What is the initial approach to a patient presenting with tachycardia?

Initial Approach to Tachycardia Workup

Begin by immediately assessing hemodynamic stability—if the patient shows acute altered mental status, ischemic chest pain, acute heart failure, hypotension, or shock, proceed directly to synchronized cardioversion without delay for diagnostic workup. 1, 2

Immediate Stabilization (First 2-3 Minutes)

Assess for hemodynamic instability by looking for: 1, 2

• Acute altered mental status
• Ischemic chest discomfort
• Acute heart failure signs
• Hypotension or shock

Simultaneously perform these actions: 3, 1

• Attach cardiac monitor
• Obtain vital signs and establish IV access
• Check oxygen saturation via pulse oximetry
• Assess for signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions, paradoxical abdominal breathing) 3
• Provide supplemental oxygen if hypoxemia or respiratory distress present, as hypoxemia commonly drives tachycardia 1, 2

Critical Decision Point: Stable vs. Unstable

If UNSTABLE (any of the above signs present):

Perform immediate synchronized cardioversion 1, 2

• Sedate if conscious and time permits 1
• Do NOT delay cardioversion to obtain 12-lead ECG 1, 2
• For wide-complex tachycardia, presume ventricular tachycardia and cardiovert immediately 2
• For witnessed, monitored unstable VT, consider precordial thump only if defibrillator not immediately available 2

If STABLE:

Obtain 12-lead ECG to define the rhythm 3, 1

Determine if heart rate >150 bpm: Rates <150 bpm are unlikely to cause symptoms unless ventricular function is impaired, suggesting the tachycardia may be compensatory rather than primary 3, 1

Identify potential reversible causes while initiating treatment: 1, 2

• Hypoxemia (most common)
• Dehydration
• Fever
• Anemia
• Pain or anxiety
• Medication effects

Algorithmic Classification Based on ECG

Step 1: Assess QRS Width 3, 1

Narrow-Complex Tachycardia (QRS <0.12 seconds):

Determine if regular or irregular: 3, 1

If regular narrow-complex:

• Consider sinus tachycardia, atrial flutter, AV nodal reentry, accessory pathway-mediated tachycardia, or atrial tachycardia 3
• For SVT: Attempt vagal maneuvers first (unless unstable or would delay treatment) 3, 4
• If vagal maneuvers fail: Administer adenosine 6 mg rapid IV push, followed by 12 mg if needed 3, 1

If irregular narrow-complex:

• Likely atrial fibrillation, multifocal atrial tachycardia, or occasionally atrial flutter 3
• CRITICAL PITFALL: Never use AV nodal blocking agents (adenosine, calcium blockers, beta-blockers) if pre-excited atrial fibrillation or flutter is present, as this accelerates ventricular response 1, 2

Wide-Complex Tachycardia (QRS ≥0.12 seconds):

Most wide-complex tachycardias are ventricular in origin 3

Differential includes: 3

• Ventricular tachycardia (most common)
• SVT with aberrancy
• Pre-excited tachycardias (Wolff-Parkinson-White syndrome)
• Ventricular paced rhythms

If regular monomorphic wide-complex of uncertain origin:

• Consider IV adenosine for both treatment and diagnosis 1
• CRITICAL PITFALL: Never give adenosine for irregular or polymorphic wide-complex tachycardia 1, 2

If presumed ventricular tachycardia:

• Amiodarone 150 mg IV over 10 minutes (repeat if VT recurs, then maintenance infusion 1 mg/min for first 6 hours) 3, 1
• Alternative: Procainamide 20-50 mg/min until arrhythmia suppressed, hypotension ensues, QRS increases >50%, or maximum 17 mg/kg given 3, 5
• Avoid procainamide if prolonged QT or CHF 3

Step 2: Special Diagnostic Considerations

If sinus tachycardia identified: Focus on treating underlying cause rather than the heart rate itself 1, 6

If pre-excitation present on resting ECG with history of paroxysmal regular palpitations: Presume AVRT and refer to electrophysiology without needing to capture the arrhythmia 2

If pre-excitation with irregular paroxysmal palpitations: Suggests atrial fibrillation, requiring urgent EP evaluation due to sudden death risk 2

Critical Pitfalls to Avoid

• Never delay cardioversion in unstable patients while obtaining 12-lead ECG 1, 2
• Never normalize heart rate in compensatory tachycardia where cardiac output depends on the rapid rate (e.g., sepsis, hypovolemia) 1, 2
• Never combine multiple AV nodal blocking agents with overlapping half-lives, as this causes profound bradycardia 1, 2
• Never use AV nodal blocking agents in pre-excited atrial fibrillation/flutter 1, 2

Post-Stabilization Management

Even if VT self-terminates, urgent cardiology consultation is required as this represents a potentially life-threatening condition 2, 6

Obtain echocardiography to evaluate for structural heart disease in patients with VT 6

For atrial fibrillation/flutter after spontaneous conversion: Assess stroke risk using CHA₂DS₂-VASc score to determine need for anticoagulation 6

Refer to electrophysiology for: 2

• Wide-complex tachycardia of unknown origin
• Clear history of paroxysmal regular palpitations
• Drug-resistant or drug-intolerant narrow-complex tachycardia
• Patients desiring freedom from long-term drug therapy

Key Clinical Insight

Research demonstrates that 77% of patients presenting with sustained VT are hemodynamically stable initially, allowing first-line antiarrhythmic drug administration; however, 51% ultimately require electrical therapy for definitive termination 7. Additionally, "stable" VT carries a 3-year mortality of 33.6%, which may exceed that of unstable VT after risk adjustment 8. Therefore, direct current cardioversion must always be immediately available in the emergency department, and all VT patients require aggressive evaluation and specialist consultation regardless of initial stability. 7, 8