Electrical Properties of the Heart

The heart generates its own electrical activity (myogenic rhythmicity). The SA node is the dominant pacemaker because it has the highest intrinsic firing rate (~100/min). Its resting membrane potential is unstable — Phase 4 (pre-potential/pacemaker potential) is a slow spontaneous depolarisation driven by an inward Na+ current through f-type (funny) channels (if), which open at negative potentials. As depolarisation reduces K+ permeability (outward iK decreases), the cell depolarises further. At around -50 to -40 mV, T-type Ca2+ channels open (iCa,T), bringing the membrane to threshold. Then L-type Ca2+ channels open (iCa,L), producing the upstroke (Phase 0). Repolarisation (Phase 3) is driven by increased K+ permeability (iK).

SA node cells lack fast voltage-gated Na+ channels, so depolarisation is slow compared with ventricular cardiomyocytes. At rest, parasympathetic dominance via vagal tone slows the SA node from 100/min to ~60-70/min (vagal braking). Sympathetic stimulation (noradrenaline → β1 → cAMP → PKA) increases if, iCa,T, and iCa,L, steepening the pacemaker potential slope and increasing HR. Parasympathetic stimulation (ACh → M2 → ↓cAMP + opens KACh channels → hyperpolarisation) decreases the slope and hyperpolarises the cell, increasing time to threshold and slowing HR. Backup pacemakers: AV node (40-50/min) and Purkinje fibres (20-30/min).

The ventricular cardiomyocyte AP has five phases. Phase 4: stable resting membrane potential (~-90 mV) maintained by outward iK. Phase 0: stimulus from adjacent cell → threshold -65 mV → fast voltage-gated Na+ channels open → rapid depolarisation to +40 mV (~1-2 ms). Phase 1: fast Na+ channels self-inactivate → slight repolarisation from transient outward K+ current (ito). Phase 2 (plateau): L-type Ca2+ channels (activated at -30 mV during Phase 0) sustain inward Ca2+ current (iCa,L), counterbalancing outward K+ (ito) → plateau at ~0 mV; this prolonged depolarisation drives contraction and is unique to cardiac muscle. Phase 3: K+ permeability increases and Ca2+ channels inactivate → repolarisation.

The long AP (~300 ms) and absolute refractory period (~250 ms) prevent tetanic contraction. Fast Na+ channels are inactivated until membrane potential returns below -20 mV. The conduction pathway: SA node → atrial muscle (0.5 m/s) → AV node (0.05 m/s, delays 0.1 s) → bundle of His (1.0 m/s) → left and right bundle branches (5.0 m/s) → Purkinje fibres (5.0 m/s) → ventricular muscle (0.5 m/s). The AV nodal delay allows complete atrial systole before ventricular contraction.