The origin of the cardiac parasympathetic fibers can be found in the medulla oblongata. These fibers are located in cells within the dorsal motor nucleus of the vagus nerve or the nucleus ambiguus. They then pass through the neck near the common carotid arteries and travel through the mediastinum to reach the postganglionic vagal cells. These cells are situated either on the surface of the heart or within its walls. The majority of vagal ganglion cells are found in the epicardial fat pads near the SA and AV nodes.

Both the right and left vagus nerves have different distributions within the heart. The right vagus nerve primarily affects the SA node, where its stimulation slows down the firing of the node and can even momentarily halt it. On the other hand, the left vagus nerve mainly inhibits the AV conduction tissue, leading to varying degrees of AV block. However, the efferent vagal fibers have overlapping distributions, meaning that left vagal stimulation also depresses the SA node while right vagal stimulation hinders AV conduction.

The SA and AV nodes are abundant in acetylcholinesterase, an enzyme responsible for the rapid breakdown of the neurotransmitter acetylcholine (ACh). When vagal stimulation is ceased, the effects of the stimulation quickly fade due to the rapid destruction of ACh. Additionally, the effects of vagal stimulation on the SA and AV nodes have a short latency period of approximately 50 to 100 milliseconds. This is because the released ACh rapidly activates specialized ACh-regulated potassium (KACh) channels in the cardiac cells. The quick opening of these channels is facilitated by the direct coupling of the muscarinic receptor to the KACh channel via a guanine nucleotide-binding protein. The combination of these two characteristics allows the vagus nerves to exert precise control over the SA and AV nodal function beat by beat.

In general, parasympathetic influences dominate over sympathetic effects at the SA node. For instance, in the absence of vagal nerve stimulation, increasing the frequency of sympathetic stimulation from 0 to 4 Hz results in an approximate increase of 80 beats per minute in heart rate. However, when the vagus nerves are stimulated at 8 Hz, the influence of increasing sympathetic stimulation frequency from 0 to 4 Hz on heart rate is minimal.

The cardiac sympathetic fibers originate in the upper five or six thoracic segments and lower one or two cervical segments of the spinal cord within the intermediolateral columns. These fibers emerge from the spinal column through the white communicating branches and enter the paravertebral chains of ganglia. The preganglionic and postganglionic neurons mainly synapse in either the stellate or middle cervical ganglia, depending on the species. Within the mediastinum, the postganglionic sympathetic and preganglionic parasympathetic fibers come together to form a complex plexus of mixed efferent nerves that supply the heart.

The postganglionic sympathetic fibers in this plexus approach the base of the heart along the adventitial surface of the great vessels. From the base of the heart, these fibers spread out as an extensive epicardial plexus to reach the different chambers. They then penetrate the myocardium, typically accompanying the coronary vessels.

In contrast to the abrupt termination of the response following vagal activity, the effects of sympathetic stimulation gradually diminish after the stimulation is discontinued.
The cardiac parasympathetic fibers originate in the medulla oblongata, in cells that lie in the dorsal motor nucleus of the vagus nerve or in the nucleus ambiguus (see ). In humans, centrifugal vagal fibers pass inferiorly through the neck near the common carotid arteries and then through the mediastinum to synapse with postganglionic vagal cells. These cells are located either on the epicardial surface or within the walls of the heart. Most of the vagal ganglion cells are located in epicardial fat pads near the SA and atrioventricular (AV) nodes.
The right and left vagus nerves are distributed to different cardiac structures. The right vagus nerve affects the SA node predominantly; stimulation of this nerve slows SA nodal firing and can even stop the firing for several seconds. The left vagus nerve mainly inhibits AV conduction tissue to produce various degrees of AV block (see ). However, the distribution of the efferent vagal fibers is overlapping in such a way that left vagal stimulation also •Fig. 18.3 Changes in Heart Rate When the Vagus and Cardiac
Sympathetic Nerves Are Stimulated Simultaneously. Thesympa depresses the SA node and right vagal stimulation impedes AV conduction.
The SA and AV nodes are rich in acetylcholinesterase, an enzyme that rapidly hydrolyzes the neurotransmitter acetylcholine (ACh). The effects of a given vagal stimulus decay very quickly (
Fig. 18.2A ) when vagal stimulation is discontinued because ACh is rapidly destroyed. In addition, vagal effects on SA and AV nodal function have a very short latency (≈50 to 100 msec) because the ACh released quickly activates special ACh-regulated potassium (KACh) channels in the cardiac cells. These channels open quickly because the muscarinic receptor is coupled directly to the KACh channel by a guanine nucleotide–binding protein. These two features of the vagus nerves—brief latency and rapid theticnerveswerestimulatedat0,2,and4Hzinthepresenceofvagalnervestimulation(Vag)at0,4,and8Hz.(ModifiedfromLevyMN,ZieskeH.J Appl Physiol. 1969;27:465.) decay of the response—enable them to exert beat-by-beat control of SA and AV nodal function.
Parasympathetic influences usually predominate over sympathetic effects at the SA node, as shown in
Fig. 18.3 . When the frequency of sympathetic stimulation increases from 0 to 4 Hz, the heart rate increases by approximately 80 beats per minute in the absence of vagal nerve stimulation (0 Hz). However, when the vagus nerves are stimulated at 8 Hz, increasing the sympathetic stimulation frequency from 0 to 4 Hz has only a negligible influence on heart rate.
The cardiac sympathetic fibers originate in the intermediolateral columns of the upper five or six thoracic segments and the lower one or two cervical segments of the spinal cord (see ). These fibers emerge from the spinal column through the white communicating branches and enter the paravertebral chains of ganglia. The preganglionic and postganglionic neurons synapse mainly in the stellate or middle cervical ganglia, depending on the species. In the mediastinum, postganglionic sympathetic and preganglionic parasympathetic fibers join to form a complicated plexus of mixed efferent nerves to the heart.
The postganglionic cardiac sympathetic fibers in this plexus approach the base of the heart along the adventitial surface of the great vessels. From the base of the heart, these fibers are distributed to the various chambers as an extensive epicardial plexus. They then penetrate the myocardium, usually accompanying the coronary vessels.
In contrast to abrupt termination of the response after vagal activity, the effects of sympathetic stimulation decay gradually after stimulation is stopped (see