What is this and how does it work?
The sinoatrial node is the primary center of automaticity. It suppresses the automaticity of lower parts of the conduction system and contractile cardiomyocytes.
In frogs, the anatomical equivalent of the SAN is the sinus venosus region, which contains Remak's ganglion. The classic physiological experiment involving the application of Stannius ligatures to a frog heart proves the presence of automaticity in various regions and demonstrates a decreasing gradient of automaticity from the venous sinus to the apex of the heart. Normally, excitation originates in the primary pacemaker—the venous sinus (SAN)—and then propagates sequentially: sinus → atria → ventricle. The contraction frequency is maximal for the given heart.
How does excitation propagate?
From the sinoatrial node, the impulse propagates in the following sequence:
- Atria — excitation travels along the atrial conducting fibers; typical atrial cardiomyocytes are excited. On the mechanogram, the small wave (PA) corresponds to atrial contraction.
- Atrioventricular node (AVN) — the impulse reaches the atrioventricular node.
- Bundle of His — from the atrioventricular node, excitation travels to the ventricles via the bundle of His; within the cardiac septum, the bundle divides into right and left branches.
- Purkinje fibers — excitation passes to the Purkinje fibers and reaches typical ventricular cardiomyocytes, causing their contraction. On the mechanogram, the large wave (VC) corresponds to ventricular contraction.
How does the autonomic nervous system regulate the node?
- Cholinergic regulation: for the sinoatrial node, M-receptors and a vagal effect (slowing of heart rate) are indicated. The target in the heart is $M_2$-cholinergic receptors. When the inhibitory influence of the vagus nerve is removed, the automaticity of the sinoatrial node increases, leading to tachycardia. At low doses, transient bradycardia is possible; the causes are stimulation of vagal centers in the central nervous system or increased acetylcholine release due to blockade of presynaptic $M_2$-receptors.
- Noradrenergic regulation: for the sinoatrial node, $\beta_1$-receptors and an increased heart rate are indicated. Cardiac effects are caused by increased $Ca^{2+}$ influx into various cardiac structures; in the sinoatrial node, automaticity increases, leading to an elevated heart rate.
Role of the SAN in extrasystoles
If an impulse arises outside the sinoatrial node, premature contractions may occur.
- Atrial extrasystole: the impulse originates in the atria outside the SAN, passes through the AVN, and propagates through the ventricles via the normal pathway. On the graphical recording, the P wave preceding the extrasystole is altered because excitation propagates through the atria atypically. The QRS complex is of normal shape and narrow, as intraventricular conduction is unimpaired.
- Ventricular extrasystole: the ectopic focus is located in the ventricle. A full compensatory pause occurs after a ventricular extrasystole. The normal impulse from the SAN reaches the ventricles while they are in a refractory state following the extrasystole, so one normal contraction is dropped. The ventricles contract only in response to the next sinus impulse. The interval encompassing the pre-extrasystolic and post-extrasystolic periods equals two normal cardiac cycles — 2 R-R.
Pacemaker concept in other systems
In P.K. Anokhin's and K.V. Sudakov's concept of the pacemaker role of hypothalamic centers, an analogy with the heart is used: just as the sinus node subjugates other cardiac automation centers with lower excitability, the motivational centers of the hypothalamus control structures at other levels of the brain. Inactivation of hypothalamic centers leads to the disintegration of the entire system of elements integrated into motivational excitation.
Class and exam questions
What does the Stannius ligatures experiment prove?
This classic experiment on the frog heart proves the presence of automaticity in various regions of the heart and demonstrates a decreasing gradient of automaticity from the venous sinus to the apex of the heart.
Why does a compensatory pause occur during ventricular extrasystole?
The normal impulse from the sinoatrial node reaches the ventricles while they are still in a refractory state following the ventricular extrasystole. Therefore, one normal contraction is skipped, and the interval combining the pre-extrasystolic and post-extrasystolic periods equals 2 R-R.
How does the vagus nerve affect the sinoatrial node?
For the sinoatrial node, a vagal effect is indicated: slowing of the heart rate. The targets in the heart are $M_2$-cholinergic receptors.
What else to study on this topic
- Atrioventricular node
- Conduction system of the heart
- Extrasystole
- Autonomic regulation of the heart
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