A 34 year-old male presents to your emergency department with palpitations. His vitals checked at triage include pulse >170; BP 112/76; sO2 98%; GCS 15
Would you give adenosine?
We presented the ECG to the medical Twitter community and asked what they would do, and what was the most likely ECG diagnosis:
Describe and interpret this ECG
ECG ANSWER and INTERPRETATION
- Regular broad-complex tachycardia, rate 174
- Typical LBBB morphology in aVR, V1 and V6
- Absence of fusion or capture beats
However, there is one feature here that is unusual for LBBB, can you spot it?
The combination of a regular broad complex tachycardia with typical LBBB morphology, and inferior axis (+90 degrees), should raise suspicion for a form of monomorphic VT known as right ventricular outflow-tract tachycardia (RVOT tachycardia).
In addition, there are other features suggestive of VT, can you spot them?
There are signs of AV dissociation, with P waves discernible at different rates to QRS complexes (sensitivity 82%, specificity 98%):
The initial R wave in V1 measures ~40ms:
- With a dominant S wave in V1, an initial R wave of > 30-40ms is also suggestive of VT (Brugada algorithm)
The differential diagnosis of a regular broad complex tachycardia is VT versus SVT with aberrant conduction (due to bundle branch block or Wolff-Parkinson-White Syndrome). For an in-depth review of differentiating between the two, see VT versus SVT.
RVOT tachycardia is a form of monomorphic VT originating from the outflow tract of the right ventricle or occasionally from the tricuspid annulus. It is most commonly a form of idiopathic VT, whereby no structural heart disease, metabolic/electrolyte abnormalities, or long QT syndrome can be found. It can also be seen in patients with Arrhythmogenic Right Ventricular Dysplasia (ARVD).
The RVOT is divided into rightward (free wall), anterior, leftward, and posterior (septal) parts. RVOT tachycardia can originate from any of these sites but all carry common ECG characteristics.
ECG features of RVOT VT:
- LBBB morphology
- Inferior axis
- rS complex in V1 and R complex in V6
- Precordial transition usually ≥ V3, with the exception of septal origin, which occurs at ≤ V3
Other general features of VT, such as AV dissociation, fusion and/or capture beats may also be present.
Back to our initial question: Would you give adenosine?
If the patient is stable, you can administer adenosine…
- Acute termination of idiopathic RVOT VT in a stable patient can be achieved by vagal manoeuvres or adenosine (6mg up to 24mg)
- IV verapamil is an alternative if the patient has adequate blood pressure
- DCCV is always the management preference if there is haemodynamic instability.
RVOT tachycardia in ARVD generally does not terminate with adenosine. Differentiation between idiopathic RVOT tachycardia and that caused by ARVD can be difficult and may rely on previous ECG findings as well as family history. In ARVD, the baseline ECG usually shows inverted T waves in right precordial leads, and when present, RV conduction delay with an epsilon wave best seen in V1-2.
What if there was still uncertainty regarding the rhythm?
In stable patients with a regular broad complex tachycardia, adenosine is useful and safe as a diagnostic and potentially therapeutic agent.
In unstable patients, if there is doubt regarding the rhythm (SVT v VT), proceed to DCCV.
- VT versus SVT
- RVOT Tachycardia
- Arrhythmogenic Right Ventricular Dysplasia (ARVD)
- Supraventricular Tachycardia (SVT)
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- Marill KA et al. Adenosine for wide-complex tachycardia: Efficacy and safety. 2009; Critical Care Medicine 37(9):2512-8. DOI: 10.1097/CCM.0b013e3181a93661
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