The heart has a specialised electrical conduction system that initiates and coordinates heartbeats in an orderly sequence. This system consists of: SA node (sino-atrial node): right atrial wall near SVC; primary pacemaker; rate 70-75/min. AV node (atrioventricular node): at the junction of atria and ventricles in the interatrial septum; delays conduction ~0.1 sec (allows atria to complete contraction and fill ventricles before ventricles contract); rate 40-60/min if SA node fails. Bundle of His (AV bundle): from AV node through fibrous AV ring (only electrical connection between atria and ventricles); divides into right and left bundle branches in the interventricular septum. Purkinje fibres: from bundle branches, spread throughout ventricular myocardium; conduct impulses rapidly (4 m/s) ensuring synchronised ventricular contraction; rate 20-40/min if both SA and AV nodes fail. The key principle: the fastest pacemaker dominates, which is why SA node normally controls heart rate.

The SA node demonstrates automaticity — the ability to spontaneously generate action potentials without external stimulation. This property arises from unique ion channel characteristics of SA node cells (also called P cells or pacemaker cells): Funny current (If): unique to pacemaker cells; inward Na+ current that slowly depolarises the membrane during diastole toward threshold — this "funny" or "pacemaker" current (via HCN channels) is responsible for the spontaneous phase 4 depolarisation. Calcium channels (T-type and L-type): contribute to the upstroke of the SA node action potential (unlike working myocardium where Na+ channels cause the rapid upstroke). No stable resting potential: SA node membrane never maintains a constant negative potential; it continuously and spontaneously depolarises (phase 4 depolarisation), reaches threshold, fires an action potential, repolarises, and immediately begins depolarising again. This cyclical spontaneous depolarisation occurs approximately 70-75 times per minute under normal conditions, producing the heartbeat rhythm.

The SA node's intrinsic rate of 70-75/min is modulated by the autonomic nervous system to allow heart rate to change with physiological demands. Parasympathetic (vagal) control: the vagus nerve (CN X) innervates the SA node and releases acetylcholine (ACh), which binds muscarinic (M2) receptors on SA node cells, increasing K+ permeability via GIRK channels (G-protein-coupled inward rectifying K+ channels), hyperpolarising the membrane and slowing the rate of diastolic depolarisation — this decreases heart rate (negative chronotropy) and is the dominant influence at rest, which is why resting heart rate (70-75/min) is lower than the SA node's intrinsic rate without autonomic input (~100/min). Sympathetic control: sympathetic nerves release noradrenaline (and the adrenal gland releases adrenaline), which binds beta-1 adrenergic receptors on SA node cells, increasing the rate of diastolic depolarisation via increased cAMP and enhanced funny current (If) — this increases heart rate (positive chronotropy). Athletes at rest: high vagal tone → resting heart rate often 45-60/min. Fight-or-flight response: high sympathetic, low parasympathetic → heart rate can reach 180-200/min.

SA node dysfunction can cause several clinically important arrhythmias. Sick sinus syndrome (SSS): failure of the SA node to generate impulses at an adequate rate, causing severe bradycardia, pauses in cardiac rhythm, or alternating bradycardia and tachycardia. Symptoms include fatigue, dizziness, syncope (fainting), and exercise intolerance. Treatment often requires permanent cardiac pacemaker implantation. The ECG shows absence of P waves during pauses or abnormal P wave morphology. Complete heart block: total failure of impulse conduction from atria to ventricles (can be at AV node or bundle branches), so atria and ventricles beat independently at their own intrinsic rates. SA node drives atria at 70-75/min; ventricles beat at the intrinsic idioventricular rate of 20-40/min. Haemodynamically unstable — usually requires emergency temporary pacing followed by permanent pacemaker. Atrial fibrillation: not an SA node problem per se, but the most common sustained cardiac arrhythmia; chaotic electrical activity originating from multiple foci in the atria replaces the organised SA node pacemaker activity, producing rapid (300-600 depolarisations/min) and irregular atrial activity with an irregularly irregular ventricular response.