Arrhythmias Comprehensive Notes

Arrhythmias: Comprehensive Clinical Notes 1. Introduction to Arrhythmias Definition: An arrhythmia is any deviation from the normal rhythm of the heart, which may present as: - Tachycardia (fast rhythm) - Bradycardia (slow rhythm) - Irregular rhythm Clinical significance: - May be asymptomatic or present with palpitations, syncope, fatigue, chest pain, dizziness, hypotension, or sudden cardiac death. - Can arise transiently (e.g., during exercise) or chronically (structural heart disease). Classification: - Supraventricular arrhythmias (SVAs) – Origin above the ventricles: - Atrial fibrillation (AF) - Atrial flutter - AV nodal reentrant tachycardia (AVNRT) - Paroxysmal supraventricular tachycardia (PSVT) - Ventricular arrhythmias (VAs) – Origin within the ventricles: - Ventricular tachycardia (VT) Ventricular fibrillation (VF) - Premature ventricular contractions (PVCs) - Conduction abnormalities: Heart blocks (first-, second-, third-degree) - Bundle branch blocks - Automaticity disorders: - Sinus node dysfunction - Ectopic pacemaker activity 2. Causes of Arrhythmias A. Disturbances in impulse generation: - SA node dysfunction (sick sinus syndrome) - Ectopic pacemaker activity (abnormal automaticity) - Triggered activity (afterdepolarizations) B. Disturbances in impulse conduction: - Functional or anatomical conduction blocks - Re-entry circuits C. Cellular and biochemical causes: - Electrolyte imbalances: Hypokalemia, hyperkalemia → altered membrane potential; Hypocalcemia, hypercalcemia → affects action potential duration - Ion channel remodeling: Changes in Na⁺, K⁺, Ca²⁺ channels alter excitability - Structural remodeling: Fibrosis, myocardial infarction, scar tissue, dilated cardiomyopathy - Defective calcium handling: SR calcium overload → DADs - Cell damage: Ischemia, infarction, myocarditis D. Other factors: - Drugs (anti-arrhythmic toxicity, digoxin, sympathomimetics) - Hormonal/metabolic conditions (thyrotoxicosis, adrenal disorders) - Genetic mutations (Long QT syndrome, Brugada syndrome) 3. Physiological Control of Automaticity A. Pacemaker potential (Phase 4) in SA node: - SA node myocytes spontaneously depolarize to threshold. - The slope of Phase 4 determines intrinsic heart rate. B. Hierarchy of pacemakers: | Pacemaker | Intrinsic rate (bpm) | |-----------|-------------------| | SA node | 60–100 | | AV node | 40–60 | | His bundle| 40–50 | | Purkinje fibers | 20–45 | C. Autonomic modulation: - Sympathetic stimulation: ↑ phase 4 slope → ↑ heart rate Parasympathetic (vagal) stimulation: ↓ phase 4 slope → ↓ heart rate D. Overdrive suppression: - Faster pacemaker (SA node) suppresses slower pacemakers (AV node, Purkinje fibers). 1 4. Normal and Abnormal Rhythms Rhythm Rate P wave QRS Clinical significance Normal sinus rhythm 60–100 1:1 P:QRS Narrow Normal Sinus tachycardia 100– 180 1:1 Narrow Physiological (exercise) or pathological (fever, HF, sepsis) Sinus bradycardia <60 1:1 Narrow Ectopic beats Variable Abnormal P or absent Wide if ventricular Premature contractions Atrial fibrillation Variable Absent Irregular Risk of stroke, palpitations Ventricular tachycardia 100– 250 Absent Wide Emergency; ↓ CO, risk of VF Ventricular fibrillation N/A Absent Chaotic Cardiac arrest Normal in athletes; vagal tone ↑ Clinical examples: - Athlete with resting HR 45 bpm → sinus bradycardia (physiological) - Post-MI patient develops PVCs → risk for VT/VF 5. Afterdepolarizations A. Early afterdepolarizations (EADs): - Occur during late phase 2 or early phase 3 of AP - Mechanism: prolonged repolarization, reduced K⁺ currents - Causes: hypokalemia, hypomagnesemia, drug-induced QT prolongation - Can trigger torsades de pointes B. Delayed afterdepolarizations (DADs): - Occur late phase 3 / early phase 4 - Mechanism: intracellular Ca²⁺ overload → spontaneous SR Ca²⁺ release - Causes: digitalis toxicity, catecholamine excess, heart failure - Can trigger ectopic beats C. Clinical implication: - If afterdepolarization reaches threshold → ectopic beats or arrhythmias 6. Conduction Blocks A. Types: - Functional: tissue is refractory, conduction temporarily blocked - Anatomical: dead tissue, scar, or fibrosis prevents conduction B. AV blocks: | Degree | ECG | Effect | |--------|-----|-------| | 1st | PR >0.2s | Delayed conduction | | 2nd (Mobitz I/Wenckebach) | Progressive PR prolongation, dropped beat | Intermittent block | | 2nd (Mobitz II) | Constant PR, dropped beat | Risk of progression to 3rd degree | | 3rd | No atrialventricular association | Independent atrial and ventricular rhythm (Purkinje takes over ~35 bpm) | C. Consequences: - Bradycardia, syncope, reduced CO - Risk of sudden cardiac death in complete block 2 7. Re-entry Arrhythmias A. Mechanism: - Non-uniform conduction and refractory periods create a circular loop - Action potential continuously circulates → tachycardia B. Pre-requisites: - Central area of conduction block (scar tissue) - Region with unidirectional block (dead myocytes, varying refractory period) C. Examples: - Atrial flutter (sawtooth pattern on ECG) - AVNRT - Ventricular tachycardia D. Clinical consequences: - Continuous depolarization → impaired cardiac output - Can progress to ventricular fibrillation → cardiac arrest 8. Pharmacology of Arrhythmias A. Cardiac glycosides: - Digoxin: ↑ vagal tone, slows AV conduction, increases inotropy - Narrow therapeutic window, risk of DAD-induced arrhythmias B. Anti-arrhythmic drugs: | Class | Mechanism | Examples | Clinical use | |-------|-----------|---------|-------------| | I | Na⁺ channel blockers | Flecainide, Lidocaine | VT, AF | | II | Betablockers | Metoprolol, Bisoprolol | AF, post-MI arrhythmia | | III | K⁺ channel blockers | Amiodarone, Sotalol | VT, VF | | IV | Ca²⁺ channel blockers | Verapamil, Diltiazem | SVT, AF rate control | C. Electrolyte therapy: - Potassium, magnesium supplementation for arrhythmia prevention - Avoid hypokalemia to reduce EADs D. Other agents: - Adenosine: AVNRT termination - Atropine: symptomatic bradycardia 9. Treatment of Life-threatening Arrhythmias A. Ventricular tachycardia / fibrillation: - Immediate defibrillation: depolarizes all myocardial tissue, terminating re-entry loops - CPR: maintain perfusion until rhythm restored - Anti-arrhythmic infusion: Amiodarone, Lidocaine B. Bradyarrhythmias: - Pacemaker insertion (temporary or permanent) C. Long-term management: - Lifestyle: reduce alcohol, caffeine, smoking - Medications: beta-blockers, anti-arrhythmics - Device therapy: ICD for recurrent VT/VF - Correct underlying causes: ischemia, electrolyte disturbances 10. Diagnostic Tools A. ECG: Evaluate P wave, QRS duration, PR interval, T wave, QT interval; Detect AF, VT, VF, conduction blocks B. Holter Monitor: Continuous 24–48 hour recording C. Event Monitor: Patient-activated, for intermittent symptoms D. Telemetry: Continuous inpatient ECG monitoring E. Blood tests: Electrolytes, renal function, thyroid function, cardiac biomarkers F. Imaging: Echocardiography (LV function), Cardiac MRI (fibrosis/scar detection) 3 11. Clinical Scenarios A. Post-MI arrhythmias: - High risk of VT/VF; monitor continuously - Treat electrolyte imbalances Consider beta-blockers, amiodarone prophylaxis B. Atrial fibrillation: - Risk of thromboembolism → anticoagulation guided by CHA₂DS₂-VASc - Rate vs rhythm control strategies C. Bradyarrhythmias in athletes: - Usually benign - Monitor if symptomatic or syncope occurs D. Drug-induced arrhythmias: - Monitor QT interval - Adjust offending medications 12. Key Mechanisms Illustrated (Diagram Placeholders) • Pacemaker hierarchy – SA → AV → His → Purkinje • Afterdepolarizations (EAD/DAD) • Re-entry loop schematic • ECG patterns – Sinus rhythm, AF, VT, VF • Management flowchart – Initial assessment → pharmacologic → electrical → long-term monitoring 13. Summary and Key Clinical Points • Arrhythmias arise from abnormal impulse generation or conduction. • Early recognition prevents morbidity and mortality. • Afterdepolarizations (EAD/DAD) and conduction blocks are important mechanisms. • Re-entry is a common cause of tachyarrhythmias. • Treatment may involve drugs, devices, and acute interventions (defibrillation). • Comprehensive management requires monitoring, risk stratification, and addressing underlying causes. • Understanding physiology, pharmacology, and clinical presentation is essential for safe and effective care. 4