Bradycardia refers to a heart rate that is slower than expected, conventionally often defined in adults as fewer than 60 beats per minute, although the numerical threshold alone does not establish disease. Slow heart rates can occur normally during sleep and in physically trained individuals because of increased vagal influence and efficient cardiovascular conditioning. Bradycardia becomes clinically important when the slow rate reflects a pathological rhythm or conduction abnormality, particularly when it reduces cardiac output and causes symptoms. Clinical interpretation therefore considers the person's age, circumstances, symptoms, medications, athletic conditioning and the specific electrical rhythm.
Sinus bradycardia occurs when the sinoatrial node continues to initiate normal impulses but at a slower frequency. Other forms arise from impaired conduction between the atria and ventricles. Atrioventricular block can be classified into degrees according to the severity and pattern of impaired conduction. In more advanced forms, atrial impulses may fail to reach the ventricles, leaving the ventricles dependent on slower subsidiary pacemakers. This can produce substantial reduction in heart rate and, in severe cases, inadequate circulation. Distinguishing sinus bradycardia from conduction block requires ECG assessment rather than relying on pulse rate alone.
Physiological Bradycardia can occur during sleep and in endurance-trained athletes. Increased parasympathetic activity can slow the sinoatrial node without indicating disease. Conversely, pathological bradycardia can result from ageing-related degeneration of the conduction system, myocardial infarction, inflammation, infiltrative disease, hypothyroidism, electrolyte abnormalities and medications such as beta blockers or some calcium-channel blockers. High vagal tone can also contribute. The same numerical heart rate can therefore be entirely appropriate in one person and clinically concerning in another.
Symptoms arise when the slow rhythm reduces effective cardiac output or fails to increase appropriately when physiological demand rises. Possible manifestations include fatigue, dizziness, exercise intolerance, weakness, confusion, near-fainting and syncope. Some people remain completely asymptomatic despite substantial bradycardia. Symptoms can also arise intermittently when pauses or blocks occur, making short ECG recordings insufficient to identify the problem. Correlating symptoms with the rhythm is therefore an important part of assessment and can require prolonged monitoring.
Evaluation generally begins with history, examination, medication review and ECG. Additional investigations may include ambulatory monitoring, blood tests for potentially reversible causes and exercise testing to assess whether heart rate increases appropriately during activity. Echocardiography can be useful when structural heart disease is suspected. Sleep-related breathing disorders may be considered in appropriate circumstances because nocturnal rhythm changes can accompany them. The objective is not merely to find a low number but to determine whether the rhythm is physiological, caused by a reversible factor or evidence of intrinsic conduction-system disease.
Treatment depends on the cause and clinical consequences. Reversible causes should be addressed where possible, such as correcting metabolic abnormalities or adjusting a causative medicine under appropriate medical supervision. Asymptomatic physiological bradycardia often requires no treatment. Persistent symptomatic bradycardia caused by significant conduction-system disease may require permanent pacemaker implantation. Temporary pacing can be used in selected acute emergencies. A pacemaker supplies appropriately timed electrical impulses when the heart's own conduction system cannot maintain an adequate rate or sequence.
Severe acute Bradycardia can produce hypotension, altered consciousness, shock or cardiac arrest when circulation becomes inadequate. Emergency management depends on the clinical condition and underlying rhythm and can involve immediate supportive measures, medications that increase heart rate and temporary pacing when indicated. A low pulse alone does not automatically constitute an emergency; the presence of poor perfusion or serious symptoms is critical. Conversely, a person with apparently modest bradycardia can require urgent assessment if there are significant pauses, advanced conduction block or haemodynamic compromise.
Bradycardia should therefore be distinguished from simply having a naturally low resting heart rate. A value below 60 bpm is a descriptive threshold rather than a diagnosis. Athletes, young healthy people and sleeping individuals can have low rates without pathology, while a normal rate does not exclude intermittent conduction disease. The important questions are whether the rhythm is appropriate for the circumstances, whether electrical conduction is normal, whether symptoms or impaired circulation are present and whether a reversible cause exists. Proper assessment prevents both unnecessary treatment of physiological bradycardia and failure to recognise clinically important conduction disorders.
