Wide QRS Tachycardia Without Visible P Waves
Diagnosis
This rhythm is most likely ventricular tachycardia (VT) and should be treated as such unless proven otherwise. 1, 2
The key diagnostic features present are:
- Wide QRS complex (>120 ms but not narrow) 1, 2
- No visible P waves, suggesting either VT with AV dissociation or a junctional/supraventricular mechanism with the P waves buried in the QRS 1
- Regular rhythm (implied by "nice heart rhythm") 1
Why This Is Likely VT
The absence of visible P waves in a wide QRS tachycardia strongly suggests AV dissociation, which is virtually diagnostic of ventricular tachycardia. 1, 2 When P waves cannot be seen, they are either:
- Dissociated from the QRS (VT with independent atrial activity) 1, 2
- Hidden within the QRS (less likely with a wide complex) 1
The American College of Cardiology emphasizes that approximately 80% of wide QRS tachycardias are ventricular in origin, particularly in patients with structural heart disease or prior myocardial infarction. 1, 2
Critical Diagnostic Pitfall
Wide QRS tachycardias are frequently misdiagnosed as supraventricular tachycardia (SVT) with aberrancy, leading to dangerous treatment errors. 3 In one study, 39% of VT cases were initially misdiagnosed, and verapamil administration in these misdiagnosed cases resulted in hemodynamic deterioration in 100% of patients. 3
Immediate Management Algorithm
Step 1: Assess Hemodynamic Stability
- If hemodynamically unstable (hypotension, altered mental status, chest pain, pulmonary edema): Immediate DC cardioversion 1, 2
- If hemodynamically stable: Proceed to Step 2 2
Important: Stable vital signs do NOT help distinguish between SVT and VT—many VT patients remain stable initially. 2
Step 2: Obtain 12-Lead ECG and Look for VT Criteria
While obtaining the ECG, prepare for cardioversion. Look for these features that confirm VT: 1, 2, 4
- AV dissociation (more QRS complexes than P waves, or P waves marching through at their own rate) 1, 2
- Absence of RS complex in ALL precordial leads (positive or negative concordance)—sensitivity 99%, specificity 97% 1, 4
- RS interval >100 ms in any precordial lead (from R onset to S nadir) 1, 2, 4
- Fusion or capture beats (diagnostic of VT) 1
Step 3: If Diagnosis Remains Uncertain, Treat as VT
The default assumption must be VT. 1, 2 For stable patients with presumed VT:
First-line pharmacologic options:
- IV procainamide (preferred) 1, 2
- IV sotalol (alternative) 1
- IV amiodarone (especially if impaired LV function or heart failure) 1, 2
Second-line:
- IV lidocaine (less effective—only 19% termination rate in one study) 5
Critical "Never Do" List
- NEVER give verapamil or diltiazem for wide complex tachycardia of uncertain etiology—this causes severe hypotension and can be fatal in VT 1, 2, 3
- NEVER give IV calcium-channel blockers and beta blockers together due to potentiation of hypotensive/bradycardic effects 1
- Use adenosine with extreme caution—it may precipitate VF in patients with coronary disease and can accelerate ventricular rate in pre-excited AF 1
Special Considerations
If History of MI or Structural Heart Disease
A positive history of previous myocardial infarction with first occurrence of wide QRS tachycardia after the infarct strongly indicates VT. 1, 2 QR complexes in the ECG indicate myocardial scar and are present in ~40% of post-MI VT cases. 1
If Pre-Excitation Suspected
If the patient has known Wolff-Parkinson-White syndrome or the wide QRS suggests pre-excited tachycardia, avoid AV nodal blocking agents (adenosine, verapamil, diltiazem, beta blockers). 1 Use DC cardioversion or IV ibutilide/flecainide if stable. 1
Post-Conversion Management
After successful termination, all patients with wide QRS tachycardia of uncertain etiology should be referred to an arrhythmia specialist for electrophysiology study and consideration of catheter ablation or ICD placement. 1, 2