Cardiac Arrhythmias
Medicine · Cardiology · lean revision notes
Cardiac Arrhythmias
Cardiac arrhythmias are disorders of impulse formation, conduction, or both, producing rates that are too fast (tachyarrhythmias), too slow (bradyarrhythmias), or irregular. NEET PG loves ECG strip recognition, the Vaughan Williams classification, DC cardioversion vs defibrillation distinctions, and pacemaker/ICD indications. This is a high-yield, image-heavy topic — train your eye on the strips.
Basic electrophysiology refresher
The conduction sequence is the spine of every arrhythmia question:
SA node → atria → AV node → bundle of His → right & left bundle branches → Purkinje fibres → ventricular myocardium
- SA node is the natural pacemaker (intrinsic rate 60–100/min), supplied by the RCA in ~60% and LCx in ~40%.
- AV node provides physiological delay (the PR segment) and is the only normal electrical bridge between atria and ventricles. Its block protects ventricles in atrial tachyarrhythmias.
- Escape pacemaker rates: AV junction 40–60/min; ventricular (Purkinje) 20–40/min. Slower escape = lower, more dangerous block.
High-yield: Phase 0 of the fast (myocardial) action potential = rapid Na⁺ influx. Phase 2 plateau = Ca²⁺ influx balanced by K⁺ efflux. Phase 3 repolarisation = K⁺ efflux. SA and AV nodal cells are "slow-response" — depolarised by Ca²⁺, hence the use of verapamil/diltiazem and adenosine to act on them.
Mechanisms of arrhythmia
- Enhanced/abnormal automaticity — e.g. sinus tachycardia, some atrial tachycardias.
- Triggered activity — early afterdepolarisations (EAD, phase 2/3, cause torsades in long QT) and delayed afterdepolarisations (DAD, phase 4, digoxin toxicity, catecholamines).
- Re-entry — the commonest mechanism (AVNRT, AVRT, atrial flutter, most VT). Requires unidirectional block + slow conduction around a circuit.
Classification of tachyarrhythmias
| Feature | Narrow-complex (QRS <120 ms) | Broad-complex (QRS ≥120 ms) |
|---|---|---|
| Origin | Supraventricular (above His) | Ventricular, or SVT with aberrancy/WPW |
| Examples | Sinus tach, AF, flutter, AVNRT, AVRT, atrial tach | VT, VF, SVT with BBB, antidromic AVRT |
| Default assumption | — | Treat as VT until proven otherwise, especially if structural heart disease/old MI |
High-yield: A regular broad-complex tachycardia in a patient with prior MI is VT in >90% of cases. Never give verapamil to a broad-complex tachycardia of uncertain origin — it can precipitate haemodynamic collapse.
Atrial fibrillation (AF)
The commonest sustained arrhythmia. ECG: absent P waves, irregularly irregular RR intervals, fibrillatory (f) waves at 350–600/min.
Causes (mnemonic "PIRATES"): Pulmonary (PE, COPD), Ischaemia/IHD, Rheumatic mitral stenosis, Anaemia/Atrial myxoma, Thyrotoxicosis, Ethanol ("holiday heart"), Sepsis/Sleep apnoea. Hypertension is the commonest overall cause in the West; mitral stenosis remains a key cause in India.
Management — two parallel goals
Rate vs rhythm: Rate control (β-blocker, diltiazem/verapamil, digoxin) is non-inferior to rhythm control for most (AFFIRM trial). Rhythm control (DC cardioversion, amiodarone, flecainide, catheter ablation) is preferred in young/symptomatic/first episodes.
Stroke prevention — CHA₂DS₂-VASc score:
| Letter | Factor | Points |
|---|---|---|
| C | Congestive heart failure/LV dysfunction | 1 |
| H | Hypertension | 1 |
| A₂ | Age ≥75 | 2 |
| D | Diabetes mellitus | 1 |
| S₂ | Prior Stroke/TIA/thromboembolism | 2 |
| V | Vascular disease | 1 |
| A | Age 65–74 | 1 |
| Sc | Sex category (female) | 1 |
High-yield: Anticoagulate if score ≥2 (men) / ≥3 (women). Score 0 (men)/1 (women) → no anticoagulation. DOACs (apixaban, rivaroxaban, dabigatran) are first-line except in mechanical valves or moderate–severe mitral stenosis, where warfarin is mandatory. Bleeding risk is gauged by HAS-BLED.
Cardioversion rule: If AF >48 h (or unknown duration) and not anticoagulated, give 3 weeks anticoagulation before and 4 weeks after cardioversion, OR do TEE to exclude LA appendage thrombus first.
Atrial flutter
ECG: sawtooth "F" waves, best seen in inferior leads (II, III, aVF), atrial rate ~300/min, ventricular rate often 150 (2:1 block).
High-yield: A regular narrow-complex tachycardia at exactly 150/min = think atrial flutter with 2:1 block. Definitive treatment = radiofrequency ablation of the cavotricuspid isthmus (success >90%).
Paroxysmal SVT (AVNRT & AVRT)
- AVNRT (commonest PSVT): re-entry within the AV node. Regular, narrow QRS, rate 150–250. P waves buried in or just after QRS (pseudo-S in inferior leads, pseudo-R′ in V1).
- AVRT: re-entry using an accessory pathway (e.g. WPW). Orthodromic (narrow QRS, common) vs antidromic (broad QRS).
Acute management flow: Vagal manoeuvres (carotid sinus massage, modified Valsalva) → IV adenosine 6 mg rapid push, then 12 mg → if fails, verapamil/diltiazem or β-blocker → DC cardioversion if unstable.
High-yield: Adenosine (ultra-short half-life ~10 s) is both therapeutic and diagnostic. Avoid in asthma (bronchospasm). Contraindicated/ineffective via AV nodal block in atrial flutter but transiently unmasks flutter waves.
Wolff-Parkinson-White (WPW) syndrome
Accessory pathway (bundle of Kent) bypasses the AV node.
ECG triad: short PR (<120 ms) + delta wave (slurred QRS upstroke) + wide QRS. WPW = pre-excitation pattern plus symptomatic tachyarrhythmia.
High-yield: AF in WPW is a medical emergency. AV-nodal blockers (adenosine, verapamil, diltiazem, digoxin, β-blockers — "ABCD") are CONTRAINDICATED because they push conduction down the accessory pathway → very fast ventricular rates → VF. Use IV procainamide / ibutilide, or synchronised DC cardioversion if unstable. Definitive cure = radiofrequency ablation of the accessory pathway.
Lown-Ganong-Levine syndrome: short PR but no delta wave (James fibres bypassing AV node into the His bundle).
Ventricular tachycardia (VT) & fibrillation (VF)
- VT: ≥3 consecutive ventricular beats ≥100/min, broad QRS. Sustained = >30 s or causing instability. Monomorphic VT usually = scar re-entry (post-MI).
- VF: chaotic, no organised QRS — pulseless → defibrillate immediately.
Polymorphic VT with long QT = Torsades de pointes ("twisting of the points" around the baseline).
High-yield: Drug of choice for haemodynamically stable monomorphic VT = IV amiodarone (procainamide also acceptable). Unstable VT with a pulse → synchronised DC cardioversion. Pulseless VT/VF → immediate unsynchronised defibrillation + CPR. Treatment of torsades = IV magnesium sulphate.
VT vs SVT with aberrancy (Brugada criteria favouring VT)
- AV dissociation, capture/fusion beats.
- QRS >140 ms (RBBB pattern) or >160 ms (LBBB pattern).
- Extreme axis (northwest axis), concordance across precordial leads.
- Positive history of structural heart disease/MI.
Bradyarrhythmias and heart blocks
AV blocks
| Type | ECG hallmark | Site | Risk |
|---|---|---|---|
| First degree | PR >200 ms, every P conducts | AV node | Benign |
| Mobitz I (Wenckebach) | Progressive PR lengthening → dropped beat | AV node | Usually benign |
| Mobitz II | Constant PR, sudden dropped QRS | His-Purkinje | Dangerous → pacemaker |
| Third degree (complete) | Complete AV dissociation, P and QRS independent | AV node or infranodal | Pacemaker |
Wenckebach footprint: grouped beating with progressively shortening RR before the pause; the pause is less than twice the preceding RR.
High-yield: Mobitz II and complete heart block need permanent pacemaker. Atropine helps nodal (narrow-complex escape) blocks but may worsen Mobitz II/infranodal block — use transcutaneous pacing/isoprenaline there. Complete heart block with a narrow QRS = junctional escape (more stable); broad QRS escape = ventricular (unstable, lower rate).
Stokes-Adams attack: transient syncope from ventricular asystole during complete heart block.
Sick sinus syndrome (tachy-brady)
Alternating sinus bradycardia/pauses and atrial tachyarrhythmias → pacemaker if symptomatic.
DC cardioversion vs defibrillation
| Synchronised cardioversion | Defibrillation | |
|---|---|---|
| Shock timing | Synced to R wave | Random (no organised QRS) |
| Used for | Unstable AF, flutter, SVT, VT with pulse | VF, pulseless VT |
| Why sync | Avoids R-on-T → VF | No R wave to sync to |
Signs of instability mandating immediate cardioversion (mnemonic): Shock (hypotension), Heart failure/pulmonary oedema, Ischaemic chest pain, Altered mental status (syncope) — "the 4 H's of haemodynamic compromise."
Vaughan Williams classification of antiarrhythmics
| Class | Action | Examples | Key exam point |
|---|---|---|---|
| Ia | Na⁺ block, ↑ APD/QT | Quinidine, Procainamide, Disopyramide | Procainamide → drug-induced lupus; quinidine → cinchonism, ↑ digoxin |
| Ib | Na⁺ block, ↓ APD | Lignocaine, Mexiletine, Phenytoin | Lignocaine = DOC for VT in ischaemia (acts on ischaemic tissue) |
| Ic | Na⁺ block, no APD change | Flecainide, Propafenone | Avoid in structural heart disease/post-MI (CAST trial ↑ mortality) |
| II | β-blockers | Metoprolol, Esmolol | Rate control, post-MI mortality benefit |
| III | K⁺ block, ↑ APD/QT | Amiodarone, Sotalol, Ibutilide, Dofetilide | Amiodarone = broadest spectrum |
| IV | Ca²⁺ channel block | Verapamil, Diltiazem | Rate control SVT/AF; avoid in WPW-AF, VT |
High-yield: Amiodarone is class III but has all four class actions. Toxicities (heavily tested): pulmonary fibrosis, thyroid dysfunction (both hypo- and hyper-, it is iodine-rich), corneal microdeposits, blue-grey skin, hepatotoxicity, optic neuritis. Monitor TFT, LFT, chest X-ray, PFTs.
Drugs NOT in Vaughan Williams: Adenosine, Digoxin, Magnesium, Atropine, Ivabradine (funny-current I_f blocker — pure rate-lowering).
High-yield: Digoxin is a positive inotrope (inhibits Na⁺/K⁺-ATPase) and negative chronotrope (↑ vagal tone at AV node). Toxicity worsened by hypokalaemia, hypomagnesaemia, hypercalcaemia, renal failure. Classic ECG: reverse-tick (scooped) ST depression; toxicity sign = paroxysmal atrial tachycardia with block, bidirectional VT. Antidote = digoxin-specific antibody (Fab) fragments.
Long QT, Brugada & channelopathies
- Congenital long QT: Romano-Ward (autosomal dominant, isolated), Jervell-Lange-Nielsen (autosomal recessive + congenital deafness). Risk = torsades/sudden death. Treat with β-blockers, avoid QT-prolonging drugs.
- Acquired long QT: drugs (macrolides, fluoroquinolones, antipsychotics, antifungals, Class Ia/III antiarrhythmics), hypokalaemia, hypomagnesaemia, hypocalcaemia.
- Brugada syndrome: SCN5A mutation; ECG = coved ST elevation V1–V3 with RBBB pattern; sudden cardiac death risk → ICD. Unmasked by fever, Na-channel blockers.
QTc cut-off (Bazett: QT/√RR): prolonged if >440 ms (men) / >460 ms (women); >500 ms = high torsades risk.
Pacemaker & ICD indications
Permanent pacemaker (PPM) indications:
- Symptomatic sinus node dysfunction / sick sinus syndrome.
- Mobitz II and third-degree (complete) AV block.
- Symptomatic Mobitz I, alternating BBB, post-MI persistent advanced block.
ICD indications: survivors of cardiac arrest (VF/unstable VT), sustained VT with structural disease, LV ejection fraction ≤35% with NYHA II–III (primary prevention), inherited channelopathies (long QT, Brugada, HOCM) at high risk.
NBG pacemaker codes (first 3 letters): chamber Paced – chamber Sensed – Response (I=inhibited, T=triggered, D=dual). Example DDD = dual-chamber sensing and pacing.
Key differentials at the bedside
Irregularly irregular narrow tachycardia → AF, atrial flutter with variable block, multifocal atrial tachycardia (MAT — ≥3 distinct P morphologies, seen in COPD). Regular narrow tachycardia at 150 → flutter (2:1) vs AVNRT vs sinus tach — adenosine differentiates. Regular broad tachycardia → VT >> SVT with aberrancy/WPW. Bradycardia with cannon a-waves in JVP → complete heart block (atria contract against closed tricuspid).
Recently asked / exam angle
- ECG strip identification is the single most common format: identify sawtooth (flutter), irregularly irregular no-P (AF), delta wave (WPW), Wenckebach, AV dissociation (complete block), torsades.
- "Drug contraindicated in AF with WPW" → adenosine/verapamil/digoxin/β-blocker (any AV-nodal blocker).
- "Synchronised vs unsynchronised shock" pairing — VF/pulseless VT = defibrillate; everything else unstable = synchronise.
- "Antiarrhythmic causing pulmonary fibrosis / thyroid dysfunction / corneal deposits" → amiodarone.
- "Class Ic post-MI increased mortality" → CAST trial / flecainide.
- "Recurrent unrefreshing torsades treatment" → IV magnesium sulphate.
- "Jervell-Lange-Nielsen" → long QT + deafness (AR).
- CHA₂DS₂-VASc and the warfarin-mandatory exceptions (mechanical valve, mitral stenosis).
- "Treatment of choice for typical atrial flutter / WPW" → radiofrequency ablation.
- Adenosine contraindicated in asthma; ineffective for VT.
Rapid revision
- Irregularly irregular + absent P waves = AF; sawtooth waves in II/III/aVF = atrial flutter.
- Regular narrow tachycardia at exactly 150/min → suspect flutter with 2:1 block.
- Adenosine 6→12 mg for SVT; ultra-short acting; avoid in asthma.
- WPW = short PR + delta wave + wide QRS; never give AV-nodal blockers in WPW-AF — use procainamide/cardioversion.
- Broad-complex regular tachy in post-MI patient = VT until proven otherwise.
- Stable VT → amiodarone; unstable VT with pulse → synchronised cardioversion; pulseless VT/VF → defibrillate.
- Torsades → IV magnesium; caused by long QT (drugs, ↓K⁺/↓Mg²⁺).
- Mobitz II & complete heart block → permanent pacemaker; atropine can worsen infranodal block.
- Wenckebach = progressive PR prolongation then dropped beat; benign, AV-nodal.
- Amiodarone toxicity: lung fibrosis, thyroid (hypo/hyper), corneal deposits, blue skin, hepatotoxicity.
- Flecainide (Ic) contraindicated in structural heart disease (CAST trial); lignocaine (Ib) = ischaemic VT.
- CHA₂DS₂-VASc ≥2 (men)/≥3 (women) → anticoagulate; mechanical valve & mitral stenosis = warfarin only; DOAC otherwise.