Arrhythmia — Types, Causes, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

A cardiac arrhythmia is any disturbance in the normal rate, rhythm, or conduction pathway of the heartbeat. The normal heart beats 60-100 times per minute in a regular sinus rhythm initiated by the sinoatrial (SA) node in the right atrium. Arrhythmias result from abnormalities in impulse formation (abnormal automaticity — ectopic foci firing inappropriately), conduction (heart block — electrical signals blocked at the AV node or His-Purkinje system), or both (re-entry circuits — electrical impulses recycling in an abnormal loop). Arrhythmias range from benign (isolated premature beats causing palpitations) to immediately life-threatening (ventricular fibrillation — requiring immediate defibrillation). Classification: supraventricular arrhythmias (originating above the bundle of His — atrial fibrillation, atrial flutter, SVT, AVNRT, WPW syndrome — generally less dangerous); ventricular arrhythmias (originating in the ventricles — ventricular tachycardia, ventricular fibrillation — potentially life-threatening); conduction disorders (sick sinus syndrome, heart block — may require pacemaker). Atrial fibrillation (AF) — the most common sustained arrhythmia — affects approximately 37 million people globally and is associated with a 5-fold increase in stroke risk, making anticoagulation management critical. Arrhythmias are responsible for approximately 350,000-500,000 sudden cardiac deaths annually in the US and Europe.

Arrhythmias result from structural heart disease, systemic conditions, medications, electrolyte disturbances, and genetic factors that alter myocardial electrophysiology. Structural causes: coronary artery disease and myocardial infarction (scarring creates re-entry circuits — substrate for ventricular tachycardia); heart failure and cardiomyopathy (dilated or hypertrophic — both strongly arrhythmogenic); valvular heart disease (mitral stenosis classically causes atrial fibrillation from left atrial dilatation); congenital heart disease; pericarditis and myocarditis. Systemic causes: hypertension (the most common cause of atrial fibrillation — left atrial enlargement); hyperthyroidism (sinus tachycardia, AF — thyroid function should always be checked in new AF); electrolyte abnormalities (hypokalaemia and hypomagnesaemia lower the ventricular fibrillation threshold — critical risk in acute MI; hypercalcaemia shortens the QT interval); hypoxia; sleep apnea (autonomic disturbance during hypoxic episodes triggers AF). Medications: digoxin toxicity; QT-prolonging drugs (antipsychotics, antibiotics — azithromycin, fluoroquinolones — antifungals — causing TdP ventricular tachycardia); sympathomimetics; alcohol excess ('holiday heart' syndrome — AF after binge drinking); caffeine excess; cocaine (ventricular fibrillation). Genetic: long QT syndrome (LQTS), Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), HCM — all cause sudden cardiac death, particularly in young people during exercise or emotional stress. Risk factors for AF specifically: age above 65 (prevalence 10-15% over 80), obesity, alcohol, hypertension, diabetes, and valvular heart disease.

Arrhythmia symptoms range from subtle to life-threatening. Common symptoms: palpitations — the most common complaint — described as racing, pounding, irregular, or missed heartbeats; lightheadedness or pre-syncope (near-fainting from transient cerebral hypoperfusion); syncope (loss of consciousness — requires urgent investigation as it may indicate a malignant arrhythmia; Stokes-Adams attacks are episodic loss of consciousness from complete heart block); breathlessness and exercise intolerance (from reduced cardiac output during tachyarrhythmia or AF); chest discomfort or chest pain (may accompany rapid arrhythmia or ischaemia triggering arrhythmia); and fatigue. Specific arrhythmia presentations: AF — typically irregular palpitations, fatigue, breathlessness, or is completely asymptomatic (detected incidentally on pulse check or ECG); SVT (AVNRT) — sudden onset and offset rapid regular palpitations (150-250 bpm), neck throbbing (from retrograde P waves causing cannon A-waves against closed tricuspid valve), often triggered by caffeine or stress; WPW syndrome — rapid palpitations that can deteriorate to AF with rapid conduction via accessory pathway causing haemodynamic collapse; ventricular tachycardia — rapid palpitations with haemodynamic compromise (dizziness, collapse, consciousness loss). Emergencies: cardiac arrest (no pulse, no consciousness, no breathing — ventricular fibrillation or pulseless VT requires immediate CPR and defibrillation); slow arrhythmia with collapse (complete heart block — may require emergency pacing).

ECG (12-lead electrocardiogram) is the cornerstone of arrhythmia diagnosis. It identifies: AF (irregularly irregular rhythm, absent P waves, fibrillatory baseline); atrial flutter (sawtooth baseline at 300 bpm with 2:1, 3:1 or 4:1 block); SVT (narrow complex tachycardia at 150-250 bpm — regular, retrograde P waves); ventricular tachycardia (broad complex tachycardia at 100-250 bpm with AV dissociation, fusion beats); heart block (PR prolongation in 1st degree; dropped beats in 2nd degree Mobitz I/II; P-QRS dissociation in 3rd degree); QTc prolongation (risk of TdP); delta wave (WPW syndrome — pre-excitation). Ambulatory ECG monitoring for intermittent symptoms: Holter monitor (24-72 hours — for frequent episodes); event recorder or loop recorder (worn for weeks — for infrequent symptoms, patient-triggered); implantable loop recorder (ILR — subcutaneous implant recording for 3 years — gold standard for very infrequent syncope). Echocardiogram: assesses structural heart disease, ventricular function (LVEF — key for ICD indication), valvular disease, and left atrial size. Electrophysiology study (EPS): invasive catheter study mapping intracardiac electrical pathways — used to diagnose and ablate SVT, WPW, VT, AF; identifies location of accessory pathways and re-entry circuits. Tilt table test for vasovagal syncope. Genetic testing for inherited arrhythmia syndromes (LQTS, Brugada, CPVT, HCM) in young patients with unexplained arrhythmia or family history of sudden cardiac death. Blood tests: thyroid function, electrolytes (K+, Mg2+), cardiac biomarkers (troponin — ischaemia), digoxin levels.

Arrhythmia treatment is tailored to type, severity, and underlying cause. Atrial fibrillation: (1) Rate control — slow ventricular rate in permanent AF using beta-blockers (bisoprolol, metoprolol), digoxin, or rate-limiting calcium channel blockers (diltiazem, verapamil); target resting HR 60-100 bpm; (2) Rhythm control — restore and maintain sinus rhythm — DC cardioversion (synchronised external electrical shock under sedation — 200-360J biphasic); pharmacological cardioversion (IV flecainide or amiodarone); long-term antiarrhythmic drugs (flecainide, propafenone for structurally normal heart; amiodarone for structural heart disease); catheter ablation (pulmonary vein isolation — PVI — isolates AF triggers in pulmonary veins; 60-80% single-procedure success rate for paroxysmal AF, 50-70% for persistent AF); (3) Stroke prevention — critical: CHA2DS2-VASc score guides anticoagulation — score 2+ in men, 3+ in women warrants direct oral anticoagulants (DOACs: apixaban, rivaroxaban, dabigatran, edoxaban — superior to warfarin in most patients with AF). SVT (AVNRT/AVRT): acute termination — Valsalva manoeuvre (syringe technique), carotid sinus massage, IV adenosine (6-12 mg — first-line — terminates 90% of SVT); long-term — catheter ablation (cure rate 95%+ for AVNRT); beta-blocker or calcium channel blocker prophylaxis. WPW: avoid AV-nodal blocking drugs (digoxin, verapamil) — can accelerate conduction down accessory pathway; definitive treatment is catheter ablation of accessory pathway (cure rate above 95%). Ventricular tachycardia: acute — IV amiodarone, lidocaine, or synchronised cardioversion (if haemodynamically stable) or defibrillation (if pulseless/unstable); long-term — ICD (implantable cardioverter-defibrillator) for secondary prevention (post-cardiac arrest or haemodynamically significant VT) or primary prevention (LVEF below 35%); antiarrhythmic drugs (amiodarone, sotalol, mexiletine); VT ablation. Bradyarrhythmias and heart block: permanent pacemaker implantation — indications include symptomatic sick sinus syndrome, second-degree Mobitz II, complete (third-degree) heart block, and symptomatic bradycardia below 40 bpm. Emergency — transcutaneous pacing or IV atropine 0.5-1 mg for acute complete heart block.

Atrial fibrillation carries a 5-fold increased risk of ischaemic stroke due to left atrial appendage thrombus formation — approximately 15–20% of all ischaemic strokes are AF-related. Tachycardia-mediated cardiomyopathy develops in sustained uncontrolled rapid arrhythmias (ventricular rate above 110 bpm chronically), causing reversible left ventricular dysfunction that can recover with rate control or ablation. Sudden cardiac death from ventricular fibrillation or pulseless ventricular tachycardia is responsible for approximately 350,000–500,000 deaths annually in the US and Europe. Heart failure can develop or worsen from reduced cardiac output during sustained tachyarrhythmias or from dyssynchrony in bundle branch block. Syncope and falls from bradyarrhythmias or vasovagal arrhythmias increase fracture risk, particularly in elderly patients. ICD therapy itself carries risks — inappropriate shocks from supraventricular tachycardia or oversensing cause significant distress and psychological impact.

Prevention targets modifiable risk factors for the most clinically important arrhythmias. AF prevention: treat hypertension (the most important modifiable risk factor for AF); achieve and maintain healthy weight (each unit increase in BMI raises AF risk by 4%); reduce alcohol consumption (abstinence or very low intake); treat sleep apnea (CPAP reduces AF burden significantly); control blood glucose and thyroid function. Sudden cardiac death prevention: pharmacological — ACE inhibitors, beta-blockers, statins, and mineralocorticoid receptor antagonists in heart failure reduce arrhythmic death; ICD implantation in high-risk patients (post-MI with LVEF below 35%, LVEF below 30-35% of any cause). For inherited arrhythmia syndromes (LQTS, Brugada, CPVT, HCM): avoid QT-prolonging medications (check www.crediblemeds.org); avoid triggers (exercise for CPVT, fever for Brugada); family screening of first-degree relatives. Avoid excessive caffeine, energy drinks, recreational drugs (cocaine, amphetamines), and alcohol. Regular exercise (30-150 minutes/week of moderate intensity) reduces AF risk; however, extreme endurance exercise (ultra-marathons, sustained heavy training) paradoxically increases AF risk ('athlete's heart' — vagally mediated AF).

Call emergency services immediately for: loss of consciousness (syncope) with or without palpitations — ventricular arrhythmia causing syncope can be immediately life-threatening; cardiac arrest (unresponsive, not breathing, no pulse — call 999 and start CPR; use a public AED if available); palpitations with chest pain, breathlessness, or severe dizziness — may indicate ischaemia-related or haemodynamically compromising arrhythmia; and sudden severe breathlessness in a patient with known AF or heart failure (acute decompensation or very rapid AF). Seek urgent (same-day) cardiology assessment for: new onset irregular pulse or palpitations lasting more than 30 minutes; first episode of rapid regular palpitations with near-collapse; palpitations in a patient with known structural heart disease (HCM, ischaemic heart disease, cardiomyopathy) or known inherited arrhythmia syndrome; new onset atrial fibrillation detected on pulse check or automated cuff — should have an ECG and urgent AF assessment for stroke risk stratification and anticoagulation decision within 24-48 hours. Do not drive if you are experiencing syncope or recurrent arrhythmia — DVLA/licensing authority notification requirements apply.