Neurohumoral Control of the Heart & Circulation - Quiz 10 Flashcards

1
Q

Where are the Autonomic Nervous System Centers located? (4)

A

spinal cord
brain stem
hypothalamus
portions of the cerebral cortex > especially of the limbic cortex, can transmit signals to the lower centers and influence autonomic control.

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2
Q

NE Order of importance in the vessels?

A

“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).

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3
Q

NE order of importance in the heart?

A

Norepinephrine (NE) released from sympathetic nerve terminals binds to postjunctional adrenoceptors (order of functional importance: β1 > β2 > α1) to increase (+) inotropy, chronotropy, and dromotropy.

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4
Q

Which Sympathetic Nerve Receptor predominantly causes Vasoconstriction?

A

Alpha-1 Receptor

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)

Also Causes:
Iris dilation
Intestinal relaxation
Intestinal sphincter contraction
Pilomotor contraction
Bladder sphincter contraction

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5
Q

What is the most important adrenoreceptor in the heart?

Not including the coronary vascular adrenoreceptors

A

Beta- 1 Receptor

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6
Q

Which Sympathetic Nerve Receptor predominantly causes increased Contractility (inotropy)?

A

Beta-1 Receptor

Activation of sympathetic efferent nerves to the heart releases the neurotransmitter norepinephrine that binds primarily to β1-adrenoceptors located in nodal tissue, conducting tissues, and myocardium

When activated by aβ1-agonistsuch as NE or EPI, heart rate is increased (positive chronotropy), conduction velocity is increased (positive dromotropy), contractility is increased (positive inotropy), and the rate of myocyte relaxation is increased (positive lusitropy).

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7
Q

Which Sympathetic Nerve Receptor predominantly causes Bronchodilation?

A

Beta-2 Receptor

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8
Q

Which catecholamine causes vasodilation in some organs?

A

Epinephrine

In a few tissues epinephrine causes vasodilation because it also has a beta-adrenergic receptor stimulatory effect, which dilates rather than constricts certain vessels.

Circulating epinephrine (EPI) binds with high affinity to smooth muscle β2-adrenoceptors to cause vasodilation in some organs; however, the effect EPI is very concentration dependent. While EPI has a higher affinity for β2 than postjunctional α1or α2-adrenoceptors, at high concentrations it does bind to the postjunctional α1and α2-adrenoceptors, which can override the vasodilatory effects of β2-adrenoceptor stimulation and produce vasoconstriction.

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9
Q

Which catecholamine is the principle vasoconstrictor?

A

Norepinephrine

Norepinephrine is the principal vasoconstrictor hormonal substance secreted at the endings of the sympathetic vasoconstrictor nerve fibers.

Norepinephrine, which acts directly on the alpha-adrenergic receptors of the vascular smooth muscle to cause vasoconstriction.

They act directly on all blood vessels, usually to cause vasoconstriction.

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10
Q

Which Parasympathetic Nerve Receptor inhibits Norepinephrine release?

A

Acetylcholine

ACh also binds to prejunctional muscarinic receptors (M2) on sympathetic nerve terminals to inhibit NE release.

Parasympathetic (vagal) nerves release acetylcholine (ACh), which binds to postjunctional M2 receptors to decrease (−) inotropy, chronotropy, and dromotropy.

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11
Q

Which Sympathetic Nerve Receptor inhibits Norepinephrine release?

A

Alpha-2

Released norepinephrine can also bind to prejunctional α2-adrenoceptors located on the sympathetic nerve terminal. These receptors inhibit norepinephrine release through a negative feedback mechanism.

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12
Q

What does stimulation of the Beta-2 Receptor cause? (7)

A
  • Vasodilation
  • Bronchodilation
  • Intestinal relaxation
  • Uterine relaxation
  • Calorigenesis
  • Glycogenolysis
  • Bladder wall relaxation
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13
Q

Beta-2 Vasodilation and Bronchodilation is mediated by which drug?

A

Epi

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14
Q

Beta-1 increased Contractility and Chronotropy has a drug affinity of ____ > ____?

A

Epi > Norepi

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15
Q

Alpha-2 Vasoconstiction and Neurotransmitter releases has a drug affinity of ____ > _____?

A

Norepi > Epi

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16
Q

Alpha-1 Vasoconstriction has a drug affinity of _____ > ______?

A

Norepi > Epi

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17
Q

What are the precursors to Epinephrine?

A

Tyrosine > Dopamine > Norepi > Epi

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18
Q

What is Inotropy?

A

Contractility

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19
Q

What is Chronotropy?

A

Heart Rate

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20
Q

What is the function of the Vasomotor Center?
Which ANS?
Nerve involved
Organ impact
Body Vessels

A

This center transmits parasympathetic impulses through the vagus nerves to the heart and sympathetic impulses through the spinal cord and peripheral sympathetic nerves to virtually all arteries, arterioles, and veins of the body.

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21
Q

What is Dromotropy?

A

Conduction velocity of AV Node

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22
Q

Functions of Parasympathetic Nervous System (7)

A
  • Constricts Pupils
  • Stimulates Saliva Flow
  • Constricts Bronchi
  • Slows Heartbeat
  • Stimulates Peristalsis and Secretion
  • Stimulates Bile Release
  • Contracts Bladder
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23
Q

Functions of Sympathetic Nervous System (8)

A
  • Dilates Pupils
  • Inhibits Saliva
  • Relaxes Bronchi
  • Accelerates Heartbeat
  • Inhibits Peristalsis and Secretion
  • Secretion of Adrenaline and Noradrenaline
  • Inhibits Bladder Contraction
  • Stimulates Orgasm
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24
Q

What is Lusitropy?

A

Rate of Myocardium Relaxation

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25
Q

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

A

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

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26
Q

The Sympathetic Nervous Systen is located where in the Thoracic-Lumbar area?

A

T1- L2

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27
Q

Parasympathetic Nerves exit the medulla as ____ preganglionic fibers that form synapses with ____ postganglionic fibers within the heart or vascular tissue.

Vagus Nerve CN X

A

Long Preganglionic Efferent Fibers

Short Postganglionic Fibers

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28
Q

What does efferent mean?

A

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 systemand the parasympathetic nervous system.

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29
Q

What does afferent mean?

A

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.

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30
Q

Where and what is the medulla? (3)

A

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.

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31
Q

What are visceral reflexes?

Visceral means soft organs

A

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.

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32
Q

What is the most important part of the autonomic nervous system for regulating the circulation is the?

A

Sympathetic nervous system

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33
Q

Sympathetic Nerves exit the medulla and travel down the spinal cord where they synapse with ____ preganglionic fibers that travel to, and synapse within, sympathetic ganglia. _____ Postganglionic efferent fibers from the ganglia travel to the heart and vasculature where they synapse at their target sites.

A

Short Preganglionic Fibers
Long Postganglionic Fibers

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.

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34
Q

Extrinsic Control of Peripheral Blood Flow is Mediated Mainly by the _____________?

A

Sympathetic Nervous System

Sympathetic stimulation of the heart increasesheart rate (positive chronotropy),inotropyandconduction 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 byalpha-adrenoceptors

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35
Q

What is the Parasympathetic Nervous System pathway?

A

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 toM2 muscarinic receptors,a subclass of cholinergic receptors . Thisproduces 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). .

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36
Q

What is the Major differnces bt/ the Sympathetic & Parasympathetic system?

A

Sympathetic: Excitatory Cardiac Effects - Innervates entire heart

Parasympathetic: , contributes importantly to regulation ofheartfunction.

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.

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37
Q

Which Catecholamine does the Adrenal Gland mostly release w/ Sympathetic Stimulation?

A

Epinephrine - 80%

Norepinephrine - 20%

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38
Q

What is the “Second Messenger” of the Sympathetic Stimulation of heart muscle cell?

A

Cyclic AMP - allows greater Ca++ influx

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39
Q

What happens intracellularly when catecholamines bind to the Beta-Adrenergic Receptor?

A

Activates Adenylyl Cyclase - Converts ATP to cAMP

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40
Q

What happens intracellularly when catecholamines bind to the Alpha-1 Receptor?

A

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

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41
Q

What is Vasopressin?

A

ADH released by Posterior Pituitary - causes vasocontriction & increases blood volume by renal fluid reabsorption

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.

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42
Q

What does the Atrial Natriuretic Peptide do?

A

Decreases SVR & CVP by decreasing release of Renin

Increases Diuresis

Decreases Blood Volume

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43
Q

How does the Baroreceptror Reflex help with Blood Pressure Regulation?

A

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

After the baroreceptor signals have entered the nucleus tractus solitarius of the medulla, secondary signalsinhibit the vasoconstrictor centerof the medulla andexcite the vagal parasympathetic center.The net effects are (1)vasodilationof the veins and arterioles throughout the peripheral circulatory system and (2)decreased heart rateandstrength of heart contraction.Therefore, excitation of the baroreceptors by high pressure in the arteries reflexlycauses the arterial pressure to decreasebecause 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.

44
Q

What is the Baroreceptor Reflex?

A

Receptors located in Cartoid Sinus & Aortic Arch

Senses blood pressure & adjusts HR, Contractility, & SVR accordingly.

45
Q

Which Reflex is dominant when blood volume is increased?

A

Bainbridge Reflex

46
Q

What surgery does Baroreceptor Reflex activation frequently cause hemodynamic changes?

A

Carotid Endarterectomy

47
Q

What else contributes to the heart rate changes seen with the Bainbridge Reflex?

A

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

48
Q

What does the Bainbridge Reflex do?

A.K.A Atrial Reflex

A

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

Increased blood volume is detected by stretch receptors located in both atria at the venoatrial junctions.

49
Q

What are Atrial Strech Receptors?

pressure vs volume?

A

Low pressure receptors that respond to stretch

Sense cardiovascular system volume

50
Q

Where are the Atrial Stretch Receptors Located?

NOT THE ONES INVOLVED WITH BAINBRIDGE

A

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

51
Q

What are the effects of Atrial Stretch Reflex that is not part of the Bainbridge Reflex?

A

Increase Urine Output

Decrease BP & Blood Volume

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.

52
Q

What drug should you use if you have a Bezold-Jarisch Reflex?

A

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.

53
Q

What is the Bezold-Jarisch Reflex?

A

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

54
Q

What is the CNS Ischemic Response?

A

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

55
Q

What are S/S of Cushings Triad? (4)

A

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

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.

56
Q

What is the Cushing Response?

A

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.

57
Q

What is Cushing’s Triad?

A

Increased ICP

Hypertension

Bradycardia

58
Q

What Receptors are involved in the Diving Reflex? (3)

A

peripheral receptors, neuronal pathways, and chemoreceptors.

59
Q

What is the Diving Reflex?

A

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.

60
Q

Where are the Peripheral Chemoreceptors located?

A

Aortic & Carotid Bodies

61
Q

Learn the Peripheral Chemoreceptors Map

A
62
Q

What is the pathway when a chemoreceptor is triggered?

A

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.

63
Q

What do the Peripheral Chemoreceptors do?

A

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

64
Q

What does ANP do to BP?

A

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.

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.

65
Q

What stimulates the Atrial Natriuretic Peptide (ANP)? (4)

A

Atrial Distention

Sympathethic Stimulation

Angiotensin II

Endothelin

66
Q

What are the Indirect effects of Hypoxia on the Circulatory System?

A

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

67
Q

What are the Direct effects of Hypoxia on the Circulatory System?

A

Profound Hypoxia causes
↓HR & ↓Contractility

Dr. Larmon said you would be near death.

68
Q

What is the Indirect effect of Hypercarbia?

A

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

69
Q

What is the Direct effect of Hypercarbia?

A

↓Contractility

70
Q

What is the “Fight or Flight” Response? (6)

A

Mass discharge of Sympathetic Nervous System

↑BP

↑Blood Glucose

↑Strength & ↑Focus

↑Coagulation

↑Metabolism

71
Q

What are the 2 Types of Acetylcholine Receptors?

A

Muscarinic Receptor

&

Nicotinic Receptor - neuromuscular junction

72
Q

How are Cardiac Contraction and Relaxation accelerated?

A

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.

73
Q

How does Neostigmine work?

A

Anti-Cholinersterase

@ Nicotinic Receptor - Reverse muscle relaxant

@Muscarinic - Bradycardia, Bronchospams, Salivation - Give Glycopyrrolate (Robinul)

74
Q

Which part of the Brainstem is the Vasomotor Center located?

A

Medulla

75
Q

Which neurotransmitter is released between the Pre-Ganglionic & Post-Ganglionic Sympathetic fibers?

A

Acetylcholine

76
Q

Which neurotransmitter is released between the Post-Ganglionic Sympathetic fibers & Target Site?

A

Norepinephrine

77
Q

Which neurotransmitter is released between the Pre-Ganglionic Sympathetic Fiber & Adrenal Medulla?

A

Acetylcholine

78
Q

Which Autonomic Nervous System innervates Blood vessels except for capillaries?

A

Sympathetic Nervous System

79
Q

What is the most important adrenoreceptor in the heart?

Not including the coronary vascular adrenoreceptors

A

Beta- 1 Receptor

80
Q

Which Sympathetic Nerve Receptor predominantly causes Bronchodilation?

A

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

81
Q

What converts Angiotensinogen to Angiotensin I?

A

Renin

82
Q

What converts Angiotensin I to Angiotensin II?

A

Angiotensin Converting Enzyme (ACE)

83
Q

Renin-Angiotensin-AldosteroneSystem

A
84
Q

Why is Renin released from the kidney? (3)

A

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

85
Q

What does Angiotensin II stimulate the Adrenal Cortex to release?

A

Aldosterone

86
Q

What is the effect that Angiotensin II has upon the body?

A

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 thetotal peripheral resistanceand to decrease sodium and water excretion by the kidneys, thereby increasing the arterial pressure.

87
Q

What do Angiotenin II and Aldosterone do to the body?

A

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

88
Q

What are Muscarinic Receptors Natural Stimulators (2) and Receptor Locations (5)?

A

Natural Stimulators
Acetycholine
Muscarine

Locations
CNS
Effector Cells stimulated by Parasympathetic- post-ganglionic neurons
Cardiac tissue
Secretory glands
Smooth muscles.

89
Q

What are Nicotinic Receptors Natural Stimulators (2) and Receptor Locations (4)?

A

Natural Stimulators
Acetycholine
Nicotine

Locations
CNS
Autonomic ganglia
Adrenal medulla
Neuromuscular junction

90
Q

M1

Location (3)

Effect (4)

Stimulatory or Inhibitory?

A

**Location **
CNS
Salivary Glands
Parietal Glands

**Effect **
CNS Excitation
Memory
Locomotor Activity
Gastric Acid Secretion

Stimulatory

↑ IP3/DAG

(IP3/DAG) can release endoplasmic reticulum calcium to change intracellular calcium concentration.

91
Q

What is Vagal Tone?

A

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.

92
Q

Where is the sinus nerve (nerve of Herring) from and where does it innervate?

A

Glossopharyngeal nerve (IX)
Carotid sinus

93
Q

M3
Location (2)

Effect (1)

Stimulatory or Inhibitory

A

Location
Smooth muscle
Exocrine glands

Effect
All smooth muscle contraction
except
Vasodilation
Glandular secretion

Stimulatory ↑ IP3/DAG

(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

94
Q

M2

Location (1)

Effect 3)

Stimulatory or Inhibitory?

A

Heart

↓cAMP
↓Rate
↓Force
↓AV Conduction

More so in atria than ventricles

Inhibitory

95
Q

An Epinephrine infusion will cause what changes to the HR, SBP and DBP?

A

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

Overall
HR Increased
SBP Increased
Diastolic Decreased

96
Q

A Norepinephrine infcusion will cause what changes to HR, SBP and DBP?

A

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.

Overall
HR transiently increases then decreases
SBP Increased
Diastolic Increased

97
Q

NE Order of importance in the vessels?

A

“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).

98
Q

The cell bodies for the preganglionic vagal efferents innervating the heart are found in which region of the brain?

A

Nucleus ambiguus

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

99
Q

Norepinephrine released by sympathetic nerves

A

Constricts blood vessels by binding to α1-adrenoceptors.

norepinephrine binds to α1-adrenoceptors located on vascular smooth muscle to stimulate vasoconstriction.

100
Q

Stimulating efferent fibers of the right vagus nerve that innervates the heart

A

Releases acetylcholine, which binds to M2 receptors.

vagus nerve is parasympathetic cholinergic and therefore releases acetylcholine.

101
Q

When a person suddenly stands up from a sitting position, their arterial pressure is found to fall initially by about 10 mm Hg; however, after 1 minute, the pressure is restored. Which of the following contributes to the restoration of arterial pressure after standing?

A

Increased sympathetic efferent nerve activity to systemic circulation

because the initial fall in pressure decreases arterial baroreceptor firing, which results in sympathetic activation of the heart and systemic vasculature to increase pressure.

102
Q

Infusion of a high dose of epinephrine following pharmacologic blockade of β-adrenoceptors will?

A

Increase systemic vascular resistance.

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.

103
Q

In an experimental protocol, intravenous infusion of acetylcholine was found to decrease mean arterial pressure and increase heart rate. These results can best be explained by

A

Systemic vasodilation followed by reflex activation of sympathetic nerves.

acetylcholine dilates blood vessels, which lowers arterial pressure and causes a baroreceptor-mediated increase in heart rate brought about by sympathetic activation.

104
Q

A hospitalized patient with acute decompensated heart failure is given a drug (neprilysin inhibitor) that increases circulating atrial natriuretic peptide by inhibiting its metabolism. What beneficial effects would this treatment have in this patient?

A

Decrease blood volume by promoting sodium loss by the kidneys

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.

105
Q

Following an automobile accident that resulted in significant hemorrhage, a 48-year-old male patient is admitted to the emergency department in critical condition with an arterial pressure of 65/45 mm Hg and a heart rate of 140 beats/min. Fluid resuscitation was augmented by administration of arginine vasopressin. The potential benefit of adding vasopressin during resuscitation is derived from its ability to

A

Increase systemic vascular resistance.