Pre-excited atrial fibrillation with haemodynamic compromise in a young man with Wolff–Parkinson–White
A 26-year-old man is brought to the emergency department with palpitations and near-syncope that began 40 minutes ago. He has had three similar but shorter episodes in the past year and one documented narrow-complex tachycardia at a walk-in clinic, treated with intravenous verapamil. Today he is pale and clammy, blood pressure 76/44 mmHg, pulse approximately 230/min irregular, respiratory rate 28/min and oxygen saturation 94% on air. The ECG shows a broad-complex, irregularly irregular tachycardia with varying QRS width, rates up to 280/min, and one short run of a very wide complex. He is drowsy but rousable. He has no known structural heart disease, takes no regular medication, and has no family history of sudden death. There is an anaesthetist and a defibrillator immediately available.
1. What is the rhythm diagnosis, and how do you manage him in the first 10 minutes?
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This is pre-excited atrial fibrillation (AF conducted antegradely down an accessory pathway) in a patient with WPW. Clues: irregularly irregular broad-complex tachycardia, varying QRS morphology, extremely fast rates (up to 280/min, exceeding the AV node's typical conduction capacity), and a history of a narrow-complex tachycardia (AVRT) in a young patient with no structural disease.
Immediate management:
- He is haemodynamically unstable (hypotension, drowsiness) - synchronised DC cardioversion is the treatment of choice. Sedate if there is time and an anaesthetist is present; if not, proceed immediately because delay risks ventricular fibrillation. Start with a biphasic 150–200 J synchronised shock and escalate.
- Apply pads, obtain IV access, monitor continuously, and have atropine/vasopressors and airway equipment ready.
- If cardioversion restores sinus rhythm, look for the delta wave in sinus rhythm and refer for electrophysiology study and ablation.
- Do not give AV nodal blocking drugs (see next question).
- Check electrolytes, thyroid function and echocardiography; screen for other causes of AF (alcohol, stimulants).
2. Which drugs must be avoided in this situation, and why? What would you use if he were stable enough for pharmacological therapy?
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Avoid verapamil, diltiazem, digoxin, adenosine and beta-blockers. They block the AV node, which in pre-excited AF reduces the competing pathway for conduction and can increase antegrade conduction down the accessory pathway, accelerating the ventricular rate and precipitating ventricular fibrillation. Adenosine can also provoke AF. Intravenous amiodarone is likewise discouraged in pre-excited AF (it can slow the accessory pathway and has been associated with deterioration). The previous verapamil at the walk-in clinic was potentially dangerous and must be documented to avoid repetition.
If the patient were stable (preserved blood pressure, no ischaemia or heart failure), pharmacological options are:
- Procainamide (slow infusion, with monitoring) - prolongs accessory pathway refractoriness.
- Ibutilide - an alternative for pharmacological cardioversion, with QT and torsades precautions.
- Direct current cardioversion remains reasonable even in stable patients.
In this patient, instability mandates electricity now. After stabilisation, arrange an electrophysiology study with radiofrequency ablation of the accessory pathway, which is curative and the definitive treatment; he should be advised to avoid competitive sports and stimulants until then and given a written plan for future episodes.
3. A junior colleague suggests giving intravenous amiodarone because the rhythm "looks like AF with aberrancy." How do you handle the diagnostic uncertainty and the team interaction?
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A broad-complex irregular tachycardia should be treated as pre-excited AF or polymorphic VT until proven otherwise - both are shocked if unstable, so the immediate action does not change. The distinction matters for drug choice and disposition.
Reasoning to share with the team:
- Irregularity with varying QRS width and rates above 250/min strongly favours pre-excited AF over VT (which is usually regular) or AF with bundle branch block (regular QRS width).
- Look for a delta wave after cardioversion, a short PR interval, and a history of palpitations in a young person. Echocardiography and eventual EPS confirm the diagnosis; accessory pathway location can be inferred from the delta wave but is not needed acutely.
- Amiodarone is not the right drug in pre-excited AF and can accelerate conduction; if the rhythm turns out to be VT, synchronised cardioversion is still correct in an unstable patient.
Team interaction: acknowledge the uncertainty explicitly, explain the physiological reason for avoiding AV nodal blockers and amiodarone, and state the plan. Document the discussion, and use it as a teaching moment rather than a public reprimand. Escalate to the on-call cardiologist and arrange early EP referral. Debrief after the event: the earlier verapamil prescription should be reviewed through the incident-reporting system as a patient-safety learning point.