There are several other tachycardia rhythms that can be seen with both stable and unstable tachycardia. These rhythms include monomorphic ventricular tachycardia and polymorphic ventricular tachycardia both of which are wide-complex tachycardias.
Wide complex tachycardias are defined as a QRS of ≥ 0.12 second. Expert consultation should be considered with these rhythms.
These wide-complex tachycardias are the most common forms of tachycardia that will deteriorate to ventricular fibrillation.
Monomorphic Ventricular Tachycardia
With monomorphic VT all of the QRS waves will be symmetrical. Each ventricular impulse is being generated from the same place in the ventricles thus all of the QRS waves look the same.
Treatment of monomorphic VT is dependent upon whether the patient is stable or unstable. Expert consultation is always advised, and if unstable, the ACLS tachycardia algorithm should be followed.
Polymorphic Ventricular Tachycardia
With polymorphic ventricular tachycardia, the QRS waves will not be symmetrical. This is because each ventricular impulse can be generated from a different location. On the rhythm strip, the QRS might be somewhat taller or wider.
One commonly seen type of polymorphic ventricular tachycardia is torsades de pointes. Torsades and other polymorphic VT are advanced rhythms which require additional expertise and expert consultation is advised.
If polymorphic VT is stable the ACLS tachycardia algorithm should be used to treat the patient. Unstable polymorphic ventricular tachycardia is treated with unsynchronized shocks (defibrillation). Defibrillation is used because synchronization is not possible.
These wide complex tachycardias tend to originate in the ventricles rather than like a normal rhythm which originates in the atria.
Top Questions Asked On This Page
Q: What are the doses for synchronized cardioversion?
A: Here are the cardioversion voltage doses:
- Narrow regular: 50-100 J
- Narrow irregular: 120-200 J biphasic or 200 J monophasic
- Wide regular: 100 J
- Wide irregular: defibrillation dose (not synchronized)”
All of this information is covered on the tachycardia algorithm page.
Q: Is it necessary to memorize the doses listed above?
A: It is necessary to understand the concepts and be familiar with the shock dosages.
The repetition that is built into the website is designed to help you become very familiar with all of the concepts and use them in emergencies.
Q: What sort of a pulse would you be feeling with a polymorphic VT?
A: You may feel a weak pulse or a strong pulse depending on how long the polymorphic VT has been going on. One thing is for sure….You won’t be feeling a pulse for very long if this rhythm continues.
Click to view more top questions
[This content is available for registered users.]
Learn more about the course…
[523.251,659.255,783.991]
[523.251,659.255,783.991]
Ventricular Tachycardia (VT) is a broad complex tachycardia originating from the ventricles. There are several different forms of VT — the most common is monomorphic VT, which originates from a single focus within the ventricles.
ECG features of monomorphic VT- Regular, broad complex tachycardia
- Uniform QRS complexes within each lead — each QRS is identical (except for fusion/capture beats)
Monomorphic VT can be difficult to differentiate from other causes of broad complex tachycardia.
Other ECG features suggestive of VT include:
- Very broad complexes (>160ms)
- Absence of typical RBBB or LBBB morphology
- Extreme axis deviation (“northwest axis”)
- AV dissociation (P and QRS complexes at different rates)
- Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration
- Fusion beats — occur when a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology
- Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen
- Josephson’s sign – Notching near the nadir of the S-wave
- Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms
- RSR’ complexes with a taller “left rabbit ear”. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller
Below are some examples of positive and negative concordance, and Brugada’s and Josephson’s sign. For more examples of the other suggestive features, see VT versus SVT.
Brugada’s sign (right): R-S interval > 100 msCauses of Monomorphic VT
- Ischaemic Heart Disease
- Dilated cardiomyopathy
- Hypertrophic cardiomyopathy
- Chaga’s Disease
- VT may impair cardiac output with consequent hypotension, collapse, and acute cardiac failure. This is due to extreme heart rates and loss of coordinated atrial contraction (“atrial kick”)
- The presence of pre-existing poor ventricular function is strongly associated with cardiovascular compromise
- Decreased cardiac output may result in decreased myocardial perfusion with degeneration into VF
- Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is required in all cases of VT
- Haemodynamically stable
- Haemodynamically unstable — e.g hypotension, chest pain, cardiac failure, decreased conscious level
This is the most important classification clinically and influences immediate management.
2. Duration- Sustained = Duration > 30 seconds, or requiring intervention due to haemodynamic compromise
- Non-sustained = Three or more consecutive ventricular complexes, terminating spontaneously in < 30 seconds
- Monomorphic
- Polymorphic VT
- Torsades De Pointes (Polymorphic with QT prolongation)
- Right Ventricular Outflow Tract Tachycardia
- Fascicular Tachycardia
- Bidirectional VT
- Ventricular Flutter
- Ventricular Fibrillation (VF)
Three mechanisms exist for initiation and propagation of ventricular tachycardia:
- Requires two distinct conduction pathways
- Under normal circumstances, impulses cancel each other out (0)
- Conduction block in one pathway develops due to myocardial scarring, usually as a result of prior ischaemia/infarction (1)
- Strong ventricular impulses from the normal/slowed pathway can re-enter the blocked region (2), creating a re-entry circuit (3)
- Occurs due to early or late after-depolarisations
- Examples include Torsades de Pointes and digitalis toxicity
- Accelerated abnormal impulse generation by a region of ventricular cells
Monomorphic VT:
- Classic monomorphic VT with uniform QRS complexes
- Indeterminate axis
- Very broad QRS (~200 ms)
- Notching near the nadir of the S wave in lead III = Josephson’s sign
Monomorphic VT:
- Very broad QRS complexes (~ 200 ms) with uniform morphology
- Fusion and capture beats are seen in the rhythm strip
- Brugada’s sign is present: the time from the onset of the QRS complex to nadir of S wave is > 100 ms (best seen in V6)
NB: The rhythm strip is recorded after the other 12 leads rather than simultaneously
Example 3Monomorphic VT:
- Very broad complexes (~ 200 ms in V5-6)
- Northwest axis (-120 degrees)
- Brugada’s sign — the distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms
- Josephson’s sign — notching near the nadir of the S wave is seen in leads II, III, aVF
- Possibly some superimposed P waves in aVF
Monomorphic VT alternating with ventricular bigeminy.
The ventricular complexes have the following features:
- Very broad QRS duration (> 160 bpm)
- Positive concordance in the precordial leads (dominant R waves in V1-6)
- Brugada’s sign – time from onset of QRS to nadir of S wave > 100 ms; best seen in leads aVR and aVL
Monomorphic VT:
- Extreme axis deviation / northwest axis is present
- -150 degree; QRS positive in aVR, negative in I + aVF
- There is a RBBB-like pattern in V1 with a taller left rabbit ear – this is very specific for VT
Monomorphic VT:
- Northwest axis
- Tall monophasic R wave in V1 with an rS complex in V6 (small R wave, big S wave) — this pattern is also very specific for VT
This ECG fulfils the Brugada Morphology Criteria for VT.
NOTE: in the presence of a dominant R wave in V1 (“RBBB morphology”), VT is diagnosed if:
- There is an RSR’ complex with a taller left rabbit ear
- There is a tall monophasic R wave
- There is an rS complex in V6 (R/S ratio < 1)
See “VT versus SVT with aberrancy” for more details.
Example 7Monomorphic VT:
- This ECG is a difficult one!
- Although there is a broad complex tachycardia (HR > 100, QRS > 120), the appearance in V1 is more suggestive of SVT with aberrancy, given that the the complexes are not that broad (< 160 ms) and the right rabbit ear is taller than the left
- However, on closer inspection there are signs of AV dissociation, with superimposed P waves visible in V1
- Also, the presence of a northwest axis and an rS complex in V6 (tiny R wave, deep S wave) indicate that this is VT
Several arrhythmias can present as a wide-complex tachycardia (QRS > 120 ms), including:
- Ventricular Tachycardia
- SVT with aberrant conduction due to bundle branch block
- SVT with aberrant conduction due to the pre-excitation syndromes
- Pace-maker mediated tachycardia
- Metabolic derangements e.g. hyperkalaemia
- Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants)
Differentiating between the various causes of wide-complex tachycardia is challenging and not always possible.
Clinical Features Suggestive of VT- Age > 35 (positive predictive value of 85%)
- Structural heart disease
- Ischaemic heart disease
- Previous MI
- Congestive heart failure
- Cardiomyopathy
- 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)
- A number of diagnostic algorithms exist to help aid in the diagnosis of VT.
- No algorithm is 100% accurate in predicating VT
- Algorithms can be complex and require specific and unfamiliar measurements to be calculated
- Flow charts for the four commonly used algorithms (ACC, Brugada, Ultra-simple Brugada, Vereckei ) can be found over at ECGpedia.org.
Remember
- If in doubt, treat as VT!
Read more about the different types of VT by following these links:
- VT versus SVT with aberrancy
- Right Ventricular Outflow Tract Tachycardia
- Polymorphic VT / Torsades De Pointes
- Fascicular VT
- Bidirectional VT
- Ventricular Flutter
- ECG Exigency 004 – a case of broad complex tachycardia.
Online
- Wiesbauer F, Kühn P. ECG Yellow Belt online course: Become an ECG expert. Medmastery
- Wiesbauer F, Kühn P. ECG Blue Belt online course: Learn to diagnose any rhythm problem. Medmastery
- Rawshani A. Clinical ECG Interpretation ECG Waves
- Smith SW. Dr Smith’s ECG blog.
Textbooks
- Mattu A, Tabas JA, Brady WJ. Electrocardiography in Emergency, Acute, and Critical Care. 2e, 2019
- Brady WJ, Lipinski MJ et al. Electrocardiogram in Clinical Medicine. 1e, 2020
- Straus DG, Schocken DD. Marriott’s Practical Electrocardiography 13e, 2021
- Hampton J. The ECG Made Practical 7e, 2019
- Grauer K. ECG Pocket Brain (Expanded) 6e, 2014
- Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography 1e, 2009
- Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric 6e, 2008
- Mattu A, Brady W. ECG’s for the Emergency Physician Part I 1e, 2003 and Part II
- Chan TC. ECG in Emergency Medicine and Acute Care 1e, 2004
- Smith SW. The ECG in Acute MI. 2002 [PDF]
- ECG Library Basics – Waves, Intervals, Segments and Clinical Interpretation
- ECG A to Z by diagnosis – ECG interpretation in clinical context
- ECG Exigency and Cardiovascular Curveball – ECG Clinical Cases
- 100 ECG Quiz – Self-assessment tool for examination practice
- ECG Reference SITES and BOOKS – the best of the rest
ECG LIBRARY
Electrocardiogram
MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Adult/Paediatric Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library. Twitter: @rob_buttner
Ed BurnsEmergency Physician in Prehospital and Retrieval Medicine in Sydney, Australia. He has a passion for ECG interpretation and medical education | ECG Library |