sinoatrial node

The SA node is composed of specialized pacemaker cells with unstable resting membrane potentials due to the 'funny current' (If, Na+ influx through HCN channels) that drives slow phase 4 depolarization, followed by phase 0 depolarization mediated by L-type Ca2+ channels (unlike the fast Na+ channels of ventricular myocytes). This automaticity gives the SA node the fastest intrinsic firing rate (~60-100 bpm), making it the dominant pacemaker; if it fails, subsidiary pacemakers (AV node ~40-60 bpm, Purkinje fibers ~15-40 bpm) take over at slower rates. The SA node is supplied by the right coronary artery (RCA) in ~60% of individuals (SA nodal branch), making SA node dysfunction a concern in RCA occlusion (inferior MI), which can cause sinus bradycardia or sinus node dysfunction. Autonomic innervation: sympathetic stimulation (β1 receptors, increased cAMP) increases the slope of phase 4 and heart rate (positive chronotropy); vagal stimulation (M2 receptors, increased K+ efflux via GIRK channels, decreased cAMP) hyperpolarizes the cell and slows heart rate (negative chronotropy) - this is the basis of normal resting vagal tone keeping HR below the SA node's intrinsic rate. Clinically relevant conditions include sick sinus syndrome (SA node dysfunction causing bradycardia-tachycardia syndrome, often in elderly, may require pacemaker), sinus arrhythmia (normal variation with respiration), and sinus tachycardia/bradycardia. Pharmacology: drugs like beta-blockers, calcium channel blockers (non-dihydropyridines), and digoxin affect SA node firing rate; ivabradine selectively blocks If channels to reduce heart rate without affecting contractility, used in heart failure and angina.