Wide-complex tachycardia with a prior LBBB: aberrancy or VT?
A 58-year-old man walks into an urgent care clinic complaining of palpitations and lightheadedness that started 25 minutes ago. He is alert, speaking in full sentences, and denies chest pain, dyspnea, or syncope. Vital signs: HR 168, BP 118/72, RR 18, SpO2 96% on room air, afebrile. The monitor shows a regular monomorphic wide-complex tachycardia with a QRS of 150 ms. A prior ECG in his chart documents sinus rhythm with a left bundle branch block, QRS 148 ms, with the same frontal-plane axis and the same precordial morphology as the current strip. An IV is in place and a 12-lead ECG has just been printed. A colleague says, "It's just his old LBBB, give adenosine and send him home," and the covering physician is 20 minutes away.
1. The monitor morphology matches his documented LBBB. Does that rule out ventricular tachycardia, and what features on the 12-lead would you use to decide?
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No. A prior bundle branch block whose morphology matches the current strip lowers the probability of VT but does not exclude it - VT can arise in a ventricle whose activation pattern happens to resemble the patient's baseline block, and the history of structural disease is itself a risk factor for VT. Treat this as undifferentiated until proven otherwise.
Features that push toward VT:
- AV dissociation (independent P waves marching through) - highly specific but often hard to see.
- Capture or fusion beats - a narrow beat or a hybrid beat proves a separate sinus-driven activation.
- QRS duration >160 ms (his 150 ms is borderline, not reassuring).
- Extreme axis (roughly −90° to ±180°), or axis shift >40° from the baseline ECG.
- Morphology atypical for his known LBBB - e.g., q wave or absent R in V6, RSR' in V6, monophasic R in V1, or an RS interval >100 ms in any precordial lead.
- Precordial concordance (all precordial leads positive or all negative).
Also confirm the rhythm is real: check a pulse, check that the leads are on the patient and not on a vibrating bed or a loose electrode. Artifact is the third differential and disappears when you look at the patient.
Practical rule: if the diagnosis is genuinely uncertain, manage as VT. Calcium channel blockers given for presumed SVT-with-aberrancy in a patient who actually has VT can precipitate collapse.
2. He remains alert with BP 118/72. What is your sequence of management now, and where does adenosine fit?
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He is stable, so there is no indication for immediate electricity. His instability criteria (hypotension, altered mentation, ischemic chest pain, acute heart failure) are all absent, and he has a documented matching baseline morphology - so this is the setting for a monitored, diagnostic-and-therapeutic attempt rather than an emergency shock.
Sequence:
- Continuous monitor, pads on the chest, defibrillator at the bedside, oxygen if needed, IV confirmed. Do this where you can manage a deterioration, i.e., not in a room you cannot resuscitate in - and he should not be sent home; he needs admission and cardiology.
- Adenosine 6 mg rapid IV push with a flush is reasonable for a regular monomorphic wide-complex tachycardia, both diagnostically and therapeutically. If the rhythm terminates and reveals sinus rhythm with his baseline LBBB, the diagnosis is AV-nodal-dependent SVT with aberrancy. If it does not terminate, that is uninformative - VT does not usually respond to adenosine.
- Alternatively, or if adenosine fails, start an antiarrhythmic infusion: amiodarone 150 mg over 10 min or procainamide 20–50 mg/min to a maximum of 17 mg/kg (avoid procainamide if QT is prolonged or LV function is poor), and call for expert consultation.
- Do not give verapamil or diltiazem for an undifferentiated wide-complex tachycardia.
- If at any point he becomes unstable, abandon the drug sequence and go to synchronized cardioversion.
3. Two minutes later he is confused, pale, and reports chest pressure; BP is 78/44. Describe exactly what you do, including device settings and what you check after the shock.
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This is now an unstable tachycardia - hypotension, altered mental status, and ischemic symptoms. Immediate synchronized cardioversion; do not delay for drugs.
Device handling:
- Press SYNC and confirm the sync markers are landing on the R waves. In a wide-complex tachycardia, marker misalignment (double-counting or missing the QRS) is common; if the machine will not sync, the rhythm is being treated as polymorphic and you should defibrillate (unsynchronized).
- Initial energy for a regular monomorphic wide-complex tachycardia: 100 J biphasic (monophasic 200 J). If it fails, escalate: 100 → 200 → 300 → maximum, or use the manufacturer's recommended step-up.
- Premedicate with a sedative/analgesic if there is time and the patient can tolerate it - but not at the expense of delay in a patient who is already hypotensive.
- Warn everyone to clear, and clear again with your own eyes.
After the shock:
- Sync mode usually reverts to unsynchronized after a discharge - re-engage SYNC before any subsequent shock for a reorganized rhythm.
- Reassess rhythm and pulse immediately; if he is now in VF or pulseless VT, switch to the cardiac arrest algorithm and unsynchronized defibrillation at maximum energy.
- If the cardioversion is successful, obtain a post-conversion 12-lead, look for ischemia (which may have driven the arrhythmia), correct electrolytes (K, Mg), and start an antiarrhythmic infusion to prevent recurrence.
- If he is temporarily unstable and cardioversion is not immediately available, treat the BP with fluids and a vasopressor but keep moving toward electricity.