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cardiac pharm - adrenergic agents Flashcards

1
Q

what are the CNS neurotransmitters

A

epi, NE, dopamine, serotonin, GABA, Ach

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2
Q

what are the natural catecholamines

A

epi, norepi, dopamine

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3
Q

what are the synthetic catecholamines

A

isoproterenol and dobutamine

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4
Q

what is the potency of catechols at alpha receptors

A

NE>epi>isoproterenol

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5
Q

what is the potency of catecholamines at the beta receptors

A

isoproterenol > epi > norepi

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6
Q

where are alpha 1 receptors found and what does activation cause

A

vasculature, gut, heart, glands

activation causes vasoconstriction and relaxation of the GI tract

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7
Q

where are alpha 2 receptors found and what does activation cause

A

found pre-synaptically in peripheral vascular smooth muscle, coronaries, brain

activation causes inhibition of NE release and inhibition of SNS outflow leading to decreased BP and HR and inhibition of CNS activity

found post-synaptically in coronaries, CNS

activation causes constriction and sedation and analgesia

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8
Q

where are beta one receptors found and what does activation cause

A

found in myocardium, SA node, ventricular conduction system, coronaries, kidney.

activation causes increase in inotropy, chronotropy, myocardial conduction velocity, coronary relaxation, and renin release

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9
Q

where are beta 2 receptors found and what does activation cause

A

found in vasc, bronchial, and uterine smooth muscle, smooth muscle of skin, myocardium, coronaries, kidneys, GI tract

causes vasodilation, bronchodilation, uterine relaxation, gluconeogenesis, insulin release, potassium uptake by cells

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10
Q

what are the 2 synthetic non-catechols

A

ephedrine and phenylephrine

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11
Q

is ephedrine indirect or direct acting

A

both

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12
Q

is phenylephrine direct or indirect acting

A

direct

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13
Q

what is a side effect of repeated doses of ephedrine

A

tachyphylaxis (aka rapidly diminishing response to successive doses of drug, rendering it less effective)

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14
Q

what is a side effect of phenylephrine related to HR

A

reflex bradycardia

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15
Q

what is the pressor of choice for OB

A

phenylephrine

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16
Q

describe alpha1 second messenger/output

A
  1. phospholipase C activated
  2. you get inositol triphosphate (IP3) and diacylglycerol (DAG)
  3. activates protein kinase C which increases free Ca2+
  4. Calmodulin activation = increased CB formation = contraction

vasoconstriction

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17
Q

describe alpha 2 second messenger/output

A
  1. inhibits adenylate cyclase
  2. decreased CAMP
  3. increased K conductance (hyperpolarization)

decreased norepi release

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18
Q

describe beta 1 and 2 second messenger/output

A
  1. activated adenylate cyclase
  2. increased CAMP
  3. increased kinase activation and phosphorylation

relaxes smooth muscle and stimulated cardiac contractility

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19
Q

what does the alpha 1 receptor activation do at the iris

A

contraction of radial muscle = dilates pupil = mydriasis

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20
Q

what does alpha 1 do at the prostate and uterus

A

contract

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21
Q

what is alpha 2’s affect on platelets

A

aggregation

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22
Q

what is alpha 2s action on vascular smooth muscle

A

post-synaptic = contraction

pre-synaptic = dilation

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23
Q

beta 1 role at kidneys

A

stimulation of renin release

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24
Q

beta 2 role at mast cells

A

decreased histamine release

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25
Q

beta 2 role at pancreas

A

increased insulin release

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26
Q

beta 2 role at liver

A

glycogenolysis

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27
Q

what does beta 2 activation do to potassium

A

increases potassium uptake

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28
Q

dopamine 1 receptor location and action

A

at smooth muscle

post synaptic: dilates renal, mesenteric, coronary, cerebral blood vessels

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29
Q

dopamine 2 receptor location and action

A

at nerve endings

pre synaptic: - modulates transmitter release, nausea and vomiting

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30
Q

what does the joint national committee on prevention, detection, and treatment of high blood pressure say is a normal BP

A

SBP <120
DBP<80

age 18-59 with no co-morbidities and 60 or older with diabetes and/or chronic kidney disease <140/90 is ok

age 60 or older with no diabetes or chronic kidney disease <150/90 is ok

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31
Q

what is the first line treatment of hypertension

A

thiazide diuretic

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32
Q

hypertensive urgency

A

DBP >120 with evidence of progressive end organ damage

goal: decrease DBP to 100-105 within 24 hours (clonidine)

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33
Q

hypertensive crisis

A

DBP > 120 with evidence of end organ failure
goal: decrease DBP to 100-105 ASAP

(nitroprusside, nitroglycerin, labetalol, fenoldapam)

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34
Q

name the alpha antagonists and whether they are competitive or non-competitive

A

competitive: phentolamine, prazosin, yohimibine

covalent bond/non-competitive: phenoxybenzamine

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35
Q

name the non-selective alpha receptor antagonists

A

phenoxybenzamine

phentolamine

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36
Q

name the alpha 1 selective antagonists

A

prazosin, terazosin, doxazosin, alfuzosin, tamsulosin

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37
Q

name the alpha 2 selective antagonist

A

yohimbine

tolazoline

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38
Q

what are the mixed alpha and beta antagonists

A

labetalol and carvedilol

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39
Q

what are the non selective beta antagonists (first generations)

A 
Propanolol
nadolol
penbutolol
pindolol
timolol
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40
Q

what are the second generation beta one selective antagonists

A 
acebutolol
atenolol
bisoprolol
esmolol
metoprolol
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41
Q

what are the third generation non selective beta antagonists

A

carteolol
carvedilol
bucindolol
labetolol

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42
Q

what are the third generation beta 1 selective antagonists

A

betaxolol
caliprolol
nebivolol

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43
Q

name a beta antagonist more selective for beta 2

A

butoxamine

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44
Q

what are the CV effects of alpha 1 antagonism

A

decreased PVR and lowered BP

postural hypotension due to failure of venous constriction upon standing

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45
Q

what are the CV effects of alpha 2 antagonism

A

increased NE release from nerve terminals results in tachycardia due to stimulation of beta receptors in the heart

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46
Q

GU effects of alpha antagonists

A

blockade in prostate and bladder cause muscle relaxation and ease micturition

\aka you can pee easier

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47
Q

alpha antagonist eye effect

A

miosis

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48
Q

alpha antagonist airway effect

A

increased nasal congestion

49
Q

phenoxybenzamine moa

A

binds covalently to alpha 1 and 2 receptors (nonselective, however more affinity for 1) to cause decreased SVR and vasodilation with less associated tachycardia

50
Q

pharmacokinetics of phenoxybenzamine

A

pro drug with 1 hour onset time

long acting with elimination half time of 24 hours

51
Q

phenoxybenzamine uses

A

for pheo patients in preop

raynauds

52
Q

preop dose of phenoxybenzamine for patients with pheo

A

0.5-1 mg/kg

53
Q

phentolamine moa

A

non selective alpha antagonist that produces a decrease in SVR and vasodilation and causes reflex mediated AND alpha-2 associated increases in HR and CO

54
Q

uses of phentolamine and associated doses

A

intraoperative management of hypertensive emergency (30-70 mcg/kg)

  • pheochromocytoma manipulation
  • autonomic hyperreflexia

extravascular administration of sympathomimetic agents (2.5-5 mg)

tola said you may see a drip in the OR of 0.1-2mg/min

55
Q

prazosin moa

A

selective alpha 1 antagonist that is less likely to cause tachycardia and dilates both arterioles and veins

56
Q

uses of prazosin

A

preop prep of patients with pheo

essential HTN (combined with thiazides)

decreasing afterload in patients with heart failure

Raynauds

57
Q

why do people use yohimibine

A

it is an alpha 2 selective blocker that increases release of norepi from post-synaptic neuron and is used for orthostatic hypotension and impotence/ED

58
Q

what are terazosin and tamsulosin and what are my biggest concerns

A

long acting selective alpha 1 antagonists that are effective in prostatic smooth muscle relaxation

orthostatic hypotension is biggest concern so prescribers should start slow so patients can adjust

59
Q

when was propanolol released according to that graph?

A

1965ish

might be a good bonus

60
Q

what do beta receptor antagonists do

A

disallow sympathomimetics from provoking a beta response on the heart, airway, blood vessels, JG cells, and pancreas

61
Q

beta antagonist effects on heart

A

bradycardia, decreased contractility, decreased conduction velocity, improve O2 supply and demand balance

62
Q

beta antagonist effects on airway

A

bronchoconstriction and bronchospasm

63
Q

beta antagonist effects on the blood vessels

A

vasoconstriction in skeletal muscles, increase PVD symptoms

64
Q

beta antagonist effects on JG cells

A

decreased renin release which is an indirect way of decreasing BP

65
Q

beta antagonist effects on pancreas

A

decreased stimulation of insulin release by epi/norepi at beta one

and then beta 2 antagonism can mask symptoms of hypoglycemia

66
Q

beta antagonist moa

A

selective binding to beta receptors

competitive and irreversible inhibition - aka large doses of agonists will overcome antagonism

67
Q

what happens to the beta adrenergic receptors in patients who chronically take beta antagonists

A

upregulation - so if we stop them suddenly perioperatively, expect hypertension/tachycardia

68
Q

which beta blocker would you choose for patients who have asthma, copd, smoking hx

A

an alpha 1 selective like metoprolol

69
Q

what is the elimination half life of esmolol

A

10 minutes

70
Q

what is the T1/2 of metop

A

3-4 hours

71
Q

what is the T1/2 of labetalol

A

5 hours

72
Q

what do we use beta blockers for

A 
treatment of hypertension
management of angina
decrease mortality in treatment of post MI patients
suppression of tachyarrythmias
prevention of excessive SNS activity
73
Q

what are some relative contraindications to beta blockers

A

pre-existing AV heart block or cardiac failure
reactive airway disease
diabetes without BS monitoring
hypovolemia (d/t decreased CO and BP)

74
Q

how should you give adrenergic antagonists to patients with pheo

A

give an alpha antagonist before you give a beta antagonist

otherwise you will drop their heart rate and they will still be working against a crazy afterload

75
Q

what detrimental CV effect can happen when you take a beta antagonist and inhalational agents

A

hypotension

76
Q

beta antagonism and IOP

A

these decrease aqueous humor production so good for patients with glaucoma because IOP is decreased

timolol

77
Q

what happens to your lipid panel with beta antagonists

A

can cause decreased concentration of HDL which may increase risk for CAD

(chronic use)

78
Q

propanolol moa

A

nonselective beta antagonist which decreases HR and contractility at beta 1 and increases vascular resistance at beta 2

79
Q

concerns for patients taking propanolol chronically

A

decreased clearance of amide LAs d/t a decrease in hepatic blood flow inhibiting metabolism in liver - risk for LA toxicity
decreased pulmonary clearance of fentanyl (both are basic lipophilic amines)

80
Q

what is the HR goal for propanolol

A

55-60

81
Q

propanolol cardiac effects

A

decreased hr, contractility, co
increased PVR, coronary vascular resistance

also decreased renin release

82
Q

dose of propanolol

A

0.0k mg/kg IV or 1-10 mg

give slowly 1mg q5min

83
Q

protein binding of propanolol

A

90-95%

84
Q

metabolism of propanolol

A

significant 1st pass effect (90-95%)

metabolized in liver

85
Q

elimination half time of propanolol

A

2-3 hours and will be increased in low hepatic blood flow states

86
Q

metoprolol moa

A

beta one selective but dose related

87
Q

metabolism and elimination of metoprolol

A

first pass effect (60%)
metabolized in liver
elimination half time = 3-4 hours

88
Q

dose of metop

A 
PO = 50-400 mg
IV = 1-15mg max
89
Q

dose of metop

A 
PO = 50-400 mg
IV = 1-15mg max
90
Q

atenolol moa

A

most selective beta 1 antagonist and thought to have the least CNS effects

advantageous to those who need beta 2

91
Q

pharmacokinetics of atenolol

A

given PO
NOT metabolized in liver
excreted in renal system and so elimination half time is increased in patients with renal disease (normally 6-7 h)

92
Q

uses of atenolol

A

antihypertensive

also given to people who get nervous public speaking

93
Q

esmolol moa

A

rapid onset and short duration beta 1 selective blocker

94
Q

onset of action of esmolol

A

60 second

95
Q

duration of action of esmolol

A

10-30 minutes

96
Q

metabolism of esmolol

A

plasma esterase

these aren’t the same ones that metabolize succ so there is no effect

97
Q

does esmolol cross BBB or placenta

A

NO it has poor lipid solubility

98
Q

esmolol used for

A

to treat HTN and tachycardia associated with DL
pheo surges
thyrotoxicosis
thyroid storm

99
Q

side effects of timolol eye gtts

A

hypotension and bradycardia and increased airway resistance

100
Q

Nadalol moa/pk

A

non selective beta blocker with no significant metabolism
renal and biliary elimination
T1/2 of 20-40h so they only take it 1x a day

101
Q

betaxolol considerations

A

cardioselective beta one blocker
elimination half time = 11-22h
single dose daily for HTN
topical for glaucoma with less risk of bronchospasm than timolol so good choice for patients with glaucoma and asthma

102
Q

labetalol moa

A

combined alpha and betal non-selective antagonist

IV B:A = 7:1
PO B:A = 3:1

decreases systemic BP via alpha 1 with attenuated reflex tachy via beta 2 blockade

so decreased HR, SVR, and BP with unaffected CO

103
Q

PK of labetalol

A

conjugation with glucuronic acid, <5% recovered unchanged in urine
elimination half life of 5-8h - prolonged in liver disease but not affected by kidney disease

104
Q

when is the max drop in BP after IV admin of labetalol

A

5-10 minutes after admin

105
Q

dose of labetalol

A

0.1-0.5 mg/kg IVP

usually give 5 mg at a time for mild hypertension in OR

106
Q

what do we use labetalol for

A

intraoperative HTN and hypertensive crisis

can be used in hypotensive technique without an increase in HR

107
Q

side effects of labetalol

A

orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia

108
Q

centrally acting agents moa

A

centrally acting partial alpha 2 agonists, acting at CNS non-adrenergic binding sites and alpha 2

reduce sympathetic outflow from vasomotor centers in the brain stem

109
Q

uses for alpha 2 agonists

A 
htn
induce sedation
decreased anesthetic reqs
improve periop hemodynamics
analgesia
110
Q

what is clonidine

A

a centrally acting alpha 2 agonist that decreases BP and CO due to decreased HR and peripheral resistance`

111
Q

risk of abrupt cessation with clonidine

A

rebound hypertension - so continue periop

112
Q

side effects of clonidine

A 
brady
sedation
dry mouth
impaired concentration
nightmares
depression
vertigo
EPS
lactation in men
113
Q

PK of clonidine

A

given PO or TD patch

50/50 hepatic metabolism and renal excretion

114
Q

withdrawal syndrome of clonidine

A

occurs with doses >1.2 mg/day
18h after d/c of last dose
lasts for 24-72 hours
treatment = rectal or TD clonidine

115
Q

ephedrine dose

A

5-10 mg IVP

116
Q

phenylephrine dose

A

100mcg/ml increments IVP

15mcg/min gtt

117
Q

epi dose

A

1-20 mcg/min

118
Q

dopamine dose

A

low (dopa) = 3-5 mcg/kg
medium (beta) = 6-10 mcg/kg
high (alpha)= >10 mcg/kg

119
Q

dobutamine dosing

A

1-20 mcg/kg/min

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