Cardiac Innervation Sympathetic

The heart is not only a mechanical pump but also a complex organ intricately regulated by the autonomic nervous system (ANS). Cardiac innervation is crucial for maintaining proper heart rate, conduction velocity, contractility, and overall cardiovascular homeostasis. Understanding cardiac innervation involves examining the sympathetic and parasympathetic inputs, as well as the cardiac plexus, which serves as a communication hub between the heart and the central nervous system.

1. Introduction

Cardiac innervation refers to the network of nerves that regulate heart function. Unlike skeletal muscle, which is voluntarily controlled, the heart is primarily under involuntary regulation by the autonomic nervous system, consisting of sympathetic and parasympathetic divisions. This regulation allows the heart to respond dynamically to various physiological demands, such as exercise, stress, or rest.

Sympathetic nervous system (SNS): Prepares the heart for “fight or flight” responses.
Parasympathetic nervous system (PNS): Promotes “rest and digest” functions.
Cardiac plexus: An intricate network of autonomic fibers that coordinate the cardiac responses and transmit signals to and from the CNS.

A thorough understanding of cardiac innervation is essential for clinicians, physiologists, and anyone studying cardiovascular pathophysiology, as dysfunctions in these pathways can lead to arrhythmias, heart failure, and other cardiac conditions.

2. Sympathetic Innervation of the Heart

The sympathetic nervous system plays a critical role in enhancing cardiac output during stress or physical activity. Its activation results in increased heart rate, stronger myocardial contractions, and accelerated conduction through the atrioventricular (AV) node.

2.1 Anatomy of Sympathetic Cardiac Innervation

Sympathetic innervation originates from the thoracic spinal cord segments T1–T5. Preganglionic sympathetic fibers exit the spinal cord via the ventral roots and enter the sympathetic chain (paravertebral ganglia). These fibers may synapse at the:

Cervical ganglia (superior, middle, and inferior cervical ganglia)
Upper thoracic ganglia (T1–T5)

Postganglionic fibers then travel through the cardiac nerves to reach the cardiac plexus. From there, they distribute to different parts of the heart:

Atria: Rich sympathetic innervation increases heart rate.
Ventricles: Enhances contractility (positive inotropic effect).
Conduction system: Speeds AV nodal conduction and increases excitability of the sinoatrial (SA) node.

2.2 Neurotransmitters and Receptors

Neurotransmitter: Norepinephrine (noradrenaline) is released at postganglionic sympathetic endings.
Receptors: Primarily β1-adrenergic receptors on cardiomyocytes and pacemaker cells.

Effects include:

Chronotropic: Increases heart rate.
Inotropic: Increases myocardial contractility.
Dromotropic: Increases conduction velocity through AV node.
Lusitropic: Enhances relaxation during diastole.

2.3 Functional Significance

Sympathetic innervation is crucial in situations requiring increased cardiac output, such as:

Exercise
Emotional stress
Hemorrhage or shock

Excessive sympathetic activity, however, can contribute to arrhythmias, hypertension, and heart failure.

3. Parasympathetic Innervation of the Heart

The parasympathetic nervous system primarily decreases heart activity, conserving energy and maintaining cardiovascular stability at rest.

3.1 Anatomy of Parasympathetic Cardiac Innervation

Parasympathetic fibers originate from the dorsal motor nucleus of the vagus nerve and the nucleus ambiguus in the medulla oblongata. These fibers travel via the vagus nerve (cranial nerve X) to reach the heart.

Key pathways include:

Right vagus nerve: Predominantly influences the SA node, reducing heart rate.
Left vagus nerve: Predominantly influences the AV node, slowing conduction.

Parasympathetic fibers synapse in intrinsic cardiac ganglia, located in and around the atria and near the SA and AV nodes. From there, postganglionic fibers distribute short distances to cardiac tissues.

3.2 Neurotransmitters and Receptors

Neurotransmitter: Acetylcholine (ACh)
Receptors: Muscarinic M2 receptors on pacemaker cells and atrial myocardium

Effects include:

Chronotropic: Decreases heart rate (negative chronotropic effect)
Dromotropic: Slows AV nodal conduction
Inotropic: Slightly decreases atrial contractility; minimal effect on ventricles

3.3 Functional Significance

Parasympathetic activity is dominant during resting states, helping to:

Reduce cardiac oxygen demand
Maintain low resting heart rate
Protect against excessive sympathetic stimulation

Enhanced parasympathetic tone is associated with lower risk of sudden cardiac death, as it stabilizes cardiac electrical activity.

4. The Cardiac Plexus

The cardiac plexus is a complex network of autonomic fibers located near the aortic arch and bifurcation of the trachea, serving as a critical hub for cardiac innervation.

4.1 Anatomy

The cardiac plexus is divided into:

Superficial cardiac plexus: Located anterior to the aortic arch, beneath the ligamentum arteriosum. Receives contributions from:
- Superior cervical sympathetic ganglion
- Vagus nerve
Deep cardiac plexus: Located posterior to the aortic arch, in front of the tracheal bifurcation, receiving fibers from:
- Thoracic sympathetic ganglia
- Vagus nerve

The plexus then sends fibers to the:

SA node
AV node
Atria and ventricles
Coronary vessels

4.2 Composition

The cardiac plexus contains:

Sympathetic fibers: Postganglionic from cervical and thoracic ganglia
Parasympathetic fibers: Preganglionic fibers from vagus nerve
Visceral afferent fibers: Convey sensory information (pain, stretch) to the CNS

4.3 Function

Acts as a relay station for autonomic control of the heart
Integrates sympathetic and parasympathetic inputs to coordinate heart rate, contractility, and conduction
Mediates reflexes, such as baroreceptor reflexes and cardiac pain perception

4.4 Clinical Significance

Cardiac plexus blocks can be used for pain management in cases of refractory angina
Dysfunction or injury can contribute to arrhythmias or autonomic dysregulation

5. Autonomic Regulation of Heart Function

Cardiac innervation does not act in isolation. The sympathetic and parasympathetic systems interact to maintain homeostasis.

5.1 Reciprocal Regulation

Sympathetic and parasympathetic activity often work in opposition:
- Sympathetic increases heart rate and contractility
- Parasympathetic decreases heart rate and conduction velocity
Vagal tone is predominant at rest, providing a baseline inhibitory influence on heart rate
During stress or exercise, sympathetic tone predominates, rapidly increasing cardiac output

5.2 Reflex Control

Several autonomic reflexes regulate heart function:

Baroreceptor reflex: Responds to changes in blood pressure
Chemoreceptor reflex: Responds to changes in oxygen and carbon dioxide levels
Cardiopulmonary reflex: Responds to changes in blood volume and venous return

These reflexes converge on the cardiac plexus and autonomic nuclei, ensuring adaptive cardiac responses.

6. Clinical Relevance

Understanding cardiac innervation is essential for diagnosing and treating cardiovascular disorders:

6.1 Arrhythmias

Excessive sympathetic activity can trigger tachyarrhythmias
Enhanced parasympathetic activity can cause bradyarrhythmias

6.2 Heart Failure

Chronic sympathetic overactivity in heart failure contributes to ventricular remodeling and progression of disease

6.3 Autonomic Dysfunction

Disorders such as diabetic autonomic neuropathy or postural orthostatic tachycardia syndrome (POTS) involve impaired cardiac innervation

6.4 Therapeutic Interventions

Beta-blockers: Inhibit sympathetic effects, reducing heart rate and myocardial oxygen demand
Vagal nerve stimulation: Explored as therapy in refractory heart failure and arrhythmias