Cardiac Plexus: Anatomy and Function

• The cardiac plexus is an autonomic network integrating neural inputs for cardiovascular regulation.
• Its intricacy stems from autonomic contributions, synaptic processing, and connections with mediastinal, cervical, and thoracic structures.
• It regulates heart rate, contraction force, and coronary blood flow via sympathetic and parasympathetic signals.

Objectives Regarding The Cardiac Plexus

• Define the cardiac plexus and its anatomical location.
• Discuss its components, including sympathetic, parasympathetic, and visceral afferent fibers.
• Explain its functional significance in regulating cardiac activity.
• Describe clinical implications, including cardiac pain and autonomic dysfunctions.

Anatomy of the Cardiac Plexus

• It comprises sympathetic, parasympathetic, and visceral afferent fibers in interconnected subplexuses.
• It's located anterior to the trachea's bifurcation and posterior to the ascending aorta and pulmonary trunk.
• It includes the superficial and deep cardiac plexus.
• The superficial cardiac plexus lies beneath the aortic arch, near the right pulmonary artery.
• The deep cardiac plexus is located between the aortic arch and the tracheal bifurcation.

Components of the Cardiac Plexus

• The main components consist of sympathetic innervation and parasympathetic innervation.

Sympathetic Innervation

• Cervical and thoracic sympathetic ganglia (T1-T4 spinal cord segments) are the source of sympathetic innervation.
• Preganglionic fibers synapse in cervical and upper thoracic ganglia, with postganglionic fibers forming cardiac nerves.
• Sympathetic innervation increases heart rate (chronotropic), contraction force (inotropic), and causes coronary vasodilation via β1-adrenergic receptors.

Parasympathetic Innervation

• The vagus nerve (CN X) provides parasympathetic innervation through cardiac branches.
• Preganglionic fibers synapse in small ganglia in the cardiac plexus or myocardium.
• Parasympathetic innervation decreases heart rate, reduces contractility, and promotes coronary vasoconstriction via muscarinic receptors (M2).

Visceral Afferents (Sensory Fibers)

• Pain fibers travel with sympathetic nerves to T1-T4 spinal segments, explaining referred pain in myocardial ischemia.
• Baroreceptor and chemoreceptor fibers travel with the vagus nerve to the brainstem for cardiovascular reflex regulation.

Subdivisions of the Cardiac Plexus

• Superficial Cardiac Plexus is located beneath the aortic arch, anterior to the right pulmonary artery.
• It receives left superior cervical sympathetic cardiac nerve (from sup.cerv ganglion) and the inferior cardiac branch of the left vagus nerve.
• Its function is to modulate aortic baroreceptor reflexes and influences coronary vasculature.

Deep Cardiac Plexus location and function

• It's between the aortic arch and tracheal bifurcation, extending to the pulmonary trunk
• Larger and more intricate compared to the superficial plexus
• It receives sympathetic fibers (cervical and upper thoracic ganglia T1-T4), parasympathetic fibers from both vagus nerves, and contributions from recurrent laryngeal nerves (secondary loops).
• It provides primary autonomic control over myocardial contractility and heart rate.

Intrinsic Cardiac Ganglia

• These are ganglionated plexuses distributed within the epicardium and myocardium, predominantly in the atria and interatrial septum.
• Key clusters include sinoatrial (SA) nodal ganglion (near superior vena cava opening), atrioventricular (AV) nodal ganglion (near the interatrial septum), and pulmonary and aortic root ganglia (modulate coronary flow).
• They function in the local processing of autonomic inputs before modulating nodal activity.

Sympathetic Contributions to the Cardiac Plexus

• Preganglionic fibers originate from the intermediolateral cell column (IML) of T1-T4 spinal segments.
• These fibers typically synapse in the superior, middle, and inferior cervical ganglia with the first to fourth thoracic sympathetic ganglia (stellate ganglion may contribute).
• Postganglionic fibers directly enter the cardiac plexus
• Major sympathetic cardiac nerves include the superior, middle, and inferior cervical cardiac nerves, plus thoracic cardiac branches (T1-T4 ganglia).

Functional Implications of Sympathetic Activation

• Increased heart rate (chronotropic effect) happens via β1-adrenergic stimulation at the SA node
• Leads to enhanced myocardial contractility (inotropic effect) via β1 activation in ventricular myocytes
• Coronary vasodilation occurs via β2-adrenergic receptors (indirect effect).
• The stellate ganglion plays a dominant role in sympathetic outflow to the heart and influences ventricular contractility and repolarization.
• The right stellate ganglion excites the SA node.

Parasympathetic Contributions to the Cardiac Plexus

• Preganglionic fibers originate from the dorsal motor nucleus (DMV) and nucleus ambiguus (NA) of the medulla.
• The vagus nerve descends along the carotid sheath and synapse within intrinsic cardiac ganglia.
• The superior and inferior cardiac branches of the vagus nerve and recurrent laryngeal contributions provide parasympathetic input.

Functional Implications of Parasympathetic Activation

• A decreased heart rate (negative chronotropic effect) stems from M2 muscarinic receptor activation at the SA node.
• Reduced myocardial contractility (negative inotropic effect) is achieved via the inhibition of cAMP in ventricular myocytes.
• Coronary vasoconstriction is achieved via direct M2-mediated effects on vascular smooth muscle.
• The right vagus nerve predominantly influences the SA node, while the left vagus affects the AV node.
• The vagus nerve exerts tonic inhibition over sympathetic activity at rest, maintaining a lower basal heart rate.

Visceral Afferent Contributions to the Cardiac Plexus: Pain Pathways

• Nociceptive fibers originate in the myocardium, traveling through sympathetic nerves to the T1-T4 dorsal root ganglia.
• These fibers project to the spinothalamic tract, explaining referred pain (chest, left arm, jaw) in angina and myocardial infarction.

Physiological Role of the Cardiac Plexus

• The cardiac plexus regulates heart rate via a balance between sympathetic and parasympathetic activity.
• Myocardial contractility is controlled by β1-adrenergic receptors (sympathetic) and muscarinic M2 receptors (parasympathetic).
• Sympathetic stimulation leads to coronary vasodilation via β2 receptors, whereas parasympathetic stimulation causes vasoconstriction.

Clinical Correlations of the Cardiac Plexus

• Visceral afferents from the heart share spinal segments with the T1-T4 dermatomes, resulting in pain referred to the left arm, chest, jaw, or neck in angina or myocardial infarction.
• Sympathetic overactivity can cause tachyarrhythmias and may contribute to sudden cardiac death, while parasympathetic dominance may lead to bradycardia/cardiac syncope.
• Clinical procedures involving the cardiac plexus include stellate ganglion blockade for refractory ventricular arrhythmias, and cardiac plexus ablation for pain relief in terminal cardiac conditions.