How should a patient with a wide‑complex tachycardia be managed, including assessment of hemodynamic stability and differentiation between ventricular tachycardia and supraventricular tachycardia with aberrant conduction?

Management of Wide Complex Tachycardia

If the diagnosis of wide complex tachycardia cannot be definitively established, treat the patient as ventricular tachycardia (VT), and if hemodynamically unstable, perform immediate synchronized cardioversion without delay. 1, 2, 3

Initial Assessment: Hemodynamic Stability

The first and most critical decision point is determining hemodynamic stability. Assess for:

• Acute altered mental status 2
• Ischemic chest discomfort 2
• Acute heart failure 2
• Hypotension or shock 2, 4
• Signs of increased work of breathing and oxygen saturation 2

For Hemodynamically Unstable Patients:

Proceed immediately to synchronized cardioversion—this is the most effective and rapid means of terminating any hemodynamically unstable wide complex tachycardia. 1, 2, 4, 3

• Do not delay cardioversion to obtain a 12-lead ECG, attempt pharmacologic therapy, or pursue additional diagnostic studies 2, 4, 3
• Sedate the patient if conscious and time permits (consider etomidate 0.2-0.3 mg/kg IV given hypotension) 4, 3
• Consider precordial thump only for witnessed, monitored unstable VT if a defibrillator is not immediately ready 2, 4
• Establish continuous cardiac monitoring, two large-bore IV lines, and continuous blood pressure monitoring 4
• All unstable patients require ICU/CCU admission and immediate cardiology/electrophysiology consultation 4, 3

For Hemodynamically Stable Patients: Diagnostic Approach

Step 1: Obtain a 12-Lead ECG

A 12-lead ECG during tachycardia is the single most critical diagnostic tool for identifying the mechanism. 1, 2

Step 2: Assess Rhythm Regularity

Determine if the wide complex tachycardia is regular or irregular. 2

Step 3: Apply Diagnostic ECG Criteria to Differentiate VT from SVT with Aberrancy

Key diagnostic features that are pathognomonic for VT:

• AV dissociation (independent P waves with ventricular rate faster than atrial rate)—look for irregular cannon A waves in jugular venous pulse and variable intensity of first heart sound on physical exam 1, 2
• Fusion or capture beats 1, 2
• Negative concordance in precordial leads (all QRS complexes negative in V1-V6) is diagnostic for VT 1

Features highly suggestive of VT:

• QRS width >140 ms with RBBB morphology or >160 ms with LBBB morphology 1, 2
• RS interval >100 ms in any precordial lead 1
• Concordance (all positive or all negative QRS deflections across V1-V6) 1, 2
• QR complexes indicating myocardial scar (present in ~40% of post-MI VT) 1

Clinical history strongly suggesting VT:

• Previous myocardial infarction with first occurrence of wide complex tachycardia after the infarct 1

Important Caveats:

• QRS width criteria are less specific in patients taking class Ia or Ic antiarrhythmic drugs, those with hyperkalemia, or severe heart failure 1
• QRS width criteria do not help differentiate VT from SVT with accessory pathway conduction 1
• Positive concordance does not exclude antidromic AVRT over a left posterior accessory pathway 1

Pharmacologic Management of Stable Wide Complex Tachycardia

First-Line Therapy:

For stable monomorphic VT without severe heart failure or acute MI:

• Procainamide is the preferred first-line agent (20-50 mg/min IV infusion until arrhythmia suppression, hypotension, QRS widening >50%, or maximum dose of 17 mg/kg) 4, 3
• Procainamide is more effective than amiodarone for early slowing and termination of VT 3
• Monitor blood pressure closely during infusion 3

For stable monomorphic VT with severe heart failure, acute MI, or impaired left ventricular function:

• Amiodarone 150 mg IV over 10 minutes is the preferred agent, followed by maintenance infusion of 1 mg/min for the first 6 hours 2, 4, 3
• Amiodarone has a better safety profile in structural heart disease but is less ideal for early conversion 3

Diagnostic/Therapeutic Consideration:

IV adenosine may be considered for undifferentiated regular stable wide complex tachycardia:

• Relatively safe and can help diagnose the underlying rhythm 2, 3
• If the rhythm terminates with adenosine, this suggests SVT with aberrancy rather than VT 3
• Use with extreme caution: adenosine may precipitate ventricular fibrillation in patients with coronary artery disease and accelerate ventricular rate in pre-excited tachycardias (atrial fibrillation with WPW) 1, 2
• Avoid in severe asthma and be aware it may precipitate atrial fibrillation in 1-15% of cases 3

Special Situations:

For polymorphic VT with long QT syndrome (torsades de pointes):

• IV magnesium is the primary treatment 4, 3
• Consider overdrive pacing or IV isoproterenol for polymorphic VT with bradycardia or pauses 4, 3

For ischemic VT or catecholaminergic VT:

• IV beta-blockers may be effective, but avoid in hypotensive states 4, 3

Critical Pitfalls to Avoid

Never use calcium channel blockers (verapamil or diltiazem) for wide complex tachycardia unless definitively proven to be SVT—they can cause hemodynamic collapse or ventricular fibrillation if the rhythm is actually VT. 1, 2, 3

Never use AV nodal blocking agents (adenosine, calcium blockers, beta-blockers) in pre-excited atrial fibrillation or flutter—they can accelerate the ventricular response. 2

Do not administer adenosine for irregular or polymorphic wide complex tachycardia. 2

Avoid using multiple AV nodal blocking agents with overlapping half-lives—this can cause profound bradycardia. 2

Do not delay cardioversion in unstable patients while waiting for 12-lead ECG or attempting pharmacologic conversion. 2, 4, 3

Avoid sotalol in patients with prolonged QT interval. 2, 4

Post-Stabilization Management

• Rapidly correct electrolyte abnormalities, particularly potassium, magnesium, and calcium 4, 3
• All patients with wide complex tachycardia require ICU/CCU admission and immediate cardiology/electrophysiology consultation 4, 3
• Consider electrophysiology study and possible catheter ablation once stabilized 4, 3
• Obtain echocardiography to evaluate structural heart disease 2
• Identify and treat reversible causes (infection/sepsis, hypoxia, myocardial ischemia, metabolic derangements) 2