1. Adrenergic Agonists and Adrenergic Blockers
Chapter 18
Adrenergic Agonists and Adrenergic Blockers
Copyright © 2015, 2012, 2009, 2006, 2003, 2000, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

2. Adrenergic Agonists Function of adrenergics Sympathetic responses
Stimulation of sympathetic nervous system or use of adrenergic drugs can cause dilation of pupils and bronchioles; increased heart rate; constriction of blood vessels; relaxation of muscles in GI tract, bladder, and uterus.
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3. Effects of Adrenergic Agonists at Receptors
Alpha1
Increases cardiac contractility, vasoconstriction
Dilates pupils, decreases salivary gland secretion
Increases bladder & prostate contraction
Alpha2
Inhibits norepinephrine release
Promotes vasodilation and decreased BP
Decreases GI motility and tone
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4. Effects of Adrenergic Agonists at Receptors (Cont.)
Beta1
Increases cardiac contractility, heart rate
Increases renin secretion, BP
Beta2
Decreases GI tone and motility
Bronchodilation
Increases blood flow in skeletal muscles
Relaxes smooth muscles of uterus
Activates liver glycogenolysis
Increases blood glucose
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5. Effects of Adrenergic Agonists at Receptors (Cont.)
Dopaminergic–located in the renal, mesenteric, coronary, and cerebral arteries
Vasodilation
Increases blood flow
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6. Neurotransmitter Inactivation
Reuptake of transmitter back into neuron
Enzymatic transformation or degradation
MAO inside neuron
COMT outside neuron
Diffusion away from the receptor
Drugs halt termination of neurotransmitter by inhibiting
Norepinephrine reuptake
Norepinephrine degradation
After the transmitter (i.e., norepinephrine) has performed its function, the action must be stopped to prevent prolonging the effect.
Two enzymes that inactivate the metabolism of norepinephrine are monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT).
Copyright © 2015, 2012, 2009, 2006, 2003, 2000, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

7. Classification of Adrenergic Agonists/Sympathomimetics
Direct-acting
Epinephrine, norepinephrine
Indirect-acting
Amphetamine
Mixed-acting
Ephedrine
Direct-acting sympathomimetics: directly stimulate adrenergic receptor
Indirect-acting sympathomimetics: stimulate release of norepinephrine from terminal nerve endings
Mixed-acting sympathomimetics: stimulate adrenergic receptor sites and stimulate release of norepinephrine from terminal nerve endings
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8. Catecholamines Catecholamines Noncatecholamines Endogenous Synthetic
Epinephrine, norepinephrine, dopamine
Synthetic
Isoproterenol, dobutamine
Noncatecholamines
Most have longer duration of action than endogenous and synthetic
Phenylephrine, metaproterenol, albuterol
Catecholamines: chemical structures of a substance that can produce a sympathomimetic response
Noncatecholamines: stimulate adrenergic receptors
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9. Epinephrine (Adrenaline)
Nonselective
Action
Alpha1 increases the blood pressure.
Beta1 increases heart rate.
Beta2 promotes bronchodilation.
Contraindications and caution
Cardiac dysrhythmias, hypertension
Hyperthyroidism
Pregnancy
Epinephrine is nonselective, as it excites three different adrenergic receptors approximately equally.
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10. Epinephrine (Cont.) Action Uses Inotropic Vasoconstrictor
Bronchodilator
Uses
Anaphylaxis, anaphylactic shock
Bronchospasms
Cardiogenic shock, cardiac arrest
Inotropic: strengthens myocardial contraction, increasing cardiac output
Vasoconstriction: increases heart rate and systolic blood pressure
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11. Epinephrine (Cont.) Side effects/adverse reactions Drug interaction
Cardiac dysrhythmias
Hypotension, flushing, reflex tachycardia
Decreased renal perfusion
Drug interaction
Beta blockers
Decrease epinephrine action
Digoxin
Causes cardiac dysrhythmias
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12. Epinephrine (Cont.) Nursing interventions
Monitor BP, heart rate, urine output.
Report tachycardia, palpitations, tremors, dizziness, hypertension.
Monitor IV site for infiltration.
Antidote: phentolamine mesylate (Regitine)
Avoid cold medicines and diet pills if hypertensive, diabetic, CAD, or dysrhythmic.
Avoid adrenergics when breastfeeding.
Avoid continuous use of adrenergic nasal sprays.
Patient should be placed on cardiac monitor for early detection of dysrhythmias.
Monitor urine output for early detection of decreased renal perfusion.
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13. Albuterol (Proventil)
Selective
Acts on beta2-adrenergic receptors
Promotes bronchodilation
Uses
Treats bronchospasm, asthma, bronchitis, COPD
Caution
Severe cardiac disease
Hypertension, hyperthyroidism
Diabetes mellitus, pregnancy
Albuterol is selective for beta2-adrenergic receptors so response is purely bronchodilation.
Refer to Table 18-2, Adrenergic Drugs (Alpha1, Beta1, and Beta2).
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14. Albuterol (Cont.) Side effects/adverse reactions Drug interaction
Tremors, nervousness, restlessness
Dizziness, reflex tachycardia
Hallucinations
Cardiac dysrhythmias
Drug interaction
May increase effect with other sympathomimetics, MAO inhibitors, and tricyclic antidepressants
Antagonize effect with beta blockers
Refer to Prototype Drug Chart 18-2, Albuterol.
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15. Nursing Process: Adrenergic Agonist
Assessment
Nursing diagnosis
Planning
Nursing interventions
Patient teaching
Cultural considerations
Evaluation
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16. Central-Acting Alpha Agonists
Clonidine (Catapres)
Selective alpha2-adrenergic agonist (sympathomimetic)
Used primarily to treat hypertension
Methyldopa (Aldomet)
Alpha-adrenergic agonist (sympathomimetic) that acts within the CNS
Taken up into the brainstem neurons and converted to methylnorepinephrine, which is an alpha2-adrenergic agonist that leads to alpha2 activation
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17. Side Effects: Adrenergic Agonists
Hypertension
Tachycardia
Palpitations
Restlessness
Tremors
Dysrhythmias
Dizziness
Urinary retention
Nausea, vomiting
Dyspnea
Pulmonary edema
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18. Adrenergic Blockers/Adrenergic Antagonists/Sympatholytics
Block effects of adrenergic neurotransmitter
Block alpha and beta receptor sites
Directly by occupying receptors
Indirectly by inhibiting release of neurotransmitters epinephrine and norepinephrine
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19. Effects of Adrenergic Blockers at Receptors
Alpha1
Vasodilation, decreased BP, reflex tachycardia
Pupil constriction
Suppresses ejaculation
Reduces contraction of smooth muscles in bladder neck and prostate
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20. Effects of Adrenergic Blockers at Receptors (Cont.)
Beta1
Reduces cardiac contractility
Decreases pulse
Beta2
Bronchoconstriction
Contracts uterus
Inhibits glycogenolysis
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21. Alpha Blockers
Drugs that inhibit a response at alpha-adrenergic receptor site
Selective
Block alpha1
Nonselective
Block alpha1 and alpha2
Action
Promote vasodilation
Use
Decrease symptoms of BPH, PVD
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22. Beta-Adrenergic Blockers
Beta blocker action
Decrease BP and pulse
Nonselective beta blockers
Blocks beta1
Blocks beta2
Bronchoconstriction
Use with caution in patients with COPD
Propranolol HCl (Inderal)
Uses
Angina, cardiac dysrhythmias, hypertension, heart failure
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23. Beta-Adrenergic Blockers (Cont.)
Nonselective propranolol
Contraindications
COPD
Side effects/adverse reactions
Impotence, decreased libido, reversible alopecia
Drug interactions
Decreased drug effects with
Phenytoin, isoproterenol, NSAIDs, barbiturates, caffeine, theophylline
Heart block may occur with
Digoxin, calcium channel blockers
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24. Beta-Adrenergic Blockers (Cont.)
Selective beta blockers
Blocks beta1 only
Decrease BP and HR
Fewer side effects
Metoprolol (Lopressor), atenolol (Tenormin)
Side effects/adverse reactions
Bradycardia, hypotension, dysrhythmias, headaches, dizziness, fainting, fatigue, mental depression, nausea, vomiting, diarrhea, blood dyscrasias, hypoglycemia
Copyright © 2015, 2012, 2009, 2006, 2003, 2000, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

25. Beta-Adrenergic Blockers (Cont.)
Intrinsic sympathomimetic activity (ISA)
Ability of certain beta blockers to bind with a beta receptor to prevent strong agonists from binding to that receptor producing complete activation
Nonselective beta blockers with ISA–carteolol, carvedilol, penbutolol, and pindolol
Selective blocker with ISA–acebutolol
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26. Beta-Adrenergic Blockers (Cont.)
Drug interactions
Decreased effects with
NSAIDs
Increased effects with
Prazosin, terazosin, atropine, anticholinergics
Increased risk of hypoglycemia with
Insulin, sulfonylureas
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27. Adrenergic Neuron Blockers
Block release of norepinephrine
Subdivision of adrenergic blockers
Used to decrease BP
Example
Reserpine (Serpalan): reduces the serotonin and catecholamine transmitters. Depletion of these neurotransmitters may lead to severe mental depression.
Adrenergic neuron blockers are drugs that block release of norepinephrine from the sympathetic terminal neurons.
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28. Nursing Process: Adrenergic Neuron Blockers
Assessment
Nursing diagnosis
Planning
Nursing interventions
Patient teaching
Cultural considerations
Evaluation
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29. Practice Question #1
When teaching a patient who has been prescribed metoprolol (Lopressor) about side/adverse effects, which is the highest priority teaching point?
Report any complaints of stuffy nose.
Instruct the patient how to take a pulse.
Check for bladder distention.
Warn of possible impotence and decreased libido.
Answer: B
Rationale: It is most important for the patient to learn how to monitor the heart rate because of the side effect of bradycardia with metoprolol.
Copyright © 2015, 2012, 2009, 2006, 2003, 2000, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

30. Practice Question #2
Stimulation of which adrenergic receptor results in dilation of vessels and decrease in blood pressure?
Alpha1
Alpha2
Beta1
Beta2
Answer: B
Rationale: When alpha2 receptors are stimulated, they inhibit the release of norepinephrine, leading to a decrease in vasoconstriction. This results in vasodilation and a decrease in blood
pressure.
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31. Practice Question #3
The nurse is teaching the patient about the side effects of atenolol (Tenormin). These include
pupillary constriction.
blood vessel dilation.
bronchospasm.
tachycardia.
Answer: C
Rationale: The side effects commonly associated with beta blockers are bradycardia, hypotension, headache, dizziness, cold extremities, hypoglycemia, and bronchospasm.
Copyright © 2015, 2012, 2009, 2006, 2003, 2000, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

32. Practice Question #4
A nurse is administering epinephrine to a patient during a cardiac arrest. The primary desired action of this medication is to
stimulate a heart rate.
decrease cerebral blood flow.
initiate respirations.
increase blood flow to the kidneys.
Answer: A
Rationale: Epinephrine is a potent inotropic (strengthens myocardial contraction) drug that increases cardiac output, promotes vasoconstriction and systolic blood pressure elevation, increases heart rate, and produces bronchodilation. High doses can result in cardiac dysrhythmias necessitating electrocardiogram (ECG) monitoring. Epinephrine can also cause renal vasoconstriction, thereby decreasing renal perfusion and urinary output.
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33. Practice Question #5
A patient has been prescribed atenolol (Tenormin). To ensure safe dosing, the nurse teaches the patient to frequently assess what parameter?
A. Daily weight
B. Heart rate
C. Urine output
D. Body temperature
Answer: B
Rationale: The side effects commonly associated with atenolol (Tenormin), which is a beta blocker, include bradycardia, hypotension, headache, dizziness, cold extremities, hypoglycemia, and bronchospasm.
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34. Practice Question #6
A patient is receiving dopamine (Intropin) intravenously. Which drug should the nurse have available to treat extravasation and tissue necrosis?
A. Norepinephrine bitartrate (Levophed)
B. Nadolol (Corgard)
C. Phentolamine mesylate (Regitine)
D. Clonidine (Catapres)
Answer: C
Rationale: The antidote for IV extravasation of dopamine is phentolamine mesylate (Regitine) 5 to 10 mg, diluted in 10 to 15 mL of saline infiltrated into the area. Norepinephrine bitartrate (Levophed) is an adrenergic agonist; nadolol (Corgard) is a beta1 and beta2 adrenergic blocker, and clonidine (Catapres) is a selective alpha2-adrenergic agonist (sympathomimetic) used primarily to treat hypertension.
Copyright © 2015, 2012, 2009, 2006, 2003, 2000, 1997, 1993 by Saunders, an imprint of Elsevier Inc.