CANTOS, JOREM BSN LEVEL II

BEGORNIA, LEIGH NCM 106 PHARMACOLOGY

BLANCO, TRICIA
DRUGS AFFECTING THE CARDIOVASCULAR SYSTEM

DRUG Generic MECHANISM OF ACTION ADVERSE EFFECTS CONTRAINDICATIONS NURSING CONSIDERATIONS

CLASSIFICATION Name

Positive Inotropic
-Group of medicines that affect the contraction of the heart muscle.

-Digoxin -Digoxin causes a positive inotropic
effect on the heart and that it causes
the heart to squeeze or contract
harder so it increases cardiac
contractility which in the end is going
to increase stroke volume another
thing it does has a negative
Chronotrophic effect on the heart
which causes the heart to be at a
slower rate it also causes a negative
dramatropic effect which is going to
cause impulses to be sent slower
through the AV node now when we
take all these actions and combine
them together what's the result for
our patient's heart is gonna squeeze
more blood out so there will be an
increase in stroke volume, therefore,
increasing cardiac output.
 Nausea  Hypersensitive to drug
 Vomiting  Digitalis-induced toxicity
 Anorexia  Ventricular fibrillation or
 Diarrhea ventricular tachycardia unless
 Mental disturbances caused by HF.
 Fatigue  Wolff-Parkinson-white
 Headache syndrome
 Thrombocytopenia  Use with extreme caution in
 Vision changes elderly with acute MI, incomplete
 Dysrhythmias AV block, sinus bradycardia,
PVCs, chronic constrictive
pericarditis, hypertrophic
cardiomyopathy, renal
insufficiency, severe pulmonary
disease, and hypothyroidism.
 Obtain baseline data (HR and
rhythm, BP, and electrolytes
level)
 Before giving the drug, take an
apical-radial pulse for 1 min.
hold dose if pulse < 60 in adult
or < 90 in infant; retake pulse
in 1 hr. If adult pulse remains <
60 or infant < 90, hold the drug
and notify the prescriber.
 Monitor potassium level,
hyperkalemia may result from
digoxin toxicity.
 Have digibind or digoxin
immune fab (antidote for
digoxin toxicity) nearby
 Educate patient to eat
potassium-rich foods to
prevent digoxin toxicity.

-Dobutamine -Acts on beta 1 receptors to cause
increases in inotropy and
chronotropic what this means is that
dobutamine will cause increases in
cardiac output with minimal effects
on vascular resistance in fact there
are very minimal effects on alpha
and beta 2 receptors that may even
cause slight decreases in systemic
vascular resistance dobutamine are
 Increased heart rate
 increased blood pressure
 ventricular ectopic activity
 Nervousness
 Headache
 Nausea
 vomiting, palpitations
 thrombocytopenia
 Swelling at the injection site.
 Acute myocardial infarction
 Unstable angina
 Left main stem disease
 Severe hypertension
 Arrhythmias
 Acute myocarditis or pericarditis
 Hypokalemia
 Idiopathic hypertrophic sub-
aortic stenosis.
 Monitor ECG, BP, pulmonary
artery wedge pressure, cardiac
output, and urine output.
 Correct hypovolemia before
drug therapy
 Monitor electrolyte levels
 Tell the patient to report all
adverse reactions.
 Instruct patient to report
discomfort at IV insertion sites.
 therefore useful in heart failure and
cardiogenic shock both of which are
characterized by decreased cardiac
output and high vascular resistance
in summary dobutamine is an
ionotropic agent that causes
increases in cardiac output and mild
decreases in systemic vascular
resistance
-Dopamine -Acts on beta 1 receptors recall that
beta 1 receptors are found primarily
in the heart and stimulating them
increases heart rate and stroke
volume in other words dopamine has
a positive chronotropic and inotropic
effect Chronotrophic means
increasing heart rate and inotropic
means increasing contractility ie
stroke volume
-Antidysrhythmics exert their effect on specific ion channels on the cardiac cell membrane which then alters the shape of the action potential and thus have inotropic, chronotropic, and toxic
-used to suppress abnormal rhythms of the heart, such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation.
Sodium Channel -Quinidine -Blocks cardiac sodium channels
Blockers Decreases conduction velocity in
atria and ventricles
 Irregular heartbeats  Pheochromocytoma  Monitor blood pressure, pulse,
 Nausea, Vomiting,  Uncorrected ventricular peripheral pulses, and urinary
 Anxiety fibrillation output at intervals prescribed
 Headache  Ventricular tachycardia by a physician. Precise
 Chills, Goosebumps  Other tachyarrhythmias measurements are essential
 Dyspnea. for accurate titration of dosage.
 Report the following indicators
promptly to a physician for use
in decreasing or temporarily
suspending dose:
The reduced urine flow rate in
absence of hypotension; ascending
tachycardia; dysrhythmias;
disproportionate rise in diastolic
pressure (marked decrease in
pulse pressure); signs of peripheral
ischemia (pallor, cyanosis, mottling,
coldness, complaints of
tenderness, pain, numbness, or
burning sensation).
Antidysrhythmic
actions as a result.
 Diarrhea  Hypersensitivity to quinine or  Check apical pulse, BP, and
 Lightheadedness cinchona derivatives cardiac monitor prior to
 Headache  Thrombocytopenic purpura administration of quinidine.
 -Depresses myocardial excitability
and contractility (negative inotropic
effect)
Beta-Blockers -Propanolol -non-selective beta adrenergic
receptor blocker that acts by
blocking beta 1 receptor on the
cardiac myocyte cell which
consequently inhibits the enzyme
adenylate cyclase this in turn inhibits
cyclic a MP synthesis and
consequently the production of PK a
leading to a decrease in calcium
influx through the voltage-gated l-
type calcium channel leading to a
 Tiredness secondary to previous quinidine
 Feeling like your heart is exposure
beating faster, chest pain  2nd or 3rd degree AV block
 Skin rash and blurred or double  Thyrotoxicosis.
vision  Acute rheumatic fever
 Subacute bacterial endocarditis
 Extensive myocardial damage
 Severe left sided heart failure
 Hypotensive states
 Myasthenia gravis
 Digoxin toxicity
 Cautious use in impaired liver or
kidney function
 Safety not established in
pregnancy or lactation (Category
C).
 Nausea  Asthma
 vomiting  Chronic obstructive pulmonary
 diarrhea disease (COPD)
 constipation  Atrioventricular (AV) block
 stomach cramps  Intermittent claudication, and
 decreased sex drive, psychosis.
impotence, or difficulty having
an orgasm
 sleep problems (insomnia); or
tired feeling.
 Monitor blood pressure. If QRS
widens > 50%, notify physician.
 Serum quinidine levels should
be between 2 – 5 mcg/ml.
 Take oral quinidine with a full
glass of water on an empty
stomach to enhance
absorption.
 If GI symptoms occur, take
quinidine with food.
 Quinidine is preferred over
procainamide for long term
suppression of dysrhythmias
due to probability of SLE
syndrome and blood
dyscrasias.
 Obtain baseline cardiac rhythm
strip, CBC, lab tests for liver
and renal functions, and blood
pressure.
 Quinidine will double digoxin
serum levels, so digoxin doses
will have to be reduced.
 Monitor patient for digoxin
toxicity.
 During conversion of atrial
fibrillation, patient may develop
thromboembolism.

 Monitor hemodynamic
parameters (HR, BP)
 May cause bradycardia, CHF,
pulmonary edema
 Masks symptoms associated
with diabetes mellitus
 Advise to change positions
slowly to prevent orthostatic
hypotension
 Instruct patient on how to take
blood pressure
 decrease in the sympathetic effect
on the my cardiac cell which is a
decrease in heart rate and
contractility furthermore propanolol
also inhibits renin secretion from the
kidney which reduces angiotensin ii
formation and subsequent
aldosterone release
-Atenolol -Inhibits stimulation of beta1-
receptor sites, located mainly in the
heart, decreasing cardiac
excitability, cardiac output, and
myocardial oxygen demand.
Atenolol also acts to decrease
release of renin from the kidneys,
aiding in reducing blood pressure. At
high doses, it inhibits stimulation of
beta2 receptors in the lungs, which
may cause bronchoconstriction.
Potassium -Amiodarone -Type III antiarrhythmic: Acts directly
Channel Blockers on cardiac cell membrane; prolongs
repolarization and refractory period;
increases ventricular fibrillation
threshold; acts on peripheral smooth
muscle to decrease peripheral
resistance
 Pharyngitis, erythematous rash,
fever, sore throat,
laryngospasm, respiratory
distress
 Dizziness, vertigo, tinnitus,
fatigue, emotional depression
 Bradycardia, CHF, cardiac
arrhythmias, sinoatrial or AV
nodal block, tachycardia,
peripheral vascular
insufficiency, claudication, CVA,
pulmonary edema, hypotension
 nausea, vomiting, fatigue
 tremor, lack of coordination,
 constipation, stomach pain
 insomnia
 headache
 decreased sex drive or
performance
 uncontrollable or unusual
movements of the body
 Cardiogenic shock, heart block
greater than first degree
 hypersensitivity to beta blockers
 overt heart failure,
 sinus bradycardia
 Hypersensitivity to drug or iodine
 Second- or third-degree heart
block who do not have a
pacemaker.
 Severe bradycardia,
hypokalemia, lactation.
 Use cautiously with thyroid
dysfunction, pregnancy.
 Stopping abruptly may result in
life threatening arrhythmias
 Monitor daily intake and output
 Advise patient to notify
physician for difficulty
breathing
 During I.V. atenolol therapy,
monitor vital signs and cardiac
rhythm closely.
 Discard parenteral mixture with
atenolol if it isn’t used within 48
hours.
 Stop atenolol and notify
prescriber if patient develops
bradycardia, hypotension, or
other serious adverse reaction.
Patient-teaching
 Take drug with meals if GI
upset occurs.
 Do not stop taking this drug
unless told to do so by a health
care provider.
 Report difficulty breathing,
night cough, swelling of
extremities, slow pulse,
confusion, depression, rash,
fever, sore throat.
 Reserve use for life-
threatening arrhythmias;
serious toxicity, including
arrhythmias, pulmonary toxicity
can occur.
 Monitor cardiac rhythm
continuously.
 Monitor for an extended period
when dosage adjustments are
made.

Calcium Channel -Verapamil -inhibits entry of calcium ions into
Blockers arterial smooth muscle cells as well
as the myocytes and conducting
tissue. These actions lead to
reversal and preventions of coronary
artery spasm, reduction in afterload
through peripheral vasodilatation
and reduction in ventricular rate in
patients with chronic atrial flutter or
fibrillation and reduction in the
occurrence of paroxysmal
supraventricular tachycardia.
Verapamil reduces BP, relieves
angina and slows AV conduction.
 Bradycardia, worsening heart
failure, transient asystole
 hypotension, pulmonary and
peripheral edema
 nausea, fatigue, dizziness,
headache, palpitation, flushing
 rashes, alopecia
 hyperprolactinaemia, increased
LFT and arthralgia.
 Potentially Fatal: Heart block
and cardiac failure in patients
with preexisting cardiac
disease. Hepatotoxicity.
 Cardiogenic shock, severe
bradycardia, severe left
ventricular dysfunction,
uncompensated heart failure,
hypotension (systolic pressure
<90 mm Hg), porphyria.
 Patients with atrial flutter or atrial
fibrillation and an accessory
bypass tract (e.g., Wolff-
Parkinson-White, Lown-Ganong-
Levine syndromes).
 2nd or 3rd degree AV block
(unless pacemaker is fitted).
 Arrange for periodic chest X-
ray to evaluate pulmonary
status (every 3–6 mo).
 Arrange for regular periodic
blood tests for liver enzymes,
thyroid hormone levels.
 WARNING: Monitor for safe
and effective serum levels
(0.5–2.5 mcg/mL).
 WARNING: Doses of digoxin,
quinidine, procainamide,
phenytoin, and warfarin may
need to be reduced one-third
to one-half when amiodarone
is started.
 Give drug with meals to
decrease GI problems.
 Arrange for ophthalmologic
examinations; reevaluate at
any sign of optic neuropathy.

 WARNING: Monitor patient
carefully (BP, cardiac rhythm,
and output) while drug is being
titrated to therapeutic dose.
 Ensure that patient swallows
SR tablets whole; patient
should not cut, crush, or chew
them.
 Monitor BP very carefully with
concurrent doses of
antihypertensives.
 Monitor cardiac rhythm
regularly during stabilization of
dosage and periodically during
long-term therapy.
 Administer SR form in the
morning with food to decrease
GI upset.
 Protect IV solution from light.

-Antianginal drugs are used to provide immediate relief from symptoms and prevent angina attacks. If your risk of having a heart attack or stroke is high, it should be possible to reduce the risk
by using a combination of medication and lifestyle changes. Guidelines recommend initial treatment with one or two antianginal drugs, plus aspirin, possibly an angiotensin-converting enzyme
inhibitor, and a statin for secondary prevention of cardiovascular disease.
Angina pectoris - chest pains due to the imbalance of oxygen supply and demand in the heart.
Nitrates -Nitroglycerin -the issue with angina that chest
pain
was the lack of oxygen supply to
oxygen demand what we need to do
is increase the oxygen supply right if
we need more oxygen we got to
figure out a way to allow the heart to
have more oxygen and in a nutshell
that's what nitrates do they allow
more oxygen to go to the heart so
here we see we have veins and
arteries that lead to and from the
heart and remember oxygen is
carried through blood cells right your
blood and your hemoglobin inside
the actual blood cell holds oxygen so
the way nitrates work is they actually
dilate the veins leading to the heart
and this is also called preload
meaning before the blood supply
and if we increase the preload if we
dilate those veins we allow more
blood to easily flow in with oxygen
so now we know that nitrates dilate
the veins allowing more blood and
more oxygen to reach the heart so
how does that actually happen right
so if we have a patient like this one
Anti-angina
 Headache, dizziness,
weakness.
 Orthostatic hypotension,
tachycardia, flushing,
palpitations, fainting.
 S.L. burning
 Nausea, vomiting.
 Cutaneous vasodilation, contact
dermatitis, rash.
 Hypersensitivity reactions.
 Hypersensitive patients
 Severe anemia
 Erectile dysfunction medications
(sildenafil [Viagra], tadalafil
[Cialis], avanafil [Stendra],
vardenafil [Levitra])
 Severe hepatic or renal disease
and use of other vasodilators
 Beta-blockers, verapamil,
diltiazem
 Monitor patients with renal or
hepatic impairment carefully for
possible drug accumulation
and adverse reactions.
 Do not drink grapefruit juice
while using this drug.

 Administer IV nitroglycerin with
extreme caution to patients
with hypotension or
hypovolemia
 Monitor patient closely for
change in levels of
consciousness and for
dysrhythmias.
 Supervise ambulation as
needed
 Take baseline BP and heart
rate with patient in sitting
position before initiation of
treatment with transdermal
preparations.
Patient-Teaching
 Spit out the rest of your
sublingual tablet as soon as
pain is completely relieved
 Be aware that pain not relieved
by 3 sublingual tablets over a
15-min period may indicate
acute MI or severe coronary
insufficiency.
 Change position slowly and
avoid prolonged standing.
 Do not breast feed while taking
 here and we give them nitroglycerin this drug without consulting
essentially what happens is that physician.
medication gets absorbed and nitric
oxide which is part of the medication
is released so that nitric oxide in our
body will allow the formation of
something called cyclic gmp or
cGMP in our body allows for smooth
muscles to relax and smooth
muscles are like our veins and
arteries now when the smooth
muscles relax we get that
vasodilation and because of that we
see an improved blood supply and
we have an increased oxygen
supply to meet the demand so
essentially again we're just
increasing that supply to the heart so
that it has efficient oxygen

Calcium Channel -Nifedipine -blocks calcium channels in the
Blockers vascular smooth muscle and cardiac
muscle preventing calcium from
entering the cells this inhibits the
muscle contraction inhibiting smooth
and cardiac muscle decreases
vascular resistance and dilates the
coronary arteries these effects
reduce blood pressure and decrease
the workload of the heart nifedipine
is used in the treatment of
hypertension and angina again
nifedipine lowers blood pressure by
relaxing the blood vessels making it
easier for the heart to pump
essentially using less oxygen
 Peripheral edema
 hypotension
 palpitations, tachycardia
 flushing
 dizziness, headache, nausea,
lethargy
 eye pain, mental depression,
visual disturbances,
 tremor, impotence, fever
 paradoxical increase in
ischemic chest pain during
initiation of treatment
 abnormalities in liver function
 Acute MI, cardiogenic shock,
acute unstable angina, treatment
of anginal attack in chronic
stable angina.
 WARNING: Monitor patient
carefully (BP, cardiac rhythm,
and output)
 Taper dosage of beta-blockers
before nifedipine therapy.
 Protect drug from light and
moisture.
Patient-Teaching
 Do not chew, cut, or crush
sustained-release tablets.
Swallow whole.
 Inform patient of the side
effects
 Report irregular heartbeat,
shortness of breath, swelling of
the hands or feet, pronounced
dizziness, constipation.

-Ranolazine -The main action of ranolazine is  Dizziness, headache, tinnitus,  Contraindicated with  Obtain baseline ECG, LFTs,
that it blocks late sodium currents in vertigo hypersensitivity to any and renal function tests before
ischemic conditions and prevents  Palpitations, peripheral edema, component of the drug; pre- starting therapy.
 excess calcium entry into the
myocardial cells. This is because the
blockage of late sodium current
reduces the amount of sodium
available for the functioning of
sodium-calcium exchanger
which facilitates the entry of calcium
into the cell.
-In addition, ranolazine is also
a partial fatty acid oxidation
inhibitor, inhibiting the beta
oxidation of fatty acids. This causes
a shift of myocardial energy
substrate from fatty acids to glucose.
Anaerobic glycolysis needs a
smaller number of oxygen molecules
for production of ATP molecules.
Hence shift of myocardial
metabolism towards glucose
utilization is beneficial to the
ischemic myocardium.
-Ranolazine is hemodynamically
neutral and does not produce any
significant alteration in heart rate or
blood pressure.
Angiotensin- -Lisinopril -Lowers blood pressure only and not
Converting the heart rate.
Enzyme (ACE) -Acts on the ACE
inhibitors -In our liver, a peptide hormone
called angiotensinogen is made,
renin which is secreted by our
kidneys converts this
angiotensinogen to angiotensin-I.
Then our lung’s blood vessel
releases the angiotensin-converting
enzyme (ACE) which converts
angiotensin-I into angiotensin-II.
-This angiotensin-II binds with a
prolonged QT interval
 Nausea, constipation, dry
mouth, vomiting, abdominal
pain
 Dyspnea
Anti-hypertensive
 Dizziness, headache, fatigue
 cough, upper respiratory tract
infection
 rash
 diarrhea, nausea, vomiting,
abdominal pain
 chest pain, weakness
 orthostatic effects; hypotension
 hyperkalemia
 impotence
 decreased hemoglobin
 increased serum creatinine.
 Potentially Fatal: Severe
existing QT prolongation,
concurrent use of QT-interval
prolonging drugs; hepatic
impairment; concurrent use of
potent or moderately potent
CYP3A inhibitors, including
diltiazem; lactation.
 Use caution in severe renal
impairment, history of ventricular
tachycardia, pregnancy.
 History of angioedema related to
previous treatment with ACE
inhibitors, hereditary or
idiopathic angioedema. Bilateral
renal artery stenosis. Pregnancy
(2nd or 3rd trimester), lactation.
 Ensure that patient swallows
tablets whole; do not cut,
crush, or let patient chew the
tablets.
 Ensure that patient continues
to use other prescribed
antianginal medications.
 Advise patient to avoid
grapefruit juice and grapefruit
products while using this drug.
 Suggest use of contraceptive
measures while taking this
drug; potential effects on a
fetus are not known.
 Advise nursing mothers that
another method of feeding the
baby will be needed while
taking this drug.
 Provide safety measures if
dizziness and lightheaded
occur.
 Monitor patients on diuretic
therapy
 Monitor patients closely in any
situation that may lead to a
decrease in BP secondary to a
reduction in fluid volume
 Arrange for reduced dosage in
patients with impaired renal
function.
 BLACK BOX WARNING:
Suggest the use of
contraceptives; if pregnancy
should occur, discontinue the
 receptor found in our kidneys, when hypotension, angioedema drug as soon as possible.
this happens it will increase
aldosterone levels which increases
sodium retention thus keeping water
inside.
-What this drug does is that it binds
with ACE preventing it from
converting angiotensin-I to
angiotensin-II.
-Decreased release of aldosterone
reduces sodium and water
reabsorption and increases their
excretion, thereby reducing blood
pressure.

Angiotensin II -Losartan -Acts on the receptor
Receptor Blockers -In our liver, a peptide hormone
(ARBS) called angiotensinogen is made,
renin which is secreted by our
kidneys converts this
angiotensinogen to angiotensin-I.
Then our lung’s blood vessel
releases the angiotensin-converting
enzyme (ACE) which converts
angiotensin-I into angiotensin-II.
-This angiotensin-II binds with a
receptor found in our kidneys, when
this happens it will increase
aldosterone levels which increases
sodium retention thus keeping water
inside.
-What this drug does is that it block
the angiotensin-II receptor which is
found in our kidneys.
--Decreased release of aldosterone
reduces sodium and water
reabsorption and increases their
excretion, thereby reducing blood
pressure.
 Dizziness, fatigue, headache,
insomnia, malaise
 Hypotension
 Nasal congestion
 Diarrhea, indigestion, nausea,
vomiting
 Thrombocytopenia
 Back pain, leg pain, muscle
spasms
 Cough, upper respiratory tract
infection
 Erythroderma
 Angioedema,
hyperkalemia, hyponatremia
 Concurrent aliskiren therapy (in
patients with diabetes)
 hypersensitivity to losartan or its
components
 Monitor BP at drug trough
 Monitor drug effectiveness
 The inadequate response may
be improved by splitting the
daily dose into a twice-daily
doses.
 Lab tests: Monitor CBC,
electrolytes, liver & kidney
function with long-term
therapy.
 Instruct patient to avoid
potassium-containing salt
substitutes.
 Advise patient to avoid
exercising in hot weather and
drinking excessive amounts of
alcohol

-blocks the reabsorption of sodium forcing sodium to be urinated
Thiazide - -work at the distal convoluted
Chlorothiazide tubules section of our kidney to
prevent sodium from being
reabsorbed into the bloodstream
these are indicated for people with
high blood pressure because once
you start peeing more and more
your blood volume becomes less
and less and if you have less blood
volume you have less blood
pressure now this also makes sense
that these agents are used for
edema because you have excess
fluid in your body and you start
urinating more and more you start
getting rid of that excess fluid.
-Potassium and water are secreted.
-Calcium is reabsorbed
Loop Diuretics -Furomeside -Strongest diuretics
-Works at the ascending loop of
henle
-Sodium, Calcium, Potassium,
Magnesium are secreted together
with the urine.
Diuretics
 Fever, respiratory distress,
anaphylactic reaction.
 Irregular heart beat, weak
pulse, orthostatic hypotension.
 Vomiting, acute pancreatitis,
diarrhea.
 Hypokalemia, hypercalcemia,
hyponatremia, hypochloremic
alkalosis, elevated cholesterol
and triglyceride levels.
 Unusual fatigue, dizziness,
mental changes, vertigo,
headache.
 Urticaria, photosensitivity, skin
rash.
 Fluid and electrolyte imbalance.
 Rashes, photosensitivity,
nausea, diarrhoea, blurred
vision, dizziness, headache,
hypotension.
 Bone marrow depression (rare),
hepatic dysfunction.
Hyperglycaemia, glycosuria,
ototoxicity.
 Potentially Fatal: Rarely,
sudden death and cardiac
arrest. Hypokalaemia and
magnesium depletion can
cause cardiac arrhythmias.
 Anuria  Lab tests: Baseline and
 Hepatic coma periodic determinations are
 Hypersensitivity to chlorothiazide indicated for blood count,
or its components, serum electrolytes, CO2, BUN,
sulfonamides, or related thiazide creatinine, uric acid, and blood
diuretics; glucose.
 Renal failure  Monitor for hyperglycemia.
 Monitor I&O rates and patterns
 Patient-teaching
 Avoid drinking large quantities
of coffee or other caffeine
drinks.
 Hypokalemia may be
prevented if the daily diet
contains potassium-rich foods.
 Anuria unresponsive to  Administer with food or milk to
furosemide prevent GI upset.
 hypersensitivity to furosemide,  Reduce dosage if given with
sulfonamides, or their other antihypertensives;
components readjust dosage gradually as
BP responds.
 Give early in the day so that
increased urination will not
disturb sleep.
 Avoid IV use if oral use is at all
possible.
 WARNING: Do not mix
parenteral solution with highly
acidic solutions with pH below
3.5.
 Discard diluted solution after
24 hr.
 Refrigerate oral solution.
 Measure and record weight to
monitor fluid changes.

Potassium-sparing -Amiloride -Aldosterone antagonist
diuretics -Work at the distal convoluted
tubules section of our kidney
-Potassium-sparing diuretics reduce
sodium re-absorption at the distal
tubule, thus decreasing potassium
secretion. Potassium-sparing
diuretics when used alone are rather
weak, hence they are used most
commonly in combination therapy
with thiazide and loop diuretics.
Anticoagulants -Heparin -Drugs that prevent the formation of
a clot by inhibiting certain clotting
factors. These drugs have no effect
on a blood clot that has already
formed. They prevent intravascular
thrombosis by decreasing blood
coagulability. Their uses vary from
preventing clot formation to
preventing the extension of an
established clot, or a thrombus.
 Headache, dizziness,
nervousness, confusion,
paresthesias, drowsiness.
 Cardiac arrhythmias, Dyspnea
 Polyuria, dysuria
Coagulation Modifiers
 Fever
 Hemorrhage, overly prolonged
clotting time, thrombocytopenia,
white clot syndrome
 Hyperkalemia
 Hypoaldosteronism
 Irritation, mild pain, hematoma,
ulceration, skin necrosis,
pruritus, urticaria, transient
alopecia.
 Chills, anaphylactoid reactions
 Hypersensitivity to amiloride
 Impaired renal function
 Serum potassium level above
5.5 mEq/L
 Therapy with another potassium-
sparing diuretic, such as
spironolactone or triamterene, or
a potassium supplement
 Hypersensitivity to heparin or its
components
 Breastfeeding, infants,
neonates, or pregnant woman
 Severe thrombocytopenia
 Uncontrolled bleeding
 Arrange to monitor serum
electrolytes, hydration, liver
and renal function.
 Arrange for potassium-rich diet
or supplemental potassium as
needed.

 Monitor for S&S of
hyperkalemia and
hyponatremia
 Lab tests: Serum potassium
levels, particularly

 Patient-Teaching
 Do not take potassium
supplements, salt substitutes,
high intake of dietary
potassium unless prescribed
by physician.
 Do not drive or engage in
potentially hazardous activities
until response to drug is
known.
 Do not breast feed while taking
this drug without consulting
physician.
 Check vital signs and monitor
for bleeding and liver enzymes
 Always check compatibilities
with other IV solutions.
 Use a heparin lock needle to
avoid repeated injections.
 Inspect injection sites for signs
of hematoma; do not massage
injection sites.
 Have protamine sulfate readily
available
 -Heparin binds with antithrombin III,
enhancing antithrombin III’s
inactivation of the coagulation
enzymes thrombin (factor IIa) and
factors Xa and XIa.
Antiplatelets -Clopidogrel -This drug class exerts its action by
decreasing the responsiveness of
platelets to stimuli that cause them
to clump or aggregate. Through this,
the formation of the platelet plug is
decreased which can be beneficial in
preventing heart attacks and
strokes.
-Carboxylesterase converts
clopidogrel to its active form which
then becomes a platelet inhibitor.
This prevents the binding of ADP to
platelet receptors (P2Y12) which
then prevents the activation of the
glycoprotein complex which will lead
to the prevention of platelet
aggregation.
Thrombolytic -Alteplase -Often used as emergency drugs
given intravenously to dissolve life-
threatening clots in blood vessels,
especially in arteries that supply the
heart, lungs, and brain, improve
blood flow, and prevent ischemic
damage to tissue and organs. They
are used to treat emergency
conditions such as ischemic strokes,
heart attacks, pulmonary embolism,
and deep vein thrombosis in the
legs.
 Fatal intracranial bleeding  Hypersensitivity
 Headache, dizziness  Active pathologic bleeding (e.g.,
 Epistaxis peptic ulcer, intracranial
 Hemorrhage hemorrhage)
 Pruritus, bruising,  Use cautiously in patients with
 Angioedema renal or hepatic impairment
 Anaphylaxis
 Internal and superficial bleeding  Active internal bleeding,
(cerebral, retroperitoneal, GU, aneurysm, bleeding diathesis,
GI). intracranial neoplasm, severe
 anaphylaxis uncontrolled hypertension
 History of stroke, intracranial or
intraspinal surgery or trauma in
past 2 months
 Recent head trauma, recent
intracranial surgery, recent
stroke, seizure activity at the
onset of stroke, subarachnoid
hemorrhage, suspicion or history
 Frequent blood tests are
necessary
Patient Teaching
 Report nose bleed, bleeding of
the gums, unusual bruising,
black or tarry stools, cloudy or
dark urine, abdominal or lower
back pain, severe headache.
 Assess for stomach ulcer or
active bleeding before
administering the drug
 Monitor vital signs and lab
values
 Instruct patient to report any
bleeding or bruising
 Monitor for S&S of excess
bleeding
 Monitor blood pressure and
heart rate and rhythm
frequently
 Protect patients from invasive
procedures
 Lab tests: Coagulation tests
including APTT, bleeding time,
PT, TT, INR, must be done
before administration of the
drug.

-These drugs are plasminogen
activators, i.e., they convert
plasminogen into active plasmin,
which breaks down the blood clot,
allows free flow of blood to the
affected areas, and supplies oxygen
and nutrients limiting the damage.
Bile Acid -Colesevelam -They bind to bile acids (which
Sequestrants contain cholesterol) in the small
intestine and prevent their re-
absorption into the body. The bound
complex is insoluble and is excreted
in the feces. A decrease in bile acid
or when the gallbladder is empty of
bile acids leads to an increase in
hepatic synthesis of bile acids from
cholesterol floating in our system.
Depletion of cholesterol increases
LDL receptor activity, therefore
increasing the removal of LDL
cholesterol from the blood.
HMG-CoA -Atorvastatin -Statins (also called HMG-CoA
Reductase reductase inhibitors) block an
Inhibitors (statins) enzyme called HMG-CoA reductase
that is involved in the synthesis of
mevalonate, a naturally occurring
substance that is then used by the
body to make sterols. By inhibiting
this enzyme, cholesterol and LDL-
cholesterol production are
decreased. Statins also increase the
number of LDL receptors on liver
cells, which enhances the uptake
and breakdown of LDL cholesterol.
Antihyperlipidemic
 Hypertension,
hypertriglyceridemia
 Oral blistering, pharyngitis,
rhinitis
 Hypoglycemia
 Abdominal distention or pain,
bowel or esophageal
obstruction, unexplained
elevated liver enzymes,
indigestion, nausea,
pancreatitis, worsening of
hemorrhoids
 Flu-like syndrome
 Headache, asthenia
 Flatulence, abdominal pain,
cramps, constipation, nausea,
dyspepsia, heartburn, liver
failure
 Sinusitis, pharyngitis
 Rhabdomyolysis with acute
renal failure, arthralgia, myalgia
of intracranial hemorrhage
 History of bowel obstruction or
pancreatitis induced by
hypertriglyceridemia,
hypersensitivity to colesevelam
or its components, serum
triglyceride level greater than
500 mg/dl
 Active hepatic disease
 Breastfeeding, pregnancy
 Hypersensitivity to atorvastatin
or its components
 Unexplained persistent rise in
serum transaminase level
 Tell patient to immediately
report bleeding, including from
the nose or gums
 Lab tests: Monitor total
cholesterol, LDL-C, HDL-C,
and triglycerides periodically.
 Monitor bowel habits, decrease
the dosage, or add stool
softener, or stop the drug if
severe constipation develops.
 Withhold drug and notify
physician for triglycerides >300
mg/dL.
 Instruct patient to take the drug
with a meal and drink plenty of
fluids.
 Know that atorvastatin should
not be used in patients taking
cyclosporine, gemfibrozil,
tipranavir plus ritonavir, or
telaprevir
 Use atorvastatin cautiously in
patients who consume
substantial quantities of alcohol
or have a history of liver
disease
 Obtain baseline liver function
test, lipid levels, and blood
glucose level.
 Notify prescriber immediately
and expect to withhold
atorvastatin therapy if a patient
develops an acute condition
suggestive of a myopathy
 Tell the patient to take the drug
at the same time each day to
maintain its effects
 Instruct patient to take a
missed dose as soon as
possible. If it’s almost time for
his next dose, he should skip
the missed dose. Tell him not
to double the dose.
 Be aware that atorvastatin is
expensive.
 Advise patients with diabetes
to monitor blood glucose levels
closely.