Overview #
- Definitions
- Ventricular Tachycardia (VT) encompasses a variety of rhythms that originate in the ventricular myocardium
- As a rule, all ventricular tachycardias are wide-complex (but not all wide-complex tachyarrhythmias are necessarily ventricular in origin)
- Prioritisation
- Emergency – Code Blue
- Key points
- Any wide-complex tachycardia should be treated as VT unless advised otherwise by a senior clinician
- The management of any arrhythmia with haemodynamic instability, acute heart failure or syncope is immediate cardioversion
References #
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Triage #
Immediate Attention
Sustained Ventricular Tachycardia (VT) is an emergency which requires immediate attention. Immediately call a Code Blue*, even if the patient is conscious, as patients in VT who have not already arrested are at high risk of of sudden cardiac arrest
* An exception is non-sustained VT (NSVT) which is described below
Causes #
As with many other tachyarrhythmias, patients often have an underlying structural change in their heart that predisposes them to this arrhythmia. This can be congenital but is most often acquired. (1)
Additionally, there is often an identifiable trigger for an episode of arrhythmia.
Underlying Factors: (3)
- Ischaemic Heart Disease, especially with prior myocardial infarction*
- Any structural heart disease (valvular disease, cardiomyopathy, etc.)
- Medications (esp. antiarrhythmics and QT prolonging drugs)
- Congenital heart disease
- Genetic syndromes (eg. Brugada, long-QT)
- Previous cardiac surgery
- Other (eg. myocarditis, sarcoidosis, etc.)
Precipitants: (6)
- Acute coronary syndrome*
- Electrolyte imbalances (especially hyperkalaemia)
- Medications (esp. antiarrhythmics and QT prolonging drugs)
- Any other Reversible Cause of Cardiac Arrest:
- Hypoxia
- Hypovolaemia/Haemorrhage/Anaemia
- Hyper/Hypo-electrolytes
- Hypo/Hyperthermia
- Thrombus – Cardiac
- Thrombus – Pulmonary
- Tamponade
- Tension Pneumothorax
- Toxins (ie. Medications, drugs)
* There should be a high suspicion for active cardiac ischaemia in any patient experiencing VT. Cardiology consultation is compulsory
Clinical features #
VT most commonly presents as pulseless cardiac arrest.
However, VT does not always cause immediate cardiac arrest. When conscious, patients are generally symptomatic (see below), but may occasionally be asymptomatic for a short period.
In general, any patient with the following signs/symptoms might have an arrhythmia, and an ECG should attempt to be captured during the episode of symptoms: (1)
- Syncope
- Dizziness
- Unexplained Hypotension
- Chest Pain
- Dyspnea
- Palpitations
Types of VT #
Monomorphic VT:
This is ‘typical’ VT and is characterised by: (2)
- Wide QRS complex
- HR >120
- Regular rhythm
- Persisting for >30 seconds

(8)
Non-Sustained VT (NSVT)
- As above but for <30 seconds (and >3 beats)

(9)
Management is inherently different to sustained VT (detailed below).
Polymorphic VT
- Constantly changing QRS morphology

(8)
A collection of VT where the QRS morphology is constantly changing. At a JMO level the management principles are very similar. Expert Cardiology advice must be consulted for further management.
Torsades de Pointes
A subset of Polymorphic VT characterised by:
- Sine wave appearance

(10)
Torsades de Pointes is always associated with underlying long QT interval. Causes of a long QT interval should be thoroughly investigated.
Artifact
Shivering artifact can appear remarkably similar to VT. Clues to differentiate include:
- Complete lack of symptoms
- Present in only 1 strip of the 12-lead ECG
- The presence of narrow QRS complexes interspersed throughout

(2)
Other VT Mimics
As alluded to earlier, not all wide-complex tachycardia is VT. The following conditions produce similar ECG patterns: (2)
- SVT with aberrancy
- AF with aberrancy
- Pre-excited AF (associated with Wolf-Parkinson-White syndrome)
- Hyperkalaemia
- Sodium channel blocker toxicity
- Pacemaker-associated Tachycardia
Diagnosing these conditions is outside the scope of this guideline. For those curious, these are some signs that confirm true VT and make a diagnosis of true VT more likely: (2)
- ‘confirm true VT’
- Capture beats
- Fusion beats
- ‘true VT more likely’
- HR > 120bpm and QRS > 120ms
- ‘Concordance’ in precordial leads
- All precordial leads positive (R waves) or negative (S waves)
- aVR is positive (dominant R wave)
- P waves and QRS complexes at different rates
In practice, decision tools such as the Brugada Algorithm summarise these features and are used to quickly confirm a diagnosis of VT.

Please see reference 11 for a more in-depth look at the Brugada algorithm including worked examples(11)
However at a JMO level, unless directed otherwise by a senior clinician, these should initially be managed using the guidelines below.
Investigations #
Initial investigations
Investigation | Significance |
VBG | This is the most useful investigation to undertake while simultaneously managing the patient. Results will be back fast enough to potentially identify a precipitant |
12-lead ECG | Confirm VT diagnosis (and differentiate true VT from VT mimics)Search for causes for VT (Ischaemia, QTc prolongation, etc.) |
Further acute investigations
These investigations might guide management to prevent a recurrence of VT
Investigation | Indication |
FBE | Identify anaemia or infection as precipitants |
UEC, CMP | Replace any electrolytes. K+ and Mg2+ are of particular importance |
Troponin | VT might be caused by ACS(Careful interpreting results: Troponin will invariably rise to a degree due to rate-related ischaemia) |
Other investigations
All cases of VT should be reviewed by the cardiology team who might advise:
Investigation | Indication |
TTE# | To investigate for underlying heart disease (if not performed recently) |
Angiogram# | Diagnostic and potentially therapeutic for coronary artery disease |
Management – Initial Response #
All episodes of VT should warrant an immediate Code Blue. While waiting for help, the patient should be initially approached with DRSABC as per BLS guidelines: (5)
- Check for Response
- Assess for Breathing & Pulse
If not breathing or no pulse, start immediate CPR as per BLS protocol.
Definitive management is:
Defibrillation as soon as possible |
Management – with adverse features #
Adverse features are defined as any of the following:
- Shock
- Syncope
- New signs of heart failure
- Signs of myocardial ischaemia
In such cases, prepare for the following: (5)
1st Line | Immediate Synchronized DC CardioversionAttempt up to 3 times |
2nd Line | Amiodarone 300mg IV, over 10-20 minutesThen, repeat synchronized DC Cardioversion |
If at any point the patient becomes pulseless or stops breathing, proceed to BLS as above.
Management – no adverse features #
Rarely, patients may present hemodynamically stable. They should still be managed immediately as their condition may quickly deteriorate: (5)
Step 1(Loading) | Amiodarone 300mg IV, over 20-60 minutes |
Step 2(Maintenance) | Amiodarone 900mg IV, over 24 hours |
While on an amiodarone infusion, patients should be transferred to CCU/ICU for monitoring, with careful attention on the patient’s QT interval
(Amiodarone can length the QT interval and hence provoke Torsade De Pointes)
If at any point the patient demonstrates adverse features, manage as above.
Management – polymorphic VT #
Polymorphic VT with adverse features should be assessed and managed the same as Monomorphic VT.
With or without adverse features, it is also worth adding on the following treatments: (7)
1st Line | Magnesium 10mmol IV, over 15 minutesConsider starting an infusion after |
2nd Line | Other options:Overdrive pacingIsoprenaline infusionLignocaine infusion |
If the rhythm is truly Torsade de Pointes, amiodarone should be avoided as it can further lengthen the QT interval. Instead, magnesium is extremely effective (even if baseline Mg levels are normal)
Even if the rhythm is another form of Polymorphic VT, magnesium might help and it also has an excellent safety profile (7)
Management – NSVT #
No immediate management necessaryInvestigate for possible precipitants |
NSVT is generally asymptomatic and identified in patients on continuous cardiac monitoring. It is commonly seen post-MI or post cardiac surgery.
Most importantly it is benign, and does not increase the risk of cardiac arrest. (4)
Reasonable steps to take if a patient has recurrent episodes:
- Investigate for VT precipitants (especially electrolytes and active ischaemia)
- Referral to Cardiology for advice (eg. for outpatient follow up, further investigation)
Contributors
Reviewing Consultant/Senior Registrar
Dr Daniel Shell
Dr Robert Stolz