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S5 - Anesthesia Pharm II - Test 2 > Sympathomimetics & Agonists > Flashcards

Sympathomimetics & Agonists Flashcards

1
Q

endogenous catecholamines

A
  • epinephrine
  • norepinephrine
  • dopamine
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2
Q

synthetic catecholamines

A
  • isoproterenol
  • dobutamine
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3
Q

synthetic noncatecholamines

A
  • ephedrine
  • amphetamine
  • phenylephrine
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4
Q

selective alpha-2 adrenergic agonists

A
  • clonidine
  • dexmedetomidine
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5
Q

selective beta-2 adrenergic agonists

A
  • albuterol
  • terbutaline
  • ritodrine
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6
Q

CV effects of SNS stimulation

A
  • increased HR
  • increased BP
  • increased contractility
  • susceptibility to ectopy
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7
Q

pulm effects of SNS stimulation

A

bronchodilation

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8
Q

effects of SNS stimulation on vasculature

A
  • vasodilation/improved blood flow to skeletal muscle
  • vasoconstriction/decreased flow to skin, GI, renal systems
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9
Q

how does SNS stimulation impact CNS

A

increased cognition

(except alpha-2 stim, which inhibits)

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10
Q

endocrine effects of SNS stimulation

A
  • lipolysis
  • glycogenolysis
  • increased blood sugar
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11
Q

how are sympathomimetics used in regional anesthesia

A
  • increase contractility or vascular tone r/t sympathetic blockade
  • to prolong regionals
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12
Q

clinical uses of sympathomimetics (5)

A
  • treat sympathetic blockade from regional blocks
  • prolong regionals
  • increase or maintain BP/prevent tissue ischemia while hypovolemia corrected
  • bronchodilation in asthmatic
  • to manage anaphylaxis
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13
Q

how does SNS stimulation affect coagulation

A

increased rate of coagulation

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14
Q

how do alpha agonists vs. alpha blockers affect your pupils

(table 13.2)

A
  • agonist: mydriasis - dilation
  • blocker: miosis (slight) - constriction

one of these days i’ll remember what these are

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15
Q

how do beta-agonists vs. blockers impact eyeballs

(table 13.2)

A
  • agonists: no clinical effect
  • blockers: decreased IOP
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16
Q

how do alpha agonists vs. blockers impact HR

(table 13.2)

A
  • agonists: reflex bradycardia
  • blockers: reflex tachycardia
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17
Q

how do beta-agonists vs. blockers impact HR

(table 13.2)

A
  • agonists: increased HR
  • blockers: decreased HR
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18
Q

how do beta agonists vs. blockers impact contractility

(table 13.2)

A
  • agonists: increased
  • blockers: decreased
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19
Q

how do beta agonists vs. blockers impact conduction velocity (table 13.2)

A
  • agonists: increased
  • blockers: decreased
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20
Q

how do alpha agonists vs. blockers impact blood vessels

(table 13.2)

A
  • agonists: constriction
  • blockers: dilation
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21
Q

how do beta agonists vs. blockers impact HR

(table 13.2)

A
  • agonists: increase
  • blockers: decrease
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22
Q

how do cholinergics affect:

  • eyes
  • heart rate, contractility, and conduction velocity
  • blood vessels
  • lungs
  • GI
  • uterus
  • liver

(table 13.2)

A
  • eyes: miosis and decreased IOP
  • dec. HR & conduction velocity
  • slightly dec. contractility
  • bronchoconstriction
  • increased GI motility and secretion
  • no effect on blood vessels, uterus, liver
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23
Q

how do beta agonists vs. blockers impact blood vessels

(table 13.2)

A
  • agonists: dilation
  • blockers: constriction
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24
Q

how do alpha and beta agonists impact the GI tract vs. alpha and beta blockers?

(table 13.2)

A
  • alpha & beta agonists decrease motility and secretion
  • alpha blockers - no effect
  • beta blockers - GI relaxation
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25
Q

how do alpha and beta agonists impact the uterus?

(table 13.2)

A
  • alpha agonist = contraction
  • beta agonist = relaxation
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26
Q

how does a sympathomimetic have direct effects?

which ones have this MOA?

A

bind to receptors and activate directly

catecholamines & phenylephrine

(both endogenous and exogenous catecholamines)

epi, NE, DA, isoproterenol, dobutamine + phenylephrine

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27
Q

how does a sympathomimetic have indirect effects?

what drugs fall in these categories?

A
  • cause release of NE from postganglionic sympathetic nerve endings (amphetamine)

or

  • block reuptake of NE to keep more in circulation (cocaine, TCAs)
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28
Q

patients who may not respond to indirect-acting sympathomimetics

A
  • denervation (heart transplant)
  • depletion (sepsis)
  • pt taking MAOIs
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29
Q

what is tachyphylaxis?

A

the greater the concentration of the sympathomimetic, the lower the number of receptors in tissues or decreased response

(need more drug for desired response)

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30
Q

how can increased concentrations of norepi result in tachyphylaxis?

A

fewer adrenergic receptors on cell membranes

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31
Q

how can albuterol lead to tachyphylaxis?

A

chronic treatment causes the number of beta 2 receptors to decrease (down-regulation)

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32
Q

which sympatomimetic given for BP has a big problem with tachyphylaxis?

A

ephedrine - might give 5mg and then when BP drops 10 min later have to give 10 mg for same resposne as before

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33
Q

what mechanism is the most responsible for termination of catecholamine effect?

A

uptake back into post-ganglionic sympathetic nerve endings

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34
Q

why are catecholamines short-lived?

A

metabolism by MAO and COMT

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35
Q

the lungs are responsible for filtering some portion of what 2 catecholamines

A

norepi & dopamine

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36
Q

metabolism of noncatecholamine sympathomimetics

A
  • inactiated by MAO only
  • no reuptake
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37
Q

which tends to last longer - catecholamines or noncatecholamines?

A

noncatecholamines

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38
Q

which receptors does epi act on

A

alpha and beta (dose dependent)

α1 = α2

β1 = β2

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39
Q

which sympathomimetic is the most potent alpha stimulant

A

epi

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40
Q

why is SQ epi absorbed more slowly than IV?

A

epi-induced vasoconstriction

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41
Q

does epi have cerebral effects?

A

no - poorly lipid-soluble, doesn’t cross BBB

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42
Q

where is epi synthesized, stored, and released from?

(Flood)

A

adrenal medulla

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43
Q

what effect of high dose epi can contribute to mortality in anaphylaxis?

A

alpha stimulation

make sure you give the correct dose and concentration :)

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44
Q

clinical uses of epi (4)

A
  • decrease absorption and prolong duration of LAs
  • treat anaphylaxis
  • treat cardiac arrest
  • increase contractility
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45
Q

what is considered a low-dose epi gtt?

receptors affected & their actions

A

.01-.03 mcg/kg/min mcg/min

  • β1: increase HR, BP, CO, inotropy
  • β2: decreased DBP d/t decreased SVR
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46
Q

why might low-dose epi decrease coronary perfusion?

A

decreased DBP

per Flood, epi enhances coronary blood flow (I guess at higher doses, doesn’t say)

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47
Q

net vascular effect of low-dose epi gtt

A
  • distribution of blood flow to skeletal muscle
  • decreased SVR
  • decreased RBF
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48
Q

moderate-dose epi gtt

receptors affected & their actions

A

.03-1.5 mcg/kg/min

or 4 mcg/min according to that stupid PDA sheet

  • β1 - increased SBP, HR, CO, inotropy
  • I guess some α too
  • increased venous return
  • increased susceptibility to arrhythmias mixed with α
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49
Q

why does moderate dose epi cause increased venous return?

A

vasoconstriction r/t high concentration of α receptors in venous vascualture

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50
Q

large dose epi gtt

receptors impacted

A

10-20 mcg/min

both beta & alpha-1

(was this the answer on the test?)

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51
Q

predominant receptor activated with high dose epi gtts

what are its effects?

A

alpha

vasoconstriction of skin, mucosa, hepatorenal vessels

decreased RBF

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52
Q

SVT is common with what dose epi gtt

A

high (>0.15 mcg/kg/min)

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53
Q

what determines epi’s overall effect on blood flow to a specific organ?

(Flood)

A

the relative balance of alpha1 & beta2 receptors in the vasculature of particular organ

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54
Q

when might epi cause bronchonstriction?

A

in a pt taking beta-blockers (especially nonselective) d/t unopposed alpha1 effects

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55
Q

how does epi affect bronchial smooth muscle?

this is due to which receptor?

A

relaxed (beta 2)

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56
Q

how does epi affect blood sugar

A

increases

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57
Q

metabolic effects of beta 2 activation with epi

Flood says its beta 1 so idk

A

increased glycogenolysis and lipolysis

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58
Q

metabolic effects of alpha-2 stimulation with epi

again, Flood says alpha 1

A

inhibits release of insulin (hyperglycemia)

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59
Q

electrolyte abnormality that may be seen with epi

why?

A

hypokalemia

stress-induced d/t activation of Na-K pump on RBCs (beta 2)

buttt hyperkalemia initially because it follows glucose out of the cell or something like that

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60
Q

ocular effects of epi

which receptor is reponsible

A

alpha-1

  • contraction of radial msucles of iris = pupil dilation
  • contraction of orbital muscles = eye bulging
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61
Q

why is BP generally increased with epi?

(Flood)

A

increase in cardiac index as well as increase in SVR

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62
Q

affects of epi on HR

(Flood)

A

initial tachycardia may be followed by decrease d/t baroreceptor reflexes

increased HR by accelerating rate of spontaneous 4 depolarization (also inc. dysrhythmias)

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63
Q

which catecholamine has the most significant metabolic effects?

A

epi

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64
Q

what is the most likely explanation for periop hyperglycemia?

(Flood)

A

release of endogenous epi resulting in glycogenolysis and inhibition of insulin secretion

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65
Q

what’s the explanation for why beta 2 agonist effects are responsible for hypokalemia?

(Flood)

A

a nonselective beta blocker (propranolol) can prevent hypokalemia but a selective beta-1 blocker (atenolol) can’t

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66
Q

how does epi affect GI/GU smooth muscle

A
  • relaxation of GI smooth muscle
  • beta - relaxation of bladder detrusor muscle
  • alpha1- contracts bladder sphincter
  • (slowed GI motility and urinary retention)
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67
Q

which receptors does norepi activate?

A

potent alpha, beta-1

α1= α2; β1>>β2

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68
Q

clinical use of norepi

A

vasoconstriction to increase SVR and BP

(ex - sepsis, coming off bypass)

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69
Q

why is it important to have a NE infiltration protocol?

(lol we def didnt have this)

A

infiltration of NE into sub-q tissue can cause necrosis d/t vasoconstriction

70
Q

which endogenous neurotransmitter is synthesized and stored in postganglionic sympathetic nerve endings and released with sympathetic nerve stimulation?

(Flood)

A

norepi

71
Q

alpha 1 effects of norepi

A
  • vasoconstriction of arterial and venous vessels of all vascular beds
  • increased SVR, MAP
  • increased venous return (at lower doses)
  • decreased HR
72
Q

venous return with higher vs. lower doses of NE

A

lower doses - increased

higher - decreased d/t constriction proximal to capillary bed (causes fluid trapping, leakage into interstitial space)

73
Q

what receptor does “low dose” norepi work on?

what are the effects of activation?

A

beta 1 selective

increased HR, increased inotropy

74
Q

receptors activated by “high dose” norepi

effects of activation

A

α1, α2, β1

increased SVR, BP

decreased HR (baroreceptor reflex)

75
Q

dose range of norepi gtt

A

0.02 - 0.4 mcg/kg/min

76
Q

according to Flood, norepi causes potent arterial and venous vasoconstriction in all vascular beds except

A

coronary arteries

77
Q

why might you see minimal changes in HR with a norepi gtt?

(Flood)

A

baroreceptor reflexes triggered by arterial vasoconstriction are counteracted by beta1 mediated increased HR

78
Q

how does norepi primarily increase MAP?

(Flood)

A

vasoconstriction

(to lesser degree by increased SV & CO)

79
Q

what effect do epi and norepi have on coronary arteries?

(Flood)

A

both dilate

80
Q

what are the metabolic effects of norepi?

A

really aren’t any

81
Q

why are resp effects not really seen with norepi?

A

no beta 2 effects

82
Q

what conditions is norepi ideal for?

when should it be used v cautiously?

A
  • ideal for sepsis or post bypass with decreased SVR
  • caution/avoid in pts with cardiogenic shock or LV failure due to increased afterload and mycocardial O2 demands
83
Q

which neurotransmitter is the immediate precursor to norepi

(Flood)

A

dopamine

84
Q

which catecholamine is described:

endogenous neurotransmitter in the central and peripheral nervous systems

A

dopamine

85
Q

receptors activated by dopamine

A

D1=D2 >> β >> α

86
Q

what dose of dopamine has an indirect sympathomimetic effect via NE release?

A

moderate (2-10 mcg/kg/min)

87
Q

what is a low dose dopamine gtt?

what receptors are activated?

A

0.5-3 mcg/kg/min

or 1-2 mcg/kg/min depending on who ya ask

D1 (Flood says D2 also)

88
Q

moderate dopamine gtt dose

what receptors are activated & where

A

3-10 mcg/kg/min

beta-1 in the heart

89
Q

CV effects of low dose dopamine gtt

A

vasodilation

may have decreased BP

Flood: diuresis, natriuresis; may have reflex increased HR d/t decreased DBP

90
Q

why does moderate dose dopamine increase CO?

A

beta-1 activation, increased inotropy

Per Flood, also: increased chronotropy, vasodilation, afterload reduction, increased stroke volume

91
Q

what is a high-dose dopamine gtt?

what receptor(s) does it act on & where?

A

10-20 mcg/kg/min

alpha-1 in peripheral vessels

92
Q

effects of alpha-1 stimulation in vascular smooth muscle with high-dose dopamine gtt?

(Flood)

A
  • arterial and venous vasoconstriction
  • increased SVR
  • increased BP
93
Q

why might dopamine be an unreliable mechanism for increasing CO in pts with chronic heart failure?

(Flood)

A

a portion of dopamine’s effect is d/t stimulation of endogenous NE release - may not work well for pts with depleted catecholamine stores

94
Q

did giving our kidney transplant patients dopamine for BP and maintaining UOP help with M&M?

A

nope, apparently not :)

95
Q

why might you have a hard time weaning a pt off the vent while they’re on a dopamine gtt?

A

inhibits ventilatory response to arterial hypoxemia

96
Q

why might a dopamine gtt increase susceptibility to arrhythmias?

A

NE release

(still less susceptible than with epi)

97
Q

how does a dopamine gtt affect myocardial O2 supply and demand

A

may make demand > supply

98
Q

indications for a dopamine gtt

A
  • increase CO in pts with low BP, inc. atrial filling pressures, and low UOP
  • “renal dose dopamine” though studies show this is a waste of time
98
Q

indications for a dopamine gtt

A
  • increase CO in pts with low BP, inc. atrial filling pressures, and low UOP
  • “renal dose dopamine” though studies show this is a waste of time
99
Q

renal effects of dopamine gtt

A

increased:

  • RBF
  • GFR
  • UOP
  • Na+ excretion (inhibits aldosterone)
100
Q

3 things that antagonize renal effects of a dopamine gtt

A
  1. arterial hypoxemia
  2. droperidol
  3. reglan
101
Q

which 2 catecholamines are useful when combined together?

why?

(Flood but I think she mentioned this)

A
  • dopamine & dobutamine
  • both are inotropic but each dilates different vascular beds
  • objective is to increase coronary perfusion and CO while decreasing afterload
102
Q

which catecholamine can depress the immune system?

(Flood)

A

dopamine

there are a bunch more details in the book but skipping since she didnt mention this

103
Q

why does dopamine interfere with ventilatory response to hypoxemia & hypercarbia?

(Flood)

A

inhibitory actions at carotid bodies

104
Q

which catecholamine is unique in that can simultaneously increase contractility, RBF, Na+ excretion, and UOP?

(Flood)

A

dopamine

105
Q

which receptors does dobutamine work on

A

beta 1 > beta 2 >>>>> alpha

106
Q

dose used for dobutamine gtt

A

0.5-15 mcg/kg/min

2-10mcg/kg/min (from PDA)

107
Q

how does dobutamine cause increase CO?

(Flood)

A

primarily by increase in SV

108
Q

how does dobutamine affect SVR and PVR?

A

both decrease

109
Q

how does dobutamine impact myocardial O2 demand vs dopamine

A

dobutamine - minimal increase in O2 demand, less imbalance in myocardial O2 supply/demand

110
Q

how does dobutamine affect coronaries?

A

coronary dilation = increased supply (balances increased demand)

111
Q

how does dobutamine affect renal perfusion?

A

does not cause renal vasodilation, but can still improve renal perfusion via increased CO

112
Q

adverse effects of high dose dobutamine

A

increased HR, dysrhythmias

113
Q

respiratory affects of dobutamine

(Flood)

A

pulmonary vasodilation may worsen V/Q mismatch

inhibits HPV

114
Q

indication for a dobutamine gtt

A

increase CO in pts with CHF

115
Q

indication for a dobutamine gtt

A

increase CO in pts with CHF

116
Q

when is it beneficial to combine dobutamine with a vasodilator?

A

significant LV failure - to decrease SVR and improve CO

117
Q

which catecholamine is the most potent beta-agonist

A

isoproterenol

118
Q

beta 1 effects of isoproterenol

A
  • increased HR
  • inotropy
  • susceptibility to dysrhythmias
119
Q

beta 2 effects of isoproterenol

A
  • decreased SVR
  • vasodilation in skeletal muscle
120
Q

overall CV effects of isoproterenol

A

decreased MAP, decreased coronary blood flow, increasd O2 demand

121
Q

why is isoproterenol no good for pts with CAD

A

decreased coronary blood flow r/t decreased MAP and increased HR

122
Q

clinical uses of isoproterenol

A
  • increase HR in pts with heart block
  • induce dysrhythmias in cath lab
  • chemical pacemaker
  • pHTN and RV dysfunction (Flood)
123
Q

how does ephedrine have both direct and indirect effects?

A
  • direct effect on beta receptors
  • indirect effect on alpha receptors from the NE release
124
Q

duration of ephedrine

A

prolonged - slow inactivation & excretion

125
Q

initial vs subsequent IV dose of ephedrine

A

general dose: 2.5 - 10 mg

increase subsequent doses to obtain same response (tachyphylaxis)

126
Q

beta 1 effects of ephedrine

A
  • increased SBP and DBP
  • increased HR
  • increased CO
  • increased contractility (principle effect)
127
Q

alpha 1 effects of ephedrine

A
  • vasoconstriction
  • decreased renal & splanchnic flow
128
Q

beta 2 effects of ephedrine

A
  • vasodilation
  • increased coronary artery & skeletal muscle flow
129
Q

potency of ephedrine vs epi

A

epi is 250x more potent

130
Q

effects of epi vs ephedrine on DBP

A

epi may decrease DBP

ephedrine increases DBP

131
Q

is SVR affected by ephedrine? why or why not?

A

may not change much as vasodilation of some vessels will offset vasoconstriciton of others

132
Q

effects of ephedrine if given to a patient on beta blockers

A

response may resemble alpha agonist

133
Q

CNS effects of ephedrine

A

crosses BBB, increases MAC

134
Q

respiratory effects of ephedrine

A

beta 2 stim = bronchodilation

135
Q

why is ephedrine maybe not the drug of choice for preggos (according to TC and not MBG, who doesn’t know shit)

A

higher incidence of fetal acidosis vs. phenylephrine

136
Q

indications for ephedrine

A
  • temporarily increase BP d/t sympathetic blockade from neuraxial
  • hypotension d/t inhaled or IV anesthesia
  • bronchodilation
  • nasal congestion
  • antiemetic (0.5 mg/kg IM)
137
Q

direct and indirect effects of phenylephrine

A
  • mostly direct effects - alpha 1
  • very small indirect effects - can evoke NE release
138
Q

CV effects of alpha 1 stimulation with phenylephrine

A
  • increased BP
  • susceptibility to dysrhythmias
  • decreased CO d/t increased afterload or reflex bradycardia
  • decreased blood flow to kidneys, skin, splanchnic system
139
Q

how does phenylephrine affect coronaries

A

increased flow d/t prolonged diastolic time

140
Q

CNS effect of phenylephrine

A

decreased cerebral O2 sat

141
Q

indications for phenylephrine

A
  • increase BP d/t sympathetic blockade or vasodilation (volatiles)
  • increase BP in pts with CAD or aortic stenosis
  • maintain BP during carotid endarterectomy
  • slow HR r/t SVT
  • nasal decongestant
  • prolong duration of spinal anesthesia
142
Q

as a rule, what is the preferred agent for treatment of hypotension in CAD?

A

phenylephrine

(increased coronary perfusion without increased HR)

143
Q

how does a phenylephrine gtt impact concurrent potassium supplementation?

(Flood)

A

stimulation of alpha receptors during acute K+ loading interferes with movement of K+ ions across cell membranes

(admin. in absence of acute K+ load doesn’t change plasma K+ concentrations)

144
Q

MOA of clonidine

A

centrally acting partial alpha 2 agonist

145
Q

CNS effects of clonidine

A
  • decreased sympathetic output from CNS
  • hyperpolarizes cell membranes in CNS (potential to decrease MAC up to 50%)
145
Q

CNS effects of clonidine

A
  • decreased sympathetic output from CNS
  • hyperpolarizes cell membranes in CNS (potential to decrease MAC up to 50%)
146
Q

does clonidine cause vasodilation or constriction?

why?

A

vasodilation via stimulation of alpha2 inhibitory neurons in medullary vasomotor center

147
Q

how does clonidine affect neuraxial blocks?

A

inhibits substance P release, blunts perception of noxious stimuli

148
Q

CV effects of clonidine

A

dose-dependent decreases in BP, HR, and CO

149
Q

does clonidine affect renal blood flow?

A

maintained, but could still have decreased renal perfusion r/t decreased BP/CO

150
Q

why is clonidine no longer used as a premed?

A

most common side effect is sedation

also issues with BP, HR, CO changes

151
Q

why might bradycardia with clonidine require treatment with an anticholinergic?

A

decreased catecholamine levels

152
Q

adverse effect of suddenly stopping clonidine

A

rebound HTN

153
Q

indications of clonidine

A
  • neuraxial analgesia
  • use as a premed
  • prolongs effects of regional anesthesia
  • to diagnose pheochromocytoma
  • treat opioid withdrawal
  • treat shivering
154
Q

benefits of clonidine in neuraxial techniques

A

analgesia without ventilatory depression, pruritis, N/V, delayed gastric emptying

155
Q

uses of clonidine as a premed

(which isn’t really done anymore)

A
  • blunts response from DL
  • decreased lability of BP/HR ((((this seems opposite of why she said we dont use it)))
  • decreases catecholamine concentrations
  • decreases MAC and IV induction requirements
  • accentuates ephedrine
  • decreases incidence of myocardial ischemic episodes in pts with CAD
156
Q

how is clonidine used to diagnose pheochromocytoma?

A

if reduced release of catecholamines from nerve endings is seen with clonidine admin (whatever that means), the patient doesn’t have pheo

157
Q

why is clonidine considered a sympatholitic?

A

decreased release of NE

158
Q

which agent can be used to treat shivering? why?

A

clonidine - inhibits central thermoregulatory control

159
Q

MOA of dexmedetomidine

(Precedex)

A

alpha 2 agonst

160
Q

AE of rapid precedex admin

A

HTN

161
Q

recommended loading dose and gtt maintenance rate of precedex

A

loading: 1 mcg/kg over 10 min
gtt: 0.2-0.7 mcg/kg/hr

162
Q

how does precedex affect MAC?

A

decreases > 90%

163
Q

which has an increased likelihood of hypotension and hypothermia - precedex or clonidine?

A

precedex

164
Q

withdrawal symptoms may be seen after precedex is used for how long?

A

24 hours

165
Q

a large IV bolus of precedex resembles what catecholamine? why?

(Flood)

A

0.25-1 mcg/kg over 3-5 min results in paradoxical HTN with decreased HR

resembles phenylephrine - resultant effect of crossover alpha 1 stim.

166
Q

MOA of albuterol

A

selective beta 2 agonist

beta 2 >> beta 1 >>>>> alpha

167
Q

2 uses of albuterol

A
  • prevent/treat bronchoconstriction in asthma or COPD
  • stop premature uterine contractions
168
Q

why might you want to avoid albuterol in hypotensive pts?

A

vasodilation can offset protective vasoconstriction

169
Q

side effects of albuterol r/t beta 2 receptors on skeletal muscles

A

tremors

170
Q

lab values that might change with acute albuterol admin

A
  • hyperglycemia
  • hypokalemia
  • hypomagnesemia

S5 - Anesthesia Pharm II - Test 2 (7 decks)

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