- norepinephrine is released from the terminal

DRUGS ACTING ON THE AUTONOMIC NERVOUS

SYSTEM
Autonomic Nervous System (ANS)
• Called involuntary or visceral nervous
system, innervates smooth muscles and
glands
• Its functions include control and regulation
of the heart, respiratory system, GI tract,
eyes and glands
• The ANS is an involuntary nervous system
over which a person has little or no control
Somatic Nervous System
• A voluntary system that innervates skeletal
muscles over which there is control
TWO SETS OF NEURONS (autonomic):
nerve ending and stimulates the cell
receptors to produce a response
PARASYMPATHETIC NERVOUS SYSTEM
- in many areas, the parasympathetic
nervous system works in opposition to the
SNS
- is called the cholinergic system, because
the neurotransmitter at the end of the
neuron that innervates the muscle is
acetylcholine
- the parasympathetic system is associated
with activities that help the body to store or
conserve energy, a “rest-and-digest”
response
SYMPATHETIC AND PARASYMPATHETIC RESPONSE OF
ORGANS

1. Afferent neurons (sensory) – send impulses to

BODY SYMPATHETIC PARASYMPATHETIC
the CNS, where they are interpreted TISSUE/ORGAN RESPONSE RESPONSE
2. Efferent neurons (motor) – receive the
Eye Dilates pupils Constricts pupils
impulses (information) from the brain and
Lungs Dilates Constricts
transmit those impulses through the final
bronchioles bronchioles and
cord to the effector organ cells increases
secretions
TWO BRANCHES OF EFFERENT PATHWAYS:
Heart Increases Decreases heart
heart rate rate
• Sympathetic nervous system
• Parasympathetic nervous system Blood Vessels Constricts Dilates blood
blood vessels vessels
Both system act on the same organs but Gastrointestinal Relaxes Increases
produce opposite responses to provide smooth peristalsis
muscles of
homeostasis (balance). Drugs act on the gastrointestinal
sympathetic and parasympathetic nervous tract
system by either stimulating or depressing Bladder Relaxes Constricts bladder
responses bladder
muscle
SYMPATHETIC NERVOUS SYSTEM Uterus Relaxes
uterine muscle
- Sometimes referred to as the “fight-or-flight”
Salivary Gland Increases
system, or the system responsible for salivation
preparing the body to respond to stress
- The SNS acts much like an accelerator,
speeding things up for action
- Also called adrenergic system because at SYMPATHETIC PARASYMPATHETIC
STIMULANTS STIMULANTS
one time it was believed that adrenaline
was the neurotransmitter that innervated Sympathomimetics Direct-acting
smooth muscle. The neurotransmitter is, (adrenergics, parasympathetics
adrenomimetics, or (cholinergics or
however norepinephrine
adrenergic agonists) cholinergic agonists)
- the adrenergic receptor organ cells are four
types: alpha1, alpha2, beta1, beta2 Action: Action:
 • Beta2-receptors – found mostly in the
Increase blood Decrease blood
pressure pressure smooth muscles of the lung, arterioles of
skeletal muscles, and the uterine muscle
Increase pulse rate Decrease pulse rate
Relax bronchioles Constrict bronchioles Relaxation of smooth muscles in the lungs =
Dilate pupils of eyes Constrict pupils of eyes bronchodilation

Relax uterine muscles Increase urinary
contraction
Increase blood sugar Increase peristalsis
Indirect-Acting
OTHER ADRENERGIC RECEPTOR
Cholinesterase
inhibitors
(Anticholinesterase)
Action:
Increase muscle tone
Increase of blood flow to the skeletal muscles
and relaxation of the uterine muscle = decrease
in uterine contraction
• Dopaminergic- located in the renal,
mesenteric, coronary and cerebral arteries.
When stimulated, vessels dilate and blood
flow increases
o Only dopamine can activate this
receptor

SYMPATHETIC PARASYMPATHETIC
RECEPTOR PHYSIOLOGIC
DEPRESSANTS DEPRESSANTS
RESPONSES
Sympatholytics Parasympatholytics
Alpha 1 Increases force of the
(adrenergic blockers, (anticholiners,
heart contraction;
adrenolytics, or cholinergic
vasoconstriction
adrenergic anatagonists, or
increases BP; mydriasis
anatagonists) antispasmodics)
occurs; salivary glands
Action: Action: decrease secretion;
increases urinary
Decrease pulse rate Increase pulse rate
bladder relaxation and
Decrease blood Decrease mucous urinary sphincter
pressure secretions contraction
Constrict bronchioles Decrease Alpha 2 Inhibits release of
gastrointestinal motility norepinephrine; dilates
Increase urinary blood vessels;
retention produces hypotension;
decreases
Dilate pupils of eyes gastrointestinal motility
and tone
Beta 1 Increases heart rate
ALPHA-ADRENERGIC RECEPTORS and force of
contraction; increases
• are located in the vascular tissues (vessels) renin secretion, which
of the muscles increases BP
• Alpha1 – receptor – arterioles and venules
Beta 2 Dilates bronchioles;
constrict, increasing peripheral resistance promotes
and blood return to the heart (increase BP) gastrointestinal and
• Alpha2-receptor – inhibits the release of NE, uterine relaxation;
leading to a decrease in vasoconstriction promotes increase in
(decrease BP) blood sugar through
glycogenolysis in liver;
• Beta1-receptors – located primarily in the
increases blood flow in
heart; increases myocardial contractility skeletal muscles
and heart rate
INACTIVATION OF NEUROTRANSMITTERS
Transmitters are inactivated by:
1. Reuptake of the transmitter back into the
neuron (nerve cell terminal)
2. Enzymatic transformation or degradation
3. Diffusion away from the receptor
CLASSIFICATION OF SYMPATHOMIMETICS
Three categories according to their effects on
organ cells:
• Direct acting sympathomimetics, which
directly stimulate the adrenergic receptor
(eg. Epi and NE)
• Indirect-acting sympathomimetics, which
stimulate the release of norepinephrine from
the terminal nerve endings
• 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
EPHEDRINE
• Is an example of a mixed-acting
sympathomimetic
• Acts indirectly by stimulating the release
of norepinephrine from the nerve
terminals and acts directly on the
alpha1, beta1 and beta2 receptors
• Is helpful to treat idiopathic orthostatic
hypotension and hypotension that results
from spinal anesthesia
• It also stimulates beta 2 receptors, which
dilate bronchial tubes, and is useful to
treat mild forms of bronchial asthma
CATHECOLAMINES
• Chemical structures of a substance (either
endogenous or synthetic) that can produce
a sympathomimetic response
• Endogenous catecholamines are
epinephrine, norepinephrine and dopamine
• Synthetic catecholamines are isoproterenol
and dobutamine
NONCATECHOLAMINES
• Examples: phenylephrine, metaproterenol,
albuterol
• Stimulate the adrenergic receptors
• Most noncatecholamines have longer
duration of action than the endogenous or
synthetic catecholamines
Many of the adrenergic drugs stimulate more than
one of the adrenergic receptor sites. An example is
epinephrine (Adrenalin), which acts on alpha 1,
beta 1 and beta 2 adrenergic receptor sites
The responses from these receptor sites include an
increase blood pressure, pupil dilation, increase in
heart rate and bronchodilation
EPINEPHRINE
• In certain types of shock, epinephrine is
useful because it increases blood pressure,
heart rate, and airflow through the lungs
through bronchodilation
• Epinephrine affects three different
adrenergic receptors, it is nonselective
• Side effects result when more responses
occur than are desired
• Sympathomimetic
• Pregnancy category: C
• Indication: to treat allergic reaction,
anaphylaxis, bronchospasm, cardiac arrest
PHARMACOKINETICS
• Can be administered SQ, IV, topically or
by inhalation, intracardiac, and
instillation methods
• It should not be given orally- it is rapidly
metabolized in the GI tract and liver
which will result to inadequate serum
levels
• Epinephrine is metabolized by the liver
and excreted in the urine
PHARMACODYNAMICS
• Is frequently used in emergencies to
treat anaphylaxis
• Epinephrine is a potent inotropic
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
 • Can also cause renal
vasoconstriction, thereby decreasing
renal perfusion and urinary output
• The onset and peak concentration
times are rapid:
o SQ/IM: Onset: 3-10 mins;
Peak: 20 mins; Duration: 20-30
mins
o IV: onset: immediate; Peak: 2-
5 mins; Duration: 5-10 mins
o Inhal: Onset: 1 min; Peak: 3-5
mins; Duration: 1-3 mins
• Clonidine and Methyldopa are selective
alpha 2 adrenergic drugs used to primarily
to treat hypertension
• The accepted theory for the action of alpha
2 drugs is that they regulate the release of
norepinephrine by inhibiting its release.
Alpha 2 drugs are also believed to produce
cardiovascular depression by stimulating
alpha 2 receptors in the CNS, leading to a
decrease in BP
ADRENERGIC AGONIST

CLASSIFICATION GENERIC NAME BRAND NAME

INTERACTIONS Alpha- and Beta- Dobutamine Dobutrex
Adrenergic drugs
Dopamine Intropin
• The use of decongestants with
Ephedrine (generic)
epinephrine has additive effect
Epinephrine Adrenalin, Sus-
• When administered with digoxin, Phrine
cardiac dysrhythmias may occur
norepinephrine Levophed
• Beta-blockers, TCA and MAOIs can
Alpha-Specific Clonidine Catapress
cause a decrease in the action of Adrenergic Agonists
Phenylephrine Neo-
epinephrine Synephrine
albuterol Proventil,
ALBUTEROL Ventolin
Arformoterol Brovana
• Is selective for beta 2 adrenergic receptors,
so the response is purely bronchodilation isoproterenol Isuprel

• Beta2-adrenergic agonist Beta-Specific Levalbuterol Xopenex

Adrenergic Agonists
• Pregnancy category: C Metaproterenol Alupent
• Indication: treat bronchospasm, asthma, Pirbuterol Maxair
bronchitis and other COPD Autohaler
Salmetrol Serevent
PHARMACOKINETICS Diskus
terbutaline Brethine
• Is well absorbed from the GI tract and is
extensively metabolized in the liver
• The half life of the drug differs slightly
according to the route of administration
(oral route is 2.5 hours; inhalation is 3.5 hours) ASSESSMENT
• Excretion: 75% excreted in the urine
• Record vital signs for future comparison.
PHARMACODYNAMICS (especially pulse and blood pressure to
monitor for possible excess stimulation of the
• The primary use of albuterol is to prevent cardiac system.)
and treat bronchospasms • Assess the drugs client take and report
• PO: onset- 30 mins; peak- 2-3 hours; possible drug-drug interactions
duration- 4-6 hours • Determine the client’s history. Most
• Inhal: onset- 5-15 mins; peak- 0.5-2 hours; adrenergic drugs are contraindicated if
duration- 3-6 hours client has cardiac dysrhythmias, narrow-
angle glaucoma or cardiogenic shock
CLONIDINE AND METHYLDOPA
• Compare the results of lab results with future
lab findings
DIAGNOSIS
• Risk for impaired tissue integrity related to
severe hypotension
• Decreased cardiac output related to
bradycardia
PLANNING
• Client’s vital signs will be within normal or
acceptable ranges
INTERVENTIONS
• Record client’s vital signs. Report signs of
increasing BP and HR. if the drug is for shock,
check BP every 3 to 5 minutes to avoid
hypertension
• Report any side effects of adrenergic drugs:
tachycardia, palpitations, tremors, dizziness,
and increased BP
• Check client’s UO and assess for bladder
distention. Urinary retention can result from
high drug dose or continuous use of
adrenergic drugs
• For cardiac resuscitation, administer
epinephrine 1:1000 IV (1mg/ mL), which may
be diluted in 10 mL of saline solution
• Monitor IV site frequently when
administering norepinephrine bitartrate or
dopamine because infiltration of these
drugs causes tissue necrosis
• Antidote for norepinephrine and dopamine
is PHENTOLAMINE MESYLATE 5 to 10 mg
diluted in 10-15 mL of saline infiltrated into
the area
• To avoid N/V, offer food to client when
giving adrenergic drugs
• Evaluate blood glucose levels because they
may be increased
GENERAL CLIENT TEACHING
• Instruct the client to read labels on all OTC
drugs for cold symptoms and diet pills. Many
of these have properties of sympathetic
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 breast milk
• Explain to the client that continuous use of
nasal sprays or drops that contain
adrenergics may result in nasal congestion
rebound (inflamed and congested nasal
tissue)
SELF-ADMINISTRATION
• Inform client and family how to administer
cod medications by sprays 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
• Direct client to use bronchodilator sprays
conservatively. If client excessively uses a
nonselective adrenergic drug that affect
beta1 and beta2- receptors, tachycardia
may occur
CULTURAL CONSIDERATIONS
• Decrease language barriers for clients with
language difficulties and for those who do
not work in the health care field by
decoding the jargon of the health care
environment
EVALUATION
• Evaluate client’s response to the adrenergic
drug. Continue monitoring client’s vital signs
and report abnormal findings
• Evaluate patient understanding on drug
therapy by asking patient to name the drug,
its indication, and adverse effects to watch
for
• Monitor patient compliance to drug therapy
ADRENERGIC BLOCKERS (ANTAGONISTS)
• Drugs that block the effects of the
adrenergic neurotransmitters
• Also called adrenergic antagonists or
sympatholytics
• They block the effects of the effects of the
sympathetic nervous system by inhibiting the
release of the neurotransmitters
norepinephrine and epinephrine
• They react with specific adrenergic receptor
sites without activating them, thus
 preventing the typical manifestations of SNS • It is contraindicated for clients with asthma
activation or second- or third-degree heart block

ALPHA-ADRENERGIC BLOCKERS PHARMACOKINETICS

• Drugs that block or inhibit the response at • Propranolol is well absorbed from the GI
the alpha receptor site tract. It crosses the blood brain barrier and
• Divided into two groups: selective that the placenta and is excreted in breast milk
blocks alpha 1 and non-selective alpha • Metabolized by the liver and has a short
blockers that blocks alpha 1 and alpha 2 half-life of 3 to 6 hours
• Can cause orthostatic hypotension and
reflex tachycardia PHARMACODYNAMICS
• Alpha beta blockers are helpful in
• By clocking both types of beta receptors,
decreasing symptoms of benign prostatic
propranolol, decreases the heart rate and
hypertrophy
blood pressure
• They promote vasodilation, causing
• It also causes the bronchial tubes to
decrease BP. If vasodilation is longstanding,
constrict and the uterus to contract
orthostatic hypotension can result
• It is available in tablets and sustained-
• Alpha blockers can be used to treat
release capsules and for IV administration
peripheral vascular disease

BETA-ADRENERGIC BLOCKERS Route Onset Peak Duration

Oral 20-30 min 60-90 6-12 H
• Commonly called as beta-blockers min
• Decreases heart rate; a decrease in BP
IV immediate 1 min 4-6 H
usually follows
• Some beta-blockers are non-selective T ½: 3-5 hours
blocking beta 1 and 2 receptors Metabolism: Liver
• Non-selective beta blockers should be used Excretion: Urine
with extreme caution in any client who has
COPD or asthma
• A selective adrenergic blocker has a great ATENOLOL
affinity for certain receptors. If the desired
effect is to decrease pulse rate and blood • Beta1 – adrenergic blocker
pressure, then selective beta1- blocker may • Pregnancy category: C
be ordered • Atenolol comes only as a tablet you take by
mouth
An intrinsic sympathomimetic causes partial • Used to treat high blood pressure, angina
stimulation of beta receptors. Certain non-selective pectoris and myocardial infarction. It can
blockers that have ISA are: carteolol, carvedilol, also help prevent heart attack or heart
penbutolol, pindolol damage after a heart attack
• After a heart attack, it reduces the amount
The selective blocker that has ISA is acebutolol
of work for your heart muscle has to do to
These agents reportedly cause fewer side effects push blood through your body
and are helpful to clients experiencing severe
PHARMACOKINETICS
bradycardia
• Well absorbed in the GI tract
PROPRANOLOL
• Protein-binding 6-16%
• Propranolol was the first beta blocker • Therapeutic half -life: 6-7 H
prescribed to treat angina, cardiac • Undergoes little or no metabolism by the
dysrhythmias, hypertension and heart failure liver, and the absorbed portion is eliminated
primarily by renal excretion
PHARMACODYNAMICS
• PO: Onset- 2-7 H; Peak- 2-4H; Duration: 24H
• IV: Onset- unknown; Peak- 5 mins; Duration-
24 H
ADRENERGIC NEURON BLOCKERS
• Drugs that block the release of
norepinephrine from the sympathetic
terminal neurons
• Classified as a subdivision of the adrenergic
blockers
• The clinical use of neuron blockers is to
decrease blood pressure
• Guanadrel sulfate (Hylorel), an example of
an adrenergic neuron blocker, is a potent
antihypertensive agent
ASSESSMENT
• Obtain baseline v/s and ECG for future
comparison. Bradycardia and decrease in
BP are common cardiac effects of beta-
adrenergic blockers/ beta blockers
• Assess if client has respiratory problems by
listening for signs of wheezing or noting
dyspnea (clients with asthma should take a
beta 1 blocker such as metoprolol
(Lopressor) and avoid nonselective beta-
blockers
• Determine the drugs that the client currently
takes
• Record client’s UO and use for future
comparison
NURSING DIAGNOSIS
• Ineffective breathing pattern related to
dyspnea
• Decreased cardiac output related to
cardiac dysrhythmias
• Risk for injury related to dizziness
PLANNING
• Client will comply with the drug regimen
• Client’s v/s will be within the desired range
INTERVENTIONS
• Monitor client’s v/s. report marked changes
such as decreased BP and HR
• 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
can occur
• Determine whether the client has diabetes
and receives a beta-adrenergic blocker;
insulin dose or oral hypoglycemic may need
to be adjusted
• Have glucagon available. Clients who take
beta-blockers do not have normal
compensatory mechanisms while in shock
states. To resuscitate such clients, glucagon
should be given in high doses to counteract
the sympatholytic effects of beta-blockers
GENERAL TEACHING
• Advise client to avoid abruptly stopping a
beta-blocker; rebound hypertension,
rebound tachycardia and angina attack
could result.
• Instruct client to comply drug regimen
• Educate clients about insulin therapy; early
warning signs of hypoglycemia may be
masked by the beta-blockers
• Direct clients to monitor blood sugar
carefully and follow diet orders when on
insulin therapy
• Teach client and family how to take BP and
HR
SIDE EFFECTS
• Encourage client t o avoid orthostatic
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 clients that certain beta blockers and
alpha blockers may cause impotence or
decreased libido, which is usually dose
related
CULTURAL CONSIDERATIONS
 • Obtain an interpreter when necessary; do
not rely on family members, who may not
fully disclose because of honor or shame
• When translation is needed, discuss the
ethnicity of the interpreter as well as the
language desired
EVALUATION
• Evaluate the effectiveness of the adrenergic
blocker
• Vital signs must be stable within the desired
range
CHOLINERGICS
- Drugs that stimulate the parasympathetic
nervous system. They mimic the
parasympathetic neurotransmitter
acetylcholine
DIRECT-ACTING CHOLINERGIC AGONISTS
• Usually used for treatment of neurogenic
bladder atony in children, relieve pressure
on glaucoma patients, and treatment of
symptoms of dry mouth in patients with
Sjogren’s Syndrome
• Are similar to Ach and react directly with
receptor sites to cause the same reaction
• Common examples include bethanechol
and pilocarpine
PILOCARPINE
• Direct-acting cholinergic drug that constricts
the pupils of the eyes thus opening the
canal of Schlemm to promote drainage of
aqueous humor (fluid)
• Used to treat glaucoma by relieving fluid
(intraocular) pressure in the eye
• Also acts on the nicotinic receptor, as does
carbachol
BETHANECHOL CHLORIDE (URECHOLINE)
• Used to treat urinary retention, abdominal
distention
• Stimulates the cholinergic receptor;
promote contraction of the bladder;
increase GI peristalsis, pupillary constriction
and bronchoconstriction
• Pregnancy category: C
PHARMACOKINETICS
• Poorly absorbed from the GI tract, most
likely excreted in the urine
PHARMACODYNAMICS
• Principal use is to promote micronutrition
(urination) by stimulating the muscarinic
cholinergic receptors to increase urine
output. The client voids approximately 30
minutes to 1.5 hours after taking an oral
dose
• Bethanechol increases peristalsis in the GI
tract. This drug should be taken on an
empty stomach
• PO: Onset- 0.5-1.5 H; Peak- 1-2 H; Duration-
4-6H
• SQ: Onset- 5-15 mins; Peak- 0.5 H; Duration-
2H
ASSESSMENT
• Note baseline v/s for future comparison
• ASSESS UO (should be > 600 mL/ day).
Report decreases in UO
• Obtain history from client health problems
such as peptic ulcer, urinary obstruction or
asthma. Cholinergics can aggravate
symptoms of these conditions
NURSING DIAGNOSIS
• Impaired urinary elimination related to
urinary retention
• Anxiety related to wheezing
• Risk for impaired skin integrity related to rash
PLANNING
• Client will have increased bladder and GI
tone after taking cholinergics
• Client will have increased neuromuscular
strength
INTERVENTIONS
• Monitor client’s v/s. HR and BP decrease
when large doses of cholinergics are taken.
Orthostatic hypotension is a side effect of a
cholinergic such as bethanechol
• Record fluid intake and output. Decreased
urinary output should be reported because
it may be related to urinary obstruction
 • Give cholinergics 1hour before or 2 hours
after meals. If client complains of gastric
pain, the drug may be given with meals
• Check serum amylase, lipase, aspartate
aminotransferase and bilirubin levels. These
laboratory values may increase slightly
when taking cholinergics
• Observe client for side effects such as
gastric pain or cramping, diarrhea,
increased salivary or bronchial secretions,
bradycardia and orthostatic hypotension
• Auscultate for bowel sounds, Report
decreased or hyperactive bowel sounds
• Auscultate breath sounds for rales or
rhonchi. Cholinergic drugs can increase
bronchial secretions
• Have IV atropine sulfate (0.6 mg) available
as an antidote for cholinergic overdose.
Early signs of overdosing include salivation,
sweating, abdominal cramps and flushing
• Note that diaphoresis may occur; linens
should be changed as needed
• Beware of the possibility of cholinergic crisis;
symptoms include muscular weakness and
increased salivation
GENERAL CLIENT TEACHING
• Instruct client to take the cholinergic as
prescribed. Compliance with the drug
regimen is essential
• Direct client to report severe side effects
such as profound dizziness or a decrease in
HR below 60 bpm
• Teach client to arise from a lying position
slowly to avoid dizziness; this is most likely a
result of orthostatic hypotension
• Encourage client to maintain effective oral
hygiene if excess salivation occurs
• Advise client to report any difficulty in
breathing as a result of respiratory distress
EVALUATION
• Determine the effectiveness of the
cholinergic or anticholinesterase drug
• Evaluate the stability of client’s v/s and note
the presence of side effects or adverse
reactions
INDIRECT- ACTING CHOLINERGIC AGENTS
• Used for myasthenia gravis and Alzheimer’s
disease
• Myasthenia gravis is a chronic muscular
disease caused by defect in neuromuscular
transmission. It is thought to be an
autoimmune disease in which antibodies to
own ACh receptors are made. A fewer
receptor sites become available, patients
begin to have progressive weakness and
lack of muscle control
• Alzheimer’s Disease is a progressive disorder
of neural degeneration leading to marked
loss of memory and the ability to carry on
activities of daily living
ANTICHOLINERGICS
• Are drugs that oppose the effects of
acetylcholine. In essence, they also block
the effects of parasympathetic nervous
system (PNS) so they are called as
parasympatholytics
• Atropine is currently the only widely used
anticholinergic drug
• Other common examples include meclizine,
scopolamine and ipratropium
• Major responses are a decrease in GI
motility, decrease in salivation, dilation of
pupils (mydriasis) and increase in pulse rate
• Other effects are decreased bladder
contraction which can result in urinary
retention, and decreased rigidity and
tremors related to neuromuscular
excitement
ATROPINE SULFATE
• The prototype drug is derived from the plant
belladonna
• It is used to depress salivation and bronchial
secretions and to dilate the bronchi, but it
can thicken respiratory secretions (causing
obstruction of airways)
• Preoperative medications to reduce
salivation, increase heart rate and dilate
pupils
• Pregnancy category: C
PHARMACOKINETICS
 • Well absorbed orally and parenterally. It
crosses the blood brain barrier and exerts its
effect on the CNS
• PO: onset- 0.5-1 H; Peak- 1-2H; Duration- 4H
• IM: onset- 10-30 mins; Peak- 0.5 H; Duration-
4H
• IV: onset- immediate; peak- 5 mins; duration-
unknown
• Instill: onset- 20-30 mins; Peak- 30-40 mins;
Duration- days
ASSESSMENT
• Obtain baseline v/s. Tachycardia is a side
effect that occurs with large doses of
anticholinergics such as atropine sulfate
• Assess UO. Urinary retention may occur
• Assess neurological status (e.g., orientation,
affect, reflexes) to evaluate any CNS effects
• Assess abdomen (e.g., bowel sounds, bowel
and bladder patterns, urinary output) to
evaluate for GI and GU adverse effects
• Monitor laboratory test results to determine
need for possible dose adjustments and to
identify potential toxicity
NURSING DIAGNOSIS
• Impaired urinary elimination related to
effects on the bladder
• Impaired oral mucous membrane related to
decreased oral secretions
• Risk for injury related to acute confusion
PLANNING
• Client’s secretions will be decreased before
surgery
• Client will not have side effects that may
become a health problem
INTERVENTIONS
• Ensure proper administration of the drug to
ensure effective use and decrease the risk
of adverse effects
• Monitor patient response (e.g., blood
pressure, ECG, urine output) for changes
that may indicate need to adjust dose
• Provide comfort measures (e.g., sugarless
lozenges, lighting control, small and
frequent meals) to help patient cope with
drug effects
• Raise bedside rails for clients who are
confused and debilitated
• Provide patient education about drug
effects and warning signs to report enhance
knowledge about drug therapy and
promote compliance
• Administer IV atropine undiluted or diluted in
10mL of sterile water
EVALUATION
• Monitor patient response to therapy
(improvement in condition being treated)
• Monitor for adverse effects (e.g.,
photophobia, heat intolerance, urinary
retention)
• Evaluate patient understanding on drug
therapy by asking patient to name the drug,
its indication, and adverse effects to watch
for
• Monitor patient compliance to drug therapy
TRIHEXYPHENIDYL HCL
• Decrease involuntary symptoms of
parkinsonism or drug-induced parkinsonism
by inhibiting acetylcholine
• It blocks cholinergic receptors to decrease
involuntary movements
PHARMACOKINETICS
• Well absorbed from the GI tract
• Therapeutic half-life is 5-10 hours
• Excretion: in urine
PHARMACODYNAMICS
• Decreases involuntary movement and
diminishes the signs and symptoms of
tremors and muscle rigidity that occur with
Parkinson’s disease and pseudoparkinsonism
• PO: onset- 1H; peak- 2-3 H; Duration- 6-12 H
ANTIHISTAMINES FOR TREATING MOTION SICKNESS
• The effects of anticholinergics on the CNS
benefit client prone to motion sickness. An
example of such an anticholinergic
classified as an antihistamine for motion
sickness is scopolamine
• It is available topically as a skin patch that is
placed behind the ear
• Prevention of motion sickness is also
provided via wrist bands and ginger gum
• Transdermal scopolamine is delivered over 3
days and is frequently prescribed for
activities such as flying, cruising on the water
and bus or automobile trips
• Other drugs are dimenhydrinate, cyclizine,
and meclizine hcl
Drugs acting on the Endocrine System
RECAP: Sympathetic Nervous System
Drugs/ Sympathomimetics
- used to mimic adrenaline
(norepinephrine & epinephrine)
4 receptor sites:
• A1- blood vessels – constricts =
increased BP
• A2= decreases BP
• B1- cardiac muscle= increases
HR- tachycardia & palpitations
• B2- bronchial airway =
bronchodilation
A1 Blocker
Effect: decrease BP
Antihypertensive agent
Example: Minipres
A2 Agonist- stimulates an action.
Effect: decrease BP
Antihypertensive agent
Example: Clonidine (Catapres)
B1 Blocker
**Most important assessment: check
HR
Effect: bradycardia
Antidote: Glucagon
Example: Propranolol (Inderal)
B2 Agonist
Bronchodilator agent
Can be used for COPD
Example: Albuterol
ENDOCRINE SYSTEM
• The endocrine system consists of
ductless glands that secrete
hormones into the bloodstream
• Hormones are chemical
substances synthesized from
amino acids and cholesterol that
act on body tissues and organs
and affect cellular activity
Two Categories:
• Proteins or small peptides
• steroids
Pituitary Glands
• also called hypophysis
• located at the base of the brain
and has two lobes, the anterior
and posterior
• anterior pituitary gland (master
gland) – it secrets hormones that
stimulate the release of other
hormones from target glands
• posterior pituitary gland- secretes
two hormones:
o ADH or vasopressin
o oxytocin
Anterior Pituitary Gland
• The anterior pituitary hormones
are:
o Thyroid Stimulating
Hormone
o Adrenocorticotropic
Hormone
o Gonadotropins- follicle
stimulating hormone and
luteinizing hormone.
• They control the synthesis and
release of hormones from thyroid,
adrenals and ovaries
• Other hormones secreted from
the anterior pituitary include
growth hormone (GH), prolactin
(PL) and melanocyte-stimulating
hormone (MSH)
Thyroid Stimulating Hormone – also called
thyrotropin hormone influences the growth
and activity of the thyroid gland
Adrenocorticotropic Hormone – regulates
the endocrine activity of the cortex portion
of the adrenal gland
Gonadotropins – gonadotropic hormones
regulate the hormonal activity of gonads
(ovaries and testes)
Growth hormone (GH)
• a general metabolic hormone
• its major effects are directed to
the growth of skeletal muscles
and long bones of the body
 • it is a protein-sparing and
anabolic hormone that causes
amino acids to be built into
proteins and stimulates most
target cells to grow in size and
divide.
POSTERIOR PITUITARY GLAND
• The posterior pituitary simply
acts as a storage area for
hormones made by
hypothalamic neurons.
• Oxytocin. Oxytocin is released
in significant amount only
during childbirth and in nursing
women; it stimulates powerful
contractions of the uterine
muscle during labor, during
sexual relations, and during
breastfeeding and also
causes milk ejection (let-down
reflex) in a nursing woman.
• Antidiuretic hormone (ADH).
ADH causes the kidneys to
reabsorb more water from the
forming of urine; as a result,
urine volume decreases and
blood volume increases; in
larger amounts, ADH also
increases blood pressure by
causing constriction of the
arterioles, so it is sometimes
referred to as vasopressin
THYROID GLAND
• Located anterior to the trachea
• Thyroid hormone often referred to
as the body’s major metabolic
hormone, is actually two active
hormones, iodine-containing
hormones, thyroxine or T4,
and triiodothyronine or T3.
o Thyroxine is the major
hormone secreted by the
thyroid follicles.
o Most triiodothyronine is
formed at the target
tissues by conversion of
the thyroxine to
triiodothyronine.
o Thyroid hormone controls
the rate at which glucose
is “burned” oxidized, and
converted to body heat
and chemical energy; it is
also important for normal
tissue growth and
development.
PARATHYROID GLANDS
• There are 4 parathyroid glands
(two pairs) that lie on the dorsal
surface of the thyroid gland.
• Secretes parathormone, or
parathyroid hormone (PTH),
which regulates the calcium
levels in the blood
• A decrease in serum calcium
stimulates the release of PTH
• PTH increases calcium levels by:
o Mobilizing calcium from
the bone
o Promoting calcium
absorption from the
intestine
o Promoting calcium
reabsorption from the
renal tubules
• Calcitonin, a hormone produced
primarily by the thyroid gland
and to a lesser extent by the
parathyroid and thymus glands,
inhibits calcium reabsorption by
bone and increases renal
excretion of calcium. Calcitonin
counteracts the action of PTH
ADRENAL GLANDS
• Located at the top of each
kidney
• Consist of two separate sections:
o adrenal medulla – releases
the catecholamines
epinephrine and
norepinephrine and is
linked with sympathetic
nervous system.
o adrenal cortex- produces
two major types of
 hormones
(corticosteroids)-
glucocorticoids (cortisol)
and mineralocorticoids
(aldosterone).
• also produces small amounts of
androgen, estrogen, and
progestin
• Glucocorticoids have a profound
influence on electrolytes and the
metabolism of carbohydrates,
protein and fat
• Glucocorticoid deficiency can
result in serious illness and even
death
PANCREAS
• Located to the left of and behind
the stomach.
• Is both an exocrine and
endocrine gland.
• Exocrine- secretes digestive
enzymes into the duodenum.
• Endocrine- has cell clusters called
islets of Langerhans.
• The alpha islet cells produce
glucagon, which regulates
glucose in the liver, and the beta
cells secrete insulin, which
regulates glucose metabolism.
• Insulin- used to control diabetes
mellitus.
Pituitary Gland- Anterior Lobe
• The anterior pituitary gland,
called the adenohypophysis,
secretes the following hormones
that target glands and tissues:
o GH- stimulates growth in
tissue and bone
o TSH- acts on the thyroid
gland
o ACTH- stimulates the
adrenal gland
o Gonadotropins (FSH & LH)-
affects the ovaries.
Growth Hormone
• Two hypothalamic hormones
regulate GH:
o Growth hormone-
releasing hormone (GH-
RH)
o Growth hormone-
inhibiting hormone (GH-IH;
somatostatin)
• GH affects body tissues and
bones; GH replacement
stimulates linear growth when
there is GH deficiency.
• GH drugs can’t be given orally.
They are inactivated by
gastrointestinal enzymes.
• SQ and IM administration of GH is
necessary.
• Prolonged GH therapy can
antagonize insulin secretion and
eventually cause diabetes
mellitus.
Drug therapy: GH deficiency
• Somatrem (Protropin) and
somatropin (Humatrope) are two
growth hormones used to treat
growth failure in children
because of pituitary GH
deficiency.
• Somatropin is a product that has
the identical amino acid
sequence as human growth
hormone.
• Somatrem also has the identical
sequence of pituitary GH plus an
additional amino acid.
Drug therapy: GH excess
• Gigantism and acromegaly
can occur with GH
hypersecretion and are
frequently caused by a
pituitary tumor. If the tumor
cannot be destroyed by
radiation, the prolactin-
release inhibitor bromocriptine
can inhibit the release of GH
from the pituitary.
 • Octreotide (Sandostatin) is a
potent synthetic somatostatin
used to suppress GH release. It
can be used alone or with
surgery or radiation.
THYROID-STIMULATING HORMONE
• The adenohypophysis secretes
TSH in response to TRH from the
hypothalamus and TSH stimulates
the thyroid gland to release T3
and T4.
• Excess TSH secretion can cause
hyperthyroidism, and a TSH
deficit can cause
hypothyroidism.
• Hypothyroidism may be caused
by a thyroid gland disorder or a
decrease in TSH secretion.
• Thyrotropin (Thytropar), a purified
extract of TSH, is used as a
diagnostic agent to differentiate
between primary and secondary
hypothyroidism.
Corticotropin, Repository Corticotropin,
Corticotropin- Zinc Hydroxide
• Drug Class:
o Pituitary
adrenocorticotropic
hormone
• Pregnancy Category: C
• Indications: to diagnose
adrenocortical disorders; acts as
an inflammatory agent; to treat
acute MS.
• Mode of action: stimulates
adrenal cortex to secrete cortisol
• Contraindications: Severe fungal
infection, heart failure, peptic
ulcer
PHARMACOKINETICS
• Rapidly absorbed following
intramuscular administration
• Stimulates adrenal gland to
secrete corticosteroids. The
aqueous and gel preparations
are well absorbed in the
circulation. Zinc is added to some
preparations.
• Therapeutic half- life: 15- 20
minutes
• Excreted in the urine.
PHARMACODYNAMICS
• Suppresses the inflammatory and
immune responses
• Also prescribed to treat adrenal
insufficiency secondary to
inadequate corticotropin
secretion
• IM: onset- <6H; peak- 6-18 H;
duration- 12-24 H
• IV: onset- unknown; peak- 1H;
duration- UK
Assessment (Pituitary Hormones)
• Obtain baseline v/s. Report
abnormal results
• Determine client’s UO and
weight
• Assess the client for infectious
process. Corticotropin suppress
signs and symptoms of infection
• Note client’s physical growth.
Compare child’s growth with
reported standards. Report
findings
Nursing Diagnoses
• Ineffective health maintenance
related to lack of ability to
maintain drug regimen
• Delayed growth and
development related to deficient
stimulation of growth hormone
Planning
• Client will be free of pituitary
disorder with appropriate drug
regimen.
Interventions
• ADH
o Monitor v/s. increased HR
and decreased systolic
pressure
 o Record UO
o Advise client to adhere
drug regimen
o Direct client to decrease
salt intake to decrease or
avoid edema
o Instruct client to report side
effects such as muscle
weakness, edema,
petechiae, ecchymosis,
decrease in growth,
decreased wound healing
and menstrual irregularities
• ACTH, Corticotropin
o Avoid administering this
drug to clients with
adrenocortical
hyperfunction.
Corticotropin stimulates
the release of cortisol from
the adrenal glands
o Observe client’s weight
o Watch carefully for
adverse effects when the
drug is discontinued
o Check lab findings.
Electrolyte replacement
may be necessary
• GH
o Monitor blood sugar and
electrolyte levels in clients
receiving GH
o Advice athletes not to
take GH because of its
side effects
o Inform client with diabetes
to closely monitor blood
sugar levels
o Instruct and teach patient
and family to monitor
client’s growth rate
Evaluation
• Evaluate effectiveness of drug
therapy.
• Monitor patient response to
therapy (maintenance of fluid
balance).
• Monitor for adverse effects (e.g.
water intoxication, GI problems).
• Evaluate patient understanding
on drug therapy by asking
patient to name the drug, its
indication, and adverse effects
to watch for.
• Monitor patient compliance to
drug therapy.
POSTERIOR LOBE
• Also called as neurohypophysis
• It secretes ADH and oxytocin
• ADH promotes water
reabsorption from the renal
tubules to maintain water
balance in the body fluids
• Diabetes Insipidus can lead to
severe fluid volume deficit and
electrolyte imbalances
• Fluid and electrolyte balance
must be closely monitored, and
ADH replacement may be
needed
• The ADH preparations vasopressin
(Pitressin) and desmopressin
acetate (DDAVP) can be
administered intranasally or by
injection
Thyroid gland
• Triiodothyronine (T3) and
Thyroxine (T4) are secreted by the
thyroid gland.
• Their functions are to regulate
protein synthesis and enzyme
activity and to stimulate
mitochondrial oxidation.
• For thyroid deficiency
(hypothyroidism), synthetic T4
and T3 may be prescribed, either
alone or in combination.
• When thyroid gland secretes an
overabundance of thyroid
hormones (hyperthyroidism),
antithyroid drugs are usually
indicated.
Hypothyroidism
• A decrease in thyroid hormone
secretion.
• Primary hypothyroidism occurs
more frequently, the cause of
which are acute or chronic
inflammation of the thyroid
gland, radioiodine therapy,
excess intake of antithyroid drugs,
and surgery.
• Myxedema is severe
hypothyroidism in the adult.
• In children, hypothyroidism can
have a congenital (cretinism) or
prepubertal (juvenile
hypothyroidism) onset.
Drug therapy: Hypothyroidism
• Levothyroxine sodium
(Levothroid, Synthroid) is the DOC
for replacement therapy for the
treatment of hypothyroidism.
• It increases the levels of T3 and
T4.
• Also used to treat simple goiter
and chronic lymphocytic
(Hashimoto) thyroiditis.
• Liothyronine (Cytomel) is a
synthetic T3 that has a short half-
life and duration of action.
• Better absorbed from GI tract
than levothyroxine, frequently
used as initial therapy for treating
myxedema.
• Liotrix (Euthroid, Thyrolar) is a
mixture of levothyroxine sodium
and liothyronine sodium in a 4:1
ratio.
LEVOTHYROXINE SODIUM
• Drug class: Thyroid hormone
• Pregnancy category: A
• Indications: to treat
hypothyroidism, myxedema and
cretinism
• Mode of action: increase
metabolic rate, oxygen
consumption and body growth
• Contraindications: Thyrotoxicosis,
myocardial infarction (MI), severe
renal disease
Pharmacokinetics
• Synthetic thyroid hormone
preparation. The GI mucosa
absorbs 50-75 % of levothyroxine.
• Therapeutic half life: 6-7 days
• Excreted in the bile and feces
Pharmacodynamics
• Increases metabolic rate,
cardiac output, protein synthesis
and glycogen use
• PO: onset- unknown; peak- 24H- 1
week; duration- 1-3 weeks
• IV: onset- 6-8H; peak- 24-48 H;
duration- unknown
Assessment
• Assessment of the thyroid from an
anterior or posterior position.
• Auscultation of the lobes of the
thyroid gland using the
diaphragm of the stethoscope if
there are abnormalities
palpated.
• Assess thyroid gland for firmness
(Hashimoto’s) or tenderness
(thyroiditis).
Nursing Diagnoses
• Activity intolerance related to
fatigue and depressed cognitive
process
• Risk for imbalanced body
temperature related to cold
intolerance
• Constipation related to
depressed gastrointestinal
function
• Ineffective breathing pattern
related to depressed ventilation
• Disturbed thought processes
related to depressed metabolism
and altered cardiovascular and
respiratory status
Planning
• To achieve a successful nursing
care plan, the following goals
should be realized:
o Increase in participation in
activities.
o Increase in
independence.
o Maintenance of normal
body temperature.
o Return of normal bowel
function.
o Improve respiratory status.
o Maintenance of normal
breathing pattern.
o Improve thought
processes.
Interventions
• Promote rest. Space activities to
promote rest and exercise as
tolerated
• Protect against coldness. Provide
extra layer of clothing or extra
blanket
• Avoid external heat exposure.
Discourage and avoid the use of
external heat source
• Mind the temperature. Monitor
patient’s body temperature
• Increase fluid intake. Encourage
increased fluid intake within the
limits of fluid restriction
• Provide foods high in fiber
• Manage respiratory symptoms.
Monitor respiratory depth, rate,
pattern, pulse oximetry and ABG
• Pulmonary exercises. Encourage
deep breathing, coughing, and
use of incentive spirometry
• Orient to present surroundings.
Orient patient to time, place,
date and events around him or
her
Evaluation
• Evaluate effectiveness of the
drug and drug compliance.
• Continue monitoring for side
effects from drug accumulation
or overdosing.
HYPERTHYROIDISM
• Is an increase in circulating T3
and T4 levels, which result from
an overactive thyroid gland or
excessive output of thyroid
hormones from one or more
thyroid nodules.
• May be mild with few symptoms
or severe = thyroid storm.
• Thyroid storm is a life-threatening
health condition that is
associated with untreated or
undertreated hyperthyroidism.
• Grave’s disease or thyrotoxicosis
is the most common type of
hyperthyroidism caused by
hyperfunction of the thyroid
gland.
• Can be treated by surgical
removal of a portion of the
thyroid gland (subtotal
thyroidectomy), radioactive
iodine therapy, or antithyroid
drugs.
• Any of these treatments can
cause hypothyroidism.
Propranolol (Inderal) can control
cardiac symptoms like
palpitations and tachycardia
that result from hyperthyroidism. It
does not lower T3 & T4.
Drug therapy: Hyperthyroidism
• The purpose of antithyroid drugs
is to reduce the excessive
excretion of thyroid hormones by
inhibiting thyroid secretion.
• The use of surgery and
radioiodine therapy frequently
leads to hypothyroidism.
• Thiourea derivatives (thioamides)
are the drugs of choice used to
decrease thyroid hormone
production; they do not destroy
 thyroid tissue but rather block
thyroid hormone action.
• Propylthiouracil (PTU) and
methimazole (Tapazole) are
effective thioamide anti thyroid
drugs. They are useful for treating
thyrotoxic crisis and in
preparation for subtotal
thyroidectomy.
• Strong iodide solution such as
Lugol’s solution have been used
to suppress thyroid function for
clients who have undergone
subtotal thyroidectomy as a result
of Grave’s disease. Sodium
iodide administered IV is useful for
the management of thyrotoxic
crisis.
ANTITHYROID AGENTS
• are drugs used to block the
production of thyroid hormone
and treat hyperthyroidism.
• This include thioamides and
iodide solutions. These groups of
drugs are not chemically related
but they both block the
formation of thyroid hormones
within the thyroid gland.
• Indications: Treatment of
hyperthyroidism; Thyroid blocking
in a radiation emergency
PHARMACOKINETICS
• Thioamides
route onset peak Duration
PO 30-60 - 2-4 H
min
T ½: 6-13H
Metabolism: -
Excretion: urine
• Iodine Solutions
route onset peak duration
PO 24H 10-15 d 6 wk
T ½: unknown
Metabolism: liver; Excretion: urine
Contraindications and Cautions
• Allergy to any component of the
drug.
• Pregnancy. Development of
cretinism. PTU is the drug of
choice for pregnant women.
• Lactation. Risk of antithyroid
activity in the infant (neonatal
goiter)
• Pulmonary edema or
tuberculosis. Contraindicated
with strong iodine products.
Interactions
• Thioamides: increased bleeding
with oral anticoagulants and PTU
• Iodine solutions: changes in the
metabolism and level of
anticoagulants, theophylline,
digoxin, metoprolol, and
propranolol
Assessment
• Assess for contraindications or
cautions (e.g. history of allergy,
renal stone, pregnancy, etc.) to
avoid adverse effects.
• Assess skin lesions; orientation and
affect; liver evaluation; serum
calcium, magnesium, and
alkaline phosphate levels; and
radiographs of bones as
appropriate, to determine
baseline status before beginning
therapy and for any potential
adverse effects.
Nursing Diagnoses
• Imbalanced nutrition: more than
body requirements related to
metabolic changes
• Risk for injury related to bone
marrow suppression
Implementation
• Administer PTU three times a day,
around the clock to ensure
consistent therapeutic levels.
• Give iodine solution through a
straw to decrease staining of
teeth; tables can be crushed.
• Provide comfort measures to help
patient cope with drug effects.
• Provide patient education about
drug effects and warning signs to
report to enhance patient
knowledge and to promote
compliance.
Evaluation
• Monitor patient response to
therapy (lowering of thyroid
hormone levels).
• Monitor for adverse effects
(bradycardia, anxiety, blood
dyscrasias).
• Evaluate patient understanding
on drug therapy by asking
patient to name the drug, its
indication, and adverse effects
to watch for.
• Monitor patient compliance to
drug therapy.
Parathyroid Glands
• Secretes the PTH which regulates
calcium levels in the blood.
• A decrease in serum calcium
stimulates the release of PTH.
• Calcitonin decreases serum
calcium levels by promoting
renal excretion of calcium.
• Parathyroid hormone agents
treat hypoparathyroidism and
synthetic calcitonin treats
hyperparathyroidism.
Hypocalcemia can be caused
by PTH deficiency, vitamin D
deficiency renal impairment or
diuretic therapy, and PTH
replacement helps correct the
calcium deficit.
• The action of PTH is to:
o promote calcium absorption
from the GI tract
o promote reabsorption of
calcium from the renal tubules
o activate vitamin D
Calcitriol
• Vit D analogue that promotes
calcium absorption from the GI
tract and secretion from bone to
the bloodstream.
• Pregnancy Category: C
• Indication: treat
hypoparathyroidism and
manage hypocalcemia in
chronic renal failure.
• Mode of action: enhancement of
calcium deposits in bones.
• Contraindications:
Hypersensitivity, hypercalcemia,
hyperphosphatemia,
hypervitaminosis D,
malabsorption syndrome.
Pharmacokinetics
• Readily absorbed from the GI
tract.
• It crosses the placenta.
• Half life is moderate (3 to 8H)
 • Excreted mostly in feces.
Pharmacodynamics
• given for the management of
hypocalcemia
• it increases serum calcium levels
by promoting calcium absorption
from the intestines and renal
tubules
• PO: onset- 2-6H; peak- 10-12 H;
duration- 3-5 days
Assessment
• Note serum calcium levels.
Report any abnormal results.
• Assess for symptoms of tetany in
hypocalcemia: twitching of
mouth, tingling and numbness of
fingers, carpopedal spasm,
spasmodic contractions and
laryngeal spasm.
Nursing Diagnoses
• Acute pain related to GI and
CNS effects
• Imbalanced nutrition: less than
body requirements related to GI
effects
Implementation
• Monitor serum calcium
concentration before and
periodically during treatment to
allow for adjustment of dose to
maintain calcium levels within
normal limit.
• Provide supportive measures
(e.g. analgesics, small and
frequent meals, help with
activities of daily living) to help
patient deal with CNS and GI
effects of the drug.
• Arrange for nutritional
consultation if GI effects are
severe to ensure nutritional
balance.
• Provide patient education about
drug effects and warning signs to
report to enhance patient
knowledge and to promote
compliance.
Evaluation
• Monitor patient response to
therapy (return of serum calcium
levels to normal).
• Monitor for adverse effects
(weakness, headache, GI
effects).
• Evaluate patient understanding
on drug therapy by asking
patient to name the drug, its
indication, and adverse effects
to watch for.
• Monitor patient compliance to
drug therapy.
Adrenal Glands
• The paired adrenal glands consist
of the adrenal medulla and
adrenal cortex.
• The adrenal cortex produces two
types of hormones
(corticosteroids):
o Glucocorticoids (cortisol)
o Mineralocorticoids
(aldosterone)
• Corticosteroids promote sodium
retention and potassium
excretion. A decrease in
corticosteroid secretion is called
adrenal hyposecretion ( adrenal
insufficiency or Addison’s
disease) and an increase in
corticosteroid secretion is called
adrenal hypersecretion (Cushing
syndrome).
Glucocorticoids : Prednisone
• Are agents that stimulate an
increase in glucose levels for
energy.
• They also increase the rate of
protein breakdown and
decrease the rate of protein
formation from amino acids to
preserve energy.
 • They are also capable of
lipogenesis, or the formation and
storage of fat in the body for
energy source.
• Pregnancy Category: C
• Indication: to decrease
inflammatory occurrence, to
treat dermatologic disorders.
Systemic use is indicated for
treatment of some cancers,
hypercalcemia associated with
cancer, hematological disorders,
and some neurological
infections.
• Mode of action: suppression of
inflammation and adrenal
function.
Pharmacokinetics
• Is readily absorbed from the GI
tract.
route onset peak Duration
PO varies 1-2H 1-1.5 d
T ½: 3.5H
Metabolism: liver
Excretion: urine
Pharmacodynamics
• The major actions of prednisone
are to suppress an acute
inflammatory process and for
immunosuppression. It prevents
cell-mediated immune reactions
o PO: onset- unknown;
peak- 1-2H; duration- 24-
36H
Contraindications
• Allergy to any component of the
drug. To prevent hypersensitivity
reactions.
• Acute infection. Can be
exacerbated by the blocking
effects of the drug on
inflammation and immune
system.
• Diabetes. Glucose-elevating
effect of the drug can disrupt
glucose control
• Other endocrine
disorders. Potential of imbalance.
Assessment
• Note baseline vital signs for
future comparison.
• Assess laboratory test results,
especially serum electrolytes
and blood sugar.
• Obtain client’s weight and urine
output to use for future
comparison.
• Assess client’s medical and
herbal history. Report if client
has glaucoma, cataracts,
peptic ulcer, psychiatric
problems or diabetes mellitus.
Glucocorticoids can intensify
these health problems.
Nursing Diagnoses
• Risk for infection related to
immunosuppression
• Risk for impaired tissue integrity
related to side effect of a rash
• Altered cardiac output related
to fluid retention
• Excess fluid volume related to
water retention
Implementation
• Determine vital signs.
• Record weight. Report weight
gain of 5lbs in several days
• Space multiple doses evenly
throughout the day to try to
achieve homeostasis.
• Taper doses when discontinuing
to give the adrenal glands a
chance to recover and produce
adrenocorticoids.
• Watch carefully for signs and
symptoms of hypokalemia.
 • Protect patient from unnecessary
exposure to infection and
invasive procedure because the
steroids suppress the immune
system, and the patient is at
increased risk for infection.
• Provide comfort measures to help
patient cope with drug effects.
• Provide patient education about
drug effects and warning signs to
report to enhance patient
knowledge and to promote
compliance.
• Monitor older adults for signs and
symptoms of increased
osteoporosis.
• Report changes in muscle
strength.
• Instruct client to avoid persons
with respiratory infections,
because these drugs suppress
the immune system.
• Encourage client to have a
MedicAlert card, tag or bracelet
stating the glucocorticoid drug
taken.
• Instruct client how to use an
aerosol nebulizer. Warn client
against overuse of the aerosol to
avoid possible rebound effect.
Herbs & Corticosteroids
• Herbal laxatives (cascara, senna)
and herbal diuretics (celery seed,
juniper) can decrease serum
potassium levels.
• Ginseng
o improves strength and
stamina; also used to
prevent cancer and DM
o if taken with
corticosteroids may cause
central nervous system
stimulation and insomnia.
• Echinacea- used for common
colds and promotes wound
healing
o may counteract the
effects of corticosteroids.
• Licorice- for chronic fatigue
syndrome & chronic hepatitis
o potentiates the effect of
corticosteroids and may
cause a substantial
decrease in serum
potassium level.
Evaluation
• monitor patient response to
therapy (e.g. relief of signs and
symptoms of inflammation, return
of adrenal function within normal
limits)
• monitor for adverse effects (e.g.
infections, skin changes, fatigue)
• evaluate patient understanding
on drug theraoy by asking
patient to name the drug, its
indication, and adverse effects
to watch for
• monitor patient compliance to
drug therapy
ANTIDIABETIC AGENTS
• any drug that works to lower
abnormally high glucose (sugar)
levels in the blood, which are
characteristic of the endocrine
system disorder known as
diabetes mellitus
DIABETES
• caused by the body’s inability to
produce or respond to the
pancreatic hormone insulin
• one of the important
physiological actions of insulin is
to control blood glucose levels.
Glucose is an important nutrient
for cellular metabolism, and cells
must receive neither too little nor
too much. A deficiency in the
pancreatic secretion of insulin, or
 lack of tissue sensitivity to the
hormone, leads to diabetes, the
primary feature of which is
elevated blood glucose levels
(hyperglycemia)
• most patients can be classified as
having either type I diabetes or
type II diabetes
• Type I (insulin dependent) – is
characterized by absolute lack of
production of insulin
• Type II (deficiency of insulin
hormone) – is characterized by
tissue resistance to the insulin that
is produced by the pancreas
ADMINISTRATION OF INSULIN
INSULIN
• Insulin is released from the beta
cells of the islets of Langerhans in
response to an increase in blood
glucose.
• Oral glucose load is more
effective in raising the serum
insulin level than an intravenous
(IV) glucose load.
• Insulin promotes the uptake of
glucose, amino acids, and fatty
acids and converts them to
substances that are stored in
body cells.
• Glucose is converted to
glycogen for future glucose
needs in the liver and muscle,
thereby lowering the blood
glucose level.
• The normal range for blood
glucose is 60 to 100 mg/ dl and
70 to 110 mg/dl for serum
glucose. When the blood
glucose level is greater than 180
mg/dl, glycosuria (sugar in the
urine) can occur.
• Increase blood sugar acts as an
osmotic diuretic, causing
polyuria. when blood sugar
remains elevated (>200 mg/dl),
diabetes mellitus occurs.
Beta Cell Secretion of Insulin
• The beta cells in the pancreas
secrete approximately 0.2 - 0.5
units/kg/daily. A client weighing
70 kilograms secretes 14 to 35
units of insulin a day.
• More insulin secretion may occur
if the person consumes a greater
caloric intake. A client with
diabetes mellitus may require 0.2
to 1 units /kg/daily.
• The higher range maybe
because of obesity, stress, or
tissue resistance.
• Insulin is a protein and cannot be
administered orally because
gastrointestinal secretions destroy
the insulin structure.
• It is administered SQ, at a 45-to-
90-degree angle. The 90-degree
angle is made by raising the skin
and fatty tissue; the insulin is
injected into the pocket
between the fat and the muscle.
In a thin person with little fatty
tissue, the 45-to-60-degree angle
is used.
• Regular insulin is the ONLY type
that can be administered IV.
• The site and depth of insulin
injection affect absorption. Insulin
absorption is greater when given
in the deltoid and abdominal
areas than when given in the
thigh and buttocks areas.
• Insulin administered SQ has a
lower absorption rate than if it is
administered IM.
• Heat and massage could
increase SQ absorption. Cooling
the SQ area can decrease
absorption.
• Insulin is usually given in the
morning before breakfast it can
be given several times a day.
 • Insulin injection sites should be
rotated to prevent lipodystrophy
which can interfere with insulin
absorption. The patient needs to
develop a side rotation pattern
to avoid this and to promote
insulin absorption
• Lipoatrophy it's a depression
under the skin surface that
primarily occurs in females and
children.
• Lipohypertrophy is a raised lump
or knot under skin surface that is LIPOHYPERTROPHY
more common in males. It is
frequently caused by repeated
injections into the same side.
• Illness and stress increase the
need for insulin. Insulin doses
should not be withheld during
illness, including infections and
stress. Hyperglycemia and
ketoacidosis may result from
withholding insulin.

LIPODYSTROPHY Types of insulin onset peak Duration

Ultra rapid 15 mins 30-60 3-4H
(Humalog) mins
Rapid acting/ 30mins- 2-4 H 6-8H
Short acting 1H
(regular insulin)
• Clear
• Ex:
Humulin
R;
Novolin R
Immediate 1-2H 6-8H 18-24H
Acting
• Ex: NPH;
Humulin
N,
Novolin N
Long Acting 3-4H 16- 30-36H
(Ultralente) 20H
LIPOATROPHY
INSULIN RESISTANCE
• Antibodies develop over time in
persons taking animal insulin. This
can slow the onset of insulin
action and extend its duration of
action. Antibody development
 can cause insulin resistance and
insulin allergy.
• Obesity can also be a causative
factor for insulin resistance .
• Skin tests with different insulin
preparations may be performed
to determine whether there is an
allergic effect . Human and
regular insulins produce fewer
allergens.
STORAGE OF INSULIN
• Unopened insulin vials are
refrigerated until needed. once
an insulin vial has been opened it
may be kept:
o at room temperature for
one month
o in the refrigerator for three
months
o Insulin is less irritating to the
tissues when injected at
room temperature.
o Insulin vials should not be
put in the freezer and
should not be placed in
direct sunlight or in a high
temperature area.
o Prefilled syringes should be
stored in the refrigerator
and should be used within
one to two weeks. Open
insulin vials lose their
strength after
approximately 3 months.
Sliding -scale insulin coverage
• Insulin may be administered in
adjusted doses that depends on
individual blood glucose test
results.
• When the diabetic client has
extreme variances in insulin
requirements (example : stress
from hospitalization, surgery,
illness, infection), adjusted dosing
or sliding scale insulin coverage
provides a more constant blood
glucose level.
• Blood glucose testing is
performed several times a day at
specified intervals (usually before
meals). A preset scale usually
involves directions for the
administration of rapid or short
acting insulin
INSULIN PUMPS
• There are two types of insulin
pumps:
o Implantable- is surgically
implanted in the
abdomen. It delivers basal
insulin infusion and bolus
doses with meals,
administered wither
intraperitoneally or IV. With
the use of implantable
insulin pumps, fewer
hypoglycemic reactions
occur, and the blood
glucose levels are
controlled
o Portable/ external insulin
pumps- also called
continuous SQ insulin
infusion, have been
available since 1983. It
keeps blood glucose levels
as close to normal as
possible. Infusions are
programmed by the client.
The client can adjust the
rate according to
changes in activity
• Glucose levels should be
monitored at least daily with or
without an insulin pump. An
alarm is sounded when incident is
not delivered.
Oral Hypoglycemic Agents
1. Sulfonylureas- Glipizide
(Glucotrol)
• group of agent used to
control blood glucose level.
 • stimulate insulin release from the
beta cells in pancreas. They
improve insulin binding to insulin
receptors and may actually
increase the number of insulin
receptors.
• Not effective for all diabetics
and may lose their effectiveness
over time with others.
• Sulfonylureas are further classified
as first-generation or second-
generation sulfonylureas.
• Use of first-generation
sulfonylureas is declining as more
effective drugs have become
available.
• Use of second-generation
sulfonylureas have several
advantages over first-generation,
including safer for patients with
renal dysfunction as they are
excreted in urine and bile,
absence of interaction to many
protein-bound drugs, and longer
duration of action.
First Generation Sulfonylureas
• They are divided into :
o Short acting – Tolbutamide
(Orinase)
o Immediate acting –
Acetohexamide (Dymelor)
o Long acting –
Chlorpropamide
(Diabinese)
Second Generation Sulfonylureas
• Glimepiride
• Glipizide – directly stimulate the
beta cells then secrete insulin,
thus decreasing the blood
glucose level
Pharmacokinetics
• Glipizide is well absorbed from
the GI tract and highly protein-
bound.
route onset peak Duration
oral 15-30 1-2H 24H
mins
Metabolism: liver
Excretion: urine
Pharmacodynamics
• Glipizide is the most common
sulfonylurea drug prescribed for
type 2 diabetes mellitus. It lowers
the blood sugar by stimulating
pancreatic beta cells to secrete
insulin
Assessment
• Assess for contraindications or
cautions (e.g. history of allergy to
the drugs, pregnancy and
lactation status, severe renal or
hepatic dynsfunction, etc.) which
are contraindications in the use
of these agents
• Perform a complete physical
assessment to establish baseline
status before beginning therapy
and to evaluate effectiveness
and any potential adverse
effects during therapy
• Assess orientation and reflexes;
baseline pulse and blood
pressure; adventitious breath
sounds; abdominal sounds and
function to monitor effects of
altered glucose levels
• Assess body systems for changes
suggesting possible
complications associated with
poor blood glucose control
• Investigate nutritional intake,
noting any problems with intake
and adherence to prescribed
diet, to help prevent adverse
reactions to drug therapy.
• Assess activity level, including
amount and degree of exercise,
which can alter serum glucose
levels and dosage needs for
these drugs.
 • Monitor blood glucose levels as
ordered to evaluate
effectiveness of drug and
glycemic control.
• Monitor results of laboratory tests,
including urinalysis, for evidence
of glycosuria, and renal and liver
function tests, to determine the
need for possible dose
adjustment and evaluate for
signs of toxicity.
Nursing Diagnoses
• Risk for unstable blood glucose
related to ineffective dosing of
antidiabetic agents
• Imbalanced nutrition: less than
body requirements related to
metabolic effects
• Disturbed sensory perception:
kinesthetic, visual, auditory, and
tactile related to glucose levels
Implementation
• Administer the drug as prescribed
in the appropriate relationship to
meals to ensure therapeutic
effectiveness.
• Ensure that patient has dietary
and exercise regimen and using
good hygiene practices to
improve the effectiveness of the
insulin and decrease adverse
effects of the disease.
• Monitor blood glucose levels and
report changes. The reference
value is 60-100mg/ dl for blood
glucose and 70-110 mg/dl for
serum glucose.
• Monitor nutritional status to
provide nutritional consultation as
needed.
• Monitor response carefully; blood
glucose monitoring is the most
effective way to evaluate dose.
• Obtain blood glucose levels as
ordered to monitor drug
effectiveness.
• Monitor patients during times of
trauma, pregnancy, or severe
stress, and arrange to switch to
insulin coverage as needed.
• Provide comfort measures to help
patient cope with drug effects.
• Provide patient education about
drug effects and warning signs to
report to enhance patient
knowledge and to promote
compliance.
Evaluation
• Monitor patient response to
therapy (stabilization of blood
glucose levels).
• Monitor for adverse effects
(hypoglycemia and
gastrointestinal distress).
• Evaluate patient understanding
on drug therapy by asking
patient to name the drug, its
indication, and adverse effects
to watch for.
• Monitor patient compliance to
drug therapy.
Nonsulfonylureas
• Biguanides are classed as non-
sulfonylureas. Metformin is the
only available biguanide for
diabetes treatment. It inhibits the
amount of glucose produced by
the liver, increases the insulin-
receptor binding and stimulates
tissue uptake of glucose.
• Metformin does not stimulate the
pancreas to make or release
more insulin so doesn't cause
hypoglycemia. Metformin is used
to treat Type 2 diabetes.
Biguanide: Metformin (Glucophage)
 • decrease the production and
increases the uptake of glucose.
It is effective in lowering blood
glucose and does not cause
hypoglycemia as the
sulfonylureas do. It has been
associated with development of
lactic acidosis and GI distress.
• metformin is approved for use in
children 10 years of age and
older. It is also being used in the
treatment of women with
polycystic ovarian syndrome
(PCOS).
• Inhibits hepatic formation of
glucose.
used to treat insulin induced
hypoglycemia when other
methods of providing glucose are
not available.
Clients with diabetes who are prone to
severe hypoglycemic reactions (insulin
shock) should keep glucagon in the
home, and family members should be
taught how to administer during an
emergency hypoglycemic reaction.
Blood glucose level begins to increase
within 5 to 20 minutes after
administration.

Glucosidase Inhibitor: Acarbose

(Precose)
• Inhibits absorption of excess
glucose from the intestine
• Is used with a proper diet and
exercise program to control high
blood sugar in people with type 2
diabetes
• Controlling high blood sugar
helps prevent kidney damage,
blindness, nerve problems, loss of
limbs, and sexual function
problems

Hyperglycemic drugs: Glucagon

• Glucagon is a hyper glycemic
hormone secreted by the alpha
cells of the islets of Langerhans in
the pancreas.
• Glucagon increases blood sugar
by stimulating glycogenolysis
(glycogen breakdown) in the
liver. It protects the body cells
especially those in the brain and
retina, by providing the nutrients
and energy needed to maintain
body function.
• Glucagon is available for
parenteral use (SQ, IM and IV),it is
Drugs Acting on the Cardiovascular System
Cardiovascular System
• Heart
• Blood Vessels (arteries & veins)
• Blood
➢ Blood rich in oxygen (O2), nutrients and
hormones move through the vessels called
arteries, which narrow to arterioles.
➢ Capillaries transport rich, nourished blood to
body cells and absorb waste products such as
carbon dioxide (CO2), urea, creatinine and
ammonia.
➢ The deoxygenated blood returns to the
circulation by the venules and veins to be
eliminated by the lungs and kidneys with other
waste products.
➢ The heart's pumping action serves as the energy
source that circulates blood to body cells.
Blockage of vessels can inhibit blood flow.
Heart
• The right atrium receives deoxygenated blood
from the circulation.
• The right ventricle pumps blood through the
pulmonary artery to the lungs for gas exchange
(carbon dioxide for oxygen).
• The left atrium receives oxygenated blood
• The left ventricle pumps the blood into the aorta
for systemic circulation
• The heart muscle, called the myocardium,
surrounds the ventricles and atria.
• The ventricles are thick-walled (especially the
left ventricle)to achieve the muscular force
needed to pump blood to the pulmonary and
systemic circulations.
• The atria are thin-walled, have less pumping
action and serve as receptacles for blood from
the circulation and lungs.
• The heart has a fibrous covering called the
pericardium, which protects it from injury and
infection .
• The endocardium is a three-layered membrane
that lines the inner part of the heart chambers.
• Four valves – two atrioventricular (tricuspid and
mitral) and two semilunar (pulmonic and aortic)-
control blood flow between the atria and
ventricles and between the ventricles and the
pulmonary artery and the aorta.
• The right coronary artery supplies blood to the
right atrium and ventricle of the heart
• the left coronary artery supplies blood to the left
atrium and ventricle of the heart .
• The left coronary artery divides near its origin to
form the left circumflex artery and the anterior
descending artery.
• Blockage to one of these arteries can result into
a myocardial infarction , or heart attack .
Conduction of Electrical Impulses
• The myocardium is capable of generating and
conducting its own electrical impulses.
• The cardiac impulse usually originates in the
sinoatrial (SA) node located in the posterior wall
of the right atrium.
• The SA node is frequently called the pacemaker,
because it regulates the heartbeat (firing off
cardiac impulses), which is approximately 60- 80
bpm in the normal adult .
• The atrio ventricular (AV) node, located in the
posterior right side of the interatrial septum, has
a continuous track of fibers called the bundle of
His, or the AV bundle.
• The AV node is called the functional pacemaker,
having an adult rate of 40 -60 bpm.
• If the SA node fails, the AV node takes over, thus
causing a slower heart rate.
• The AV node sends impulses to the ventricles.
• These two conducting systems (SA node and AV
node)can act independently of each other .
• The ventricle can contract independently 30 to
40 times per minute.
➢ Drugs that affect cardiac construction include:
calcium, digitalis preparations, and quinidine
and its related preparations.
➢ The autonomic nervous system (ANS) and drugs
that stimulate or inhibit it influence heart
contractions .
➢ The sympathetic nervous system and the drugs
that stimulate it increases heart rate; the
parasympathetic nervous system and the drugs
that stimulate it decrease heart rate.
 Regulation of Heart Rate and Blood Flow Cardiac Glycosides
• The heart beats approximately 60-80 times per • are cardiotonic agents from foxglove or digitalis
minute in an adult, pumping blood into the plants.
systemic circulation • They exert their effects on the cardiac muscles
• As blood travels, resistance to blood flow by affecting levels of intracellular calcium. In
develops an arterial pressure increases. turn, the contractility of the muscles is
• The average systemic arterial pressure, known as increased.
blood pressure, is 120/80 mmhg. DIGOXIN (Lanoxin)
• Arterial blood pressure is determined by • Pregnancy Category: C
peripheral resistance and cardiac output, the • Indication: The treat HF, atrial tachycardia,
volume of blood expelled from the heart in one flutter or fibrillation.
minute, which is calculated by multiplying the • Mode of Action: inhibits sodium- potassium
heart rate by the stroke volume: ATPase, promoting increased force of cardiac
• CO (Cardiac Output) = HR (Heart Rate) x SV contraction, cardiac output and tissue perfusion;
(Stroke Volume) decreases ventricular rate.
CIRCULATION • Contraindications: Ventricular dysrhythmias,
There are two types of circulation: second or third- degree heart block.
• Pulmonary • Caution: AMI, renal disease, hypothyroidism,
• Systemic or peripheral. hypokalemia
• With pulmonary circulation, the heart pumps Pharmacokinetics
deoxygenated blood from the right ventricle route onset peak Duration
through the pulmonary artery to the lungs. Oral 30-120 min 2-6 H 6-8 d
• In this situation, the artery carries blood that has IV 5-30 min 1-5 H 4-5 d
a high concentration of carbon dioxide . T ½ : 30-40 H
• Oxygenated blood returns to the left atrium by Metabolism: N/A
the pulmonary vein. Excretion: urine (unchanged)
• With systemic or peripheral circulation, the
heart pumps blood from the left ventricle to the Pharmacodynamics
aorta and into the general circulation . • In clients with a failing heart, cardiac glycosides
• Arteries and arterioles carry the blood to increased myocardial contraction, which
capillary beds . increases cardiac output and improves
• Nutrients in the capillary blood or transferred to circulation and tissue perfusion. because these
cells in exchange for waste products. Blood drugs decrease conduction through the AV node,
returns to the heart through venules and veins. the heart rate decreases.
BLOOD • The onset and peak actions of oral an (IV) digoxin
• Blood is composed of plasma, red blood cells vary.
(erythrocytes), white blood cells (leukocytes) and • The therapeutic serum level is 0.5 to 2.0 ng/ml
platelets . for digoxin.
• Plasma, made up of 90% water and 10% solutes, • To treat HF, the lower serum therapeutic level
constitute 55% after total blood volume . should be obtained, and for atrial flutter or
• The major function of blood is to provide fibrillation the higher therapeutic serum levels
nutrients, including oxygen to body cells. are required.
• Most of the oxygen is carried on the hemoglobin • PO: Onset: 1-5H
of red blood cells. Peak: 6-8H
• White blood cells are the major defense Duration: 2-4 days
mechanism of the body, an act by engulfing • IV: Onset: 5-30 mins
microorganisms. They also produce antibodies. Peak: 1-5H
• The platelets are large cells that cause blood to Duration: 2-4 days
coagulate. Adverse Effects
• RBCs have a lifespan of approximately 120 days, • CNS: headache, weakness, drowsiness, vision
whereas the lifespan of a WBC is only 2- 24 changes (most commonly reported:
hours. seeing yellow halo around objects)
• CV: arrhythmias
 • GI: GI upset, anorexia
NURSING ALERT!
• Signs and Symptoms of digitalis toxicity:
o Anorexia
o N/V
o Malaise
o Depression
o Irregular heart rhythms (e.g. heart block,
heart arrhythmias, and ventricular
tachycardia)
Interactions
• Digoxin immune Fab or DigiFab: antidote; these
antibodies bind molecules of digoxin, making
them unavailable at site of action. Used when
serum digoxin is >10 ng/mL and serum
potassium is >5 mEq/L.
• Verapamil, amiodarone, quinine, erythromycin,
tetracycline, cyclosporine: increased
therapeutic and toxic effects of digoxin.
Combination of digoxin with any of these drugs
would warrant decrease in dose of digoxin to
prevent toxicity.
• Potassium-losing diuretics: increased risk of
cardiac arrhythmias
• Thyroid hormones, metoclopramide,
penicillamine: decreased therapeutic effects of
digoxin. Increasing the dose of digoxin is
important.
• Cholestyramine, charcoal, colestipol, antacids,
bleomycin, cyclophosphamide,
methotrexate: decreased absorption of digoxin.
In this case, digoxin must be taken 2-4 hours
after taking any of these drugs.
• St. John’s wort, psyllium: decreased therapeutic
effect of digoxin
• Ginseng, hawthorn, licorice: increased risk of
digoxin toxicity
Assessment
• Assess for the mentioned contraindications to
this drug (e.g. renal insufficiency, acute MI,
hypersensitivity, etc.) to prevent potential
adverse effects.
• Conduct thorough physical assessment before
beginning drug therapy to establish baseline
status, determine effectivity of therapy and
evaluate potential adverse effects.
• Obtain baseline status for weight while noting
recent manifestations that increase or decreases
to determine patient’s fluid status.
• Assess closely patient’s heart rate and blood
pressure to identify cardiovascular changes that
may warrant a change in digoxin drug dose.
• Auscultate heart sounds to note the presence of
abnormal sounds and possible conduction
problems.
• Determine urinary pattern and output to assess
gross indication of renal function.
• Obtain baseline electrocardiogram (ECG) to
identify heart rate and rhythm.
• Monitor serum electrolyte and renal function
test results to determine whether changes in
drug dose is needed or not
Nursing Diagnoses
• Risk for fluid volume deficit related to increased
renal perfusion as effect of the drug
• Decreased cardiac output related to inefficient
myocardial contractility
• Ineffective tissue perfusion related to decreased
blood flow to different parts of the body
Implementation
• Check drug dose and preparation carefully
to avoid medication errors because drug has
narrow safety margin.
• Do not administer drug with food and antacids
to prevent decreased in drug absorption.
IMPORTANT! Count apical pulse for one full
minute before administering drug to monitor for
adverse effects.
• Drug is withheld if pulse is less than 60 beats per
minute in adults and 90 beats per minute in
infants.
• Apical pulse is taken after one hour and if it
remains low, nurse must document it, withhold
the dose, and inform doctor.
Implementation
• Assess pulse rhythm to detect arrhythmias which
are early signs of drug toxicity.
• Weigh the patient daily to monitor for fluid
retention and HF. Assess dependent areas for
presence of edema and note its degree of pitting
to assess severity of fluid retention.
APICAL PULSE
 Implementation
• Monitor serum digoxin level as ordered
(normal: 0.5-2 ng/mL) to evaluate therapeutic
dosing and development of adverse effects.
• Provide comfort measures (e.g. small frequent
meals for GI upset, instituting safety measures
for drowsiness and weaknesses, and providing
adequate room lighting for patients with visual
disturbances) to help patient tolerate drug
effects.
• Promote rest periods and relaxation
techniques to balance supply and demand of
oxygen.
• Ensure maintenance of emergency drugs and
equipment at bedside (e.g. potassium salts
and lidocaine for arrhythmias, phenytoin for
seizures, atropine in case of clinically
significant low heart rate, and cardiac monitor)
to promote prompt treatment in cases of
severe toxicity.
• Educate patient on drug therapy including drug
name, its indication, and adverse effects to
watch out for to enhance patient
understanding on drug therapy and thereby
promote adherence to drug regimen.
Evaluation
• Monitor patient response to therapy through
assessing manifestations of HF, arrhythmia,
and serum level of digoxin.
• Monitor for adverse effects (e.g. visual
changes, HF, and arrhythmias).
• Evaluate patient understanding on drug
therapy by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
Types of Angina Pectoris
ANTIDOTE for Cardiac /Digitalis Glycosides
• Digoxin immune Fab (Ovine, Digibind) may be
given to treat severe digitalis toxicity. This agent
binds with dioxin to form complex molecules
that can be excreted in the urine; digoxin is
unable to bind at the cellular site of action.
• signs and symptoms of digoxin toxicity should be
reported promptly to the health care provider.
• Serum dioxin levels should be closely monitored.
Digitalis toxicity may result in first degree second
degree or complete heart block
Phosphodiesterase Inhibitors
• aid in increasing force of myocardial contractility
through their enzyme-blocking effect. This in
turn, increases the flow of calcium into the
myocardial cells.
• The two drugs in this group are inamrinone
lactate (Inocor) and milrinone lactate
(Primacor). These drugs increase stroke volume
and cardiac output and promote vasodilation.
• They are administered IV for no longer than 48
to 72 hours.
• Severe cardiac dysrhythmias might result from
the use of phosphodiesterase inhibitors, so the
client's ECG or electrocardiogram and cardiac
status should be monitored.
Antianginal Drugs
● aid in increasing force of myocardial contractility
through their enzyme-blocking effect. This in
turn, increases the flow of calcium into the
myocardial cells.
● The two drugs in this group are inamrinone
lactate (Inocor) and milrinone lactate (Primacor).
These drugs increase stroke volume and cardiac
output and promote vasodilation.
● They are administered IV for no longer than 48
to 72 hours.
● Severe cardiac dysrhythmias might result from
the use of phosphodiesterase inhibitors, so the
client's ECG or electrocardiogram and cardiac
status should be monitored.
● Are used to treat angina pectoris.
● used primarily to restore the balance between
the oxygen supply and demand of the heart.
● These drugs dilate the coronary vessels to
increase the flow of oxygen to the ischemic
regions.
● They also decrease the workload of the heart so
the organ would have less demand for oxygen.
• The frequency of anginal pain depends on many
factors, including the type of angina.
• There are three types of angina:
o Classic (stable): occurs with stress or
exertion
o Unstable (preinfarction): occurs
frequently over the course of a day with
progressive severity.
o Variant (Prinzmetal, vasospastic):
occurs during rest.
• The first two types are caused by a narrowing or
partial occlusion of the coronary arteries; variant
angina is caused by vessel spasm (vasospasm).
• Unstable angina often indicates an impending
MI.
Nonpharmacologic Measures to Control Angina • Mode of action: decreases myocardial demand
• AVOID: for oxygen; decreases preload by dilating veins,
o Avoid heavy meals indirectly decreasing afterload.
o Smoking • Contraindications: Marked hypotension, AMI,
o Extremes in weather changes increased intracranial pressure, severe anemia
o Strenuous exercise • Side effects: N/V, headache, dizziness, syncope,
o Emotional upset weakness, flush, confusion, pallor, rash, dry
• Proper nutrition, moderate exercise (only after mouth.
consulting with the health care provider), • Adverse reactions: hypotension, reflex
adequate rest and relaxation techniques should tachycardia, paradoxical bradycardia
be used as preventive measures
Types of antianginal drugs Pharmacokinetics/Pharmacodynamics
• Antianginal drugs increase blood flow either by route onset Duration
increasing oxygen supply or by decreasing IV 1-2 min 3-5 min
oxygen demand by the myocardium. Sublingual 1-3 min 30-60 min
• Three types of antianginals are: tablet
o Nitrates – reduction of venous tone, Translingual 2 min 30-60 min
which decreases the workload of the spray
heart and promotes vasodilation. Transmucosal 1-2 min 3-5 min
o Beta Blockers & tablet
o Calcium Channel Blockers - Decrease Oral SR tablet 20-45 min 8-12h
the workload of the heart and decrease Topical 30-60 min 4-8h
oxygen demands. Ointment
• Nitrates are usually given subcutaneously and Transdermal 30-60 min 24h
intravenously as needed. if the heart pain T ½: 1-4 min
continues, a better blocker is given Metabolism: liver
intravenously, and if the client is unstable to Excretion: Kidney (urine)
tolerate beta blockers, a calcium blocker may
be substituted. Assessment
• Presence of mentioned contraindications and
Nitrates cautions.
• are antianginal agents that provide fast action • Skin color and integrity, especially for
to directly relax smooth muscles and depress transdermal or topical forms of nitrates
muscle tone without affecting nerve activity. • Pain and activity level
• Nitrates reduce preload and myocardial • Neurological status (level of consciousness,
muscle tension by dilating the veins. They affect, reflexes, etc.)
reduce afterload by dilating the arteries. • Cardiopulmonary status (BP; take heart rate in
• Both of these actions lower oxygen demand by full minute)
decreasing the workload of the heart. • Electrocardiogram as ordered
Therapeutic Action • Laboratory tests (e.g. CBC, liver and kidney
• The main effect is drop in systemic blood function tests, etc.)
pressure.
• It compensates by increasing blood flow to ECG PLACEMENT
healthy arteries and veins because affected Nursing Diagnoses
vessels already lose their elasticity. • Decreased cardiac output related to vasodilation
and hypotensive effects of the drug
Nitroglycerin • Risk for Injury related to adverse effects on
• Drug class: Antianginal neurological and cardiovascular status
• Trade names: Nitrostat, NTG, Nitrol Nitrate • Ineffective Tissue Perfusion related to low
• Pregnancy Category: C oxygen supply to myocardial cells
• Indication: to control angina pectoris (anginal
pain)
Implementation • Propranolol is the prototype drug of this class. It
• Instruct patient not to swallow sublingual is used for treatment of angina and syncope.
preparations to ensure therapeutic effects. Take • Nebivolol, the newest adrenergic blocking agent
three tablets with a 5-minute interval, for a total does not produce the same adverse effects seen
of three doses. If the pain does not subside, seek in propranolol.
medical help. Pharmacokinetics
• Ask for presence of burning sensation to ensure route onset peak Duration
drug potency. oral 15 min 90 min 15-19h
• Protect drug from sunlight to maintain drug IV Immediate 60-90 15-19h
potency. min
• For sustained release forms, take drug with T ½: 3-4h
water and do not crush for these preparations Metabolism: liver
need to reach GIT intact. Excretion: kidney (urine)
• Rotate injection sites and provide skin care as • food increases bioavailability of propranolol
appropriate to prevent skin abrasion and • Propanolol is the only drug under this class
breakdown that can cross the blood-brain barrier
• Avoid abrupt stop of long-term therapy. Taper Contraindications and Cautions
doses for 4-6 weeks to prevent myocardical • Bradycardia, heart block, and cardiogenic shock
infarction – blocking effect of drugs exacerbates these
• Provide comfort measures; small frequent conditions
meals, appropriate room temperature and • Pregnancy and lactation – potentially harmful
lights, noise reduction, ambulation assistance, effects to the fetus or neonate
reorientation, and skin care • Diabetes, chronic obstructive pulmonary disease
Evaluation (COPD), thyrotoxicosis, and peripheral vascular
• Monitor patient response to therapy (pain diseases – blocking effect prevents maintaining
assessment). homeostatic requirements of these diseases
• Monitor for presence of mentioned adverse Adverse Effects
effects. • CNS: emotional depression, dizziness, fatigue,
• Monitor for effectiveness of comfort measures. sleep disturbances
• Monitor for compliance to drug therapy • GI: gastric pain, nausea, vomiting, colitis,
regimen. diarrhea
• Monitor laboratory tests. • CV: heart failure, reduced cardiac output,
arrhythmia
Beta-Blockers • Respiratory: dyspnea, cough, bronchospasm
• Beta-adrenergic blockers are drugs which block Interactions
or lyse the effects of sympathetic stimulation. • Clonidine: increased rebound hypertension
Hence, they are also called as sympatholytics. • NSAIDs: decreased antihypertensive effects
Therapeutic action • Epinephrine: hypertension followed by
• Main effects include decreased blood pressure,
bradycardia
contractility and heart rate by blocking the beta-
• Ergot alkaloids: peripheral ischemia
receptors in the heart and juxtaglomerular
apparatus of the kidneys. These combined • Insulin and oral hypoglycemic agents: alteration
effects reduce the oxygen demand of the heart. in blood glucose levels without the patient
• Usually used in therapy with nitrates because of experiencing manifestations of hypo- or
reduced adverse effects and increased exercise hyperglycemia
tolerance.
Assessment
• Not indicated for variant angina because
therapeutic effect of drugs can cause vasospasm. • Assess for presence of mentioned
Indications contraindications and cautions.
• Nadolol is used for management of chronic • Assess neurological status to determine
angina. It is the drug of choice in angina patients
presence of neurological adverse effects. Focus
with hypertension.
on level of orientation and sensory function.
 • Monitor blood pressure and heart rate calcium ions, thereby altering arterial and
accurately. Be sure to count the heart rate in one cardiac muscle action potentials.
full minute. • They basically produce vasodilation and relief of
• Auscultate lungs to determine presence of spasm.
possible respiratory adverse effects. • They do not increase lipid levels.
• Check color and sensation of extremities. • Serve as a substitute for classic and variant
angina when beta-blockers and nitrates are
Measure capillary refill. This is to evaluate
contraindicated.
presence of insufficiencies in the peripheral
Therapeutic Action
vascular system. • By blocking contractions, loss of muscle tone and
• Monitor laboratory test results (e.g. electrolyte vasodilation occur, consequently decreasing
levels and renal function tests) to ascertain risk peripheral resistance.
for arrhythmia and discern whether dose • Relieves vasospasm in variant angina, thereby
adjustment is needed. increasing blood flow to the heart.
• Can block atherosclerotic process in endothelial
CAPILLARY REFILL TIME cells
• normal = < 2 seconds Indications
• Treatment of variant angina, chronic angina and
Diagnosis effort-associated angina
• Decreased Cardiac Output related to decreased Pharmacokinetics
heart rate, blood pressure, and contractile route onset peak Duration
properties of the heart Oral 30-60 min 2-3h 2-4h
• Ineffective Tissue Perfusion related to decreased SR, ER 30-60 min 6-11h Varies
blood flow to the heart IV immediate 2-3 min varies
• Risk for Injury related to possible alterations in T ½: SR (3.5-6h); ER (6-7h)
CNS while on drug therapy Metabolism: liver
Implementation Excretion: kidney (urine)
• Give drug as ordered following safe and
appropriate administration to ensure Contraindications and Cautions
therapeutic effects. • Allergy to drugs
• Provide comfort measures: ambulation • Heart block and sick sinus syndrome –
assistance, raised siderails, appropriate room conduction problems in these diseases may be
light and temperature, and rest periods exacerbated by slow conduction effect of drugs
• Monitor cardiopulmonary status closely to • Renal and hepatic dysfunctions – alteration with
detect possible alterations in vital signs which
metabolism and excretion of drugs
signal need for dose adjustment and to prevent
• Heart failure – worsened by decreased cardiac
related adverse effects.
output effect of the drug
• Educate client about the need to not abruptly
stop therapy as this can lead to rebound Adverse Effects
hypertension and myocardial infarction.
Evaluation • CNS: dizziness, lightheadedness, fatigue, and
• Monitor patient response to therapy. headache
• Monitor for presence of mentioned adverse • GI: nausea, hepatotoxicity effect of the drug
effects. • CV: hypotension, bradycardia, peripheral edema
• Monitor for effectiveness of comfort measures. • EENT: flushing, rash
• Monitor for compliance to drug therapy
regimen. Interactions
• Monitor laboratory tests.
• Cyclosporine with diltiazem: increased serum
Calcium-Channel Blocker level and toxicity of cyclosporine
• Calcium-channel blockers are drugs which block
heart contraction by inhibiting movement of
 • Cyclosporine with verapamil: heart block and
digoxin toxicity. Verapamil increases level of
digoxin.
• Digoxin with verapamil: depressed myocardial
conduction
• General anesthesia with verapamil: serious
respiratory distress
Assessment
• Assess for presence of mentioned
contraindications and cautions.
• Inspect skin color and integrity to determine
presence of adverse effects on skin.
• Assess the patient’s complaint of pain and the
activity level prior to and after the onset of pain
to aid in identifying possible contributing factors
to the pain and its progression.
• Monitor cardiopulmonary status closely as the
drug can cause severe effects on these two body
systems.
Nursing Diagnosis
• Decreased Cardiac Output related to
hypotension and vasodilating effect of the drugs
• Risk for Injury related to cardiovascular and CNS
adverse drug effects
Implementation
• Monitor blood pressure and heart rate and
rhythm to detect possible development of
adverse effects.
• Provide comfort measures for the patient to
tolerate side effects (e.g. small frequent meals
for nausea, limiting noise and controlling room
light and temperature to prevent aggravation of
stress which can increase demand to the heart,
etc.)
• Educate client on measures to avoid angina
attacks (e.g. diet changes, rest periods, etc.)
• Emphasize to the client the importance of strict
adherence to drug therapy to ensure maximum
therapeutic effects.
Evaluation
• Monitor patient response to therapy.
• Monitor for presence of mentioned adverse
effects
• Monitor for effectiveness of comfort measures.
• Monitor for compliance to drug therapy
regimen.
• Monitor laboratory tests.
Antiarrhythmic Drugs
• address arrhythmia by altering cells’
automaticity and conductivity.
• All cells in the heart are capable of undergoing
spontaneous contractions (automaticity).
Therefore, these cells are capable of
generating excitatory impulses.
• Disruptions in the conduction of these
impulses affect contractility of the heart as
well as the volume of blood pumped by the
heart each minute (cardiac output).
• Arrhythmia is the term applied for disruptions
that interfere with generation of impulses and
conduction of these impulses to the
myocardium.
Arrhythmias
• Arrhythmias (also called dysrhythmias)
involve changes in the automaticity and
conductivity of the heart cells.
• To better understand this condition, there are
two concepts vital to be mastered:
conductivity and automaticity.
o Conductivity: is the property of the
heart cells to transmit spontaneous
impulses starting from the sinoatrial
 (SA) node, activating all parts of the
heart muscle almost spontaneously.
o Conductivity is the basis of cardiac
contraction and relaxation, allowing
the heart to beat.
Heart Arrythmia
• Different areas of the specialized conductive
system include:
o SA node – impulse generation of 60-100
impulses per minute
o AV node – 40-50 impulses per minute
o Ventricular muscle cells – 10-20
impulses per minute
• Automaticity: is the property of the heart cells
to undergo spontaneous depolarization during
Types of arrhythmias
relaxation. This is because at this
• Depending on factors causing them, here are
point, potassium flows out of the cell
different types of arrhythmias:
while sodium moves inside: the condition
o Changes in rate: tachycardia,
necessary to produce an action potential.
bradycardia
• Here are the five phases of action potential:
o Stimulation from ectopic focus:
o Phase 0 – depolarization phase; stage in
premature atrial contractions (PACs),
which cell reaches point of stimulation.
premature ventricular contractions
This phase is characterized by open
(PVCs), atrial flutter and/or fibrillation
sodium gates and sodium ions rushing
(AF), ventricular fibrillation
towards the cell leading to action
o Alterations in conduction through the
potential. There is absence of charge
muscle: heart blocks, bundle branch
difference between the outside and the
block
inside of the membrane.
• It can be triggered by the following: electrolyte
o Phase 1 – a very short period wherein
disturbances, decreased oxygen supply to the
concentration of sodium equalizes
cells, structural damage of the conduction
inside and outside of the cell
system, drug effects, acidosis, and lactic acid
o Phase 2 – plateau phase; stage in which
accumulation.
cell is trying to go back to its resting
Class I antiarrhythmics
stage (repolarization). The cell becomes
• This class blocks sodium channels in the cell
less permeable to sodium, potassium
membrane during action potential. Subgroup
begins to leave the cell, and calcium
under this class is based on their mechanism in
starts to enter the cell.
blocking sodium channels.
o Phase 3 – rapid repolarization phase;
• These class are local anesthetics and membrane-
stage in which the sodium gates are
stabilizing agents because of their ability to bind
closed and potassium flows out of the
more quickly to sodium channels.
cell.
Therapeutic Action
o Phase 4 – resting phase; stage in which
sodium-potassium pump restores the • Class I antiarrhythmics stabilize cell membrane
cell’s resting membrane potential in by depressing phase 0 of action potential. They
preparation for the next action bind to sodium channels and change the
potential. duration of action potential of the cells.
• Class IA drugs depress phase 0 and prolong
duration of action potential.
• Class IB drugs somewhat depress phase 0 and
shorten duration of action potential.
• Class IC drugs markedly depress phase 0 and
extremely slows conduction but has little effect
on the duration of action potential.
Indications
• Primarily indicated for decreasing workload of
the heart and relieving HF
• Digoxin is especially indicated for atrial flutter,
atrial fibrillation, and paroxysmal atrial
tachycardia.
Pharmacokinetics
Route Onset Peak Duration
IM
IV
T ½: 10 min, then 1.5-3 h
Metabolism: liver
Excretion: urine
Contraindications and Cautions
• Allergy to Class I antiarrhythmics. Prevent
severe hypersensitivity reactions.
• Bradycardia, heart block. Unless an artificial
pacemaker is in place, the conduction-altering
effect of drug can lead to total heart block.
• HF, hypotension, shock. Exacerbated by effects
of drug on action potential.
• Electrolyte imbalance. Can alter drug
effectiveness
• Renal, hepatic dysfunction. Interfere with drug
bioavailability and excretion
• Pregnancy and lactation. Can cause potential
adverse effects to the fetus or neonate.
Adverse Effects
• CNS: dizziness, drowsiness, fatigue, twitching,
mouth numbness, slurred speech, vision
changes, tremors
• CV: arrhythmias, hypotension, vasodilation,
potential for cardiac arrest
• Respiratory: respiratory depression
• Hema: bone marrow depression
• EENT: rash, hypersensitivity reactions, hair loss
Interactions
• Digoxin, beta-blockers: increased risk for
developing arrhythmias
• Quinidine with digoxin: quinidine competes with
digoxin at renal transport sites so it can increase
chances of developing digoxin toxicity
• Cimetidine: increased Class Ia toxicity
• Anticoagulants: increased risk of bleeding
Class II antiarrhythmics
• This class interferes with action potential by
blocking beta receptors in the heart and kidneys.
This, in turn, blocks phase 4 of action potential.
Class II antiarrhythmics are beta-adrenergic blockers.
Therapeutic Action
• Class II antiarrhythmics engage in competitive
inhibition of beta receptors specifically found in
the heart and kidneys. For this reason, there is
decreased in heart rate, excitability, and cardiac
output. Conduction through AV node also slows
down. In the kidneys, release of renin is
decreased.
• These effects decrease blood pressure and the
stabilize the highly-excitable heart. As a result,
workload of the heart is lessened.
Indications
• This class is specifically indicated for treatment
of supraventricular tachycardia and premature
ventricular contractions (PVCs).
Pharmacokinetics
Route Onset Peak Duration
Oral 20-30 min 60-90 min 6-12 h
IV Immediate 1 min 4-6h
T ½: 3-5h
Metabolism: Liver
Excretion: urine
Contraindications and Cautions
• Sinus bradycardia (<45 beats per minute), heart
block. Exacerbated by the therapeutic effects of
the drug.
• HF, cardiogenic shock, asthma, respiratory
depression. Exacerbated by blocking beta
receptors.
• Pregnancy and lactation. Can cause potential
adverse effects to the fetus or neonate.
• Diabetes, thyroid dysfunction. Altered by
blockade of beta-receptors
• Renal, hepatic dysfunction. Interfere with
bioavailability and excretion of drugs.
Adverse Effects
• CNS: dizziness, fatigue, dreams, insomnia
• CV: arrhythmias, hypotension, bradycardia, AV
blocks, alteration in peripheral perfusion
• Respiratory: bronchospasm, dyspnea
• GI: anorexia, diarrhea, constipation, nausea,
vomiting
• Other: loss of libido, decreased tolerance to
exercise, alterations in blood glucose level
Interactions
• Verapamil: increased adverse drug effects
• Insulin: increased hypoglycemia
Class III antiarrhythmics
• This class prolongs and slows down the outward
movement of potassium during phase 3 of action
potential. These drugs act directly on the heart
 muscles to prolong repolarization and refractory • This class blocks the movement of calcium
period. towards the cell membrane.
• All of these drugs are proarrhythmic and have Therapeutic Action
the possibility of inducing arrhythmias. • Class IV antiarrhythmics depress action potential
Therapeutic Action generation and slows down phases 1 and 2 of
• Class III antiarrhythmics’ ability to prolong action potential. This action slows down both
refractory period and repolarization increases conduction and automaticity.
the threshold for ventricular fibrillation. Indications
• These are used to treat life-threatening • Other uses of diltiazem and verapamil include
arrhythmias for which no other drugs have been treatment for hypertension and angina.
effective. Pharmacokinetics
• This class can also act on peripheral tissues to Route Onset Peak Duration
decrease peripheral resistance. Oral 30-60 min 2-3h 6-8h
Indications IV Immediate 2-3 min Unknown
• Amiodarone is the drug of choice for ventricular T ½: 3.5-6h
fibrillation and pulseless ventricular tachycardia. Metabolism: Liver
Pharmacokinetics Excretion: Urine
Route Onset Peak Duration
Oral 2-3d 3-7h 6-8h Contraindications and Cautions
IV Immediate 20 min Infusion • Allergy to calcium-channel blockers. Prevent
T ½: 10d hypersensitivity reactions.
Metabolism: Liver • Heart block (sick sinus syndrome). Unless an
Excretion: urine artificial pacemaker is in place, heart blocks can
be exacerbated by the effects of the drug.
Contraindications and Cautions
• HF, hypotension. Exacerbated by hypotensive
• AV Block. Ibutilide and dofetilide exacerbate this
effect of the drug.
health condition.
• Pregnancy, lactation. Potential adverse effects
• Renal, hepatic dysfunction. Interfere with
bioavailability and excretion of drugs. to neonate or fetus.
• Shock, hypotension, respiratory depression, • Renal, hepatic dysfunction. Interfere with
prolonged QT interval. Depressed action bioavailability and excretion of drugs.
potentials can worsen these health problems.
Adverse Effects
Adverse Effects
• CNS: weakness, dizziness, fatigue, depression,
• CNS: weakness, dizziness
headache
• CV: arrhythmias, HF
• CV: hypotension, shock, edema, HF, arrhythmia
• GI: nausea, vomiting, GI distress
• Amiodarone is associated with liver toxicity, • GI: nausea, vomiting, GI distress
ocular abnormalities, and very serious cardiac Interactions
arrhythmias. • Verapamil with beta-blockers: increased risk of
Interactions
cardiac depression
• Digoxin, quinidine: increased toxic drug effects
• Digoxin: additive slowing of AV node conduction
• Antihistamines, phenothiazines, tricyclic
antidepressants: increased risk of • Atracurium, pancuronium, vecuronium:
proarrhythmias increased respiratory depression
• Dofetilide combined with ketoconazole, • Increased risk of cardiac depression if IV
verapamil, cimetidine: increased risk for adverse preparation of these drugs were given 48 hours
drug effects within administration of IV beta-adrenergic
• Sotalol combined with antacids, NSAIDs, and blockers.
aspirin: loss of effectiveness of sotalol • Diltiazem can increase serum level of
Class IV antiarrhythmics cyclosporine.
• Include two calcium-channel blockers, namely:
diltiazem and verapamil.
Nursing Considerations for Antiarrhythmics
Assessment
• Assess for the mentioned contraindications to
this drug
• Conduct thorough physical assessment before
beginning drug therapy
• Assess patient’s neurological status to
determine potential CNS drug effects.
• Assess cardiac status closely
• Monitor respiratory rate, rhythm, and depth to
assess for respiratory depression and detect
changes associated with development of HF.
• Monitor laboratory test results including
complete blood count, renal and liver function
tests to determine the need for possible change
in dose and identify toxic effects.
Nursing Diagnoses
• Decreased cardiac output related to cardiac
effects of the drug
• Ineffective tissue perfusion related to decreased
blood flow to different parts of the body
• Altered sensory perception related to CNS drug
effects
• Risk for injury related to weakness and dizziness
Implementation
• Titrate the dose to the smallest amount enough
to manage arrhythmia to decrease the risk of
drug toxicity.
• Monitor cardiac rhythm closely to detect
potentially serious adverse effects and to
evaluate drug effectiveness.
• Provide comfort and safety measures (e.g.
raising side rails, adequate room lighting, noise
control) to help patient tolerate drug effects.
• Ensure maintenance of emergency drugs and
equipment at bedside to promote prompt
treatment in cases of severe toxicity
• Educate patient on drug therapy
Evaluation
• Monitor patient response to therapy through
assessment of cardiac output and rhythm.
• Monitor for adverse effects (e.g. sedation,
respiratory depression, CNS effects).
• Evaluate patient understanding on drug therapy
by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
Diuretics
• are drugs that primarily increase the excretion
of sodium.
• To some extent, they also increase the volume of
urine produced by the kidneys. By blocking the
absorptive capacity of cells lining the renal
tubules for sodium, intravascular volume and
the eventual leaking of fluid from capillaries is
reduced and prevented.
• It is used in the management of diseases like
glaucoma, hypertension, and edema in heart
failure, liver failure, and renal diseases.
Edema
• Edema is the accumulation of fluids in the
interstitial spaces. It can be typically seen in
patients with heart failure (HF), cirrhosis and
other liver diseases, and renal diseases.
• Edema in HF is caused by activation of the renin-
angiotensin system due to an inefficient
pumping activity of the heart. As a result, blood
volume increases, and sodium is retained.
Hypertension
• is persistent higher-than-normal blood pressure
and is primarily idiopathic (no known cause).
• When not acted upon promptly, this can lead to
multiple organ failure and severe cardiovascular
complications.
• Diuretic agents are used in management of
hypertension to reduce blood pressure by
decreasing circulating fluid volume and sodium.
Glaucoma
• is an eye disease that is characterized by
increased intraocular pressure (IOP), which is the
pressure inside the eyes.
• When not acted upon promptly, high IOP can
damage optic nerve and cause irreversible
blindness.
• Diuretic agents are used in the management of
glaucoma by enhancing the osmotic pull to
effectively remove some fluid in the eye,
decreasing the IOP.
Thiazide and Thiazide-like Diuretics
• belong to a chemical class of drugs
called sulfonamides. Thiazide-like diuretics have
different chemical structure but work in the
same mechanism as that of thiazide diuretics.
• This is among the most commonly used class of
diuretics.
Therapeutic Action
• It causes active pumping out of chloride from the
cells lining the ascending limb of Loop of Henle
and distal tubule by blocking the chloride pump.
Since sodium passively moves with chloride to
maintain electrical neutrality, both sodium and
chloride are excreted in the urine.
Indication
• Considered to be a milder form of diuretics
compared to loop diuretics.
• First-line drugs for management of essential
hypertension.
Pharmacokinetics
Route Onset Peak Duration
Oral 2h 4-6h 6-12h
T ½: 5.6-14h
Metabolism: Liver
Excretion: urine
Contraindications and Cautions
• Allergy to loop diuretics. Prevent severe
hypersensitivity reactions.
• Fluid and electrolyte imbalances. Can be
potentiated by the changes in fluid and
electrolyte levels caused by diuretics.
• Severe renal failure, anuria. May prevent
diuretics from working; can precipitate crisis
stage due to blood flow changes brought about
by diuretics.
• Systemic lupus erythematosus (SLE). Can
precipitate renal failure because the disease
already causes changes in glomerular filtration.
• Glucose tolerance abnormalities and diabetes
mellitus. Worsened by glucose-elevating effect
of some diuretics
• Gout. Already reflects abnormality in tubular
reabsorption and secretion.
• Liver disease. Could interfere with drug
metabolism and lead to drug toxicity.
• Bipolar disorder. Can be exacerbated by calcium
changes brought about by the use of this drug.
• Pregnancy, lactation. Can cause potential
adverse effects to the fetus and baby. Routine
use of this drug in pregnancy is not appropriate
and should be used only when there is
underlying pathological conditions. For lactating
women, an alternative method of feeding should
be instituted.
Adverse Effects
• CNS: weakness
• CV: hypotension, arrhythmias
• GI: GI upset
• GU: hypokalemia (can precipitate
hyperglycemia), hypercalcemia, hyperuremia,
slightly-alkalinized urine (can lead to bladder
infections)
Interactions
• Cholestyramine or colestipol: decreased
absorption of diuretics; must be taken separated
by at least 2 hours.
• Digoxin: increased risk for digoxin toxicity
because of changes in serum potassium levels
• Quinidine: increased risk for quinidine toxicity
• Antidiabetic agents: decreased effectivity of
antidiabetics
• Lithium: increased risk for lithium toxicity
Loop Diuretics
• This type of diuretics exerts its main effect on the
loop of Henle. Hence, so named.
• Referred to as high-ceiling diuretics because
they are capable of causing greater degree of
diuresis compared to other types.
Therapeutic Action
• Blocks the action of chloride pump in the
ascending limb of the loop of Henle, where 30%
of sodium is normally reabsorbed. This causes
decreased reabsorption of chloride and sodium.
• Exerts the same effect on the descending limb of
loop of Henle and distal tubule causing sodium-
rich urine.
Indications
• Indicated for treatment of acute HF, acute
pulmonary edema, and edema associated with
HF or with renal or liver disease, and
hypertension.
• Drug of choice when rapid and extensive diuresis
is needed. It can produce a fluid loss up to 20
pounds per day.
• Proven to be effective even with the presence of
acid-base disturbances, renal failure, electrolyte
imbalances, and nitrogen retention.
 • Also used in the treatment of pulmonary edema
but its effect only influences the blood that
reaches the nephrons.
• Ethacrynic acid is used less frequently in the
clinical setting because newer drugs are more
potent and reliable.
Pharmacokinetics
Interactions
• Aminoglycosides or cisplatin: increased
ototoxicity effect of loop diuretics
• Anticoagulants: increased anticoagulation
effects
• Indomethacin, ibuprofen, salicylates and other
NSAIDs: decreased antihypertensive effects and
loss of sodium

Route Onset Peak Duration Carbonic Anhydrase Inhibitors

Oral 60 min 60-120 min 6-8h
IV, IM 5 min 30 min 2h
T ½: 120 min
Metabolism: Liver
Excretion: Urine
Contraindications and Cautions
• Allergy to thiazides and sulfonamides. Prevent
severe hypersensitivity reactions.
• Electrolyte depletion. Can be potentiated by the
changes in fluid and electrolyte levels caused by
diuretics.
• Severe renal failure, anuria. Exacerbated by the • Relatively mild diuretics
effects of the drug.
• Systemic lupus erythematosus (SLE). Can Therapeutic Action
precipitate renal failure because the disease
• Inhibits the action of the enzyme carbonic
already causes changes in glomerular filtration.
anhydrase, the catalyst for the formation of
• Glucose tolerance abnormalities and diabetes sodium bicarbonate stored as alkaline reserve in
mellitus. Worsened by glucose-elevating effect the renal tubules and is important for the
of some diuretics excretion of hydrogen.
• Gout. Already reflects abnormality in tubular
• It slows down the movement of hydrogen ions
reabsorption and secretion. which leads to greater amount of sodium and
• Hepatic coma. Exacerbated by fluid shifts bicarbonate lost in the urine.
associated with drug use.
• Pregnancy, lactation. Can cause potential Indications
adverse effects to the fetus and baby. Routine
• Most often used for the treatment of glaucoma.
use of this drug in pregnancy is not appropriate
Inhibition of carbonic anhydrase results in
and should be used only when there is
decreased secretion of aqueous humor of the
underlying pathological conditions. For lactating
eyes.
women, an alternative method of feeding should
• Also used as adjunct to other diuretics when
be instituted.
more intense diuresis is needed.
Adverse Effects
Pharmacokinetics
• CNS: dizziness
Route Onset Peak Duration
• CV: hypotension
Oral 1h 2-4h 6-12h
• GI: GI upset Sustained- 2h 8-12h 18-24h
• GU: hypokalemia (can precipitate release oral
hyperglycemia), increased bicarbonate excretion IV 1-2 min 15-18 min 4-5h
(can lead to alkalosis), hypocalcemia and tetany T ½: 5-6h
• EENT: ototoxicity, reversible loss of hearing Metabolism: Liver; Excretion: Urine
Contraindications and Cautions
• Allergy to carbonic anhydrase inhibitors,
thiazides, antibacterial sulfonamides. Prevent
severe hypersensitivity reactions.
• Chronic noncongestive angle-closure
glaucoma. Not effectively treated by this drug.
• Fluid and electrolyte imbalance, renal or
hepatic disease, adrenocortical insufficiency,
respiratory acidosis, chronic obstructive
pulmonary disease (COPD). Could be
exacerbated by fluid and electrolyte changes
caused by these drugs.
• Pregnancy, lactation. Can cause potential
adverse effects to the fetus and baby. Routine
use of this drug in pregnancy is not appropriate
and should be used only when there is
underlying pathological conditions. For lactating
women, an alternative method of feeding should
be instituted.
Adverse Effects
• CNS: paresthesia, confusion, drowsiness
• CV: hypotension
• GU: hypokalemia (can precipitate
hyperglycemia), increased loss of bicarbonate
(can lead to metabolic acidosis)
Interactions
• Salicylate, lithium: increased excretion of these
drugs
Potassium-Sparing Diuretics
• Less powerful than loop diuretics but they retain
potassium instead of wasting it.
• Typically used for patients who have high risk for
hypokalemia associated with diuretic use.
Therapeutic Action
• This type of diuretics causes a loss of sodium
while promoting the retention of potassium.
• Spironolactone acts as aldosterone antagonist
which blocks the action of aldosterone in the
distal tubule. On the other hand, amiloride and
triamterene block potassium secretion through
the tubule.
Indications
• This is often used as adjuncts with thiazide or
loop diuretics or in patients who are especially at
risk if hypokalemia develops.
• Spironolactone is the drug of choice for
treating hyperaldosteronism typically seen in
patients with liver cirrhosis and nephrotic
syndrome.
Pharmacokinetics
Route Onset Peak Duration
Oral 24-48h 48-72 h 48-72h
T ½: 20h
Metabolism: Liver
Excretion: Urine (unchanged)
Contraindications and Cautions
• Allergy to potassium-sparing diuretics. Prevent
severe hypersensitivity reactions.
• Hyperkalemia, renal disease,
anuria. Exacerbated by the effects of the drug.
• Pregnancy, lactation. Can cause potential
adverse effects to the fetus and baby. Routine
use of this drug in pregnancy is not appropriate
and should be used only when there is
underlying pathological conditions. For lactating
women, an alternative method of feeding should
be instituted.
Adverse Effects
• CNS: lethargy, confusion, ataxia
• CV: arrhythmias
• Musculoskeletal: muscle cramps
• GU: hyperkalemia, increased loss of bicarbonate
(can lead to metabolic acidosis)
• Associated with various androgen effects such as
hirsutism, gynecomastia, deepening of the voice,
and irregular menses.
Interactions
• Salicylates: decreased diuretic effect
Osmotic Diuretics
• This type of diuretic exerts their therapeutic
effect by pulling water into the renal tubule
without loss of sodium.
• Only one osmotic diuretic is currently
available, mannitol (Osmitrol).
Therapeutic Action • Perform a thorough physical assessment to
• Mannitol is a sugar that is not well reabsorbed by establish baseline data before drug therapy
the tubules and it acts to pull large amounts of begins, to determine effectiveness of therapy,
fluid into the urine due to the osmotic pull and to evaluate for occurrence of any adverse
exerted by large sugar molecule. effects associated with drug therapy.
• This also pulls fluid into the vascular system from • Inspect skin (note presence of edema and status
extravascular spaces like aqueous humor. of skin turgor) to determine hydration status and
have a baseline data for effectiveness of drug
Indications
therapy.
• Mannitol is usually used in acute situations when
• Assess cardiopulmonary status (blood pressure,
it is necessary to decrease IOP before eye
pulse rate, heart and lung sounds, etc.) to
surgery or during acute attacks of glaucoma.
evaluate fluid movement and state of hydration.
• Diuretic of choice in cases of increased cranial
It is also to monitor the effects on the heart and
pressure or acute renal failure due to shock, drug
lungs.
overdose, or trauma.
• Obtain an accurate body weight to provide
• Also available as an irrigant in transurethral
baseline to monitor fluid balance.
prostatic resection and other transurethral
• Monitor intake and output and voiding patterns
procedures.
to evaluate fluid balance and renal function.
Pharmacokinetics • Evaluate liver status to determine potential
Route Onset Peak Duration problems in drug metabolism.
IV 30-60 min 1h 6-8h • Monitor the results of laboratory tests (e.g.
Irrigant Rapid Rapid Short serum electrolyte levels especially potassium
T ½: 15-100 min and calcium, uric acid and glucose levels, etc.) to
Metabolism: N/A determine drug’s effect.
Excretion: urine (unchanged)
• Monitor liver and renal function tests to identify
need for possible dose adjustment and toxic
Contraindications and Cautions
effects.
• Renal disease, anuria, pulmonary congestion,
intracranial bleeding, dehydration, Nursing Diagnoses
HF. Exacerbated by large shifts in fluid related to • Impaired urinary elimination related to drug
drug use. effect
• Pregnancy, lactation. Can cause potential • Imbalanced nutrition: less than body
adverse effects to the fetus and baby. requirements related to GI upset and metabolic
changes
Adverse Effects • Risk for deficient fluid volume related to increase
fluid volume excretion
• CNS: light-headedness, confusion, headache
• Risk for injury related to changes in fluid volume
• CV: hypotension, cardiac decompensation,
and electrolyte balance
shock Implementation
• GI: nausea, vomiting • Administer drug with food or milk if GI upset is a
• GU: fluid and electrolyte imbalance problem to buffer drug effect on the stomach
• Most common and potentially dangerous lining.
adverse effect related to an osmotic diuretic is • Administer intravenous diuretics slowly to
the sudden drop in fluid levels. prevent severe changes in fluid and electrolytes.
Nursing Considerations for Diuretic Drugs • Administer oral form early in the day to prevent
increased urination during sleep hours.
Assessment • Monitor patient response to drugs through vital
• Assess for the mentioned cautions and signs, weight, serum electrolytes and hydration
contraindications to evaluate effectiveness of drug therapy.
 • Assess skin condition to determine presence of
fluid volume deficit or retention.
• Provide comfort measures (e.g. skin care,
nutrition referral, etc.) to help patient tolerate
drug effects.
• Provide safety measures (e.g. adequate lighting,
raised side rails, etc.) to prevent injuries.
• Educate client on drug therapy to promote
compliance.
Evaluation
• Monitor patient response to therapy (e.g.
weight, urinary output, edema changes, blood
pressure).
• Monitor for adverse effects (e.g. electrolyte
imbalance, hyperglycemia, hyperuricemia, acid-
base disturbances, etc).
• Evaluate patient understanding on drug therapy
by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
Antihypertensive Drugs
• affect different areas of blood pressure control
so in most cases, these agents are combined for
synergistic effect.
• Ninety percent of cases of hypertension have no
known cause. Therefore, the main action of
antihypertensive agents is to alter the body’s
regulating mechanisms (e.g. baroreceptors,
renin-angiotensin-aldosterone system, etc.)
responsible for maintaining normal blood
pressure.
• Different people have different responses
towards hypertensive agents because
hypertension is multifactorial. For an instance,
the presence of comorbidities (e.g. diabetes,
myocardial infarction, etc.) may make some
antihypertensives not suitable for treatment.
Hypertension
• Is an increase in blood pressure such that the
systolic pressure is greater than 140MM HG and
diastolic pressure is greater than 90MM HG .
• Essential hypertension is the most common type
affecting 90% of persons with high blood
pressure
• The exact origin of essential hypertension is
unkown however contributing factors include:
Categories
• A category rating the severity of hypertension
has been devised and the classifications of blood
pressure are as follows:
o Normal – systolic: <120 mmHg; diastolic:
<80 mmHg
o Elevated – systolic: 120-129 mmHg;
diastolic: <80 mmHg
o Stage 1 Hypertension – systolic: 130-139
mmHg; diastolic: 80-89 mmHg
o Stage 2 Hypertension – systolic: less
than or equal to 140 mmHg; diastolic:
less than or equal to 90 mmHg
ACE INHIBITORS
• Angiotensin-converting enzymes inhibitors
(ACE Inhibitors) are antihypertensive agents
that act in the lungs to prevent the conversion of
angiotensin I into angiotensin II, which is a
potent vasoconstrictor.
Therapeutic Action
• By preventing the production of angiotensin II
which is a potent vasoconstrictor and a
stimulator of aldosterone release, blood
pressure is decreased with resultant loss of
serum sodium and fluid but with a slight increase
in serum potassium.
Indications
• Primarily indicated for hypertension and can be
used alone or in combination with other drugs.
• Aside from its indication in treating
hypertension, it is also combined with diuretics
and digoxin in the treatment of heart failure and
left ventricular dysfunction. The resultant effect
is decreased in peripheral resistance and blood
volume leading to decreased cardiac workload.
• It is also approved for treatment of diabetic
nephropathy, in which the renal artery is being
damaged by diabetes. It is thought that
decreased in stimulation of angiotensin
receptors in the kidney will slow down the
damage in the renal artery.
Pharmacokinetics
Route Onset Peak
Oral 15 min 30-90 min
T ½: 2h
 Metabolism: Liver
Excretion: Urine
Contraindications and Cautions
• Allergy to ACE inhibitors. Prevent severe
hypersensitivity reactions.
• Renal impairment. Decreased renal blood flow
effect of these drugs can exacerbate renal
impairment.
• Heart failure. Changes in hemodynamics caused
by these drugs can exacerbate heart failure.
• Hyponatremia and hypovolemia. Can be
exacerbated by the therapeutic effects of the
drug.
• Pregnancy and lactation. Can cause potential
adverse effects to the fetus and can decrease
milk production. Pregnant women are advised to
use barrier type of contraceptives while taking
this drug.
Adverse Effects
• GI: irritations, ulcer, constipation, liver injury
• GU: renal insufficiency, renal failure, proteinuria
• CV: reflex tachycardia, chest pain, heart failure,
cardiac arrhythmias
• EENT: rash, alopecia, dermatitis, photosensitivity
• Captopril is associated with sometimes-fatal
pancytopenia, cough, and GI distress.
Interactions
• Allopurinol: increased risk for hypersensitivity
• NSAIDs: increased risk for decreased
antihypertensive effects
Assessment
• Assess for the mentioned contraindications to
this drug (e.g. renal impairment, hyponatremia,
hypovolemia, etc.) to prevent potential adverse
effects.
• Obtain baseline status for weight, vital signs,
overall skin condition, and laboratory tests like
renal and hepatic function tests, serum
electrolyte, and complete blood count (CBC)
with differential to assess patient’s response to
therapy.
Nursing Diagnoses
• Decreased cardiac output related to effect of
drug in increasing fluid volume excretion
• Impaired skin integrity related to dermatological
effects of the drug
• Increased risk for infection related to potential
decreasing effect of drug to circulating blood
cells
Implementation
• Educate patient on importance of healthy
lifestyle choices which include regular exercise,
weight loss, smoking cessation, and low-sodium
diet to maximize the effect of antihypertensive
therapy.
• Administer drug on empty stomach one hour
before or two hours after meal to ensure
optimum drug absorption.
• Monitor renal and hepatic function tests to alert
doctor for possible development of renal and/or
hepatic failure as well as to signal need for
reduced drug dose.
• Monitor for presence of manifestations that
signal decreased in fluid volume (e.g. diarrhea,
vomiting, dehydration) to prevent exacerbation
of hypotensive effect of drug.
• Educate patient and family members about
drug’s effect to the body and manifestations that
would need reporting to enhance patient
knowledge on drug therapy and promote
adherence
Evaluation
• Monitor patient response to therapy through
blood pressure monitoring.
• Monitor for adverse effects (e.g. hypotension,
arrhythmias, renal failure, cough, and
pancytopenia).
• Evaluate patient understanding on drug therapy
by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
Angiotensin II – Receptor Blockers
• ARBs are antihypertensive agents that exert
their action by blocking vasoconstriction and
release of aldosterone through selective
blocking of angiotensin II receptors in vascular
smooth muscles and adrenal cortex.
Therapeutic Action
• The main action is to block the blood pressure
raising effect of the renin-angiotensin-
aldosterone system (RAAS).
Indications
• Like ACE inhibitors, they can also be used alone
for treatment of hypertension or in combination
with other antihypertensive agents.
• Utilized in treatment of heart failure for patients
who do not respond to ACE inhibitors.
• By blocking the effects of angiotensin receptors
in vascular endothelium, these drugs are able to
slow down the progress of renal disease in
patients with type 2 diabetes and hypertension.
Pharmacokinetics
Route Onset Peak Duration
Oral Varies 1-3h 24h
T ½: 2h
Metabolism: Liver
Excretion: Urine
Contraindications and Cautions
• Allergy to ARBs. Prevent severe hypersensitivity
reactions.
• Renal and hepatic impairment. Can alter
metabolism and excretion of drugs which can
increase the risk for toxicity.
• Hypovolemia. Can be exacerbated by the drug’s
action on blocking important life-saving
compensatory mechanisms.
• Pregnancy and lactation. Can cause potential
adverse effects to the fetus and potential
termination of pregnancy between second and
third trimester. It is still not known whether ARBs
can enter breast milk but it is generally not
allowed in lactating women because of potential
adverse effects to the neonate.
Adverse Effects
• CNS: headache, dizziness, syncope, weakness
• Respiratory: symptoms of upper respiratory
tract infections (URTI), cough
• GI: diarrhea, abdominal pain, nausea, dry mouth,
tooth pain
• EENT: rash, alopecia,
• dry skin
Interactions
• Phenobarbital, indomethacin, rifamycin: loss of
effectiveness of ARBs
• Ketoconazole, fluconazole, diltiazem: decreased
antihypertensive effects of ARBs
Implementation
• Educate patient on importance of healthy
lifestyle choices which include regular exercise,
weight loss, smoking cessation, and low-sodium
diet to maximize the effect of antihypertensive
therapy.
• Administer drug with food to prevent GI distress
associated with drug intake.
• Monitor renal and hepatic function tests to alert
doctor for possible development of renal and/or
hepatic failure as well as to signal need for
reduced drug dose.
• Provide comfort measures (e.g. quiet
environment, relaxation techniques, etc.) to help
patient tolerate drug effects.
• Educate patient and family members about
drug’s effect to the body and manifestations that
would need reporting to enhance patient
knowledge on drug therapy and promote
adherence.
Evaluation
• Monitor patient response to therapy through
blood pressure monitoring.
• Monitor for adverse effects (e.g. skin reactions,
cough, headache, etc.)
• Evaluate patient understanding on drug therapy
by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
Vasodilators Adverse Effects

• Direct vasodilators are used when the previous • CNS: headache, dizziness, anxiety
drugs mentioned are not effective. • CV: reflex tachycardia, heart failure, edema,
• These antihypertensive agents are reserved for chest pain
severe hypertension and hypertensive • GI: nausea, vomiting, GI upset
emergencies. • EENT: rash, lesions (e.g. minoxidil is associated
with abnormal hair growth.)
Therapeutic Action
• Nitroprusside is metabolized into cyanide so it
• These antihypertensive agents exert their effect can cause cyanide toxicity characterized by
by acting directly on smooth muscles. dyspnea, ataxia, loss of consciousness, distant
Consequently, there will be muscle relaxation heart sounds, and dilated pupil.
and vasodilation. Both of these will cause drop in • Nitroprusside suppresses iodine uptake which
blood pressure. leads to development of hypothyroidism.

Indications Interactions

• these drugs are only used for hypertension • Each drug in this group act differently on the
cases that do not respond to other drug body so each drug should be checked for
therapies. potential drug-to-drug and drug-to-food
• Nitroprusside is used in maintaining controlled interactions.
hypotension during surgery.
Nursing Assessment
• Nitroprusside is administered intravenously;
hydralazine is available for oral, intravenous, and • Assess for the mentioned contraindications to
intramuscular use; and minoxidil is available for this drug (e.g. drug allergy, CAD, cerebral
oral use only. insufficiency etc.) to prevent potential adverse
effects.
Pharmacokinetics
• Obtain baseline status for weight, vital signs,
Route Onset Peak Duration overall skin condition, and laboratory tests like
IV 1-2 min Rapid 1-10 min renal and hepatic function tests, and serum
T ½: 2 min electrolyte to assess patient’s response to
Metabolism: Liver therapy.
Excretion: Urine
Contraindications and Cautions Nursing Diagnoses

• Allergy to direct vasodilators. Prevent severe
hypersensitivity reactions.
• Cerebral insufficiency. Can be exacerbated by
drug’s action to cause sudden drop in blood
pressure.
• Peripheral vascular disease, CAD, heart failure,
tachycardia. These conditions can be
exacerbated by sudden drop in blood pressure.
• Pregnancy and lactation. Can cause potential
adverse effects to the fetus and should not be
used unless the benefit to the mother clearly
outweighs the risk to the fetus. The drug can
enter the breast milk and can cause potential
adverse effects to the neonate.
• Decreased tissue perfusion related to changes in
volume of blood pumped out by the heart
• Acute pain related to GI distress, headache, and
skin effects of the drug
Implementation
• Educate patient on importance of healthy
lifestyle choices which include regular exercise,
weight loss, smoking cessation, and low-sodium
diet to maximize the effect of antihypertensive
therapy.
• Monitor blood pressure and heart rate and
rhythm closely
• Provide comfort measures for the patient to
tolerate side effects (e.g. small frequent meals
for nausea, limiting noise and controlling room
 light and temperature to prevent aggravation of
stress which can increase demand to the heart,
etc.)
• Monitor patient for any manifestations that
could decrease fluid volume inside the body (e.g.
vomiting, diarrhea, excessive sweating, etc.) to
detect and treat excessive hypotension.
• Educate patient and family members about
drug’s effect to the body and manifestations that
would need reporting
• Emphasize to the client the importance of strict
adherence to drug therapy to ensure maximum
therapeutic effects.
Evaluation
• Monitor patient response to therapy through
blood pressure monitoring.
• Monitor for presence of mentioned adverse
effects (e.g. hypotension, GI distress, skin
reactions, etc.)
• Monitor for effectiveness of comfort measures.
• Monitor for compliance to drug therapy
regimen.
• Monitor laboratory tests.
Drugs Affecting Coagulation (Anticoagulants,
Antiplatelets, Thrombolytics)
• These groups of drugs affect clot formation and
resolution by hindering different steps in clotting
formation which include:
o altering the formation of platelet plug
(antiplatelet drugs)
o interfering the clotting cascade and
thrombin formation (anticoagulant
drugs)
o stimulating the plasmin system to break
down the formed clot (thrombolytic
agents).
Thromboembolic and Hemorrhagic Disorders
• Disorders that directly affect coagulation
process are divided into two main categories:
o thromboembolic disorders, which
involve overproduction of clots
o hemorrhagic disorders, which is
characterized by ineffective clotting
process leading to excessive bleeding.
• Thromboembolic disorders include medical
conditions (e.g. CAD) which involve
overproduction of clots which result into
decreased blood flow and total vessel occlusion.
Manifestations include hypoxia, anoxia, and
even necrosis.
• These disorders are treated by drugs that
interfere with normal coagulation process to
prevent formation of clots.
• On the other hand, less common hemorrhagic
disorders is characterized by excessive bleeding.
These are treated by drugs that promote the
clotting process. Some of these conditions
include:
o Hemophilia: characterized by genetic
lack of clotting factors
o Liver disease: characterized by non-
production of proteins and clotting
factors necessary for clot formation
o Bone marrow disorders: characterized
by insufficient quantity of platelets
rendering them ineffective
Antiplatelet Agents
• This drug class exerts its action by decreasing
the responsiveness of platelets to stimuli that
cause it to clump or aggregate. Through this,
formation of platelet plug is decreased.
Therapeutic Action
• By blocking receptor sites on the platelet
membrane, platelet adhesion and aggregation
is inhibited.
• Also, platelet-platelet interaction as well as
interaction of platelets to clotting chemicals
are prevented.
Indications
• Primarily indicated for cardiovascular diseases
that have potential for development of vessel
occlusion.
• Other indications include maintenance of
arterial and venous grafts, preventing
cerebrovascular occlusion, and including them as
adjunct to thrombolytic therapy for treatment of
myocardial infarction.
• One drug, anagrelide, blocks the production of
platelets in the bone marrow.
Pharmacokinetics
Route Onset Peak Duration
Oral 5-30 min 0.25-2h 3-6h
T ½: 15 min – 12h
 Metabolism: Liver
Excretion: Bile
Adverse Effects
• CNS: headache, dizziness, weakness
• GI: GI distress, nausea
• Skin: skin rash
• Hema: bleeding (oftenly occurs while brushing
the teeth)
• Interactions
• Increased risk of bleeding if combined with
another drug that affects blood clotting.
Contraindications and Cautions
• Allergy to antiplatelet agents. Prevent severe
hypersensitivity reactions.
• Known bleeding disorder. Increased risk of
excessive blood loss
• Recent surgery. Increased risk of bleeding in
unhealed blood vessels
• Closed head injuries. Increased risk of bleeding
in injured blood vessels of the brain
• History of thrombocytopenia. Anagrelide
decreased bone marrow production of platelets.
• Pregnancy, lactation. Generally inadvisable
because of potential adverse effects to fetus or
neonate
Nursing Assessment
• Assess for the mentioned contraindications to
this drug (e.g. hypersensitivity, acute liver
disease, pregnancy etc.) to prevent potential
adverse effects.
• Conduct thorough physical assessment before
beginning drug therapy to establish baseline
status, determine effectivity of therapy, and
evaluate potential adverse effects.
• Obtain baseline status for complete blood count
and clotting studies to determine any potential
adverse effects.
Nursing Diagnoses
• Disturbed sensory perception related to CNS
effects
• Acute pain related to CNS and GI effects
• Risk for injury related to CNS effects and
bleeding tendencies
Implementation
• Administer drug with meals to relieve GI upset.
• Provide comfort measures for headache
because pain due to headache may decrease
patient compliance to treatment regimen.
• Educate patient on ways to promote safety like
using electric razor, soft-bristled toothbrush,
and cautious movement because any injury at
this point can precipitate bleeding.
• Educate patient on drug therapy including drug
name, its indication, and adverse effects to
watch out for to enhance patient understanding
on drug therapy and thereby promote
adherence to drug regimen.
Evaluation
• Monitor patient response to therapy (e.g.
increased bleeding time, prevention of occlusive
events).
• Monitor for adverse effects (e.g. bleeding,
headache, GI upset).
• Evaluate patient understanding on drug therapy
by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
Anticoagulants
• By interfering with clotting cascade and
thrombin formation, anticoagulants are able to
interfere with the normal clotting process.
Therapeutic Action
• Warfarin, an oral agent in this class, reduces
Vitamin K-dependent clotting factors. As a result,
clotting process is prolonged.
• Two new oral agents, dabigatran and
rivaroxaban, directly inhibits thrombin (last step
in clotting process) and factor Xa, respectively.
• Heparin and antithrombin block formation of
thrombin from prothrombin.
Indications
• Among the many indications for this drug class
include: stroke and systemic emboli risk
reduction, nonvalvular atrial fibrillation, and
deep vein thrombosis.
• Heparin is used for prevention of blood clots in
blood samples, dialysis, and venous tubing. It
also does not enter breastmilk so it is the
anticoagulant of choice for lactating women.
 • Antithrombin is a naturally-occurring disease, pregnancy etc.) to prevent potential
anticoagulant and is a natural safety feature in adverse effects.
the clotting system. • Conduct thorough physical assessment before
beginning drug therapy to establish baseline
Pharmacokinetics
status, determine effectivity of therapy, and
Route Onset Peak Duration evaluate potential adverse effects.
IV Immediate Minutes 2-6h • Obtain baseline status for complete blood count
Subcutaneous 20-60 min 2-4h 8-12h and clotting studies to determine any potential
T ½: 30-180 min adverse effects
Metabolism: cells
Excretion: Urine Nursing Diagnoses

• Ineffective tissue perfusion related to blood loss

Contraindications and Cautions • Disturbed body image related to direct drug
toxicity characterized by rash and alopecia
• Allergy to anticoagulants. Prevent severe • Risk for injury related to bleeding tendencies and
hypersensitivity reactions. bone marrow depression
• Known bleeding disorder, recent
trauma/surgery, presence of indwelling Implementation
catheters, threatened abortion, GI ulcers. These
• Assess for signs signifying blood loss (e.g.
conditions can be compromised by increased
petechiae, bruises, dark-colored stools, etc.) to
bleeding tendencies.
determine therapy effectiveness and promote
• Pregnancy, lactation. Warfarin is a prompt intervention for bleeding episodes.
contraindication.
• Establish safety precautions (e.g. raising side
• Adverse Effects rails, ensuring adequate room lighting, padding
• Warfarin is associated with alopecia, dermatitis, sides of bed, etc.) to protect patient from injury.
bone marrow depression, and less frequently • Maintain antidotes on bedside (e.g. protamine
with prolonged and painful erections. sulfate for heparin, Vitamin K for warfarin) to
• Direct drug toxicity is characterized by nausea, GI promptly treat drug overdose.
upset, diarrhea, and hepatic dysfunction. • Evaluate effectiveness by monitoring the
Interactions following blood tests: prothrombin time (PT)
and international normalized ratio (INR) for
• Anticoagulants, salicylates, penicillin, WARFARIN; and whole blood clotting time
cephalosporin: increased bleeding if combined (WBCT) and activated partial thromboplastin
with heparin time (APTT) for HEPARIN.
• Nitroglycerin: decreased anticoagulation if • Educate patient on drug therapy
combined with heparin
• Cimetidine, clofibrate, glucagon, erythromycin: Evaluation
increased bleeding if combined with warfarin • Monitor patient response to therapy (e.g.
• Vitamin K, phenytoin, rifampin, barbiturates: increased bleeding time)
decreased anticoagulation if combined with • Monitor for adverse effects (e.g. bleeding, bone
warfarin marrow depression, alopecia, etc.).
• Antifungals, erythromycin, phenytoin, rifampin: • Evaluate patient understanding on drug therapy
alteration in metabolism of dabigatran and by asking patient to name the drug, its
rivaroxaban indication, and adverse effects to watch for.
Nursing Assessment • Monitor patient compliance to drug therapy.

• Assess for the mentioned contraindications to

this drug (e.g. hypersensitivity, acute liver
Thrombolytic Agents • Hypersensitivity reaction (uncommon) is
characterized by rash, flushing, and
• Thrombolytic agents promote clot resolution,
bronchospasm.
the process of activating the plasmin system to
break down the thrombus or clot that has been Interactions
formed.
• Anticoagulant, antiplatelet: increased risk of
Therapeutic Action bleeding

• The conversion of plasminogen to plasmin is the Nursing Assessment

body’s natural anticlotting system. Thrombolytic
• Assess for the mentioned contraindications to
agents’ action to activate this promotes
this drug (e.g. hypersensitivity, acute liver
breakdown of fibrin threads and dissolution of
disease, CVA within 2 months, etc.) to prevent
formed clots.
potential adverse effects.
• It is necessary to prevent vessel occlusion and
• Conduct thorough physical assessment before
therefore, to deliver adequate blood flow to
beginning drug therapy to establish baseline
body systems.
status, determine effectivity of therapy, and
Indications evaluate potential adverse effects.
• Obtain baseline status for complete blood count,
• For treatment of acute MI, pulmonary embolism,
fecal occult blood test (FOBT), and clotting
and acute ischemic stroke.
studies to determine any potential adverse
• Also for clearing of occluded intravenous
effects.
catheters and central venous access devices.
Nursing Diagnoses
Pharmacokinetics
• Decreased cardiac output related to cardiac
route onset peak Duration arrhythmias and potential for bleeding
IV immediate End of N/A • Risk for injury related to clot-dissolving effects
injection Implementation
T ½: unknown • Assess for signs signifying blood loss (e.g.
Metabolism: plasma petechiae, bruises, dark-colored stools, etc.) to
Excretion: unknown determine therapy effectiveness and promote
prompt intervention for bleeding episodes.
• Establish safety precautions (e.g. raising side
Contraindications and Cautions
rails, ensuring adequate room lighting, padding
• Contraindications and Cautions sides of bed, etc.) to protect patient from injury.
• Allergy to thrombolytics. Prevent severe • Evaluate effectiveness by monitoring
hypersensitivity reactions. coagulation studies to adjust drug dose
• Known bleeding disorder, recent appropriately.
trauma/surgery, acute liver disease, • Educate patient on drug therapy including drug
cerebrovascular accident within 2 months, GI name, its indication, and adverse effects to
ulcers. These conditions can affect normal watch out for to enhance patient understanding
clotting factors and normal plasminogen on drug therapy and thereby promote
production. adherence to drug regimen.
• Pregnancy, lactation. Potential adverse effects Evaluation
to fetus or neonate. • Monitor patient response to therapy (e.g.
Adverse Effects dissolution of blood clot and return of blood
flow)
• CV: cardiac arrhythmias, hypotension • Monitor for adverse effects (e.g. bleeding,
• Hema: bleeding (most common) anemias, hypotension, etc.).
 • Evaluate patient understanding on drug therapy
by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
Antihyperlipidemic Drugs
• Antihyperlipidemic Drugs lower serum levels of
cholesterol and various lipids.
• They are also called as lipid-lowering agents;
these drugs provide effective treatment for
hyperlipidemia (increased lipid level in the
blood).
• The incidence of coronary artery disease (CAD),
the most common cause of death among adults,
is higher in people with hyperlipidemia.
• High level of lipids and triglyceride is associated
with metabolic syndrome consist of insulin
resistance, abdominal obesity, hypertension,
and proinflammatory and prothrombotic states.
Coronary Artery Disease (CAD)
• Coronary artery disease (CAD) is the most
common type of heart disease in the United
States.
• It is sometimes called coronary heart disease or
ischemic heart disease.
• For some people, the first sign of CAD is a heart
attack.
• CAD is caused by plaque buildup in the walls of
the arteries that supply blood to the heart (called
coronary arteries) and other parts of the body.
• Plaque is made up of deposits of cholesterol and
other substances in the artery.
• Plaque buildup causes the inside of the arteries
to narrow over time, which can partially or totally
block the blood flow.
• This process is called atherosclerosis.
Bile Acid Sequestrants
• These drugs are used to normalize high serum
level of cholesterol.
Therapeutic Action
• Bile acid sequestrants exert their effect in the
intestines by binding into bile acids which
contain a high level of cholesterol.
• The resultant insoluble complex formed by this
combination is then excreted through feces.
• As this happens, more LDL segments from the
circulation will be absorbed by the intrahepatic
circulation to make more bile acids.
Indications
• Bile Acid Sequestrants are used as the treatment
for primary hypercholesterolemia (high
cholesterol and high LDL) as an adjunct to diet
and exercise.
• Cholestyramine is also used to treat pruritus
associated with partial biliary obstruction.
Pharmacokinetics
• Not absorbed systemically and is excreted in the
feces.
Contraindications and Cautions
• Allergy to bile acid sequestrants. Prevent severe
hypersensitivity reactions.
• Complete biliary obstruction. Prevent bile from
being secreted into the intestines.
• Abnormal intestinal function. Aggravated by
the presence of bile acid sequestrants.
• Pregnancy and lactation. Potential decrease in
absorption of fat and fat-soluble vitamins can be
detrimental to fetus or neonate.
Adverse Effects
• CNS: headache, anxiety, fatigue, drowsiness
• GI: GI upset, constipation, fecal impaction,
nausea, aggravated hemorrhoids
• Hema: increased bleeding time, decreased
production of clotting factors
• Musculoskeletal: muscle aches, muscle pains
• Other: rash, fat-soluble vitamin deficiencies
• Interactions
• Bile acid sequestrants delay the absorption of
thiazide diuretics, corticosteroids, digoxin,
warfarin, and thyroid hormones. Therefore, if
needed, these drugs are taken 1 hour before or
4-6 hours after a meal
Assessment
• Assess for the mentioned contraindications
• Conduct thorough physical assessment before
beginning drug therapy
• Obtain baseline status for weight
 • Assess neurological status, particularly
orientation and alertness to determine any CNS
effects.
• Assess bowel elimination patterns, including
frequency of stool passage and stool
characteristics to monitor the development of
constipation and possible fecal impaction.
• Assess closely patient’s heart rate and blood
pressure to identify cardiovascular changes that
may warrant change in drug dose
• Inspect abdomen for distention and auscultate
bowel sounds to assess for changes in GI
motility.
• Monitor results of laboratory tests, particularly
serum cholesterol and lipid levels to evaluate the
effectiveness of drug therapy.
Nursing Diagnoses
• Acute pain related to CNS and GI effects
• Risk for injury related to CNS drug effects and
potential for bleeding
• Altered elimination pattern related to
constipation
Implementation
• Administer powdered agents already mixed
with fluids to ensure drug effectiveness.
• Instruct client not to chew, crush, and cut
tablets because these drugs are meant to be
broken down in the intestines and premature
crushing will render active ingredients
ineffective.
• Administer drug before meals to ensure that
drug is in the GI tract together with food.
• Administer other drugs 1 hour before or 4-6
hours after bile acid sequestrants to avoid drug
interactions.
• Arrange for a bowel program to effectively
address constipation if it ever occurs.
• Instruct patient to increase oral fluid intake and
dietary fiber intake to prevent constipation.
• Provide comfort measures
• Educate patient on drug therapy
Evaluation
• Monitor patient response to therapy (serum lipid
and cholesterol levels).
• Monitor for adverse effects (e.g. headache,
vitamin deficiency, and increased bleeding
times.
• Evaluate patient understanding on drug therapy
by asking the patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
HMG-CoA Reductase Inhibitors
• Drugs under this classification are chemically-
modified compounds from the products of fungi.
• This drug group increases the cell absorption of
LDL by blocking the enzyme (HMG-CoA
reductase) regulating the rate-limiting step in
the synthesis of cholesterol. With this alteration
in fat metabolism, HDL increases slightly.
• PREGNANCY CATEGORY X - For women who are
pregnant, this drug class is contraindicated
(pregnancy category X)
Therapeutic Action
• In a sense, HMG-CoA reductase inhibitors block
the completion of cholesterol synthesis in the
body.
• These are primarily indicated as adjunct
medicine with diet and exercise for treatment of
high cholesterol and LDL levels in the blood.
Indications
• Pravastatin, lovastatin, and simvastatin are
indicated for patients with documented CAD to
slow progression of the disease.
• Together with these three agents, atorvastatin is
used as prophylaxis for first myocardial
infarction attack for patients with multiple risk
factors for CAD.
Pharmacokinetics
Route Onset Peak Duration
Oral Slow 1-2h 20-30h
T ½: 14h
Metabolism: Liver
Excretion: Bile
Contraindications and Cautions
• Allergy to HMG-CoA reductase inhibitors.
Prevent severe hypersensitivity reactions.
• Active liver disease. Exacerbated by drug’s
therapeutic effect and has potential to lead to
severe liver failure.
 • Pregnancy, lactation. Potential for drug adverse
effects to fetus or neonate.
• Impaired endocrine function. Problems can
arise due to alteration in the formation of steroid
hormones.
• Renal impairment. Caution is given to patients
taking other statins and close monitoring in
instituted. Atorvastatin is not affected by renal
diseases.
Adverse Effects
• CNS: headache, dizziness, insomnia, fatigue,
blurred vision, cataract development
• CV: increased risk for cardiovascular effects with
simvastatin started at 80 mg for new patients
• GI: flatulence, nausea, vomiting, cramps,
abdominal pain, constipation
• Hepatobiliary: increase liver enzymes, acute
liver failure with use of atorvastatin and
fluvastatin
Interactions
• Cyclosporine, erythromycin, gemfibrozil, niacin,
antifungal drugs: increased risk for
rhabdomyolysis
• Digoxin, warfarin: increased serum levels and
resultant toxicity of HMG-CoA reductase
inhibitors
• Oral contraceptives: increased serum estrogen
• Grapefruit juice: increased serum levels and
resultant toxicity
Assessment
• Assess for the mentioned contraindications to
this drug (e.g. hypersensitivity, acute liver
disease, pregnancy etc.) to prevent potential
adverse effects.
• Conduct thorough physical assessment before
beginning drug therapy to establish baseline
status, determine effectivity of therapy, and
evaluate potential adverse effects.
• Obtain baseline status for weight while noting
recent manifestations that increases or
decreases to determine patient’s fluid status.
• Assess neurological status with particular focus
on consciousness, reflexes, and affect.
• Assess closely patient’s heart rate and blood
pressure to identify cardiovascular changes that
may warrant change in drug dose.
• Assess bowel patterns to determine possibility
of developing constipation and resultant fecal
impaction.
Nursing Diagnoses
• Disturbed sensory perception related to CNS
effects
• Risk for injury related to CNS effects
Implementation
• Administer drug at bedtime to maximize
effectiveness of the drug because peak of
cholesterol synthesis is from midnight to 5 AM.
However, atorvastatin can be given at any hour
of the day.
• Monitor serum cholesterol and LDL levels to
determine effectiveness of drug therapy.
• Monitor results of liver functions tests to
determine possible liver damage.
• Ensure patient has initiated a 3–6-month diet
and exercise program before initiating drug
therapy to ensure need for drug therapy.
• Emphasize the importance of lifestyle
changes to the patient to decrease risk of CAD
and promote drug effectiveness.
• Provide comfort and safety measures
• Educate patient on drug therapy
Evaluation
• Monitor patient response to therapy as
evidenced by normal serum cholesterol and LDL
levels, absence of first MI, and slowing of CAD
progression.
• Monitor for adverse effects (e.g. cataracts,
rhabdomyolysis, and acute liver disease).
• Evaluate patient understanding on drug therapy
by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
Cholesterol Absorption Inhibitors
• Cholesterol absorption inhibitors are used to
treat high cholesterol in people who cannot take
a statin. This medicine lowers total cholesterol
and LDL (bad) cholesterol.
• This medicine is used along with lifestyle changes
including diet and exercise to lower cholesterol.
• Ezetimibe (Zetia) lowers total cholesterol and
LDL cholesterol levels in people who have high
 cholesterol. This medicine can improve
cholesterol levels, but it has not been proved to
lower the risk of a heart attack or a stroke.
• A drug that combines ezetimibe and simvastatin
(Vytorin) lowers total cholesterol and LDL levels.
But taking Vytorin may not limit hardening of the
arteries (atherosclerosis) any better than the
statin medicine alone. But the combination of
ezetimibe and simvastatin can lower LDL levels
more than simvastatin alone
Therapeutic Action
• Acting on the brush border of intestines,
cholesterol absorption inhibitors block the
absorption of dietary cholesterol.
• Consequently, less cholesterol goes to the liver
and it increases the cholesterol clearance to
make up for the drop.
Indications
• Adjunct to diet and exercise as a monotherapy or
in combination with HMG-CoA inhibitors or bile
acid sequestrants.
• Used in combination with statins to treat
homozygous familial hypercholesterolemia.
Pharmacokinetics
Route Onset Peak
Oral Moderate 4-12h
T ½: 22h
Metabolism: Liver, small intestine
Excretion: Urine, feces
Contraindications and Cautions
• Allergy to cholesterol absorption inhibitors.
Prevent severe hypersensitivity reactions.
• Liver disease, pregnancy, lactation: not used if
combined with statins because of the effects of
statins to these health conditions. Effect of this
class to fetuses and neonates is not known.
Adverse Effects
• CNS: headache, dizziness, fatigue
• Respiratory: upper respiratory tract infection
(URI)
• GI: mild abdominal pain, diarrhea
• Musculoskeletal: muscle aches and pains, back
pain
Interactions
• Cholestyramine, fenofibrate, antacid,
gemfibrozil: elevated serum level of cholesterol
absorption inhibitors
• Cyclosporine: increased toxicity of cholesterol
absorption inhibitors
• Fibrates: increased risk for development of
cholelithiasis
• Warfarin: increased serum warfarin levels
Assessment
• Assess for the mentioned contraindications to
this drug
• Conduct thorough physical assessment before
beginning drug therapy.
• Assess neurological status. Give with
a particular focus on orientation and reflexes to
determine CNS drug effects.
• Assess closely patient’s heart rate and blood
pressure. To identify cardiovascular changes
that may warrant a change in drug dose.
• Assess bowel patterns. To determine
the possibility of developing constipation and
resultant fecal impaction.
• Monitor laboratory test results of serum
cholesterol, LDL, and liver function. To
determine the potential for drug adverse effects
and monitor effectiveness of therapy.
Nursing Diagnoses
• Disturbed sensory perception related to CNS
effects
• Acute pain related to side-effect of drugs as
evidenced by headache, myalgia, and GI distress
• Risk for injury related to CNS effects
Implementation
• Monitor serum cholesterol and LDL levels. To
determine the effectiveness of drug therapy.
• Monitor results of liver functions tests. To
determine possible liver damage.
• Ensure patient has initiated a 3–6-month diet
and exercise program before initiating drug
therapy. To ensure the need for drug therapy.
• Emphasize the importance of lifestyle
changes. To the patient to decrease the risk of
CAD and promote drug effectiveness.
• Provide comfort and safety measures.
• Educate patient on drug therapy.
EVALUATION
• Monitor patient response to therapy as
evidenced by normal serum cholesterol and LDL
levels.
• Monitor for adverse effects (e.g. muscle pains,
respiratory infections, headache).
• Evaluate patient understanding on drug
therapy by asking patient to name the drug, its
indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.
 DRUGS AFFECTING THE RENAL SYSTEM

What composes the renal system?

Renal system is composed of the:

1. Kidneys and the structures of the urinary tract
2. the uterus
3. the urinary bladder
4. the urethra

What are the 4 four major functions of the renal system in the body?

1. Maintaining the volume and composition of body fluids within normal ranges,
including the following functions:

-clearing nitrogenous wastes from the protein metabolism

-maintaining acid-base balance and electrolyte levels
-excreting various drugs and drug metabolites

2. Regulating Vitamin D activation, which helps to maintain and regulate calcium levels

3. Regulating blood pressure through the Renin-Angiotensin-Aldosterone System

4. Regulating red blood cell production through the production and secretion of
erythropoietin

What is DIURETIC agents?

- Thought simply as increasing amount of urine produced by the kidney

- Its clinical significance: Increase SODIUM EXCRETION by preventing
reabsorption of sodium

What are the 5 classes of diuretics? (each working at a slightly different site in the
nephron)

T hiazide & thiazide like

L oop
C arbonic anhydrase
P otassiumsparing
O smotic
What is a fluid rebound?
 Patient takes diuretic and stops taking water

Decrease blood volume

Activates the Sense by the osmotic

RAA mechanism center of the brain

ADH is released- hold water- rebound edema

DRUG THERAPY ACROSS THE LIFESPAN

1. Children

 Hydrochlorothiazide and chlorothiazide have established pediatric

dosing guidelines
 Furosemide- care should be taken not to exceed 6 mg/kg per day
 Ethacrynic acid- should not be used in infants
 Bumetanide- may be used for children who are taking other ototoxic
drugs, including antibiotics, and may cause less hypokalemia

2. Adult
*Chronic diuretic therapy
 Weight taking (same scale, same clothes, same time)- to check fluid
retention and sudden fluid loss
 Maintain fluid intake- to prevent fluid rebound
 potassium losing
 potassium sparing

A. OSMOTIC DIURETICS
Example:
1. Mannitol (Osmitrol)- sugar which pulls large amount of fluid into the urine-
IV use
2. Urea (Ureaphil)- IV
3. Glycerin (Osmoglyn) 0 oral & suppository

Action:
Acts of the proximal tubule and loop of Henle, to create an osmotic force that
pulls water into the nephron and increased the excretion of nearly all electrolytes

Indication:

Prevention of acute renal failure, reduce intracranial pressure, decrease

intraocular pressure and acute glaucoma, to prevent the oliguric phase of renal
failure, to promote the movement of toxic substances through the kidney

Contraindications:

Renal disease and anuria from several renal disease, pulmonary congestion,
intracranial bleeding dehydration and CHF

Adverse Effects:

Related to the sudden drop in fluid levels, hypotension, hypovolemia, heart

failure, pulmonary congestion, phlebitis at side of administration, headache,
blurred vision, dizziness, disorientation, convulsion, N/V, light headedness

Nursing Considerations:

 Administer oral drug with food or milk to buffer the drug effect on the
stomach lining if GI upset is a problem
 Administer intravenous diuretics slowly to prevent severe changes in
fluid and electrolytes
 Continuously monitor urinary output, cardiac response, and heart rhythm
of patients receiving intravenous diuretics to monitor for rapid fluid switch
and potential electrolyte disturbances leading to cardiac arrhythmia
 Switch to the oral form, which is less potent and easier to monitor, as soon
as possible, as appropriate
 Administer oral form EARLY IN THE DAY so that increased urination will
NOT INTERFERE WITH SLEEP
 Monitor dose carefully and reduce the dose of one or both drugs if given
with antihypertensive agents; loss of fluid volume can precipitate
hypotension.
 Monitor the patients response to the drug (e.g., blood pressure, urinary
output, weight, serum electrolytes, hydration, periodic blood glucose
monitoring) to evaluate the effectiveness of the drug and monitor for
adverse effects.
 Assess WEIGHT DAILY to evaluate fluid balance.
  Check skin turgor to evaluate for possible fluid volume deficit, and assess
edematous areas for changes, including a decrease in amount or degree
of pitting
 Provide comfort measures, including skin care and nutrition consultation

B. CARBONIC ANHYDRASE INHIBITORS

*mild diuretic
1. acetazolamide (Diamox)
2. dichlorphenamide (Daramide, Oratrol)
3. methazolamide (Neptazane)

ACTION

Diuretics that block the effects of carbonic anhydrase slow down the movement of
hydrogen ions; as a result, more SODIUM and BICARBONATE are lost in the urine

What is Carbonic anhydrase?

Is an enzyme and catalyst for the formation of sodium bicarbonate, which is stored as
the alkaline reserve in the renal tubule, and for the excretion of hydrogen, which results
in a slightly acidic urine.

INDICATIONS

 Adjunct to other diuretic

 Used to decrease intraocular fluid pressure in open angle glaucoma
 reversing severe renal hypoperfusion

CONTRAINDICATIONS

 allergy to the drug or antibacterial sulfonamides or thiazides

 chronic non-congestive angle closure glaucoma

ADVERSE EFFECTS

 metabolic acidosis (bicarbonate is lost)

 hypokalemia, paresthesias (tingling), confusion dehydration
 blood dyscrasias, pancytopenia, hemolytic anemia, aplastic anemia
 flaccid paralysis
NURSING CONSIDERATIONS

C. LOOP DIURETICS or HIGH CEILING DIURETICS

1. furosemide (Lasix)- most commonly used
2. eumetanide (Bumex)
3. ethacrynic acid (Edecrin)- the 1st loop diuretic
4. torsemide (Demadex)

ACTION

 Acts on the ascending limb of the loop of Henle to BLOCK THE

REABSORPTION OF SODIUM CHLORIDE and WATER
 can provide fluid loss up to 20 lbs/day
 excretion of potassium is increased

INDICATIONS

 acute congestive heart failure

 acute pulmonary edema
 used to reduce the edema associated with heart failure, hepatic cirrhosis, or
chronic renal failure

CONTRAINDICATIONS

 Allergy, electrolyte depletion, Anuria, severe renal failure, hepatic coma, and
pregnancy
 Lactation

ADVERSE EFFECTS

hypocalcemia and tetany, alkalosis- drop in serum pH when Bicarbonate is lost in the
urine, postural hypotension and dizziness, dehydration, serious hypokalemia, bloody
dyscrasias ototoxicity, circulatory collapse, hyperglycemia

D. THIAZIDE DIURETICS & THIAZIDE LIKE

 Thiazide belong to SULFONAMIDES
 Thiazide like has different chemical structures but work in the same
way with thiazide used to manage essential hypertension
 Short Acting: chlorothiazide (Diuril), hydrochlorothiazide (HydroDiuril,
HCTZ) most commonly used
  Intermediate-Acting: bedroflumethiazide (Naturetin), benzthiazide
(Aquatag, Exna, Hydrex), hydroflumethiazide (Diucardin, Saluron),
metolazone (Zaroxolyn, Mykrox), quinethazone (Hyrdromox)
 Long acting chlorthalidone (Hygroton), polythiazide (Renese)

ACTION

 Blocks the CHLORIDE pump and SODIUM passively moved with CHLORIDE
 Chloride is (-) , Sodium is (+)
 Thereby excreting both the chloride and sodium

INDICATIONS

 Treatment of mild to moderate hypertension

 Indicated for edema due to mild to moderate heart failure, liver failure and renal
failure

CONTRAINDICATIONS

Allergy to thiazides or sulfonamides, fluid or electrolyte imbalance, renal and liver

disease

ADVERSE EFFECTS

Serious hypokalemia: weakness, muscle cramps and arrhythmias, hypercalcemia, uric

acid excretion is decreased, gout, electrolyte depletion: hyponatremia, dehydration,
hypotension, hyperglycemia, coma, bloody dyscrasias, alkalinized urine

E. POTASSIUM SPARING DIURETICS

1. eplerenone (Inspra)
2. amiloride hydrochloride (Midamor)
3. spironolactone (Aldactone)- drug of choice for hyperaldosteronism
4. Traiamterene (Dyrenium)

ACTION

Acts on the late distal tubule and collecting ducts to BLOCK REABSORPTION OF
SODIUM and REDUCE EXCRETION OF POTASSIUM (sodium-potassium exchange)
blocking exchange of sodium for K and hydrogen ions in the distal tubule, increasing
sodium and chloride excretion without increasing K excretion.
Indication

 Primary use is in combination with thiazide or loop diuretics to minimize potassium

loss, hyperaldosteronism (a condition seen in cirrhosis of the liver and nephritic
syndrome

Contraindication

 Allergy to the drug, hyperkalemia, renal disease or anuria; patients taking amiloride
or triamterene

Adverse Effects

 Hyperkalemia- lethargy, confusion, ataxia, muscle cramps and cardiac

arrhythmias, dehydration, hyponatremia, agranulocytosis, and other blood
dyscrasias
 Drug to drug: if loop is taken with salicylates, it slows the effect of diuretic

Nursing Responsibilities

 Administer with food or milk

 Administer IV drug slowly
 Protect the drug from light
 Discard diluted drug after 24 hours
 Continuously monitor urine output, cardiac response, and HR of pxs receiving
intravenous diuretics
 Switch to oral form as soon as possible
 Measuring I&O and daily weights
 Administer early in the day
 Monitor the px response to drug
 Monitor Na and K values, BP, K intake
 Observe for changes in LOC, dizziness, fatigue, and postural hypotension
 Observe for signs of hypersensitivity reaction
 Monitor hearing and vision

DRUGS ACTING ON THE RENAL SYSTEM

A. URINARY TRACT ANTI-INFECTIVES

 norfloxacin (Noroxin)- newer and broader spectrum
 nalidixic acid (NegGram)
 nitrofurantoin (Furadantin)
Action

 act specifically in the urinary tract to destroy Gram (-) bacteria (causes most UTI)
either through acidification of the urine (ideal for chronic UTI) or direct antibiotic
effect

Indication

 chronic UTI, adjunctive therapy in acute cystitis and pyelonephritis

 prophylaxis with urinary tract anatomical abnormalities and residual urine
disorders

Contraindication

 allergy

Adverse Effects

 n/v, diarrhea, anorexia

 baldder irritation, dysuria, pruritus, urticarial
 headache, dizziness, nervousness and confusion

Nursing Considerations

 ensure that culture and sensitivity are performed before therapy begins and
repeated if the response is not as expected
 administer the drug with food
 institute safety precautions if px experiences CNS effects
 advice px to continue the full course of the drug ordered
 encourage the px to drink lots of fluids
 educate px with chronic UTI
 avoid food that cause an alkaline ash and produce an alkaline urine (citrus juices,
fruits, and antacids)
 drink high-acid cranberry juice
 void immediately after sexual intercourse
 women should avoid baths if possible, especially bubble baths
 wipe front to back and never back to front which introduces E. coli and other agents
to the urethra

B. URINARY TRACT ANTISPAMODICS

 oxybutynin (Ditropan)- oral and dermal patch
 tolterodine (Detrol, Detrol LA)
 trospium- the newest drug approved

Action

 relieve spasms by blocking parasympathetic activity and relaxing the detrusor and
other urinary tract muscles
 spasms: dysuria, nocturia & suprapubic pain

Indication

* spasms (cystitis, prostatitis, urethritis, neurogenic bladder)

Contraindications

 allergy, pyloric or duodenal obstruction or recent surgery

 obstructive urinary tract problems
 glaucoma, myasthenia gravis, or acute hemorrhage

Adverse Reactions

 nausea, vomiting, dry mouth

 nervousness, tachycardia
 vision changes

Nursing Considerations

 arrange for appropriate ttt of any underlying UTI

 arrange for an ophthalmological examination
 institute safety precautions if the px experiences CNS effects
 encourage the px to continue ttt for the underlying cause of the spasm

C. URINARY TRACT ANALGESIC

 phenazopyridine (Azo Standard, Baridium)- is a dye that is used to relieve urinary
tract pain

Action

 exerts a direct topical analgesic effect on the urinary tract mucosa

 Indication

 relieve symptoms such as burning, urgency, frequency, pain, discomfort

Contraindication

 allergy and serious renal dysfunction

Adverse Reactions

 GI upset, headache, rash

 A reddish-orange coloring of the urine (due to the drug’s chemical actions in the
system), renal or hepatic toxicity

Nursing Considerations

 Arrange for appropriate treatment of any underlying UTI

 Caution the px that urine may be reddish brown and may stain fabrics
 Administer the drug with food

D. BLADDER PROTECTANT
 pentosanpolysulfate sodium (Elmiron)

Action

 A heparin like compound that has anticoagulant and fibrinolytic effects

 adheres to the bladder wall mucosal membrane and acts as a buffer to control
cell permeability

INDICATION

 decrease pain and discomfort associated with interstitial cystitis (Chronic

inflammation of the interstitial connective tissue of the bladder that may extend
into deeper tissue)

CONTRAINDICATIONS

 Increased risk of bleeding

 History of heparin-induced thrombocytopenia
ADVERSE REACTIONS

 bleeding

NURSING CONSIDERATIONS

 Establish the presence of interstitial cystitis by biopsy or cystoscopy before

beginning therapy
 Administer the drugs on an empty stomach
 Monitor bleeding times periodically during therapy

E. DRUGS FOR TREATING BENIGN PROSTATIC HYPERPLASIA

1. alfuzosin (Xatral)
2. finasteride (Proscar)
3. tamsulosin (Flomax)
4. terazosin (Hytrin)

ACTION

 Alpha adrenergic blockers (tamsulosin, alfuzosin, terazosin) block post synaptic

alpha adrenergic receptors that results in dilation of arterioles & veins thereby
relaxing the bladder and urinary tract
 Androgen hormone inhibitor (finasteride and dutasteride) inhibit the intracellular
enzyme that converts testosterone to a potent androgen dihydrostestosterone
(DHT)- which the prostate gland depends on for development and maintenance

INDICATION: BPH

CONTRAINDICATION: allergy to the drug

ADVERSE EFFECT

 headache, fatigue, dizziness, postural dizziness, lethargy, tachycardia,

hypotension, GI upset, sexual dysfunction
 Finasteride and dutasteride: decreased libido, impotence and sexual dysfunction

NURSING CONSIDERATION:

>Determine the presence of BPH

>Administer the drug without regard to meals