AVNRT differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2] Ramyar Ghandriz MD[3]

Overview

AV nodal reentrant tachycardia is diffrentiated mostly by ECG. diseases that may lead to tachycardia and how to differentiate them is discussed below.

Differentiating AV nodal reentrant tachycardia from other Diseases

Supraventricular tachycardias must be differentiated from each other because the management strategies may vary:

AV Nodal Reentry Tachycardia

  • Rate: In adults the range is 140-250 bpm, but in children the rate can exceed 250 bpm.
  • Rhythm: Regular
  • P waves: The p wave is usually superimposed on or buried within the QRS complex
  • PR interval: The PR interval cannot be calculated as the p wave is generally obscured by the QRS complex. In uncommon AVNRT, the p wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the p wave can appear just before the QRS complex.
  • QRS complex: Less than 0.12 seconds, consistent, and normal in morphology in the absence of abberant conduction, QRS alternans may be present
  • Response to Maneuvers: May break with adenosine or vagal maneuvers
  • Epidemiology and Demographics: Accounts for 60%-70% of all SVTs. 80% to 90% of cases are due to antegrade conduction down a slow pathway and retrograde up a fast pathway.

Atrial Fibrillation

  • Rate: 110 to 180 bpm
  • Rhythm: Irregularly irregular
  • P waves: Absent, fibrillatory waves
  • PR interval: Absent
  • QRS complex: Less than 0.12 seconds, consistent, and normal in morphology in the absence of abberant conduction
  • Response to Maneuvers: Does not break with adenosine or vagal maneuvers
  • Epidemiology and Demographics: More common in the elderly, following bypass surgery, in mitral valve disease, hyperthyroidism

Atrial Flutter

  • Rate: 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) bpm, but 150 is most common
  • Rhythm: Regular
  • P waves: Sawtooth pattern of P waves at 250 to 350 beats per minute
  • PR interval: Varies depending upon the magnitude of the block, but is short
  • QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
  • Response to Maneuvers: Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
  • Epidemiology and Demographics: More common in the elderly, after alcohol

AV Reciprocating Tachycardia

  • Rate: More rapid than AVNRT
  • Rhythm:
  • P waves:
  • PR interval:
  • QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
  • Response to Maneuvers: May break with adenosine or vagal maneuvers
  • Epidemiology and Demographics: More common in males, whereas AVNRT is more common in females, Occurs at a younger age

Junctional Tachycardia

Multifocal Atrial Tachycardia

Sinus Node Reentry Tachycardia

Sinus tachycardia

  • Rate: Greater than 100.
  • Rhythm: Regular.
  • P waves: Upright, consistent, and normal in morphology (if no atrial disease)
  • PR interval: Between 0.12–0.20 seconds and shortens with increasing heart rate
  • QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
  • Response to Maneuvers:
  • Epidemiology and Demographics:

Ventricular Tachycardia

Wolff-Parkinson-White syndrome

  • Pathophysiology: Anatomically and functionally, the fast and slow pathways of AVNRT should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW) syndrome or atrioventricular re-entrant tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium in close proximity to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings, they provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
  • Rate:
  • Rhythm:
  • P waves: In WPW with orthodromic conduction due to a bypass tract, the p wave generally follows the QRS complex, whereas in AVNRT, the p wave is generally buried in the QRS complex.
  • PR interval:
  • QRS complex: In WPW there is a delta wave and evidence of ventricular preexcitation if there is conduction to the ventrilce via antegrade conduction down an accessory pathway. It should be noted, however, that in some patients with WPW, a delta wave and pre-excitation may not be present because bypass tracts do not conduct antegrade.
  • Response to Maneuvers: May break in response to procainamide, adenosine, vagal maneuvers
  • Epidemiology and Demographics:
  • Risk Factors: None, an inhereted disorder
Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrioventricular nodal reentry tachycardia (AVNRT)[1][2][3][4]
  • Regular
  • 140-280 bpm
  • Slow-Fast AVNRT:
    • Pseudo-S wave in leads II, III, and AVF
    • Pseudo-R' in lead V1.
  • Fast-Slow AVNRT
  • Slow-Slow AVNRT
  • Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)
  • Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • QRS alternans may be present
Atrial Fibrillation (AFib)[5][6]
  • Irregularly irregular
  • Absent
  • Fibrillatory waves
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 2.7–6.1 million people in the United States have AFib
  • 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
Atrial Flutter[7]
  • Regular or Irregular
  • 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
  • Sawtooth pattern of P waves at 250 to 350 bpm
  • Biphasic deflection in V1
  • Varies depending upon the magnitude of the block, but is short
  • Less than 0.12 seconds, consistent, and normal in morphology
  • Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Multifocal Atrial Tachycardia[8][9]
  • Irregular
  • Atrial rate is > 100 beats per minute
  • Varying morphology from at least three different foci
  • Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Premature Atrial Contractrions (PAC)[10][11]
  • Regular except when disturbed by premature beat(s)
  • 80-120 bpm
  • Upright
  • > 0.12 second
  • May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node
  • Ashman’s Phenomenon:
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[12][13]
  • Regular
  • Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm
  • Less than 0.12 seconds
  • A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway
  • A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.
Ventricular Fibrillation (VF)[14][15][16]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[17][18]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent
  • Absent
  • Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
  • Wide complex, QRS duration > 120 milliseconds
  • 5-10% of patients presenting with AMI


References

  1. ↑ Katritsis DG, Josephson ME (August 2016). "Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia". Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
  2. ↑ Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). "Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway". Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
  3. ↑ "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
  4. ↑ Schernthaner C, Danmayr F, Strohmer B (2014). "Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias". Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
  5. ↑ Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). "The ECG as a tool to determine atrial fibrillation complexity". Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
  6. ↑ Harris K, Edwards D, Mant J (2012). "How can we best detect atrial fibrillation?". J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
  7. ↑ Cosío FG (June 2017). "Atrial Flutter, Typical and Atypical: A Review". Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  8. ↑ Scher DL, Arsura EL (September 1989). "Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment". Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
  9. ↑ Goodacre S, Irons R (March 2002). "ABC of clinical electrocardiography: Atrial arrhythmias". BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
  10. ↑ Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). "Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome". J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
  11. ↑ Strasburger JF, Cheulkar B, Wichman HJ (December 2007). "Perinatal arrhythmias: diagnosis and management". Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
  12. ↑ Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). "Evaluation and management of wolff-Parkinson-white in athletes". Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  13. ↑ Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). "Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues". Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
  14. ↑ Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). "Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction". J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
  15. ↑ Samie FH, Jalife J (May 2001). "Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart". Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
  16. ↑ Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). "Sudden cardiac death: epidemiology and risk factors". Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
  17. ↑ Koplan BA, Stevenson WG (March 2009). "Ventricular tachycardia and sudden cardiac death". Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  18. ↑ Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.

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