What is the appropriate management for a hypotensive patient presenting with a Wolff‑Parkinson‑White (WPW) pattern?

Management of Hypotension in Wolff-Parkinson-White Pattern

A hypotensive patient with WPW pattern requires immediate synchronized electrical cardioversion if the hypotension is caused by pre-excited atrial fibrillation or rapid tachyarrhythmia, as this is a Class I emergency intervention to prevent ventricular fibrillation and sudden cardiac death. 1

Critical Initial Assessment

The first step is to determine whether the hypotension is caused by:

• Pre-excited atrial fibrillation with rapid ventricular response – characterized by wide QRS complexes (≥120 ms), irregular rhythm, and ventricular rates often exceeding 200 beats per minute 2
• Orthodromic AVRT – narrow-complex regular tachycardia that can cause hemodynamic compromise 3
• Other causes unrelated to the WPW pattern – such as sepsis, hypovolemia, or cardiogenic shock from structural heart disease 3

The presence of a wide, irregular tachycardia in a hypotensive patient with known or suspected WPW must be assumed to be pre-excited atrial fibrillation until proven otherwise, as misdiagnosis can be fatal. 2

Immediate Management Algorithm

If Hemodynamically Unstable (Hypotensive, Altered Mental Status, Chest Pain, Pulmonary Edema)

• Perform immediate synchronized electrical cardioversion without delay – this is the only appropriate intervention and takes absolute priority over pharmacological therapy 1, 3
• Do not waste time attempting pharmacological conversion in an unstable patient 1
• Cardioversion prevents progression to ventricular fibrillation, which occurs when atrial fibrillation conducts rapidly through the accessory pathway (shortest pre-excited R-R interval <250 ms) 3

If Hemodynamically Stable Despite Hypotension

If the patient is hypotensive but maintaining adequate perfusion (alert, no chest pain, no pulmonary edema):

• For wide-complex irregular tachycardia (pre-excited AF):

  • Administer intravenous procainamide as first-line pharmacological therapy (Class I recommendation) – it blocks the accessory pathway and can produce transient complete AV block, markedly reducing ventricular rate 1, 2
  • Alternative: intravenous ibutilide (Class I recommendation) 1, 2
  • Second-line options: Class IC agents (flecainide, propafenone) if procainamide/ibutilide unavailable 1

• For narrow-complex regular tachycardia (orthodromic AVRT):

  • Attempt vagal maneuvers first 3
  • Administer intravenous adenosine (6 mg rapid IV push, then 12 mg if needed) – safe and effective for terminating orthodromic AVRT when QRS is narrow 3
  • Alternative: AV-nodal blocking agents (beta-blockers, calcium-channel blockers) are effective in this setting 3

Absolutely Contraindicated Medications in Pre-Excited Atrial Fibrillation

Never administer the following drugs if the QRS is wide (≥120 ms), as they can precipitate ventricular fibrillation and sudden death: 1, 2

• Digoxin – shortens accessory pathway refractory period and accelerates ventricular response 1
• Non-dihydropyridine calcium-channel blockers (diltiazem, verapamil) – facilitate anterograde conduction over the accessory pathway 1
• Intravenous beta-blockers (metoprolol, esmolol, propranolol, atenolol) – ineffective for rate control and may worsen accessory-pathway conduction 1
• Adenosine when QRS ≥120 ms – will not terminate the arrhythmia and may precipitate ventricular fibrillation 1
• Amiodarone – can accelerate conduction through the accessory pathway in WPW, use only with extreme caution 2

These medications slow conduction through the AV node while leaving the accessory pathway unchanged, leading to unopposed rapid ventricular rates and risk of ventricular fibrillation. 1

Critical Diagnostic Pitfall

If hypotension is present but the rhythm is sinus with a WPW pattern (delta waves visible), the hypotension is NOT caused by the WPW pattern itself. 3 In this scenario:

• Search for alternative causes of hypotension (sepsis, bleeding, cardiomyopathy, medication effects) 3
• The WPW pattern is an incidental finding and should not distract from standard hypotension management 3
• Avoid AV-nodal blocking agents even in sinus rhythm if there is any possibility of atrial fibrillation developing 1

Post-Stabilization Management

Once the patient is stabilized:

• Refer for catheter ablation of the accessory pathway – this is the definitive first-line treatment (Class I recommendation) for all symptomatic WPW patients, with success rates exceeding 95% and major complication rates of 0.1–0.9% 1, 3
• Ablation is mandatory for patients who present with atrial fibrillation, syncope, or hemodynamic compromise 1
• Do not discharge the patient on long-term AV-nodal blocking agents, as these are contraindicated in WPW with the potential for pre-excited atrial fibrillation 1

Special Consideration: Iatrogenic Bradycardia

If the hypotension is accompanied by bradycardia rather than tachycardia:

• This is most commonly iatrogenic from inappropriate administration of AV-nodal blocking agents 3
• Immediately discontinue all beta-blockers, calcium-channel blockers, digoxin, and amiodarone 3
• The WPW pattern itself does not cause bradycardia; search for co-existing sinus node dysfunction or medication effects 3
• If symptomatic bradycardia persists, standard bradycardia protocols apply (atropine, temporary pacing) 3

Key Clinical Principle

The combination of hypotension and WPW pattern demands immediate rhythm assessment: if the rhythm is a wide-complex irregular tachycardia, assume pre-excited atrial fibrillation and cardiovert immediately; if the rhythm is narrow-complex regular tachycardia, treat as orthodromic AVRT with adenosine; if the rhythm is sinus, the hypotension is unrelated to WPW and requires standard evaluation. 1, 3, 2