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Ventricular tachycardia

Table of Contents

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

InvestigationSignificance
VBGThis 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 ECGConfirm 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

InvestigationIndication
FBEIdentify anaemia or infection as precipitants
UEC, CMPReplace any electrolytes. K+ and Mg2+ are of particular importance
TroponinVT 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:

InvestigationIndication
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 LineImmediate Synchronized DC CardioversionAttempt up to 3 times
2nd LineAmiodarone 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 LineMagnesium 10mmol IV, over 15 minutesConsider starting an infusion after
2nd LineOther 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

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