What are the common ECG rhythms, how are they identified on an ECG, and what are the recommended management steps for each?

ECG Rhythms: Identification and Management

The most critical first step in managing any cardiac rhythm is determining patient stability—unstable patients with wide-complex tachycardia should be presumed to have ventricular tachycardia and receive immediate cardioversion. 1

Systematic Approach to ECG Rhythm Identification

Step 1: Assess Patient Stability

Before analyzing the rhythm, determine hemodynamic status:

• Unstable signs: Hypotension, altered mental status, chest pain, acute heart failure, syncope
• Stable: Alert, adequate perfusion, tolerating rhythm

Step 2: Determine QRS Width

Narrow-Complex Tachycardias (QRS <120 ms)

These are almost always supraventricular in origin 2. Analyze systematically:

Regular Narrow-Complex Tachycardias:

• No visible P waves, regular RR: Most likely AVNRT (atrioventricular nodal reentrant tachycardia)

  • Look for pseudo R' wave in V1 or pseudo S wave in inferior leads 3, 2

• P wave in ST segment (RP <90 ms): Most likely AVRT (atrioventricular reentrant tachycardia) 4

• RP interval longer than PR interval: Consider atypical AVNRT, permanent junctional reciprocating tachycardia (PJRT), or atrial tachycardia 2

• Atrial rate exceeds ventricular rate: Atrial flutter or atrial tachycardia 3

Irregular Narrow-Complex Tachycardias:

• Absolutely irregular RR intervals, no distinct P waves, atrial cycle length <200 ms: Atrial fibrillation 5
• Variable P-wave morphology: Multifocal atrial tachycardia (MAT) 4
• Atrial flutter with variable AV conduction 3

Wide-Complex Tachycardias (QRS ≥120 ms)

Critical distinction: Assume VT until proven otherwise 1. The differential includes:

• Ventricular tachycardia (VT)
• SVT with aberrancy (bundle branch block)
• Pre-excited tachycardia (accessory pathway conduction)
• Ventricular paced rhythms

Regular Wide-Complex Tachycardia:

• AV dissociation or fusion complexes present: Diagnostic of VT 3
• Concordance in precordial leads (all positive or all negative): Suggests VT or pre-excitation 3
• Apply Brugada criteria or Vereckei algorithm for systematic differentiation 3

Irregular Wide-Complex Tachycardia:

• Atrial fibrillation with aberrancy
• Pre-excited atrial fibrillation (WPW syndrome)
• Polymorphic VT/torsades de pointes 1

Management Algorithms

Unstable Tachycardia (Any Type)

1. Immediate synchronized cardioversion 1
2. If rhythm deteriorates to VF or polymorphic VT: Unsynchronized defibrillation 1
3. Precordial thump may be considered for witnessed, monitored unstable VT if defibrillator not immediately available (Class IIb) 1

Stable Narrow-Complex SVT

1. Vagal maneuvers first 2
2. Adenosine (preferred AV nodal blocker due to short half-life) 1
3. Alternative AV nodal blockers: calcium channel blockers or beta-blockers 1
4. Avoid AV nodal blockers in pre-excited atrial fibrillation/flutter (can accelerate ventricular response and cause hemodynamic collapse) 1

Stable Wide-Complex Tachycardia

1. Obtain 12-lead ECG 1
2. Consider expert consultation 1
3. If regular and monomorphic, adenosine is relatively safe for both diagnosis and treatment (Class IIb) 1
4. Do NOT give adenosine for irregular or polymorphic wide-complex tachycardia 1

Ventricular Tachycardia (Stable)

Amiodarone is the preferred agent:

• 150 mg IV over 10 minutes 1
• Can repeat as needed up to 2.2 g/24 hours 1
• Effective for monomorphic VT, especially in patients with coronary disease and poor ventricular function 1

Alternative agents:

• Sotalol 1.5 mg/kg IV over 5 minutes (avoid if prolonged QT) 1
• Lidocaine is less effective than amiodarone, procainamide, or sotalol—consider second-line 1

Pre-excited Atrial Fibrillation (WPW)

Critical pitfall: This is a life-threatening rhythm requiring specific management:

• NEVER use AV nodal blockers (adenosine, calcium channel blockers, beta-blockers, digoxin) 1
• These can paradoxically accelerate ventricular response and precipitate VF
• Use antiarrhythmic medications (amiodarone, procainamide, or sotalol) for rate control 1
• If unstable: Immediate cardioversion 1

Atrial Fibrillation

ECG characteristics: Absolutely irregular RR intervals, no distinct P waves, atrial cycle length <200 ms when visible 5

Rate control options:

• Beta-blockers or non-dihydropyridine calcium channel blockers (effective at rest and exercise) 5
• Digoxin (effective only at rest, less effective during exercise) 5

Important consideration: Conversion to sinus rhythm may cause thromboembolic complications without appropriate anticoagulation precautions 1

Common Pitfalls to Avoid

1. Misdiagnosing VT as SVT with aberrancy: Can be fatal if verapamil/diltiazem given for VT 2
2. Using AV nodal blockers in pre-excited AF: Can precipitate ventricular fibrillation 1
3. Combining long-acting AV nodal blockers: Can cause profound bradycardia 1
4. Giving adenosine for irregular wide-complex tachycardia: Contraindicated 1
5. Assuming stable vital signs rule out VT: Hemodynamic stability does not differentiate SVT from VT 2

Documentation Requirements

Always obtain:

• 12-lead ECG during tachycardia when possible (should not delay treatment if unstable) 2
• 12-lead ECG in sinus rhythm for comparison 3
• Minimum: rhythm strip from monitor/defibrillator before cardioversion 2

The systematic approach of assessing stability → QRS width → regularity → P-wave relationship provides a reliable framework for identifying and managing the vast majority of cardiac rhythms encountered in acute care settings.