Wide Complex Tachycardia

Wide Complex Tachycardia

Introduction

  • Wide complex tachycardia is defined as a rate of > 100 with QRS > 120ms. 
    • Wide QRS represents slow activation of the ventricles that does not use the rapid His-Purkinje system of the heart.
  • There are 5 classic causes of wide complex tachycardia mechanisms:
    • Classic Causes of Wide Complex Tachycardia
      1. Ventricular Tachycardia
      2. SVT with aberrancy (usually SVT with RBBB or LBBB)
      3. Pre-Excitation
      4. Pacing
      5. Artifact

      (Another commonly cited cause is massive ST elevation)

  • When facing a WCT, it is important to remember that VT is the cause in 80% of the cases
    • If the patient has ischemic heart disease, then VT is the cause in 90% of the cases. 
  • General Approach:
    • Misdiagnosing SVT as VT would lead to treating with cardioversion and amiodarone.  This is aggressive treatment for SVT, but it’s not harmful.
    • Misdiagnosing VT as SVT and treating it with IV beta blockers and diltiazem would lead to hemodynamic instability in 100% of the time, thereby producing harm.  
  • Since a large majority of WCTs are VT (80%), especially in patients with ischemic or structural heart disease, and VT therapies are effective for both VT and SVT, it is more than reasonable to treat all WCT as VT if the diagnosis is uncertain.  

Basics

  • Wide QRS complex suggests ventricular activation by:
    • Impulse originating outside the normal conduction system, below the level of the AV node
    • Impulse conducted down an abnormal His-Purkinje system (HPS)
    • Pre-excitation with anterogradely conducted impulse over a bypast tract (BT)

Approach

  1. Assess the hemodynamic stability of the patient
    • If unstable, presume VT and treat accordingly
    • If stable, monitor continuously, as status can change
  2. Evaluate ECG features and generate a differential diagnosis
  3. Narrow the differential using clinical history, physical exam, ECG and diagnostic maneuvers

Diagnosis: Hx/Px/Labs

  1. History:

    • Some historical elements can help suggest an etiology of WCT:
      • Older patients (>35) are more likely to have VT
      • Patients with underlying cardiac disease are more likely to have VT
      • Medications:
        • Class IA and IC can cause aberration of SVT (by their property of use dependency)
        • QTc prolonging agents can predispose to polymorphic VT
        • Digoxin most commonly causes VT (monomorphic or bidirectional)
      • Symptoms and hemodynamic status are not helpful in establishing the diagnosis in WCT

    Physical Exam:

    • Look for evidence of heart disease, or manifestation of peripheral vascular disease (e.g., stroke)
    • Evidence of AV dissociation on physical exam:
      • Variable intensity and appreciation of S1
      • Cannon A waves – imply contraction of atrium against a close AV valve (AV dissociation)
      • Fluctuation in blood pressure (variation in atrial contribution to end diastolic filling)

    Laboratory Investigations:

    • Assess for evidence of ischemia (cardiac biomarkers)
    • Assess for electrolyte derangement (particularly magnesium and potassium)
    • Assess levels of drugs were appropriate (digoxin, antiarrhythmics, etc)
    • Toxicology screen

Diagnostic Maneuvers

  • Only should be done for hemodynamically unstable patients with crash cart ready to deliver cardioversion if necessary.
  • Vagal maneuvers – can produce transient AV block, which can terminate some re-entrant SVTs.  
  • Adenosine
    • Very helpful diagnostically to distinguish VT from SVT.
    • Adenosine will result in a transient AV block, which may terminate some re-entrant SVTs, or block conduction to the ventricles to reveal atrial activity (such as atrial tachycardia).
    • Adenosine generally has no effect on VT.
    • Start with 6mg adenosine IV followed by rapid IV saline flush.  If no effect, dose is doubled to 12mg IV.  If no effect, then can be doubled to 24mg IV.
      • With each injection warn the patient about the sensation of adenosine, and check to ensure the IV line is functional.
      • No response to 24mg of adenosine generally means the tachycardia is insensitive to adenosine, and does not require the AV node in its mechanism (VT). 
    • NOTE: Some VT rhythms are adenosine sensitive, particularly outflow tract idiopathic VT. 

ECG Assessment: VT vs. SVT with aberrancy

  • Two most important differential diagnoses of WCT are VT and SVT with aberrancy.  Other differential diagnoses are often easily excluded:
    • Pacing is easily ruled out with clinical history, physical exam, and absence of pacing spikes. 
    • Artifact can also be ruled out, as it often produces non-physiologic signals on ECG, often in a single lead.   
    • Pre-excitation (pre-excited SVT) is quite rare.  The best tool is to look at the baseline ECG for evidence of pre-excitation.  Pre-excitation of ventricles starts in the basal area, which produces a positive QRS in most precordial leads. 
  • There are numerous scoring systems and algorithms developed to distinguish these two entities.  (Brugada criteria, Vereckei algorithm, Lead II criteria, etc..).  All of these algorithms are derived from the core principles, which we teach here.  We recommend you become familiar with the Brugada criteria, since it is well known and frequently tested on exams.
  • A useful approach is to start with a presumed diagnosis of VT, which will be correct 80-90% of the time.  Significant proof is needed to dissuade you towards SVT.
  • Principle #1: AV dissociation proves VT
    • Highly favours VT (Spec 98%, Sens 82%), but only seen in 20-50% of VTs (Brugada et al 1992)
    • AV dissociation proves that atria and ventricles are independently activated.
      • A variation of this includes AV association but finding more QRSs than P-waves (see example).  This proves that atria are not needed for the mechanism of the arrhythmia.
    • Inability to find P-waves, or finding a 1:1 association between QRSs and P-waves is not helpful as both SVT and VT can produce this.  About 30% of VTs conduct retrogradely to the atria, and have a 1:1 VA relationship.  Whether the diagnosis is SVT (atrial driving the ventricles) or VT (ventricles driving the atria) cannot be determined with a 1:1 AV relationship. 
    • TIP: Look for P-waves in leads with the smallest QRS.  Best leads are II, V1, V2, I, and III.
    • Advanced Tip: Look for wobble in the cycle length to see whether A or V move first, which tells you which one is driving the other
  • Principle #2: Concordance proves VT
    • If all precordial leads demonstrate positive R-waves with no negative components, then VT is diagnosed.  Similarly if all precordial leads are negative (QS waves) with no positive component, VT is diagnosed. 
    • This is the most specific criterion (Sp 100%, Sn 21%), but is frequently absent and is not helpful.  
    • There is no variation of LBBB or RBBB that can produce this pattern, hence VT is highly likely.

 Principle #3: QRS is completely identical to the sinus QRS highly suggests SVT. 

  • Baseline ECG often establishes baseline conduction abnormalities
  • WCT that has an identical QRS to sinus rhythm suggests that the ventricles are being activated in an identical way to sinus rhythm, which is most commonly SVT.
  • This does not absolutely rule out VT due to the following exceptions:
    • Septal VT with early access to the His-Purkinje system.
    • Bundle branch reentrant (BBR) VT and interfascicular reentrant VT, which is only seen in patients with severe left ventricular dysfunction, and baseline bundle branch block (+/- fascicular block).

Principle #4: QRS with right superior axis (aka “extreme right axis” or “northwest axis”) is highly indicative of VT.

  • There is no combination of bundle branch block or fascicular block that can produce this axis change. 
  • Initial positive force in aVR also suggests highly unusual initial activation of the ventricles.

In absence of above principles, use QRS Morphology Criteria

  • In absence of above findings, we end up with QRS morphology criteria asking the most basic question: How likely is this QRS morphology to represent LBBB or RBBB (+/- fascicular block)? 
  • Note that QRS morphology is probabilistic, and is diagnostically weaker because:
    1. It relies on the learner’s ability to identify a “typical” aberrancy pattern on a 12-lead ECG (BBB or fascicular blocks).  We often suggest learners draw each lead of typical BBBs on blank paper. 
    2. Highly unusual aberrancy patterns are frequently encountered.  We have also seen VT morphology highly resembling BBB.
  • Numerous studies have assessed aberrancy patterns (LBBB and RBBB-type), and found features that are “typical” and “atypical” for a BBB, associated with sensitivity/specificity for each.  These features include:
    1. LBBB and RBBB generally have rapid onset, representing conduction down the functioning bundle.  Slow onset of QRS favours VT.
      • Brugada demonstrated R-S time of 100ms as a cutoff (measured beginning of R to the nadir of the S in V1-V2).
    2. In cases of RBBB-type morphology (positive terminal QRS in V1)
      • RBBB has rSR’ morphology –> the first r is never larger in amplitude compared to R’.  If it is, suspect VT.
      • RBBB should have a large positive component (R), and a small negative component (S) in V6.  Absence of an R in V6, or an R that is smaller than S in V6 is unusual for an RBBB, and suggests VT. 
      • RBBB QRS duration is typically < 140ms, anything longer suggests VT.
        • NOTE: This is a soft criteria, since many VTs are narrow and many BBBs are wide.
    3. LBBB-type morphology (negative termianl QRS in V1)
      • LBBB generally has a negative component in V1.  Downstroke of the S wave in V1 is smooth, and presence of notching on the downstroke suggests VT. 
      • LBBB QRS duration is typically < 160ms, anything longer suggests VT (very soft criteria).
  • Note on fusion and capture beats:
    • Fusion beats: Simultaneous activation of ventricle by supraventricular impulse and ventricular beat resulting in intermediate QRS morphology
    • Capture beats: QRS complex identical to underlying sinus rhythm occurs during the WCT – intermittent “capture” of ventricular activation by the normal conduction system
    • Capture of fusion beats are rare, and suggest a diagnosis of VT.  However, VT often can fuse with ventricular ectopy creating the appearance of capture and fusion beats. 
    • NOTE: Capture and fusion beats are important to understand because they frequently show up on exams.

Algorithms

  • There are many well-validated algorithms to distinguish VT from SVT.  However, we frown upon blindly memorizing algorithms because they are easy to forget, can be tricky to apply, and carry numerous pitfalls that are often forgotten. 
  • All algorithms are based on the principles we laid out above.  We feel that understanding the pathophysiologic explanation for each principle will will establish a more durable and valuable skill set compared to memorizing an algorithm. 
  • However, algorithms are often frequently discussed by physicians, and are often found on exams.  The most popular one is the Brugada Criteria.  As an exercise, identify the above principles as steps in this brugada criteria:
  • Step 1: Absence of RS complex in precordial leads (concordance)
    • YES –> VT
    • NO –> Go to Step 2
  • Step 2: R to S interval >100msec in at least 1 precordial lead (slow activation)
    • YES –> VT
    • NO –> Go to Step 3
  • Step 3: AV dissociation present
    • YES –> VT
    • NO –> Go to Step 4
  • Step 4: Morphology criteria (above) for VT present in leads V1-V2 AND V6 (see table)
    • YES –> VT
    • NO –> SVT
  • Other algorithms: (1) Bayesian, (2) Vereckei, (3) Griffith, (4) aVR, (5) Lead II R-waves Peak Time.

Acute Management

General Approach

  1. Determine if patient is stable or unstable
  2. Unstable patient:
    • If patient is unstable but pulse present – Start with synchronized cardioversion when possible, otherwise deliver unsynchronized shock
    • If pulseless – begin CPR and deliver high-energy countershock, follow ACLS algorithm
  3. Stable patient:
    • Attempt diagnostic maneuvers as above
    • Establish etiology and treat accordingly (below)
    • Avoid using IV beta-blockers, CCB or digoxin if etiology of WCT unestablished as it may precipitate hemodynamic collapse
AHA ALCS Guidelines 2018
 AHA Guidelines: Stable Vs. Unstable 
  • Hypotension
  • Acutely altered mental status
  • Signs of shock
  • Ischemic chest discomfort
  • Acute heart failure
AHA Definition of “Sustained” VT
AHA 2017 Guideline
  • Sustained – VT >30 s or requiring termination due to hemodynamic compromise
  • Non-sustained VT – ≥ 3 beats terminating spontaneously
  • Monomorphic – Same QRS morphology throughout the tachycardia

Acute Termination of VT:

NOTE: If the patient has stable wide QRS tachycardia, consideration should be given to confirming the diagnosis of VT with adenosine.  Otherwise, acute termination options include: 

  1. Electrical cardioversion
    • Preferred for hemodynamically unstable or unconscious patients
    • Synchronized cardioversion if QRS and T-wave readily discernible; otherwise, unsynchronized cardioversion (according to ACLS)
    • If the patient is awake sedation MUST be administered.  Generally midazolam (+/- fentanyl) is preferred in this case due to minimal effects on blood pressure.  Ketamine is also an option, but is less frequently used due to emergence reactions.
    • ***IMPORTANT NOTE: Electrical cardioversion should never be performed on a conscious patient.  A conscious patient has enough cardiac output to perfuse the brain, and can tolerate sedation. If they do not tolerate sedation and become unstable/unconscious, then an urgent cardioversion is indicated.  Cautious use of phenylephrine can help offset the vasodilating effect of sedatives and should be ready to be given as boluses during sedation of hypotensive patients. 
  2. Pharmacological cardioversion
    • Preferred in patients with stable sustained VT
    • Procainamide
      • Loading dose: 20-50mg/minutes until arrhythmia stops or a maximum dose of 17mg/kg is delivered. Maintenance dose at 1-4mg/minute
      • More effective than Amiodarone (PROCAMIO trial)
      • Can be used for ischemic and non-ischemic cardiomyopathy
    •  Amiodarone
      • Dose: 150mg IV over 10 minutes, followed by 1mg/minute for 6 hours, then 0.5mg/minute for 18 hours (or can switch to oral).  Total: 900mg (1 bag)
      • Most commonly used, as clinicians are most familiar with it
    •  Lidocaine:
      • Dose: 1-1.5 mg/kg bolus, can repeat a 0.5-0.75mg/kg bolus q5-10 minutes (for a maximum dose of 3mg/kg), then follow by a continuous infusion at 1-4mg/minute
      • Less effective of the 3 options, and often added as an adjunct to Procainamide or Amiodarone. 
      • Theoretically more effective in ischemic VT (in cells with metabolic acidosis).
      • NOTE: Oral version of IV lidocaine is mexiletine.
      •  
Acute Treatment of Sustained Monomorphic VT
Acute Treatment of Sustained Polymorphic VT

Treatment of VT Storm:

VT Storm Definition (AHA 2017)
VT/VF storm (electrical storm or arrhythmic storm) refers to a state of cardiac electrical instability that is defined by ≥3 episodes of sustained VT, VF, or appropriate shocks from an ICD within 24 h
  • Once patient is out of VT, there are THREE pillars of VT storm management to prevent further VT:
    1. Anti-Arrhythmic Medications:
      • Amiodarone (most common)
      • Procainamide (most effective)
      • Lidocaine (least effective, fewest side effects)
    2. Beta-blockade
      • Propranolol PO 40mg q6hours for first 48 hours)
        • Best evidence from RCT
        • More effective than metoprolol (Chatzidou et al 2018 JACC)
      • Metoprolol PO up to 100mg BID or 60mg TID PO
      • Esmolol IV: 0.5 mg/kg bolus, 0.05 mg/kg/min
        • Easily titratable (halflife is 9 min)
        • Best choice if patient is hemodynamically unstable.
    3. Sedation
      • NOTE: this is an extremely important, and most often forgotten step
      • The patient must be RAAS -1 or -2 (Wakes to speak with you, but falls asleep when you leave the room)
      • Benzodiazepines (common choices are lorazepam 1-3mg q8h or midazolam IV 1-2mg/hr)
      • Propofol (most effective anti-arrhythmic), but requires intubation if patient is too sedated
    4. Other: Treat underlying substrate
      • Remove offending agents (QTc prolonging drugs)
      • Correct electrolyte derangements
      • Revascularization in acute ischemia
    5. NOTE: Revascularization for patients with VT storm
      • Monomorphic VT is usually caused by a macro-reentry circuit involving areas of scar in patients with poor LV function (< 30-35%).  In rare cases, VT can be triggered by ischemia. 
      • In the absence of objective evidence of ongoing ischemia, urgent angiography is of limited value in the acute treatment of VT storm.
      • However polymorphic VT and VF are frequently caused by ischemia, and urgent revascularization may be of benefit. 

Refractory VT Storm

  • Options for VT storm refractory to medical therapy:
    1. Sedation with propofol and intubation
      • Sedation with propofol is highly effective in settling electrical storm.  Intubation may be indicated for airway protection if higher doses of propofol are needed. 
      • Ensure all discussions of goals of care, cardiac transplantation, and potential ablation procedures are completed prior to sedation. 
    2. Cardiac Transplantation
      • This is definitive management for a patient in VT storm.  A discussion about cardiac transplantation MUST be initiated as early as possible because a transplant assessment and workup must be completed. 
    3.  Goals of care discussion
      • Especially important if the patient is > 70yo and unlikely to be eligible for cardiac transplantation. 
    4. Catheter ablation
      • Overall ablation can be attempted as a bailout procedure.  It may have limited efficacy, especially in patients with large amount of scar burden or non-ischemic cardiomyopathy, which have patchy scar with numerous foci of VT substrate.
      • Ablation may not be possible if the patient is too unstable to tolerate catheter access of the left ventricle. 
    5. Stellate Ganglion block and Sympathetic Denervation (option in centres experienced in stellate ganglion blockade and

Patients with pacemakers/ICD:

  • Pacemaker mediated tachycardia (PMT) is a rare form of WCT in patients with a dual chamber pacemaker.  The pacemaker tracks a retrograde A from the prior V-pace to create a re-entry loop, or a pacemaker is rapidly pacing the V in an attempt to track an intrinsic atrial arrhythmia.
  • Patients with suspected pacemaker mediated tachycardia (PMT) can be easily treated by temporarily applying a magnet to the device.  The magnet will activate “magnet mode”, which will disable sensing and revert pacemaker function to asynchronous fixed-rate mode (usually 80 bpm). This will terminate any PMT rhythms, and the patient should revert to normal rhythm once magnet is removed. 
  • NOTE: PMT is rare in modern medicine due to various anti-PMT device algorithms.

Long Term Management

2020 Canadian Cardiovascular Society/Canadian Heart Rhythm Society Position Statement on the Management of Ventricular Tachycardia and Fibrillation in Patients With Structural Heart Disease

Authors

  • Primary Authors: Dr. Yehia Fanous (MD, Internal Medicine Resident), Dr. Pavel Antiperovitch (MD, FRCPC, EP Fellow)
  • Author/Reviewer: pending
  • Staff Reviewer: pending
  • Copy Editor: pending
  • Last Updated: Dec 14, 2020
  • Comments or questions please email feedback@cardioguide.ca
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