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Apex > Unit 2 Autonomic Nervous System > Flashcards

Unit 2 Autonomic Nervous System Flashcards

1
Q

List 3 forms of extracellular signals?

A

Chemical
Electrical
Mechanical

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2
Q

What are the 4 classifications of receptors?

A

Ion channel
G-Protein Coupled Receptor
Enzyme Linked Receptor
Intracellular receptor

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3
Q

Describe an ion channel

Example

A

An ion conducting pore that opens and closes to control ions flowing along their concentration gradient.
Voltage-gated sodium channel in the neuron

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4
Q

What are the 2 ways a GPCR can work?

Example

A
  1. It opens or closes an ion channel
  2. It activates or inhibits an enzyme inside the cell

Alpha-1 receptor in vascular smooth muscle

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5
Q

Describe an enzyme linked receptor.

Example

A

The receptor is also an enzyme
At rest the catalytic domain is inactive
When the signal binds the catalytic domain becomes activated

Insulin receptor in skeletal muscle (linked to tyrosine kinase)

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6
Q

Describe an intracellular receptor.

Examples

A

A signal diffuses through the cell membrane and binds to the receptor located inside the cell.

Steroids bind to receptors in the cytoplasm
Thyroid hormone binds to receptors in the cell nucleus

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7
Q

What is the general flow of events with a GPCR?

A

First messenger > GPCR > Effector > Second messenger > Cellular response

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8
Q

What is a ligand (GPCR)?

A

The first messenger that binds to the GPCR. Can be endogenous or exogenous.

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9
Q

Where is the GPCR?

A

In the cell membrane, making it accessible from outside the membrane

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10
Q

How many subunits does the G-protein have?

A

3:
Alpha
Beta
Gamma

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11
Q

What is the function of the protein on the GPCR?

A

The G-protein either stimulates or inhibits an effector (enzyme or channel)

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12
Q

What are the G-proteins? What do each do?

A

Gs: stimulatory
Gq: stimulatory
Gi: inhibitory

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13
Q

What happens with a ligand binds to the GPCR?

A

The ligand-receptor interaction activates the G-protein.
This causes the alpha subunit to dissociate from the beta and gamma subunits.
The alpha subunit of a Gs or Gq will turn on an effector, while the alpha subunit of a Gi protein will turn off an effector.
When the ligand unwinds from the receptor, the alpha subunit rejoins the beta and gamma subunits, and its interaction with the effector ends.

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14
Q

What is the function of the effector (GPCR)?

A

To activate the second messenger

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15
Q

Name 2 enzymatic effectors

A

Adenylate cyclase

Phopholipase C

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16
Q

Name 2 ion channel effectors

A

GABA-A

M2 receptors at the SA node

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17
Q

List the 5 second messengers

A
  1. Cyclic adenosine monophosphate (cAMP)
  2. Cyclic guanosine monophosphate (cGMP)
  3. Inositol triphosphate (IP3)
  4. Diacylglycerol (DAG)
  5. Calcium ion (Ca+2)
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18
Q

Mnemonic for Gq GPCR?

A 
Gq’s HAV 1 M&M
Gq stimulates phospholipase C
PLC turns on IP3, Ca+2, DAG
Histamine 1
Alpha 1
Vasopressin 1
Muscarinic 1
Muscarinic 3 (apex also says 5)
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19
Q

Mnemonic for Gi GPCR?

A 
Gi MAD2
Gi inhibits adenylate cyclase 
Adenylate cyclase turns off ATP and cAMP
Muscarinic 2 (apex also says 4)
Alpha 2
Dopamine 2
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20
Q

Mneumonic for Gs GPCR?

A 
Gs does all the rest
Gs stimulates adenylate cyclase
Adenylate cyclase turns on ATP and cAMP
Beta 1 and 2
Dopamine 1
Vasopressin 2
Histamine 2
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21
Q

Nicotinic receptors are located where? What type of signal transduction?

A

ANS ganglia, NMJ, and CNS

Ion channels

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22
Q

Which dopamine receptors are presynaptic and which are postsynaptic?

A

Pre: D2
Post: D1

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23
Q

Which vasopressin receptors are in the vasculature and which are in the renal tubules?

A

Vasculature: V1

Renal tubules: V2

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24
Q

ANS receptors and physiologic action of the heart? PNS?

A

SNS:
Myocardium B1
Conduction system B1
Increased contractility, HR, and conduction speed
The cardiac accelerator fibers arise from T1-T4

PNS:
Myocardium M2
Conduction system M2
Decreased contractility, HR, conduction speed
Vagus nerve CN X
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25
Q

ANS receptors and physiologic action of vasculature

A

SNS:
Arteries a1 > a2 -> vasoconstriction
Veins a2 > a1 -> vasoconstriction

PNS:
No parasympathetic receptors

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26
Q 
ANS receptors and physiologic action of specific vascular beds:
Myocardium
Skeletal muscle
Renal
Mesenteric
A

Myocardium: B2 -> vasodilation; no PNS receptors
Skeletal muscle: B2 -> vasodilation; no PNS receptors
Renal: DA -> vasodilation; no PNS receptors
Mesenteric: DA -> vasodilation; no PNS receptors

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27
Q

ANS receptors and physiologic action of the bronchial tree

A

SNS:
B2 -> bronchodilation
Beta 2 receptors are not innervated, instead they respond to catecholamines in the systemic circulation or in the airway (inhaled)

PNS:
M3 -> bronchoconstriction

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28
Q

ANS receptors and physiologic action of the kidney

A

SNS:
Renal tubules: a2 -> diuresis (ADH inhibition)
Renin release: B1 -> increased renin release

PNS:
No receptors

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29
Q

ANS receptors and physiologic action of the eye

A

SNS:
Sphincter muscle (iris): no SNS receptor
Radial muscle (iris): a1 -> contraction (mydriasis)
Ciliary muscle: B2 -> relaxation (far vision)

PNS:
Sphincter muscle: M -> contraction (miosis)
Radial muscle: no PNS receptor
Ciliary muscle: M -> contraction (near vision)

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30
Q

ANS receptors and physiologic action of the GI

A 
SNS:
Sphincters: a1 -> contraction
Motility & tone: a1 / a2 / B1 / B2 -> Decrease
Salivary glands: a2 -> decrease 
Gallbladder & ducts: B2 -> relaxation
PNS:
Sphincters: M -> relaxation
Motility & tone: M -> increase
Salivary glands: M -> increase 
Gallbladder & ducts: M -> contraction
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31
Q

ANS receptors and physiologic action of the pancreas

A

SNS:
Islet B cells: a2 -> decrease insulin release and B2 -> increase insulin release

PNS: no receptors

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32
Q

ANS receptors and physiologic action of the liver

A

SNS:
a1 / B2 -> increase serum glucose

PNS: no receptors

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33
Q

ANS receptors and physiologic action of the uterus

A

SNS:
a1 -> contraction
B2 -> relaxation

PNS: no receptors

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34
Q

ANS receptors and physiologic action of the bladder

A

SNS:
Trigone & sphincter: a1 -> contraction
Detrusor: B2 -> relaxation

PNS:
Trigone & sphincter: M -> relaxation
Detrusor: M -> contraction

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35
Q

ANS receptors and physiologic action of the sweat glands

A

SNS: a1 -> increase secretion
PNS: M -> increase secretion

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36
Q

Describe alpha 1 stimulation in the eye

A

Alpha 1 stimulation -> radial muscle contraction -> mydriasis (pupil dilation)

Radial muscle dilates pupil = ready to go = SNS

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37
Q

Describe muscarinic stimulation in the eye

A

Muscarinic stimulation -> sphincter muscle contraction -> miosis (pupil contraction

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38
Q

Location of the alpha 2 receptor is throughout the body, but what 3 ways can these locations be classified?

A

Presynaptic
Postsynaptic
Nonsynaptic

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39
Q

What are presynaptic alpha 2 receptors?

A

These are NE releasing neurons in the CNS and PNS (negative feedback mechanism reduces NE release)

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40
Q

Where are postsynaptic alpha 2 receptors located?

A

In smooth muscle and several organs

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41
Q

Where are nonsynaptic alpha 2 receptors found?

A

Platelets

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42
Q

Where are alpha 2 receptors in the nervous system found and what is their physiologic effect? (5)

A 
Medulla: decrease SNS tone
Vagus nerve: increase PNS tone
Locus coeruleus: sedation, hypnosis
Spinal cord (dorsal horn): analgesia
???: antishivering
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43
Q

What the is physiologic effect of alpha 2 receptors in the vasculature?

A

Vasoconstriction

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44
Q

What is the physiologic effect of alpha 2 receptors in the renal tubules?

A

Inhibits ADH (diuresis)

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45
Q

What is the physiologic effect of alpha 2 receptors in the pancreas?

A

Decrease insulin release

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46
Q

What is the physiologic effect of alpha 2 receptors in the platelets?

A

Increase platelet aggregation

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47
Q

What is the physiologic effect of alpha 2 receptors in the salivary glands?

A

Dry mouth

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48
Q

What is the physiologic effect of alpha 2 receptors in the GI tract?

A

Decrease gut motility

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49
Q

Dexmedetomidine is a centrally acting alpha-2 agonist that reduces SNS tone and causes sedation, MAC reduction, analgesia, bradycardia, and vasodilation; what happens with rapid administration?

A

It can stimulate postsynaptic alpha-2 receptors in the arterial and venous circulations leading to vasoconstriction and hypertension.

  • the CNS effect temporarily lags behind
  • once it kicks in the central alpha-2 effect overpowers the peripheral alpha-2 effect
  • therefore, it is possible to see a transient rise in BP
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50
Q

What enzyme metabolizes cyclic adenosine monophosphate? Into what?

A

Phosphodiesterase III

AMP - adenosine monophosphate

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51
Q

Inhibiting PDE III and increase cAMP benefits:

A
  1. In the cardiac muscle cell, cAMP augments myocardial performance by:
    - increasing intracellular calcium and the force of contraction
    - increasing the rate of relaxation by accelerating the return of calcium to the sarcoplasmic reticulum (lusitropy)
  2. In the vascular smooth muscle cell, cAMP inhibits myosin light chain kinase causing:
    - vasodilation
    - decreased SVR
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52
Q

PDE III inhibitors are also called ______.

Example

A

Inodilators

Milrinone

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53
Q

PDE III inhibitors augment myocardial performance independently of the SNS, making them useful in what 4 situation?

A

BB induced myocardial depression
Acute heart failure
Unresponsiveness to IV catecholamines
Anytime the combination of increased inotropy and reduced afterload would be desirable

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54
Q

What is the prototype nonselective phosphodiesterase inhibitor?

A

Theophylline

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55
Q

What is the primary neurotransmitter in the SNS?

A

Norepinephrine

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56
Q

Sympathetic neurons synthesize NE from what 2 substances?

A

Tyrosine - an amino acid obtained from diet

Phenylalanine (converted to tyrosine first)

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57
Q

Tyrosine is transported into the adrenergic nerve terminal and converted to DOPA by what enzyme? What is significant about this step?

A

Tyrosine hydroxylase

This occurs in the cytoplasm and is the rate limiting step in NE synthesis

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58
Q

DOPA is converted to dopamine by what enzyme?

A

DOPA decarboxylase

This also occurs in the cytoplasm

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59
Q

Dopamine is transported into a synaptic vesicles and is converted to NE by what enzyme?

A

Dopamine beta-hydroxylase

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60
Q

In the adrenal medulla, most of the NE is converted to epinephrine by what enzyme?

A

Phenylethanolamine-N-methyltransferase

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61
Q

The adrenal medulla secretes about ___% epinephrine and ____% NE into the circulation

A

80% EPI

20% NE

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62
Q

Describe NE release

A
  1. The action potential depolarizes the nerve terminal
  2. Voltage-tasted calcium channels open, and calcium flows into the nerve terminal
  3. Increased neuronal calcium causes NE vesicles to fuse with the nerve terminal and release NE into the synaptic cleft via exocytosis
  4. NE inhibits its release by stimulating the pre-synaptic alpha-2 receptor
  5. NE can augment its release by stimulating the pre-synaptic beta-2 receptor
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63
Q

What are the 3 ways that NE can be removed from the synaptic cleft? Which is the most important?

A

Reuptake into the presynaptic neuron (accounts for 80%)
Diffusion away from the synaptic cleft
Reuptake by extraneural tissue

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64
Q

Reuptake of NE is blocked by what 2 drugs?

A

Tricyclic antidepressants

Cocaine

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65
Q

What 2 enzymes metabolize NE and EPI? What is the final metabolic byproduct?

A 
Monoamine oxidase (MAO)
Catechol-O-methyltransferase (COMT)

Final byproduct of NE and EPI metabolism is vanillylmandelic acid (VMA)

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66
Q

An elevated vanillylmandelic acid (VMA) level in the urine aids in the diagnosis of what?

A

Pheochromocytoma

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67
Q

Where are the principle sites of metabolism of catecholamines that have entered circulation?

A

Liver and kidneys

Only ~5% of NE is excreted unchanged in the urine

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68
Q

Vanillylmandelic acid (VMA) has another name

A

3-methoxy-4-hydroxymandelic acid

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69
Q

What is the primary neurotransmitter in the parasympathetic nervous system?

A

Acetylcholine

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70
Q

Acetylcholine stimulates how many different receptor types? What are they and where are they found?

A

3:
Nicotinic type N (nerve): preganglionic fibers at autonomic ganglia (SNS & PNS), central nervous system
Nicotinic type M (muscle): neuromuscular junction
Muscarinic: postganglionic PNS fibers at effector organs, central nervous system

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71
Q

Nicotinic receptors are what type of receptor? Muscarinic receptors are what type?

A

Nicotinic: ion channels
Muscarinic: GPCR

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72
Q

Describe Ach synthesis

A
  1. Choline is transported from the blood into the cytoplasm of the nerve terminal
  2. Acetyl Coenzyme A is produced in the mitochondria and released into the cytoplasm
  3. In the presence of the enzyme choline acetyltranferase, choline and acetyl CoA are joined to form acetylcholine
  4. Acetylcholine is packed into vesicles
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73
Q

Describe the release of Ach

A
  1. The action potential depolarizes the nerve terminal
  2. Voltage-gated Ca+2 channels open and allow an influx of Ca+2 into the nerve terminal
  3. Ca+2 is required for Ach vesicles to fuse with the nerve terminal and release Ach via exocytosis into the synaptic cleft
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74
Q

Why does Mg+2 cause muscle weakness and act synergistically with NMB?

A

Mg+2 is an antagonist of Ca+2 at the presynaptic nerve terminal

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75
Q

Describe Ach metabolism

A
  1. Acetylcholinesterase is positioned around the cholinergic receptor and quickly hydrolyzes Ach after it unbinds from the receptor
  2. The byproducts are choline and acetate
  3. Choline is transported back into the nerve terminal via reuptake and will serve as substrate for further Ach synthesis
  4. Acetate diffuses away from the synaptic cleft
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76
Q

Preganglionic nerve fibers in the SNS are what type of nerve fibers?

A

Myelinated B fibers

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77
Q

Postganglionic nerve fibers in the SNS are what type of fibers?

A

Unmyelinated C fibers

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78
Q

List the 5 components of the autonomic reflex arc

A 
Sensor
Afferent pathway
Control center
Efferent pathway
Effector
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79
Q

What structures receive the bulk of sensory input from the body? (3)

A

Hypothalamus
Brainstem
Spinal cord

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80
Q

Compare and contrast the architecture of the SNS and PNS efferent pathways

A

SNS:
Preganglionic: short, myelinated, B-fibers, releases Ach
Postganglionic: long, unmyelinated, C-fibers, releases NE (except sweat glands, piloerector muscles and some vessels release Ach)

PNS:
Preganglionic: long, myelinated, B-fibers, release Ach
Postganglionic: short, unmyelinated C-fibers, release Ach

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81
Q

The SNS originates where? What spinal nerves? Where are the cell bodies? Where do the axons exit?

A

Thoracolumbar
T1 - L3
Cell bodies arise from the intermedia lateral region of the spinal cord
Axons exit via the ventral root

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82
Q

Where is the ganglia of the SNS?

A

Near the spinal cord

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83
Q

Post to preganglionic ratio of the SNS

A

30: 1 -> post-synaptic amplification contributes mass response

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84
Q

SNS preganglionic fibers

A

Short
Myelinated
B-fibers

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85
Q

Post ganglionic SNS fibers

A

Long
Unmyelinated
C-fibers

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86
Q

Neurotransmitter and ganglia in SNS

A

Ach

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87
Q

Receptor at the ganglia is SNS

A

Nicotinic type N

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88
Q

Neurotransmitter from postganglionic fiber in SNS

A

NE (except sweat glands, piloerectory muscles, so vessels release Ach)

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89
Q

Receptor at effect organ in SNS

A

Alpha
Beta
Dopamine
Muscarinic (for the Ach exceptions)

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90
Q

The PNS originates where? What spinal nerves? What cranial nerves?

A

Craniosacral
CN III, VII, IX, X
S2 - S4

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91
Q

Where is the ganglia in the PNS?

A

Near or inside the effector organ

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92
Q

What is the post to preganglionic ration in the PNS?

A

1-3 : 1 -> precise control of each organ

93
Q

Preganglionic fiber in the PNS

A

Long
Myelinated
B-fiber

94
Q

Postganglionic fiber in the PNS

A

Short
Unmyelinated
C-fiber

95
Q

Neurotransmitter at the ganglia in the PNS

96
Q

Receptor at the ganglia in the PNS

A

Nicotinic type N

97
Q

Neurotransmitter from postganglionic fiber in the PNS

98
Q

Receptor at effector organ in PNS

A

Muscarinic

99
Q

In the SNS the preganglionic sympathetic fibers exit the spinal cord via the what? Through what do the fibers enter the sympathetic chain?

A

Ventral nerve roots

White communicating rami

100
Q

Once inside the sympathetic chain, what are the 3 paths a preganglioic fiber can take to synapse with a postganglionic fiber?

A
  1. It will synapse with the postganglionic fiber and exit at the same level
  2. It will ascend or descend the sympathetic chain, then synapse at another level before exiting
  3. It will bypass the sympathetic chain entirely and synapse in a collateral ganglion
101
Q

After synapsing in the ganglia, the postganglionic fiber will travel where?

A

To its respective effector organ

102
Q

Fibers that innervate the sweat glands, piloerector muscle, and blood vessels to the skin and muscles take a different path than the rest of the SNS postganglionic fibers, what path do they take?

A

After exiting the sympathetic chain, the re-enter the spinal nerve via the grey communicating rami, and then they travel alongside somatic nerves towards their effector organ

103
Q

What provides sympathetic innervation to the ipsilateral upper extremity and a portion of the head and neck?

A

Stellate ganglion

104
Q

Stellate ganglion blockade

A

Treatment of upper extremity sympathetic dystrophy
Complex regional pain syndrome
Increase blood flow to the upper extremity
Often an unintended consequence of a brachial plexus block

105
Q

What manifests from blockade of the Stellate ganglion?

A

Horner’s syndrome:
Ptosis, anhidrosis, miosis, and enophthalmos
Mnemonic: Very Homely PAM- vasodilation Horner ptosis anhidriosis miosis

106
Q

Name 2 areas of the adrenal gland and what they secrete

A

Medulla: catecholamines
Cortex: glucocorticoids, mineralocorticoids, androgens

107
Q

How is the innervation of the adrenal medulla different from the typical SNS efferent architecture?

A

There is no postganglionic fiber.
The preganglionic fibers release Ach onto the chromaffin cells, and the chromaffin cells release EPI and NE into the systemic circulation at a ratio of 80% to 20% respectively

108
Q

Chromaffin cells are derived from what type of tissue?

A

Neural tissue

109
Q

At rest, the adrenal medulla secretes how much EPI? NE?

A

EPI: 0.2 mcg/kg/min
NE: 0.05 mcg/kg/min

110
Q

How long do catecholamines remain in the blood stream compared who the synaptic cleft?

A

Remain the bloodstream 5 - 10 times longer than in the synaptic cleft

111
Q

What is a pheochromocytoma?

A

A catecholamine secreting tumor (mostly NE) that usually originates in the chromaffin tissue in the adrenal gland

112
Q

Classic presentation of pheochromocytoma

A

Excessive SNS activation: headache, diaphoresis, tachycardia

113
Q

What is the hemodynamic management of a patient with pheochromocytoma? What must you do FIRST?

A

You must block alpha before you block beta!
Alpha antagonists commonly used:
-nonselective - phenoxybenzamine, phentolamine
-alpha-1 selective - doxazosin, prazosin

114
Q

What problems arise from blocking the beta receptor first with pheochromocytoma?

A

Beta-2 blockade inhibits skeletal muscle vasodilation and increases SVR
Beat-1 blockade reduces inotropy and can precipitate CHF in the setting of increased SVR

115
Q

Once the tumor is removed what happens to catecholamine levels?

A

They all go with it, prepare for hypotension and hypoglycemia

116
Q

Sympathetic stimulation causes hepatocytes to release what 2 things into systemic circulation?

A

Glucose and potassium

117
Q

What happens to the GLU released by the liver with SNS stimulation?

A

It provides substrate for aerobic metabolism, but for cells to utilize GLU insulin must be present, so it would make sense that SNS stimulation causes the pancreas to release insulin from the beta cells

118
Q

What happens to the potassium released by the liver with SNS stimulation?

A

Initially K+ released from the liver causes the serum K+ to rise - short lived.
SNS stimulation causes adrenal medulla to secrete catecholamines into circulation.
When EPI binds to the B2 receptor on skeletal muscle and RBCs, it activates the Na/K pump and shifts K+ into the cells -> decrease in serum K+

119
Q

Name 4 ways to shift K+ into the cell

A

Alkalosis
Beta-2 agonists (albuterol, ritodrine, epi)
Theophylline (methylxanthines)
Insulin (activating the Na/K exchanger: epi or insulin)

120
Q

Name 4 ways to shift K+ out of the cell

A 
Acidosis (activating H+/K+ exchanger) 
Cell lysis (rhabdomyolysis) 
Hyperosmolarity 
Succinylcholine (nicotinic type-m agonism)
121
Q

What is the baroreceptor reflex?

A

It regulates short term BP control

  • when BP rises the BRR decreases HR, contractility and SVR
  • when BP falls the BRR increases HR, contractility and SVR
122
Q

If the baroreceptor reflex regulates short term BP, what regulates longer term BP?

A

RAAS and ADH

123
Q

Where are the stretch receptors for the baroreceptor reflex?

A

Carotid sinus

Transverse aortic arch

124
Q

On what nerve is afferent information from the stretch receptors in the carotid sinus sent?

A

Nerve of Hering -> glossopharyngeal nerve -> nucleus tractus solitarius in the medulla

125
Q

On what nerve does the stretch receptors in the transverse aortic arch send afferent information?

A

Vagus nerve -> nucleus tractus salitarius in the medulla

126
Q

What is the main control center for the baroreceptor reflex?

A

The vasomotor center in the medulla and in the pons

127
Q

What are the 4 key functions of the vasomotor center?

A

Vasoconstriction
Vasodilation
Cardiac stimulation
Cardiac inhibition

128
Q

List 3 clinical examples of the baroreceptor reflex and their result

A

Carotid endarterectomy - manipulation of carotid sinus may cause bradycardia.
Mediastinoscopy - pressure from the scope on the transverse aortic arch may cause bradycardia.
Phenylephrine - agonism of the alpha-1 receptor increase SVR and BP, the baroreceptor reflex increase vagal tone causing the HR to decrease.

129
Q

How do VAs affect the baroreceptor reflex? Which one affects it this way the least and why?

A

Decrease effectiveness of baroreceptor reflex in a dose-depends fashion.
ISO has mild beta-1 agonist properties, it impairs the baroreceptor reflex the least.

130
Q

How does thiopental affect the baroreceptor reflex

A

Preserves baroreceptor function - causes SVR to decrease with a compensatory rise in HR

131
Q

How does propofol affect the baroreceptor reflex?

A

Depresses baroreceptor function

132
Q

How does ketamine affect the baroreceptor reflex?

A

It activates the SNS and will cause an increased HR with a minimal change is SVR. If catecholamine reserve is exhausted, direct myocardial depressant effects may be unmasked.

133
Q

How does Etomidate affect baroreceptor reflex?

A

Usually an unchanged HR with a small decrease in SVR, hypovolemia patients may experience hypotension following Etomidate

134
Q

How does hydralazine affect the baroreceptor reflex?

A

Intact. It is a potent vasodilator, the reduction in SVR is countered with an increase in HR via the BRR.

135
Q

How does nitroprusside and Nitroglycerine affect the baroreceptor reflex?

A

Preserved BRR

136
Q

How do beta adrenergic blockers affect the baroreceptor reflex?

A

By antagonizing the beta-1 receptor in the heart, BB may, depending on the extent of beta blockade, prevent a compensatory rise in HR in the setting of hypotension. Labetalol also antagonizes the alpha-1 receptor and may increase the risk of Orthostatic hypotension

137
Q

How does norepinephrine affect the baroreceptor reflex?

A

Its effect on HR is dose-dependent. In lower doses the beta-1 chronotrophic effects prevail. As the dose increase, the alpha-1 vasoconstrictive effects overshadow the beta-1 effects. The net results is a baroreceptor-mediated fall in HR.

138
Q

How do epi, dobutamine, isoproterenol and dopamine affect the baroreceptor reflex?

A

They all increase HR regardless of their dose.

139
Q

Drugs that decrease BP and increase HR, BRR is _____

A

Preserved
Hydralazine
Thiopental

140
Q

Drugs that increase BP and decrease HR, BRR is ______

A

Preserved

Norepinephrine

141
Q

Drugs that decrease BP and HR, BRR is _____

A

Inhibited
Labetalol
Sevoflurane

142
Q

Drugs with variable response, HR can increase, decrease, stay the same, or stop entirely):

143
Q

What is the Bezold-Jarisch Reflex?

A

Slows HR in the setting of profound hypovolemia (preload is too low)

144
Q

What is the Bainbridge reflex?

A

Increases HR in the setting of venous congestion (preload is too high)

145
Q

What is the stimulus for Bezold-Jarisch reflex?

A

Venous return too low

Myocardial ischemia

146
Q

What is the purpose of the Bezold-Jarisch reflex?

A

Allows empty heart time to fill

A slow heart is a better perfused heart

147
Q

Where are the sensors for the Bezold-Jarisch reflex?

A

Left ventricle (but also in other cardiac chambers)

148
Q

What is the afferent nerve for the Bezold-Jarisch reflex?

A

Vagus: unmyelinated C fibers

149
Q

What is the control center for the Bezold-Jarisch reflex?

A

Medulla: vasomotor center

150
Q

What the the efferent nerve for the Bezold-Jarisch reflex?

A

Vagus stimulation

151
Q

What is the effector site(s) for the Bezold-Jarisch reflex?

A

SA node: decrease HR

AV node: decrease CV

152
Q

What is the clinical response of the Bezold-Jarisch reflex?

A

Triad: bradycardia, hypotension, coronary artery dilation

153
Q

What is the treatment for Bezold-Jarisch reflex?

A

Restore preload: IVF, T-burg, elevate legs above head

Increase HR: atropine, ephedrine, epinephrine

154
Q

List 4 examples that will stimulate Bezold-Jarisch reflex?

A

Profound hypotension
Massive hemorrhage
Cardiac arrest under spinal anesthesia
Shoulder arthroscopy and interscalene block and epi in LA and sitting position

155
Q

What it the stimulus for the Bainbridge reflex?

A

Venous return too high

156
Q

What is the purpose of the Bainbridge reflex?

A

Minimizes venous congestion and promotes forward flow

157
Q

Where are the sensors for the Bainbridge reflex?

A

SA node (SA node stretch directly increases its firing rate)
Right ventricle
Pulmonary veins

158
Q

What is the afferent nerve for the Bainbridge reflex?

A

Vagus: unmyelinated C fibers

159
Q

What is the control center for the Bainbridge reflex?

A

Medulla: vasomotor center

160
Q

What is the efferent nerve for the Bainbridge reflex?

A

Vagus inhibition

161
Q

What is the effect site for the Bainbridge reflex?

A

SA node: increase HR

162
Q

What is the clinical response of the Bainbridge reflex?

A

Tachycardia

163
Q

What is the treatment for Bainbridge reflex?

A

None needed

164
Q

What are examples that will trigger the Bainbridge reflex?

A

Autotransfusion during childbirth

Very rapid administration of IVF

165
Q

Other than triggering the Bainbridge reflex, what other 2 things does cardiac congestion lead to?

A
  1. Decreased ADH release from the posterior pituitary gland

2. Increased atrial natriuretic peptide release -> diuresis -> decreases intravascular volume

166
Q

What is another name for the oculocardiac reflex? Why?

A

Five & dime reflex:
Afferent limb: CN V - trigeminal nerve
Efferent limb: CN X - vagus nerve

167
Q

What stimuli can trigger the oculocardiac reflex?

A

Traction to the extraocular muscles (especially the medial rectus)
Strabismus surgery - particularly in children
Pressure on the globe
Pressure on the conjunctiva
Ocular trauma
Pressure on the orbital tissue that remains following enucleation
A retrobulbar block can either cause or prevent the oculocardiac reflex

168
Q

What is the afferent limb of the oculocardiac reflex?

A

Long & short ciliary nerve -> ciliary ganglion -> ophthalmic division V1 of trigeminal nerve (CN V) -> gasserian ganglion

169
Q

What is the control center for the oculocardiac reflex?

A

Medulla: vasomotor center

170
Q

What is the efferent limb of the oculocardiac reflex?

A

Vagus (CN X)

171
Q

What is the effector organ of the oculocardiac reflex?

A

Heart: M2 receptor at SA and AV nodes

172
Q

What is the clinical presentation of the oculocardiac reflex?

A 
Bradycardia 
Hypotension
Junctional rhythm 
AV block
Asystole
173
Q

List 3 factors that worsen severity of the oculocardiac reflex?

A

Hypoxemia
Hypercarbia
Light anesthesia

174
Q

What is the treatment for oculocardiac reflex?

A

Ask surgeon to remove stimulus
Administer 100% O2, ensure proper ventilation, and deepen anesthetic
Administer an anticholinergic such as atropine or glycopyrrolate

175
Q

The oculocardiac reflex will fatigue with subsequent occurrences. T/F

176
Q

Will anticholinergic pretreatment help prevent oculocardiac reflex?

A

Barash says no

Nagelhout says yes for peds

177
Q

What is the Cushings reflex?

A

A sign of intracranial hypertension
Presentation: Hypertension, bradycardia, and irregular respirations
HTN is attempt to restore CPP
Bradycardia is from the baroreceptor reflex’s response to HTN
Irregular respirations are the result of brainstem compression

178
Q

What is the celiac reflex?

A

It is initiated by traction to the mesentery or other abdominal organs.
It is mediated by the vagus nerve.
It causes bradycardia and hypotension.

179
Q

What is the chemoreceptor reflex?

A

It is stimulated by hypoxia and hypercarbia.

It increases minute ventilation and SNS tone.

180
Q

What is the primary determinant of cardiac output in the patient with a heart transplant? What is the consequence of this?

A

The transplanted heart is severed from autonomic influence, so the HR is determined by the intrinsic rate of the SA node. This explains with these patients often have a resting tachycardia (HR = 100-120 bpm).
If CO is the product of HR and SV and the HR is fixed, then CO becomes dependent on preload. Indeed, CO is highly dependent on cardiac filling. This feature makes these patients very sensitive to hypovolemia.

181
Q

What drugs can be used to augment HR in the patient with a heart transplant?

A

Central to understanding this is knowing there is no autonomic input from the cardiac accelerator fibers (T1-T4) or the vagus nerve.
Drugs that directly stimulate the SA node can be sued to increase HR: epi, isoproterenol, glucagon.
Drugs that indirectly simulate the SA node can NOT be used: atropine, glycopyrrolate, ephedrine

182
Q

Any reflex that requires ANS innervation will be disrupted in the denervated heart, except for which reflex? Why?

A

Bainbridge reflex, because SA node stretch will directly increase SA node firing rate

183
Q

What is the most common cause of cardiac denervation in non-cardiac surgery patients?

A

Diabetes (diabetic autonomic dysfunction)

184
Q

What is a glomangioma?

A

Glomus tumor: originates from neural crest cells, usually not malignant.
Tend to grow in the neuroendocrine tissues that lay near carotid artery, aorta, glossopharyngeal nerve, and the middle ear.

185
Q

What substance(s) do glomaniomas secrete and what are their effects? What are your primary concerns for anesthetic?

A

They secrete several vasoactive substances that can lead to exaggerated hyper- or hypotension.

  • Norepinephrine (similar to pheochromocytoma): HTN
  • Serotonin and kallikrein (similar to carcinoid tumor): bronchoconstriction< HA, HTN, flushing, and diarrhea
  • Histamine or bradykinin: bronchoconstriction and hypotension
  • these tumors do not release epi because they lack the enzyme that converts NE to epi (phenylethanolamine N-methyltransferase)
  • Octreotide can be used to treat carcinoid-like s/sx
  • Cranial nerve dysfunction can cause swallowing impairment, aspiration of gastric contents, and airway obstruction
  • Surgical dissection fo a glomus tumor that has invaded the internal jugular vein increases the risk of air embolism
186
Q

What are the anesthetic consideration for multiple system atrophy? Aka?

A

Shy-Drager syndrome: causes degeneration of locus coeruleus, intermedia lateral column of the spinal cord (where the cell bodies for the SNS efferent nerves live), and the peripheral autonomic nerves.
S/sx reflect autonomic dysfunction: orthostatic hypotension, urinary retention, impotence, and bowel dysfunction.
Death from cerebral hypoperfusion usually occurs within 8 years of initial diagnosis.
Autonomic dysfunction contributes to hemodynamic instability during anesthesia. Hypotension is treated with volume resuscitation and direct acting sympathomimetics. Indirect acting adrenergic agonists (ephedrine) and possibly ketamine can cause an exaggerated hypertensive response.

187
Q

What receptors does norepinephrine affect?

A

Dose dependent affinity for:
Alpha-1
Alpha-2
Beta-1

188
Q

Low dose vs high dose norepinephrine?

A

Dose: 0.02 - 0.04 mcg/kg/min
Low dose range: beta-1 selective (increases HR and inotropy)
High dose range: stimulates alpha-1, alpha-2, and beta-1 receptors (increase SVR -> increase BP -> decreases HR via baroreceptor reflex)

189
Q

Norepinephrine is ideal for low ____ states, like sepsis or CPB hypotension due to low _______.

A

SVR

Afterload

190
Q

Why should norepinephrine be avoided in cardiogenic shock?

A

Because it increases afterload and MVO2 (myocardial oxygen consumption)

191
Q

What should be done if norepinephrine extravasation occurs?

A

Inject area with phentolamine 2.5-10 mg in 10mL of diluent to vasodilate the affected region.
A stellate ganglion block is another option.

192
Q

Compare and contrast low, intermediate, and high dose epinephrine.

A

Low dose 0.01-0.03 mcg/kg/min: beta-1, beta-2 (increased HR, CO and inotropy, decreased SVR and wide pulse pressure)
Intermediate dose 0.03-0.15 mcg/kg/min: mixed alpha and beta effects
High dose > 0.15 mcg/kg/min: alpha effects predominate, and supraventricular tachyarrhythmias are common

193
Q

What effects does epi have on bronchials?

A

Bronchodilation

194
Q

What effect does epi have on mast cells?

A

Mast cell stabilization - useful for anaphylaxis

195
Q

What effect does epi have on LAs?

A

Prolongs duration of LAs

196
Q

What effect does epi have on serum glucose?

A

Increases serum glucose

197
Q

What effect does epi have on serum K+?

A

Causes hypokalemia due to transcellular potassium shift

198
Q

Compare and contrast low, intermediate, and high dose dopamine

A

Low dose 1-2 mcg/kg/min: renal vasodilation and increased RBF (BP may decrease as more CO is delivered to the kidneys).
Intermediate dose 2-10 mcg/kg/min: cardiac stimulation (increased HR, inotropy and CO)
High dose 10-20 mcg/kg/min: vasopressor effect (alpha effects overshadow DA and beta effects)

199
Q

Does renal dose dopamine reduce morbidity or mortality and prevent renal failure?

A

No, no, and no.

200
Q

What receptors does isoproterenol stimulate? Dose?

A

Beta-1 and beta-2 receptors

0.02-0.05 mcg/kg/min

201
Q

Describe the cardiovascular effects of isoproterenol

A

Cardiac stimulation - increased HR, inotropy and CO
Vasodilation decreases SVR
The reduction in SVR can be so severe as to drop DBP, and this can impair CPP (CPP = AoDBP - LVEDP)
This makes it a poor choice for septic shock
It can cause severe dysrhythmias and tachycardia

202
Q

List 4 clinical indications for isoproterenol

A

Chemical pacemaker for bradycardia unresponsive to atropine
Heart transplant
Treatment of bronchoconstriction
Cor pulmonale

203
Q

What receptors does dobutamine stimulate? Dose? Effects?

A

Potent beta-1 and mild beta-2 agonist
0.5-15 mcg/kg/min
Cardiac stimulation - increased HR, inotropy, and CO

204
Q

What receptors does phenylephrine stimulate?
Dose
Infusion

A

Non-catecholamine that selects for alpha-1 receptors (no beta effects)
Bolus dose 20-100 mcg
Infusion 10-200 mcg/min

205
Q

What cardiovascular effects does phenylephrine have?

A

Increases SVR
Increases coronary perfusion pressure
Reflex bradycardia
Useful for conditions where increased afterload is required, such as hypertrophic cardiomyopathy or tetralogy of Fallot

206
Q

What receptors does ephedrine stimulate?

Dose

A

Non-catecholamine with direct and indirect effects at alpha-1, alpha-2, beta-1 and, beta-2
IV dose 5-10 mg
IM dose 25-50 mg

207
Q

What cardiovascular effects does ephedrine have?

A

Increases HR, inotropy, CO, and SVR
Uses endogenous catecholamine stores from the presynaptic sympathetic nerve
Multiple doses can cause tachyphylaxis (progressively smaller response to a given dose after multiple administrations)

208
Q

In what situations should ephedrine NOT be used to treat hypotension?

A

Does not work well when neuronal catecholamine stores are depleted (sepsis) or absent (heart transplant)
Risk of hypertensive crisis in patient on MAO inhibitors
Conditions where increased HR or contractility is detrimental to hemodynamics

209
Q

Where is vasopressin produced? What releases vasopressin?

A

Produced by hypothalamus

Released by the posterior pituitary gland

210
Q

How does vasopressin increase BP?

A

Vasopressin restores BP in 2 ways:
V1 receptor stimulation causes intense vasoconstriction
V2 receptor stimulation increases intravascular volume by stimulating the synthesis and insertion of aquaporins into the walls of the collecting ducts. This increases water (but not solute) reabsorption and lowers serum osmolarity.

211
Q

What is the important difference between aldosterone and vasopressin?

A

Aldosterone increases water and sodium reabsorption (serum osmolarity is unchanged); vasopressin only increases water reabsorption so serum osmolarity is lowered

212
Q

Vasopressin bolus? Infusion? Overdose?

A

IV bolus 0.5-1 unit
IV infusion 0.01-0.04 units/min
Overdose can cause hyponatremia and seizures

213
Q

What is the first line treatment for ACEI or ARB induced vasoplegia that’s refractory to catecholamines? Second line therapy?

A

First: Vasopressin
Second: Methylene blue

214
Q

Mnemonic for Beta-1 selective beta antagonists

A

MABE AB

Metoprolol
Atenolol
Betaxolol
Esmolol

Acebutolol
Bisoprolol

215
Q

Non selective beta antagonists (6)

A 
Carvedilol
Labetalol
Nadolol 
Pindolol 
Propranolol
Timolol
216
Q

Clinical uses of BBs (8)

A 
Essential HTN
Angina pectoris
Coronary artery dz
Myocardial ischemia
Dysrhythmias
Congestive heart failure
Hyperthyroidism
Migraine headaches
217
Q

What is the primary site of metabolism of the commonly used BBs? What are 2 exceptions?

A

Most BBs depend on the liver as their primary site of metabolism.
Exceptions:
Esmolol - RBC esterases
Atenolol - eliminated by the kidneys

218
Q

What are the cardiovascular effects of BBs?

A

Reduce HR, inotropy, conduction velocity, and myocardial oxygen demand

219
Q

What is the significance of NON-selective BBs?

A

Increase airway resistance, in patients with asthma a cardio selective BB is the best option.

220
Q

What BBs antagonize the alpha-1 receptor?

A

Labetalol block beta to alpha 7:1

Carvedilol block beta to alpha 10:1

221
Q

How can BB overdose be treated?

A 
Glucagon
Calcium
PDE III inhibitors
Epinephrine
Isoproterenol 
Cardiac pacing
222
Q

Prop BB may reduce the risk of what? But increase the risk of what?

A

Reduce risk: cardiac morbidity and mortality

Increase: stroke, bradycardia, and hypotension

223
Q

Which BBs have LA properties? What is another name for this?

A

Membrane stabilizing properties is another way of saying that a drug has local anesthetic-like effects.
This effect reduces the rate of rise of the cardia action potential, however it probably only occurs when these drugs reach toxic levels.
Propranolol
Acebutolol

224
Q

What is intrinsic sympathomimetic activity? Which drugs exert this effect?

A

BB that exert a partial agonist effect, while simultaneously blocking other agonists that have a higher affinity for the beta receptor are said to have intrinsic sympathomimetic activity.
Labetalol
Pindolol

225
Q

List 4 alpha antagonists

A

Phenoxybenzamine
Phentolamine
Prazosin
Yohimbine

226
Q

Describe Phenoxybenzamine

A

Long acting, non-selective, noncompetitive antagonist of the alpha-1 and alpha-2 receptor.
Causes vasodilation by decreasing SVR.
Impairs the NE regulating effect of the presynaptic alpha-2 receptor -> reflex tachycardia.
Its primary role is to manage HTN in the patient with pheochromocytoma 0.5-1 mg/kg PO.
Side effects: orthostatic hypotension and nasal congestion.

227
Q

Describe phentolamine

A

Short-acting, non-selective, competitive antagonist of the alpha-1 and alpha-2 receptor.
It causes vasodilation by decreasing SVR.
It impairs the NE regulating effect of the presynaptic alpha-2 receptor -> reflex tachycardia.
Clinical uses include tx of pheochromocytoma or autonomic hyperreflexia 30-70 mcg/kg IV.
Can also be injected into tissue surrounding an infiltrated IV containing a vasoconstrictor 2.5-10 mg in 10mL diluent.

228
Q

Describe prazosin

A

Selective alpha-1 blocker.
Causes vasodilation by decreasing SVR.
Does not impact NE regulating effect of the presynaptic alpha-2 receptor so no reflex tachycardia.
Clinical uses: essential HTN, especially in patients with benign prostatic hypertrophy.

229
Q

Describe yohimbine

A

An herb that antagonizes the alpha-2 receptor.
Increases sympathetic tone by increasing NE release from the presynaptic nerve terminal.
Used to treat orthostatic hypotension.
Overdose leads to tachycardia and HTN.

Apex (46 decks)

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