Antiarrhythmics

Clinical approach (perioperative)

• Treat the patient first: ABCDE, oxygen, analgesia/sedation, correct precipitating causes
  • Common precipitants: hypoxia, hypercarbia, acidosis, pain, sepsis, myocardial ischaemia, electrolyte disturbance (K+, Mg2+, Ca2+), drug effects (volatile agents, catecholamines), hypovolaemia
• Define rhythm: narrow vs broad complex; regular vs irregular; haemodynamic stability
  • Unstable features: hypotension, shock, syncope, chest pain/ischaemia, acute heart failure
• Immediate actions (ALS-aligned):
  • Unstable tachyarrhythmia: synchronised DC cardioversion (sedate/anaesthetise if time)
  • Pulseless VT/VF: defibrillation + CPR + adrenaline + amiodarone per ALS
  • Bradycardia with adverse features: atropine first-line; consider pacing; adrenaline/isoprenaline infusion if needed
• Drug choice depends on mechanism: AV nodal dependent vs atrial vs ventricular; structural heart disease; QT interval; accessory pathway
  • AF with WPW (pre-excited AF): avoid AV nodal blockers (adenosine, verapamil/diltiazem, beta-blockers, digoxin); use procainamide (where available) or DC cardioversion; amiodarone use varies by guideline—seek senior/cardiology advice

Common perioperative scenarios → typical drug options

• Regular narrow complex SVT (AVNRT/AVRT) stable
  • Vagal manoeuvres → adenosine IV bolus; if recurrent consider beta-blocker or verapamil (if no LV dysfunction/hypotension)
• Atrial fibrillation/flutter with rapid ventricular response (stable)
  • Rate control: beta-blocker (e.g., metoprolol/esmolol) or diltiazem/verapamil; digoxin if sedentary/HF (slow onset)
  • Rhythm control: amiodarone (especially if structural heart disease) or DC cardioversion if unstable/recent onset with symptoms
• Monomorphic VT (with pulse)
  • Unstable: synchronised DC cardioversion
  • Stable: amiodarone IV; consider lidocaine (especially ischaemia-related) if amiodarone unavailable/ineffective; correct K+/Mg2+
• Torsades de pointes / polymorphic VT with prolonged QT
  • Magnesium sulfate IV; stop QT-prolonging drugs; correct hypokalaemia; consider overdrive pacing/isoprenaline if bradycardia-related; defibrillate if unstable/pulseless
• Symptomatic bradycardia
  • Atropine IV; if ineffective consider transcutaneous pacing, adrenaline infusion, or isoprenaline; treat reversible causes (e.g., high spinal, vagal stimulus, beta-blocker toxicity)

Vaughan Williams classification (mechanism-led)

• Class I: Na+ channel blockers (membrane stabilisers) → slow phase 0 upstroke in fast-response tissue (atria/ventricles/His-Purkinje)
  • IA (e.g., quinidine, procainamide, disopyramide): moderate Na block + K block → ↑ AP duration, ↑ QT
  • IB (e.g., lidocaine, mexiletine): weak Na block, preferential for ischaemic/depolarised tissue → ↓ AP duration
  • IC (e.g., flecainide, propafenone): strong Na block → marked conduction slowing, little APD change; proarrhythmic in structural heart disease
• Class II: beta-blockers → ↓ cAMP, ↓ Ca2+ currents; slow AV nodal conduction, ↑ AV nodal refractoriness
  • Useful for rate control (AF), SVT prevention, catecholamine-driven arrhythmias; post-MI mortality benefit
• Class III: K+ channel blockers → prolong repolarisation (phase 3) → ↑ AP duration, ↑ ERP, often ↑ QT
  • Amiodarone (multi-class), sotalol (also beta-blocker), dofetilide/ibutilide (less common UK periop)
• Class IV: non-dihydropyridine Ca2+ channel blockers (verapamil, diltiazem) → slow AV nodal conduction
  • Avoid in severe LV dysfunction, hypotension; dangerous with beta-blockers (heart block/asystole risk)
• Unclassified/others: adenosine, digoxin, magnesium, atropine, ivabradine (sinus node), potassium
  • Adenosine: AV nodal block; Digoxin: ↑ vagal tone + Na/K ATPase inhibition; Mg2+: stabilises myocardium (torsades, digoxin-related arrhythmias)

Key drugs (high-yield properties)

• Adenosine
  • MOA: A1 receptor activation → ↑ K+ efflux, ↓ Ca2+ influx → transient AV nodal block; very short half-life (~10 seconds)
  • Indications: termination/diagnosis of regular narrow complex SVT (AVNRT/AVRT); diagnostic for broad complex tachycardia if regular monomorphic and stable (with caution)
  • Dose: rapid IV bolus via large vein + flush (e.g., 6 mg → 12 mg → 12 mg); consider lower dose via central line or post-transplant
  • Adverse: flushing, chest tightness, bronchospasm, transient asystole/AV block; may precipitate AF (dangerous in WPW)
  • Interactions: antagonised by methylxanthines (theophylline/caffeine); potentiated by dipyridamole; increased sensitivity in denervated transplanted heart
• Amiodarone
  • MOA: predominantly Class III (K+ block) but also Na+ block, beta-blockade, Ca2+ block → slows conduction, prolongs refractoriness; relatively low torsades risk vs other Class III
  • Indications: VF/pulseless VT (ALS), stable VT, AF rhythm control (esp. structural heart disease/HF), refractory SVT
  • IV dosing (typical): 300 mg in arrest after 3rd shock; for perfusing arrhythmia 150 mg over 10 min then infusion (e.g., 1 mg/min for 6 h then 0.5 mg/min)
  • Acute adverse (IV): hypotension (solvent-related vasodilation), bradycardia, AV block; phlebitis/extravasation
  • Chronic adverse: thyroid dysfunction (hypo/hyper), pulmonary toxicity, hepatotoxicity, corneal deposits, photosensitivity/blue-grey skin, neuropathy; very long half-life (weeks)
  • Interactions: increases warfarin effect (↑ INR) and digoxin levels; additive bradycardia with beta-blockers/verapamil
• Lidocaine (lignocaine) – antiarrhythmic use
  • Class IB Na+ blocker; preferential effect in ischaemic ventricular tissue; reduces automaticity
  • Indications: ventricular arrhythmias (esp. ischaemia-related) when amiodarone unsuitable; not effective for atrial arrhythmias
  • Adverse: CNS toxicity (tinnitus, perioral numbness, seizures), drowsiness; cardiovascular depression at high levels
  • PK: high hepatic extraction; reduced clearance in low cardiac output, liver disease; active metabolites
• Beta-blockers (e.g., esmolol, metoprolol, propranolol)
  • MOA: Class II; reduce sympathetic drive; slow SA rate and AV conduction; reduce triggered activity (catecholamine-mediated)
  • Esmolol: ultra-short acting (ester hydrolysis by RBC esterases) useful perioperatively for SVT/AF rate control, hypertension/tachycardia
  • Adverse/contra: bradycardia, AV block, hypotension, bronchospasm (non-selective), acute decompensated HF; caution with verapamil/diltiazem
• Verapamil / Diltiazem
  • MOA: Class IV; AV nodal slowing (useful for SVT and AF rate control)
  • Avoid: WPW with AF (may accelerate ventricular response), severe LV dysfunction, hypotension; dangerous with beta-blockers
• Digoxin
  • MOA: inhibits Na+/K+ ATPase → ↑ intracellular Ca2+ (inotropy) + ↑ vagal tone → slows AV node
  • Use: AF rate control in HF/sedentary patients; slow onset; less effective in high sympathetic states (sepsis, perioperative stress)
  • Toxicity: arrhythmias (atrial tachycardia with block, ventricular ectopy), GI upset, confusion, xanthopsia; risk ↑ with hypokalaemia, hypomagnesaemia, renal failure, drug interactions (amiodarone, verapamil, macrolides)
  • Treatment of severe toxicity: digoxin-specific antibody fragments; magnesium for arrhythmias; correct K+ (careful—may rise after Fab)
• Magnesium sulfate
  • Use: torsades de pointes, long QT-related ventricular ectopy, digoxin-related arrhythmias; also for eclampsia
  • Adverse: flushing, hypotension, bradycardia, respiratory depression at high levels; potentiates neuromuscular blockade
• Atropine
  • MOA: competitive muscarinic antagonist → reduces vagal tone → increases SA rate and AV conduction
  • Use: symptomatic bradycardia; less effective in high-grade infranodal block; may worsen ischaemia by increasing HR
  • Adverse: tachycardia, dry mouth, urinary retention, delirium; can precipitate angle-closure glaucoma

Electrophysiology & ECG effects (link to drug class)

• PR interval reflects AV nodal conduction: prolonged by beta-blockers, verapamil/diltiazem, digoxin, adenosine
• QRS duration reflects ventricular depolarisation/conduction: widened by Class I (especially IC) and severe hyperkalaemia
• QT interval reflects repolarisation: prolonged by Class IA and many Class III (sotalol, dofetilide); amiodarone prolongs QT but torsades risk comparatively lower
• Torsades risk increased by: prolonged QT, bradycardia, hypokalaemia, hypomagnesaemia, female sex, structural heart disease, drug interactions

Perioperative considerations

• Anaesthetic interactions: volatile agents and hypokalaemia can increase arrhythmogenicity; catecholamines (e.g., adrenaline infiltration) can trigger SVT/VT
• Regional/neuraxial: high spinal → bradycardia/hypotension (treat with fluids, vasopressors, atropine; consider adrenaline infusion)
• Electrolytes: aim K+ high-normal and Mg2+ normal in patients with AF/VT history; correct before giving QT-prolonging drugs
• Structural heart disease: avoid flecainide/propafenone in ischaemic heart disease or LV dysfunction; prefer amiodarone for rhythm control
• Anticoagulation: AF management includes stroke prevention; perioperative decisions depend on CHA2DS2-VASc and bleeding risk (not an antiarrhythmic effect but commonly examined in viva context)