Chapter 30: Adrenergic Agonists

DRUG LIST

ALPHA – AND - BETA ALPHA -SPECIFIC ADRENERGIC BETA-SPECIFIC ADRENERGIC

ADRENERGIC AGONISTS AGONISTS AGONISTS
Dobutamine Clonidine (alpha2 – specific) Albuterol
Dopamine Midodrine Arformoterol
Ephedrine Phenylephrine (P) Formoterol
Epinephrine (P) Indacaterol
Norepinephrine Isoproterenol (P)
Levalbuterol
Metaproterenol
Olodaterol
Salmeterol
Terbutaline
ADRENGERIC AGONIST  naturally occurring catecholamine
 treatment of shock
 “sympathomimetic” drug  stimulates the heart and blood pressure but
o mimics effect of SNS also causes a renal and splanchnic arteriole
 a drug that stimulates the adrenergic receptors dilation that increases blood flow to the kidneys,
of the sympathetic nervous system, either preventing the diminished renal blood supply
directly (by reacting with receptor sites) or and possible renal shutdown
indirectly (by increasing norepinephrine levels)
 can affect both the alpha- and beta-receptors, Epinephrine / norepinephrine
or they can act at specific receptor sites
 use of adrenergic agonists varies from  naturally occurring catecholamines that interact
ophthalmic preparations for dilating pupils to with both alpha- and beta-adrenergic receptors
systemic preparations used to support  used for the treatment of shock and to stimulate
individuals experiencing shock the body after cardiac arrest and for immediate
relief of anaphylaxis
ALPHA – AND – BETA ADRENERGIC AGONISTS
Dobutamine
 Drugs that are generally sympathomimetic
 stimulate all of the adrenergic receptors; that is,  synthetic catecholamines
they affect both alpha- and beta-receptors  acts at both receptor sites
 Some of these drugs are naturally occurring  has a slight preference for beta1- receptor sites
catecholamines  treatment of heart failure because it can
increase myocardial contractility without much
Drugs in Focus change in rate and does not increase the
oxygen demand of the cardiac muscle

Ephedrine

 synthetic catecholamines
 stimulates the release of norepinephrine from
nerve endings and acts directly on adrenergic
receptor sites
 Many over-the-counter (OTC) cold products
contain ephedrine or pseudoephedrine

Pharmacokinetics
Therapeutic actions
 absorbed rapidly after injection or passage
 Heart rate increases with increased myocardial through mucous membranes
contractility  metabolized in the liver
 bronchi dilate, and respirations increase in rate  excreted in the urine
and depth  given intravenously (IV) to achieve rapid onset
 blood vessels constrict, causing an increase in of action (emergency situation)
blood pressure
 intraocular pressure decreases contraindications
 glycogenolysis
o breakdown of stored glucose to  known hypersensitivity (hypersensitivity
reactions)
increase blood glucose level
 pheochromocytoma (systemic overload of
 pupils dilate
catecholamines could be fatal)
 sweating can increase
 tachyarrhythmias or ventricular fibrillation
Indications (increased heart rate and oxygen consumption
usually caused by these drugs could
 treatment of hypotensive states or shock, exacerbate these conditions)
bronchospasm, and some types of asthma  hypovolemia (fluid replacement would be the
treatment for the associated hypotension)
Dopamine
  halogenated hydrocarbon general anesthetics
(sensitize the myocardium to catecholamines
and could cause serious cardiac effects

cautions

 peripheral vascular disease (atherosclerosis,

Raynaud disease, diabetic endarteritis)
 pregnancy and lactation

Adverse effects

 associated with the drugs’ effects on the SNS

o arrhythmias, hypertension,
palpitations, angina, and dyspnea ALPHA – SPECIFIC ADRENERGIC AGONISTS
related to the effects on the heart and
cardiovascular (CV) system  “alpha-agonists”
 nausea, vomiting, and constipation related to  Specifically stimulating to alpha-receptors
the depressant effects on the gastrointestinal within SNS, causing body responses seen
(GI) tract when alpha-receptors are stimulated
 headache, sweating, feelings of tension or
anxiety, and piloerection related to sympathetic Drugs in focus
stimulation
 Hypokalemia
o result of the release of aldosterone
that occurs with sympathetic
stimulation and the resultant loss of
potassium
 muscle cramps Therapeutic actions
o related to the shift in potassium
 all of these drugs cause vasoconstriction, care  result from the stimulation of alpha-receptors
must be taken to avoid extravasation of any within the SNS
infused drug
o necrosis and cell death Phenylephrine

Drug – drug interaction  potent vasoconstrictor and alpha1-agonist

 little or no effect on the heart or bronchi
 Increased effects of tricyclic antidepressants  used in many combination cold and allergy
(TCAs) and monoamine oxidase inhibitors products
(MAOIs) can occur because of the increased  Parental: used to treat shock or shock-like
norepinephrine levels or increased receptor states, to overcome paroxysmal
stimulation supraventricular tachycardia, to prolong local
 increased risk of hypertension if alpha- and anesthesia, and to maintain blood pressure
beta-adrenergic agonists are given with any during spinal anesthesia
other drugs that cause hypertension, including  Topical: treat allergic rhinitis and to relieve the
herbal therapies and OTC preparations symptoms of otitis media
 lose effectiveness if combined with any  Ophthalmic: dilate the pupils for eye
adrenergic antagonist examination, before surgery, or to relieve
elevated eye pressure associated with
glaucoma
 effective in constricting topical vessels and
decreasing the swelling, signs, and symptoms
of rhinitis

Clonidine

 stimulates CNS alpha2-receptors

 leads to decreased sympathetic outflow from
the CNS because the alpha2-receptors
moderate the release of norepinephrine from
the nerve axon
 available in oral and transdermal forms for use
to control hypertension and as an injection for
epidural infusion to control pain in cancer
patients
 associated with many more CNS effects (bad
Nursing Consideration dreams, sedation, drowsiness, fatigue,
headache)
 cause extreme hypotension, heart failure, and
bradycardia due to its decreased effects of the
sympathetic outflow from the CNS

pharmacokinetics

 well absorbed from all routes of administration

  reach peak levels in a short period—20 to 45  Clonidine has a decreased antihypertensive
minutes effect if taken with TCAs
 metabolized in the liver  Clonidine combined with propranolol result to
 excreted in the urine paradoxical hypertension
 transdermal form of clonidine is slow-release  Midodrine can precipitate increased drug
and has a 7-day duration of effects, so it only effects of digoxin, beta blockers, and many
needs to be replaced once a week antipsychotics
 Phenylephrine can be given intramuscularly  adrenergic agonist will lose effectiveness if
(IM), subcutaneously, IV, orally, and as a nasal combined with any adrenergic antagonist
or an ophthalmic solution

Contraindications

 presence of allergy to the specific drug

 severe hypertension or tachycardia (possible
additive effects)
 narrow – angle glaucoma (exacerbated by
arterial constriction)
 no adequate studies about use during
pregnancy and lactation

Caution

 CV disease or vasomotor spasm (aggravated

by the vascular effects of the drug)
 thyrotoxicosis or diabetes (thyroid - stimulating
and glucose-elevating effects of sympathetic
stimulation)
 renal or hepatic impairment (interfere with
metabolism and excretion of the drug)

Adverse Effects Nursing considerations

 CNS effects:
o feelings of anxiety, restlessness,
depression, fatigue, strange dreams,
and personality changes
o Blurred vision and sensitivity to light
may occur because of the pupil
dilation that occurs when the
sympathetic system is stimulated
 CV effects: arrhythmias, ECG changes, blood
pressure changes, and peripheral vascular
problems
 GI effects: Nausea, vomiting, and anorexia can
occur related to the depressant effects of the
SNS
 GU effects: decreased urinary output, difficulty
urinating, dysuria, and changes in sexual
function related to the sympathetic stimulation
of these systems

These drugs should not be stopped suddenly BETA – SPECIFIC ADRENERGIC AGONISTS
- adrenergic receptors will be sensitive to catecholamines  beta2-specific agonists and are used to
manage and treat bronchial spasm, asthma,
- sudden withdrawal can lead to tachycardia,
and other obstructive pulmonary conditions
hypertension, arrhythmias, flushing, and even death
 specifically stimulating to beta-receptors within
- Avoid these effects by tapering the drug over 2 to 4 days SNS, causing body responses seen when beta-
when it is being discontinued receptors are stimulated

if phenylephrine is given IV, care should be taken to avoid Drugs in Focus

extravasation

vasoconstricting effects of the drug can lead to necrosis

and cell death in the area of extravasation

Drug – drug interaction

 Phenylephrine combined with MAOIs can

cause severe hypertension, headache, and
hyperpyrexia
 Increased sympathomimetic effects occur when
phenylephrine is combined with TCAs
  Pulmonary effects: difficulty breathing,
coughing, and bronchospasm to severe
pulmonary edema
 GI effects: GI upset, nausea, vomiting, and
anorexia
 Hypokalemia
o result of the release of aldosterone
that occurs with sympathetic
stimulation and the resultant loss of
potassium
 sweating, pupil dilation, rash, and muscle
cramps that occur as a result of the potassium
shift

drug – drug interaction

 Increased sympathomimetic effects can be

expected if this drug is taken with other
sympathomimetic drugs
 Decreased therapeutic effects can occur if this
drug is combined with beta-adrenergic blockers

Therapeutic actions & indications

 effects of isoproterenol are related to its

stimulation of all beta-adrenergic receptors
 increased heart rate, conductivity, and
contractility
 bronchodilation
 increased blood flow to skeletal muscles and
splanchnic beds
 relaxation of the uterus
 isoproterenol exerts a “coronary steal” effect,
diverting blood away from injured or hypoxic
areas of the heart muscle, an effect that can
increase the size and extent of an evolving
myocardial infarction

pharmacokinetics Nursing considerations

 rapidly distributed after injection

 metabolized in the liver
 excreted in the urine
 half-life is relatively short—less than 1 hour

contraindications

 presence of allergy to the drug or any

components of the drug
 pulmonary hypertension (exacerbated by the
effects of the drug)
 anesthesia with halogenated hydrocarbons
(sensitize the myocardium to catecholamines
and could cause a severe reaction)
 eclampsia, uterine hemorrhage, and
intrauterine death (complicated by uterine
relaxation or increased blood pressure)
 pregnancy and lactation

Caution

 diabetes, thyroid disease, vasomotor problems,

degenerative heart disease, or history of stroke
(exacerbated by the sympathomimetic effects
of the drug)
 severe renal impairment (alter excretion of the
drug)

adverse effects

 CNS effects: restlessness, anxiety, fear,

tremor, fatigue, and headache. CV effects can
include tachycardia, angina, myocardial
infarction, and palpitations