Tachycardia Work-Up: Evaluation, Investigations, and Initial Management
Begin by immediately assessing hemodynamic stability—if the patient shows acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or shock, proceed directly to synchronized cardioversion without delay. 1, 2
Initial Assessment and Stabilization
Immediate Actions (First 2-3 Minutes)
- Attach cardiac monitor, establish IV access, and measure blood pressure to enable rapid intervention if the patient decompensates 1, 2
- Assess oxygenation via pulse oximetry and look for signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions) 3
- Provide supplemental oxygen if saturation is inadequate or respiratory distress is present 1, 2
- Obtain a 12-lead ECG immediately if the patient is stable enough—this is the single most critical diagnostic tool and should not be delayed unless the patient is unstable 3, 1
Critical Decision Point: Stable vs. Unstable
If unstable (altered mental status, chest pain with ischemia, acute heart failure, hypotension, or shock), perform immediate synchronized cardioversion without waiting for further workup 1, 2. Sedate if conscious and time permits 1.
A common pitfall is delaying cardioversion in unstable patients while obtaining a 12-lead ECG—stability determines urgency, not diagnostic curiosity 1.
Diagnostic Investigations for Stable Patients
ECG Analysis: The Cornerstone of Diagnosis
The 12-lead ECG during tachycardia reveals the mechanism and guides treatment 3, 1. Analyze systematically:
1. Determine regularity: Regular vs. irregular rhythm 1, 2
- Irregular narrow-complex: Likely atrial fibrillation, multifocal atrial tachycardia, or atrial flutter with variable block 3
- Regular narrow-complex: Consider AVNRT, AVRT, atrial flutter with fixed block, or atrial tachycardia 3
- Regular wide-complex: Ventricular tachycardia until proven otherwise 1, 2
2. Measure QRS duration: Narrow (<120 ms) vs. wide (≥120 ms) 3, 1
3. For wide-complex tachycardia, look for VT-specific features:
- AV dissociation (independent P waves with ventricular rate faster than atrial rate)—this is pathognomonic for VT 3, 1
- Fusion or capture beats—also pathognomonic for VT 1
- Concordance in precordial leads (all QRS complexes positive or all negative in V1-V6)—strongly suggests VT 3, 1
- QRS width >140 ms with RBBB morphology or >160 ms with LBBB morphology—favors VT 1
4. For narrow-complex tachycardia, examine P wave location:
- P wave buried in or immediately after QRS (pseudo S wave in inferior leads, pseudo R' in V1): Typical AVNRT 3
- P wave in early ST segment (short RP): Orthodromic AVRT 3
- P wave closer to next QRS (long RP): Atypical AVNRT, PJRT, or atrial tachycardia 3
5. Check baseline ECG (when in sinus rhythm) for:
- Pre-excitation pattern (short PR, delta wave)—indicates WPW syndrome and mandates immediate electrophysiology referral 3, 4
Additional Investigations
- Basic metabolic panel: Check for hypokalemia and hypomagnesemia, which predispose to arrhythmias 2
- Thyroid function (TSH): Exclude hyperthyroidism as a reversible cause 4
- Complete blood count: Assess for anemia or infection 4
- Troponin: If chest pain or ischemic symptoms present 1
- Echocardiogram: Evaluate for structural heart disease, especially if recurrent episodes or considering long-term management 3, 4
- Ambulatory monitoring (Holter or event recorder): Essential for patients with recurrent paroxysmal symptoms to capture episodes 3, 4
Initial Management Algorithm
For Unstable Patients (Any Wide or Narrow Complex)
Immediate synchronized cardioversion is the only appropriate intervention 1, 2. For witnessed, monitored unstable VT, consider precordial thump if defibrillator not immediately ready 1.
For Stable Regular Narrow-Complex Tachycardia
Step 1: Vagal maneuvers (Valsalva maneuver preferred over carotid massage, especially in elderly) 2, 5
Step 2: Adenosine 6 mg rapid IV push followed immediately by saline flush 1, 2
- If no response after 1-2 minutes, give 12 mg rapid IV push 3, 1
- Success rate approximately 93% for AVNRT and AVRT 2
- Critical contraindication: Do NOT use adenosine if pre-excitation (WPW) with atrial fibrillation/flutter—this can accelerate ventricular response and cause cardiac arrest 1
Step 3: If adenosine fails, consider:
- Beta-blockers (most effective for rate control) 2
- Non-dihydropyridine calcium channel blockers (diltiazem or verapamil) 2
For Stable Regular Wide-Complex Tachycardia
Treat as ventricular tachycardia unless proven otherwise—administering verapamil or diltiazem for presumed SVT when the rhythm is actually VT can cause hemodynamic collapse or ventricular fibrillation 1.
Option 1: Amiodarone 150 mg IV over 10 minutes for confirmed or presumed VT 3, 1, 2
- Follow with maintenance infusion of 1 mg/min for first 6 hours 3
Option 2: Adenosine can be used diagnostically for regular monomorphic wide-complex tachycardia of uncertain origin 1, 2
- Use with extreme caution: May precipitate ventricular fibrillation in patients with coronary artery disease 1, 2
- Never use for irregular or polymorphic wide-complex tachycardia 1
Option 3: Procainamide 20-50 mg/min until arrhythmia suppressed, hypotension occurs, QRS widens >50%, or maximum dose 17 mg/kg reached 3
- Avoid if prolonged QT or heart failure 3
For Irregular Narrow-Complex Tachycardia (Atrial Fibrillation/Flutter)
Rate control is the priority:
Critical warning: If pre-excitation is present on baseline ECG, avoid all AV nodal blocking agents (adenosine, calcium blockers, beta-blockers, digoxin)—these can paradoxically accelerate ventricular response through the accessory pathway 1
Special Considerations and Pitfalls
Heart Rate Interpretation
- Heart rates <150 bpm are unlikely to cause symptoms unless ventricular function is impaired 3, 1, 2
- Sinus tachycardia (gradual onset/termination) requires treatment of underlying cause (fever, dehydration, infection, hypotension), not antiarrhythmic therapy 3, 2
- PSVT (abrupt onset/termination) is frequently misdiagnosed as panic disorder because symptoms are nearly identical 4, 5
Common Dangerous Pitfalls
- Using multiple AV nodal blocking agents with overlapping half-lives—can cause profound bradycardia 1
- Normalizing heart rate in compensatory tachycardias where cardiac output depends on rapid rate (e.g., hypovolemia, sepsis) 1
- Administering adenosine for irregular or polymorphic wide-complex tachycardia 1
- Assuming anxiety without proper cardiac evaluation in patients with recurrent paroxysmal palpitations 4
When to Refer to Cardiac Electrophysiology
Immediate/urgent referral indicated for: 3, 2, 4
- Pre-excitation on resting ECG with history of paroxysmal palpitations (WPW syndrome)
- Wide-complex tachycardia of unknown origin
- Recurrent episodes of regular, paroxysmal palpitations with abrupt onset/termination
- Drug resistance or intolerance
- Patients desiring to be free of long-term drug therapy
Identify and Correct Reversible Causes
While initiating treatment, simultaneously address: 1, 2
- Hypoxia
- Hypokalemia and hypomagnesemia (correct to reduce arrhythmia risk)
- Infection/sepsis
- Hypovolemia/hypotension
- Myocardial ischemia
- Metabolic derangements