Cardiac Arrhythmias

1. Definition

2. Etiology & Predisposing Factors

Structural / Cardiac Disease

• Coronary artery disease / MI — sinus bradycardia occurs in 10–15% of acute MI patients; ventricular arrhythmias arise from ischemic scars; reentrant VT is strongly associated with myocardial fibrosis
• Heart failure / Cardiomyopathy — structural remodeling (fibrosis), electrophysiologic remodeling, and neural (autonomic) remodeling all contribute
• Valvular disease, myocarditis, pericarditis, congenital heart disease
• Hypertrophy — increased wall stress and ionic remodeling raise arrhythmic risk

Systemic / Extra-Cardiac

• Electrolyte disturbances — hypokalemia, hypomagnesemia, hypocalcemia
• Metabolic — hypoxia, hypothyroidism (myxedema), hypothermia, sepsis
• Autonomic — excessive vagal tone (vasovagal syncope, carotid sinus hypersensitivity), sympathetic activation (catecholamine excess, emotional stress)
• Elevated intracranial pressure, meningitis, intracranial tumors, cervical/mediastinal tumors
• Neurally mediated — eye surgery, coronary arteriography, vomiting reflex

Drug / Toxic

• Antiarrhythmics themselves — proarrhythmia (e.g., class IA/IC agents, TdP from QT-prolonging drugs)
• Beta-blockers, calcium channel blockers, digoxin, amiodarone — can cause bradyarrhythmias
• Sympathomimetics — catecholamines, cocaine, thyroid hormone excess
• Other — lithium, clonidine, propafenone, parasympathomimetic drugs; even ophthalmic beta-blocker drops can cause SA/AV nodal abnormalities in elderly patients

Genetic / Channelopathies

• Long QT syndrome (LQTS) — mutations in K⁺ or Na⁺ channel genes → prolonged APD → EADs → TdP
• Short QT syndrome, Brugada syndrome, CPVT, HCM, ARVC
• Remodeling through autonomic remodeling (nerve sprouting, denervation) amplifies dispersion of refractoriness

3. Mechanisms

A. Abnormal Automaticity

• Normal automaticity: SA node fires spontaneously due to pacemaker current (I_f — "funny current") via HCN channels
• Enhanced automaticity: ectopic foci in atria, AV junction, or ventricles discharge faster than the SA node
• Antiarrhythmic drugs suppress ectopic firing by depressing diastolic depolarization slope, shifting threshold voltage, or hyperpolarizing resting membrane potential

B. Triggered Activity

• Early afterdepolarizations (EADs): occur during phases 2–3 of the action potential, caused by APD prolongation (e.g., LQTS, hypokalemia, QT-prolonging drugs); mediated by reactivation of L-type Ca²⁺ or late Na⁺ currents → TdP
• Delayed afterdepolarizations (DADs): occur after full repolarization (phase 4), caused by cytosolic Ca²⁺ overload (digitalis toxicity, catecholamine excess, heart failure) via SR Ca²⁺ release → transient inward current

C. Reentry

1. Two anatomically or functionally distinct pathways
2. Unidirectional block in one pathway
3. Sufficient conduction slowing in the other to allow the blocked pathway to recover

4. Classification

By Rate

By Site of Origin

Supraventricular Arrhythmias (SVA)

• Sinus node: Sinus bradycardia, sinus tachycardia, sinus arrhythmia, sick sinus syndrome (SSS), sinoatrial block
• Atrial: Atrial premature complexes (APCs), atrial tachycardia (AT), atrial flutter, atrial fibrillation (AF)
• AV junctional: Junctional rhythm, AV nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT — e.g., WPW syndrome)

Ventricular Arrhythmias

• Premature ventricular complexes (PVCs)
• Ventricular tachycardia (VT): monomorphic, polymorphic
• Ventricular flutter and ventricular fibrillation (VF)
• Torsades de pointes (TdP) — polymorphic VT in setting of prolonged QT

Conduction Disturbances

• SA block: first-, second-, third-degree
• AV block:
  • First-degree (prolonged PR > 200 ms)
  • Second-degree Mobitz type I (Wenckebach — AV nodal)
  • Second-degree Mobitz type II (infranodal — His-Purkinje)
  • Third-degree (complete heart block)
• Bundle branch blocks (LBBB, RBBB), fascicular blocks

By Duration

• Paroxysmal (self-terminating)
• Persistent (requires cardioversion)
• Permanent (cardioversion not feasible or elected)

5. Clinical Features / Symptoms

• Sinus bradycardia is asymptomatic in healthy young adults and athletes (HR may fall to 35–40 bpm during sleep); symptomatic only when cardiac output is inadequate
• Tachyarrhythmia-induced cardiomyopathy can develop from persistent, untreated tachycardia — with potential normalization of LV function after successful treatment
• Second-degree AV nodal block (proximal to His) without structural disease follows a benign course in younger patients but carries poor prognosis in structural heart disease

6. Diagnosis

History & Physical

• Onset, duration, associated symptoms (syncope, chest pain)
• Drug history (QT-prolonging agents, digoxin, stimulants)
• Family history (LQTS, SCD, HCM, ARVC)

12-Lead ECG

• P wave morphology and PR interval → SA/AV node function
• QRS duration and morphology → bundle branch block, VT vs. SVT with aberrancy
• QT interval → LQTS risk
• Delta waves → pre-excitation (WPW)
• ST-T changes → ischemic substrate

Ambulatory Monitoring

• Holter monitor (24–48 h) — for frequent arrhythmias
• Event recorder / loop recorder — for infrequent paroxysmal events
• Implantable loop recorder (ILR) — for cryptogenic syncope, long-term monitoring
• Smartwatch/wearable — emerging tool; validated for AF detection (Apple Heart Study)

Electrophysiology Study (EPS)

• Invasive catheter-based mapping of intracardiac electrograms (A, H, V)
• Distinguishes site of AV block (AV node vs. His-Purkinje)
• Assesses inducibility of VT, identifies mechanism (reentry vs. triggered)
• Guides radiofrequency (RF) catheter ablation

Additional Studies

• Echocardiogram — structural substrate (EF, wall motion, LVH, ARVC)
• Cardiac MRI — fibrosis (late gadolinium enhancement) → reentrant VT substrate
• Stress testing — CPVT, catecholaminergic VT, ischemia-related arrhythmias
• Tilt-table test — neurally mediated (vasovagal) syncope
• Carotid sinus massage — carotid sinus hypersensitivity
• Labs — electrolytes (K⁺, Mg²⁺, Ca²⁺), thyroid function, drug levels

AV Block Localization Clues

• Type I (Wenckebach): response to vagal stimulation/atropine → suggests AV nodal site; generally benign
• Type II (Mobitz): carotid sinus massage improves, atropine worsens → suggests His-Purkinje site; more ominous, higher risk of progression to complete block
• Very long PR intervals (>200 ms) are more likely from AV nodal delay

7. Treatment

Pharmacologic — Antiarrhythmic Drugs (AADs)

A modified Vaughan Williams classification (2018+) encompasses classes 0–VII including connexin modulators and upstream targets (atrial structural remodeling). No new agents have been FDA-approved in the US since dronedarone (2009).

• Drug effects depend on tissue type, heart rate (use-dependence), membrane potential, autonomic tone, genetics, and age
• Reverse use dependence (class III agents): QT prolongation is greater at slow rates → TdP risk
• AADs suppress arrhythmias by: (a) reducing automatic pacemaker rate, (b) eliminating afterdepolarizations, or (c) converting unidirectional block to bidirectional block or increasing conduction velocity to eliminate reentry

Non-Pharmacologic

Cardioversion / Defibrillation

• Electrical cardioversion (DC): synchronized shock for AF, flutter, hemodynamically unstable VT
• Defibrillation: unsynchronized shock for VF/pulseless VT
• Chemical cardioversion: ibutilide (IV) or dofetilide for AF/flutter

Cardiac Pacing

• Temporary pacing: hemodynamically significant bradycardia, post-arrest bradycardia, complete AV block
• Permanent pacemaker (PPM): SSS, symptomatic bradycardia, Mobitz II or third-degree AV block, chronotropic incompetence
  • Atropine: 0.5 mg IV initially for acute sinus bradycardia; ineffective for His-Purkinje block
• Cardiac resynchronization therapy (CRT): HF with LBBB and reduced EF

Implantable Cardioverter-Defibrillator (ICD)

• Primary prevention: EF ≤35% despite optimal therapy (NYHA II–III)
• Secondary prevention: survivors of VF/hemodynamically unstable VT
• Delivers anti-tachycardia pacing (ATP) and/or high-energy shocks
• ICD with CRT (CRT-D) for HF with ventricular dyssynchrony

Catheter Ablation (Radiofrequency / Cryoablation)

• AVNRT / AVRT / WPW: success rate ~95%; first-line in symptomatic patients
• Atrial flutter: isthmus ablation, >95% success
• AF: pulmonary vein isolation (PVI); increasingly first-line in paroxysmal AF
• Idiopathic VT (structurally normal heart): ~85% success
• Post-infarction VT: >70% free from recurrence; guided by 3D electroanatomic mapping (CARTO, EnSite NavX)
• Complications (up to 3%): vascular injury, heart block, tamponade, stroke, valve damage

Surgical

• Maze procedure (surgical AF ablation)
• Left cardiac sympathetic denervation (LCSD) for refractory CPVT/LQTS
• Left atrial appendage occlusion (WATCHMAN) for AF + CHA₂DS₂-VASc ≥ 2 with anticoagulation contraindication

Specific Arrhythmia Syndromes — Targeted Management

Summary