VT or SVT with aberrancy?

Vigneshvarprashanth Umapathy1,*, S. Aravindakumar2, Priyanka B3

1Resident Internal Medicine, Kauvery Hospital, Tennur, Trichy, India

2Chief Consultant Interventional Cardiologist, Kauvery Heart City, Trichy, India

3Duty Medical Officer, Department of Cardiology, Kauvery Heart City, Trichy, India

*Correspondence: worldofuv@gmail.com

Background

A drug given for the treatment of supraventricular tachycardia (SVT) may be detrimental to a patient with ventricular tachycardia (VT) making the differential diagnosis in wide-QRS tachycardia quite critical. Wide-QRS complex tachycardias (QRS duration >0.12 s) often pose a diagnostic and therapeutic challenge. Errors are made, as many of us wrongly consider VT unlikely if the patient is hemodynamically stable. However, ECG findings can quickly and accurately distinguish VT in more than 90% of cases. We discuss this ECG to explore various factors that differentiate VT from SVT with aberrancy.

Case Presentation

A 71-year-old gentleman, euglycemic and normotensive, known to have complete heart block, s/p permanent pacemaker implantation (PPI) – dual chamber (DDDR) (done 4 months back), normal coronaries with slow flow, presented with complaint of palpitations for 1 day, which was sudden in onset and persistent. There was no associated chest pain, sweating, vomiting, or syncope. There was no history of fever or dyspnoea. On examination, he was conscious, oriented, and afebrile, BP: 100/60 mmHg, HR: 164/min, RR: 24/min, SpO2: 94% on RA. ECG showed wide QRS regular tachycardia with a rate of 161/min.

tachycardia-1

ECG 1: On admission – Wide QRS regular tachycardia with a heart rate of 161/min.

The challenge in the ER was to find out whether it was ventricular tachycardia (VT) or supraventricular tachycardia (SVT) with aberrancy, as both differ in management. A diagnosis of VT was made based on the Brugada algorithm and other factors supporting VT, and amiodarone infusion was started. ECHO revealed severe LV dysfunction, RV dysfunction, moderate MR, and moderate TR.

Clinical factors and ECG features of our patient suggesting VT
1 Elderly age
2 Valvular heart disease (ECHO)
3 Absence of typical RBBB or LBBB morphology
4 Very broad complexes > 160ms
5 Negative concordance in precordial leads
6 Brugada sign
7 Josephson sign
8 Brugada criteria: Presence of RS interval >100ms in precordial leads and morphology criteria satisfied the Brugada criteria to make a diagnosis of VT.

Troponin T was positive. Creatinine was elevated, suggesting type 1 cardio-renal syndrome. His VT persisted even after 21 hours of amiodarone infusion. However, heart rate reduced to 139/min.

tachycardia-2

ECG 2: Taken after 21 hours of amiodarone infusion – Wide QRS regular tachycardia with a heart rate of 139/min.

He had recurrent vomiting. His serum bilirubin, SGOT, and SGPT levels were markedly raised. Ischemic hepatitis was considered. In view of persistent VT even after amiodarone infusion, development of cardio-renal syndrome and ischemic hepatitis, DC cardioversion was done. ECG showed a return of ventricular paced rhythm with a rate of 70/min. His creatinine levels decreased. He gradually became better and was discharged.

tachycardia-3

ECG 3: Taken post DC shock – return of ventricular paced rhythm; heart rate of 70/min.

Discussion

Clinical factors associated with VT or SVT

 

VT SVT
Age > 35 (positive predictive value of 85%) Previous ECGs show a bundle branch block pattern with identical morphology to the broad complex tachycardia
Structural heart disease Previous ECGs show evidence of WPW (short PR < 120ms, broad QRS, delta wave)
Ischaemic heart disease The patient has a history of paroxysmal tachycardias that have been successfully terminated with adenosine or vagal manoeuvres
Previous MI
Family history of sudden cardiac death (suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia that are associated with episodes of VT)

ECG features increasing the likelihood of VT

  1. Absence of typical RBBB or LBBB morphology
  2. Extreme axis deviation (“northwest axis”): QRS positive in aVR and negative in I and aVF
  3. Very broad complexes > 160ms
  4. AV dissociation:
  5. P and QRS complexes at different rates
  6. P waves are often superimposed on QRS complexes and may be difficult to discern
  7. Capture beats: Occur when the sinoatrial node transiently “captures” the ventricles in the midst of AV dissociation, producing a QRS complex of normal duration
  8. Fusion beats: Occur when a sinus and ventricular beat coincide to produce a hybrid complex
  9. Positive concordance throughout the precordial leads
  10. Negative concordance throughout the precordial leads
  11. RSR’ complexes with a taller left rabbit ear:
  12. This is the most specific finding in favour of VT
  13. This is in contrast to RBBB, where the right rabbit ear is taller
  14. Brugada sign: Distance from onset of R wave to nadir of S wave is > 100ms in leads V1-6
  15. Josephson sign: Notching/slurring near the nadir of the S wave

Brugada criteria

For difficult cases, the Brugada criteria can be used to distinguish between VT and SVT with aberrancy. The algorithm is followed from top to bottom – if any of the criteria are satisfied, then VT is diagnosed.

tachycardia-4

Our patient fulfilled two of the above criteria:

1. RS interval >100ms in precordial lead

2. Morphology criteria

Morphology criteria of Brugada algorithm for VT

Broad complex tachycardia with RBBB morphology Appearance in V1-2

With a positive R wave in V1/V2, three patterns are indicative of VT:

  • Smooth monophasic R wave
  • Notched downslope to the R wave – the taller left rabbit ear
  • A qR complex (small Q wave, tall R wave) in V1

Appearance in V6

In V6, the following patterns are consistent with VT:

  • QS complex: Completely negative complex with no R wave
  • R/S ratio < 1
    • Small R wave, deep S wave
    • Indicates VT only if LAD is also present
Broad complex tachycardia with LBBB morphology Appearance in V1-2

With a dominant S wave in V1, the following three features are diagnostic of VT:

  • Initial R wave > 30-40 ms duration.
  • Notching or slurring of the S wave (Josephson sign)
  • RS interval (time from R wave onset to S wave nadir) > 60-70 ms

Appearance in V6

The presence of Q waves in V6 is indicative of VT.

There are two possible patterns of this:

  • QS waves in V6 (as with RBBB-like patterns) – Very specific for VT
  • qR complex in V6 (small q wave, large R wave)

Hemodynamic stability should not be used to differentiate VT from SVT with aberrant conduction as it is not universally associated with SVT with aberrancy and is not indicative of rhythm classification.

To conclude, careful interpretation of a 12-lead ECG is necessary to establish a correct diagnosis. Knowledge about Brugada criteria could come in handy in the ER to make a quick diagnosis of VT or SVT with aberrancy. Drugs used to treat SVT like adenosine and calcium channel blockers could worsen VT. But drugs used to treat VT like procainamide and amiodarone can be effective in the treatment of SVT with aberrancy. Therefore, when in doubt it’s better to treat as VT.

References

 

 

Vigneshvarprashanth

Dr. Vigneshvarprashanth Umapathy

Resident Internal Medicine

Aravindakumar

Dr. S. Aravindakumar

Chief Consultant Interventional Cardiologist

Priyanka

Dr. B. Priyanka

Duty Medical Officer

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