Autonomic Nervous System

Agent
SUBDIVISIONS OF THE PERIPHERAL
NERVOUS SYSTEM
Sympathetic and Parasympathetic
Effects on Body Tissues
Sympathetic and Parasympathetic
Effects on Body Tissues
 Adrenergic agonist
• Called Sympathomimetic drug–
mimics the effect of SNS
• Are related to their stimulation of
adrenergic receptor sites
• Varies from ophthalmic preparation
for dilating pupils to systemic
preparation – support individuals
experiencing shock
Alpha & Beta ADRENERGIC
AGONIST
• A & B agonists – stimulates all
adrenergic receptors
• Agents that affects both A & B
sites include dobutamine,
dopamine, ephedrine, epinephrine,
metaminol, norepinephrine.
Effects of activation of alpha1, alpha2,
beta1 and beta2 Receptors
Effects of activation of alpha1, alpha2,
beta1 and beta2 Receptors
Effects of activation of alpha1, alpha2,
beta1 and beta2 Receptors
Effects of activation of alpha1, alpha2,
beta1 and beta2 Receptors
 Pharmacokinetic
• Generally absorbed rapidly after
injection or passage through
mucous membrane.

• Used via IV when in emergency to

achieve rapid onset of action.
 Contraindication
• Contraindicated to patients who have
known hypersensitivity to prevent
reaction.
• Pheochromocytoma – can be fatal due
to systemic overload of catecholamine
• Tachyarrhythmias & ventricular
fibrillation – increase HR and O2
consumption
• Hypovolemia
 Adverse Effect
• Since it can cause vasoconstriction,
care must be taken to avoid
extravasation of any infused drugs.

• Extravasation can lead to necrosis

and cell death.
Drug-drug interaction
• Increase effects of tricyclic
antidepressants and MAOIs –
increased norepinephrine levels
and stimulation.
• Increase risk of hypertension if
given with any drug that can cause
hypertension. (herbal or OTC)
 ALPHA –SPECIFIC
ADRENERGIC AGONISTS
 Mechanism of Action
• Central alpha-2 agonists stimulate
alpha-2 adrenergic receptors in the
brain, resulting in decreased
sympathetic outflow, cardiac output,
and peripheral resistance.
• These agents may cause fluid
retention, and in most cases,
combination with a diuretic can be
considered.
 Adverse Effect
• These agents may cause fluid
retention, sedation, and dry mouth.
They should be avoided in patients
with heart failure.
• The first-dose effect of dizziness and
syncope is possible. Abrupt cessation
should be avoided due to the risk for
rebound HTN, which is higher in
patients also taking a beta blocker
Beta-Adrenergic Agonist
• Beta2-adrenergic agonists
stimulate beta2-adrenergic
receptors, increasing the
production of cyclic 3′5′ adenosine
monophosphate (cAMP).
• Increased cAMP relaxes airway
smooth muscle and increases
bronchial ciliary activity.
Beta-Adrenergic Agonist
• All beta2-adrenergic agonists have
slight cardiovascular stimulatory
effects including increased heart
rate, increased force of cardiac
contractility, and increased cardiac
conductivity. 
 Adverse Effect
• Adverse effects of beta2-adrenergic
receptor stimulation include
increased skeletal muscle activity,
central nervous system stimulation,
hyperglycemia, and hypokalemia.
 Contraindication
• Contraindicated in persons with a
history of hypersensitivity to beta-
adrenergic agonists or any
component of the formulation.
• Should be used with caution in
patients with known cardiovascular
disease, diabetes mellitus,
glaucoma, hyperthyroidism, or
seizure disorders. 
 Adverse Effect
• Serious adverse events associated
with SABAs include paradoxical
bronchospasm, anaphylaxis,
hypersensitivity reaction,
angioedema, hypertension,
hypotension, angina, cardiac
arrest, arrhythmia, hypokalemia,
and hyperglycemia.
 Adverse Effect
• Serious adverse events associated
with LABAs include paradoxical
bronchospasm, asthma
exacerbation, asthma related death,
laryngospasm, hypersensitivity
reaction, anaphylaxis, hypertension,
hypotension, angina, cardiac arrest,
arrhythmia, hypokalemia, and
hyperglycemia.
 Interaction
• Other sympathomimetic drugs (e.g.,
catecholamines, catecholamine
analogs, amphetamines) increase the
risk for beta2-adrenergic agonist adverse
effects and toxicities. 
• Nonselective and higher doses of beta1-
selective adrenergic blocking drugs
diminish the bronchodilator effects of
the beta2-adrenergic agonists
 NON-SELECTIVE
ADRENERGIC BLOCKER
• Primarily used to treat cardiac-
related condition.
• Competitively blocks the effects of
norepinephrine at both receptors.
• Results in lower BP, slower PR, and
increased renal perfusion with
decreased renin levels.
• Indicated for HTN, alone or with
diuretics.
NURSING PROCESS
Assessment:
•Assess for contraindication or
cautions
•Perform PA
•Assess V/S – pulse and BP
•Auscultate lungs
•Monitor urine output and laboratory
test.
 ALPHA1-SELECTIVE
ADRENERGIC BLOCKING
AGENTS
• Causes decrease in vascular tone
and vasodilation, leads to fall in BP.
• Since it doesn’t block the
presynaptic a-2 receptors, the reflex
tachycardia that accompanies a fall
in BP, does not occur.
 BETA-BLOCKERS
• Beta blockers are very effective in
managing angina.
• They reduce the workload of the heart
and decrease overall myocardial oxygen
demand and consumption through
antagonism of adrenergic receptors.
• This is accomplished by a reduction in
the heart rate and myocardial
contractility, both at rest and during
periods of normal exercise.
• Nitrates and beta blockers have
complementary effects on myocardial
oxygen supply and demand and
therefore are often used together.
• Because beta blockers reduce the
heart rate, they can be used to
control the reflex tachycardia that
sometimes occurs with the
administration of nitrates. 
• Beta antagonists that block only beta-1 receptors
are considered cardioselective beta blockers. Those
that block both beta-1 and beta-2 receptors are
nonselective. 

• Beta-1-receptor blockade is desirable in a patient

with angina because it causes a slowing of the heart
rate and a reduction in myocardial contractility.

• These effects reduce myocardial oxygen demand

and therefore improve and prevent anginal
symptoms. 
• Blockage of beta-2 receptors can
lead to bronchoconstriction;
therefore, nonselective beta
blockers should be used with
caution in patients with
uncontrolled or unstable reactive
airway disease.
 Contraindication
• Beta blockers are relatively
contraindicated and therefore should be
used cautiously in patients with
preexisting bradycardia because beta
blockade may lower the heart rate
further.
• Should not be used if a patient is
experiencing an acute episode of
decompensated heart failure.
 Adverse Effects
• Beta blockers have the potential to adversely
affect cardiac function. 
• These effects include slowing the sinoatrial
node and atrioventricular (AV) conduction,
leading to symptomatic bradycardia and
heart block.
•  If the patient has preexisting cardiac
conduction system disease, a preparation
with some intrinsic beta-agonist activity may
be chosen to minimize these adverse
events.