What Is It and How Does It Work?
The sinoatrial node is the primary center of automaticity. It suppresses the automaticity of downstream components of the conduction system and contractile cardiomyocytes.
In frogs, the anatomical analogue of the SAN is the sinus venosus, which houses Remak's ganglion. The classical physiological experiment involving Stannius ligatures applied to a frog heart proves the presence of automaticity in various heart regions and demonstrates a descending gradient of automaticity from the venous sinus to the cardiac apex. Normally, excitation originates in the primary pacemaker—the venous sinus (SAN)—and then propagates sequentially: sinus → atria → ventricles. The contraction frequency is maximal for this heart.
How Does Excitation Spread?
From the sinoatrial node, the impulse propagates in the following sequence:
- Atria — excitation travels along the atrial conducting pathways, exciting typical atrial cardiomyocytes. On a mechanocardiogram, the small wave (PA) corresponds to atrial contraction.
- Atrioventricular node (AV node) — the impulse reaches the atrioventricular junction.
- Bundle of His — from the AV node, excitation travels to the ventricles via the bundle of His; within the interventricular septum, the bundle divides into right and left bundle branches.
- Purkinje fibers — excitation transitions to the Purkinje fibers and reaches typical ventricular cardiomyocytes, triggering their contraction. On a mechanocardiogram, the large wave (VC) corresponds to ventricular contraction.
How Does the Autonomic Nervous System Regulate the Node?
- Cholinergic regulation: M-receptors and a vagal effect are associated with the sinoatrial node, leading to a decrease in heart rate (bradycardia). The cardiac target consists of $M_2$ muscarinic receptors. When vagal inhibitory influence is removed, SAN automaticity increases, leading to tachycardia. At low doses, transient bradycardia may occur due to stimulation of vagal centers in the CNS or increased acetylcholine release resulting from presynaptic $M_2$ receptor blockade.
- Noradrenergic regulation: $\beta_1$ receptors and heart rate acceleration are associated with the sinoatrial node. Cardiac effects are driven by increased $Ca^{2+}$ influx into various cardiac structures; automaticity increases within the sinoatrial node, elevating the heart rate.
Role of the SAN in Extrasystoles
If an impulse originates outside the sinoatrial node, premature contractions (extrasystoles) may occur.
- Atrial extrasystole: The impulse originates in the atria outside the SAN, passes through the AV node, and propagates to the ventricles via the normal pathway. On an ECG trace, the P wave preceding the extrasystole is altered because atrial activation is atypical. The QRS complex has a normal, narrow shape because intraventricular conduction is unimpaired.
- Ventricular extrasystole: The ectopic focus of excitation is located in the ventricle. A full compensatory pause follows a ventricular extrasystole. The normal sinus impulse from the SAN reaches the ventricles while they are still in a refractory period following the extrasystole, causing one normal contraction to be dropped. The ventricles contract only in response to the subsequent sinus impulse. The interval combining the pre-extrasystolic and post-extrasystolic periods equals two normal cardiac cycles (2 R–R).
The Pacemaker Concept in Other Systems
In P.K. Anokhin and K.V. Sudakov's concept of the pacemaker role of hypothalamic centers, an analogy to the heart is used: just as the sinus node subjugates other cardiac automaticity centers with lower excitability, motivational hypothalamic centers control structures at other levels of the brain. Disruption of hypothalamic centers leads to the disintegration of the entire system of elements united into motivational arousal.