Normal cardiac activation starts in the sinoatrial node. Abnormal rhythms usually arise from pathology affecting the cardiac conduction system.
Normal activation and autonomic control
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Spontaneous depolarisation in the sinoatrial node initiates the cardiac cycle, followed by sequential activation of the atria and ventricles through specialised conducting tissues.
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Parasympathetic vagal activity decreases heart rate. Sympathetic activity increases it through cardiac sympathetic nerves and circulating catecholamines.
Three mechanisms of tachycardia
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Increased automaticity involves spontaneous depolarisation of an ectopic focus in the atria, atrioventricular junction or ventricles, often in response to catecholamines.
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Single ectopic depolarisations produce premature beats; repeated depolarisation produces atrial, junctional or ventricular tachycardia.
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Re-entry is initiated by an ectopic beat and sustained by a re-entry circuit. It causes most tachyarrhythmias.
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Triggered activity is secondary depolarisation arising from an incompletely repolarised cell membrane. It can cause ventricular arrhythmias in patients with coronary artery disease.
Rhythm origin and QRS complexes
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Arrhythmias may be supraventricular, arising from sinus, atrial or junctional sites, or ventricular in origin.
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Supraventricular rhythms usually have narrow QRS complexes because ventricular depolarisation follows the normal sequence through the atrioventricular node, bundle of His, bundle branches and Purkinje fibres.
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Ventricular arrhythmias usually have broad QRS complexes because activation spreads slowly through myocardial cells rather than rapidly through Purkinje fibres.
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Supraventricular tachycardia can occasionally produce broad complexes and mimic ventricular tachycardia when bundle branch block or an additional atrioventricular connection is present.