palpitations & presyncope…

the case.

A 54 year old female presents to ED with an ‘odd sensation’ in her chest. This has been occurring intermittently for 2 months but has now increased in frequency & severity. She reports 3 episodes earlier today associated with nausea, clamminess & presyncope.

She is post-menopausal & has a history of poorly-controlled type 2 diabetes and hypertension. Her initial ECGs & troponins are unremarkable, so she is admitted to the observation-unit for an exercise-stress test the following morning.

Whilst awaiting the treadmill, she reports a recurrence of her symptoms. She has a glistening sweat & appears pale.

This ECG is captured whilst she is symptomatic….

ECG#1 (odd & pale)

[DDET Interpret this ECG…?]

Broad complex, regular tachycardia !!

  • Rate.
      • ~188bpm
  • Rhythm.
      • Regular ventricular rate. P-waves not present.
  • Axis.
      • Right-shifted, inferior axis [ +103*]
  • Intervals.
      • PR – n/a
      • QRS ~ 140 msec
      • QTc ~ 530 msec
  • Extras:
      • Atypical LBBB pattern
          • qS in V1
            • S-wave notching (Josephson’s sign)
            • S-wave duration ~70-80 msec
          • rS pattern [V2-3]
          • unusual rSR’ pattern [V5-6]
      • No obvious features of AV-dissociation.

Ventricular tachycardia with atypical LBBB pattern & right-inferior axis.

This is suggestive of right ventricular outflow tract VT.


[DDET What happens next ?!?]

By the time the rhythm is recognised & bought to the attention of medical staff – she has spontaneously reverted….

This is her post-reversion 12-lead ECG.

ECG#2 (feeling better)



[DDET Interpret ECG #2 …]

  • Rate.
      • ~ 78 bpm.
  • Rhythm.
      • Regular (sinus).
      • PVCs following every second QRS.
  • Axis.
      • QRS: normal [~ +70]
      • PVCs: rightward [~ +103*]
  • Intervals.
      • PR: ~160 msec (normal)
      • QRS: ~100 msec (normal)
      • QTc: ~520msec.
  • Extras.
      • No obvious ST/T-wave changes.
      • PVCs are of identical configuration to those seen in the prior ECG.
          • atypical LBBB pattern with right-inferior axis.

Sinus rhythm with prolonged QTc. Regular PVCs from focus identical to prior VT.

I’ve had some assistance this week from Dr Adam Lee, Cardiology Registrar & colleague of mine who had the following salient points to make regarding these ECG’s.

ECG 1:
” There are good criteria for aberrant SVT vs VT, particularly Vereckei’s aVR rule and the traditional Brugada ( [especially] Step 4!)…but probably the most pragmatic initial step is to ask “does it look like typical RBBB/LBBB?” If the answer is no, then it’s very likely to be VT (although can’t exclude non-specific IVCD). In this case, the negative high lateral leads (I, aVL) are very atypical for traditional LBBB and so is the funny Rsr’ (‘left rabbit ear’) in the lateral chest leads. “

ECG 2:
” The fact the ventricular ectopics in sinus rhythm have an identical QRS morphology to that of the tachycardia makes VT nearly certain. For a VEB to have identical morphology to an aberrant conducted supraventricular beat would be an exceedingly rare coincidence. The caveat is you need to make sure it is a true VEB not an atrial ectopic conducted with aberrancy (which it could do, given ectopics by definition are early beats and therefore may occur when parts of the conduction system are still refractory). The key is to examine for a P-wave prior to the wide beat and you usually need to scrutinise the preceding T-wave to see if it’s hidden in it. In this case, the preceding T-wave looks identical to the one before so there is definitely no P wave; it’s therefore a VEB. This also hints that the VT is of a focal origin, rather than due to a macro-re-entrant circuit (like typical scar related VTs).”


[DDET Tell me more…]

Right Ventricular Outflow Tract Ventricular Tachycardia (RVOT-VT)


  • Outflow tract VT’s are commonly seen in patients with no evidence of structural heart disease.
      • 80-90% from RVOT. The other ~10% from LVOT.
  • Impulses originate from (or near) the RVOT.
      • Results in a LBBB morphology (ventricular depolarisation spreading from right to left) with a right inferior axis.
  • Thought to be a result of cyclic AMP triggering.
      • May explain its response to adenosine & beta-blockers.
  • Can be mistakenly labeled as SVT with aberrancy.


  • Commonly presents with chest pain, dyspnoea, palpitations or presyncope (rarely, with frank syncope)
      • Exercise or emotional stress (or any hyperadrenergic state) can precipitate the tachycardia.
      • Women have increase in symptoms related to changes in hormonal status.


  • LBBB pattern.
  • Inferior (right-ward) axis.
  • Other features of VT.
      • AV dissociation
      • ‘fusion’ & ‘capture’ beats.

It is important to examine the ‘normal’ ECG for the features of arrhythmogenic right ventricular dysplasia (ARVD) which also results in LBB-morphology VT (w/ inferior axis).

  • ARVD is associated with epsilon waves, T-wave inversion (V1-3) & a prolonged S-wave upstroke (V1-3) amongst others.



  • Vagal manoeuvres (valsalva or carotid massage).
  • Pharmacology.
      • Adenosine
      • Verapamil
  • Cardioversion (if at all unstable).

This type of VT is usually sensitive to adenosine;
It is the textbook example of why you cannot claim that “wide complex tachycardia reverted with adenosine, therefore it must be SVT”.


  • Pharmacology.
      • Beta-blockers & Calcium-channel blockers.
      • Class Ia, Ic & III anti-arrhythmics have been trialled.
  • Radiofrequency ablation.
      • Curative in 90% of cases.
      • Reserved for drug-refractory cases or those with potentially malignant forms of dysrhythmia.


  • The prognosis of truly idiopathic outflow-tract VT is benign & the vast majority of patients in the long-term do not develop structural heart disease or sudden cardiac death.
  • Sudden death is rare !
      • However – it is known that small percentages of patients with frequent ventricular arrhythmias develop LV dysfunction & there are case reports of patients in cardiac arrest or polymorphic VT following the initial diagnosis of benign outflow tract VTs.


Dr Lee also wanted to impart the following for us “ED folk”…
” [RVOT-VT] falls under the umbrella of “benign VTs”. The VT is usually well tolerated haemodynamically and these patients do not need ICDs long term. However, from an ED point of view, you can’t be too cocky. RVOT VT can look very similar to the VT of ARVC (arrhythmogenic right ventricular cardiomyopathy) which can be fatal. First principles still apply –> if pt is haemodyanamically compromised, just shock.”


[DDET Patient progress…]

  • Admitted to Coronary Care. Electrolytes optimised. Commenced on beta-blocker.
  • Coronary angiogram on Day 2 of admission = normal !
  • Cardiac MRI = normal !
  • Electrophysiology study.
      • VT from RVOT (anterior area).
      • Ablation attempted, however unsuccessful due to patient movement & presence of polymorphic PVCs.

She is currently on slow-release verapamil, awaiting a repeat EPS study under general anaesthesia.


[DDET References.]

  1. Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
  2. Prystowsky EN et al. Ventricular arrhythmias in the absence of structural heart disease. J Am Coll Cardiol. 2012 May 15;59(20):1733-44.
  3. Saliba WI, Natale A. Ventricular tachycardia syndromes. Med Clin North Am. 2001 Mar;85(2):267-304.
  4. LifeInTheFastLane.com – Right ventricular outflow tract (RVOT) tachycardia.

Thanks again to Dr Adam Lee for his assistance and contribution to this post.


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