HBF-II LEC 02 Gross Anatomy ANS Thorax Lecture Slides 2024 PDF

Autonomics of the Thorax Paul Walker, Ph.D. Professor & Director- Gross Anatomy Dept Ophthalmology, Visual & Anatomical Sciences [email protected] Functional Summary of the Thoracic Autonomics Heart Cardiac muscle exhibits spontaneous contractility. Pacem...

Autonomics of the Thorax Paul Walker, Ph.D. Professor & Director- Gross Anatomy Dept Ophthalmology, Visual & Anatomical Sciences [email protected] Functional Summary of the Thoracic Autonomics Heart Cardiac muscle exhibits spontaneous contractility. Pacemaker control is exerted by the SA and AV nodes which are innervated by autonomic fibers. Autonomic nerves modify the rate & strength of each contraction of cardiac muscle, and thus control cardiac output. SANS increases heart rate and strength of contraction. PANS decreases heart rate and strength of atrial contraction. Lungs Smooth muscle of the bronchial tree is innervated by autonomic nerves, and this changes the lumen patency of the airways. SANS causes bronchodilation. PANS causes bronchoconstriction. Autonomic innervation of mucus glands and blood vessels also provides moisture and warmth to the airways. SANS dries out the airways and PANS moistens them. Esophagus SANS inhibits peristalsis and constricts smooth muscle of blood vessels. PANS stimulates peristalsis and mucous secretions. Autonomics of GI system will be discussed later in the HBF-II course. Functional Summary of the Thoracic Autonomics Visceral Sensory Fibers Visceral afferent (VA) sensory fibers transmit information from thoracic organs to the CNS. These fibers are found in the same autonomic nerve plexuses that also carry visceral efferent (VE) motor fibers to thoracic organs. An autonomic nerve plexus (e.g. cardiac plexus) contains both visceral efferent (VE: SANS & PANS) and visceral afferent (VA) fibers. Visceral sensory (VA) fibers carry information from stretch (volume) baroreceptors that sense changes in distension in the walls of the airways and major vessels (aorta arch, carotid arteries). Fibers also carry information from chemoreceptors located in the carotid arteries that detect O2 and CO2 levels in the blood. There are also visceral sensory (VA) fibers that transmit pain or other irritant information from the heart and lungs. We will discuss the contribution of these fibers to referred pain toward the end of this lecture.  Gross View of Thoracic Autonomics Anterior view of the Posterior Mediastinum with the heart, lungs, pulmonary arteries, vena cava removed. Esophagus, trachea, main bronchii and aorta remain in view. The left vagus nerve is prominent in the diagram. The vagus nerve provides parasympathetic innervation to the thoracic viscera. The sympathetic trunk and ganglia important for heart & lung regulation are also illustrated. Also shown are the cardiac, pulmonary, and esophageal nerve plexuses that transmit autonomic nerves to the thoracic viscera and also return visceral sensory information to the CNS. How do we make sense of this diagram? Fig 1  Schematic Organization of the Thoracic Autonomics SANS The upper half (T1-T6) of the thoracic spinal cord is the location of preganglionic neurons of the SANS cell column that regulate the thoracic viscera (heart, lungs, esophagus). PANS The brainstem originates the vagus nerve (CN X), which contains preganglionic PANS axons to the thoracic viscera (heart, lungs, esophagus). Fig 2  Summary of the Autonomic Regulation of the Cardiopulmonary System SANS NE b1 Ach NE NE Upper Thoracic SANS Preganglionic SANS Postganglionic b2 Spinal Cord VE Sympathetic Ganglion Located Along the Ach M2 Sympathetic Trunk CNS PNS NE b2 PANS NE a Ach Ach M3 PANS Preganglionic Ach Brainstem PANS Postganglionic Vagus Nerve (CN X) Terminal Parasympathetic Ganglion VE Located in the Organ Fig 3  SANS Innervation of the Heart Preganglionic SANS neurons originate from sympathetic column in the upper part of thoracic spinal cord. Most sources say T1-T4. Preganglionic SANS axons leave via ventral roots and travel into spinal nerves Axons enter sympathetic ganglia via white rami communicans Upper Thoracic Fig 4  SANS Innervation of the Heart Preganglionic SANS axons enter the sympathetic trunk via white rami communicans at the same spinal level as their cell body origin. Once in the trunk, they: Synapse in the ganglion at the level they entered. Pass through the ganglia and ascend in the sympathetic trunk into the neck to synapse in cervical sympathetic ganglia. Upper Thoracic Fig 4 SANS Innervation of the Heart Postganglionic axons leave the cervical sympathetic ganglia directly as cervical sympathetic nerves of the cardiac plexus. These travel from neck region to thorax Postganglionic axons leave the thoracic sympathetic ganglia directly as thoracic sympathetic nerves of the cardiac plexus. These are already located in thorax. Upper Thoracic SANS causes increased heart rate and increased force of contraction via beta- adrenergic (b1, b2) receptors. SANS also induces coronary artery vasodilation in a mechanism that is coupled to increased metabolic demand of heart muscle. Clinical Note: Beta blockers are antihypertensive medicines that suppress of beta- Fig 4 adrenergic receptor-mediated signaling. PANS Innervation of the Heart Preganglionic PANS neurons are Preganglionic PANS axons travel located in the brainstem (medulla). in the vagus nerve (CN X). Vagus n. gives off cervical & thoracic cardiac parasympathetic branches which travel with the sympathetic axons as part of the cardiac plexus. Preganglionic PANS axons synapse in terminal PANS ganglia located deep to the epicardium of the heart. Postganglionic PANS fibers innervate specialized cardiac muscle in SA and AV nodes and thus affect atrial contractility. PANS causes decreased heart rate and decreased force of atrial contraction via muscarinic M2 receptors. PANS also reduces Upper Thoracic coronary artery blood flow due to decreased metabolic demand of heart muscle. Fig 5 Autonomic Innervation of the Lungs Postganglionic SANS fibers innervate bronchiolar and vascular smooth muscle of the pulmonary tree as well as mucus glands. Receptors in SANS pulmonary targets are: b2 adrenergic receptors- enhance airflow by producing bronchodilation. a adrenergic receptors- reduce mucus secretion (via vasoconstriction). Clinical Note: Inhalant bronchodilators that act at b2 adrenergic receptors are commonly used to treat asthma. These agents are mixed with corticosteroids, which are incorporated to blunt the inflammatory response. Fig 6 Autonomic Innervation of the Lungs PANS preganglionic axons from the vagus nerve destined to innervate the lungs distal to the primary bronchus diverge from the cardiac plexus and distribute along anterior and posterior surfaces of the primary bronchi. They track along the pulmonary tree distally to reach the terminal bronchioles. Postganglionic PANS fibers also innervate bronchiolar and vascular smooth muscle of the pulmonary tree as well as mucus glands. Receptors in PANS pulmonary targets are: M3 muscarinic receptors constrict bronchiole smooth muscle to produce bronchoconstriction and also increase mucus secretion. Fig 6 Visceral Afferents- Baroceptor Reflex When a person moves from reclining to standing posture, the resultant pooling of blood in the lower half of the body is countered by vasoconstriction in certain organs to drive blood to appropriate areas (e.g. brain) while also increasing cardiac output. This baroreceptor reflex functions as a buffer to maintain blood pressure during sudden changes in posture. Orthostatic Hypotension- failure to maintain blood pressure when transitioning to the upright position. Causes dizziness and fainting. Often occurs in the elderly. Diseases affecting baroreceptor reflex: Familial Dysautonomia- loss of visceral afferents traveling in the vagus nerve Multiple System Atrophy- loss of preganglionic SANS in the spinal cord Fig 7 Visceral Afferents- Chemoreception Reflex The chemoreceptor reflex maintains homeostasis of blood gases by regulating respiration, cardiac output and blood flow through peripheral vessels. This detects changes in partial oxygen pressure (PO2) and partial carbon dioxide pressure (PCO2). A brainstem chemoreceptor reflex pathway activates SANS when PO2 drops and PCO2 rises resulting in an increase in cardiac output and increased peripheral vascular tone. These changes also decrease blood flow to skeletal muscle and viscera, but blood flow to brain remains unchanged preserving vital functioning of the CNS. The cardiovascular component of the chemoreceptor reflex is closely matched with respiration mediated by the phrenic nerve innervation of the diaphragm. Under different circumstances, this system regulates the cardiovascular system in ways that you wouldn’t predict. For example, holding the breath does not increase heart rate when PCO2 levels rise, but rather causes the heart rate to decrease. Fig 7  Visceral Afferents- Sensing Organ Damage Pain fibers from the thoracic viscera are in the same autonomic plexuses that contain SANS and PANS fibers. Cell bodies of these VA neurons are found in the in dorsal root ganglion (DRG) at upper thoracic spinal levels. There are also somatic afferent (SA) sensory neuronal cell bodies in these DRGs that transmit cutaneous information from skin dermatomes. Upper Thoracic Therefore, the spinal cord receives both visceral afferent and somatic afferent pain signals. T1-T4 Skin Dermatomes Fig 8 Visceral Afferents- Sensing Organ Damage Visceral afferent (VA) signals from damaged heart muscle are brought into the spinal cord at the same levels that receive somatic afferent (SA) sensory information from skin dermatomes. This creates an interesting phenomenon called ‘referred pain’, where afferent signals originating from damaged heart muscle are perceived as pain coming from skin surface (chest, arm, neck). Others types of referred pain include: From the lungs- typically reported to the shoulder (scapular) region. From the diaphragm- referred more superiorly to the neck region because the afferent pain fibers from the diaphragm travel with motor fibers of the phrenic nerve (C3-C5). Acid reflux of esophagus is likely related to referred pain to central T5-T6 dermatome regions (epigastric) and is commonly called ‘heart burn’. Fig 9