A topic in the Open Knowledge Graph — a free, open map of 15,290 topics and the order to learn them in.
Cardiac arrhythmias result from three mechanisms: abnormal automaticity (ectopic pacemakers firing faster than SA node), triggered activity (early after-depolarization from calcium overload or repolarization abnormalities, delayed after-depolarization from DAD), and reentry (circular conduction around anatomic or functional block). Structural disease (scar, fibrosis) and ion channel dysfunction (congenital long QT, short QT, Brugada) predispose to arrhythmias. Ischemia, acute inflammation, and electrolyte derangements trigger arrhythmias in structurally normal hearts.
Use action potential diagrams showing early (during repolarization) and delayed (after repolarization complete) after-depolarizations. Understand the reentry circuit requires unidirectional block and slow conduction. Study Vaughan-Williams classification of antiarrhythmic agents by their ion channel targets.
Automaticity does not require abnormal ion channels—any cell capable of reaching threshold can generate an ectopic rhythm. Reentry requires both unidirectional block AND slow conduction; fast conduction throughout the circuit prevents reentry. Long QT syndrome increases risk of torsade de pointes, not standard VT.
Your understanding of the cardiac action potential is the foundation for everything here. Normal cardiac rhythm depends on the SA node acting as the dominant pacemaker because it depolarizes faster than any other cardiac tissue — its slope of phase 4 spontaneous depolarization is steepest. Arrhythmias arise when this hierarchy breaks down. The three mechanisms — abnormal automaticity, triggered activity, and reentry — are distinct failure modes of cardiac electrical architecture.
Abnormal automaticity arises when ischemia, hypoxia, or electrolyte abnormalities partially depolarize non-pacemaker cells. When the resting membrane potential drifts from −90 mV to approximately −60 mV, the funny current (If) and calcium channels that drive spontaneous depolarization begin to activate even in cells like ventricular myocytes that are normally quiescent. These cells then fire on their own schedule, generating ectopic beats that interrupt the SA node's rhythm. Hypercalemia and ischemia are classic triggers: both reduce the magnitude of the resting membrane potential, nudging cells into the range where automaticity is possible.
Triggered activity requires a preceding action potential — hence "triggered." It comes in two forms. Early after-depolarizations (EADs) occur during phase 2 or 3 of the action potential, when repolarization is prolonged (long QT) and the L-type calcium channels, which inactivated normally, can recover and reactivate before repolarization completes. The result is a secondary upstroke riding on the tail of the first action potential. EADs are the mechanism of torsades de pointes — a distinctive polymorphic ventricular tachycardia that "twists" around the baseline. Delayed after-depolarizations (DADs) occur after repolarization is complete, driven by calcium overload. When sarcoplasmic reticulum calcium is excessive (as in digoxin toxicity or catecholamine excess), spontaneous calcium release through ryanodine receptors drives the sodium-calcium exchanger to expel calcium while importing sodium, generating an inward current that can reach threshold and fire an ectopic beat.
Reentry is geometrically elegant and clinically the most common sustained arrhythmia mechanism. Imagine electrical wavefront traveling down two pathways around an anatomic obstacle (a scar, valve ring, or accessory pathway). In a normal heart, the wavefront meets in the middle after going around both paths and extinguishes — both pathways have similar conduction velocities and refractory periods. Reentry requires two conditions to coexist: unidirectional block in one pathway (the wavefront cannot go forward but can be entered from behind) and slow conduction in the other pathway (slow enough that by the time the wavefront traverses it, the blocked pathway has recovered its excitability). The wavefront then re-enters the blocked pathway retrograde and circles indefinitely, producing a sustained tachycardia. Ablation therapy destroys the circuit by eliminating one of the pathways; antiarrhythmic drugs interrupt reentry by either slowing conduction further (making the circuit too slow to sustain itself) or prolonging refractoriness (so the circuit never finds excitable tissue to re-enter). Understanding which mechanism underlies a particular arrhythmia directly determines which class of antiarrhythmic therapy is appropriate.