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

Initial Approach to Managing a Patient with Tachycardia

The first critical step is to immediately assess hemodynamic stability by looking for acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension (systolic BP <90 mmHg), or shock—if any of these are present, perform immediate synchronized cardioversion without delay. 1, 2, 3

Immediate Actions for All Tachycardia Patients

While assessing stability, simultaneously:

• Attach cardiac monitor and obtain vital signs 1, 2
• Establish IV access 1, 2
• Check oxygen saturation via pulse oximetry 1, 2
• Provide supplemental oxygen if hypoxemia or respiratory distress is present, as hypoxemia commonly drives tachycardia 1, 2
• Identify potential reversible causes (hypoxemia, hypovolemia, electrolyte abnormalities, myocardial ischemia, drug toxicity) 2

Critical Decision Point: Unstable vs. Stable

If Hemodynamically UNSTABLE:

Perform immediate synchronized cardioversion—this is the most effective and rapid means of terminating any hemodynamically unstable tachycardia, whether narrow or wide complex. 4, 3

• Sedate the patient if conscious and time permits, but do not delay cardioversion if extremely unstable 2, 3
• Do NOT delay cardioversion to obtain a 12-lead ECG 2, 3
• For wide-complex tachycardia in unstable patients, presume ventricular tachycardia and cardiovert immediately 2, 3
• Avoid adenosine in hypotensive patients (systolic BP <90 mmHg) as it can worsen hypotension 3
• After successful cardioversion, obtain 12-lead ECG, consider amiodarone prophylaxis to prevent recurrence, and consult cardiology urgently 3

If Hemodynamically STABLE:

Obtain a 12-lead ECG to define the rhythm and proceed with algorithmic classification. 1, 2

Algorithmic Classification Based on ECG (Stable Patients)

Step 1: Assess QRS Width

NARROW-Complex Tachycardia (QRS <120 ms)

For regular narrow-complex tachycardia:

1. First-line: Vagal maneuvers (Valsalva maneuver for 10-30 seconds with patient supine, or carotid sinus massage for 5-10 seconds after confirming no bruit, or ice-cold wet towel to face) 4, 2

   • Success rate approximately 28% when switching between techniques 4

2. If vagal maneuvers fail: Adenosine 6 mg rapid IV push, followed by 12 mg if needed 4, 2

   • Terminates AVNRT in approximately 95% of patients and orthodromic AVRT in 90-95% 4
   • Adenosine is the preferred agent due to rapid onset and short half-life 4
   • Contraindicated in severe asthma 4
   • Use with extreme caution if diagnosis unclear—may precipitate ventricular fibrillation in patients with coronary artery disease or accelerate ventricular rate in pre-excited tachycardias 4, 2

3. Alternative agents: IV diltiazem, verapamil, or beta-blockers (if adenosine fails or contraindicated) 4, 2

   • Avoid in suspected systolic heart failure or if VT/pre-excited AF cannot be excluded 4

4. If pharmacologic therapy fails: Synchronized cardioversion 4

Critical pitfall: Never use AV nodal blocking agents (adenosine, calcium channel blockers, beta-blockers) in pre-excited atrial fibrillation or flutter—this can accelerate ventricular response and cause ventricular fibrillation 2

WIDE-Complex Tachycardia (QRS ≥120 ms)

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. 4, 2

Diagnostic clues favoring VT:

• AV dissociation (pathognomonic for VT when present—look for irregular cannon A waves in jugular venous pulse and variable intensity of first heart sound) 2
• Fusion or capture beats (pathognomonic for VT) 2
• QRS >140 ms with RBBB morphology or >160 ms with LBBB morphology 2
• RS interval >100 ms in any precordial lead 4
• Negative concordance in precordial leads (diagnostic for VT) 4
• History of previous myocardial infarction with first wide-complex tachycardia after infarct strongly indicates VT 4

Management approach:

1. For regular monomorphic wide-complex tachycardia of uncertain origin: IV adenosine can be used for both diagnosis and treatment 2

   • However, electrical cardioversion should be immediately available as adenosine may precipitate VF 4

2. For presumed VT: Amiodarone 150 mg IV over 10 minutes 2, 5

   • Note: Antiarrhythmic effect may take up to 30 minutes, making it unsuitable for unstable patients 3
   • Monitor for hypotension (most common adverse effect, occurs in 16% of patients) 5

3. If pharmacologic therapy fails or patient becomes unstable: Immediate synchronized cardioversion 4

Special consideration for pre-excited atrial fibrillation:

• Presents as irregular wide-complex tachycardia with varying QRS morphology 4
• If unstable: Immediate synchronized cardioversion 4
• If stable: Ibutilide or IV procainamide (not adenosine, calcium channel blockers, or beta-blockers) 4

Post-Stabilization Management

• Even if VT self-terminates, urgent cardiology consultation is required as this represents a potentially life-threatening condition 1
• Obtain echocardiography to evaluate for structural heart disease in patients with VT 1
• Refer to electrophysiology for: wide-complex tachycardia of unknown origin, clear history of paroxysmal regular palpitations, drug-resistant or drug-intolerant narrow-complex tachycardia, and patients desiring freedom from long-term drug therapy 1

Key Clinical Pitfalls to Avoid

• Delaying cardioversion in unstable patients while waiting for 12-lead ECG 2
• Using multiple AV nodal blocking agents with overlapping half-lives, which can cause profound bradycardia 2
• Administering adenosine for irregular or polymorphic wide-complex tachycardia 2
• Normalizing heart rate in compensatory tachycardias (e.g., sinus tachycardia from hypovolemia, sepsis, hypoxemia) where cardiac output depends on rapid rate—treat the underlying cause instead 2
• Heart rates <150 bpm are unlikely to cause symptoms unless ventricular function is impaired, so focus on identifying and treating underlying causes 2