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

Arrhythmia refers to any abnormality in the heart's electrical conduction system resulting in an irregular, too-fast (tachyarrhythmia — above 100 bpm), or too-slow (bradyarrhythmia — below 60 bpm) heart rhythm. The heart's normal conduction system relies on an organised electrical pathway: sinus node (SA node) → atrioventricular node (AV node) → His-Purkinje system → ventricular myocardium. Any disruption of impulse generation or conduction at any level can cause arrhythmia. The most common clinically significant arrhythmia is atrial fibrillation (AF) — characterised by chaotic atrial electrical activity (350-600 impulses per minute) causing an 'irregularly irregular' ventricular response — affecting 37 million people globally and responsible for up to 30% of all ischaemic strokes. Other major types include: atrial flutter (regular saw-tooth atrial activity at 250-350 bpm with 2:1 or 3:1 block); supraventricular tachycardia (SVT — paroxysmal regular narrow complex tachycardia at 150-250 bpm, including AVNRT and AVRT in Wolff-Parkinson-White syndrome); ventricular tachycardia (VT — broad complex tachycardia from ventricular focus, potentially haemodynamically compromising); ventricular fibrillation (VF — completely chaotic ventricular activity causing cardiac arrest); and bradyarrhythmias including sick sinus syndrome and atrioventricular (AV) block (first, second, third-degree/complete heart block). Arrhythmias range from benign incidental findings to immediately life-threatening emergencies requiring resuscitation.

Arrhythmias arise from structural, metabolic, or functional disturbances in the cardiac conduction system. Structural and ischaemic causes: coronary artery disease and myocardial infarction (scar tissue forms re-entry circuits — the most common substrate for VT and VF); heart failure (chamber dilation stretches conduction tissue); hypertension (the leading modifiable risk factor for atrial fibrillation — causes left atrial enlargement and fibrosis); valvular heart disease (particularly mitral stenosis and regurgitation — AF); hypertrophic cardiomyopathy (a major cause of sudden cardiac death from VF in young people); and congenital heart defects (ASD, VSD — associated with SVTs and AF). Metabolic and electrolyte causes: hypokalaemia (low potassium — below 3.5 mmol/L — the most important electrolyte abnormality predisposing to VF and torsades de pointes); hypomagnesaemia; hypocalcaemia; hyperthyroidism (causes AF in 10-15% of cases — particularly in elderly). Toxic and iatrogenic causes: excess alcohol ('holiday heart' — AF precipitated by binge drinking); caffeine in excess; cocaine and amphetamines (cause VT, VF); certain medications (QT-prolonging drugs — antipsychotics, macrolides, antimalarials, methadone; digoxin toxicity — bradyarrhythmias and AV block; flecainide or sotalol proarrhythmia). Autonomic and functional causes: vagal AF (triggered by rest, sleep, or large meals — common in highly trained athletes); adrenergic AF (triggered by exercise, stress, or caffeine — in younger patients). Genetic conditions: inherited channelopathies — long QT syndrome (LQTS — KCNQ1/KCNH2/SCN5A gene mutations causing prolonged ventricular repolarisation and torsades de pointes VT); Brugada syndrome (SCN5A — ST elevation V1-V3, VF risk); catecholaminergic polymorphic VT (CPVT — CASQ2/RYR2 mutations); Wolff-Parkinson-White syndrome (accessory pathway — risk of AF degenerating into VF). Risk factors for AF specifically: age over 65 (prevalence 10-15%), obesity, sleep apnoea, alcohol use, male sex, structural heart disease, diabetes, and hypertension.

Arrhythmia symptoms depend on the type, rate, duration, and haemodynamic impact of the rhythm disturbance. Many arrhythmias are asymptomatic and detected incidentally — CLL is often diagnosed on a routine FBC; AF may be found on routine ECG or a wrist-based smartwatch. Symptomatic presentations: palpitations — awareness of the heartbeat as fluttering, racing, pounding, or irregular sensations; patients often describe paroxysmal SVT as a sudden 'switch-on, switch-off' rapid regular heartbeat; AF as an irregular 'fish-flopping' or chaotic sensation; VT as a sudden onset of rapid thudding. Dizziness and presyncope — from reduced cardiac output during fast arrhythmias or from cerebral hypoperfusion during bradyarrhythmias. Syncope (fainting) — Stokes-Adams attacks in complete heart block: sudden loss of consciousness without warning from abrupt cessation of ventricular rate; fainting during exertion in inherited arrhythmia syndromes (LQTS, CPVT, HCM) is a red flag for VF risk. Dyspnoea and exercise intolerance — from reduced cardiac output and pulmonary venous congestion in fast AF, VT, or tachycardia-induced cardiomyopathy. Chest pain — from myocardial ischaemia precipitated by fast rates in patients with coronary artery disease. Sudden cardiac arrest — ventricular fibrillation or pulseless VT causes loss of consciousness, absent pulse, and absence of effective circulation within seconds — immediately fatal without CPR and defibrillation. Asymptomatic AF specifically: detected by 12-lead ECG, Holter, or wearable devices — estimated 10-30% of AF is subclinical; still carries the same stroke risk as symptomatic AF. Bradyarrhythmias: fatigue, exercise intolerance, near-fainting, cold extremities, and confusion from reduced cardiac output.

A standard 12-lead ECG is the primary diagnostic tool — it records the heart's electrical activity in 12 spatial planes, identifying rhythm abnormalities including AF (absent P-waves, irregularly irregular QRS complexes), flutter (sawtooth atrial activity at 250-350 bpm), heart block (PR prolongation, dropped beats, AV dissociation), VT (broad complex tachycardia), SVT (narrow complex tachycardia), pre-excitation (delta wave — Wolff-Parkinson-White), Brugada pattern (coved ST elevation in V1-V2), and QTc prolongation. For intermittent palpitations or unexplained syncope: ambulatory ECG monitoring — 24 or 48-hour Holter monitor records continuously; 2-4 week event monitor (patient-activated when symptomatic); wearable 14-day patch monitor (Zio patch — superior detection of paroxysmal AF); implantable loop recorder (ILR — subcutaneous device implanted in the left parasternal area under local anaesthetic; battery life 3-4 years; wirelessly transmits to a remote monitoring centre) — the gold standard for infrequent unexplained syncope. Echocardiogram (transthoracic or transoesophageal/TOE): assesses structural heart disease underlying arrhythmia; TOE is the gold standard before cardioversion to exclude left atrial appendage thrombus in AF; cardiomyopathy identification guides ICD suitability. Exercise stress test: for exercise-induced arrhythmias; excludes ischaemia precipitating VT. Electrophysiology study (EPS): invasive catheter-based mapping of cardiac electrical pathways — identifies accessory pathways (WPW), defines the mechanism of SVT (AVNRT vs AVRT), and guides ablation; inducibility of VT guides ICD programming. Blood tests: TFTs (hyperthyroidism in new AF); electrolytes (K+, Mg2+, Ca2+ — hypokalaemia and hypomagnesaemia in VF risk); cardiac biomarkers (troponin — myocardial injury in haemodynamically compromised tachyarrhythmia); and drug levels (digoxin toxicity — therapeutic level 0.8-2.0 nmol/L).

Treatment is tailored to the specific arrhythmia type, haemodynamic stability, and underlying cause. Atrial fibrillation management has four pillars: (1) Rate control: beta-blockers (bisoprolol, metoprolol), rate-limiting calcium channel blockers (verapamil, diltiazem), or digoxin — target resting heart rate below 110 bpm (lenient) or below 80 bpm (strict) depending on symptoms and heart function. (2) Rhythm control: DC cardioversion (synchronised electrical shock, 200 J biphasic) for haemodynamically unstable AF or elective restoration of sinus rhythm; chemical cardioversion with flecainide ('pill-in-the-pocket') for paroxysmal AF in structurally normal hearts; maintenance antiarrhythmics include flecainide (for structurally normal heart), sotalol, or amiodarone (broadest efficacy but most side effects — pulmonary toxicity, thyroid dysfunction, hepatotoxicity with long-term use). (3) Anticoagulation: oral anticoagulants are the most important treatment to prevent AF-related stroke — direct oral anticoagulants (DOACs: apixaban 5 mg twice daily, rivaroxaban 20 mg once daily, edoxaban, dabigatran) are preferred over warfarin for non-valvular AF due to better efficacy-safety profile and no INR monitoring; prescribe when CHA2DS2-VASc score is 2+ in men and 3+ in women. Left atrial appendage occlusion (Watchman device) for anticoagulation-unsuitable patients. (4) Catheter ablation: pulmonary vein isolation (PVI) for paroxysmal and persistent AF — increasingly used as first-line rhythm control in symptomatic young patients; success rate 70-85% for paroxysmal AF at 1 year. SVT: vagal manoeuvres (Valsalva, carotid sinus massage); IV adenosine 6 mg (terminating AVNRT/AVRT in 90%); radiofrequency catheter ablation is curative in 95%+ of typical SVT. VT/VF: haemodynamically unstable VT/VF — immediate DC cardioversion/defibrillation (200 J); stable VT — IV amiodarone or procainamide; implantable cardioverter-defibrillator (ICD) for VT/VF survivors or high-risk patients (ischaemic cardiomyopathy with EF below 35%). Bradyarrhythmias: permanent pacemaker implantation for symptomatic sick sinus syndrome or complete heart block.

Untreated atrial fibrillation carries a 5-fold increased risk of ischaemic stroke — blood clots form in the non-contracting left atrial appendage (LAA) and embolise to the brain, causing cardioembolic stroke; AF-related strokes are typically severe and disabling due to large clot size; anticoagulation reduces stroke risk by approximately 65-70% (warfarin) to 70-80% (DOACs). AF also causes tachycardia-induced cardiomyopathy — sustained rapid ventricular rates above 100-130 bpm progressively impair left ventricular function, causing heart failure in some patients; rate control reverses this cardiomyopathy in most cases. Untreated persistent ventricular tachycardia degenerates into ventricular fibrillation — causing sudden cardiac death in minutes without defibrillation; VT in the context of structural heart disease (ischaemic cardiomyopathy EF below 35%) carries 20-30% annual SCD risk without ICD. Untreated complete heart block causes recurrent Stokes-Adams attacks (sudden syncopal episodes without warning from ventricular standstill), progressive cardiac failure, and cardiac arrest. Uncontrolled arrhythmias cause significant reduction in exercise capacity, quality of life, cognitive function (from cerebral hypoperfusion), and increase hospital admissions, healthcare costs, and all-cause mortality.

Manage cardiovascular risk factors rigorously: control hypertension (the largest modifiable risk factor for AF — target blood pressure below 130/80 mmHg significantly reduces AF burden and stroke risk); treat diabetes with good HbA1c control; achieve and maintain a healthy BMI (obesity increases AF risk by 50% and VT risk from cardiomyopathy); treat obstructive sleep apnoea (CPAP therapy reduces AF recurrence post-ablation by 40-50%). Limit alcohol — even moderate consumption of 14 or more units per week significantly increases AF risk and triggers acute episodes; abstinence is optimal for AF patients. Regular moderate aerobic exercise (150-300 minutes per week) reduces overall arrhythmia risk; paradoxically, extreme endurance exercise (marathon and ultra-marathon running, competitive cycling) increases AF risk in healthy middle-aged men. Maintain adequate hydration and electrolyte levels — hypokalaemia from diuretics is a preventable cause of VF. Quit smoking — nicotine increases sympathetic tone and AF risk. For patients with diagnosed arrhythmias: take anticoagulants (DOACs) and antiarrhythmic medications exactly as prescribed without missing doses; attend regular cardiology and anticoagulation reviews; and carry an emergency card or medical alert wristband.

Call emergency services (999/112) immediately for: sudden collapse or loss of consciousness (possible ventricular fibrillation or haemodynamically compromising VT — cardiac arrest); palpitations with chest pain, severe breathlessness, or extreme dizziness or fainting; any suspected stroke symptoms (facial droop, arm weakness, slurred speech) — AF patients are at 5-fold elevated stroke risk. Seek urgent same-day cardiology or A&E assessment for: new irregular heartbeat or rapid palpitations lasting more than 30 minutes; first episode of rapid regular palpitations causing near-collapse; very slow pulse (below 40 bpm) with dizziness or near-fainting; and any known arrhythmia patient experiencing unusual symptoms or deterioration. If you have been diagnosed with AF: attend all scheduled anticoagulation and cardiology appointments — AF-related stroke is largely preventable with appropriate anticoagulation, and any interruption in anticoagulation significantly increases stroke risk.