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2-Pharm Exam 3 > Sympathomimetic Drugs > Flashcards

Sympathomimetic Drugs Flashcards

1
Q

Define sympathomimetics.

A

Drugs that activate adrenergic receptors

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2
Q

What are adrenergic agonists?

A

a group of drugs that mimic the action of endogenous norepinephrine and epinephrine

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3
Q

What is the origin of adrenergic agonists?

A

stem from a broad class of compounds known as catecholamines (“amines”) that function as neurotransmitters or hormones

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4
Q

What are considered sympathomimetics drugs (6)?

A

Synthetic catecholamines, synthetic noncatecholamines, selective β-2 adrenergic agonists, cardiac glycosides, phosphodiesterase inhibitors, calcium

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5
Q

What are naturally occurring catecholamines?

A

Epinephrine, Norepinephrine, Dopamine

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6
Q

Review pathway of catecholamine biosynthesis.

A
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7
Q

Review catecholamine synthesis at the cellular level.

A

Slide 6

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8
Q

Review sympathetic nervous system.

A

Slide 7.

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9
Q

What is the tissue location for Alpha 1 adrenergic receptors?

A
  • most vacular smooth muscle (innervated)
  • pupillary dilator muscle
  • Pilomotor smooth muscle
  • Prostate
  • Heart
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10
Q

What is the action for Alpha 1 adrenergic receptors?

A
  • Vasocontraction
  • dilates pupils (mydriasis)
  • erects hair
  • contraction
  • increases force of heart contraction
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11
Q

What is the tissue location for Alpha 2 adrenergic receptors?

A
  • Postsynaptic CNS adrenoceptors
  • Platelets
  • adrenergic and cholinergic nerve terminals (Presynaptic)
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12
Q

What is the actions for Alpha 2 adrenergic receptors?

A
  • decrease SNS outflow
  • Aggregation of platelets
  • inhibition of transmitter release
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13
Q

What is the location for beta 1 adrenergic receptors?

A
  • heart
  • kidney (juxtaglomerular cells)
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14
Q

What is the action for beta 1 adrenergic receptors?

A
  • increases HR
  • cardiac contractility
  • AV node conduction increase
  • inreases renin release
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15
Q

What is the location for beta 2 adrenergic receptors (not innervated)?

A
  • respiratory, uterine and vascular (skeletal muscle vessels and vessels to the liver) smooth muscle
  • skeletal muscle
  • human liver
  • heart
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16
Q

What is the action for beta 2 adrenergic receptors (not innervated)?

A
  • promotes smooth muscle relaxation
  • promotes potassium uptake
  • activates glycogenolysis= increased glucose
  • increases heart rate
  • increases cardiac contractility
  • increases AV nodal conduction
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17
Q

What is the action and location for Beta 3 adrenergic receptors (not innervated)?

A
  • Tissue: fat cells
  • Actions: activates lipolysis
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18
Q

What is the action and location for D1 adrenergic receptors (not innervated)?

A
  • Tissue: smooth muscle
  • Actions: dilates renal blood vessels
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19
Q

Review classification and comparactive pharmacology of sympathomimetics.

A
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20
Q

Review adrenoceptors diagram.

A
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21
Q

What is the etiology of epinephrine?

A

Fight or Flight neurotransmitter, Hormone secreted from the adrenal medulla

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22
Q

What is the metabolism of epinephrine?

A

metabolized by catechol-O-methyl transferase (COMT) and monoamine oxidase (MAO)

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23
Q

What are the properties of epinephrine?

A

Many clinical uses reflect its alpha, β-1, and β-2 properties

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24
Q

What is the location of epinephrine alpha receptors?

A

Alpha receptors mainly in cutaneous, splanchnic, renal vascular beds

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25
Q

What receptor target predominates at higher doses of epinephrine?

A

α-1 (vasoconstriction) predominates at higher doses versus β-2 (vasodilation - skeletal muscles)

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26
Q

What are the Beta 1 effects of epinephrine?

A

chronotropic and inotropic effects: Increases HR by accelerating the rate of spontaneous phase 4 depolarization which also increases likelihood of cardiac dysrhythmias

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27
Q

Describe the cardiac action potential cycle.

A
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28
Q

What are the kidney effects of epinephrine?

A

Decrease in renal blood blow; increased renin

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29
Q

Epinephrine is _____ potent compared to Norepinephrine.

A

2-10x more potent

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30
Q

What are the endocrine effects associated with Epinephrine?

A

Significant effects on metabolism (liver glycogenolysis; inhibition of insulin); hyperglycemia

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31
Q

Why is hypokalemia and dysrhythmias a concern with Epinephrine administration?

A

Movement of K+ into the cell (β-2 activates Na-K ATP pump in skeletal muscle) may later offset with stimulating K release from liver

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32
Q

What effect does Epinephrine have on the eye?

A

Mydriasis

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33
Q

What is the smooth muscle effects of Epinephrine?

A
  • β-adrenergic smooth muscle relaxation
  • Hepatosplanchnic vasoconstriction
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34
Q

What is the coagulation effects of Epinephrine?

A

Potent platelet aggregator; increase Factor V activity

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35
Q

Describe the dosing of Epinephrine.

A
  • 0.01-0.03 mcg/kg/min (beta effects)
  • 0.03-0.15 mcg/kg/min (alpha and beta)
  • 0.15-0.3 mcg/kg/min (alpha)
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36
Q

What is the onset of Epinephrine?

A

< 1min

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37
Q

When is the peak effect of Epinephrine seen?

A

peak 2-5 min

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38
Q

What is the duration of Epinephrine?

A

duration 5-10 min

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39
Q

What are the airway smooth muscle effects of Epinephrine (2)?

A
  1. B-2 receptor stimulation causes relaxation of bronchial smooth muscles
  2. B-2 receptor stimulation increases intracellular concentrations of cyclic AMP and decreases release of vasoactive mediators asso/w bronchial asthma
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40
Q

Epinephrine has the most significant effect on metabolism of all the __________

A

catecholamines

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41
Q

What is Beta 1 receptor stimulation from Epinephrine associated with?

A

Beta-1 receptor stimulation increases liver glycogenolysis (which results from activation of hepatic phosphorylase enzyme) and adipose tissue lipolysis (which results from activation of triglyceride lipase which accelerates breakdown of triglycerides to form free fatty acids & glycerol)

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42
Q

What is alpha 1 receptor stimulation from Epinephrine associated with?

A

Alpha-1 stimulation inhibits release of insulin

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43
Q

What does infusion of Epinephrine increase (5)?

A
  • increase plasma concentrations of glucose
  • increase cholesterol
  • increase phospholipids & LDLs
  • epi can also inhibit peripheral glucose uptake d/t inhibition of insulin secretion
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44
Q

What is the explanation for perioperative hyperglycemia associated with Epinephrine?

A

Release of endogenous epinephrine and the resulting glycogenolysis and inhibition of insulin secretion is most likely explanation

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45
Q

Review the clinical uses of epinephrine.

A
  • Life-threatening allergic reactions/anaphylaxis
  • Severe asthma
  • Bronchospasm
  • ACLS protocols
  • Hemodynamic instability
  • Promotes inotropy during CPB weaning
  • Sepsis
  • Additive to local anesthetics
  • Used in local anesthetics for field blocks to promote a bloodless surgical field
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46
Q

How does epinephrine treat hemodynamic instability?

A

promotes myocardial contractility & increases SVR

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47
Q

How does epinephrine help treat sepsis?

A

used as single agent or in combo with norepinephrine to maintain BP

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48
Q

What effect does epinephrine have when added to local anesthetics?

A

to decrease systemic absorption & prolong duration of action for regional anesthetics

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49
Q

Where is norepinephrine stored?

A

stored in postganglionic sympathetic nerve endings; immediate precursor to epinephrine

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50
Q

What does norepinephrine stimulate?

A

stimulates β-1 and α-1 adrenergic receptors

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51
Q

What is the comparison of norepinephrine and epinephrine?

A

Equal in potency to epi in β-1 but minimal β-2 effects

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52
Q

What is the primary MOA of norepinephrine?

A

Potent α-1 agonist (intense venous/arterial vasoconstriction except coronaries)

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53
Q

What is a potent side effect of norepinephrine potent a-1 agonist effect?

A

Can result in metabolic acidosis

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54
Q

What effect does norepinephrine show that is greater than epinephrine?

A

Greater than epi: SVR, B/P (the MAP increase, SV, CO result primarily by vasoconstriction than direct cardiac effects as epi)

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55
Q

What does norepinephrine lack?

A

Lacks the metabolic effects of epinephrine

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56
Q

What is the infuse dose of norepinephrine for refractory hypotension?

A
  • Infusions (Levophed) 2-16 mcg/min to treat refractory hypotension
  • Dose: 0.01-0.2 mcg/kg/min
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57
Q

What is the onset of norepinephrine?

A

Onset: 1 min

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58
Q

What is the peak of norepinephrine?

A

peak 1-2 min

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59
Q

What is the duration of norepinephrine?

A

2-10 min

60
Q

What is the half-life of norepinephrine?

A

1 minute

61
Q

What is the primary metabolism of norepinephrine?

A

Primary elimination is hepatic

62
Q

What is the minor metabolism of norepinephrine?

A

Minor metabolized by catechol-O-methyl transferase (COMT) and monoamine oxidase (MAO)

63
Q

What is the metabolite for norepinephrine? What is a possible marker for?

A

urinary metabolite vanillylmandelic acid (VMA)- urinary marker for possible pheochromocytoma

64
Q

What is a concern with norepinephrine?

A

Concerns with extravasation

65
Q

What is the first line agent for septic shock?

A

Used as a vasoconstrictor (1st line agent in septic shock)

66
Q

What population should norepinephrine be used with caution?

A

Caution with right heart failure (increase in venous return and increase in pulmonary artery pressure)

67
Q

Why is norepinephrine inotropic use limited?

A

Inotropic use limited by potent vasoconstriction

68
Q

What can norepinephrine cause?

A
  • Can cause tachycardia
  • Organ ischemia: end-organ vasoconstriction of renal, splanchnic and peripheral beds
69
Q

What must norepinephrine be used with?

A

Must be used with adequate hydration

70
Q

What is Dopamine a precursor to?

A

Immediate precursor to NE, Important neurotransmitter

71
Q

What does Dopamine regulate?

A

Regulates cardiac, vascular and renal function

72
Q

What receptors does Dopamine work at?

A

alpha, β, dopaminergic (1, 2, & 3)

73
Q

What is true about the administration of dopamine?

A

Effects cannot be predicted on dosing, must titrate to effect

74
Q

What is the dosing recommendations for Dopamine?

A
  • 1-2 mcg/kg/min (renal: D1; D2)
  • 2-10 mcg/kg/min (cardiac: beta)
  • 10-20 mcg/kg/min (vasopressor: alpha)
75
Q

What is the onset of Dopamine?

A

Onset 2-4 min

76
Q

What is the peak of Dopamine?

A

2-10 min

77
Q

What is the duration of Dopamine?

A

duration < 10 min

78
Q

What drug interactions occur with Dopamine?

A

Affected by tricyclics and MAOI’s

79
Q

What is the effects of Dopamine?

A
  • Less dysrhythmogenic than EPI but increase tachycardia
80
Q

What must Dopamine be mixed with?

A

Must reconstituted in D5W

81
Q

What is the precursor to Dopamine?

A

Immediate precursor is L-dopa (levodopa)

82
Q

What is the metabolism of Dopamine?

A

Metabolized by both COMT and MAO

83
Q

What are the clinical uses of Dopamine?

A

Clinical uses: to increase cardiac output in patients w/ decreased cardiac contractility, low systemic BP, & low urine output; can simultaneously increase myocardial contractility, renal blood flow, GFR, excretion of sodium, and UOP

84
Q

What side effect is most common with Dopamine?

A

Dysrhythmias more common

85
Q

What is the first line treatment for cardiogenic shock?

A

cardiogenic shock, norepi is still preferred and asso/w lower mortality rate

86
Q

What is true about the concept of “renal-dose” Dopamine?

A

dopamine’s effects based on dose alone are unpredictable; “renal-dose” dopamine has now been shown to be inaccurate and not efficacious in preventing acute renal failure and is no longer recommended for “renal protection”

87
Q

What are the CV effects of Dopamine?

A

tachycardia, potential ventricular dysrhythmias, may predispose to myocardial ischemia d/t tachycardia, increasing contractility, increasing afterload, & precipitating coronary artery vasospasm, increases peripheral vascular resistance and PAPs

88
Q

What can Dopamine predispose patients to and why?

A

myocardial ischemia d/t tachycardia

89
Q

What is unqiue about Dopamine?

A
  • Unique in being able to increase CO, renal blood blow, GFR, excretion of Na, and urine output
90
Q

What can dopamine be used in conjunction with? What effect does this combination have?

A

May be used in conjunction with dobutamine (afterload reduction from skeletal and cutaneous beds)

91
Q

Describe the renal effects of dopamine.

A
  • Direct and indirect renal effects
  • diuretic
  • Activation of D2 in inner medullary collecting ducts stimulates PGE2 which antagonizes ADH, aldosterone
92
Q

There is ___________ renal protection for “renal dose dopamine” for at risk patients- can be detrimental.

A

No proven

93
Q

What is Isoproterenol?

A

Synthetic catecholamine- potent β1 and β2

94
Q

What is the infusion dose of Isoproterenol?

A
  • 1-5 mcg/min (infusion)
  • Nagelhout 0.015-0.15 mcg/kg/min
95
Q

What is the effect of Isoproterenol?

A
  • Decreased diastolic pressure
  • increased HR
  • cardiac dysrhythmias lead to decrease in coronary blood flow at same time of increased demands with HR and contractility
96
Q

What is an negative effect associated with Isoproterenol? Why?

A
  • lead to ischemia
  • cardiac dysrhythmias lead to decrease in coronary blood flow at same time of increased demands with HR and contractility
97
Q

What is the clinical uses for Isoproterenol?

A
  • heart block
  • increase heart rate for pacemaker and ablation procedures
  • Decrease pulmonary HTN for RV dysfunction
98
Q

What is Dobutamine?

A

Synthetic catecholamine: derived from isoproterenol racemic mixture

99
Q

What are the properties of Dobutamine?

A

Potent β1, weak β2 adrenergic activity with alpha at higher doses

100
Q

What is the MOA of Dobutamine?

A

Increase intracellular Ca++ (inotrope)

101
Q

What is the main clinical properites of Dobutamine?

A
  • Main clinical use is an inotrope as lacks significant vasoconstriction
  • Chronotropic at SA and AV node (more at higher doses)
102
Q

What can dobutamine increase? What effect can this have on patients with heart failure?

A

Increase in myocardial consumption but may be reduced with heart failure as a result of improved contractility, LVEDP, and decreased wall tension

103
Q

What hemodynamic reductions occur with Dobutamine?

A

Modest reductions in pulmonary artery pressure and vascular resistance (β2)

104
Q

What can Dobutamine worsen?

A

Can worsen VQ mismatching

105
Q

What effect does Dobutamine have coronary artery vessels?

A

Coronary artery dilation (sometimes used w/dopamine)

106
Q

What receptors does Dobutamine not work on?

A
  • Does not work on dopamine receptors
107
Q

What is the dose of Dobutamine?

A

Dose: 2-20 mcg/kg/min

108
Q

Why is Dobutamine used for CHF and weaning off bypass?

A

Increase myocardial contractility (β1 and alpha 1), used for CHF and weaning off bypass

109
Q

How can Dobutamine contribute to heat loss?

A

Modest peripheral dilation (β2)- can contribute to heat loss- vasodilation limited at higher doses

110
Q

What test can Dobutamine be used for?

A

Dobutamine stress tests for ischemia

111
Q

What are the most common hemodynamic adverse effects of Dobutamine?

A

tachycardia, tachydysrhythmias

112
Q

Compare and contrast dopamine and dobutamine.

A
113
Q

What are the properties of Ephedrine?

A
  • Direct stimulating alpha and β-adrenergic receptors
  • Indirect by stimulating release of endogenous NE
114
Q

What is the onset of Ephedrine?

A

Onset < 1 min

115
Q

What is the peak of Ephedrine?

A

peak 2-5 min

116
Q

What is the duration of Ephedrine?

A

duration 5-10 min

117
Q

What is the metabolism of Ephedrine?

A

Up to 40% unchanged in urine; some deaminated by MAO in liver

118
Q

What effect does Ephedrine have on blood sugar?

A

Does not induce hyperglycemia

119
Q

What effect does Ephedrine have on the eyes?

A

Mydriasis

120
Q

What is the common clinical use of Ephedrine?

A

treat anesthesia-related hypotension

121
Q

What are the effects of Ephedrine?

A

Has antiemetic effects, used for asthma, decongestant

122
Q

What is the formularies for Ephedrine?

A

Given IV, IM, PO

123
Q

Why is Ephedrine not prefered for pregnant women?

A

Replaced by phenylephrine in parturients (achieves a higher umbilical pH)

124
Q

What are the CV effects of Ephedrine?

A

CV effects similar to epinephrine: less intense and last longer

  • Increase in BP, HR, cardiac output
125
Q

What are the boluses doses for Ephedrine?

A

5-10 mg boluses

126
Q

What are the effects of Ephedrine?

A
  • Renal and splanchnic blood flow decreased; coronary and skeletal increased
127
Q

What receptor leads to the CV effects of Ephedrine?

A

CV effects primarily via β1 receptors (with β-blockage, resembles more alpha-adrenergic stimulation)

128
Q

What is a potential issue with Ephedrine?

A

Tachyphylaxis can be an issue

129
Q

What is Phenylephrine similar to?

A

Mimics the effects of NE but less potent and longer lasting

130
Q

What is the properties of Phenylephrine?

A

Direct alpha-1 (mostly venous vasoconstriction)

131
Q

What is Phenylephrine used for?

A

Uses for anesthesia-induced hypotension (example: regional blockade, inhaled anesthetics, etc

132
Q

What are the cardiac effects of Phenylephrine?

A
  • CNS stimulation minimal (advantageous for patients that you wish to avoid increased HR such aortic stenosis)
  • Can result in a reflex baroceptor response (decreased HR)
  • The increase in afterload and drop in HR can decrease CO
133
Q

What is the dose of Phenylephrine?

A

Boluses 50- 100 mcg, infusions 20-100 mcg/min (0.15-0.75 mcg/kg/min per Nagelhout)

134
Q

What is the relationship between potassium and Phenylephrine?

A

Concurrent K loading with a phenylephrine drip can raise serum K even higher

135
Q

What can an inadvertent overdose of Phenylephrine cause?

A
  • may be accentuated with β blockade
  • can result in pulmonary edema and irreversible CV collapse
136
Q

Is phenylephrine overdose a problem in the OR?

A

Usually not a problem in the OR (overshoot in HTN transient)

137
Q

What issue has occurred with Phenylephrine when given given in the OR?

A

Amps of undiluted phenylephrine have been given in the OR- mediation error!

138
Q

What are the clinical manifestations of Phenylephrine overdose?

A

severe HTN, asystole, pulmonary edema, CV collapse

139
Q

What is the treatment for phenylephrine-induced hypertensive crisis?

A
  • with a B-adrenergic blocking drug is contraindicated
  • Best to treat with vasodilators such as NTG, SNP, phentolamine
140
Q

What is the drug dilutition process for ephedrine?

A
  • Ephedrine: 50mg/1mL ampule (typical concentration of ampule located in anesthesia drug pyxis/drug cart); usual dose = 5mg - 10mg IV bolus
  • Obtain 5mL syringe, draw up 4mL NS, then draw up 1mL (50mg) of ephedrine from ampule: new diluted concentration = 10mg/1mL
141
Q

What is important to do about all medications in the OR?

A

LABEL SYRINGE W/CORRECT DRUG LABLE AND CONCENTRATION!

142
Q

What is the typical dose of phenylephrine?

A

usual dose = 50mcg - 100mcg IV bolus

143
Q

What is the typical concentration of phenylephrine in the OR?

A

Phenylephrine (Neosynephrine): 10mg/1mL vial (typical concentration of vial located in anesthesia drug pyxis/drug card (this concentration is 10,000mcg!)

144
Q

What is the drug dilution process of phenylephrine?

A
  • Obtain 10mL syringe, draw up 9mL NS, then draw up 1mL (10mg) of phenylephrine from vial; this concentration is now 1mg (1000mcg)/1mL - ***label this syringe with correct concentration: 1mg/1mL – this concentration still needs to be diluted once again
  • Obtain another 10mL syringe, draw up 9mL NS, then put 1mL of the 1mg (1000mcg)/1mL concentration into this syringe; this will produce a new diluted concentration = 100mcg/1mL
  • This is called a double wash or double dilution technique
145
Q

What is the alternative drug dilution for phenylephrine?

A

Alternatively, can put 1-vial (10mg) into 250mL NS bag = 40mcg/1mL (2-vials into 250mL NS bag = 80mcg/1mL)

2-Pharm Exam 3 (14 decks)

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