🫀 Mirza's Cardiology Notes

Ventricular Tachycardia (VT)

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  • Ventricular tachycardia (VT) is a wide complex arrhythmia of ventricular origin, defined as ≥ 3 consecutive beats at a rate of more than 100 beats per minute.
  • Sustained VT is defined as tachycardia that continues for > 30 seconds or leads to hemodynamic compromise within 30 seconds.
  • Non-sustained VT (NSVT) lasts less than 30 seconds and does not cause hemodynamic instability.
  • On the basis of QRS morphology, VT is divided into monomorphic and polymorphic ventricular tachycardia. 1
  • Monomorphic VT
    • characterized by a single, stable QRS morphology with no beat-to-beat variation 1
  • Polymorphic VT
    • characterized by beat-to-beat variation in QRS shape and multiple QRS morphologies. 1
    • Torsades de Pointes is a form of polymorphic VT that occurs in the setting of the long QT interval, characterized by waxing and waning of QRS amplitude, giving it the name “twisting of the points.” 1
    • Bidirectional VT is another form of polymorphic VT and has a characteristic beat-to-beat change in the QRS axis. 1
      • Commonly seen in the setting of digitalis toxicity and patients with catecholaminergic polymorphic ventricular tachycardia (CPVT). 1
  • Accelerated atrioventricular rhythm (AIVR) is a monomorphic ventricular tachycardia, referred to as a sign of successful reperfusion, and it has a strong association with infarct size. 1
  • DDx includes ischemic heart disease (most common cause), ischemic/non-ischemic dilated cardiomyopathy, adult and congenital structural heart disease, inherited cardiac channelopathies, infiltrative cardiomyopathy, electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia), illicit drugs such as cocaine or methamphetamine, and digitalis toxicity. 1
  • RR intervals are usually regular (but may be irregular).
  • In VT, capture/fusion complexes result when a P wave occurs at the appropriate timing to allow for conduction through the AV node with at least partial capture of the ventricles. When seen, these complexes help establish the presence of AV dissociation (independent atrial and ventricular rhythms).
  • Work-up should include a 12-lead ECG in sinus rhythm
    • helps diagnose the underlying cause of ventricular tachycardia, e.g., myocardial ischemia/infarction, long QT syndrome, hypertrophic cardiomyopathy, Brugada syndrome, and ARVC. 1

Electrocardiogram (ECG) for VT

  • Wide R-R interval
    • Monomorphic VT: width unchanged
    • Polymorphic VT: width is more variable. If the intervals are not the same or irregular?
  • VT should not be irregular, if it is, then you should think of Atrial Fibrillation (AFib) or Pre-excited AFib/WPW
  • ECG Findings that support Dx of VT
    • Capture beats (also known as Dressler beats)
    • Fusion complexes
    • Precordial concordance (positive/negative)
    • AV Dissociation
    • aVR criteria (extreme/northwest axis deviation)
    • R-to-S interval > 100 ms in precordial leads

Predict Origin of Ventricular Arrhythmias

Algorithm source: 2

Fusion Complexes

  • The P-wave preceding the fusion complex is often easy to identify and can then be “marched out“ to identify other P waves associated with the atrial rhythm. This may be useful to identify AV dissociation.

Brugada Criteria

Original paper 📄 3

  1. Is there AV dissociation (independent P/QRS, capture beats, fusion beats)?
    1. Yes = VT
    2. Do the P waves march out?
  2. If no, is there an RS in any precordial lead (V1-V6)?
    1. No = VT
    2. You have to have absence of RS complex in all 6, i.e. if you see an RS complex in any precordial lead, then this criteria is not satisfied
  3. If yes, is QRS onset to nadir of S wave > 100 msec in any precordial lead?
    1. Yes = VT
    2. Caveat: rate-related aberrancy → at faster HR bundle can fool you into thinking it’s wider than it really is
  4. If no, are there morphologic criteria* for VT in both V1 and V6?
    1. Yes = VT
  5. If no, Supraventricular tachycardia

Vereckie Algorithm

Basel Algorithm

Mimickers

SVT with RBBB Aberrancy

This example: Only wide in V1, V2 because hx of RBBB. Other leads, QRS is narrow.

This example: Without baseline ECG you could get tricked. The axis is northwest (negative in I, negative in II, aVF, negative in aVR). The reason this is SVT with aberrancy is because the axis didn’t change from baseline. If you look at the baseline ECG, then you see they had northwest axis to begin with.

Sinus Tachycardia with RBBB Aberrancy

Footnotes

  1. https://www.ncbi.nlm.nih.gov/books/NBK532954/ ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9

  2. Enriquez A, Baranchuk A, Briceno D, Saenz L, Garcia F. How to use the 12-lead ECG to predict the site of origin of idiopathic ventricular arrhythmias. Heart Rhythm. 2019 Oct;16(10):1538-1544. doi: 10.1016/j.hrthm.2019.04.002. Epub 2019 Apr 4. PMID: 30954600. ↩

  3. A New Approach to the Differential Diagnosis of a Regular Tachycardia With a Wide ORS Complex. Pedro Brugada, MD; Josep Brugada, MD; Lluis Mont, MD; Joep Smeets, MD; and Erik W. Andries, MD. Circulation 1991;83:1649-1659 ↩

  4. Moccetti F, Yadava M, Latifi Y, et al. Simplified integrated clinical and electrocardiographic algorithm for differentiation of wide QRS complex tachycardia. JACC: Clinical Electrophysiology. 2022;8(7):831-839. doi:10.1016/j.jacep.2022.03.017 ↩

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