways in long RP’ tachycardia. Circulation. 1987;76:21-31.

27. Zipes DP. Clinical application of the electrocardiogram. J Am Coll Cardiol. 2000;36:1746-1748.

28. Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias-executive summary. Circulation. 2003;108:1871-1909.

29. Farre J, Wellens HJJ. The value of electrocardiogram in diagnosing site of origin and mechanism of supraventricular tachycardia Wellens HJJ, Kulbertus HE, eds. What’s New in Electrocardiography. Boston, Mass: Martinus Nijhoff; 1981:131.

30. Ho YL, Lin LY, Lin JL, et al. Usefulness of ST-segment elevation in lead aVR during tachycardia for determining the mechanism of narrow QRS complex tachycardia. Am J Cardiol. 2003;92:1424-1428.

31. Zhong YM, Guo JH, Hou AJ, et al. A modified electrocardiographic algorithm for differentiating typical atrioventricular node reentrant tachycardia from atrioventricular reciprocating tachycardia mediated by concealed accessory pathway. Int J Clin Pract. 2006;60:1371-1377.

32. Riva SI, Della Bella P, Fassini G, et al. Value of analysis of ST segment changes during tachycardia in determining type of narrow QRS complex tachycardia. J Am Coll Cardiol. 1996;27:1480-1485.

33. Green M, Heddle B, Dassen W, et al. Value of QRS alteration in determining the site of origin of narrow QRS supraventricular tachycardia. Circulation. 1983;68:368-373.

34. Kalbfleisch SJ, el-Atassi R, Calkins H, et al. Differentiation of paroxysmal narrow QRS complex tachycardias using the 12-lead electrocardiogram. J Am Coll Cardiol. 1993;21:85-89.

35. Morady F. Significance of QRS alternans during narrow QRS tachycardias. Pacing Clin Electrophysiol. 1991;14:2193-2198.

PRACTICE RECOMMENDATIONS

•Analyze P wave axis, morphology, and timing for help in diagnosing narrow QRS complex tachycardia. C

•Review the modes of onset and termination for clues to the specific type of tachycardia, including features such as the rate of acceleration and the response to medication and the Valsalva maneuver. C

•Compare a baseline 12-lead EKG with one taken during an episode of tachycardia, looking for clues to the mechanism of the arrhythmia. C

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

WATCH THE VIDEO

Sinus tachycardia educational video for patients

Courtesy of: WirelessDx

Go to http://www.wirelessdx.com/sinustachycardia.htm

Narrow QRS complex tachycardias—rhythms with a rate >100 beats per minute (bpm) and a QRS duration <120 ms—are frequently encountered in both inpatient and outpatient settings. Therapeutic strategy ranges from simple reassurance to acute inpatient intervention, depending on the specific arrhythmia.

Early and accurate diagnosis is paramount to avoid unnecessary testing, ensure timely management, and prevent complications and long-term adverse outcomes. While most narrow QRS complex tachycardias are easily diagnosed, some pose a diagnostic challenge.

This review can help. We start with a summary of the various types of narrow QRS complex tachycardias, accompanied in some cases with 12-lead electrocardiogram (EKG) strips. Next, we highlight key characteristics to consider in the differential and provide an algorithm to help you zero in on the diagnosis.

FAST TRACK

The relative duration of RP and PR intervals, P wave position, and ST segment elevation in lead aVR are among the characteristics to consider in the differential diagnosis.

Narrow QRS complex tachycardias: What you’ll find

Narrow QRS complex tachycardias fall into 2 broad categories: those that are sinus node-generated, and those that are not. Here’s a look at both.

Sinus node-generated tachycardias
Sinus node tachycardia (FIGURE 1), the most common arrhythmia,¹ is an appropriate response to physiologic or emotional stress or disease processes. It is defined as a heart rate >100 bpm with the presence of P waves of normal sinus morphology on a 12-lead EKG.

FIGURE 1
Sinus tachycardia

The P waves show normal sinus morphology. Note superior-to-inferior axis with positive P deflections in leads II, III, and aVF.

Inappropriate sinus tachycardia is a nonparoxysmal arrhythmia with a resting daytime heart rate >100 bpm (or an average heart rate >90 bpm over a 24-hour period), normal P wave morphology, and an exaggerated response to physical activity.^2,3 What distinguishes it from simple sinus tachycardia is the disproportionate degree of the arrhythmia to the level of physiologic stress.

Inappropriate sinus tachycardia is a diagnosis of exclusion, established only after other reversible pathologic or pharmacologic causes of tachycardia, such as hyperthyroidism, pheochromocytoma, infection, or theophylline toxicity, have been ruled out. Possible mechanisms may include autonomic dysfunction with increased cardiac sympathetic or reduced vagal output.⁴

Paroxysmal orthostatic tachycardia syndrome (POTS) is an abnormal sinus tachycardia response to an upright position.^5,6 It is diagnosed by a heart rate ≥120 bpm or an increase ≥30 bpm within 5 minutes of standing up or being on a tilt table, with simultaneous development of orthostatic symptoms, such as dizziness, light-headedness, or even syncope, without the corresponding drop in blood pressure. Symptoms usually resolve after the patient assumes a supine position. The presentation may overlap with that of inappropriate sinus tachycardia, although patients with POTS usually develop autonomic symptoms such as constipation, tremor, or heat/cold intolerance, as well.^7,8

Sinus node reentry tachycardia is a paroxysmal tachycardia with a normal P wave on a 12-lead EKG. The paroxysmal nature of the arrhythmia and a positive response to atropine and vagal maneuvers, as well as identification by electrophysiologic studies, differentiate this condition from inappropriate sinus tachycardia.⁹

Nonsinus node-generated tachycardias
Focal atrial tachycardia (FIGURE 2) is caused by an automatic, triggered, or microreentrant mechanism that can be localized to a specific area of atrial tissue.¹⁰ The diagnosis can often be made by a careful review of the EKG, which will reveal P waves that differ from those of the sinus beat.¹¹ This can be tricky, however, as a P wave on a 12-lead EKG from a focal point close to the sinoatrial node may resemble that of a normal sinus rhythm.

FIGURE 2
Focal atrial tachycardia

The P waves differ from those of the sinus beat. Note the positive P wave in lead aVR.

The atrial rate associated with this condition can vary from 120 to 300 bpm, depending on the focus, and may be associated with variable degrees of atrioventricular (AV) block. The crista terminalis in the right atrium and pulmonary vein ostia are frequent origins of focal atrial arrhythmias.^12,13