Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Measure QT accurately, distinguish congenital from acquired long-QT states and treat torsades without adding further QT-prolonging risk.
The QT interval represents ventricular depolarisation and repolarisation. Rate correction is imperfect: Bazett overcorrects at high rates and undercorrects at low rates, so repeat measurements and clinical context matter.
Long QT can be congenital or acquired. Before labelling an inherited syndrome, review every medicine and supplement, correct electrolytes and repeat the ECG; a concealed inherited predisposition may nevertheless be unmasked by an acquired trigger.
Torsades management differs from other broad-complex tachycardias. Magnesium and removal of the QT trigger are central, while recurrent pause-dependent episodes may need the heart rate raised with pacing or isoprenaline.
Pathogenic variants that reduce repolarising potassium current or increase inward current prolong ventricular action potentials. Expression varies, so a carrier may have an intermittently normal resting QT.
Several prescribed, over-the-counter or recreational drugs delay repolarisation, especially in combination or when metabolic inhibition raises concentrations. Overdose and unrecognised interactions increase risk further.
Hypokalaemia, hypomagnesaemia and hypocalcaemia reduce repolarisation reserve or prolong repolarisation. Vomiting, diarrhoea and diuretics may cause losses, while renal dysfunction can alter electrolytes and increase exposure to renally cleared QT-prolonging medicines.
Slow rates, atrioventricular block and short–long–short sequences lengthen repolarisation and favour early afterdepolarisations. This is particularly important in recurrent acquired torsades.
Reduced outward potassium current or excessive inward sodium or calcium current prolongs the ventricular action potential. The surface ECG reflects this as a lengthened QT interval.
Prolonged action potentials permit abnormal depolarisation before repolarisation is complete. Bradycardia, pauses, electrolyte depletion and medicines make these triggered beats more likely.
Different myocardial regions recover at different times, creating electrical heterogeneity. A premature ventricular beat arising during prolonged repolarisation can then initiate and sustain a shifting polymorphic rhythm.
In the setting of QT prolongation, polymorphic ventricular tachycardia develops with QRS complexes appearing to twist around the baseline. Episodes may stop spontaneously, recur after another pause or cause immediate haemodynamic collapse.
Sustained or unstable torsades can degenerate into ventricular fibrillation, eliminating effective cardiac output. Cerebral hypoperfusion causes syncope or seizure-like movement before cardiac arrest and death.
A repeated QTc at or above 480 ms without a drug or electrolyte explanation supports LQTS, but diagnosis can also rest on a validated score or pathogenic variant.
Polymorphic broad complexes wax and wane in amplitude and appear to twist around the baseline, often after a short-long-short sequence.
Exertional or emotion-triggered syncope, events after sudden noise, nocturnal events, unexplained seizures and a family history of LQTS or sudden death are important.
Recent QT-prolonging drugs, overdose, diarrhoea/vomiting, diuretics, renal dysfunction and bradycardia point to a modifiable trigger.
Unresponsiveness with absent normal breathing and no definite pulse converts the problem from torsades-with-a-pulse to VF/pulseless-VT ALS.
Notched, broad or low-amplitude T waves and prominent U waves can make the end of repolarisation hard to define; use a consistent tangent method and expert review.
Acute myocardial ischaemia can cause polymorphic ventricular tachycardia without preceding QT prolongation. Ischaemic symptoms, dynamic ST-segment change and a QT that is not prolonged outside the arrhythmia point to a different mechanism and management pathway.
Exercise or emotional stress triggers bidirectional or polymorphic ventricular arrhythmia, often with a normal resting ECG and QT. Exercise testing through a specialist pathway helps discriminate.
Brugada syndrome confers ventricular-fibrillation risk through a spontaneous or provoked type 1 right-precordial ST-segment pattern rather than QT prolongation. Fever or sodium-channel-blocking medicines may reveal the phenotype.
Primary epilepsy can explain recurrent convulsive episodes, but self-terminating torsades also causes cerebral hypoperfusion and tonic movements. Sudden triggers, family history and rhythm correlation are discriminating.
Prominent U waves, broad or notched T waves and automated mismeasurement may falsely lengthen QTc. Consistent manual measurement in a clear lead and repeat ECG reduce the risk of misdiagnosis.
Brief self-terminating torsades abruptly reduces cerebral perfusion, causing collapse and sometimes convulsive movement. Falls, driving incidents and repeated misdiagnosis as epilepsy can compound harm.
Torsades may fail to terminate and degenerate into ventricular fibrillation. Without rapid defibrillation, absent cardiac output causes irreversible neurological injury and sudden cardiac death.
Persistent QT-prolonging factors and pause dependence can produce closely recurring torsades episodes. Repeated instability requires monitored withdrawal of culprit medicines, correction of electrolytes and treatment of bradycardia, with immediate defibrillation capability.
Adding another QT-prolonging medicine or failing to correct electrolyte loss can extend repolarisation further. Some antiarrhythmics may therefore aggravate rather than suppress torsades.
Congenital LQTS may remain silent until a trigger causes syncope or arrest. Without specialist family assessment, genetically susceptible relatives may continue avoidable medicine or trigger exposure.
ESC notes substantial inter-observer variation even among experts. Automated QTc is a prompt to inspect the tracing, not the final diagnosis.
IV magnesium can suppress torsades even when the measured serum magnesium is not low.
A short-long-short sequence and bradycardia favour recurrent torsades; temporary pacing or isoprenaline reduces pauses while causes are corrected.
MHRA warnings emphasise additive risk from combining QT-prolonging medicines and from hypokalaemia or hypomagnesaemia.
Brief cerebral hypoperfusion from self-terminating torsades can cause convulsive movements; obtain a cardiac and family history in unexplained seizures.
A confirmed inherited diagnosis changes assessment of first-degree relatives even when they feel well.
Accepting an automated QTc without checking QRS onset, T-wave end and heart rate.
Diagnosing congenital LQTS before correcting drugs and electrolytes.
Giving amiodarone to polymorphic VT with QT prolongation.
Waiting for a low serum magnesium result before treating torsades.
Treating an ICD as a substitute for beta-blocker adherence and trigger avoidance.
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A monitored patient has recurrent self-terminating polymorphic VT, QTc 560 ms and a pulse. Potassium replacement has started. Which immediate drug is recommended by the current RCUK tachyarrhythmia algorithm?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem ·
Give with ECG and blood-pressure monitoring; toxicity risk rises in severe renal impairment. This RCUK dose is the resuscitation regimen.
Can increase myocardial oxygen demand and provoke arrhythmia; specialist use only. It is generally avoided as a strategy for congenital catecholamine-triggered LQTS unless an expert identifies a specific indication.