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CRNA Pharmacology > Alpha and Beta Adrenergic Receptor Antagonists > Flashcards

Alpha and Beta Adrenergic Receptor Antagonists Flashcards

1
Q

What are the 2 Non-selective A1 and A2 receptor antagonists ?

A

1) Phentalomine

2) Phenoxybenzamine

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2
Q

What are the 4 Selective A1 Antagonists?

A

1) Prazosin (Minipress)
2) Terazosin (Hytrin)
3) Doxazosin (Cardura)
4) Alfuzosin (Uroxatral)

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3
Q

What are the 2 Selective A1a antagonists?

A

1) Tamsulosin (Flomax)

2) Silodosin (Rapaflo)

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4
Q

What is the only A2 antagonist?

A

Yohimbine

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5
Q

Alpha-1 Adrenergic Receptor Blockade Effects

A

1) Inhibits endogenous catecholamines or sympathomimetics amine induced vasoconstriction resulting in vasodilation
2) Vasodilation causes ↓ BP due to ↓ in PVR
3) Baroreceptor-mediated reflex response cause ↑ in HR, CO and fluid retention
4) Baroreflexes are exaggerated if the antagonist also blocks alpha 2 receptors (binding alpha2 receptors on nerve endings usually inhibits NE release)

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6
Q

Alpha-2 Adrenergic Receptor Blockade Effects

A

↑ Sympathetic flow from CNS and release of NE from nerve endings which in turn stimulates A1 and B1 receptors leading to ↑ BP and HR.

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7
Q

Effect of using the following Sympathomimetic when the patient has been on an Alpha-1 Blocker chronically:

1) Phenylephrine + Alpha-1 Blocker
2) Norepinephrine + Alpha-1 Blocker
3) Epinephrine + Alpha-1 Blocker

A

1) Phenylephrine (A1) + Alpha-1 Blocker = pressor response can be almost completely suppressed
2) Norepinephrine (A1,A2,B1) + Alpha-1 Blocker = Causes maximal cardiac stimulation and pressor response is only incompletely blocked b/c of residual stimulation of cardiac β1 receptors by NE
3) Epinephrine (A1, A2, B1, B2) + Alpha-1 Blocker = pressor response may be transformed to vasodepressor effects (↓ blood pressure) b/c of residual stimulation of β2 receptors in the vasculature with resultant vasodilation by epinephrine

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8
Q

Non-cardiovascular effects of Alpha Adrenergic Receptor Antagonists

A

1) A2 antagonist - Inhibition of insulin secretion

2) A1 antagonist - ↑ GI motility and prevention of ejaculation or cause impotence

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9
Q

Phentolamine Characteristics

A

1) Nonselective (A1 and A2), competitive, reversible antagonist.
2) IV form causes vasodilation and ↓ in BP within 2 mins and lasts 10 to 15 mins
3) ↓ in BP causes baroreceptor response which ↑ CO and HR
4) Can be administered IV or IM

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10
Q

Phentolamine Metabolization

A

Primarily by the liver

~13% of drug is excreted unchanged in the urine

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11
Q

Phentolamine Clinical Uses

A

1) Prevention or Tx of acute HTN due to pheochromocytoma and ANS hyperreflexia
2) Pre-op prevention of HTN - 5mg IV or IM (1mg for children) 1 or 2 hrs before surgery
3) Prevention or Tx of dermal necrosis following extravasation of catecholamines (5-10 mg

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12
Q

Which class of drugs should never be used in conjunction with Phentolamine?

A

Beta Blockers

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13
Q

Phenoxybenzamine (Dibenzyline) Characteristics

A

1) Nonselective (A1 and A2), irreversible antagonist.
2) Binding is insurmountable - once alpha blockade has been established, even massive doses of sympathomimetics are ineffective until Phenoxybenzamine is terminated by metabolism
3) Only available PO
4) Slow onset of action (up tp 60 mins to reach peak effect)

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14
Q

Phenoxybenzamine (Dibenzyline) cardiovascular effects

A

1) Hypotension (most common)
2) Orthostatic hypotension
3) Tachycardia
4) ↑ CO via baroreceptorreflex
5) ↑ Blood flow to skin, mucosa

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15
Q

Phenoxybenzamine (Dibenzyline) non- cardiovascular effects

A

1) Crosses the placenta
2) decreases blood sugar
3) Glycogenolysis
4) Miosis
5) Sedation, drowsiness and fatigue
6) Nasal stuffiness
7) Unable to ejaculate

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16
Q

Explain the warning for Phenoxybenzamine relating to the administration of B1 and B2 agonists?

A

Phenoxybenzamine binds and IRREVERSIBLY blocks A1 and A2 receptors, which leaves beta-adrenergic receptors unopposed. Administration of agonist that stimulate B1 and B2 receptors may, therefore, produce an exaggerated hypotensive response (B2) and tachycardia (B1).

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17
Q

Phenoxybenzamine Clinical Uses

A

1) Pre-op Tx of pressure and sweating in PTs with pheochromocytoma (start 1-3 wks prior to surgery)
2) Control of autonomic hyperreflexia in PTs with spinal cord transection

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18
Q

Phenoxybenzamine Dosing

A

1) Initially 10mg PO BID

2) Increase dose every other day to 20-4mg 2 to 3 times a day until optimal dosage is obtained

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19
Q

Under which circumstances should you NEVER operate on a phenochromocytoma patient?

A

If they have not had adequate blockade first

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20
Q

Yohimbine Caracteristics

A

1) Selective A2 receptor antagonist
2) Blocks A2 receptors on presynaptic nerve endings
3) Allows more release of NE from nerve ending
4) Causes increase in HR and BP
5) Used for body building and impotence

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21
Q

Selective A1 Adrenergic Receptor Antagonists characteristics

A

1) Competitive and reversible
2) Inhibit all 3 subtypes of post synaptic receptors (A1a, A1b, A1d)
3) They do not bind A2 receptors and release NE from nerve endings

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22
Q

Selective A1 Adrenergic Receptor Antagonists clinical uses

A

Tx of HTN and BPH

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23
Q

Selective A1 Adrenergic Receptor Antagonists Cardiovascular Effects

A

1) ↓ SVR which ↓ after load and BP
2) ↓ Venous return = ↓ preload, can ↓ CO
3) Greater vasodilation at veins when compared to arteries
4) No baroreceptor reflex

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24
Q

Selective A1 Adrenergic Receptor Antagonists Adverse Effects

A

Dizziness, headache and hypotension(most common)

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25
Q

Tamsulosin (Flomax) and Siladosin (Rapaflo) MOA

A

1) Both selective, competitive postsynaptic A1a antagonist
2) Slecetively inhibits A1a receptors in bladder and prostate
3) Improves urinary flow without causing peripheral vascular smooth muscle relaxation
4) Both have minimal effect on BP

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26
Q

Tamsulosin (Flomax) and Siladosin (Rapaflo) Side Effect

A

1) Nasal decongestion/rhinitis
2) Headache
3) Dizziness
4) Low risk of Hypotension

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27
Q

Beta Adrenergic Receptor Antagonist Effect

A

Antagonism results in decreased activation of the adenylate cyclase which decreases the concentrations of cAMP

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28
Q

How can Beta Adrenergic Receptor Antagnists agents be distinguished from one another?

A

By the following properties:

1) Relative affinity for B1 and B2 receptors (Beta selectivity)
2) Intrinsic Sympathomimetic activity (ISA)
3) Differences in lipid solubility
4) Membrane-stabilizing effects (Local anesthetic activity)
5) Differences in pharmacokinetic profile (ADME)

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29
Q

Examples of Non-selective Beta Antagonists agents

A

1) Propanolol
2) Nadolol
3) Sotalol
4) Timolol
5) Carvedolol
6) Labetalol
7) Carteolol
8) Pindolol

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30
Q

Which pts are safer with cardioselective drugs vs nonselective

A 
Asthma
COPD
Asthma
diabetes
PAD (prevents B2 action of vasodilation)
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31
Q

Is selectivity pure in B blockers

A

no, it just means that they are less likely to affect non selective receptor.
drugs tend to lose their selectivity with higher doses

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32
Q

Which receptors do the following sympathomimetics bind to:

1) NE
2) EPI
3) Dopamine
4) Isoproterenol
5) Phenylephrine
6) Dobutamine
7) Ephedrine

A

1) NE - A1, A2, B1
2) EPI - A1, A2, B1, B2
3) Dopamine - A1, A2, B1
4) Isoproterenol - B1, B2
5) Phenylephrine - A1
6) Dobutamine - A1, A2, B1
7) Ephedrine - A1, B1, B2

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33
Q

Why do Tamsulosin (Flomax) and Siladosin (Rapaflo) Side Effect have such a low risk of hypotension?

A

Because they target A1a receptors only located in bladder and prostate. A1b and A1d are located in arteries and veins do not get affected by this these 2 drugs.

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34
Q

If PT has intraop hypotension who’s been on flomax, and you want to correct BP with phenylephrine, would you give a lower, normal or higher dose of phenylephrine?

A

normal - hypotension was not caused by antagonism of A1b and A1d receptors in blood vessels. Flomax only antagonizes A1a receptors in bladder and prostate.

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35
Q

Would you give a lower, normal, or higher dose to someone who has overdosed on beta blockers and is experiencing symptomatic bradycardia?

A

Higher does - because you have to out-compete the antagonist (BB) already onboard.

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36
Q

Examples of Selective Beta-1 Antagonists (aka cardioslelective agents)

A

1) Metoprolol
2) Atenolol
3) Esmolol
4) Acebutolol
5) Bisoprolol
6) Nebivolol
7) Betaxolol

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37
Q

Why are Selective Beta-1 Antagonists (aka cardioslelective agents) a better choice for OR use by anesthesia than over their non-selective counter parts

A

They do not antagonize B2 receptors and have less chance of causing bronchospasm

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38
Q

What is Intrinsic Sympathomimetic Activity (ISA) regarding Beta Antagonists

A

Means the BB has a partial agonist effect if concentration of endogenous NE is low (as in resting states)
when endogenous NE is high, BB effects will still be present
ISA agents can cause less direct myocardial depression and less brady

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39
Q

bottom line for ISA B blockers in anesthesia

A

never use ISA BBs in anesthesia unless as a last resort

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40
Q

pure antagonist vs partial antagonist

A

partial antagonist signifies the presence of ISA

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41
Q

Effect of Beta blockers with high lipid solubility

A

Cross BBB and decrease SNS outflow (↓ HR and CO)
at risk for neurologic sequelae such as:
seizures (overdose)
delerium
lethargy
nightmares/vivid dreams

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42
Q

Highly lipophilic Beta Blockers

A

1) Prpanolol

2) Nebivolol

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43
Q

Membrane Stabilizing Effect (MSA)

A

membrane stabilizing effect
ability to inhibit myocardial fast Na+ channels, which widens QRS and potentiates arrhythmias
only detectable in overdose situations

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44
Q

B Blockers with MSA

A 
Acebutolol
Betaxolol
Metoprolol
Pindolol
Propanolol
Carvedilol
Labetalol
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45
Q

B Blockers with primary Hepatic and secondary Renal clearance

A

Timolol, Pindolol, Acebutolol, Betaxolol

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46
Q

B blockers with Hepatic clearance only

A

Propanolol, Metoprolol, Labetalol, Nebivolol

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47
Q

B Blockers that undergo Renal clearance only

A

Cartelol, Nadolol, Atenolol, Sotalol

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48
Q

halflife of esmolol

A

9 mins

49
Q

B-blockers with intrinsic sympathomimetic activity (ISA)

A

Labetalol
Acebutolol
Pindolol

50
Q

B blocker uses

A 
essential HTN
manage CHF
angina pectoris
Acute coronary syndrome
hypertrophic obstructive coronary syndrome
intraoperative myocardial ischemia
suppress cardiac dysrhythmias
ventricular rate control in afib/flutter
migraine prophylaxis
pheochromocytome (always alpha-block first)
open angle glaucoma (topical)
51
Q

perioperative Beta blocker Use

A

sometimes used perioperatively in pts at risk for myocardial ischemia and to decrease mortality associated with the operation. i.e.

known CAD
positive preop stress test
LV hypertrophy
Diabetes

52
Q

General resting HR goal with perioperative B blockade

A

65 to 80 bpm

53
Q

Beta Blockers’ MOA

A
  • 1) ↓ Slope of phase 4 spontaneous depolarization
    2) ↓ Automaticity
    3) ↓ Sinus rate
    4) Slows AV nodal conduction velocity, ↑refractory period of the AV node, and lengthens PR interval
    5) Negative chronotropic , dromotropic and inotropic effects
54
Q

Effect of Beta blockers with high lipophilicity (propranolol) on baroreceptor reflex?

A

resets the baroreceptor reflex downward, leading to a decreased total PVR (meaning its harder for the reflex to respond to decreases in TPR)

55
Q

(T/F?) ALL Beta Blockers lower BP?

A

True - its due to ↓ PVR which leads to ↓ afterload

56
Q

do B blockers reduce BP in pt with normal BP?

A

not generally

they work best in the presence of preexisting increased SNS activity

57
Q

Why is a beta blocker use in reduced EF a core measure?

A

they reduce rate of LV hypertrophy development by:
decreasing PVR (afterload) and thereby reducing myocardial oxygen demand
decreased HR increases diastolic filling time, improving vent function and coronary perfusion
overall, relationship between myocardial oxygen supply and demand is improved

58
Q

When is the effect of B blockers highest?

A

In the presence of increased SNS outflow:
exercise
cardiac failure

59
Q

Can B blockers block the effects of Ca++, glucagon, or digoxin?

A

No, they all used alternate pathways that do not involve the B receptors

60
Q

which agents reduce portal pressure

A

classic nonselective B blockers (blocking B2 reduces splachnic vasoconstriction, reducing blood flow)
propanolol
nadolol

61
Q

what B blockers are avoided in diabetic pts

A 
non selective (use Lopressor if possible)
B2 blockade decreases glycogenolysis and pancreatic glucagon stimulation
62
Q

B blockers in hypoglycemia

A

all B blockers all can mask effect of catecholamine secreted during hypoglycemia, blunting visible effects (tachy, tremor, nervousness)

63
Q

B blocker induced hyperkalemia

A

very rare, really only pertinent in overdose

64
Q

which drug has highest risk of CNS effects

A

Propanolol? (most lipophilic)

can cause memory loss and depression in addition to fatigue, lethargy and vivid dreams

65
Q

preferred B blockers in gestation

A

low lipophilic (will not cross placenta)

66
Q

adverse side effects in B antagonists

A

similar for all, but vary in magnitude and selectivity, ISA, degree of CNS penetration, method of excretion, etc.

67
Q

relationship between B blocker effects and anesthesia drugs

A

additive effects may occur

68
Q

B antagonist contraindications

A

sinus brady
2nd of 3rd degree HB
cardiogenic shock
decompensated HF
sick sinus syndrome
non selective B antagonists are contraindicated in bronchial asthma/bronchospastic disease
cardioselective B blockers may be used, but should be used with caution

69
Q

Why are non-selective BBs avoided in the PT with PVD

A

Can cause cold hands and feet syndrome - bind and blocks B2 receptors in veins and arteries, causing vasoconstriction which ↓ circulation in the periphery.

70
Q

all B blockers have what non life threatening side effect with a potentially negative psychosocial effect

A

sexual dysfunction

71
Q

B blockers with anesthetic agents

A

myocardial depression exacerbation (enflurane is the worst) (least with isoflurane, sevoflurane, desflurane)
always avoid ketamine
can be used safely in perioperative period

72
Q

Is B blocker held for surgery

A

never hold without a good reason
IV dose can be given if pt was NPO
risk of SNS overactivity with missed doses, increases risk of MI

73
Q

which B blcoker should not be used perioperatively with inhaled anesthetics

A

Timolol - profound bradycardia has been observed in concomitant use

74
Q

interaction of ketamine and B blockers

A

ketamine stimulates SNS, increasing SVR and afterload
B blockers prevent myocardial contractility increase, and HF may ensue
(similar to reason Epi is not used with B blockers)

75
Q

which inhaled anesthics have the least additive effects with B blockers?

A

isoflurane
sevoflurane
desflurane

76
Q

B blocker use in rebound HTN with withdrawal of clonidine

A

B1 and B2 receptors will be blocked, but not Alpha receptors, causing an unopposed alpha vasoconstriction, making their HTN worse.

77
Q

B blockers with digoxin or Ca Channel blockers

A

use with caution: risk of bradycardia and heart block since both slow AV conduction and decrease HR

78
Q

B blocker overdose treatment

A

First - Glucagon 2-10 mg IVP followed by 5 mg/hr (drug of choice)
Second - IV fluids, Atropine, CaCL2, catecholamines (high doses)

79
Q

four B blockers that must know because they are commonly used in anesthesia setting

A

non selecrtive: propranolol, labetalol

selective: esmolol, metoprolol

80
Q

Propanolol

A

lacks ISA
equal B1 and B2
highly lipophilic
strong membrane stabilizing at high doses
extensive FPE (multiple CYP 450 ezymes in liver)
high degree of individual variation of FPE

81
Q

Propanolol’s active metabolite

A

4-Hydroxypropanolol

82
Q

Propanolol clearance

A

primarily CYP 450
active metabolite 4-hydroxypropranolol
inactive metabolites
can reduce its own clearance due to decreased hepatic blood flow
high FPE necessitates much higher oral dose

83
Q

what is the major factor in metabolization of propranolol

A

clearance greatly decreased in decreased blood flow

84
Q

Propranolol protein binding

A

~90%

heparin and other high protein binding drugs increase free drug

85
Q

propranolol onset and administration rate

A

onset: up to 15 min IV

no faster than 1mg/min, or slow IV infusion over 30 min.

86
Q

Propanolol Dosing

A

0.25mg to 5mg IV

87
Q

propranolol effects on coronary perfusion

A

B2 blockade causes some coronary vasoconstriction
decrease in HR and contractiliy decreaases myocardial oxygen demand
net effect is still a decrease in myocardial ischemia

88
Q

propanolol effects with local anesthetics

A

decreases -amide clearance due to decreased hepatic blood flow AND inhibiting metabolism in liver
increases toxicity of bupivicaine and lidocaine

89
Q

propanolol and clearance of opioids

A

substantially decreases FPE effect of fentanyl (2-4x as much reaches systemic circulation)

90
Q

Should you decrease, keep the same, or increase the dose of fentanyl when a patient is on propranolol?

A

decrease it

91
Q

Metoprolol pharmacokinetics

A 
Dose 1-5mg IV
onset: 1-5 min
peak effect: 20 min
duration: 5-8 hrs (highly variable)
highly metabolized in liver (CYP 450)
92
Q

Atenolol

A

no ISA
no MSA
low lipophilic
highly hydrophilic (high renal clearance)***

93
Q

Esmolol dosing

A

ventricular rate control in Afib/flutter
noncompensatory sinus tach
short term treatment of tachycardia/HTN in periop based on physician’s judgment

94
Q

Esmolol Immediate control dosing for tachy/HTN in OR

A 
1 mg/kg bolus over 30 sec
followed by 150 mcg/kg/min infusion if needed
max infusion rate: 
200 mcg/kg/min for tachy
300 mcg/kg/min for HTN
95
Q

Esmolol Gradual control dosing for tachy/HTN in OR

A

500 mcg/kg IV over 1 min

followed by 4 min infusion at 50 mcg/kg/min

96
Q

Esmolol Metabolism

A

metabolism occurs via esterases in cytosol of RBC’s

97
Q

Esmolol in gestation

A

can cross placental barrier in high doses and/or extended use

98
Q

Esmolol half life/duration/onset

A

9 min
10-30 min
2-5 min

99
Q

Esmolol most common side effects

A

hypotension (dose related)

diaphoresis

100
Q

Esmolol in hypovolemic patients

A

can attenuate reflex tachycardia, increasing risk of hypotension

101
Q

Esmolol and Sux

A

blockade is prolonged

moderately prolonged clinical duration and recovery in mivacurium as well

102
Q

Esmolol and propofol

A

significantly decreases propofol required to prevent pt movement in response to surgical skin incision
esmolol potentiates propofol (decreasing the dosing requirements)

103
Q

Esmolol effect on injectable anesthetics

A

decreases dosing requirements

specifically propofol as well as others

104
Q

Esmolol and catecholamines

A

B Blocking in presence of A stimulation can cause reduced CO in face of high SVR even in low doses

105
Q

most highly cardiac selective agent

A

Nebivolol

106
Q

Nebivolol

A

highest degree of B1 selectivity

endothelial NO-mediated vasodilation activity and antioxidant properties

107
Q

Labetalol MOA

A

comptetitive antagonist at A1, B1, B2, and partial B2 agonist

108
Q

Labetalol vs phentolamine and propranolol

A

1/10th to 1/5th A1 effect as phentolamine

1/4th to 1/3rd B effect as propranolol

109
Q

ratio of Labetolol Beta to A1 blockade in oral and IV doses

A

3: 1 in oral dose
7: 1 in IV dose

110
Q

Best clinical use for labetalol

A

when a pt is both tachycardic and hypertensive

111
Q

what is the dose for continuous IV infusion for labetalol

A

It is NEVER given continuously

112
Q

Labetalol onset/peak/duration

A

onset: 2-5 min IV
peak: 5-15
duration: 2-4 hrs

113
Q

Labetalol starting dose

A

5-20 mg IV repeated every 10-15 min until desired effect is achieved

114
Q

Labetalol uses

A

drug of choice when A and B blockade are needed:
catecholamine overdose
rebound HTN after clonidine withdrawal
pheochromocytoma

Other uses:
angina pectoris
aortic dissection
attenuate surgical stimulation of SNS (HR and BP)

115
Q

Labetalol use in pregnancy

A

little placental transfer due to poor lipid solubility

no change in uterine blood flow

116
Q

Labetalol adverse effects

A

hypotension (most common)

117
Q

Coreg (Carvedilol)

A

competitive antagonist at A1, B1, B2

118
Q

coreg uses

A

CHF management
LV dysfunction following MI
HTN

119
Q

Drug of choice for pregnancy induced hypertensive crisis

A

Labetalol
poor lipid solubility
uterine blood flow not altered

CRNA Pharmacology (8 decks)

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