Wide Complex Tachycardia (WCT) – Study Notes

Definition

• WCT = HR >120 bpm AND QRS >120 ms.

• Always a “get out of your seat” diagnosis → evaluate immediately.

1. Initial Approach

• Check stability:

  • Hypotension

  • Altered mental status

  • Shock (ashen, poor perfusion)

  • Ischemic chest discomfort

  • Acute heart failure

• If unstable → synchronized cardioversion (electricity).

• If stable → workup and treat (while pads are on).

2. Differential Diagnosis of Stable Regular WCT

1. Ischemia (e.g., STEMI → cath lab)

2. Hyperkalemia (tx: calcium, insulin/glucose, dialysis, bicarbonate if acidemic)

3. Drugs/toxins (e.g., tricyclics → bicarbonate)

4. Ventricular Tachycardia (VT) – ~80% of WCT

5. SVT with aberrancy (bundle branch block conduction)

⚠️ Assume VT until proven otherwise (safer, guideline-supported).

3. Key Cases

• Hyperkalemia → very wide bizarre QRS.

• Ischemia-induced VT → chest pain + ST elevations.

• Young patient VT → e.g., RVOT tachycardia (don’t assume young = SVT).

4. Mechanisms

• VT: rhythm originates in ventricle → inefficient conduction → wide QRS.

• SVT w/ aberrancy: atrial rhythm + bundle branch block → wide.

• Toxins/hyperkalemia: diffuse conduction disturbance.

5. Why Assume VT?

• Algorithms (e.g., Brugada criteria) are hard, unreliable (≈75% accuracy).

• Risk of harm if misdiagnosed:

  • VT → mistaken for SVT → wrong meds (e.g., diltiazem) → dangerous.

  • SVT → mistaken for VT → just more workup, not harmful.

• Guidelines (ESC 2019, AHA 2020): Default to VT.

6. Adenosine Use

• Can use if: stable, regular, monomorphic WCT.

• Never use if: unstable, irregular, polymorphic (e.g., WPW, torsades).

• Role: May unmask SVT/atrial flutter; sometimes converts SVT.

• ⚠️ Do NOT use conversion as diagnostic of SVT → ~10% of true VT may respond to adenosine.

7. Medications & Treatment (Stable WCT)

• Always: pads on, IV, O₂, monitor, crash cart ready.

• Synchronized cardioversion is always an option (even if stable).

• Drug therapy:

  • Procainamide (preferred in ED; safest & most effective)

  • Amiodarone (widely used; slower onset, more long-term use)

  • Sotalol (option but less common)

  • Lidocaine (sometimes used, esp. ischemia-related VT)

Evidence:

• PROCAMIO trial: Procainamide > Amiodarone (67% vs 38% termination, fewer adverse events).

• ESC 2019 → Procainamide (IIa), Amiodarone (IIb).

• AHA 2020 → Procainamide, Amio, Sotalol all IIb.

8. Recurrent VT (Electrical Storm)

• Definition: ≥3 episodes of sustained VT/VF or ≥3 ICD shocks within 24 hrs.

• Causes: ischemia, drugs, thyroid, ↓K, ↓Mg, ↑sympathetic tone.

• Treatment:

  • Cardioversion if needed.

  • Amiodarone, lidocaine.

  • Non-selective beta-blockers (e.g., propranolol, esmolol) → reduce sympathetic drive.

  • Avoid epinephrine (worsens storm).

Summary – Stable Regular WCT

1. If unstable → cardiovert.

2. If stable → assume VT unless clearly ischemia, hyperkalemia, or drugs.

3. Pads on, IV, monitor, ready to shock.

4. Adenosine may help unmask rhythm, but never rule out VT if it works.

5. Procainamide = best choice in ED. Amiodarone/sotalol also acceptable.

6. Recurrent VT = think electrical storm → consider beta-blockers.

7. Young patients can have VT too!