Version 1.0 — Published July 2026
Quick Answer
ECG tachyarrhythmias contribute 5-7 image-based MCQs per NEET PG paper across medicine, cardiology, and emergency medicine. Five patterns recur reliably year after year:
- Sinus tachycardia — HR over 100 with normal P before every QRS + normal PR + normal QRS; treat the cause, not the rate
- SVT (supraventricular tachycardia) — narrow QRS regular tachycardia at 150-250 bpm with no visible P; algorithm — vagal → adenosine 6 mg then 12 mg → beta-blocker or CCB → DC cardioversion if unstable
- Atrial fibrillation — irregularly irregular narrow QRS with no distinct P waves; CHA2DS2-VASc for anticoagulation; DOAC first-line except mechanical valve or moderate-to-severe MS (warfarin)
- Monomorphic ventricular tachycardia (VT) — wide QRS over 120 ms regular at 100-250 bpm with AV dissociation, fusion beats, capture beats; amiodarone if stable, synchronised DC cardioversion 100 J if unstable, defibrillation if pulseless
- Wolff-Parkinson-White (WPW) — short PR under 120 ms + delta wave + wide QRS; pre-excited AF is life-threatening — DO NOT give AV nodal blockers (adenosine, CCB, beta-blocker, digoxin) — use procainamide or DC cardioversion; catheter ablation of accessory pathway is curative
Locking these 5 patterns plus 3-5 additional PYQ strips (multifocal atrial tachycardia, atrial flutter with 2:1 conduction, Torsades de Pointes, junctional tachycardia, ventricular fibrillation) over 2-3 weeks moves accuracy from 40 to 85 percent in tachyarrhythmia MCQs.
Why ECG tachyarrhythmia MCQs are high-yield for NEET PG
Tachyarrhythmias cut across medicine, cardiology, emergency medicine, and anaesthesia. NEET PG, INI-CET, and FMGE feature ECG strips in 5-7 questions per paper, often paired with a classical vignette (young student with palpitations, elderly with new AF after alcohol binge, patient in shock with wide-QRS rhythm, unconscious diver rescued with polymorphic VT, young athlete with WPW-related pre-excited AF) to test pattern recognition, mechanism identification, and management algorithms.
The management decision often hinges on distinguishing narrow-QRS from wide-QRS tachycardias, regular from irregular rhythms, and recognising the specific WPW trap where AV nodal blockers accelerate the arrhythmia. Timing of DC cardioversion (immediate for unstable, deferred for stable), choice of antiarrhythmic (amiodarone for VT, adenosine for SVT, procainamide for WPW-AF), and long-term therapy (ablation, ICD, DOAC anticoagulation) all appear in the exam.
Drilling these 5 patterns plus 3-5 additional PYQ strips over 2-3 weeks moves accuracy from 40 to 85 percent.
Foundational approach before the MCQs
Systematic ECG tachycardia read
| Step | What to look at | Common findings |
|---|
| Rate | Count QRS in 6 seconds x 10; over 100 = tachycardia | Sinus vs re-entrant vs automatic |
| QRS width | Narrow (under 120 ms) = SVT-family; wide (over 120 ms) = VT until proven otherwise | Narrows the differential dramatically |
| Rhythm regularity | Regular vs irregularly irregular (AF) vs regularly irregular (atrial flutter with variable block) | AF is the classic irregularly irregular |
| P waves | Present? Morphology? Rate? Relationship to QRS? | Sinus vs atrial vs junctional vs AV dissociation |
| PR interval | Normal 120-200; short PR + delta wave = WPW pre-excitation | WPW pattern |
| QRS morphology | RBBB or LBBB pattern in wide; monomorphic vs polymorphic | VT vs SVT with aberrancy; polymorphic VT vs Torsades |
| AV dissociation | Independent P waves marching through QRS | Pathognomonic for VT in wide-QRS tachy |
| Fusion / capture beats | Occasional narrow QRS or hybrid QRS during wide-QRS tachy | Strong evidence for VT |
| Extreme axis | Right superior (quadrant 4) axis in wide-QRS tachy | Favours VT |
| Precordial concordance | All positive or all negative V1-V6 in wide-QRS tachy | Favours VT |
Narrow vs wide QRS tachycardia — differential
| Feature | Narrow-QRS tachycardia | Wide-QRS tachycardia |
|---|
| QRS width | Under 120 ms | Over 120 ms |
| Origin | SVT family (atrial, AV nodal, AV re-entrant) | Ventricular (VT, VF) or SVT with aberrancy or pre-excitation |
| Common causes | Sinus tachy, SVT (AVNRT, AVRT), AF, atrial flutter, MAT, atrial tachycardia | Monomorphic VT, polymorphic VT/Torsades, VF, SVT with BBB or aberrancy, pre-excited AF/AVRT |
| Treatment approach | Vagal + adenosine + rate control | Amiodarone or DC cardioversion; NEVER AV nodal blocker if WPW-AF suspected |
MCQ 1: 22-year-old medical student with sudden palpitations at 190 bpm during exam stress
ECG strip description: [12-lead ECG of a 22-year-old female medical student. The rhythm strip shows a regular narrow-complex tachycardia at 192 bpm. The QRS is narrow at 84 ms with normal morphology and no bundle branch block. P waves are not clearly visible — there is a subtle pseudo-R wave in V1 and pseudo-S in leads II, III, aVF (retrograde P waves inscribed at the terminal part of the QRS, characteristic of AVNRT). PR is not measurable. QT normal for the rate. No ST-segment depression. No delta wave. On the strip, at 8 seconds, the tachycardia terminates abruptly after adenosine 6 mg IV bolus — a pause of 2.4 seconds, then sinus rhythm at 96 bpm with normal PR 152 ms and no delta wave.]
Clinical vignette: A 22-year-old female medical student presents to the emergency department with sudden onset palpitations that started 45 minutes ago during her ongoing NEET PG mock examination. She reports rapid regular pounding in the chest, mild dyspnoea, chest tightness, and lightheadedness, but no syncope, no chest pain, no fever, no thyroid symptoms. She has had 3 similar episodes over the past year, each self-terminated within 20-40 minutes; she has never sought medical attention before. She is on no medications, denies alcohol/tobacco/substance use, has no family history of sudden cardiac death or channelopathy. On arrival — HR 192, BP 108/68, RR 20, SpO2 99 percent. Alert and oriented. No pallor. JVP not raised. Chest clear. S1 S2 regular but very rapid, no murmur, no S3. No peripheral oedema. Thyroid exam normal. Baseline ECG (after tachycardia termination) is normal. Echocardiogram shows structurally normal heart with normal LV function.
Options:
- (a) AV nodal re-entrant tachycardia (AVNRT) — vagal manoeuvres and adenosine, then electrophysiology study with slow-pathway ablation
- (b) Sinus tachycardia due to anxiety — reassurance and beta-blocker
- (c) Atrial fibrillation with rapid ventricular response — rate control with metoprolol and anticoagulation
- (d) Ventricular tachycardia — amiodarone and ICD
Correct answer: (a) AV nodal re-entrant tachycardia (AVNRT) — vagal manoeuvres and adenosine, then electrophysiology study with slow-pathway ablation
Reasoning: The ECG shows classical supraventricular tachycardia (SVT) — regular narrow-QRS tachycardia at 192 bpm, no visible P waves (retrograde P waves buried within or just after the QRS producing a pseudo-R in V1 and pseudo-S in inferior leads — the classical signature of AVNRT, the commonest SVT mechanism accounting for 60 percent). The abrupt termination with adenosine (which produces transient AV block breaking the re-entry loop) confirms it was an AV nodal-dependent re-entrant tachycardia. The absence of a delta wave on the sinus ECG post-conversion rules out WPW-related AVRT.
Management follows the stepwise algorithm — she is haemodynamically stable, so start with vagal manoeuvres (modified Valsalva with leg raise per REVERT trial 2015 has 43 percent success vs 17 percent for traditional; carotid sinus massage if young and no bruit; ice-water face immersion for the diving reflex). If vagal fails, adenosine 6 mg IV rapid bolus followed by 20 mL saline flush via a proximal large-bore cannula; if no response in 1-2 minutes, 12 mg, then another 12 mg if still no response. Warn the patient of transient flushing, chest tightness, and impending-doom feeling — these are expected and last under 30 seconds. Long-term management — electrophysiology study with radiofrequency slow-pathway ablation is curative with 95 percent success and under 1 percent risk of AV block requiring pacemaker; recommended for recurrent symptomatic episodes. Alternatives — chronic pill-in-pocket diltiazem or flecainide, or daily beta-blocker.
Sinus tachycardia would have visible sinus P before every QRS and would be gradual in onset. AF would be irregularly irregular. VT would be wide-QRS with AV dissociation and adenosine typically does not terminate VT.
Teaching pearl — SVT management algorithm and AVNRT vs AVRT:
| Step | Action | Notes |
|---|
| 1. Haemodynamic assessment | Unstable → immediate synchronised DC cardioversion 50-100 J | Hypotension, altered LOC, chest pain, heart failure |
| 2. Vagal manoeuvres | Modified Valsalva (leg raise), carotid massage, ice water | 43 percent success with modified Valsalva |
| 3. Adenosine | 6 mg IV rapid bolus → 12 mg → 12 mg | Large-bore proximal IV + saline flush; contraindicated in asthma, WPW pre-excited AF |
| 4. Rate-slowing drug | Metoprolol 5 mg IV or diltiazem 15-20 mg IV | Avoid in wide-QRS of uncertain origin |
| 5. DC cardioversion | If drug-refractory or becoming unstable | Synchronised 50-100 J biphasic |
| 6. Long-term | Catheter ablation of AVNRT slow pathway or AVRT accessory pathway | 95 percent success; curative |
| Feature | AVNRT | AVRT (Orthodromic) |
|---|
| Frequency | 60 percent | 30 percent |
| Mechanism | Dual AV nodal pathways (slow-fast re-entry) | Accessory pathway (Kent bundle) — down AV node, up accessory |
| QRS | Narrow (usually) | Narrow (orthodromic) or wide (antidromic) |
| P wave | Retrograde buried in QRS (pseudo-R V1, pseudo-S II III aVF) | Retrograde after QRS (short RP tachycardia) |
| Sinus ECG post-conversion | Normal | Delta wave (WPW) if manifest AVRT |
| Ablation target | Slow pathway (near coronary sinus os) | Accessory pathway (mapped anywhere on the AV groove) |
MCQ 2: 68-year-old man post-alcohol binge with irregularly irregular narrow QRS at 128 bpm
ECG strip description: [12-lead ECG of a 68-year-old man presenting the morning after a heavy alcohol binge. The rhythm strip shows a narrow-complex irregularly irregular tachycardia at an average ventricular rate of 128 bpm (RR intervals vary from 340 ms to 620 ms — no two consecutive RR intervals are the same). No distinct P waves are visible — instead there are irregular chaotic low-amplitude fibrillatory f waves best seen in lead V1 and the inferior leads. QRS width 88 ms (narrow). QT within normal limits (adjusted for the varying RR). No ST-segment abnormalities. No T-wave abnormalities. No delta wave. The 12-lead shows normal QRS morphology in all leads.]
Clinical vignette: A 68-year-old male retired banker presents to the emergency department the morning after a heavy family celebration where he consumed approximately 500 mL of whiskey over 5 hours. He woke with palpitations, mild breathlessness, and lightheadedness. Past history — hypertension on amlodipine (well controlled BP historically at 128/80), no diabetes, no known heart disease, no previous arrhythmia, no thyroid disorder. Family history — brother had a stroke at 72 years old. Social — occasional alcohol on weekends, quit smoking 15 years ago. On arrival — HR 128 irregular, BP 138/82, RR 20, SpO2 97 percent, weight 82 kg. Alert. No pallor. JVP not raised. Chest clear. Heart sounds irregular with variable intensity, no S3 or S4, no murmur. Abdomen normal. No peripheral oedema. Labs — CBC normal, K 3.8, Mg 1.9, Ca 9.1, creatinine 1.0, TSH 2.1 (normal), trop I negative. Echocardiogram shows preserved LV function (EF 58 percent), left atrium mildly dilated at 42 mm, no LA thrombus on transthoracic echo (transesophageal not yet performed), no valve pathology.
Options:
- (a) New-onset atrial fibrillation — rate control with metoprolol, CHA2DS2-VASc score for anticoagulation, and rhythm control strategy discussion
- (b) Multifocal atrial tachycardia — treat underlying COPD and correct electrolytes
- (c) Ventricular tachycardia — amiodarone and cardioversion
- (d) Sinus tachycardia with frequent premature atrial complexes — no specific treatment
Correct answer: (a) New-onset atrial fibrillation — rate control with metoprolol, CHA2DS2-VASc score for anticoagulation, and rhythm control strategy discussion
Reasoning: The ECG shows classical atrial fibrillation — the diagnostic triad of (1) irregularly irregular narrow-QRS rhythm (no two consecutive RR intervals the same), (2) no distinct P waves (replaced by chaotic low-amplitude fibrillatory f waves), (3) variable ventricular rate typically 100-160 bpm (this patient at 128 is uncontrolled). The clinical picture is textbook holiday heart syndrome — new-onset AF precipitated by alcohol binge, particularly common in middle-aged and elderly patients with mild atrial substrate (hypertension, mild LA dilatation).
Management has three arms — (1) rate control — start with metoprolol 25-50 mg PO BD titrated to resting HR under 110 (lenient control per RACE II trial 2010 is non-inferior to strict control under 80 for most stable patients); diltiazem is alternative if beta-blocker contraindicated. (2) Anticoagulation decision using CHA2DS2-VASc — this patient scores C (0, no HF) + H (1, hypertension) + A2 (2, age 75 not met; A 65-74 = 1) + D (0) + S (0) + V (0) + Sc (0, male) = 2 → anticoagulate with DOAC (apixaban 5 mg BD, rivaroxaban 20 mg OD, dabigatran 150 mg BD, or edoxaban 60 mg OD — first-line over warfarin for non-valvular AF; safer, no INR monitoring, fewer intracranial bleeds). HAS-BLED assessment for bleeding risk (H 1 + A 0 + S 0 + B 0 + L 0 + E 1 + D 0 = 2) is moderate; anticoagulation still indicated. (3) Rhythm control discussion — for first episode of new-onset AF with alcohol trigger and structurally near-normal heart, either strategy is reasonable — DC cardioversion within 48 hours of onset without prior TEE if certain of duration, OR anticoagulate for 3 weeks then TEE-guided cardioversion. Chemical cardioversion with flecainide or ibutilide (only in structurally normal heart) or amiodarone (structural heart disease) is an alternative. Long-term rhythm control with catheter ablation (pulmonary vein isolation) is an option for symptomatic paroxysmal AF per CABANA and EAST-AFNET-4 trials.
MAT would show 3+ distinct P wave morphologies, typically in COPD. VT is wide-QRS. Sinus tachycardia with PACs would have visible sinus P waves.
Teaching pearl — CHA2DS2-VASc scoring and DOAC vs warfarin choice:
| Letter | Criterion | Points |
|---|
| C | Congestive heart failure or LV dysfunction | 1 |
| H | Hypertension | 1 |
| A2 | Age 75 or over | 2 |
| D | Diabetes | 1 |
| S2 | Prior stroke, TIA, or thromboembolism | 2 |
| V | Vascular disease (MI, PAD, aortic plaque) | 1 |
| A | Age 65-74 | 1 |
| Sc | Sex female | 1 |
- Score 0 male or 1 female — no anticoagulation
- Score 1 male (non-sex) — consider anticoagulation (weak recommendation)
- Score 2+ male or 3+ female — anticoagulate
| Scenario | Anticoagulation choice |
|---|
| Non-valvular AF | DOAC first-line (apixaban, rivaroxaban, dabigatran, edoxaban) over warfarin |
| Mechanical heart valve | Warfarin only (DOAC contraindicated — RE-ALIGN trial showed harm) |
| Moderate-to-severe rheumatic mitral stenosis | Warfarin only (INVICTUS-VKA trial 2022) |
| CrCl under 15 mL/min or dialysis | Warfarin or apixaban (with reduced dose) |
| Cancer-associated thrombosis | Rivaroxaban, apixaban, or LMWH |
| Active liver disease | Warfarin with caution |
| Antiphospholipid syndrome | Warfarin only (TRAPS trial 2018 — rivaroxaban worse) |
MCQ 3: 62-year-old post-MI man with wide-QRS tachycardia at 180 bpm, hypotension, and altered mental status
ECG strip description: [12-lead ECG of a 62-year-old man with a history of anterior wall MI 2 years ago and EF 32 percent, brought to the emergency in shock. The rhythm strip shows a regular wide-complex tachycardia at 180 bpm with QRS width of 156 ms and a monomorphic morphology (every QRS complex has an identical shape). The QRS has a right bundle branch block-like pattern in V1 with a tall monophasic R and a wide slurred S in V6. There is evidence of AV dissociation — sinus P waves visible at a rate of about 80 bpm marching through the wide-QRS complexes at varying PR relationships (some just before, some on top of, some just after). Two fusion beats are visible at seconds 4 and 9 — hybrid QRS complexes intermediate between the sinus QRS and the VT QRS. One capture beat at second 12 — a narrow QRS conducted from a sinus impulse during a brief receptive window. QRS axis is right superior (quadrant 4) at −120 degrees. Precordial leads show positive concordance (all QRS complexes upright in V1-V6). No delta wave in the pre-tachycardia sinus rhythm (available from prior ECG).]
Clinical vignette: A 62-year-old male truck driver with a documented anterior wall STEMI 2 years ago (residual EF 32 percent on echo, on optimal medical therapy — aspirin, atorvastatin, ramipril, bisoprolol) is brought by his family to the emergency in a state of confusion and near-syncope that began 30 minutes ago. On arrival — HR 180 regular, BP 78/48, RR 26, SpO2 92 percent on room air. He is diaphoretic, cool peripheries, altered mental status (GCS 13, oriented to person only), with cannon a-waves visible in the JVP (indicating AV dissociation). Chest — bibasal crackles, no wheeze. Heart — very rapid, S1 variable in intensity (varying atrial contribution). No new murmur. Extremities cold, capillary refill 4 seconds. Bedside ECG shows the wide-QRS tachycardia described above. Bedside echo shows severely reduced LV function (EF around 28 percent) with anterior wall akinesia and no new pericardial effusion. Labs pending; last K on discharge was 4.2, Mg 2.0.
Options:
- (a) Monomorphic ventricular tachycardia with haemodynamic instability — immediate synchronised DC cardioversion 100 J biphasic
- (b) SVT with rate-related aberrancy — adenosine 6 mg IV
- (c) Pre-excited atrial fibrillation from occult WPW — procainamide
- (d) Sinus tachycardia with bundle branch block — treat the underlying cause
Correct answer: (a) Monomorphic ventricular tachycardia with haemodynamic instability — immediate synchronised DC cardioversion 100 J biphasic
Reasoning: The ECG shows textbook monomorphic ventricular tachycardia (VT) — wide QRS over 120 ms (156 ms here), regular, monomorphic, with multiple features that are pathognomonic or highly favouring VT over SVT with aberrancy:
- AV dissociation — independent P waves marching through the QRS complexes at their own rate (pathognomonic)
- Fusion beats — hybrid QRS complexes from partial sinus depolarisation during a brief window (highly specific)
- Capture beats — occasional narrow QRS from a sinus impulse capturing the ventricle
- Right superior axis (quadrant 4) — favours VT
- Positive concordance in precordium — all QRS upright in V1-V6, favours VT
- QRS width over 140 ms with RBBB pattern — favours VT
- Cannon a-waves in JVP clinically — visible sign of AV dissociation
- History of structural heart disease (prior MI, reduced EF) — strong prior probability of VT
The patient is haemodynamically unstable (hypotension SBP under 90, altered mental status, cool peripheries, pulmonary oedema) — this mandates immediate synchronised DC cardioversion at 100 J biphasic (200 J if monophasic device). Sedate briefly with midazolam or etomidate if time permits and BP allows. If the initial shock fails, escalate to 150 J, then 200 J. Post-cardioversion, start amiodarone infusion (150 mg IV over 10 minutes, then 1 mg/min for 6 hours then 0.5 mg/min) to prevent recurrence. Correct any reversible causes — electrolytes (K target over 4.5, Mg over 2.0), ischaemia (get an urgent trop, ECG for STEMI, consider coronary angiography), medication triggers, catecholamine excess.
Long-term management — this patient meets criteria for secondary prevention ICD (sustained VT in the setting of structural heart disease without a completely reversible cause). Primary prevention ICD is also indicated for EF under 35 percent with symptomatic heart failure post-MI at least 40 days ago (SCD-HeFT, MADIT-II). Consider catheter ablation of the VT substrate if recurrent VT despite ICD (VANISH trial supports ablation over drug escalation).
Adenosine is unlikely to terminate VT and giving it to WPW pre-excited AF can be catastrophic — never use adenosine as a diagnostic tool in wide-QRS tachycardia of uncertain origin. Pre-excited AF is irregularly irregular. Sinus tachycardia with BBB has a preceding sinus P for every QRS.
Teaching pearl — features favouring VT over SVT with aberrancy in wide-QRS tachycardia:
| Feature | Favours VT |
|---|
| AV dissociation | Pathognomonic (independent P waves) |
| Fusion beats | Pathognomonic |
| Capture beats | Pathognomonic |
| QRS width over 140 ms (RBBB pattern) or over 160 ms (LBBB pattern) | Strong |
| Extreme axis (right superior / quadrant 4) | Strong |
| Positive or negative concordance in precordium | Strong |
| History of structural heart disease (MI, cardiomyopathy, EF under 35) | Strong prior probability |
| Age over 35 with sudden wide-QRS tachycardia | Favours VT |
| Brugada morphology criteria | Application of specific algorithm |
When in doubt, treat wide-QRS tachycardia as VT. Never give AV nodal blocking drugs (adenosine, verapamil, diltiazem, digoxin) to a wide-QRS tachycardia of uncertain origin — if it is pre-excited AF from occult WPW, you can precipitate VF.
MCQ 4: 74-year-old on erythromycin with recurrent syncope and twisting wide-QRS at 240 bpm
ECG strip description: [12-lead ECG of a 74-year-old woman on prolonged erythromycin for a chronic respiratory condition. The initial ECG (pre-syncope) shows sinus rhythm at 62 bpm with a grossly prolonged QT interval — QTc 580 ms (normal under 440 in women), broad-based bifid T waves, and prominent U waves in V2-V4. The rhythm strip during the syncopal episode captured on cardiac telemetry shows a polymorphic ventricular tachycardia at approximately 240 bpm with QRS complexes that twist around the isoelectric baseline — the QRS amplitude and axis rotate cyclically over 5-10 beats producing the classical spindle-and-node appearance of Torsades de Pointes. The episode is initiated by a short-long-short RR sequence (a PVC after a compensatory pause). The episode terminates spontaneously after 12 seconds. Post-episode, sinus bradycardia at 54 bpm with persistent long QT.]
Clinical vignette: A 74-year-old female retired schoolteacher with COPD (on inhaled tiotropium and formoterol) presents with her third syncopal episode in 48 hours. She was recently started on erythromycin 500 mg QID for 10 days for a suspected atypical pneumonia by her family physician, along with ondansetron for post-viral nausea and fluconazole for suspected oral thrush. Past history — hypertension on furosemide and amiloride (diuretic), hypothyroidism on levothyroxine 75 mcg. On arrival — HR 54, BP 122/76, RR 20, SpO2 96 percent. Alert. She reports the syncope was sudden onset without prodrome, brief (under 30 seconds), with rapid recovery. Labs — K 2.8 (low), Mg 1.4 (low), Ca 8.2, TSH 2.4, glucose 92, trop I negative. Baseline ECG shows the long QT and post-episode telemetry captured the Torsades described above.
Options:
- (a) Drug-induced Torsades de Pointes on long QT background — IV magnesium sulfate 2 g, correct hypokalaemia, stop all QT-prolonging drugs
- (b) Ventricular fibrillation — immediate defibrillation and CPR
- (c) Monomorphic VT from ischaemia — amiodarone
- (d) SVT with rate-related aberrancy — adenosine
Correct answer: (a) Drug-induced Torsades de Pointes on long QT background — IV magnesium sulfate 2 g, correct hypokalaemia, stop all QT-prolonging drugs
Reasoning: The ECG shows classical Torsades de Pointes — polymorphic ventricular tachycardia with the pathognomonic twisting of the QRS around the isoelectric baseline (points-turning appearance), initiated by a short-long-short RR sequence (a PVC after a compensatory pause is the classic trigger of pause-dependent Torsades on a long-QT substrate). The baseline QTc of 580 ms is grossly prolonged (normal under 440 in women, over 500 is high risk, over 550 is very high risk). The clinical picture combines multiple QT-prolonging drugs (erythromycin, ondansetron, fluconazole), electrolyte disturbances (hypokalaemia 2.8, hypomagnesaemia 1.4 from chronic diuretic use), and a bradycardic sinus rhythm creating pause-dependent triggers.
Management — (1) if pulseless or unstable at the time of Torsades, immediate defibrillation (Torsades is polymorphic and often does not synchronise well — use unsynchronised defibrillation at 200 J biphasic). This episode terminated spontaneously so she is stable now. (2) IV magnesium sulfate 2 grams IV over 15 minutes, repeatable, regardless of the serum Mg level — magnesium suppresses early afterdepolarisations that trigger Torsades. (3) Correct hypokalaemia — IV KCl replacement to target K over 4.5 mEq/L, correct hypomagnesaemia to over 2.0. (4) Stop ALL QT-prolonging drugs immediately — erythromycin, ondansetron, fluconazole; switch to non-QT-prolonging alternatives (azithromycin has less QT effect than erythromycin but still some; ceftriaxone for pneumonia if bacterial; metoclopramide for nausea has less QT effect but caution). (5) If pause-dependent recurrence, overdrive pacing at 90-110 bpm to shorten QT and prevent recurrence, OR isoproterenol infusion (only in acquired long QT; contraindicated in congenital long QT syndrome which is exacerbated by catecholamines). (6) Monitor QT continuously.
Ventricular fibrillation is chaotic without organised QRS. Monomorphic VT has uniform QRS. Adenosine is for SVT, not polymorphic VT.
Teaching pearl — Torsades de Pointes causes and management:
Causes of long QT (leading to TdP):
| Category | Examples |
|---|
| Congenital long QT syndromes | LQT1 (KCNQ1), LQT2 (KCNH2), LQT3 (SCN5A); Jervell-Lange-Nielsen (with deafness), Romano-Ward |
| Class Ia antiarrhythmics | Quinidine, procainamide, disopyramide |
| Class III antiarrhythmics | Sotalol, ibutilide, dofetilide (amiodarone rarely) |
| Macrolides | Erythromycin, clarithromycin (azithromycin less) |
| Fluoroquinolones | Moxifloxacin (most), ciprofloxacin, levofloxacin |
| Azoles | Fluconazole, itraconazole, voriconazole |
| Antipsychotics | Haloperidol, ziprasidone, quetiapine, thioridazine (withdrawn) |
| Antiemetics | Ondansetron, domperidone (withdrawn many countries) |
| Other | Methadone, TCAs, cocaine, arsenic trioxide |
| Electrolytes | Hypokalaemia, hypomagnesaemia, hypocalcaemia |
| Bradycardia | Complete heart block with slow escape (pause-dependent TdP) |
| Other conditions | Anorexia nervosa, hypothyroidism, hypothermia, subarachnoid haemorrhage |
Management summary:
| Step | Action |
|---|
| 1. Immediate if unstable | Defibrillation (unsynchronised, 200 J biphasic) |
| 2. IV magnesium sulfate 2 g | Regardless of serum Mg; repeatable |
| 3. Correct electrolytes | K over 4.5, Mg over 2.0 |
| 4. Stop QT-prolonging drugs | Comprehensive review; switch alternatives |
| 5. Overdrive pacing 90-110 bpm | For pause-dependent recurrent TdP |
| 6. Isoproterenol | Acquired long QT only; contraindicated in congenital LQT |
| 7. Long-term congenital LQT | Beta-blocker (nadolol or propranolol); ICD if high risk; avoid triggers |
MCQ 5: 28-year-old male athlete collapses with irregular wide-QRS at 260 bpm; baseline ECG shows short PR and delta wave
ECG strip description: [Two ECGs of a 28-year-old male competitive athlete. Baseline ECG (obtained 6 months earlier during a pre-participation medical) shows sinus rhythm at 76 bpm with a short PR interval of 104 ms (normal 120-200 ms), a delta wave (slurred initial upstroke of the QRS best seen in V4-V6 and lateral leads) blending into a wide QRS of 128 ms, and secondary T-wave changes opposite to the QRS deflection direction — the classical Wolff-Parkinson-White (WPW) pattern. The current ECG at presentation shows an irregularly irregular wide-complex tachycardia at 260 bpm with varying QRS width and morphology (some QRS complexes are maximally wide with prominent delta waves representing conduction almost entirely down the accessory pathway; others are narrower and less pre-excited representing partial fusion with AV nodal conduction). The RR intervals are chaotic and short (some as short as 200 ms — a red flag for imminent VF). There is no sign of monomorphic QRS or organised P waves. The pattern is diagnostic of pre-excited atrial fibrillation in WPW.]
Clinical vignette: A 28-year-old male competitive cricketer collapses on the ground during a match with sudden syncope followed by rapid palpitations on regaining partial consciousness. He has a known WPW ECG pattern discovered on a pre-participation medical 6 months ago but was asymptomatic and had not undergone electrophysiology risk stratification. He was cleared for play on the basis of being asymptomatic. Family history — no known SCD; father alive at 62. Post-collapse, ambulance monitoring shows the pre-excited AF at 260 bpm described above. On arrival in the emergency — HR 260, BP 84/52, RR 26, SpO2 93 percent, diaphoretic, pale, drowsy but arousable. He was resuscitated with IV fluids en route. On the monitor, the wide-QRS irregular rhythm continues.
Options:
- (a) Pre-excited atrial fibrillation in WPW — DO NOT give AV nodal blockers; give IV procainamide or perform synchronised DC cardioversion; catheter ablation of accessory pathway definitively
- (b) SVT with rate-related aberrancy — adenosine 6 mg IV bolus
- (c) Monomorphic ventricular tachycardia — amiodarone infusion
- (d) Regular atrial flutter with 1:1 conduction — beta-blocker
Correct answer: (a) Pre-excited atrial fibrillation in WPW — DO NOT give AV nodal blockers; give IV procainamide or perform synchronised DC cardioversion; catheter ablation of accessory pathway definitively
Reasoning: The ECG shows the most dangerous scenario in WPW — pre-excited atrial fibrillation. The features are — (1) known WPW baseline ECG (short PR, delta wave, wide QRS), (2) irregularly irregular wide-QRS tachycardia at very high rate (260 bpm), (3) varying QRS width and morphology (varying degrees of pre-excitation as impulses conduct in variable proportions over the accessory pathway vs the AV node), (4) very short RR intervals (under 250 ms) which is a red flag for imminent degeneration into VF.
Why this is life-threatening — the accessory pathway (bundle of Kent) does NOT have the AV node's protective decremental conduction (the AV node slows down as it gets bombarded, providing intrinsic rate-limiting). In pre-excited AF, chaotic atrial impulses can conduct 1:1 over the accessory pathway at extremely high rates, producing the very fast irregular wide-QRS rhythm and risking degeneration to VF and sudden cardiac death.
The critical DO-NOT rule — NEVER give AV nodal blocking drugs (adenosine, verapamil, diltiazem, beta-blockers, digoxin) to pre-excited AF. Blocking the AV node removes the parallel slower conduction pathway and forces MORE of the atrial impulses down the accessory pathway, ACCELERATING the ventricular rate and precipitating VF. This is one of the most-tested pharmacology traps in cardiology.
Correct management — (a) if unstable (as in this patient — hypotension, altered LOC), synchronised DC cardioversion at 200 J biphasic is the immediate treatment; (b) if stable, IV procainamide 20-50 mg/min up to 17 mg/kg total — slows accessory pathway conduction and often converts to sinus rhythm; IV ibutilide is an alternative; IV amiodarone is controversial (some centres avoid it in pre-excited AF because it can slow AV nodal conduction as well and may not adequately block the accessory pathway). Long-term definitive treatment is electrophysiology study with catheter ablation of the accessory pathway — 95+ percent success with radiofrequency ablation, low complication rate, curative.
For asymptomatic WPW pattern, the risk of sudden cardiac death is around 0.1 percent per year but higher in young patients, athletes, and those in high-risk occupations (pilots, commercial drivers). EP study risk stratification should be considered — a shortest pre-excited RR under 250 ms in AF on EP study is a high-risk feature warranting prophylactic ablation. This patient should have had risk stratification 6 months ago; going forward, he needs urgent ablation.
Adenosine to this rhythm would be catastrophic. Monomorphic VT is regular and monomorphic. Atrial flutter is regular with sawtooth flutter waves.
Teaching pearl — WPW management summary:
| Scenario | Correct approach | AVOID |
|---|
| Symptomatic AVRT (orthodromic, narrow QRS) | Vagal → adenosine → beta-blocker or CCB; ablation long-term | — |
| Symptomatic AVRT (antidromic, wide QRS) | Procainamide IV; DC cardioversion if unstable; ablation | Adenosine, CCB, digoxin |
| Pre-excited AF (irregular wide-QRS) | DC cardioversion (unstable) or procainamide/ibutilide (stable); ablation | ALL AV nodal blockers — adenosine, verapamil, diltiazem, beta-blocker, digoxin |
| Asymptomatic WPW ECG pattern | EP study risk stratification in young, athletes, high-risk occupations; ablation if high-risk features (short pre-excited RR under 250 ms in AF; multiple accessory pathways) | Complacency |
| Definitive long-term | Catheter ablation of the accessory pathway | Chronic drugs (relative) |
Common pitfalls in ECG tachyarrhythmia MCQs
Five frequent error patterns appear in NEET PG dissection of tachyarrhythmia strips.
Pitfall 1: Giving adenosine or AV nodal blockers to wide-QRS tachycardia of uncertain origin
If the QRS is wide and you cannot definitively rule out VT or pre-excited AF from WPW, do NOT give adenosine, verapamil, diltiazem, or digoxin. In pre-excited AF, these accelerate the accessory pathway conduction and can precipitate VF. In VT, adenosine typically does not terminate the rhythm but produces transient AV block that masks fusion beats and capture beats making later diagnosis harder. Default rule — wide-QRS tachycardia is VT until proven otherwise; treat with amiodarone, procainamide, or DC cardioversion.
Pitfall 2: Missing AV dissociation in wide-QRS tachycardia
AV dissociation (independent P waves marching through the QRS complexes) is pathognomonic for VT. Look carefully in the leads with clearest P waves (II, V1) and use calipers to trace the P-P intervals. Cannon a-waves in the neck are the clinical bedside sign of AV dissociation. Fusion beats and capture beats are the ECG signs.
Pitfall 3: Missing the delta wave in a sinus ECG that later goes into AF
A patient with paroxysmal AF or SVT should have their baseline sinus ECG reviewed for WPW — the short PR and delta wave may be subtle in lateral leads. If present, it changes the entire management approach — avoid AV nodal blockers in future AF episodes, refer for EP study and ablation.
Pitfall 4: Confusing SVT with rate-related aberrancy vs true VT
SVT with rate-related aberrancy (usually LBBB or RBBB from rate-dependent conduction delay) can look wide-QRS. Features favouring SVT — QRS width under 140 ms, LBBB or RBBB morphology exactly matching the patient's baseline BBB, no AV dissociation, response to vagal manoeuvres. When in doubt, treat as VT — the cost of over-treating SVT as VT is small (adenosine or beta-blocker later); the cost of under-treating VT as SVT can be fatal.
Pitfall 5: Under-anticoagulating AF in Indian rheumatic mitral stenosis patients
DOACs are first-line for non-valvular AF. However, in moderate-to-severe rheumatic mitral stenosis (still common in India), the INVICTUS-VKA trial (2022) demonstrated that DOACs are inferior to warfarin — warfarin is required. Mechanical valves also mandate warfarin (RE-ALIGN trial with dabigatran was stopped for harm). Do not switch a rheumatic-AF patient from warfarin to DOAC without a valve assessment.
How to study ECG tachyarrhythmias for NEET PG
- Memorise the 5 patterns in this article cold — sinus tachy, SVT, AF, VT, WPW
- Review 3-5 additional PYQ strips — MAT, atrial flutter with 2:1 (rate 150 is the classic clue for 2:1 flutter), Torsades de Pointes, junctional tachycardia, ventricular fibrillation
- Learn the WPW DO-NOT rule cold — no AV nodal blockers in pre-excited AF, ever
- Learn the CHA2DS2-VASc components and the DOAC-vs-warfarin choice matrix
- Learn the SVT algorithm cold — vagal → adenosine 6 → 12 → 12 → beta-blocker or CCB → DC cardioversion
- Pair each pattern with its clinical trigger — young female with SVT, alcohol binge with AF, post-MI with VT, QT-prolonging drugs with Torsades, athlete with WPW pre-excited AF
- Practice reading strips in a stepwise algorithm — rate → QRS width → regularity → P waves → PR interval → axis → AV dissociation → fusion/capture → cause → treatment
- Use spaced repetition — 1d, 3d, 7d, 14d, 30d review of the same 30-40 high-yield ECG strips
- Practice in the question bank — NEETPGAI offers a tagged ECG tachycardia set; do 20-30 questions per day for 2-3 weeks
Key takeaways
- ECG tachyarrhythmias contribute 5-7 image MCQs per NEET PG paper
- SVT — narrow QRS regular at 150-250 bpm; vagal → adenosine → beta-blocker → cardioversion; ablation curative
- AF — irregularly irregular narrow QRS with no P; CHA2DS2-VASc for anticoagulation; DOAC first-line except mechanical valve or rheumatic MS
- VT — wide QRS regular with AV dissociation, fusion, capture; amiodarone if stable, DC cardioversion if unstable; ICD long-term
- WPW pre-excited AF — irregularly irregular wide QRS with varying width; NEVER give AV nodal blockers; procainamide or DC cardioversion; ablate the accessory pathway
- Torsades de Pointes — polymorphic VT on long QT; IV magnesium 2 g, correct K and Mg, stop QT drugs
- Wide-QRS tachycardia is VT until proven otherwise
- Never give adenosine or AV nodal blockers to wide-QRS tachycardia of uncertain origin
Frequently Asked Questions
How is SVT diagnosed on ECG and what is the stepwise management algorithm?
Supraventricular tachycardia (SVT) on ECG shows a narrow QRS (under 120 ms) regular tachycardia at 150-250 bpm, usually without visible P waves (the retrograde P is buried within the QRS or produces a pseudo-R in V1 or pseudo-S in inferior leads), and abrupt onset and termination (paroxysmal). The two commonest mechanisms are AV nodal re-entrant tachycardia (AVNRT — 60 percent, due to dual AV nodal pathways with a slow-fast re-entry loop) and AV re-entrant tachycardia (AVRT — 30 percent, due to an accessory pathway between atria and ventricles, orthodromic conduction down the AV node and up the accessory pathway produces narrow QRS; antidromic conduction down the accessory and up the AV node produces wide QRS mimicking VT). Management follows a stepwise algorithm — (1) assess haemodynamic stability. If unstable (hypotension, altered mental status, chest pain, heart failure signs), immediate synchronised DC cardioversion at 50-100 J. If stable, proceed to (2) vagal manoeuvres — Valsalva manoeuvre (traditional or modified Valsalva with leg raise, which has 43 percent success vs 17 percent traditional per REVERT trial 2015), carotid sinus massage (only after excluding carotid bruit, one side at a time, 5-10 seconds), or ice-water face immersion (diving reflex, most effective in young). If vagal fails, (3) adenosine 6 mg IV rapid bolus followed by 20 mL saline flush (via a proximal large-bore cannula); if no response, second dose 12 mg, then third dose 12 mg. Adenosine has a 5-10 second half-life and causes transient AV block that terminates re-entrant SVT. Warn the patient of the flushing, chest discomfort, and impending doom feeling. If adenosine fails, (4) rate-slowing IV drugs — beta-blocker (metoprolol 5 mg IV) or non-dihydropyridine calcium channel blocker (diltiazem 15-20 mg IV, verapamil 5-10 mg IV) — avoid these in wide-QRS tachycardia of uncertain origin. If persistently unstable or drug-refractory, (5) synchronised DC cardioversion. Long-term therapy — catheter ablation of the AVNRT slow pathway or AVRT accessory pathway is curative with 95 percent success and low complication rates. Chronic pill-in-pocket for infrequent episodes is diltiazem or flecainide. NEET PG tests the vagal-adenosine-cardioversion algorithm and the AVNRT-vs-AVRT distinction.
How is atrial fibrillation diagnosed and how do you decide anticoagulation using CHA2DS2-VASc?
Atrial fibrillation (AF) on ECG shows an irregularly irregular narrow QRS rhythm with no distinct P waves (replaced by chaotic low-amplitude fibrillatory f waves best seen in V1 or the inferior leads) and variable ventricular response typically 100-160 bpm (uncontrolled) or under 100 (controlled). The irregular irregularity is the diagnostic hallmark — no two RR intervals are the same. Classifications include paroxysmal (self-terminates within 7 days), persistent (over 7 days), long-standing persistent (over 1 year), and permanent (accepted, no rhythm control attempt). Workup for new-onset AF includes echocardiogram (structural heart disease, valve pathology, LV function, left atrial size, LA thrombus), thyroid function (hyperthyroidism causes AF), electrolytes, glucose, alcohol history, sleep apnoea screen, and BP control. Management has two axes — rate control (beta-blockers first-line, diltiazem or verapamil second-line if beta-blocker contraindicated, digoxin as add-on especially in heart failure — target resting rate under 110 for lenient control or under 80 for strict; RACE II trial 2010 supported lenient control) vs rhythm control (DC cardioversion for acute, amiodarone or flecainide for chemical cardioversion, catheter ablation via pulmonary vein isolation for symptomatic paroxysmal AF — CABANA and EAST-AFNET-4 trials support ablation-first strategy in appropriate patients). Anticoagulation is decided by the CHA2DS2-VASc score — Congestive heart failure (1), Hypertension (1), Age 75+ (2), Age 65-74 (1), Diabetes (1), Stroke/TIA/thromboembolism (2), Vascular disease including MI/PAD/aortic plaque (1), Sex-female (1). Score 0 in men or 1 in women — no anticoagulation. Score 1 in men (excluding sex) — consider anticoagulation (weak). Score 2+ in men or 3+ in women — anticoagulate. Bleeding risk assessed by HAS-BLED (Hypertension, Abnormal renal/liver function, Stroke, Bleeding history, Labile INR, Elderly over 65, Drugs/alcohol) — score 3+ is high risk but does NOT contraindicate anticoagulation; it flags patients for closer monitoring and modifiable risk factor optimisation. DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) are first-line over warfarin for non-valvular AF — safer, no INR monitoring, fewer intracranial bleeds. Warfarin remains preferred in mechanical heart valves and moderate-to-severe mitral stenosis (rheumatic AF, still prevalent in India). Rheumatic AF is a specific Indian context — usually secondary to rheumatic mitral stenosis, needs warfarin with INR target 2.5-3.5 (higher than 2-3 for non-valvular). NEET PG tests the irregular irregular rhythm as diagnostic, CHA2DS2-VASc scoring, DOAC preference for non-valvular AF, and warfarin for rheumatic/mechanical valve AF.
How is monomorphic ventricular tachycardia diagnosed and how does management differ from SVT with aberrancy?
Monomorphic ventricular tachycardia (VT) on ECG shows a wide QRS (over 120 ms, usually over 140 ms) regular tachycardia at 100-250 bpm with QRS morphology that is uniform (monomorphic — every QRS looks the same). Features that favour VT over SVT with aberrancy include (a) AV dissociation (independent P waves marching through the QRS complexes at a slower rate — pathognomonic), (b) capture beats (occasional narrow QRS conducted from the atrium during a brief window when the ventricle happens to be receptive), (c) fusion beats (a hybrid QRS that is intermediate between the sinus QRS and the VT QRS, occurring when a sinus impulse partially depolarises the ventricle just as the VT does), (d) extreme axis deviation (right superior axis, quadrant 4), (e) concordance in the precordial leads (all QRS complexes in V1-V6 pointing in the same direction — either all positive or all negative), (f) QRS width over 160 ms with LBBB pattern or over 140 ms with RBBB pattern, (g) history of ischaemic heart disease or structural heart disease (favours VT strongly — the Brugada algorithm plus the age-plus-structural-disease heuristic gives over 90 percent VT probability). Wide-QRS tachycardia should be treated as VT until proven otherwise — assume VT unless there is strong evidence for SVT with aberrancy. Management — (1) assess haemodynamic stability. If unstable (hypotension, altered mental status, chest pain, heart failure), immediate synchronised DC cardioversion at 100 J (biphasic) or 200 J (monophasic). If pulseless, defibrillation at 200 J biphasic per ACLS. If stable, (2) amiodarone 150 mg IV over 10 minutes, then infusion 1 mg/min for 6 hours then 0.5 mg/min — first-line for stable VT. Alternative — procainamide 20-50 mg/min IV (per PROCAMIO trial 2016, procainamide had a better safety profile than amiodarone for stable VT). Lidocaine is second-line, especially in ischaemic VT. Correct reversible causes — electrolytes (potassium, magnesium), ischaemia (revascularisation), drug toxicity (digoxin, QT-prolonging drugs). (3) After acute termination, long-term therapy — ICD (implantable cardioverter defibrillator) for secondary prevention of sudden cardiac death in any patient with sustained VT/VF in the absence of a completely reversible cause. Primary prevention ICD indicated for EF under 35 percent with symptomatic heart failure (SCD-HeFT, MADIT-II trials), and for hypertrophic cardiomyopathy with risk factors (5-year sudden death risk over 6 percent). Catheter ablation for recurrent VT despite ICD or drug therapy. NEET PG tests the AV dissociation as pathognomonic, the amiodarone-vs-cardioversion algorithm, and the ICD indications.
What is Wolff-Parkinson-White syndrome and why is pre-excited atrial fibrillation dangerous?
Wolff-Parkinson-White (WPW) syndrome refers to the ECG pattern of pre-excitation caused by an accessory pathway (bundle of Kent) between the atria and the ventricles, plus symptoms of tachyarrhythmia. The classical ECG triad is (1) short PR interval under 120 ms (rapid conduction over the accessory pathway bypasses the AV nodal delay), (2) delta wave (slurred upstroke of the QRS from initial slow depolarisation of ventricular myocardium via the accessory pathway before the AV nodal impulse arrives and takes over), (3) wide QRS over 120 ms (from the combined activation via accessory pathway and AV node). Repolarisation abnormalities (secondary T-wave changes opposite to the QRS direction) are common. The accessory pathway is a congenital muscle bridge that bypasses the normal AV nodal delay and creates a substrate for re-entrant tachyarrhythmias — most commonly AV re-entrant tachycardia (AVRT) which is orthodromic (down the AV node, up the accessory — narrow QRS, most common) or antidromic (down the accessory, up the AV node — wide QRS, mimics VT). The most dangerous scenario is pre-excited atrial fibrillation. When AF occurs in a WPW patient, chaotic atrial impulses can conduct at very high rates (over 250 bpm) over the accessory pathway which does not have the AV node's protective decremental conduction — producing a very fast, irregularly irregular wide-QRS tachycardia that can degenerate to ventricular fibrillation and sudden death. Recognition on ECG — irregularly irregular wide-QRS tachycardia at 250+ bpm with varying QRS width (some fully pre-excited over the accessory, some partially fused with AV nodal conduction). Absolutely do NOT give AV nodal blocking drugs (adenosine, verapamil, diltiazem, beta-blockers, digoxin) — blocking the AV node forces more of the atrial impulses down the accessory pathway, accelerating the ventricular rate and precipitating ventricular fibrillation. Correct management is (a) if unstable — synchronised DC cardioversion 200 J biphasic; (b) if stable — procainamide or ibutilide IV (both slow accessory pathway conduction). Long-term — catheter ablation of the accessory pathway is definitive and curative with 95+ percent success. Asymptomatic WPW ECG pattern (Wolff-Parkinson-White pattern without arrhythmia) is generally low risk but should undergo EP study risk stratification, especially in high-risk occupations (pilots, athletes, drivers) and patients under 35. NEET PG tests the short-PR-delta-wave-wide-QRS triad, the pre-excited AF danger, the DO-NOT-give-AV-nodal-blocker rule, and the catheter ablation curative approach.
What is Torsades de Pointes and how is it managed?
Torsades de Pointes (TdP, literally 'twisting of the points') is a polymorphic ventricular tachycardia characterised by QRS complexes that appear to twist around the isoelectric baseline, changing amplitude and direction cyclically. It occurs on a background of prolonged QT interval (over 500 ms is high risk, over 550 ms is very high risk). Causes of prolonged QT include (a) congenital long QT syndromes (LQT1 due to KCNQ1 potassium channel, LQT2 due to KCNH2, LQT3 due to SCN5A sodium channel — Jervell-Lange-Nielsen syndrome with sensorineural deafness, Romano-Ward without), (b) drug-induced (Class Ia antiarrhythmics — quinidine, procainamide, disopyramide; Class III — sotalol, amiodarone (rare), ibutilide, dofetilide; macrolides — erythromycin, clarithromycin; fluoroquinolones — moxifloxacin, ciprofloxacin; azoles — fluconazole; antipsychotics — haloperidol, ziprasidone, quetiapine; antiemetics — ondansetron, domperidone; methadone; TCAs), (c) electrolyte disturbances — hypokalaemia, hypomagnesaemia, hypocalcaemia, (d) bradycardia (pause-dependent TdP, seen in complete heart block with slow escape), (e) anorexia nervosa, hypothyroidism, hypothermia. TdP often self-terminates but can degenerate to ventricular fibrillation and sudden cardiac death. Management — (1) if pulseless or unstable, immediate defibrillation (Torsades is polymorphic and does not synchronise well — use unsynchronised defibrillation), (2) IV magnesium sulfate 2 grams IV over 15 minutes is first-line, repeatable, regardless of serum magnesium level, (3) correct hypokalaemia (target K over 4.5 mEq/L), hypocalcaemia, (4) stop all QT-prolonging drugs, (5) if pause-dependent, overdrive pacing to a rate of 90-110 bpm to shorten QT and prevent recurrence, or isoproterenol infusion (in acquired long QT only, contraindicated in congenital LQT), (6) long-term for congenital long QT — beta-blockers (nadolol or propranolol, especially in LQT1 and LQT2; ICD for high-risk patients with previous cardiac arrest, syncope on beta-blockers, or genetic high-risk mutations), avoid QT-prolonging drugs, avoid triggers (exertion for LQT1, auditory startle for LQT2, sleep for LQT3). NEET PG tests the twisting QRS morphology, the long QT background, the drug list, the IV magnesium first-line management, and the congenital LQT beta-blocker plus ICD algorithm.
This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: July 2026
