Arrhythmia is an abnormality of the heart's electrical rhythm, including abnormalities of rate, regularity, impulse formation or conduction. The term encompasses a very broad range of conditions, from harmless extra beats that occur in healthy people to life-threatening ventricular rhythms that can prevent effective circulation. A rhythm can be too fast, too slow or irregular, and some arrhythmias arise from abnormal impulse generation while others result from abnormal conduction through the heart. Arrhythmias can occur in structurally normal hearts or in association with coronary disease, cardiomyopathy, valve disease, congenital abnormalities, electrolyte disturbances, medications and many other conditions.
Normal cardiac rhythm begins with electrical impulse generation in the sinoatrial node, followed by conduction through the atria, atrioventricular node and specialised ventricular conduction pathways. Arrhythmias can result from abnormal automaticity, triggered activity, re-entry circuits or disturbances of conduction. Re-entry occurs when an electrical impulse repeatedly circulates through tissue under particular conduction and refractory conditions and is an important mechanism in several tachyarrhythmias. Abnormal electrical activity can originate in the atria, atrioventricular junction or ventricles. The anatomical origin and electrophysiological mechanism strongly influence symptoms, treatment and risk.
Common symptoms include palpitations, awareness of heartbeat, dizziness, breathlessness, fatigue, chest discomfort and fainting. Some arrhythmias cause no symptoms and are discovered during routine examination or ECG monitoring. Symptoms do not reliably indicate the seriousness of an arrhythmia: a person can feel dramatic palpitations from a relatively benign rhythm, while a dangerous ventricular arrhythmia may cause sudden collapse with little warning. Clinical interpretation therefore requires identifying the actual rhythm rather than judging risk from the subjective sensation alone.
Electrocardiography is central to Arrhythmia diagnosis because it records the heart's electrical activity and can show rate, rhythm, conduction intervals and characteristic waveform patterns. A short resting ECG may fail to capture intermittent arrhythmias, so ambulatory monitoring can be used for longer periods. Holter monitoring records continuously, while event or patch-based devices can monitor over longer intervals depending on the technology. Implantable loop recorders can provide prolonged monitoring in selected cases. Wearable devices can identify possible irregular rhythms but generally require clinical confirmation when a diagnosis has significant consequences.
Treatment depends entirely on the rhythm, symptoms, underlying heart condition and associated risks. Some benign or minimally symptomatic rhythms require reassurance and monitoring rather than treatment. Other arrhythmias can be managed with medicines that alter heart rate or electrical conduction, catheter ablation that destroys or isolates the tissue responsible for an abnormal circuit, or implanted devices that pace or defibrillate the heart. Treatment can also involve correcting precipitating factors such as electrolyte abnormalities, thyroid disease, medication effects or acute myocardial ischaemia.
Bradyarrhythmias and tachyarrhythmias represent broad physiological groupings within Arrhythmia. Bradyarrhythmias involve abnormally slow rates or conduction disturbances, whereas tachyarrhythmias involve excessively rapid rhythms. Atrial fibrillation is a particularly common irregular atrial rhythm and carries an increased risk of thromboembolic stroke. Ventricular tachycardia and ventricular fibrillation arise from the ventricles and can be life-threatening because they may severely reduce effective cardiac output. The distinction between supraventricular and ventricular arrhythmias is therefore clinically important because their mechanisms and emergency implications differ.
Arrhythmia risk can be increased by structural heart disease, myocardial scarring, inherited electrical disorders, electrolyte abnormalities, certain medicines, stimulant exposure and acute physiological stress. Long QT syndromes and other inherited channelopathies can predispose to dangerous ventricular rhythms despite relatively normal cardiac structure. Scar tissue following myocardial infarction can also provide pathways that support re-entry and ventricular tachycardia. Risk assessment consequently considers both the rhythm itself and the condition of the underlying myocardium.
Arrhythmia is not synonymous with an irregular heartbeat because some abnormal rhythms are regular but excessively fast or slow, while some irregular pulse patterns can arise from several different mechanisms. Premature beats can occur occasionally without indicating serious disease, whereas persistent or symptomatic rhythm abnormalities require appropriate assessment. The clinical importance of an Arrhythmia depends on its origin, duration, ventricular response, effect on circulation, associated disease and potential for progression. Diagnosis is fundamentally electrical, but treatment frequently requires addressing the structural, metabolic or systemic factors that created the conditions for abnormal rhythm.
