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NUNA 681(pharm) > CV Drugs- Adrenergic-receptor Antagonists > Flashcards

CV Drugs- Adrenergic-receptor Antagonists Flashcards

1
Q

alpha-adrenergic antagonists- MOA: binds

A

competitively or covalently with alpha receptors

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2
Q

alpha-adrenergic antagonists- MOA: prevent the effect of

A

catecholamines and other alpha agonists form entering with the alpha receptor

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3
Q

alpha-adrenergic antagonists- MOA: located in

A

the heart and peripheral vasculature

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4
Q

alpha-adrenergic antagonists- effects

A
  1. vasodilation (orthostatic hypotension)
  2. reflex tachycardia
  3. blocks inhibition of insulin secretion
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5
Q

alpha-adrenergic antagonists- side effects prevent use as

A

essential antihypertensives

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6
Q

alpha-adrenergic antagonists- if beta blockade is not present,

A

maximal cardiac stimulation is allowed

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7
Q

phentolamine (Regitine)- MOA

A

competitive binding

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8
Q

phentolamine (Regitine)- blockade is

A

nonselective, alpha 1 and alpha 2

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9
Q

phentolamine (Regitine)- effects: vasodilation- __ blockade and direct action on __

A

alpha1

vascular smooth muscle

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10
Q

phentolamine (Regitine)- cardiac effects

A

cardiac stimulation (increased HR and CO)

reflex and alpha 2 blockade (blocks negative feedback of NE)

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11
Q

phentolamine (Regitine)- side effects

A
  1. dysrhythmias
  2. angina
  3. hyperperistalsis
  4. abdominal pain
  5. diarrhea due to parasympathetic tone
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12
Q

phentolamine (Regitine)- uses

A
  1. acute HTN emergencies, pheochromocytoma
  2. accidental infiltration of a sympathomimetic (5-15 mg in 10ml)
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13
Q

phentolamine (Regitine)- onset

A

2 min

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14
Q

phentolamine (Regitine)- duration

A

10-15 min

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15
Q

phenoxybenzamine (Dibenzyline)- MOA

A

irreversible covalent binding to alpha-receptors

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16
Q

phenoxybenzamine (Dibenzyline)- blockade

A

nonselective, alpha1>alpha2

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17
Q

phenoxybenzamine (Dibenzyline)- effects: vasodilation

A

orthostatic hypotension exaggerated with hypovolemia, HTN

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18
Q

phenoxybenzamine (Dibenzyline)- effects: impariment of

A

compensatory vasoconstriction (lower BP with hypovolemia and vasodilation drugs like volatile agents)

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19
Q

phenoxybenzamine (Dibenzyline)- __ CO

A

increased

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20
Q

phenoxybenzamine (Dibenzyline)- very little change in

A

renal blood flow even with decreased BP

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21
Q

phenoxybenzamine (Dibenzyline)- prevents the inhibition of

A

insulin secretion

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22
Q

phenoxybenzamine (Dibenzyline)- causes pupil

A

constriction

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23
Q

phenoxybenzamine (Dibenzyline)- chronić use may cause

A

sedation

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24
Q

phenoxybenzamine (Dibenzyline)- __ congestion

A

nasal

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25
Q

phenoxybenzamine (Dibenzyline)- uses

A
  1. control BP in pheochromocytoma
  2. in trauma patients, used to reverse vasoconstriction (shock), only after volume replacement
  3. Raynaud’s syndrome
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26
Q

phenoxybenzamine (Dibenzyline)- onset

A

up to 60 min (IV)

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27
Q

phenoxybenzamine (Dibenzyline)- elimination 1/2 life

A

24 hours (duration can last up to 4 days)

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28
Q

prazosin (Minipress)- MOA

A

competitive, reversible binding with alpha receptors

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29
Q

prazosin (Minipress)- blockade

A

selective alpha 1 antagonist

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30
Q

prazosin (Minipress)- effects

A
  1. vasodilation of both arterioles and veins
  2. less reflex tachycardia (alpha 2 not blocked)
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31
Q

prazosin (Minipress)- uses

A
  1. HTN
  2. severe CHF
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32
Q

prazosin (Minipress)- onset

A

within 2 hours

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33
Q

prazosin (Minipress)- duration

A

10-24 hours

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34
Q

doxazosin (Cardura)- blockade

A

selective, alpha 1 antagonist

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35
Q

doxazosin (Cardura)- dose

A

once daily

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36
Q

doxazosin (Cardura)- peak

A

2-3 hours

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37
Q

doxazosin (Cardura)- elimination 1/2 life

A

22 hours

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38
Q

doxazosin (Cardura)- indications

A
  1. BPH
  2. HTN
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39
Q

beta-adrenergic antagonist- MOA: competitive binding to __ to block __

A

beta receptors

the effect of catecholamines and agonist on the heart and smooth muscles of airways and blood vessels

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40
Q

beta-adrenergic antagonists- prolonged or chronic use of beta blockers causes

A

up-regulation of beta receptors

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41
Q

classifications of beta-adrenergic antagonists

A
  1. nonselective
  2. cardioselective
  3. partial antagonist
  4. pure antagonist
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42
Q

nonselective beta-adrenergic antagonists block

A

both beta 1 and beta 2 (timolol and propranolol)

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43
Q

cardioselective beta-adrenergic antagonists block

A

beta 1 (metoprolol, atenolol, esmolol)

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44
Q

beta-adrenergic antagonists partial antagonists

A

intrinsic sympathomimetic effect (less myocardial depression and HR reduction)

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45
Q

beta-adrenergic antagonists put antagonist

A

no sympathomimetic effect

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46
Q

selectivity of beta-adrenergic antagonists is

A

dose-related; if a big enough dose of a carioselective beta-blocker is give, the effect can impact beta-2 receptors

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47
Q

beta 1 blockade removes

A

sympathetic stimulation to the heart

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48
Q

beta 1 blockade effects

A
  1. negative inotropic effects
  2. negative chronotropic effects
  3. negative dromotropic effects
  4. increased in lusitropy
  5. decrease in bathmotropy
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49
Q

beta 1 blockade negative inotropic effects

A

myocardial depression

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50
Q

beta 1 blockade negative chronotropic effects

A

slows HR, sinus rate

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51
Q

beta 1 blockade negative dromotropic effects

A
  1. slows the conduction of impulse through the AV node
  2. slows rate of phase 4 depolarization
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52
Q

beta 1 blockade increase in lusitropy effects

A

ventricular relaxation

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53
Q

beta 1 blockade decrease in bathmotrophy effects

A

reduced degreee of excitability

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54
Q

beta 2 blockade effects

A
  1. vasoconstriction
  2. unopposed alpha vasoconstriction can cause decreased LV ejection
  3. bronchoconstriction
  4. prevents glycogenolysis, blocks tachycardia related to hypoglycemia, alters fat metabolism (lipolysis)
  5. inhibits uptake of K into skeletal muscle cells (increased serum K)
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55
Q

effects of beta-adrenergic antagonists- additive __ with anesthetics

A

myocardial depressant effects but safe to continue

hal>iso

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56
Q

effects of beta-adrenergic antagonists- CNS

A

cross BBB- fatigue, lethargy, vivid dream, memory loss, depression

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57
Q

effects of beta-adrenergic antagonists- cross placenta so

A

fetal bradycardia, hypotension, hypoglycemia

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58
Q

effects of beta-adrenergic antagonists- GI

A

nausea, vomiting, diarrhea

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59
Q

effects of beta-adrenergic antagonists- chronic use

A

fever, rash, myopathy, alopecia, thrombocytopenia

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60
Q

contraindications to beta-blockade-

A
  1. AV heart block
  2. hypovolemia
  3. COPD
  4. diabetic
  5. PVD, Raynaud’s syndrome, alpha-adrenergic agonist
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61
Q

contraindications to beta-blockade- AV heart block

A

slowed conduction may be enhanced

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62
Q

contraindications to beta-blockade- hypovolemia

A

eliminates tachycardia that is compensating for decrease in volume

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63
Q

contraindications to beta-blockade- COPD

A

increased airway resistance (nonselective or high doses)

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64
Q

contraindications to beta-blockade- diabetic

A

mask signs of hypoglycemia (nonselective or high doses)

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65
Q

contraindications to beta-blockade- PVD, Raynaud’s syndrome, or alpha-adrenergic agonists

A

vasoconstriction unopposed (nonselective), cold extremities

66
Q

signs/symptoms of an overdose of beta-adrenergic antagonist

A
  1. bradycardia
  2. low cardiac output
  3. hypotension
  4. cariogenic shock
  5. bronchospasm
  6. prolonged intraventricular conduction of impulses
  7. hypoglycemia- rarely
67
Q

overdose of beta-adrenergic antagonist TREATMENT

A
  1. atropine 7 mcg/kg IV (0.5 mg IV) first
  2. isoproterenol 2-25 mcg/min (with nonselective beta-blockers)
  3. dobutamine
  4. glucagon and CaCl
  5. if heart rate dose not increase with drugs, a pacemaker
  6. hemodialysis
68
Q

dobutamine is used for overdose of beta-adrenergic antagonist TREATMENT when

A

when beta-blockade is from a beta-blocker with no sympathomimetic effects

69
Q

glucagon (1-10mg) overdose of beta-adrenergic antagonist TREATMENT is

A

drug of choice due to independent action; effects smooth muscle and cardiac contractility

70
Q

CaCl (250mg-1gm) for overdose of beta-adrenergic antagonist TREATMENT to

A

increase cardiac function independent of the blocked receptors

71
Q

acute withdrawal of beta-blockade

A
  1. increased sympathetic stimulation due to up-regulation of beta receptors
  2. profound hypertension, tachycardia, contractility
72
Q

acute withdrawal of beta blockade occurs within

A

24-48 hours

73
Q

during acute withdrawal of beta-blockade, avoid

A

continued preop beta-blockade therapy; infusion of propranolol 3 mg/hr IV

74
Q

treatment of HTN with beta-adrenergic antagonists

A
  1. decrease HR, decrease CO
  2. decrease contractility in larger doses
  3. with vasodilatory, prevention of reflex tachycardia
  4. decrease renin, decrease aldosterone, prevention of Na/water retention
75
Q

management of angina pectoris with beta-adrenergic antagonists

A

decreased myocardial oxygen consumption- decreased HR, contractility

76
Q

post-MI infection use of beta-adrenergic antagonists- historically

A

decreases mortality and reinfarctions
1. increases changes of survival 20-40%
2. begin within 5-28 days after MI and continue for 1-3 years
3. within 12 hours of onset of infarct may actually decrease infarct size and dysrhythmias

77
Q

post-MI infection use of beta-adrenergic antagonists- not with

A

acute coronary syndrome with ST elevation or cariogenic shock

78
Q

post-MI infection use of beta-adrenergic antagonists- both selective and nonselective drugs have __; nonselective have an effect on __

A

cardioprotective effects

K (prevents reduction) and may decrease dysrhythmias

79
Q

cardiac dysrhythmias use of beta-adrenergic antagonists- decrease activity of

A

SA node and conduction through the AV node

80
Q

cardiac dysrhythmias use of beta-adrenergic antagonists- slow

A

depolarization of ectopic pacemakers

81
Q

cardiac dysrhythmias use of beta-adrenergic antagonists- suppresses both

A

supraventicular and ventricular ectopy

82
Q

cardiac dysrhythmias use of beta-adrenergic antagonists- rapid suppression of

A

excessive sympathetic stimulation (thyrotoxicosis, pheochromocytoma, period stress)

83
Q

prevention of excessive sympathetic nervous system activity use of beta-adrenergic antagonists- minimizes repose to

A

laryngoscopy

84
Q

prevention of excessive sympathetic nervous system activity use of beta-adrenergic antagonists- __ cardiomyopathies

A

hypertrophic obstructive

85
Q

prevention of excessive sympathetic nervous system activity use of beta-adrenergic antagonists- __ and __

A

pheochromocytoma, hyperthyroidism

86
Q

prevention of excessive sympathetic nervous system activity use of beta-adrenergic antagonists- TOF, minimizes

87
Q

prevention of excessive sympathetic nervous system activity use of beta-adrenergic antagonists- prevent __ with vasodilation use in deliberate hypotension

A

reflex tachycardia

88
Q

prevention of excessive sympathetic nervous system activity use of beta-adrenergic antagonists- public speaking

89
Q

management of CHF (metoprolol, carvedilol, bisoprolol) use of beta-adrenergic antagonists-

A
  1. improve EF
  2. increase survival rate in HF
  3. doses initially small and gradually increase
90
Q

use of beta-adrenergic antagonists that cause cardio protection during surgery-

A
  1. improvement of the myocardial oxygen supply-demand balance
  2. decrease oxygen requirements by slowing HR and decreasing contractility
  3. blocks catecholamines from the receptors to avoid increased sympathetic 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
91
Q

periop beta blockers are recommended for patients who

A

are receiving beta-blocker for the treatment of conditions with ACC/AHA Class I indication for the drug

92
Q

periop beta blockers are probably recommended in patients who

A
  1. undergoing vascular surgery who suffer from CAD or show ischemia on preop testing
  2. in the presence of CAD or high cardiac risk (more than one risk factor) who are undergoing intermediate-risk surgery
  3. when preop assessment for vascular surgery identifies high cardiac risk (more than one risk factor)
93
Q

the usefulness of beta-blockers is uncertain in patients

A
  1. undergoing vascular surgery with no risk factors who are not currently taking beta-blockers
  2. undergoing either immediate-risk procedures or vascular surgery with a single clinical risk factor in the absence of CAD
94
Q

beta blockers are not to be given

A
  1. high-dose beta blockers without titration are not useful and may be harmful to patients not currently taking beta-blockers who are undergoing surgery
  2. patients undergoing surgery who have an absolute contraindication to beta blockade
95
Q

periop beta blockade should be continued

A

in patient on chronic treatment

96
Q

periop beta blockade with cardiac surgery benefit

A

reduces risk of SVT, vent arrhythmias

97
Q

periop beta blockade, should they be indicated perioperatively, should be started

A

between 30 days and 1 weeks before surgery or days to weeks before surgery

98
Q

periop beta blockade, titration of beta blocker to __ and __ is necessary in order to minimize or reduce the risk of hypotension

A

heart rate 60-80 beats per minute

systolic arterial pressure > 100 mmHg

99
Q

periop beta blockade for non cardiac

A

no benefit, reduction in arrhythmias, acute MI is offset by increase in mortality, stroke

100
Q

propranolol (Inderal) blockade

A

nonselective, pure antagonist, beta 1 = beta 2

101
Q

propranolol (Inderal) effects

A
  1. decreases HR and contractility (and CO)
  2. increase peripheral vascular resistance (beta 2), including coronary vascular resistance
102
Q

propranolol (Inderal) dose

A

0.05 mg/kg IV in increments of 0.5-1 mg every 5 minutes

103
Q

propranolol (Inderal) metabolism

104
Q

propranolol (Inderal) clearance is decreased with __

A

decrease in hepatic blood flow; it can decrease its own metabolism

105
Q

propranolol (Inderal) elimination 1/2 life

106
Q

propranolol (Inderal)- special effects on LA

A

the metabolism of amide LA is decreased by propranolol due to decreased CO and more

107
Q

propranolol (Inderal)- special effects on fentanyl

A

enters the circulation of a patient on propranolol due to decreased pulmonary uptake

108
Q

Nadolol (Corgard)- is

A

nonselective

109
Q

Nadolol (Corgard)- duration of action

A

long; given once daily

110
Q

Nadolol (Corgard)- metabolism

A

75% excreted unchanged by the kidneys, in the bile

111
Q

Nadolol (Corgard)- elimination 1/2 life

A

20-40 hours

112
Q

timolol is

A

nonselective

113
Q

timolol- is used for

A

topical eye gets for glaucoma

114
Q

timolol- side effects

A

bradycardia and hypotension caused by gets during anesthesia

115
Q

timolol- can cause

A

apnea in neonates with immature blood brain barrier

116
Q

metoprolol (Lopressor)- blockade

A

selective for beta1- receptors

117
Q

metoprolol (Lopressor)- effects

A

blocks inotropic and chronotropic responses

118
Q

metoprolol (Lopressor)- beta 2 receptors remain unblocked allowing

A

bronchodilation, vasodilation, and metabolic stability (unless higher doses are used)

119
Q

metoprolol (Lopressor)- bolus

A

5mg IV (if HR > 80); 2.5 mg IV (if HR 60-80); hold if HR <60 or SBP < 100mmHg

120
Q

metoprolol (Lopressor)- metabolism

121
Q

metoprolol (Lopressor)- elimination 1/2 life

122
Q

most selective beta 1 antagonist

A

atenolol (Tenormin)

123
Q

atenolol (Tenormin) elimination

A

renal excretion

124
Q

atenolol (Tenormin) elimination 1/2 life

125
Q

atenolol (Tenormin) does not interfere with __ so can be given with caution to __

A

metabolism

diabetic patients

126
Q

betaxolol blockade

A

beta 1 antagonist

127
Q

betaxolol is an alternative to

A

timolol (nonselective)

128
Q

betaxolol reduces

A

elevated as well as normal intraocular pressure, whether or not accompanied by glaucoma

129
Q

betaxolol __ effects with clinical doses

A

minimal pulmonary and cardiac

130
Q

bisoprolol blockade

A

beta 1 antagonist

131
Q

bisoprolol prominent effect

A

decreased HR

132
Q

bisoprolol is used for treatment of

A

essential HTN, mild to moderate CHF

133
Q

esmolol (Brevibloc) blockade

A

selective beta 1 antagonist

134
Q

esmolol (Brevibloc) dose

A

0.5 mg/kg IV over 60 seconds

135
Q

esmolol (Brevibloc) onset

A

within 5 minutes

136
Q

esmolol (Brevibloc) duration

A

10-30 minutes

137
Q

esmolol (Brevibloc) metabolism

A

rapid hydrolysis by plasma esterases (independent of renal and hepatic function)

138
Q

esmolol (Brevibloc) elimination 1/2 life

139
Q

esmolol (Brevibloc) uses: protection against

A

tachycardia and hypertension related to laryngoscopy- give esmolol 150 mg 2 minutes prior to laryngoscopy; better protection than lidocaine or fentanyl against HR

140
Q

esmolol (Brevibloc) uses: __, __, __ induced CV toxicity

A

pheochromocytoma, thyrotoxicosis, cocaine-induced

141
Q

esmolol (Brevibloc) uses: __ and __ cardiomyopathy

A

TOF and hypertrophic obstructive

142
Q

esmolol (Brevibloc) uses: __ surgery

A

cardiac surgery off bypass

143
Q

esmolol (Brevibloc) uses: to reduce requirements of

A

propofol, opioids

144
Q

esmolol (Brevibloc) uses: ECT dose

A

500 mcg/kg/min

145
Q

labetalol (Normodyne, Trandate)- blockade

A

selective alpha 1 and nonselective beta 1 and beta 2

146
Q

labetalol (Normodyne, Trandate)- 1/4 to 1/3 as potent as __ in beta blockade

A

propranolol

147
Q

labetalol (Normodyne, Trandate)- CV effects

A
  1. decreases SVR (vasodilation- alpha 1 antagonists and beta 2 agonist effect)
  2. prevents reflex tachycardia (bc beta 1)
  3. unchanged CO
148
Q

labetalol (Normodyne, Trandate)- dose

A

0.1-0.5 mg/kg IV

149
Q

labetalol (Normodyne, Trandate)- onset of peak effect

A

5-10 minutes

150
Q

labetalol (Normodyne, Trandate)- metabolism

A

conjugation of glucuronic acid (hepatic)

151
Q

labetalol (Normodyne, Trandate)- elimination 1/2 life

152
Q

labetalol (Normodyne, Trandate)- uses

A
  1. HTN emergencies, increased SNS activity, pheochromocytoma
  2. angina pectoris
  3. controlled, deliberate hypotension
153
Q

labetalol (Normodyne, Trandate)- side effects, most common

A

orthostatic hypotension

154
Q

labetalol (Normodyne, Trandate)- __spasm from __

A

bronchospasm

nonspecific beta

155
Q

labetalol (Normodyne, Trandate)- from beta effects

A

CHF, bradycardia, heart block (incidence and severity decreased)

156
Q

labetalol (Normodyne, Trandate)- chronic use necessitates

A

addition of diuretic from fluid retention

157
Q

carvedilol (Coreg)- blockade

A

alpha 1 blocking activity, non selective beta blocking (no intrinsic beta agonist effect (different from labetalol)

158
Q

carvedilol (Coreg)- metabolites produce

A

weak vasodilation effect

159
Q

carvedilol (Coreg)- indicated for

A

CHF and essential HTN

160
Q

carvedilol (Coreg)- is shown to

A

decrease mortality with CHF

NUNA 681(pharm) (12 decks)

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