Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

S5 - Anesthesia Pharm II - Test 2 > Adrenergic Antagonists > Flashcards

Adrenergic Antagonists Flashcards

1
Q

MOA of alpha-adrenergic antagonists

A
  • binds competitively or covalently with alpha receptors
  • prevents the effects of catecholamines and other alpha agonists from interacting with the alpha receptor
  • located in the heart and peripheral vasculature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

effects of alpha-adrenergic antagonists

A
  • vasodilation (orthostatic hypotension)
  • reflex tachycardia
  • blocks inhibition of insulin secretion (hypoglycemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what prevents the use of alpha-adrenergic antagonists as essential antihypertensives?

A

their side effects

(tachycardia, hypoglycemia, orthostatic hypotension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what happens if taking an alpha-adrenergic antagonist if there is no beta-blockade?

A

maximal cardiac stimulation is allowed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MOA of phentolamine (Regitine)

A

competitive binding

non-selective - alpha1 and alpha2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does phentolamine (Regitine) affect vasculature, HR & CO?

A
  • vasodilation-alpha1 blockade and direct action on vascular smooth muscle
  • cardiac stimulation - increased HR and CO
  • reflex and α2 blockade - blocks neg. feedback of NE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

side effects of phentolamine (Regitine)

A
  • dysrhythmias
  • angina
  • hyper- peristalsis
  • abdominal pain
  • diarrhea (due to parasympathetic tone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

uses of phentolamine (Regitine)

A
  • acute HTN emergencies
  • pheochromocytoma
  • accidental infiltration of a sympathomimetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

dose of phentolamine (Regitine) to use for infiltration?

A

5-15 mg in 10 ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

phentolamine (Regitine)

onset and duration

A

onset: 2 min
duration: 10-15 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

phentolamine (Regitine)

bolus/loading dose and infusion dose

A

bolus/loading: 30-70 mcg/kg (1-5 mg)

infusion: 1-10 mcg/kg/min (300 mg in 500 mL of LR or NS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MOA of phenoxybenzamine (Dibenzyline)

A

irreversible covalent binding to α-receptors

nonselective; alpha1 > alpha2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CV effects of phenoxybenzamine (Dibenzyline)

A
  • vasodilation – orthostatic hypotension exaggerated with hypovolemia, HTN
  • impairment of compensatory vasoconstriction (lower BP with hypovolemia and vasodilating drugs like volatile agents)
  • increased CO
  • very little change in renal blood flow even with decreased BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

with phenoxybenzamine (Dibenzyline) is renal autoregulation maintained?

A

yep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

non-CV effects of phenoxybenzamine (Dibenzyline)

A
  • prevents the inhibition of insulin secretion
  • pupil constriction
  • chronic use may cause sedation
  • nasal congestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

uses of phenoxybenzyamine (Dibenzyline)

A
  • control BP in pheochromocytoma
  • in trauma patients, used to reverse vasoconstriction (shock), only after volume replacment
  • Raynaud’s syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

phenoxybenzamine (Dibenzyline) onset, duration, and elimination t½

why is the onset time longer than some of the other drugs in this class?

A

onset: up to 60 min IV
duration: can last up to 4 days

elim t½: 24 hours

longer onset bc prodrug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is one thing to be cautious of when using phenoxybenzamine (Dibenzyline)?

A

the prolonged half-life can lead to accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MOA of prazosin (Minipress)

A

competitive, reversible binding with alpha receptor

selective – α1 antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

effects of prazosin (Minipress) on vasculature and HR

A
  • vasodilation of both arterioles and veins
  • less reflex tachycardia (alpha2 not blocked)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

uses of prazosin (Minipress)

A
  • HTN
  • severe CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

prazosin (Minipress) onset and duration

A

onset: within 2 hrs
duration: 10-24 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MOA of doxazosin (Cardura)

A

selective alpha1 antagonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

doxazosin (Cardura)

dosing, peak time, elimination t½

A

daily dosing

peak: 2-3 hrs

elim t½: 22 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

indications for doxazosin (Cardura)

A
  • benign prostatic hypertrophy
  • hypertension treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MOA of beta-adrenergic antagonists

A
  • competitive binding to beta receptors
  • block the effect of catecholamines and agonists on the heart and smooth muscles of airways and blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

prolonged or chronic use of beta-blockers can cause what?

A

up-regulation of beta receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

non-selective beta-adrenergic antagonists

A
  • propranolol
  • timolol
  • nadolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

cardioselective beta-adrenergic antagonists

receptor blocked and examples

A
  • blocks beta1 at normal doses, large doses can impact beta2 receptors too
  • metoprolol
  • atenolol
  • esmolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

effect of partial beta-adrenergic antagonist

A
  • intrinsic sympathomimetic effect
  • less myocardial depression and HR reduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is a pure beta-adrenergic antagonist?

A

b-adrenergic antagonist with no sympathetic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

effects of beta1 blockade

*long

A

removes sympathetic stimulation to the heart

  • negative inotropic effects - myocardial depression
  • negative chronotropic effects - slows HR, sinus rate
  • negative dromotropic effects - slows the conduction of impulse through the AV node, slows rate of phase 4 depolarization
  • increase in lusitropy - ventricular relaxation
  • decrease in bathmotropy - reduced degree of excitability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

effects of beta2 blockade

A
  • vasoconstriction
  • unopposed alpha vasoconstriction can cause decreased LV ejection
  • bronchoconstriction
  • prevents glycogenolysis, blocks tachycardia related to hypoglycemia, alters fat metabolism (lipolysis)
  • inhibits uptake of K into skeletal muscle cells (increased serum K)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

effects of beta2 blockade in patient with pre-existing obstructive airway disease

A

exaggerated airway resistance effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what patient population needs to avoid non-selective beta-blockers? why?

(other than airway disease pts)

A
  • diabetics
  • symptoms of hypoglycemia are masked and glycogen can’t be broken down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

effects seen with cardioselective vs non-selective beta-blockers when given SCh?

A
  • ** not demonstrated in pts
  • selective - K+ will increase, but will return to normal later
  • non-selective - K+ will increase and stay increased due to inhibit uptake into skeletal muscle cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

potential effects of beta-adrenergic antagonists with anesthetic agents

A
  • potential additive myocardial depressant effects
  • safe to continue - benefits of continuing outweigh the risks
  • halothane > isoflurane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

CNS effects of beta-adrenergic antagonists

A
  • cross blood/brain barrier →
  • fatigue
  • lethargy
  • vivid dreams
  • memory loss
  • depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

beta-adrenergic effects on fetus

A

Cross placenta →

  • fetal bradycardia
  • fetal hypotension
  • fetal hypoglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

GI effects of beta-adrenergic antagonists

A
  • nausea
  • vomitting
  • diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

effects of chronic use of beta-adrenergic antagonists

A
  • fever
  • rash
  • myopathy
  • alopecia
  • thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

contraindications to beta-blockers and why

*long (7)

A
  • AV heart block – slowed conduction may be enhanced
  • hypovolemia – eliminates tachycardia that is compensating for decrease in volume
  • COPD – increased airway resistance (nonselective or high doses)
  • diabetes – mask signs of hypoglycemia (nonselective or high doses)
  • peripheral vascular disease, Raynaud’s syndrome, or alpha-adrenergic agonist - vasoconstriction unopposed (nonselective), cold extremities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

effects seen with beta-adrenergic antagonist overdose

A
  • bradycardia
  • low cardiac output
  • hypotension
  • cardiogenic shock
  • bronchospasm
  • prolonged intraventricular conduction of impulses
  • hypoglycemia - rarely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

overdose of beta adrenergic antagonist - treatment order

(no doses)

A
  1. atropine
  2. isoproterenol
  3. dobutamine
  4. glucagon
  5. calcium chloride
  6. pacemaker
  7. hemodialysis (only for minimally protein-bound renally excreted beta-blockers)

AID Generally Can …? idk. i tried.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

dose of atropine to use for beta-blocker overdose?

A

7 mcg/kg IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

dose of isoproterenol to use for beta-blocker overdose?

A

2-25 mcg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

dose of glucagon to use for beta-blocker overdose?

A

1-10 mg

48
Q

dose of CaCl to use for beta-blocker overdose?

A

250 mg - 1 g

49
Q

what two drugs should be avoided when treating a beta-blocker overdose?

why?

A
  • epi and dopamine
  • alpha1 vasoconstriction occurs at the high doses required to overcome the beta blockade
50
Q

MOA of glucagon for beta-blocker overdose treatment

A
  • not via beta receptors
  • stimulates adenylate cyclase - increases cAMP
  • especially effective in life-threatening bradycardia
51
Q

considerations for beta-blocker overdose if patient needs a pacemaker

A
  • myocardial thresholds may be raised to prevent capture
  • may have to increase settings
52
Q

what causes acute withdrawal symptoms of beta-blockade?

symptoms and timing?

A
  • increased sympathetic stimulation due to up-regulation of beta receptors
  • within 24-48 hours
  • profound hypertension, tachycardia, contractility
53
Q

how to avoid acute withdrawal symptoms of beta-blockade?

A
  • continue preoperative beta-blockade therapy
  • infusion of propranolol 3 mg/hr IV
54
Q

uses of beta-blockers (6)

(not intra-op uses)

A
  • treatment of HTN
  • management of angina
  • post-MI
  • dysrhythmias
  • prevent excessive SNS activity
  • management of CHF
55
Q

MOA for beta-blockers treating HTN

A
  • decrease HR, decrease CO
  • decrease contractility in larger doses
  • with vasodilator, prevention of reflex tachycardia
  • decrease renin, decrease aldosterone, prevention of Na, water retention
56
Q

MOA of beta-blockers in mgt of angina

A
  • decreased myocardial oxygen consumption
    • decreased HR, contractility
57
Q

MOA of beta-blockers for post-MI treatment

*long

A
  • decreases mortality and reinfarctions
  • increases chances of survival 20-40%
  • within 12 hours of onset of infarct may actually decrease infarct size and dysrhythmias
  • not used with acute coronary syndrome with ST-elevation or cardiogenic shock
  • both selective and nonselective drugs have a cardioprotective effect
  • nonselective effect on K (prevents reduction) may decrease dysrhythmias
58
Q

MOA of beta-blockers for treatment of dysrhythmias

A
  • decrease activity of SA node and conduction through the AV node
  • slows depolarization of ectopic pacemakers
  • suppresses both supraventricular and ventricular ectopy
  • rapid suppression of excessive sympathetic stimulation (thyrotoxicosis, pheochromocytoma, perioperative stress)
59
Q

uses of beta-blockers for prevention of excessive SNS activity

A
  • minimizes response to laryngoscopy
  • hypertrophic obstructive cardiomyopathies
  • pheochromocytoma, hyperthyroidism
  • tetralogy of Fallot – minimize cyanosis
  • prevent reflex tachycardia with vasodilation use in deliberate hypotension
  • public speaking - anxiety
60
Q

beta-blockers use in management of congestive heart failure?

drugs used?

A
  • improve EF
  • increase survival rate in chronic HF
  • doses initially small and gradually increase
  • metoprolol, carvedilol, bisoprolol
61
Q

non-cardiac surgery patients that benefit from use of beta-blockers intra-op

what benefit is seen?

A
  • rhinoplasties - decreased post op pain
    • decreased pain and morphine use when esmolol given
    • less variation in HR, BP for first 3 hours
  • lap choles - decreased intra-op and post-op analgesic need with esmolol given during case
    • less analgesic/opioid needed
    • less PONV

“modulation of the sympathetic component of pain”

62
Q

benefits of beta-blockers for cardiac patients

A
  • reduced 30 day mortality in coronary surgery
  • reduced peri-op ischemia, mortality, CV complications for up to 2 years post-op
  • improved M&M in CABG pts
63
Q

effect of beta-blockers in elderly pts having non-cardiac surgery

A
  • reduced analgesic requirements
  • faster recovery from anesthesia
  • improved hemodynamic stability
64
Q

pre-op beta-blockate to uncontrolled hypertensive pts reduced myocardial ischemia how much?

A

from 28% to 2%

65
Q

T/F: beta-blockade reduces perception of noxious stimuli and has an anxiolytic effect

A

true

66
Q

effects of beta-blockade that cause cardioprotection during surgery (6)

*long

A
  1. improves the myocardial oxygen supply-demand balance
  2. decreases oxygen requirements by slowing HR and decreasing contractility
  3. blocks catecholamines from the receptors to avoid increased SNS stimulation
  4. prolongs diastole and increases time for oxygen delivery
  5. suppression of dysrhythmias – improves long-term mortality
  6. increase blood flow to ischemic myocardium
67
Q

no idea how to put this on a card…. so there’s some POISE info on the back of this

A

POISE = Peri-Operative Ischemic Evaluation

  • randomized, controlled clinical trial
  • 8,351 patients, 190 hospitals
  • 23 countries
  • pts accepted from 2002-2007
  • non-cardiac surgical procedures
  • > 45 years of age
  • hospitalized at least 24 hours post-op
68
Q

what drug did patients receive during the POISE trial?

overall results?

A
  • metoprolol ER 2-4 hrs before surgery continued for 30 days
  • increased risk of stroke, bradycardia, hypotension, and all cause mortality
  • decreased risk of non-fatal MI
69
Q

what was thought to be the cause of the increased risk of strokes from beta-blockers in the POISE trial?

A

hypotension causing ischemic strokes

70
Q

ACCF/AHA recommendations for peri-op beta-blockers

A

peri-op beta-blockers recommended in patients who are already receiving beta-blockers

71
Q

ACCF/AHA “probably recommends” peri-op beta-blockers in what patients?

A
  1. pts undergoing vascular surgery who suffer from CAD or show ischemia on peri-op testing
  2. in the presence of CAD or high cardiac risk (> 1 risk factor) who are undergoing intermediate-risk surgery
  3. where pre-op assessment for vascular surgery identifies high cardiac risk (>1 risk factor)
72
Q

ACCF/AHA says the use of peri-op beta-blockers is uncertain in what patients?

A
  • pts undergoing vascular surgery with no risk factors who are not currently taking beta-blockers
  • pts undergoing either immediate-risk procedures or vascular surgery with a single clinical risk factor in the absence of CAD
73
Q

time when ACCF/AHA says to not give beta-blockers?

A
  • high-dose beta-blockers without titration are not useful and may be harmful to patients not currently taking beta-blockers who are undergoing surgery
  • patients undergoing surgery who have an absolute contraindication to beta-blockade
74
Q

if beta blockers are indicated peri-operatively, when should they be started?

not that it’s even up to us..

A

“should be started between 30 days and 1 week before surgery or days to weeks before surgery”

75
Q

if using beta-blockers intra-operatively, what is necessary to minimize the risk of hypotension?

what are our HR/BP goals?

A

titrate to minimize risk

HR goal 60-80 bpm

systolic arterial pressure > 100 mmHg

76
Q

if pt is on beta-blockers pre-op, do we ever d/c them prior to surgery?

A

nope never

77
Q

overall outcomes of peri-op beta-blockers in a non-cardiac pt?

A

no benefit

reduction in arrhythmias and acute MI is offset by an increase in mortality and strokes

78
Q

if pt having cardiac surgery, what is the benefit of peri-op beta-blockers?

A

reduced risk of SVT and ventricular arrhythmias

79
Q

what is propranolol (Inderal)?

effects seen?

A
  • * gold standard - 1st bb
  • non-selective, pure antagonist, beta1=beta2
  • decreased HR and contractility (& CO)
  • increases peripheral vascular resistance (B2), including coronary resistance
80
Q

effects of coronary O2 supply/demand from propranolol (Inderal)?

A

decreased O2 requirement is bigger than decreased coronary blood flow due to increased vascular resistance

supply > demand

81
Q

propranolol (Inderal) dose

A

0.05 mg/kg IV in increments of 0.5-1.0 mg q 5 minutes

82
Q

propranolol (Inderal) metabolism and elimination t½

A
  • hepatic - it can decrease its own metabolism (clearance is decreased with decreases in hepatic blood flow)
  • elim t½: 2-3 hours
83
Q

propranolol (Inderal) special effects

A
  • metabolism of amide local anesthetics is decreased by propranolol due to decreased CO and more (?)
  • more fentanyl enters the circulation of a pt on propranolol due to decreased pulmonary uptake
84
Q

nadolol (Corgard)

selectivity, duration, metabolism, elimination t½?

A
  • nonselective beta-adrenergic antagonist
  • long duration: once daily
  • metabolism: 75% unchanged by kidneys, in the bile
  • elim t½: 20-40 hrs
85
Q

timolol

selectivity, typical use, side effects?

A
  • non-selective beta-adrenergic antagonist
  • usually used in eye drops for glaucoma

side effects:

  • bradycardia and hypotension can be seen when combined with anesthesia
  • can cause apnea in neonates (d/t immature BBB)
86
Q

metoprolol (Lopressor)

selectivity, effects?

A
  • beta-1 selective beta-blocker
  • blocks inotropic and chronotropic response
  • beta-2 unblocked - causes bronchodilation, vasodilation, and metabolic stability
  • can cause beta 2 blockade at high doses
87
Q

dose of metoprolol (Lopressor)

A

if HR > 80: 5 mg IV

if HR 60-80: 2.5 mg IV

hold if HR < 60 or SBP < 100

88
Q

metabolism and elimination t½ of metoprolol (Lopressor)

A

metabolism: hepatic

elim t½: 3-4 hours

89
Q

what is the most selective beta-1 antagonist?

A

atenolol (Tenormin)

90
Q

atenolol (Tenormin)

selectivity, elimination and t½

A
  • MOST selective beta1 antagonist
  • elimination: renal excretion
  • elim ½ life: 6-7 hours
91
Q

patient population where it would be advantageous to use atenolol (Tenormin) and why

A
  • diabetics
  • doesn’t interfere with metabolism

*but if it accumulates it can cause problems

(im guessing bc then it can hit beta2 too? thoughts?)

92
Q

betataxolol

selectivity, uses, benefits?

A
  • cardioselective - beta1 antagonist
  • uses: reduced elevated or normal IOP, whether or not if there’s glaucoma
  • benefits: less systemic effects vs atenolol, minimal pulmonary and cardiac effects at clinical doses
93
Q

bisoprolol

selectivity, main effect, uses?

A
  • cardioselective - beta1 antagonist
  • prominent effect: decreased HR
  • uses: treatment of essential HTN, mild-moderate CHF
94
Q

esmolol (Breviblock)

selectivity?

dose?

A
  • selective beta1 antagonist
  • dose: 0.5mg/kg IV over 60 seconds
95
Q

esmolol (Breviblock)

onset and duration

A

onset: within 5 min (sooner per TC)
duration: 10-30 min (shorter per TC)

96
Q

esmolol (Breviblock)

metabolism and elimination t½

A

metabolism: rapid hydrolysis by plasma esterases *independent of renal and hepatic function

elim t½: 9 min

97
Q

uses of esmolol (Breviblock)

*long

A
  • protection against tachycardia and hypertension related to laryngoscopy
  • pheochromocytoma, thyrotoxicosis, cocaine-induced cardiovascular toxicity
  • tetralogy of Fallot and hypertrophic obstructive cardiomyopathy
  • cardiac surgery – off bypass
  • reduce requirements of propofol, opioids
  • electroconvulsive therapy
98
Q

dose and timing of esmolol (Breviblock) if giving for laryngoscopy

A

150 mg given 2 minutes prior

99
Q

esmolol vs lidocaine or fentanyl for laryngoscopy

A

better protection than lidocaine or fentanyl against HR

100
Q

dose of esmolol for electroconvulsive therapy

A

500 mcg/kg/min

101
Q

caution when treating excessive SNS activity from cocaine or systemic absorption of topical epi due to what potential outcome?

A

fulminant pulmonary edema and irreversible cardiac collapse

cant increase HR or contractility to handle the increase in afterload

102
Q

what is receptors are affected by labetolol (Normodyne, Trandate)?

potency compared to propranolol?

A
  • selective alpha1 antagonist
  • nonselective beta1 and beta2 antagonist
  • also apparently some intrinsic beta 2 agonism :|
  • alpha to beta block ratio is 1:7
  • ¼-⅓ as potent as propranolol for beta-blocking effects
103
Q

CV effects of labetalol (Normodyne, Trandate)

A
  • decreases SVR (vasodilation from alpha1antagonist and beta2 agonist effects)
  • prevents reflex tachycardia
  • unchanged CO
104
Q

labetalol (Normodyne, Trandate)

dose and onset

A

dose: 0.1-0.5 mg/kg IV
onset: peak effect in 5-10 min

105
Q

labetalol (Normodyne, Trandate)

metabolism and elimination t½

A

metabolism: conjugation of glucuronic acid (hepatic)

elimination t½: 5-8 hrs

106
Q

uses of labetalol (Normodyne, Trandate)

A
  • hypertensive emergencies
  • increased sympathetic activity
  • pheochromocytoma
  • angina pectoris
  • controlled, deliberate hypotension
107
Q

side effects of labetalol (Normodyne, Trandate) (6)

A
  • orthostatic hypotension – most common
  • bronchospasm – nonspecific beta (offset by alpha block?)
  • congestive heart failure - beta *
  • bradycardia - beta *
  • heart block – beta *
  • fluid retention (chronic use necessitates addition diuretics)

*likely incidence and severity decreased

108
Q

esmolol vs labetalol

receptors effected

A

esmolol: selective beta1
labetalol: nonselective beta, alpha1

109
Q

esmolol vs labetalol

duration

A

esmolol: short (9 min)
labetalol: prolonged (5-8 hrs)

110
Q

esmolol vs labetalol

metabolism

A

esmolol: plasma esterases, organ independent
labetalol: hepatic

111
Q

esmolol vs labetalol

onset

A

esmolol: rapid (within 5 min)
labetalol: slower (5-10 min)

112
Q

which is better for deliberate hypotension - esmolol or labetalol?

A

esmolol

113
Q

which has an increased risk of “bleeders” that didnt show up with lower BP - esmolol or labetalol?

~need to reword this later pls excuse

A

labetalol

114
Q

carvedilol (Coreg)

receptors affected?

A
  • alpha1 blocking activity
  • nonselective beta-blocking (no intrinsic beta-agonist effects)
  • metabolites produce weak vasodilating effects
115
Q

uses for carvedilol (Coreg)

A
  • CHF
  • essential HTN
  • shown to decrease mortality with CHF

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions