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CV Exam III > Adrenergic Receptor Agonists and Antagonists Used to Treat Cardiovascular Disease > Flashcards

Adrenergic Receptor Agonists and Antagonists Used to Treat Cardiovascular Disease Flashcards

1
Q

Epinephrine Agonist

A

(a1, a2, b1, b2, b3)

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2
Q

pressor agents do what?

A

support BP

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3
Q

Norepinephrine Agonist

A

(a1, a2, b1, b3)

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4
Q

Isoproterenol Agonist

A

(b1, b2, b3)

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5
Q

Dobutamine Agonist

A

b1

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6
Q

Fenoldopam Agonist

A

D1

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7
Q

Clonidine Agonist

A

a1

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8
Q

Methyldopa Agonist

A

a2

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9
Q

Prazosin Antagonist

A

a1

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10
Q

Phentolamine Antagonist

A

a1,a2

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11
Q

Phenylephrine agonist

A

Alpha receptors

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12
Q

Beta Receptor Antagonists

Nonselective

A

Propranolol

Nadolol

Timolol

  • Pindolol
  • Carteolol

Sotalol

*= Intrinsic Sympathomimetic Activity (ISA)

b1 b2 and b3

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13
Q

Beta Receptor Antagonists

Cardioselective

A

Atenolol

*Acebutolol

Metoprolol

b1 over b2

advantages to pts with diabetes and asthma

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14
Q

Beta Receptor Antagonists

Third Generation

A

Labetalol

Carvedilol

Betaxolol

Carteolol

tratment of mi and chf

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15
Q

Para Neurotransmitters

A

Pre- Ach N

Post- Ach M

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16
Q

Sympathetic sweat glands Neurotransmitters

A

Pre- Ach N

Post- Ach M

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17
Q

Sympathetic Cardiac and smooth muscle gland cells and nerve terminals neurotransmitters

A

Pre- Ach N

Post- NE a and b

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18
Q

Sympathetic Renal vascular smooth muscle neurotransmitters

A

Pre- Ach N

Post- D1

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19
Q

Somatic skeletal muscle neurotransmitters

A

Pre- Ach N

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20
Q

Dopamine Effects

CNS

A

D1, D2, D3, D4, D5

Essential neurotransmitter in many different neural circuits

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21
Q

Dopamine Effects

Renal Afferent Blood Vessels

A

D1–Dilation

Increase blood flow to kidney

need in shock so you can increase blood flow to kidney

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22
Q

Dopamine Effects

Nerve Endings

A

D2–Modulate neurotransmitter release

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23
Q

Baroreceptor Reflex Control of Heart Rate and Blood Pressure

b1
muscarinic
a1
b2

A

b1 - stimulation of heart rate & force

muscarinic - decrease in heart rate

a1 - vasoconstriction

b2 - vasodilation

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24
Q

a1-Adrenergic Agonists

A

a1-adrenergic agonists are Pressor Agents

Phenylephrine (Neosynephrine) Prototype
Over-the–counter nasal decongestant

Midodrine (Pro Amatine)
oral –pts w/ autonomic insufficiency

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25
Q

Mixed Acting Alpha agonists

A

Metaraminol (Aramine)

have direct alpha receptor agonist properties and release norepi from nerve ending

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26
Q

pressor agents do what?

A

increase BP

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27
Q

Phenylephrine (prototype alpha agonist)

A

Effects:

vasoconstriction

increase peripheral resistance; increase BP

increased blood pressure causes reflex bradycardia (blocked by atropine)

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28
Q

Phenylephrine (prototype alpha agonist)

Uses

A

to maintain BP in hypotensive states
spinal anesthesia

paroxysmal atrial tachycardia
induces baroreceptor reflex slowing of rate

Nasal decongestant –over the counter cough and cold medications

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29
Q

Phenylephrine (prototype alpha agonist)

can also be used through iv

A

for pressor agent bc of its alpha effects

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30
Q

Dopamine (Intropin)

A

Important neurotransmitter in CNS

CNS receptors: D1, D2, D3, D4, D5

Peripheral receptors: D1, b1, a1

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31
Q

Dopamine (Intropin)

Pharmacological effects

A

blood vessels: vasodilates renal, coronary, & mesenteric vascular beds (D1 receptors)

increase blood flow to kidney

heart: mild increase in rate & force (partial agonist b1 and increases release of NE)

blood vessels: high doses cause vasoconstriction & increased BP (a1)-in the situation of “shock”, this is an undesirable effect bec. Decrease tissue perfusion

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32
Q

Dopamine (Intropin)

Dose Dependancy

A

at low levels d1 is kicked in for renal

hihger levels with b1 receptor in heart

at really ighg it will cause vaso from alpha 1

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33
Q

Dopamine (Intropin)

Clinical Uses

A

Shock; cardiogenic shock, unstable CHF

Increases cardiac output and enhances perfusion of kidney

Must monitor BP carefully because higher infusion rate or dose causes vasoconstriction and decreased tissue perfusion

Sometimes used in manage acute crisis in chronic CHF

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34
Q

Dobutamine (Dobutrex)

A

b1-selective agonist

actually complicated b1 agonist, a1 agonist/antagonist

inotropic agent to increase co

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35
Q

Dobutamine (Dobutrex)

Clinically mostly b1 effects

A

positive inotropic & some increase in rate

Cardiac output increases

little vascular effect

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36
Q

Dobutamine (Dobutrex)

Clinical uses

A

Clinical Use: cardiogenic shock, MI, CHF

short term treatemnt to give th heart a boost

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37
Q

Dobutamine (Dobutrex)

AE

A

may increase size of infarct

potential arrhythmias

Increases the work/O2
requirement

after crisis it can exacerbate the ischemia

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38
Q

a1-selective Receptor Blockers

Clinical Use

A

2ndor 3rdline treatment of essential hypertension; added to other agents from different class

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39
Q

a1-selective Receptor Blockers

Effects

A

Effects

↓PVR, ↓venous return, ↓ preload

Usually do not ↑ heart rate or cardiac output

Do not ↑ NE release (no a2 block) (good bc you arent limiting ne release)

Favorable effects on lipids
↓LDL & triglycerides; ↑HDL

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40
Q

a1-selective Receptor Blockers

AE

A

Can cause marked postural hypotension & syncope, orthostatic hypotension, especially with initial doses

Usually given at bedtime to minimize hypotensive effects

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41
Q

a1-selective Receptor Blockers

Drug list

A

Prazosin(Minipress)

Terazosin(Hytrin)

Doxazosin(Cardura)

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42
Q

Prazosin(Minipress)

A

100x a1 selective

Short t1/2, BID or TID dosing, titrate upward

Prototype?

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43
Q

Terazosin(Hytrin)

A

Like prazosin but long t1/2 & high bioavailability allows QD dosing

44
Q

Doxazosin(Cardura)

A

Like prazosin but long t1/2 & high bioavailability allows QD dosing

45
Q

bReceptor Antagonists 1st Generation bBlockers

A

Nonselective = both b1and b2blocked

Propranolol(prototype)(inderol)

Nadolol

Timolol

*Pindolol
partial agonist

*Carteolol
partial agonist

Sotalol

*ISA =intrinsic 
sympathomimetic activity (or partial agonist)
46
Q

b1-selective bBlockers 2nd Generation

A

b1-selective = Cardioselective

Atenolol (prototype)

Metoprolol (prototype)

Bisoprolol (used for CHF)

Esmolol -very short acting (surgery to control tachycardia)

Others
Acebutolol
partial agonist, ISA

47
Q

Non-selective Vasodilating bBlockers 3rd Generation

A

Alpha and Beta Blockers

Labetolol

Carvedilol

Vasodilating

Carteolol

Bucindolol (not available in USA)

48
Q

b1-selective, vasodilating 3rd Generationb Blockers

A

Betaxolol

Carteolol

Others not yet available in USA
Celiprolol
Nebivolol
Bopindolol
Nipradilol
Bevantolol
Tilisolol
49
Q

Mechanisms of Vasodilation Activated by 3rdGeneration bBlockers

A

Block Ca - block contraction

increase camp and cgmp - vasodilation

block ROS - antioxidant

50
Q

bBlockers: Clinical Uses

A

Hypertension

Congestive Heart Failure

Arrhythmias

Thyrotoxicosis:

dotn work as well in black people

51
Q

bBlockers: Clinical Uses

Hypertension

A

Decreases CO and produces slowdecrease in peripheral resistance.

Ischemic Heart Disease: Angina, myocardial infarction, acute coronary syndromes(give aspirin and beta blocker). Reduces cardiac work and O2consumption.

MI & Post-MI prophylaxis

protects against arrhythmias & limits infarct size

Acute MI: assess LV function

5-12 days after MI, reduces O2demand & spread of infarct zone

52
Q

bBlockers: Clinical Uses

Congestive Heart Failure

A

Improves morbidity and mortality

53
Q

bBlockers: Clinical Uses

Arrhythmias

A

sinus tachycardia and supraventricular ectopic beat

Recurrent VT, VF -especially when due to ischemia

54
Q

bBlockers: Clinical Uses

Thyrotoxicosis

A

hyperthyroid patients have Increased b receptor sensitivity

Beta blockers reduces sensitivity of myocardium to adrenergic stimulation in hyperthyroid patients.

Adjunctive treatment for anxiety (panic) attacks
reduces peripheral sympathetic signs and symptoms, e.g., palpitations

Migraine headache (Prophylactic treatment)

Pheochromocytoma

55
Q

B blocker Mechanisms

A

competitive antagonists at b-1, b-2, & b-3 receptors. bblockers differ in their degree of receptor selectivity

56
Q

Properties of Beta Adrenergic Receptor Blockers

A

bblockers differ in relatively lipid solubility; this effects their relative distribution to the CNS

These drugs differ in their bioavailability, biotransformation, and thus their pharmacokinetic properties

Somebblockers have intrinsic sympathomimetic activity (ISA), i.e., partial agonist activity

Some bblockers at high therapeutic doses may also have a non-receptor related quinidine-like or membrane-stabilizing effects.

57
Q

Beta Blocker Pharmacological effects

A

The effect of antagonists are due to blocking existing sympathetic tone.

Effects are greater if sympathetic tone is high, e.g., during stress (MI) or exercise.

Effects are different in normal subjects compared to patients with hypertension or myocardial ischemia.

58
Q

Beta Blocker Pharmacological effects

Heart

A

Decreases:

heart rate and cardiac output

exercise tolerance

rate of depolarization of ectopic pacemakers

O2demand

AV nodal conduction (can produce AV block)

infarct size & re-infarction-prevent sudden death

59
Q

Beta blocker cv short term effects

A

-↓CO, ↓HR

PVR ↑ to maintain BP as a result of blockade of b2 receptors & compensatory reflexes

60
Q

Beta blocker cv long term effects

A

PVR returns to initial values or ↓ in patients with hypertension (HTN)

a/bblockers –CO is maintained with greater ↓ in PVR

61
Q

Rhythm and Automaticity

bblockers

A

↓sinus rate

↓spontaneous rate of depolarization of ectopic pacemakers

Slow conduction velocity in the atria and AV node

↑ functional refractory period of AV node

62
Q

B Blocker Effects on Exercise Tolerance

A

bblockers blunt the increase in HR and contractility that normally occurs with exercise

Cardiac output (CO) is less affected because stroke volume is increased

bblockers decrease work capacity

b1-selective agents have lesser effects on exercise tolerance than nonselective agents

Coronary blood flow increases during exercise to meet the demands of the heart

Increased catecholamines during exercise or stress (MI) increase the work of the heart and myocardial oxygen demand

Patients with coronary artery disease have fixed narrowing of these vessels which attenuates the expected increase in flow, leading to myocardial ischemia.

why beta selective agents are good they dont cause this

63
Q

Beta Blocker Myocardial Oxygen Consumption

A

bblockers decrease myocardial oxygen demand

However, b blockers may tend to↑ oxygen demand by increasing end-diastolic pressures and systolic ejection time period

Usually, the net effect is to improve the relationship between cardiac supply and demand; exercise tolerance is improved in patients with angina, whose capacity to exercise is limited by chest pain

64
Q

Beta Blocker Antihypertensive Effects

A

bblockers do not usually lower BP in patients with normal BP but are effective treatment for patients with HTN

Mechanisms for this effect are not well understood

65
Q

Beta blocker Effects on Plasma Renin

A

Catecholamines stimulate b1 receptors in kidney juxtoglomerular apparatus to increase release of renin; bblockers block this increase in renin

Relevance of this effect to BP lowering is not clear.

However, BP is decreased the most in pts with elevated renin

bblockers are effective in lowering BP in patients with low or normal renin levels

Pindolol is an effective antihypertensive agent even though it has little effect on renin levels

66
Q

Bblocker Antihypertensive Mechanisms

A

Although bblockade would not be expected to decrease contractility of vascular smooth muscle, long term administration of these drugs to hypertensive pts ultimately leads to ↓ PVR

The mechanism for this effect is not known, but ↓ PVR in the face of persistent reduction in CO appears to account for much of the antihypertensive effect.

A CNS effect has been hypothesized –but there is little evidence to support this idea and drugs that penetrate into the CNS poorly are still effective.

67
Q

Bblocker

Peripheral Vasodilation Effects

These drugs produce peripheral vasodilation through a variety of mechanisms

A
  1. ↑NO
    1. Activate b2 receptors
    2. Block of a1 receptors
    3. Block Ca++entry
    4. Open K+ channels
    5. Antioxidant activity
    6. Antiproliferative effects
68
Q

Vasodilating bblockers also are associated with a decreased incidenceof

A

Bronchospasm, impaired lipid metabolism, impotence, reduced regional blood flow, increased vascular resistance, and withdrawal symptoms.

A lower incidence of these adverse effects is particularly beneficial in patients with insulin resistance, diabetes mellitus, and metabolic syndrome.

These effects are also being intensively investigated in relation to treatment of patients with congestive heart failure and peripheral arterial disease.

69
Q

Non-selective vasodilating bblockers

A

Carteolol, carvedilol, bucindolol, labetolol

70
Q

b1-selective vasodilating bblockers

A

Betaxolol, celiprolol, nebivolol

71
Q

Don’t give beta blockers to ?

72
Q

bblockers are effective in reducing the severity and frequency of attacks of

A

exertional angina & in improving survival in patients who have had an MI.
Not useful for vasospastic angina –may worsen

73
Q

Timolol, metoprolol, atenolol, and propranolol have been shown to exert

A

cardioprotective effects

74
Q

B blocker Treatment of Ischemic Heart Disease Angina and MI Beneficial effects due to

A

Fall in myocardial oxygen demand& increased flow to ischemic areas

↓HR, ↓contractility, ↓arterial BP (especially during exercise or stress

75
Q

B blocker Treatment of Ischemic Heart Disease Angina and MI is beneficial in all patients

76
Q

B blocker Treatment of Ischemic Heart Disease Angina and MI can result in profound decreases in left ventricular function.

A

In patients with limited cardiac reserve who are critically dependent on sympathetic stimulation

77
Q

B blocker Treatment of Ischemic Heart Disease Angina and MI Both acute and long-term treatment with bblockers has been repeatedly shown to

A

decrease mortality from MI by as much as 25% or more.

78
Q

B blocker Treatment of Ischemic Heart Disease Angina and MI Antiarrhythmic effects

A

are also beneficial in MI patients

79
Q

Beta blockers CHF Prevention

A

prevent HF in >50%, strokes reduced by >38%, occurrence of CAD and other CV events significantly decreased, improve ventricular remodeling

80
Q

Beta blockers CHF Mortality rates reduced

A

65% by carvedilol, 34% by metoprolol, 33% by bisoprolol –hospitalization reduced

81
Q

Beta blockers CHF increase

A

LVEF, cause beneficial remodeling of heart

82
Q

Beta blockers CHF use only in

A

stable CHF (class II & III), gradually titrate dose

83
Q

Beta blockers CHF pts also treated with

A

diuretic, ACE inhibitors, & digoxin

84
Q

Beta Blocker Relative Contraindications

A

Bronchial Smooth Muscle

Block sympathomimetic bronchodilation
precaution or contraindication in asthma & COPD

Metabolic

Blocks beta receptor effects on lipolysis and glycogenolysis.

May mask signs of hypoglycemia, e.g., tachycardia, BP changes, tremor. Delays recovery from insulin-induced hypoglycemia.

85
Q

Beta blocker Side Effects

A

Common:

dizziness, fatigue, diarrhea, constipation, nausea, depression, sexual dysfunction, bizarre dreams

Severe but rare
purpura, rash, fever

May Interfere with SGOT and BUN tests

Chronic use VLDL & ↓HDL
effects vary among agents

86
Q

bblockers sudden withdrawal

A

rebound hypertension, anginal attack & possibly MI if drug suddenly withdrawn after chronic therapy. Beta receptor synthesis is increased by beta blocker use. Example of receptor up-regulation, supersensitivity.

87
Q

bblockers Other contraindication

A

Acute treatment of decompensated heart failure; 2nd and 3rd degree heart block, and cardiogenic shock.

88
Q

bBlockers: Drug Interactions

A

Other hypotensive medications
reserpine, guanethidine, methyldopa

Other antiarrhythmic agents
calcium channels blockers
lidocaine

Insulin and oral hypoglycemic drugs
prolongs hypoglycemia and masks signs

Masks symptoms of hyperthyroidism

89
Q

Other Nonselective bBlockers

A

Nadolol (Corgard)

Timolol (Blocadren)

Pindolol (Visken)

Carteolol

90
Q

Nadolol (Corgard)

A

longer acting; once-per-day dosing

91
Q

Timolol (Blocadren)

A

more potent than propranolol

92
Q

Pindolol (Visken)

A

partial agonist; partial blockade
less incidence of rebound hypertension
less bradycardia

93
Q

Carteolol

A

has vasodilating properties

94
Q

b1-Selective Blockers

A

All are more potent at b1 than b2 receptors
at higher doses, block b2 as well
lessen risk of bronchospasm -still contraindicated in asthmatic
do not usually prolong hypoglycemia

Atenolol(Tenormin)

Metoprolol(Lopressor, Topral XL)

Acebutolol (Sectral)

Bisoprolol(Zebeta)

95
Q

Atenolol(Tenormin)

A

hypertension

96
Q

Metoprolol(Lopressor, Topral XL)

A

hypertension, CHF

97
Q

Acebutolol (Sectral)

A

partial agonist, hypertension, arrhythmias

98
Q

Bisoprolol(Zebeta)

A

clinical trials show dramatic benefits in CHF

99
Q

Esmolol (Brevibloc)

A

Very rapid onset & short duration of action

b1-selective

Used as IV infusion for peri-operative tachycardia and hypertension, arrhythmias

Used in electroconvulsive therapy

100
Q

Labetolol (Normodyne,Trandate)

A

Selective a 1blocker

Nonselective b1 & b2 blocker

Partial agonist at b2

Clinical Uses:
hypertension
pheochromocytoma

101
Q

Carvedilol (Coreg)

A

Nonselective b-blocker + a-blocker

Very lipid soluble

Also has antioxidant properties

Very dramatic results in CHF clinical trials
Decreased mortality by 65%

102
Q

a2-selective Receptor AgonistsCentrally Acting Antihypertensive Agents

A

Brain stem a2-receptors
Control (inhibit) sympathetic outflow to periphery
Decrease sympathetic tone

sympatholytic agents

103
Q

Methyldopa (Aldomet)

A

False neurotransmitter concept

Converted to methyl-NE

stored in vesicles instead of NE

released & acts as a centrally acting a2-agonist

Decreases central sympathetic outflow & decreases blood pressure

A preferred drug to treat hypertension in pregnancybecause of its safety

104
Q

Methyldopa (Aldomet)

A

Many side effects –sedation, dry mouth, sexual dysfunction

105
Q

Clonidine (Catapres) overview

A

An a2-adrenergic receptor agonist

IV-increase BP (peripheral a2B) followed by decreased BP (central a2A)

Oral -decreased BP (decreased C.O., preload)

Patch -same as oral

106
Q

Clonidine (Catapres) clinical use

A

Essential hypertension (very little use now)

adjunct for narcotic, alcohol, & tobacco withdrawal and many other “off label” uses

107
Q

Clonidine (Catapres) side effects

A

dry mouth, sedation, impotence

sudden withdrawal causes hypertensive crisis

CV Exam III (17 decks)

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