Nervous System & The Heart – Comprehensive Study Notes

Overview of the Nervous System

• Two major anatomical divisions

  • Central Nervous System (CNS)

  • Brain & spinal cord

  • Integrative and command center for all neural activity

  • Directly modulates cardiovascular centers in the medulla (e.g., the nucleus ambiguus and dorsal motor nucleus of the vagus)

  • Peripheral Nervous System (PNS)

  • All neural structures outside the CNS

  • Conduit for sensory input and motor output

  • Sub-divided into:

    • Somatic Nervous System

    • Voluntary, conscious control

    • Skeletal muscle activation (e.g., purposeful limb movement)

    • Autonomic Nervous System (ANS)

    • Involuntary, homeostatic control

    • Regulates vital organ function (heart, lungs, GI tract, glands, etc.)

Autonomic Nervous System – Core Concepts

• Maintains internal physiological balance (homeostasis)

• Two primary, antagonistic branches provide rapid bidirectional control:

  • Sympathetic Nervous System (SNS) – “Fight or Flight”

  • Parasympathetic Nervous System (PNS) – “Rest & Relax” / “Rest & Digest”

• Both branches share preganglionic neurons that release acetylcholine (ACh) onto nicotinic receptors, but differ in their post-ganglionic neurotransmitters & receptor sub-types

• Overall cardiovascular impact summarized by the equation: {\Delta CO} = {\Delta HR} \times {\Delta SV}

  • SNS predominately raises HR and SV → ↑ cardiac output

  • PNS predominately lowers HR → ↓ cardiac output

Sympathetic Division – Anatomy, Chemistry & Effects

• Thoracolumbar outflow: neuron cell bodies in the lateral horns of T1–L2 spinal cord segments

• Primary neurotransmitters: epinephrine (Epi) & norepinephrine (NE)

  • Post-ganglionic neurons release NE

  • Adrenal medulla (modified sympathetic ganglion) releases \approx 80\% Epi, 20\% NE directly into circulation for systemic effect

• Key systemic responses (classic “fight or flight”):

  • Pupil dilation (mydriasis) → improved vision in low light

  • ↑ Heart rate (positive chronotropy) & ↑ contractility (positive inotropy)

  • Bronchodilation → increased airflow

  • ↓ GI motility & secretions → resource allocation away from digestion

  • Glycogenolysis & lipolysis → mobilizes energy substrates

• Clinical metaphor: Pressing the car’s accelerator

  • Rapid energy expenditure to confront danger or stress

Adrenergic Receptor Sub-types

• Alpha Receptors

  • \alpha_1 – Vascular smooth muscle

  • Activation → vasoconstriction → ↑ systemic vascular resistance (SVR) → ↑ blood pressure (BP)

  • \alpha_2 – Presynaptic & some vascular smooth muscle sites

  • Presynaptic activation → ↓ NE release (negative feedback)

  • Postsynaptic vascular effect variable; some vasodilation

• Beta Receptors

  • \beta_1 – Primarily cardiac

  • Location: SA node, AV node, atrial & ventricular cardiomyocytes

  • Effects: ↑ HR, ↑ conduction velocity, ↑ contractility → ↑ CO

  • \beta_2 – Vascular & bronchial smooth muscle

  • Vasodilation of skeletal muscle/coronary vessels → ↑ blood flow where needed most

  • Bronchodilation → ↓ airway resistance

Parasympathetic Division – Anatomy, Chemistry & Effects

• Craniosacral outflow: brainstem nuclei (CN III, VII, IX, X) & spinal cord S2–S4

• Primary neurotransmitter: acetylcholine (ACh)

  • Post-ganglionic release of ACh onto muscarinic receptors

• Key systemic responses (classic “rest & relax”):

  • Pupil constriction (miosis)

  • ↓ Heart rate (negative chronotropy) & ↓ conduction velocity at AV node

  • Bronchoconstriction & ↑ bronchial secretions

  • ↑ GI motility & secretions → optimizes digestion

  • Promotes glycogenesis & energy storage

• Clinical metaphor: Pressing the car’s brake

  • Conserves energy & facilitates restorative processes

Muscarinic Receptor Sub-types (Cardio-pulmonary Focus)

• M_2 (heart)

  • SA & AV nodes

  • Activation opens K\textsuperscript{+} channels → hyperpolarization → slows pacemaker activity

• M_3 (lungs & glands)

  • Smooth-muscle contraction → bronchoconstriction

  • Glandular secretion (e.g., bronchial mucus)

Nicotinic Receptors – Shared Autonomic Feature

• Ionotropic, ligand-gated Na\textsuperscript{+}/K\textsuperscript{+} channels

• Present at all autonomic ganglia (sympathetic & parasympathetic) and neuromuscular junctions

• Rapid excitation of post-ganglionic neurons upon ACh binding

• Pharmacological note: Ganglionic blockers (e.g., hexamethonium) broadly inhibit both SNS & PNS output

The Vagus Nerve (Cranial Nerve X)

• Nicknamed “wandering nerve” due to extensive distribution

• Longest cranial nerve; spans brainstem to transverse & descending colon

• Cardiac innervation

  • SA node → slows pacemaker rate

  • AV node → prolongs refractory period

  • Limited ventricular fibers → mild negative inotropy

• Clinical relevance

  • Vagal maneuver (e.g., carotid sinus massage, Valsalva) can terminate supraventricular tachycardia by transiently increasing vagal tone

  • Excessive vagal stimulation → bradycardia, syncope (e.g., vasovagal episodes)

Cardiovascular Integration & Real-World Examples

• Baroreceptor reflex

  • ↓ BP detected → ↓ afferent firing from carotid/aortic baroreceptors → ↓ vagal & ↑ sympathetic outflow → ↑ HR & vasoconstriction → restores BP

  • Can be expressed mathematically: \Delta BP \propto \Delta (HR \times SV \times SVR)

• Exercise

  • Initial parasympathetic withdrawal → rapid HR increase

  • Subsequent sympathetic activation → sustained ↑ HR, contractility, and peripheral vasoconstriction with selective \beta_2-mediated vasodilation in active muscles

• Pharmacology

  • \beta-blockers (e.g., metoprolol) selectively antagonize \beta_1 → ↓ HR & contractility; beneficial in hypertension, angina, heart failure

  • \alpha_1 agonists (e.g., phenylephrine) used to raise BP during anesthesia-induced hypotension

  • Muscarinic agonists (e.g., bethanechol) stimulate GI motility, whereas atropine (muscarinic antagonist) is first-line for symptomatic bradycardia

• Pathophysiology

  • Autonomic neuropathy (e.g., in diabetes) → resting tachycardia, orthostatic hypotension from impaired ANS compensatory responses

Ethical / Philosophical Considerations

• Autonomic responses showcase the body’s intrinsic survival mechanisms; understanding them raises questions about pharmaceutical “override” of natural processes

• Use of performance-enhancing adrenergic agents in sports presents ethical dilemmas

• Managing end-of-life care: balancing sympathetic stimulants to maintain BP vs. allowing natural decline

Key Numbers & Equations (Cheat-Sheet)

• Sympathetic origin: T1-L2 spinal segments

• Parasympathetic cranial components: CN III, VII, IX, X

• Vagus nerve = cranial nerve X (10)

• Cardiac output: CO = HR \times SV

• Mean arterial pressure approximation: MAP \approx \frac{1}{3} (SBP - DBP) + DBP

• Normal resting HR values

  • Parasympathetic tone dominant: \approx 60–80\, \text{bpm}

  • Sympathetic surge (exercise/stress): may exceed 180\, \text{bpm} in athletes

References

• Cleveland Clinic (2025). “Vagus Nerve.”

• Gordan, R., Gwathmey, J., & Lai-Hua, X. (2015). “Autonomic and Endocrine Control of Cardiovascular Function.”

• Mastenbjork, M., & Meloni, S. (2024). “Pharmacology Review.”