Neurohumoral Control of the Heart & Circulation - Quiz 10 Flashcards

Question

Where is the Parasympathetic Nervous System located in the Cranio-Sacral area?

Answer 1

CN III (Occulomotor) VII (Facial) IX (Glossopharyngeal nerve) X (Vagus)

Answer 2

**Long** Preganglionic Efferent Fibers **Short** Postganglionic Fibers

Answer 3

conducted or conducting **outward or away from something** (for nerves, the central nervous system; for blood vessels, the organ supplied). The efferent autonomic signals are transmitted to the various organs of the body through two major subdivisions called the sympathetic nervous system and the parasympathetic nervous system.

Answer 4

conducting or conducted **inward or toward something** (for nerves, the central nervous system; for blood vessels, the organ supplied). The central nervous system receives sensory (afferent) input from peripheral sensors and from sensors within the brain.

Answer 5

It sits right about the spinal cord on the lower brainstem. It is the inner part of your adrenal gland. It releases hormones that regulate your autonomic nervous system.

Answer 6

subconscious sensory signals from visceral organs can enter the autonomic ganglia, the brain stem, or the hypothalamus and then return subconscious reflex responses directly back to the visceral organs to control their activities.

Answer 7

Sympathetic nervous system

Answer 8

Short Preganglionic Fibers Long Postganglionic Fibers ## Footnote Axons from sympathetic neurons leave the medulla, travel down the spinal cord and synapse within the intermediolateral cell column of the spinal cord, and then exit at specific thoracolumbar levels (T1–L2) These **preganglionic fibers (short compared to preganglionic parasympathetic fibers)** then synapse within sympathetic paravertebral ganglia (cervical, stellate, and thoracolumbar sympathetic chain) located on either side of the spinal cord or they synapse within prevertebral ganglia located within the abdomen (celiac, superior mesenteric, and inferior mesenteric ganglia) **Postganglionic sympathetic fibers (long compared to postganglionic parasympathetic fibers)** travel to target organs where they innervate arteries and veins; capillaries are not innervated. Small branches of these efferent nerves are found in the adventitia (outer) layer of blood vessels. Varicosities, which are small enlargements along the sympathetic nerve fibers, are the site of neurotransmitter release.

Answer 9

Sympathetic Nervous System ## Footnote Sympathetic stimulation of the heart increases heart rate (positive chronotropy), inotropy and conduction velocity (positive dromotropy). Sympathetic adrenergic nerves travel along arteries and nerves and are found in the adventitia (outer wall of a blood vessel). Varicosities, which are small enlargements along the nerve fibers, are the site of neurotransmitter (norepinephrine) release. **Capillaries receive no innervation**. Activation of vascular sympathetic nerves causes contraction of the vascular smooth muscle and vasoconstriction of arteries and veins mediated by alpha-adrenoceptors

Answer 10

The heart is innervated by parasympathetic cholinergic nerves derived from the **vagus nerves**. **Acetylcholine (ACh)** released by these fibers binds to **muscarinic receptors in the cardiac muscle, especially at the SA and AV nodes** that have a large amount of vagal innervation. **ACh released by vagus nerve binds to M2 muscarinic receptors, a subclass of cholinergic receptors** . This produces **negative chronotropy and dromotropy in the heart, as well as negative inotropy and lusitropy in the atria (the negative inotropic and lusitropic effects of vagal stimulation are relatively weak in the ventricles)**. .

Answer 11

**Sympathetic**: Excitatory Cardiac Effects - Innervates entire heart **Parasympathetic**: , contributes importantly to regulation of heart function. ## Footnote The parasympathetic nervous system (PNS) controls homeostasis and the body at rest and is responsible for the body's "rest and digest" function. The sympathetic nervous system (SNS) controls the body's responses to a perceived threat and is responsible for the "fight or flight" response.

Answer 12

Epinephrine - 80% Norepinephrine - 20%

Answer 13

Cyclic AMP - allows greater Ca++ influx

Answer 14

Activates Adenylyl Cyclase - Converts ATP to cAMP

Answer 15

Activates Phospholipase to increase Ca++ into vessel smooth muscle causing vasoconstriction

Answer 16

ADH released by Posterior Pituitary - causes vasocontriction & increases blood volume by renal fluid reabsorption ## Footnote The posterior pituitary is stimulated to release Vasopressin by the following: Angiotensin II Hyperosmolarity Decreased atrial stretch receptor firing. Sympathetic stimulation Vasopressin causes the following: Vasoconstriction with resulting increased blood pressure. Renal fluid reabsorption with resulting increased blood volume.

Answer 17

Decreases SVR & CVP by decreasing release of Renin Increases Diuresis **Decreases Blood Volume**

Answer 18

Senses and buffers changes in blood pressure If this reflex was not present, then daily blood pressure variation would be about 3 times greater Helps with postural changes in BP Works in both directions Responds much more to a rapidly changing pressure ## Footnote After the baroreceptor signals have entered the nucleus tractus solitarius of the medulla, secondary signals inhibit the vasoconstrictor center of the medulla and excite the vagal parasympathetic center. The net effects are (1) vasodilation of the veins and arterioles throughout the peripheral circulatory system and (2) decreased heart rate and strength of heart contraction. Therefore, excitation of the baroreceptors by high pressure in the arteries reflexly causes the arterial pressure to decrease because of both a decrease in peripheral resistance and a decrease in cardiac output. Conversely, low pressure has opposite effects, reflexly causing the pressure to rise back toward normal.

Answer 19

Receptors located in Cartoid **Sinus** & Aortic Arch Senses blood **pressure** & adjusts HR, Contractility, & SVR accordingly.

Answer 20

Bainbridge Reflex

Answer 21

Carotid Endarterectomy

Answer 22

A small portion of the heart rate increase is due to stretch of the SA node (not mediated by atrial stretch receptors)

Answer 23

Infusion of volume causes an increase in heart rate due to activation of atrial stretch receptors which causes medullary center activation of sympathetic output to the SA node Slow Baseline HR = Increase HR w/ fluid Fast Baseline HR = Decreased HR w/ fluid ## Footnote Increased blood volume is detected by stretch receptors located in both atria at the venoatrial junctions.

Answer 24

Low pressure receptors that respond to stretch Sense cardiovascular system **volume**

Answer 25

Vena cava - right atrial junction Pulmonary vein - left atrial junction

Answer 26

Increase Urine Output Decrease BP & Blood Volume ## Footnote In the right atrium, the stretch receptors occur at the junction of the venae cava In the left atrium, the junction is at the pulmonary veins. Increasing stretch of the receptors stimulates both an increase in heart rate and a decrease in vasopressin (a.k.a. anti-diuretic hormone - ADH) secretion from posterior pituitary. This decrease in vasopressin secretion results in an increase in the volume of urine excreted, serving to lower BP. In addition, stretching of atrial receptors increases secretion of atrial natriuretic peptide (ANP), which promotes increased water and sodium excretion through the urine.

Answer 27

Ephedrine is the most logical choice of single drug to correct the changes because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anesthesia.

Answer 28

Happens when there is a Strong Contraction of underfilled ventricle Causes Bradycrdia & Hypotension This reflex plays a role in **blood pressure regulation** Probably involved in: Bradycardia and hypotension during coronary reperfusion Bradycardia and hypotension with myocardial ischemia/infarction Bradycardia during profound hypovolemia Syncope in severe aortic stenosis Possibly involved in: Cardiac arrest during spinal anesthesia Vasovagal syncope

Answer 29

Arterial pressure elevation in response to cerebral ischemia. When this excitation occurs, the systemic arterial pressure often rises to a level as high as the heart can possibly pump. Your body is trying to save your brain. Results from decreased blood flow to the vasomotor center in the Medulla. Increased local concentration of CO2 causes SNS stimulation in the Medulla. Causes increased BP. It is a very powerful activator of the SNS. This effect is believed to be caused by failure of the slowly flowing blood to carry carbon dioxide away from the brain stem vasomotor center

Answer 30

Widened pulse pressure Bradycardia Irregular respirations (also known as Cheyne–Stokes respirations) Cheyne-Stokes respirations consist of periods of slow, deep breaths followed by periods of apnea, when breathing comes to a complete stop. Hypertension, or increased blood pressure **Additional symptoms** Headaches Vomiting Blurred vision Weakness Changes in behavior or level of consciousness ## Footnote To compensate for the lack of oxygen, the **sympathetic nervous system** is activated, causing an increase in systemic blood pressure and an initial increase in heart rate. The increased blood pressure then signals the carotid and aortic baroreceptors to activate the **parasympathetic nervous system**, causing the heart rate to decrease.

Answer 31

Type of **CNS Ischemic Response** that results from increased pressure of the cerebrospinal fluid around the brain in the cranial vault. When the **CSF pressure rises to equal the arterial pressure, it compresses the whole brain, as well as the arteries in the brain, and cuts off the blood supply to the brain.** This action initiates a CNS ischemic response that causes the arterial pressure to rise. When the **arterial pressure has risen to a level higher than the cerebrospinal fluid pressure, blood will flow once again into the vessels of the brain to relieve the brain ischemia.**

Answer 32

Increased ICP Hypertension Bradycardia

Answer 33

peripheral receptors, neuronal pathways, and chemoreceptors.

Answer 34

The diving reflex is the body’s physiological response to submersion in cold water and includes selectively shutting down parts of the body in order to conserve energy for survival. The diving reflex is a complex cardiovascular-respiratory response to immersion. This multireflex response in animals consists of **apnea; bradycardia (the experimental parameter most often measured); peripheral vasoconstriction (resulting in preferential perfusion of the brain and heart); decreased cardiac output (with a maintained or increased stroke volume); and an increase in mean arterial blood pressure.** These cardiovascular alterations act in a manner that **conserves oxygen for the heart and brain**. **Mammalian Diving Reflex In Children** In children the mammalian diving reflex is more significant due to the following reasons: 1. They have a much smaller body surface area and will become hypothermic much faster. 2. Their metabolic needs are often higher than an adult.

Answer 35

Aortic & Carotid Bodies

Answer 36

Excites nerve fibers, along with the baroreceptors, that pass through Hering's Nerve and the vagus nerve into the vasomotor center of the brain stem. This excites the vasomotor center and elevates arterial pressure back towards normal. This reflex is not a powerful control of atrial pressure until it falls below 80 mmHg. This makes this reflex become important at lower pressures to prevent further decreases.

Answer 37

**Primarily Respiration Regulation** and **Increases SVR & MAP** Decreased PaO2 tension & Increased PCO2/hydrogen ion excess that excites vasomotor center d/t **decreased BP** May occur when arterial pressure falls below a crtical level d/t inadequate bloodflow to the chemoreceptors. Helps get BP back to a normal level. Activated when MAP \< 80 mmHg

Answer 38

ANP decreases **SVR** and **CVP** which results in **decreased blood pressure**. ANP decreases release of Renin thereby decreasing Angiotensin II. It also decreases Aldosterone release by the adrenal cortex. ANP increases GFR and produces diuresis and natriuresis. The net result is **decreased blood volume**. ## Footnote ANP is involved in the long-term regulation of sodium and water balance, blood volume, and arterial pressure (Fig. 6-13). Most of its actions are the opposite of angiotensin II, and therefore, ANP is a counterregulatory system for the renin–angiotensin–aldosterone system.

Answer 39

Atrial Distention Sympathethic Stimulation Angiotensin II Endothelin

Answer 40

**Sympathetic Nervous System** activation causing **↑HR, ↑Contractility, & ↑SVR**

Answer 41

Profound Hypoxia causes ↓HR & ↓Contractility ## Footnote Dr. Larmon said you would be near death.

Answer 42

**Sympathetic Nervous System** activation causing **↑HR, ↑Contractility, & ↑SVR**

Answer 43

↓Contractility

Answer 44

Mass discharge of Sympathetic Nervous System ↑BP ↑Blood Glucose ↑Strength & ↑Focus ↑Coagulation ↑Metabolism

Answer 45

Muscarinic Receptor & Nicotinic Receptor - neuromuscular junction

Answer 46

Cardiac contraction and relaxation are both accelerated by **catecholamines and adenylyl cyclase activation** Norepinephrine and epinephrine bind to beta-receptors on the heart which leads to activation of the enzyme adenylyl cyclase. This in turn leads to production of cyclic-AMP from ATP. cAMP activates a protein kinase that phosphorylates calcium channels and allows greater entry of calcium into the cardiac muscle cell. **This allows greater Ca++ influx** cAMP is the second messenger in this system. Relaxation is also enhanced (lusitropy) **Phosphorylation of Phospholamban which enhances Ca++ uptake by the Sarcoplasmic Reticulum** Phosphorylation alters the structural conformation of a protein, causing it to become either activated or deactivated, Phospholamban is a key regulator of cardiac contractility and modulates SR Ca2+ sequestration by inhibiting the SR Ca2+-ATPase (SERCA) in its dephosphorylated state.

Answer 47

Anti-Cholinersterase @ Nicotinic Receptor - Reverse muscle relaxant @Muscarinic - Bradycardia, Bronchospams, Salivation - Give Glycopyrrolate (Robinul)

Answer 48

Acetylcholine

Answer 49

Norepinephrine

Answer 50

Acetylcholine

Answer 51

Sympathetic Nervous System

Answer 52

Beta- 1 Receptor

Answer 53

Beta-2 Receptor Vasodilation Bronchodilation Intestinal relaxation Uterine relaxation Calorigenesis Glycogenolysis Bladder wall relaxation

Answer 54

Angiotensin Converting Enzyme (ACE)

Answer 55

in response to **sympathetic stimulation, hypotension, and decreased sodium delivery**.

Answer 56

Aldosterone

Answer 57

Causes vasoconstriction which leads to increased arterial blood pressure. Powerfully constricts the **small arterioles**. If this constriction occurs in an isolated tissue area, the blood flow to that area can be severely depressed. However, the real importance of angiotensin II is that it normally **acts on many of the arterioles of the body at the same time** to **increase the total peripheral resistance and to decrease sodium and water excretion by the kidneys**, thereby **increasing the arterial pressure**.

Answer 58

promote sodium and fluid retention which leads to increased blood volume.

Answer 59

**Natural Stimulators** Acetycholine Muscarine **Locations** CNS Effector Cells stimulated by Parasympathetic- **post**-ganglionic neurons Cardiac tissue Secretory glands Smooth muscles.

Answer 60

**Natural Stimulators** Acetycholine Nicotine **Locations** CNS Autonomic ganglia Adrenal medulla Neuromuscular junction

Answer 61

**Location ** CNS Salivary Glands Parietal Glands **Effect ** CNS Excitation Memory Locomotor Activity Gastric Acid Secretion Stimulatory ↑ IP3/DAG ## Footnote (IP3/DAG) can release endoplasmic reticulum calcium to change intracellular calcium concentration.

Answer 62

Increased activity of neurons reduces sinoatrial (SA) nodal firing (negative chronotropy) and slows AV nodal conduction (negative dromotropy). It is important to note that under normal resting conditions, these neurons are tonically active, thereby producing what is termed “vagal tone” on the heart, resulting in resting heart rates significantly below the intrinsic firing rate of the SA nodal pacemaker. Afferent nerves, particularly from peripheral baroreceptors that enter the medulla through the NTS, modulate the activity of these vagal neurons. Excitatory interneurons from the NTS, which normally are excited by tonic baroreceptor activity, stimulate vagal activity.

Answer 63

Glossopharyngeal nerve (IX) Carotid sinus

Answer 64

**Location** Smooth muscle Exocrine glands **Effect** All smooth muscle contraction **except** Vasodilation Glandular secretion Stimulatory ↑ IP3/DAG ## Footnote (IP3/DAG) can release endoplasmic reticulum calcium to change intracellular calcium concentration. M3 receptors in the coronary arteries can respond to vagal activation by dilating

Answer 65

Heart ↓cAMP ↓Rate ↓Force ↓AV Conduction More so in atria than ventricles Inhibitory

Answer 66

A low dose of epinephrine increases heart rate and arterial pulse pressure (it increases systolic and decreases diastolic pressure) with little change in mean arterial pressure. These changes occur because low concentrations of epinephrine preferentially bind to cardiac β1-adrenoceptors (produces cardiac stimulation) and vascular β2-adrenoceptors (produces systemic vasodilation). Mean pressure does not change very much because the increase in cardiac output is offset by the decrease in systemic vascular resistance. **Low Doses (1-2 mcg/min) Beta-2** Stimulate Alpha-1 in the skin, mucosa and hepatorenal system while Beta-2 receptors are stimulated in the skeletal muscle. Beta-2 effects in peripheral vasculature predominate. Decreased SVR and distribution of blood to skeletal muscle. MAP remains essentially the same. **Intermediate Doses (4 mcg/min) Beta-1** Increased HR, contractility and increased CO Increased automaticity may lead to dysrhythmias **High Doses (>10 mcg/min) Alpha-1** Most potent activator of Alpha-1 receptors Reflex can occur ## Footnote Overall HR Increased SBP Increased Diastolic Decreased

Answer 67

Norepinephrine increases mean arterial pressure and arterial pulse pressure; heart rate transiently increases (β1-adrenoceptor stimulation) and then decreases owing to baroreceptor reflex activation of vagal efferents to the heart. Mean arterial pressure rises because norepinephrine binds to vascular α1-adrenoceptors, which increases systemic vascular resistance.” **Primarily Alpha-1** **Beta-1 are overshadowed by its Alpha-1 (contractility improves over HR) No Beta-2 effects CO may increased at low doses High Doses may decrease CO because of increased afterload and baroreceptor-mediated reflex bradycardia. ## Footnote Overall HR transiently increases then decreases SBP Increased Diastolic Increased

Answer 68

“Norepinephrine (NE) released from sympathetic nerve terminals binds to postjunctional adrenoceptors (order of functional importance: α1 > α2 > β2). NE binding to postjunctional α-adrenoceptors causes increased (+) vascular tone (vasoconstriction), whereas binding to β2-adrenoceptors causes decreased (−) vascular tone (vasodilation).

Answer 69

Nucleus ambiguus ## Footnote the nucleus ambiguus of the medulla contains cell bodies for the vagus nerves.

Answer 70

Constricts blood vessels by binding to α1-adrenoceptors. ## Footnote norepinephrine binds to α1-adrenoceptors located on vascular smooth muscle to stimulate vasoconstriction.

Answer 71

Releases acetylcholine, which binds to M2 receptors. ## Footnote vagus nerve is parasympathetic cholinergic and therefore releases acetylcholine.

Answer 72

Increased sympathetic efferent nerve activity to systemic circulation ## Footnote because the initial fall in pressure decreases arterial baroreceptor firing, which results in sympathetic activation of the heart and systemic vasculature to increase pressure.

Answer 73

Increase systemic vascular resistance. ## Footnote high dose of epinephrine binds to both β2- and α-adrenoceptors on blood vessels. Therefore, if the β2-adrenoceptors (which produce vasodilation) are blocked, the α-adrenoceptors can produce vasoconstriction and increased systemic vascular resistance unopposed by the β2-adrenoceptors.

Answer 74

Systemic vasodilation followed by reflex activation of sympathetic nerves. ## Footnote acetylcholine dilates blood vessels, which lowers arterial pressure and causes a baroreceptor-mediated increase in heart rate brought about by sympathetic activation.

Answer 75

Decrease blood volume by promoting sodium loss by the kidneys ## Footnote atrial natriuretic peptide produces natriuresis and diuresis, both of which are beneficial to the acutely decompensated heart failure patient who has excessive accumulation of fluid that can cause pulmonary and systemic edema.

Answer 76

Increase systemic vascular resistance.

Neurohumoral Control of the Heart & Circulation - Quiz 10 Flashcards

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