Autonomic Nervous System

 Central Nervous System (CNS) – consists of brain and spinal cord

 Peripheral Nervous System (PNS) – located outside the brain & spinal cord, is made up of
two divisions: the autonomic & the somatic
 After interpretation by the CNS, the PNS receives stimuli & initiates responses to stimuli
Autonomic Nervous System (ANS)
 also called the visceral system, innervates (acts on) smooth muscles & glands. Its functions
include control & regulation of the heart, respiratory system, GIT, bladder, eyes, & glands
 Is an involuntary NS over which a person has little or no control. We breathe, our hearts beat,
& peristalsis occurs without us realizing it.
 2 sets of neurons in autonomic component of the PNS are the:
1. Afferent (sensory) neurons
2. Efferent (motor) neurons
Autonomic Nervous System
 Afferent (sensory) neurons – send impulses to the CNS, where they are interpreted
 Efferent (motor) neurons – receive the impulses (information) from the brain & transmit
those impulses through the spinal cord to the effector organ cells. The efferent pathways in the
ANS are divided into two branches: the sympathetic & the parasympathetic nerves, which
are collectively called the sympathetic nervous system & the parasympathetic nervous
system.
 The sympathetic & parasympathetic nervous systems act on the same organs but produce
opposite responses to provide homeostasis (balance). Drugs act on the sympathetic &
parasympathetic NS by either stimulating or depressing responses.
Sympathetic Nervous System
 Isalso called the adrenergic system because, at one time, it was
believed that adrenaline was the neurotransmitter that innervated the
smooth muscle. The neurotransmitter is, however, norepinephrine.
 The adrenergic receptor organ cells are of 4 types: Alpha1, alpha2,
beta1, beta2. . Norepinephrine is released from the terminal nerve
ending & stimulates the cell receptor to produce a response.
Parasympathetic Nervous System
 Isalso called the cholinergic 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 alkaloids nicotine &
muscarine, respectively.
 Acetylcholine stimulates the receptor cells to produce a response, but
the enzyme, acetylcholinesterase, may inactivate acetylcholine before
it reaches the receptor cell.
Parasympathetic Nervous System
 Drugs that mimic (imitate) the neurotransmitters norepinephrine and
acetylcholine produce a response opposite to each other in the same organ. For
example, an adrenergic drug (sympathomimetic ) increases the heart rate,
whereas a 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.
 Sympathetic and Parasympathetic Responses to Drugs

Sympathetic Parasympathetic Responses

Sympathomimetic Parasympathomimetic Opposite response

Sympatholytic Parasympatholytic Opposite response

sympathomimetic Parasympatholytic Similar response

Sympatholytic Parasympathomimetic Similar response

 Autonomic Nervous System: Sympathetic and Parasympathetic Nervous System
Sympathetic Stimulants Parasympathetic Stimulants
Sympathomimetics (adrenergics, adrenomimetics, or Direct-Acting
adrenergic agonists) Parasympathomimetics (cholinergic or 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, adrenolytics, or Parasympatholytics (anticholinergics, cholinergic
adrenergic antagonists) antagonists, or antispasmodics)
Action: Action:
Decrease pulse rate Increase pulse rate
Decrease BP Decrease mucous secretions
Constrict bronchioles Decrease GI motility
Increase urinary retention
Dilate pupils
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.
Alpha-adrenergic Receptors
 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:
1. Relaxation of the smooth muscles of the lungs, resulting in a decrease in uterine contraction.
2. An increase in blood flow to the skeletal muscles
3. Relaxation of the uterine muscle, resulting in a decrease in uterine contraction.
 Dopaminergic – another adrenergic receptor and is located in the renal, mesenteric, coronary,
and cerebral arteries. When this receptor is stimulated, the vessels dilate and blood flow
increases. Only dopamine can activate this receptor.
 Effects of Adrenergics at Receptors
Receptor Physiologic Responses

Alpha1 Increases force of heart contraction; vasoconstriction increases BP;

mydriasis (dilation of pupils) occurs; salivary glands decrease secretion;
bladder and prostate capsule increases contraction and ejaculation

Alpha2 Inhibits the release of norepinephrine; dilates blood vessels; produces

hypotension; decreases GI motility and tone

Beta1 Increases heart rate and force of contraction; increases renin secretion,
which increases BP

Beta2 Dilates the bronchioles; promotes GI and uterine relaxation; promotes

increase in blood sugar through glycogenolysis in the liver; increases blood
flow in the skeletal muscles
Classification of Sympathomimetics/Adrenomimetics

3 categories according to their effects on organ cells:

1. Direct – acting sympathomimetics – which directly stimulate the adrenergic
receptor (e.g., epinephrine or norepinephrine)
2. indirect – acting sympathomimetics – which stimulates the release of
norepinephrine from the terminal nerve endings (e.g., ampethamine)
3. Mixed-acting sympathomimetics – both direct and indirect acting, which
stimulate the adrenergic receptor sites and stimulate the release of
norepinephrine from the terminal nerve endings
Classification of Sympathomimetics/Adrenomimetics

Example:

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
 also stimulates beta2 - receptors which dilate bronchial tubes, and is useful to treat
mild forms of bronchial asthma
Classification of Sympathomimetics/Adrenomimetics

 Example:

Catecholamines
 Are the chemical structures of a substance (either endogenous or synthetic) that can produce as
sympathomimetic response
 Examples of endogenous catecholamines are epinephrine, norepinephrine, and dopamine
 Synthetic catecholamines are isoproterenol and dobutamine

Noncatecholamines
 E.g., phenelephrine, metaproterenol, albuterol – stimulate the adrenergic
receptors. Most noncatecholamines have a longer duration of action than the
endogenous or synthetic catecholamines.
Classification of Sympathomimetics/Adrenomimetics
 Examples:
Epinephrine
 Stimulate more than one of the adrenergic receptor sites
 Acts on alpha1-, alpha2-, and beta2 – receptor sites
 Responses from these receptor sites include an increase in BP, pupil dilation, increase in heart rate (tachycardia),
and bronchodilation. Because epinephrine affects three different adrenergic receptors, it is not selective; in other
words, it is considered nonselective to one receptor.
 frequently used in emergencies to combat anaphylaxis, which is life-threatening allergic response.
 It is a potent inotropic (force of muscular contraction) drug that causes the blood to constrict; thus, the BP
increases, the heart rate increases, and the bronchial tubes dilate.
 High doses can result in cardiac dysrhythmias; therefore, ECG should be monitored
 Can also cause renal vasoconstriction, thereby, decreasing renal perfusion and urinary output.
Classification of Sympathomimetics/Adrenomimetics

 Examples:

Albuterol (Albuterol sulfate – Proventil, Ventolin)

 Selective for beta2 – adrenergic receptors, so the response is purely bronchodilation
 An asthmatic client may therefore respond better by taking albuterol than isoproterenol
because its primary action is on the beta2 – receptor.
 Primary use is to prevent and treat bronchospasms. With inhalation, the onset of action is
faster than with oral administration, although the duration of action is the same for both oral
and inhalation preparations.
 Tremors, restlessness, and nervousness may occur when high doses are taken – s/e are most
likely caused by reflex effect of beta1 – receptors.
 If albuterol is taken with MOAI, a hypertensive crisis may occur.
Classification of Sympathomimetics/Adrenomimetics

 Example:

Isoproterenol Hydrochloride (Isuprel)

 An adrenergic drug, activates beta1- and beta2 – receptors
 More specific than epinephrine because it acts on two different adrenergic
receptors but is not completely selective.
 The response in beta1 and beta2 stimulation is bronchodilation and an increase
in heart rate. For example, when a client takes isoproterenol to control asthma
for dilating the bronchi, an increase in heart rate also occurs as a result of beta1
stimulation.
 When used excessively, severe tachycardia can result.
Classification of Sympathomimetics/Adrenomimetics

 Example:
Clonidine and Methyldopa
 Clonidine (Catapres) and methyldopa (Aldomet) are selective alpha2 – adrenergic drugs that
are primarily used to treat hypertension.
 The accepted theory for the action of alpha2 drugs is that they regulate the release of
norepinephrine by inhibiting its release.
 Alpha2 are also believed to produce a cardiovascular depression by stimulating alpha2
receptors in the CNS leading to a decrease in BP
 side effects commonly associated with adrenergic drugs include hypertension, tachycardia,
palpitations, dysrhythmias, tremors, dizziness, urinary difficulty, n/v.
Nursing Process – Adrenergic Agonist
ASSESSMENT
 Record v/s for future comparison. Epinephrine stimulates alpha1 (increase BP),
beta1 (increases heart rate), and beta2 (dilates bronchial tubes) receptors.
Isoproterenol (Isuprel) stimulates the beta1 and beta2 receptors. Albuterol
(Proventil) stimulates the beta2 – receptor
 Assess the drugs client takes and report possible drug-drug interactions. Beta-
blockers decrease the effect of epinephrine.
 Determine the client’s health history. Most adrenergic drugs are contraindicated if
the client has cardiac dysrhythmias, narrow-angled glaucoma, or cardiogenic shock.
 Evaluate the results of laboratory values and compare with future laboratory
findings.
Nursing Process – Adrenergic Agonist
NURSING DIAGNOSIS
 Risk for impaired tissue integrity
 Decreased cardiac output
PLANNING
 Client’s v/s will be closely monitored and will be within normal or acceptable ranges.
NURSING INTERVENTIONS
 Record client’s v/s. report sign of increasing BP and increasing pulse rate. If client receives an alpha-adrenergic
drug intravenously for shock, the BP should be checked every 3 to 5 minutes or as indicated to avoid severe
hypertension.
 Report the s/e of adrenergic drugs, such as tachycardia, palpitations, tremors, dizziness and increase BP.
 Check client’s urinary output and assess for bladder distention. Urinary distention can result from high drug dose
or continuous use of adrenergic drugs.
Nursing Process – Adrenergic Agonist
NURSING INTERVENTIONS
 For cardiac resuscitation, administer epinephrine 1:1000 IV (1mg/ml), which may be diluted
in 10 ml of saline solution (prescribed).
 Monitor IV site frequently when administering norepinephrine bitartate (Levaterenol) or
dopamine (Intropin) because infiltration of these drugs causes tissue necrosis. These drugs
should be diluted sufficiently in IV fluids. An antidote for norepinephrine (Levophed) and
dopamine is phentolamine mesylate (Regitine) 5 to 10 mg, diluted in 10 to 15 ml of saline
infiltrated into the area.
 Offer food to client when giving adrenergic drugs to avoid n/v.
 Evaluate laboratory test results. Blood glucose levels may increased.
Nursing Process – Adrenergic Agonist
CLIENT TEACHING
General
 Instruct client to read labels on all OTC drugs for cold symptoms and diet pills. Many of these have properties of
sympathetic (adrenergic, sympathomimetics) drugs and should not be taken if client is hypertensive or has
diabetes mellitus, cardiac dysrhythmias, or coronary artery disease.
 Advise mothers not to take drugs that contain sympathetic drugs while nursing infants. These drugs pass into the
breastmilk.
 Explain to client that continuous use of nasal spray or drops that contain adrenergics may result to in nasal
congestion rebound (inflamed and congested nasal tissue).
 Inform client and family how to administer cold medications by spray or drops in the nostrils. Spray should be
used with the head in an upright position. The use of nasal spray while lying down can cause systemic absorption.
Coloration of nasal spray or drops might indicate deterioration.
ADRENERGIC BLOCKERS (ANTAGONISTS or
SYMPATHOLYTICS)
 Drugs that block the effects of the adrenergic neurotransmitter.
 They act as antagonists to the adrenergic agonists by blocking the alpha– and beta- receptor
sites. They block the effects of the neurotransmitter either directly by occupying the alpha- or
the beta- receptors or by inhibiting the release of the neurotransmitter’s norepinephrine and
epinephrine.
 Three sympatholytic receptors are alpha1, beta1, and beta2.
ALPHA-ADRENERGIC BLOCKERS (ALPHA BLOCKERS)
 drugs that block or inhibit a response at the alpha-adrenergic receptor site
 Alpha-blocking agents are divided into two groups:
1. Selective alpha-blockers – that blocks alpha1
2. Non-selective alpha blockers – that block alpha1 and alpha2
ADRENERGIC BLOCKERS (ANTAGONISTS or
SYMPATHOLYTICS)
ALPHA-ADRENERGIC BLOCKERS (ALPHA BLOCKERS)
 Can cause orthostatic hypotension and reflex tachycardia, many of these drugs are not as
frequently prescribed as the beta blockers, are helpful in decreasing symptoms of benign
prostatic hypertrophy (BPH).
 Promote vasodilation, thus causing a decrease in BP. If vasodilation is long-standing,
orthostatic hypotension can result. Dizziness may also be a symptom of a drop in BP. As the
BP decreases, pulse rate usually increases to compensate for the low BP and inadequate blood
flow.
 Can be used to treat peripheral vascular disease (e.g., Raynaud’s disease). Vasodilation occurs
permitting more blood flow to the extremities
 s/e include cardiac dysrhythmias, flush, hypotension, and reflex tachycardia.
 Effects of Adrenergic Blockers
Receptor Responses

Alpha1 Vasodilation: decreases BP; reflex tachycardia

might result; miosis (constriction of pupil)
occurs; suppresses ejaculation; reduces
contraction of the smooth muscles in the
bladder neck and prostate gland

beta1 Decreases heart rate; reduces force of

contraction
beta2 Constricts bronchioles; contracts uterus; inhibits
glycogenolysis, which can decrease blood sugar
Beta – Adrenergic Blockers
 Commonly called beta-blockers, decrease heart rate; a decrease in BP usually follows.
 Some of the beta-blockers are nonselective blocking both beta1- and beta2 - receptor.
 Not only does the pulse rate decrease because of beta1 – blocking, but bronchoconstriction also occurs
 Nonselective beta-blockers (beta1 and beta2) should be used with extreme caution in any client who has chronic
obstructive pulmonary disease (COPD) or asthma.
 If the desired effect is to decrease the pulse rate and BP, then a selective beta1- blocker, such as metoprolol
tartrate (Lopressor), may be ordered.
 Are useful in treating cardiac dysrhythmias, mild hypertension, mild tachycardia, and angina pectoris
 s/e include bradycardia, dizziness, hypotension, h/a, hyperglycemia, intensified hypoglycemia, and
agranulocytosis. Usually s/e are dose related.
Beta – Adrenergic Blockers
Propranolol hydrochloride (Inderal)
 First beta-blocker prescribed to treat angina, cardiac dysrhythmias, and hypertension.
 Although it is still prescribed today, it has many s/e, partly because of its nonselective response in blocking both
beta1- and Beta2 – receptors. It is contraindicated for clients with asthma or second- or third- degree heart block.
 extensively metabolized in liver (hepatic first-pass); thus, only a small amount of the drug reaches the systemic
circulation
 Well-absorbed from GIT. It crosses the blood-brain barrier and the placenta and is found in breast milk.
 By blocking both types of beta-receptors, propranolol decreases the heart rate and, secondarily the BP. It also
causes the bronchial tubes to constrict and the uterus to contract.
 Many drugs interact with 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 PROCESS: ADRENERGIC NEURON
BLOCKERS
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 PROCESS: ADRENERGIC NEURON
BLOCKERS
NURSING INTERVENTIONS
• Determine whether client has diabetes and receives a beta-adrenergic blocker; the insulin dose or oral
hypoglycemic may need to be adjusted.
• Client who take beta-blockers do not have normal compensatory mechanisms while in states of shock. To
resuscitate such clients, glucagon must be given in high doses to counteract the sympatholytic effects of beta-
blockers.
CLIENT TEACHING
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.
NURSING PROCESS: ADRENERGIC NEURON
BLOCKERS
• 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) hypotension by slowly rising from supine or
sitting position to standing.
• Inform client and family of possible mood changes when taking beta-blockers. Mood changes
can include depression, nightmares, and suicidal tendencies.
• Warn male that certain beta-blockers (e.g., propranolol, metoprolol, pindolol) and alpha
blockers (e.g., prazosin) may cause impotence or a decrease in libido. Usually the problem is
dose related.