Autonomic Nervous System effector organ cells.

The
efferent pathways in the ANS
Central Nervous System (CNS) are divided into two
– consists of brain and spinal branches: the sympathetic &
cord the parasympathetic nerves,
Peripheral Nervous System which are collectively called
(PNS) – located outside the the sympathetic nervous
brain & spinal cord, is made up system & the
of two divisions: the autonomic parasympathetic nervous
& the somatic system.
❖ After interpretation by the CNS, ► The sympathetic &
the PNS receives stimuli & parasympathetic nervous
initiates responses to stimuli systems act on the same organs
Autonomic Nervous System (ANS) but produce opposite
✔ also called the visceral responses to provide
system, innervates (acts on) homeostasis (balance). Drugs
smooth muscles & glands. Its act on the sympathetic &
functions include control & parasympathetic NS by either
regulation of the heart, stimulating or depressing
respiratory system, GIT, responses.
bladder, eyes, & glands Sympathetic Nervous System
✔ Is an involuntary NS over ► Is also called the adrenergic
which a person has little or no system because, at one time, it
control. We breathe, our hearts was believed that adrenaline
beat, & peristalsis occurs was the neurotransmitter that
without us realizing it. innervated the smooth muscle.
✔ 2 sets of neurons in autonomic The neurotransmitter is,
component of the PNS are the: however, norepinephrine.
• Afferent (sensory) neurons ► The adrenergic receptor
• Efferent (motor) neurons organ cells are of 4 types:
Alpha1, alpha2, beta1, beta2. .
► Afferent (sensory) neurons – Norepinephrine is released
send impulses to the CNS, from the terminal nerve ending
where they are interpreted & stimulates the cell receptor
► Efferent (motor) neurons – to produce a response.
receive the impulses
(information) from the brain & Parasympathetic Nervous System
transmit those impulses ► Is also called the cholinergic
through the spinal cord to the system because the
 neurotransmitter at the end of
the neuron that innervates the
muscle is acetylcholine.
► Cholinergic receptors at organ
cells are either nicotinic or
muscarinic, meaning that they
are stimulated by the alkaloid’s
nicotine & muscarine,
respectively.
► Acetylcholine stimulates the Sympathetic and Parasympathetic Responses to
receptor cells to produce a Drugs
response, but the enzyme,
acetylcholinesterase, may Sympathetic Parasympathetic Response
s
inactivate acetylcholine before
it reaches the receptor cell. sympathomimeti Parasympathomimeti Opposite
❖ Drugs that mimic (imitate) the c c response
neurotransmitters
norepinephrine and Sympatholytic Parasympatholytic Opposite
response
acetylcholine produce a
response opposite to each sympathomimeti Parasympatholytic Similar
other in the same organ. For c response
example, an adrenergic drug
(sympathomimetic ) increases Sympatholytic Parasympathomimeti Similar
the heart rate, whereas a c response
cholinergic
(parasympathomimetic)
decreases heart rate.
❖ A drug that mimics the
sympathetic NS & a drug that
blocks the parasympathetic NS
can cause similar responses in
the organ. For instance, the
sympathomimetic and the
parasympatholytic drugs
both increase the heart rate;
the adrenergic blocker and
the cholinergic drug both
decrease the heart rate.
Autonomic Nervous System: Sympathetic and Parasympathetic Nervous System
Sympathetic Stimulants Parasympathetic Stimulants

Sympathomimetics (adrenergics, Direct-Acting

adrenomimetics, or adrenergic Parasympathomimetics (cholinergic or
agonists) cholinergic Agonists)
Action: Action:
Increase BP Decrease BP
Increase pulse rate Decrease pulse rate
Relax bronchioles Constrict bronchioles
Dilates pupils of eye Increase urinary contraction
Relax uterine muscles Increase peristalsis
Increase blood sugar Indirect-Acting
Cholinesterase Inhibitors (anticholinesterase)
Action:
Increase muscle tone

Sympathetic Depressants Parasympathetic Depressants

Sympatholytics (adrenergic blockers, Parasympatholytics (anticholinergics,

adrenolytics, or adrenergic cholinergic antagonists, or antispasmodics)
antagonists) Action:
Action: Increase pulse rate
Decrease pulse rate Decrease mucous secretions
Decrease BP Decrease GI motility
Constrict bronchioles Increase urinary retention

Adrenergic & Adrenergic Blockers
► Two groups of drugs that
affect the sympathetic NS: the
adrenergics (sympathomimetic
or adrenomimetics) and the
adrenergic blockers
(parasympatholytics or
adrenolytics).
ADRENERGICS
✔ Drugs that stimulate the
sympathetic NS
✔ Also called adrenergic
agonists, sympathomimetics,
or adrenomimetics because
they mimic the sympathetic
neurotransmitters (i.e.,
norepinephrine and
epinephrine). They act on one
or more adrenergic receptor
sites located on the cells of
smooth muscles, such as the
heart, bronchial walls, GIT,
urinary bladder, and ciliary
muscle of the eye.
✔ There are many adrenergic
receptors; the 4 main
receptors are alpha1, alpha2,
beta1, and beta2 , which
mediate the major responses.
Alpha-adrenergic Receptors
► Located in the vascular tissue
(vessels) of smooth muscles.
► When alpha1 – receptor is
stimulated, the arterioles and
venule constrict, thereby
increasing peripheral
resistance and blood return to
the heart. Circulation is
improved and BP is increased.
When there is too much
stimulation, the blood flow
decreased to the vital organs.
► The alpha2-receptor is located
in the postganglionic
sympathetic nerve endings.
When stimulated, it inhibits
the release of
norepinephrine thus leading
to a decrease in
vasoconstriction. This results
in a decrease in BP.
► The beta1-receptor are located
primarily in the heart.
Stimulation of beta1- receptor
increases myocardial
contractility and heart rate.
► The beta2 - receptors are
found mostly in the smooth
muscles of the lung, the
arterioles of skeletal
muscles, and the uterine
muscle. Stimulation of beta2 –
receptor causes:
• Relaxation of the smooth
muscles of the lungs,
 resulting in a decrease in dilates blood
uterine contraction. vessels; produces
• An increase in blood flow to hypotension;
the skeletal muscles decreases GI
• Relaxation of the uterine motility and tone
muscle, resulting in a
decrease in uterine Beta1 Increases heart
contraction. rate and force of
Dopaminergic – another contraction;
adrenergic receptor and is located increases renin
in the renal, mesenteric, coronary, secretion, which
and cerebral arteries. When this increases BP
receptor is stimulated, the vessels
dilate and blood flow increases. Beta2 Dilates the
Only dopamine can activate this bronchioles;
receptor. promotes GI and
Effects of Adrenergic at Receptors uterine
relaxation;
Receptor Physiologic promotes
Responses increase in blood
Alpha1 Increases force of sugar through
heart glycogenolysis in
contraction; the liver;
vasoconstriction increases blood
increases BP; flow in the
mydriasis skeletal muscles
(dilation of
pupils) occurs;
salivary glands
decrease
secretion;
bladder and
prostate capsule
increases
contraction and
ejaculation
Alpha2 Inhibits the
release of
norepinephrine;
 Ephedrine
✔ Mixed-acting
sympathomimetics
Acts indirectly by stimulating the
release of norepinephrine from the
nerve terminals and acts directly on
the alpha1-, beta1-, and beta2-
receptors.
✔ Helpful to treat idiopathic
orthostatic hypotension and
hypotension that results from
spinal anesthesia
Classification of ✔ also stimulates beta2 -
Sympathomimetics/Adrenomimet receptors which dilate
ics bronchial tubes, and is useful
► 3 categories according to to treat mild forms of bronchial
their effects on organ cells: asthma
• Direct – acting ► Example:
sympathomimetics – which Catecholamines
directly stimulate the ✔ Are the chemical structures of
adrenergic receptor (e.g., a substance (either
epinephrine or endogenous or synthetic) that
norepinephrine) can produce as
• indirect – acting sympathomimetic response
sympathomimetics – which ✔ Examples of endogenous
stimulates the release of catecholamines are
norepinephrine from the epinephrine, norepinephrine,
terminal nerve endings (e.g., and dopamine
ampethamine) ✔ Synthetic catecholamines are
• Mixed-acting isoproterenol and dobutamine
sympathomimetics – both Noncatecholamines
direct and indirect acting, ✔ E.g., phenelephrine,
which stimulate the metaproterenol, albuterol –
adrenergic receptor sites and stimulate the adrenergic
stimulate the release of receptors. Most
norepinephrine from the noncatecholamines have a
terminal nerve endings longer duration of action than
the endogenous or synthetic
Example: catecholamines.
► Examples: response is purely
Epinephrine bronchodilation
✔ Stimulate more than one of the ✔ An asthmatic client may
adrenergic receptor sites therefore respond better by
✔ Acts on alpha1-, alpha2-, and taking albuterol than
beta2 – receptor sites isoproterenol because its
✔ Responses from these receptor primary action is on the beta2 –
sites include an increase in BP, receptor.
pupil dilation, increase in heart ✔ Primary use is to prevent and
rate (tachycardia), and treat bronchospasms. With
bronchodilation. Because inhalation, the onset of action
epinephrine affects three is faster than with oral
different adrenergic receptors, administration, although the
it is not selective; in other duration of action is the same
words, it is considered for both oral and inhalation
nonselective to one receptor. preparations.
✔ frequently used in ✔ Tremors, restlessness, and
emergencies to combat nervousness may occur when
anaphylaxis, which is life- high doses are taken – s/e are
threatening allergic response. most likely caused by reflex
✔ It is a potent inotropic (force of effect of beta1 – receptors.
muscular contraction) drug ✔ If albuterol is taken with
that causes the blood to MOAI, a hypertensive crisis
constrict; thus, the BP may occur.
increases, the heart rate ► Example:
increases, and the bronchial Isoproterenol Hydrochloride
tubes dilate. (Isuprel)
✔ High doses can result in cardiac ✔ An adrenergic drug, activates
dysrhythmias; therefore, ECG beta1- and beta2 – receptors
should be monitored ✔ More specific than epinephrine
✔ Can also cause renal because it acts on two different
vasoconstriction, thereby, adrenergic receptors but is not
decreasing renal perfusion and completely selective.
urinary output. ✔ The response in beta1 and beta2
► Examples: stimulation is
Albuterol (Albuterol sulfate – bronchodilation and an
Proventil, Ventolin) increase in heart rate. For
✔ Selective for beta2 – example, when a client takes
adrenergic receptors, so the isoproterenol to control
 asthma for dilating the bronchi, rate), and beta2 (dilates
an increase in heart rate also bronchial tubes) receptors.
occurs as a result of beta1 Isoproterenol (Isuprel)
stimulation. stimulates the beta1 and beta2
✔ When used excessively, receptors. Albuterol (Proventil)
severe tachycardia can stimulates the beta2 – receptor
result. ✔ Assess the drugs client takes
► Example: and report possible drug-drug
Clonidine and Methyldopa interactions. Beta-blockers
✔ Clonidine (Catapres) and decrease the effect of
methyldopa (Aldomet) are epinephrine.
selective alpha2 – adrenergic ✔ Determine the client’s health
drugs that are primarily used history. Most adrenergic drugs
to treat hypertension. are contraindicated if the client
✔ The accepted theory for the has cardiac dysrhythmias,
action of alpha2 drugs is that narrow-angled glaucoma, or
they regulate the release of cardiogenic shock.
norepinephrine by inhibiting ✔ Evaluate the results of
its release. laboratory values and compare
✔ Alpha2 are also believed to with future laboratory findings.
produce a cardiovascular
depression by stimulating
alpha2 receptors in the CNS
leading to a decrease in BP NURSING DIAGNOSIS
❖ side effects commonly ✔ Risk for impaired tissue
associated with adrenergic integrity
drugs include hypertension, ✔ Decreased cardiac output
tachycardia, palpitations, PLANNING
dysrhythmias, tremors, ✔ Client’s v/s will be closely
dizziness, urinary difficulty, monitored and will be within
n/v. normal or acceptable ranges.
NURSING INTERVENTIONS
Nursing Process – Adrenergic ✔ Record client’s v/s. report sign
Agonist of increasing BP and increasing
ASSESSMENT pulse rate. If client receives an
✔ Record v/s for future alpha-adrenergic drug
comparison. Epinephrine intravenously for shock, the BP
stimulates alpha1 (increase should be checked every 3 to 5
BP), beta1 (increases heart
 minutes or as indicated to ✔ Instruct client to read labels on
avoid severe hypertension. all OTC drugs for cold
✔ Report the s/e of adrenergic symptoms and diet pills. Many
drugs, such as tachycardia, of these have properties of
palpitations, tremors, dizziness sympathetic (adrenergic,
and increase BP. sympathomimetics) drugs and
✔ Check client’s urinary output should not be taken if client is
and assess for bladder hypertensive or has diabetes
distention. Urinary distention mellitus, cardiac dysrhythmias,
can result from high drug dose or coronary artery disease.
or continuous use of ✔ Advise mothers not to take
adrenergic drugs. drugs that contain sympathetic
NURSING INTERVENTIONS drugs while nursing infants.
✔ For cardiac resuscitation, These drugs pass into the
administer epinephrine 1:1000 breastmilk.
IV (1mg/ml), which may be ✔ Explain to client that
diluted in 10 ml of saline continuous use of nasal spray
solution (prescribed). or drops that contain
✔ Monitor IV site frequently adrenergics may result to in
when administering nasal congestion rebound
norepinephrine bitartate (inflamed and congested nasal
(Levaterenol) or dopamine tissue).
(Intropin) because infiltration ✔ Inform client and family how to
of these drugs causes tissue administer cold medications by
necrosis. These drugs should spray or drops in the nostrils.
be diluted sufficiently in IV Spray should be used with the
fluids. An antidote for head in an upright position.
norepinephrine (Levophed) The use of nasal spray while
and dopamine is phentolamine lying down can cause systemic
mesylate (Regitine) 5 to 10 mg, absorption. Coloration of nasal
diluted in 10 to 15 ml of saline spray or drops might indicate
infiltrated into the area. deterioration.
✔ Offer food to client when giving ADRENERGIC BLOCKERS
adrenergic drugs to avoid n/v. (ANTAGONISTS or
✔ Evaluate laboratory test SYMPATHOLYTICS)
results. Blood glucose levels ► Drugs that block the effects of
may increased. the adrenergic
CLIENT TEACHING neurotransmitter.
General
► They act as antagonists to the orthostatic hypotension can
adrenergic agonists by result. Dizziness may also be a
blocking the alpha– and beta- symptom of a drop in BP. As
receptor sites. They block the the BP decreases, pulse rate
effects of the neurotransmitter usually increases to
either directly by occupying compensate for the low BP and
the alpha- or the beta- inadequate blood flow.
receptors or by inhibiting the ✔ Can be used to treat peripheral
release of the vascular disease (e.g.,
neurotransmitter’s Raynaud’s disease).
norepinephrine and Vasodilation occurs permitting
epinephrine. more blood flow to the
► Three sympatholytic extremities
receptors are alpha1, beta1, ✔ s/e include cardiac
and beta2. dysrhythmias, flush,
ALPHA-ADRENERGIC BLOCKERS hypotension, and reflex
(ALPHA BLOCKERS) tachycardia.
✔ drugs that block or inhibit a Effects of Adrenergic Blockers
response at the alpha- Receptor Responses
adrenergic receptor site Alpha1 Vasodilation:
✔ Alpha-blocking agents are decreases BP;
divided into two groups: reflex
• Selective alpha-blockers – tachycardia
that blocks alpha1 might result;
• Non-selective alpha blockers miosis
– that block alpha1 and alpha2 (constriction of
ALPHA-ADRENERGIC BLOCKERS pupil) occurs;
(ALPHA BLOCKERS) suppresses
✔ Can cause orthostatic ejaculation;
hypotension and reflex reduces
tachycardia, many of these contraction of
drugs are not as frequently the smooth
prescribed as the beta blockers, muscles in the
are helpful in decreasing bladder neck
symptoms of benign prostatic and prostate
hypertrophy (BPH). gland
✔ Promote vasodilation, thus beta1 Decreases heart
causing a decrease in BP. If rate; reduces
vasodilation is long-standing, force of
 contraction ► s/e include bradycardia,
beta2 Constricts dizziness, hypotension, h/a,
bronchioles; hyperglycemia, intensified
contracts hypoglycemia, and
uterus; inhibits agranulocytosis. Usually s/e
glycogenolysis, are dose related.
which can Propranolol hydrochloride
decrease blood (Inderal)
sugar ✔ First beta-blocker prescribed
to treat angina, cardiac
Beta – Adrenergic Blockers dysrhythmias, and
► Commonly called beta- hypertension.
blockers, decrease heart ✔ Although it is still prescribed
rate; a decrease in BP usually today, it has many s/e, partly
follows. because of its nonselective
► Some of the beta-blockers are response in blocking both
nonselective blocking both beta1- and Beta2 – receptors. It
beta1- and beta2 - receptor. is contraindicated for clients
► Not only does the pulse rate with asthma or second- or
decrease because of beta1 – third- degree heart block.
blocking, but ✔ extensively metabolized in
bronchoconstriction also liver (hepatic first-pass); thus,
occurs only a small amount of the drug
► Nonselective beta-blockers reaches the systemic
(beta1 and beta2) should be circulation
used with extreme caution in ✔ Well-absorbed from GIT. It
any client who has chronic crosses the blood-brain barrier
obstructive pulmonary disease and the placenta and is found
(COPD) or asthma. in breast milk.
► If the desired effect is to ✔ By blocking both types of beta-
decrease the pulse rate and BP, receptors, propranolol
then a selective beta1- blocker, decreases the heart rate and,
such as metoprolol tartrate secondarily the BP. It also
(Lopressor), may be ordered. causes the bronchial tubes to
► Are useful in treating cardiac constrict and the uterus to
dysrhythmias, mild contract.
hypertension, mild tachycardia, ✔ Many drugs interact with
and angina pectoris propranolol: phenytoin,
isoproterenol, NSAIDs,
 barbiturates, and xanthines
(caffeine, theophylline)
decrease the drug effect of
propranolol.
✔ When propranolol is taken
with digoxin or a calcium
blocker, atrioventricular
(AV) block may occur.
Adrenergic Neuron Blockers
► Drugs that block the release of
norepinephrine from the
sympathetic terminal neurons
► Classified as a subdivision of
beta-adrenergic blockers
► Clinical use is to decrease BP
► Guanethidine monosulfate
(Ismelin) and guanadrel sulfate
(Hylorel), examples of
adrenergic neuron blockers,
are potent antihypertensive
agents.
NURSING PROCESS: ADRENERGIC
NEURON BLOCKERS
ASSESSMENT
• Obtain baseline v/s and ECG
for future comparison.
Bradycardia and decrease in
BP are common cardiac effects
of beta-adrenergic blockers.
Beta-adrenergic blockers are
frequently called beta-blockers
because they block beta1 and
beta2 (nonselective) or beta1
(cardiac selective) receptors.
• Assess whether client has
respiratory problems by
listening for signs or
wheezing or Inoting dyspnea
(difficulty in breathing). If
the beta-blocker is
nonselective, not only does
the pulse rate decrease but
also bronchoconstriction can
result. Client with asthma
should take beta1 blocker
such as metoprolol (Lopressor)
and avoid nonselective beta-
blockers.
• Determine the drugs client
currently takes. Report if any
are phenothiazines, digoxin,
calcium channel blockers, or
other antihypertensives.
• Record client’s urine output
and use for future comparison.
NURSING DIAGNOSIS
• Decreased cardiac output
• Impaired tissue integrity
PLANNING
• Client will comply with drug
regimen.
• Client’s v/s will be within the
desired range.
NURSING INTERVENTIONS
• Monitor client’s v/s. Report
marked changes such as
marked decreases in BP and
pulse rate.
• Administer IV propranolol
undiluted or diluted in D5W.
• Note any complaints of
excessive dizziness or
lightheadedness
• Report any complaint of stuffy
nose. Vasodilation results from
the use of alpha-adrenergic
blockers, and nasal congestion
may occur.
NURSING INTERVENTIONS hypotension by slowly rising
• Determine whether client has from supine or sitting position
diabetes and receives a beta- to standing.
adrenergic blocker; the insulin • Inform client and family of
dose or oral hypoglycemic may possible mood changes when
need to be adjusted. taking beta-blockers. Mood
• Client who take beta-blockers changes can include
do not have normal depression, nightmares, and
compensatory mechanisms suicidal tendencies.
while in states of shock. To • Warn male that certain beta-
resuscitate such clients, blockers (e.g., propranolol,
glucagon must be given in high metoprolol, pindolol) and
doses to counteract the alpha blockers (e.g., prazosin)
sympatholytic effects of beta- may cause impotence or a
blockers. decrease in libido. Usually, the
CLIENT TEACHING problem is dose related.
General
• Advise client to avoid abruptly
stopping a beta-blocker;
rebound hypertension,
rebound tachycardia, or an
angina attack could result.
• Instruct client to comply with
the drug regimen.
• Educate clients about insulin
therapy that early warning
signs of hypoglycemia (e.g.,
tachycardia, nervousness) may
be masked by the beta-blocker.
• Direct clients on insulin
therapy to monitor their blood
sugar carefully and to follow
diet orders.
SELF-ADMINISTRATION
• Teach client and family how to
take pulse and BP.
SIDE EFFECTS
• Encourage client to avoid
orthostatic (postural)