CARDIOVASCULAR

AGENTS

Group 1
Pharmacology
 ❑ OBJECTIVE

❖ Classes of drugs used to treat

cardiovascular disorders.
❖ Uses and varying actions of this
drugs.
❖ Absorption, distribution,
metabolization, and excretion of
these drugs.
❖ Drug interaction and adverse
reactions to these drugs.
 UNIT XIV: CARDIOVASCULAR
AGENTS
1 3
Chapter 42 Chapter 44
Cardiac Glycosides,
Antianginals, & Anti 2 Anti hypertensives
dysrhythmics
Chapter 43

4 5
Diuretics

Chapter 45 Chapter 46
Anticoagulants, Antihyperlipidemic &
Antiplatelets, & Peripheral Vasodilators
Thrombolytic
 ❑ INTRODUCTION
Drugs and the Cardiovascular System
❖ Components of the cardiovascular system
include the heart, arteries, capillaries,
veins, and lymphatics. These structures
transport life-supporting oxygen and
nutrients to cells,
remove metabolic waste products, and carry
hormones from one part of the
body to another. Because this system
performs such vital functions, any problem
with the heart or blood vessels can seriously
affect a person’s health.
01

CARDIAC GLYCOSIDES,
ANTIANGINALS, &
ANTIDYSRHYTHMICS
 ❑ OBJECTIVES
❖ Differentiate the actions of cardiac
glycosides, antianginal drugs, and
antidysrhythmic drugs.

❖ Describe the signs and symptoms of

digitalis toxicity.
❖ Compare the side effects and adverse
reactions of nitrates, beta blockers, calcium
channel blockers, quinidine, and
procainamide.
❖ Apply the nursing process, including patient
teaching, related to cardiac glycosides,
antianginal drugs, and antidysrhythmic
drugs.
❑ 3 GROUP OF DRUGS

1. Cardiac Glycosides

2. Antianginals

3. Antidysrhythmics
CARDIAC GLYCOSIDES
 ❑ DIGITALIS: WILLIAM WITHERING

❖ Digitalis is a cardiac glycoside used to

treat certain heart conditions such as
congestive heart failure (CHF) and heart
rhythm problems (atrial arrhythmias).
Digitalis works directly on the heart muscle
to strengthen and regulate the heartbeat.
 ❑ DIGITALIS: WILLIAM WITHERING
❖ Discovered in the year 1775, by a Scottish
Doctor, William Withering.
❖ Withering tried out various formulations of
digitalis plant extracts on 163 patients, and
found that if he used the dried, powdered
leaf, he got amazingly successful results.
❖ He introduced its use officially in 1785.
❑ HEART FAILURE / PUMP FAILURE
❖ The Myocardium weakens & enlarges,
losing its ability to pump blood through
the heart & into systemic circulation.
❑ CHF (CONGESTIVE HEART FAILURE)
❖ Compensatory mechanisms fail & the
peripheral & lung tissue are congested.
❑ CAUSES OF HEART FAILURE:
1. Chronic Hypertension
2. Myocardial Infarction
3. Coronary Artery Disease
4. Valvular Heart Disease
5. Congenital Heart Disease
6. Arteriosclerosis
❑ LEFT SIDED HEART FAILURE
❖ LV does not contract sufficiently to pump
the returned blood from the lungs & LA out
through the aorta into peripheral circulation.
❖ RESULT: Excessive amount of blood back-
up into the lung tissue.
❖ Usually the patient will experience SOB &
Dyspnea.
❑ RIGHT SIDED HEART FAILURE
❖ Occurs when the heart does not
sufficiently pump the returned blood
into the RA for systemic circulation.
❖ RESULT: Blood & its constituents are
backed-up into peripheral tissues,
causing peripheral edema.
❑ MYOCARDIAL HYPERTROPHY
❖ Resulting in cardiomegaly. It can be a
major problem associated with
progressive heart failure.
❑ CARDIAC PHYSIOLOGY OF HF
❖ There is an increase in preload &
afterload.
❑ PRELOAD
❖ Results from an excess of Blood Volume
in the ventricle at the end of the diastole.
❑ AFTERLOAD
❖ It is an additional pressure or force in the
ventricular wall cathe used by excess
resistance in the aorta.
❑ CARDIAC GLYCOSIDES
❖ Also called Digitalis Glycosides
❖ This group of drugs inhibit NaK pump,
resulting in an increase in intracellular
Na.
❖ This increase leads to an influx of Ca,
causes the Myocardium to contract
more efficiently.
 ❑ 3 EFFECTS OF DIGITALIS
PREPARATIONS ON MYOCARDIUM

1. Positive Inotropic Action

2. Negative Chronotropic Action
3. Negative Promo tropic Action
 ❑ INCREASED MYOCARDIAL
CONTRACTILITY (PIO)
❖ Strengthens cardiac peripheral, & kidney
function by enhancing CO, decreasing
preload, improving blood flow to the
periphery & kidneys, decreasing edema, &
promoting fluid excretion.
❖ Result: fluid retention in the lungs 7
extremities is decreased.
❑ DIGOXIN ( a secondary drug for HF)
❖ Digoxin is used to treat heart failure and
abnormal heart rhythms (arrhythmias).
It helps the heart work better and it helps
control your heart rate.
❖ Digoxin does not prolong life. It acts by
increasing the force & velocity of
Myocardium systolic contraction.
❑ 1st LINE DRUGS USED TO TREAT
HF:
1. Intravenous Inotropic Agents
❖ Dopamine

❖ Dobutamine

2. Phosphodiesterase Inhibitors
❖ Milrinone
❑ OTHER DRUGS PRESCRIBED FOR
HEART FAILURE
1. Oral Diuretics
2. Beta blockers
3. ACE Inhibitors
4. ARB’s
5. Calcium Channel Blockers
6. Vasodilators
 ❑ OTHER USES OF CARDIAC
GLYCOSIDES
❑ Atrial Fibrillation
❖ Cardiac dysrhythmia with rapid
uncoordinated contractions of atrial
myocardium.
❑ Atrial Flutter
❖ Cardiac dysrhythmia with rapid
contractions of 200-300 bpm.
When Cardiac Glycosides cannot convert
Atrial Fibrillation to normal heart rhythm, the
goal is to slow the heart rate by decreasing
electrical impulses through the AV node.
 ❑ ATRIAL FIBRILLATION
MANAGEMENT
Calcium Channel Blocker
❖ e.g. verapamil (Calan)

❑ Atrial Fibrillation

May lead to THROMBOEMBOLI

❖ warfarin (Coumadin) is prescribed

concurrently with other drug therapy.

 ❑ NONPHARMACOLOGIC MEASURES
TO TREAT HEART FAILURE
1. Limit salt intake to 2 g/day (1 teaspoon).
2. Decrease alchohol intake (1 drink/day), or
completely avoid it if possible.
3. Avoid smoking
4. Mild exercise
5. Restricting fluids in some conditions.
6. Manage normal BMI
 ❑ LABORATORY TESTS

1. Atrial Natriuretic Hormone/ Peptide

2. Brain Natriuretic Peptide
❑ ATRIAL NATRIURETIC HORMONE/
PEPTIDE
❖ Reference value: 20-77 pg/ml; 20-77
ng/L (SI units)
Elevated ANH/P
❖ May confirm heart failure.
❖ ANH/P, is secreted from the atria of the heart &
acts as antagonist to renin & aldosterone.
❖ It is released during expansion of the atrium,
produces vasodilation, & increase glomerular
filtration rate.
❖ Result: large volume of urine that decreases
BV & BP.
 ❑ BRAIN NATRIURETIC PEPTIDE
❖ Reference Values:
❖ Desired Value: <100 pg/ml
❖ Positive Value: >100 pg/ml
❖ BNP, is primarily secreted from atrial
cardiac cells, & when tested, aids in
diagnosis of heart failure rather than lung
dysfunction.
❖Diagnosing HF is difficult in peron with lung
disease who are experiencing dyspnea, &
in those who are obese or older.
❑ Elevated BNP

❖ Helps differentiate that dyspnea is due to

HF rather than lung dysfunction.

BNP is higher in old aged individual.
❖

However, it is markedly higher in an

individual with HF (i.e. 400 pg/ml).
DIGOXIN
 ❑ PRONE TO DIGITALIS TOXICITY

❖ Older Adults
❑ Cardio Toxicity
❖ Is a serious adverse reaction to Digoxin
❖ Result: Ventricular Dysrhythmias
❑ 3 CARDIAC-ALTERED FUNCTIONS
THAT CONTRIBUTE TO DIGOXIN-
INDUCED VENTRICULAR
DYSRHYTHMIAS
1. Suppression of AV conduction
2. Increased automaticity
3. Decreased refractory period in
ventricular muscle.
 ❑ TREATMENT FOR DIGOXIN INDUCED
VENTRICULAR DYSRHYTHMIAS

1. Antidysrhythmic Phenytoin
2. Lidocane
❖ should be limited to short term

treatment.
 ❑ ANTIDOTE FOR CARDIAC
DIGITALIS GLYCOSIDES
❖ SEVERE DIGITALIS TOXICITY

Antidote: Digoxin Immune Fab (ovine,

Digibind)
❖ Implementation: Signs & symptoms should

be reported immediately.
Serum digoxin levels should be closely
monitored.
❖ Digitalis toxicity may lead result in 1st
degree, 2nd degree, or complete heart
attack.
 ❑ DRUG INTERACTIONS

BEWARE OF:
❖ Drugs with digitalis preparations.

❖ Drugs and/or supplements that decreases

potassium.
❖ Cortisone preparations, taken

systematically.
 ❑ OTHER AGENTS USED TO TREAT
HEART FAILURE
1. Vasodilators
2. ACE Inhibitors
3. ARB’s
4. diuretics (thiazide, furosemide)
5. spironolactone (Aldactone)
6. Some Beta Blockers
❑ VASODILATORS
❖can be used to treat heart failure.

❖decrease venous blood return to the heart,

resulting in a decrease in cardiac filling,

ventricular stretching (preload), & oxygen
demand on the heart.
 ❑ ARTERIOLAR DILATORS ACT IN 3
WAYS
1. To reduce cardiac afterload, which
increases CO.
2. To dilate arterioles of the kidneys,
which improves renal perfusion &
increase fluid loss.
3. Improve circulation to the skeletal
muscles.
 ❑ ACE INHIBITORS
❖ Usually prescribed for HF.
❖ Dilates venules & arterioles, improving
renal blood flow & decreases blood fluid
volume.
❖ It also moderately decrease the release
of aldosterone, which in turn decreases
Na & fluid retention.
Increases K levels, so serum K levels
❖

should be closely monitored, especially

if K-sparring diuretics (e.g.
spironolactone (Aldactone)) are being
taken concurrently.
 ❑ ARB’s

Such as valsartan (Diovan) &

❖

condesartan (Antacand) have been

approved for HF in patients who can’t
tolerate ACE Inhibitors.
 ❑ DIURETICS

❖1st line drug treatment for reducing fluid

volume.
❖They are frequently prescribed with

dogoxin or other agents.

 ❑ Spironolactone (Aldactone)

(Aldactone), a potassium-sparing diuretic, is

❖

used in treating moderate to severe HF.

Aldosterone secretions are increased in HF.
This promotes body loss of potassium and
magnesium needed by the heart and
increases sodium and water retention.
❖With dosage control, beta blockers have
been shown to improve cardiac
performance.
❖ Examples of Beta Blockers that

Improves Cardiac Performance:

1.Carvedilol (Coreg)
2.Metoprolol (Lopressor, Toprol-XL)
3.Bsoprolol (Zebeta)
❖Doses should be low initially and
gradually increased.
❖It may take 1 to 3 months for a

beneficial effect to develop.

 ❑ Nesiritide (Natrecor)
❖It is an atrial natriuretic peptide hormone that
inhibits antidiuretic hormone (ADH) by
increasing urine sodium loss. Its effect in
correcting HF is achieved by promoting
vasodilation, natriuresis, and diuresis.
❖It is useful for treating patients who have acute

decompensated HF with dyspnea at rest or who

have dyspnea with little physical exertion.
 ❑ BiDil
❖ a combination of hydralazine (for BP) and
isosorbide dinitrate (a dilator to relieve heart
pain) has received FDA approval for treating
HF, especially in African Americans. African
Americans have more than twice the rate of
HF as whites, and a research study has
shown this drug to be effective in treating HF
in the African-American population.
ANTIANGINAL DRUGS
❑ Antianginal drugs
❖ are used to treat angina pectoris.
❑ Angina Pectoris
❖ This is a condition of acute cardiac pain
caused by inadequate blood flow to the
myocardium due to either plaque
occlusions within, or spasms of the
coronary arteries.
❖Referred pain felt in the neck and left arm
commonly occurs with severe angina
pectoris.
❖Anginal attacks may lead to MI (heart

attack).
❖Anginal pain usually lasts for only a few

minutes.
 ❑ TESTS THAT MIGHT BE NEEDED
TO DETERMINE CORONARY
ARTERY BLOCKAGE:
1.Stress tests
2.Echocardiogram
3.cardiac profile laboratory tests
4.cardiac catheterization
❑ TYPES OF ANGINA PECTORIS:

1. Classic (stable)
2. Unstable (preinfarction)
3. Variant (Prinzmetal, vasospastic)
❑ Classic (stable)
❖ Occurs with predictable stress or Exertion.

❑ Unstable (preinfarction)

❖Occurs frequently with progressive severity

unrelated to activity; unpredictable regarding

stress/exertion and intensity.
❑ Variant (Prinzmetal, vasospastic)

❖ Occurs during rest.

❑ NONPHARMACOLOGIC MEASURES TO
CONTROL ANGINA
1. Avoid heavy meals
2. Smoking
3. Extreme weather exchange
4. Strenuous exercise
5. Emotional upset
6. Proper nutrition
7. Moderate exercise
❑ PREVENTIVE
MEASURES
1. Adequate rest
2. Relaxation
techniques
 ❑ ANTIANGINAL DRUGS

❖ Antianginal drugs increase blood flow

either by increasing oxygen supply or
by decreasing oxygen demand by the
myocardium.
 ❑ 3 TYPES OF ANTIANGINAL
DRUGS
1. Nitrates
2. Beta Blockers
3. Nitrates
 ❑ NITRATES
❖developed in the 1840s
❖The 1st agents used to relieve angina.

❖It affect coronary arteries and blood vessels in

the venous circulation, which then causes

generalized vascular and coronary vasodilation.
❖This group of drugs reduces myocardial

ischemia but can cause hypotension.

NURSING PROCESS
ANTIDYSRHYTHMIC
DRUGS
 ❑ CARDIAC DYSRHYTHMIAS
❖A cardiac dysrhythmia (arrhythmia) is
defined as any deviation from the normal
rate or pattern of the heartbeat.
❖This includes:

❖Bradycardia

❖Tachycardia

❖Irregular
❑ ECG (ELECTROCARDIOGRAM)
❖An ECG is a record of electrical events
within the heart.
❖It can be used to detect abnormal

heart rates or rhythm, abnormal

conduction pathways, hypertrophy or
atrophy of the heart, and the
approximate location of damaged
cardiac muscle.
 ❑ A NORMAL ECG IS CONSIST OF:
1. P wave (arterial depolarization)
2. QRS complex (ventricular depolarization)
3. T wave (ventricular repolarization)
❑ PQ interval
❖ Atrial contraction occurs
❑ QT interval
❖ during the and the ventricle contract and
relax.
❑ Atrial dysrhythmias
❖ prevent proper filling of the ventricles and
decrease cardiac output by 33%.
❑ Ventricular dysrhythmias
❖ are life-threatening because ineffective
filling of the ventricle and ineffective
pumping results in decreased or absent
cardiac output.
❑ Ventricular Tachycardia
❖ ventricular fibrillation is likely to occur,
followed by death.
❖ Cardiopulmonary resuscitation (CPR)
is necessary to treat these patients.
❑ Cardiac dysrhythmias

❖ frequently follow an MI (heart attack) or

can result from hypoxia, hypercapnia,
thyroid disease, coronary artery disease,
cardiac surgery, excess catecholamines,
or electrolyte imbalance.
❑ CARDIAC ACTION POTENTIALS

❖ Cardiac action potentials are transient

depolarizations followed by
repolarizations of myocardial cells.
 ❑ 5 PHASES OF ACTION POTENTIAL OF A
VENTRICULAR MYOCYTE DURING THE
COURSE OF A HEARTBEAT
1. Phase 0
2. Phase 1
3. Phase 2
4. Phase 3
5. Phase 4
2

DIURETICS
 ❑OBJECTIVES

❖ After completion of this chapter you will

be able to:
❖ Compare the action and uses of
thiazide, loop, and potassium-sparing
diuretics.
❖Differentiate side effects and adverse
reactions related to thiazide, loop, and
potassium-sparing diuretics.
❖Apply the nursing process for the

patient taking thiazide, loop, and

potassium-sparing diuretics.
 ❑ DIURETICS
❖ Two main purposes: to decrease
hypertension and to decrease fluid
retention o edema (peripheral and
pulmonary) in heart failure and renal
or liver disorders.
Work by reducing the ability of the
❖

kidney to reabsorb salt and water from

the urine and into the body thereby
increasing the production and output of
urine (diuresis).
❖ Sodium and water reabsorption occur
throughout the renal tubular segments.
❖ Every 1 and half hours, our body’s total
volume of extracellular fluid (ECF)
goes through the part of the kidneys
called glomeruli for cleansing - the
first process for urine formation.
❖ Glomeruli - small particles such as
electrolytes, drugs, glucose, and
waste products from protein
metabolism are filtered
❖Normally 99% of the filtered sodium that
passes through the glomeruli is
reabsorbed;
❖ 50% to 55% of sodium reabsorption

occurs in the proximal tubules.

❖ 35% to 40% in the loop of Henle.
❖ 5% to 10% in the distal tubules.
❖ <3 in the collecting tubules .
Diuretics that act on the tubules closest
❖

to the glomeruli have the greatest

effect in causing natriuresis – increase
sodium excretion in the urine.
Diuretics have an antihypertensive
❖

effect it promotes sodium and water

loss by blocking sodium and chloride
reabsorption that causes a decrease in
fluid volume and lowering blood
pressure.
Many diuretics cause the loss of other
❖

electrolytes, including potassium,

magnesium, chloride, and bicarbonate.
The diuretics that promote potassium
excretion are classified as potassium-
wasting diuretics and the diuretics that
promote potassium retention is called
potassium -sparing diuretics
❑ Five categories of diuretics:
❖Thiazide and thiazide-like
❖ Loop or high-ceiling

❖Osmotic

❖ Carbonic anhydrase inhibitor

❖Potassium-sparing
 ❑ THIAZIDES AND THIAZIDE-
LIKE DIURETICS
❖Act on the distal convoluted renal
tubule, to promote sodium, chloride, and
water excretion.
❖Used to treat hypertension and

peripheral edema.
❖Not effective for immediate diuresis and
should not be used to promote fluid loss
in patients with severe renal
dysfunction.
❖Used primarily for patients with normal

renal function
❖Moderately potent diuretics and most
frequently prescribe
❖Thiazide cause a loss of sodium,

potassium, and magnesium, but it

promotes calcium reabsorption and also
affect glucose tolerance that may result
to;
❖Hypercalcemia - a higher than normal
level of calcium in the blood.
❖Hyperglycemia – a elevated level of

sugar glucose in the blood (high blood

sugar).
❖ Thiazides are divided into three groups,
according to their duration of action:
short-acting, intermediate-acting, and
long-acting.
❑ Table 43 – 1 DIURETICS
 ❑ Hydrochlorothiazide

❖ Hydrochlorothiazide has been

combined with selected angiotensin-
converting enzyme ACE inhibitors,
beta-blockers, alpha-blockers,
angiotensin II blockers, and centrally
acting sympatholytic to control
hypertension.
❑ PROTOTYPE DRUG CHART 43-1
 ❑ Side Effects and Adverse
Reactions
❖ Side effects and adverse reactions of
thiazides include electrolyte
imbalances;
❖Hypokalemia (low serum potassium)
❖Hypercalcemia (elevated serum

calcium)
❖Hypomagnesemia (low serum

magnesium)
❖Bicarbonate loss
❖Hyperglycemia (elevated blood sugar)
❖Hyperuricemia (elevated serum uric acid

level)
❖Hyperlipidemia (elevated blood lipid

level)
❖ Other side effects include:
dizziness, headache, nausea,
vomiting, constipation, urticaria, or
hives (rare), and blood dyscrasias
(rare).
 ❑ Contraindications
❖Thiazides are contraindicated for use in
renal failure (hepatic disease).
❖Patient who has symptoms of severe

kidney impairment or shutdown .

 ❑ Nursing Process:
Assessment before administering the drug

❖ Assess vital signs, weight, urine output,

and serum chemistry values (electrolytes,
glucose, uric acid) for baseline levels.
❖Check peripheral extremities for
presence of edema.
❖Obtain a history of drugs and herbal

supplements taken daily.

 ❑ Implementation
Administered oral diuretics in the
❖

morning to avoid nocturia (nighttime

urination) and sleep interruption.
❑ Assessment after administering
the drug
❖Assess and monitor daily the fluid status,
BP, pulse and any signs of electrolyte
imbalance.
❖Signs and symptoms of hypokalemia and

serum potassium levels.

❖Serum calcium and uric acid levels.
❖Signs and symptoms of digitalis toxicity

(bradycardia, nausea, vomiting, visual

changes).
❑ LOOP (HIGH CEILING) DIURETICS
❖Used in the treatment of edema due to
heart failure, liver disease and kidney
disease.
❖Work by inhibiting the sodium-potassium-

chloride co-transporter in the thick

ascending loop of Henle .
❖Loop diuretics have a great saluretic
(sodium chloride–losing) or natriuretic
(sodium-losing) effect and can cause rapid
diuresis, decreasing vascular fluid volume
and causing a decrease in cardiac output
and blood pressure.
❖The most potent diuretics.
❖The onset of action of loop diuretics
occurs within 30 to 60 minutes
❖Loop diuretics should not be prescribed if

a thiazide could alleviate body fluid

excess.
❑ Prototype Drug Chart 43-2
Furosemide
❖ Furosemide- is a frequently
prescribed diuretic for patients whose
creatinine clearance is less than
30/min and for those with end-stage
renal disease.
 ❑ Side Effects and Adverse
Reactions
Adverse effects for loops diuretics
❖

typically occur from electrolyte

imbalances secondary to the diuresis
effects which include: hypokalemia,
hyponatremia, hypocalcemia,
hypomagnesemia, and hypochloremia.
❑ Table 43-3 lists the physiologic and
laboratory changes associated with
loop diuretics.
 ❑ OSMOTIC DIURETICS
❖Increase the osmolality (concentration)
and sodium reabsorption in the proximal
tubule and loop of Henle.
❖Sodium, chloride, potassium (to a lesser

degree), and water are excreted.

Used to prevent kidney failure, to
❖

decrease intracranial pressure (ICP)

(e.g., in cerebral edema), and to
decrease intraocular pressure (IOP)
(e.g., in glaucoma).
 ❑ Mannitol
Mannitol elevates blood plasma
❖

osmolality, resulting in enhanced flow of

water from tissues, including the brain
and cerebrospinal fluid, into interstitial
fluid and plasma.
❖A potent osmotic potassium-wasting
diuretic frequently used in emergency
situations such as ICP and IOP.
❖Most frequently prescribed osmotic

diuretic.
❑ Table 43-4 DIURETICS: LOOP,
OSMOTICS, AND CARBONIC
ANHYDRASE INHIBITORS
 ❑ Side Effects and Adverse Reactions

The side effects and adverse reactions of

❖

mannitol include: fluid and electrolyte

imbalance, pulmonary edema from rapid
shift of fluids, nausea, vomiting, tachycardia
from rapid fluid loss, and acidosis.
 ❑ Contraindications

❖Mannitol must be given with extreme

caution to patients who have heart disease
and HF.
❖It should be immediately discontinued if the

patient develops HF or renal failure.

 ❑ CARBONIC ANHYDRASE
INHIBITORS
The carbonic anhydrase inhibitors block
❖

the action of the enzyme carbonic

anhydrase, which is needed to maintain
the body’s acid-base balance (hydrogen
and bicarbonate ion balance).
❖Inhibition of this enzyme causes
increased sodium, potassium, and
bicarbonate excretion.
❖Used primarily to decrease IOP in

patients with open-angle (chronic)

glaucoma and not used in narrow-angle
or acute glaucoma.
Other uses include diuresis,
❖

management of epilepsy, and treatment

of high-altitude or acute mountain
sickness.
❑ Side Effects and Adverse Reactions

❖Can cause fluid and electrolyte

imbalance, metabolic acidosis, nausea,
vomiting, anorexia, confusion,
orthostatic hypotension, and crystalluria.
 ❑ Contraindications

Should not be used in patients with

❖

hepatic disease, such as cirrhosis or

impaired hepatic function.
 ❑ POTASSIUM-SPARING
DIURETICS
Used as mild diuretics or in combination
❖

with another diuretic (e.g.,

hydrochlorothiazide, antihypertensive
drugs).
❖To prevent low levels of potassium
(hypokalemia) occurring when other
diuretics are used
❖Act primarily in the collecting duct renal

tubules and late distal tubule to promote

sodium and water excretion and
potassium retention.
 ❑ Spironolactone (Aldactone)

An aldosterone antagonist it blocks the

❖

action of aldosterone and inhibits the

sodium potassium pump (i.e., potassium is
retained and sodium is excreted).
❖It prevents our body from absorbing too
much salt and keeps your potassium
levels from getting too low.
❖Used to treat heart failure, hypertension,

or hypokalemia.
❑ Prototype Drug Chart 43-3
Spironolactone.
NOTE: Spironolactone, amiloride,
triamterene, and eplerenone should not
be taken with ACE inhibitors and
angiotensin II receptor blockers (ARBs)
because they can also increase serum
potassium levels.
❑ TABLE 43-5 DIURETICS:
POTASSIUM-SPARING
❑ Side Effects and Adverse Reactions

❖The main side effect of these drugs is

hyperkalemia (increased levels of
potassium in the blood).
❖Caution must be used when giving

potassium-sparing diuretics to a patient

with poor renal function.
GI disturbances (anorexia, nausea,
❖

vomiting, diarrhea, and numbness and

tingling of the hands and feet) can
occur.
 3

ANTIHYPERTENSIVES
 ❑ OBJECTIVES:
❖Differentiate the pharmacologic action of the
various categories of antihypertensive
drugs.
❖Compare the side effects and adverse

reaction to sympatholytics, direct acting

vasodilators, and angiotensin antagonists.
❖Apply the nursing process related to
antihypertensives including nursing
interventions and teaching.
❖Describe the blood pressure guidelines

for determining hypertension.

 ❑ HYPERTENSION
❖ Is an increase in blood pressure such that
the systolic pressure is greater than 140
mm Hg and the diastolic pressure is greater
than 90 mm Hg.
❖Essential Hypertension- is the most

common type, affecting 90% of persons

with high blood pressure.
Exact origin of hypertension cases are
❖

related to renal and disorders and are

classified as Secondary hypertension.
 ❑ SELECTED REGULATORS OF
BLOOD PRESSURE

Kidneys and blood vessels strive to

❖

regulate and maintain a “normal" blood

pressure.
Other hormones that contribute to blood
❖

pressure regulation are anti diuretics

hormone (ADH), Arterial natriuretic
peptide (ANP) hormone, and brain
natriuretic peptide (BNP) hormone.
ADH – is produced by the
❖

hypothalamus and is stored and release

by the posterior pituitary gland
(Neurohypophysis).
 ❑ PHYSIOLOGIC RISK FACTORS
❖Physiologic risk factors contribute to
hypertension.
Such as:
❖ A diet high in saturated fat and simple

carbohydrates can increase blood

pressure.
❖Alcohol increases renin secretion causing
the production of angiotensin II
❖Obesity affects the Sympathetic and

cardiovascular system by increasing cardiac

output, stroke volume, and left ventricular
filling.
 ❑ CULTURAL RESPONSES TO
ANTIHYPERTENSIVE AGENTS
❖African American are more likely to develop

hypertension at an earlier age than white

Americans.
❖They also have a higher mortality rate from

hypertension than the white population.

Antihypertensive drugs that are
❖

effective for Americans are Alpha

blockers and calcium channel blockers
(Calcium blockers).
 ❑ HYPERTENSION IN OLDER ADULTS

By 65 years of age, 26% of men and 30%

❖

of women are hypertensive. Between 65 &

75 years of age, 30% of men, and 45% of
women are hypersensitive. Both systolic
and diastolic hypertension are associated
with increased cardiovascular morbidity and
mortality.
Orthostatic (Pastural) hypertension is
❖

one of the troublesome side effects of

antihypertensive agents in adults
especially Frail or institutionalized
person.
This includes restricting dietary sodium
❖

to 2400 mg daily, avoiding tobacco,

modifying diet, exercising, and
decreasing stress.
 ❑ NONPHARMACOLOGIC CONTROL
OF HYPERTENSION

A sufficient decrease in blood pressure

❖

can be accomplished by nonpharmacologic

methods.
Nondrug methods to decrease blood
❖

pressure include stress-reduction

technique, exercise, salt restriction,
decrease alcohol ingestion, and
smoking cessation.
Nonpharmacologic method should be
❖

combined with antihypertensive drugs to

control hypertension.
 ❑ GUIDELINES OF HYPERTENSION
Blood pressure guidelines for determining
❑

hypertension have been revised and are

contained in the Seventh Report of the Joint
National Committee on Prevention,
Detection, Evaluation, and Treatment of
High Blood Pressure, or JNC 7.
❖Normal blood pressure is less than 120/80
mm Hg.
❖Prehypertension defined as systolic blood

pressure (SBP) of 120 to 139 and diastolic

blood pressure (DBP) of 80 to 89.
❖Stage 1. Hypertension falls between 140/90
and 159/99.
❖Stage 2. Hypertension is 160/100 or

greater.
According to JNC 7 (Joint National
❖

Committee), if the blood pressure is greater

than 20/10 mm Hg above goal, a drug
regimen should be started.
 ❑ PHARMACOLOGIC CONTROL OF
HYPERTENSION
❖An individual approach to the treatment of
hypertension is used by many health care
providers.
❖All drugs are considered “initial agents"

when first prescribed for hypertension.

❖Antihypertensive drug, used either singly or
in combination with other drugs, are
classified into six categories:
1. Diuretics
2. Sympatholytics (Sympathetic
depressants)
3. Direct-acting arteriolar
vasodilators
4. ACE inhibitors
5. Angiotensin II receptor blockers
(ARBs)
6. Calcium channel blockers
 1.DIURETICS
❖ Promote sodium depletion, which
decreases extracellular fluid volume
(ECFV).
❖ Diuretics are effective as first line drug
for treating mild hypertension.
❖ Diuretics examples:
Hydrochlorothiazide diuretics,
Thiazide diuretics, Loop (high-
ceiling) diuretics.
 2. Sympatholytics (Sympathetic
depressants)
❖ Sympatholytics comprise five groups of

drugs:
1. Beta adrenergic blockers
2. Centrally acting Alpha, agonist
3. Alpha-adrenergic blockers
4. Adrenergic neuro blockers
(Peripherally acting sympathologic)
5. Alpha and beta, adrenergic
blockers
 ❑ BETA-ADRENERGIC BLOCKERS

❖Frequently called “Beta Blockers”, are

used as antihypertensive drugs or in
combination with a diuretics.
❖Beta blockers reduce heart rate,

contractility, and renin release

Types of Beta blockers

❖ Nonselective beta blockers: Propranolol

(Inderal), and Carvedilol (Coreg) inhibit
beta1, (heart) and beta2 (bronchial)
receptor.
Cardioselective beta blockers- block beta
❖

receptors. Acebutolol (Sectral) l, Atenolol

(Tenormin), Betaxolol (Kerlone), Bisoprolol
(Zebeta), Metoprolol (Lopressor).
❖The real value of beta selectivity is in
maintaining renal blood flow and minimizing
the hypoglycemic effects of beta blockage.
❖Beta blockers should not be used by

patients with second or third degree

atrioventricular (AV) block or sinus
bradycardia.
Noncardioselective beta blockers such
❖

as propranolol (Inderal) should not be

given to a patient with chronic
obstructive pulmonary disease (COPD).
❖Onset of action usually 30 minutes or less,
and the duration of action is 6 to 12 hours.
❖Peak time is 20 minutes compared with 1.5

hours orally and duration of action is 4 to 10

hours.
 ❑ Side effects and adverse reaction

❖Decrease pulse rate

❖Decrease blood pressure (and with

noncardioselective beta and beta blockers)

bronchospasm.
❖Infraction of rebound hypertension, angina,
dysrhythmias, and myocardial infraction.
❖Beta blockers can cause insomnia,

depression, fatigue, nightmare, and sexual

dysfunction.
 ❑ Antihypertensive: Beta Blockers
Nursing Process:
Assessment
❖ Obtain a medication and herbal history
from patient.
❖ Obtain vital signs. Report abnormal blood
pressure and bradycardia. Compare vital
signs baseline finding.
Check laboratory values related to renal
❖

and liver function periodically

.
 ❑ Nursing diagnosis

❖Decrease cardiac output related to

variations in blood pressure readings.
❖Noncompliance with drug regimen related

to cost of multiple drugs ordered.

❖Sexual dysfunction related to side effect
of beta blockers.
❖Deficient knowledge related to

inexperience with beta blockers.

 ❑ Nursing planning

❖Patient’s blood pressure will be decreased

or will return to normal value
❖Patient states he or she will take medication

as prescribed.
❖Patient will verbalize importance of

following beta blockers regimen.

 ❑ Nursing intervention
❖Monitor vital signs, especially blood
pressure and pulse.
❖Monitor laboratory results, especially BUN,

serum creatinine, AST, and LDH.

 ❑ Evaluation

❖Evaluate effectiveness of drug therapy(

decreased blood pressure, absence of side
effects).
❖Determine that patient adheres to drug

regimen.
 ❑ CENTRALLY ACTING APLHA,
AGONISTS

❖Centrally acting alpha, agonist decrease

the sympathetic response from the
brainstem to the peripheral vessels.
They stimulates the aloha receptors, which
❖

decreases Sympathetic activity: Increase

vagus activity, decrease cardiac output, and
decrease serum epinephrine,
norepinephrine, and renin release.
Drugs example: Methyldopa, clonidine
❖

and guanfacine.
 ❑ Side effects and adverse reaction

❖Drowsiness
❖Dry mouth

❖Dizziness

❖Slow heart rate (bradycardia)

❑ ALPHA-ADRENERGIC BLOCKERS
This group of drugs blocks the alpha-
❖

adrenergic receptors (Alpha blockers),

resulting in vasodilation and decreased
blood pressure.
❖Useful in treating hypertension in patients
with lipid abnormalities.
❖Selective alpha-adrenergic are: (Prazosin,

Terazosin, and doxazosin) are mainly used

to produce blood pressure and can be used
to treat benign prostatic hypertrophy.
Pharmacokinetics-Prazosin is highly
❖

protein bound and when it is given with

other highly protein bound drugs, the
patient should be assessed for adverse
reactions.
❖ Pharmacodynamics- Selective alpha-
adrenergic blockers dilate the arterioles
and venules, decreasing peripheral
resistance and lowering blood pressure.
 ❑ Side effects and adverse reaction
❖ Orthostatic hypotension
❖ Dizziness
❖ Faintness
❖ Light headedness
❖ Increase heart rate, which may occur
with first dose
❖ Nausea
❖ Headache
❖ Drowsiness
❖ Nasal congestion caused by
vasodilation
❖ Edema
❖ Weight gain
 ❑ Side effects of phenlolamine
❖ Hypotension
❖ Reflex tachycardia caused by the
severe decrease in blood pressure
❖ Nasal congestion caused by
vasodilation and GI disturbances.
 ❑ Drug interaction

Occur when alpha adrenergic blockers are

❖

taken with anti inflammatory drugs and

nitrates. ( Nitroglycerin for angina)
 ❑ ANDRENERGIC NEURO BLOCKERS
(PERIPHERAL ACTING
SYMPTHOLYTICS)
❖Adrenergic neuro blockers are potent

antihypertensive drugs that block

norepinephrine release from the
sympathetic nerve ending, causing
decrease in norepinephrine release that
results in lowering of blood pressure
❖ The most potent drug is Reserpine
❖ Adrenergic neuro blockers are
considered the last choices for
treatment of chronic hypertension
Example of alpha1 and beta1 blocker is
❖

Labetalol (Normodyne)
❖ Common side effects of these drug
are:
❖ Orthostatic hypotension
❖ GI disturbance
❖ Nervousness
❖ Dry mouth
❖ Fatigue
 ❑ Nursing process

Assessment
❖ Obtain a medication history from patient,
including current drugs.
❖ Obtain baseline vital signs and weight for
future comparison.
Check urinary output. Report if it is
❖

decreased (less than 600 mL/day),

because drug is contraindicated if renal
disease is present
 ❖ Nursing diagnosis

❖ Risk for activity intolerance related to drug

regimen and/or cardiac status.
❖ Deficient knowledge related to drug
regimen.
❖ Ineffective sexuality pattern related to beta-
blocker or other drug Therapy.
 ❑ Planning

❖ Patient’s blood pressure will decrease.

❖ Patient will follow proper drug regimen.
 ❖ Nursing interventions

Monitor vital signs. Desired therapeutic effect

❖

of prazosin may not fully occur for 4 weeks.

Sudden marked decrease in blood pressure
and tachycardia should be reported.
❖ Check daily for fluid retention in
extremities and weight gain. Prazosin
may cause sodium and water
retention.
 ❑ Evaluation
❖ Evaluate effectiveness of drug in
controlling blood pressure; side effects
should be absent.
❖ Evaluate patient’s adherence to
medication schedule.
❖ Evaluate patient’s knowledge of
medication.
 3. DIRECT-ACTING ARTERIOLAR
VASODILATORS
❖ Act by relaxing the smooth muscles of
blood vessels, mainly the arteries, causing
vasodilation.
❖ Vasodilators are potent antihypertensive
drug.
Two direct-acting vasodilators: Hydralazine
and Minoxidil.
❖ Beta blockers are frequently prescribed

with arteriolar vasodilators to decrease the

heart rate.
Also Nitroprusside is very potent
❖

vasodilators that rapidly decrease blood

pressure.
 ❑ Side effects and adverse reaction
❖ Effects of hydralazine are: Reflex
tachycardia, palpitations, edema, nasal
congestion, headache, dizziness, GI
bleeding, lupus-like symptoms, and
neurologic symptoms (Tingling,
Numbness).
❖Effects of Minoxidil: Tachycardia, edema,
and excess hair growth
❖Nitroprusside can cause: Tachycardia,

palpitations, restlessness, agitation,

nausea, and confusion.
4. ANGIOTENSIN-CONVERTING ENZYME
INHIBITORS (ACE INHIBITORS)
❖ ACE inhibitors inhibit ACE, which in turn

inhibits the formation of angiotensin II

(vasoconstrictor) and blocks the release of
aldosterone.
❖These drugs can be used in patients
who have elevated serum renin levels.
❖ACE inhibitors are used primarily to

heart hypertension; also effective in

treating heart failure.
ACE inhibitors are: Benazepril (lotensin),
❖

Captopril (capoten), Enalapril maleate

(vasulec), Fosinopril (monipril), Lisinopril
(prinivil,Zestril), Moexipril (univasc),
Perindopril (acean), Quinapril (accupril),
Ramipril (Atlace), Trandolapril (mavik).
 ❑ Side effects and adverse reaction

❖ Primarily side effects of the ACE inhibitors

is constant, irritated cough.
❖ Others: Nausea, vomiting, diarrhea,
headache, dizziness, fatigue, insomnia,
serum potassium excess (hyperkalemia),
tachycardia
Effect of angiodema are: swelling face,
❖

tongue, lips, mucus membranes, larynx,

extremity edema
 ❑ Nursing process

Assessment
❖ Check laboratory values sings for serum
protein, albumin, blood urea nitrogen
(BUN) , Creatinine, potassium, and white
blood cell count, and compare with future
serum levels.
 ❑ Nursing diagnosis

❖ Deficient knowledge related to drug

regimen.
❖ Anxiety related to hypertensive state.
❖ Risk for falls related to orthostatic
hypotension .
 ❑ Planning

Patient will be free from moderate to severe

❖

side effects. Angioedema, cough,

dysgeusia, weakness, hyperkalemia,
orthostatic hypotension, and renal
impairment may occur as side effects.
 ❑ Nursing intervention

Monitor laboratory tests related to renal

❖

function (BUN, creatinine, protein) and blood

glucose levels. Caution: watch for
hypoglycemic reaction in patients with
diabetes mellitus . Urine may be checked in
the morning using a dipstick.
Report to health care provider occurrences
❖

of bruising, petechiae, and/or bleeding.

These may indicate a severe adverse
reaction to an angiotensin antagonist such
as captopril.
 ❑ Evaluation

❖Evaluate effectiveness of drug Therapy

(absence of severe side effects, blood
pressure return to desired range).
❖ valuate patient’s renal function.
 5.ANGIOTENSIN II RECEPTOR
BLOCKERS

❖ Similar to ACE inhibitors in that way they

prevent the release of aldosterone
(sodium retaining hormone)
❖ARBs cause vasodilation and decrease
peripheral resistance.
❖Example of ARBs: Losartan (cozaar),

Valsartan (diovan), Irbesartan (Avapro),

Candesartan cilexetil (atacand),
Telmesartan (micardis).
 ❑ Pharmacokinetics
❖Valsartan prescribed primarily to manage
hypertension.
❖The combination drug diovan HCT contains

valsartan plus a low dose of

hydrochlorothiazide.
❖The half-life is 6 to 9 hours.
❖Drug excreted in urine and feces.
 ❑ Pharmacodynamics

❖Valsartan is potent vasodilator it blocks the

binding of angiotensin II to the AT, receptor
found in many tissues.
❖Peak time is 4 to 6 hours

❖Long duration action is 24 hours

 ❑ Direct renin inhibitor

❖The first FDR approved direct renin inhibitor

for treating hypertension is Aliskiren
(Tekturna)
❖Aliskiren binds with renin, causing a

reduction of angiotensin II and aldosterone

levels.
 6.CALCIUM CHANNEL BLOCKERS
❖ Calcium channel blockers, also called
“Calcium antagonist and calcium
blockers”, block the calcium channel in
the VSM, promoting vasodilation
❖Calcium blockers are highly protein bound
but have a short half-life.
❖Slow calcium channel are found in the

myocardium (heart muscle) and vascular

smooth muscle (VSM) cells.
 ❑ 3 Groups of Calcium Blockers

Diphenylalkylarine (verapamil)- is used

❖

to treat chronic hypertension, angina

pectoris, and cardiac dysrhythmias.
Benzothiazepines (diltiazem -
❖

verapamil and diltiazem act on the

arterioles and the heart.
Dihydropyridine (amlodipine)- are the
❖

largest group of calcium channel

blockers and consist of seven drugs, six
of these are used to control
hypertension.
❖Calcium blocker nimodipine- is used to
prevent ischemic brain injury due to
vasospasm that often accompanies
subarachnoid hemorrhage.
❖Nifedipine (procardia)- decreased blood

pressure in order adults and in those with

low serum renin values.
 Nifedipine and verapamil are potent
calcium blockers.
❖ Pharmacokinetics- Amlodipine

(Norvasc) highly protein bound and it

absorbed by GI tract.
❖Pharmacodynamics- Amlodipine may
be used alone or with other
antihypertensive drugs.
❖ This drug has a long duration of
action, so it is prescribed only once a
day.
 ❑ Side effects and adverse reaction

❖ Dizziness
❖ Drowsiness
❖ Cough (rare)Blurred vision
❖ Headache
❖ Diarrhea
❖ Insomnia
❖ Arthralgia, fatigue
 ❑ Reactions:

❖ Orthostatic hypertension
❖ Hypoglycemia
❖ Hyperkalemia
❖ Life threatening
❖ Renal dysfunction
4
ANTICOAGULANTS,
ANTIPLATELETS, &
THROMBOLYTIC
 ❑ OBJECTIVES
❖ Compare the action for anticoagulants,
antiplatelets, and thrombolytics.
❖ Differentiate the side effects and adverse

reactions of anticoagulants, antiplatelets, and

thrombolytics.
Apply the nursing process, including
❖

patient teaching, for anticoagulants.

 ❑ ANTICOAGULANTS

Anticoagulants are used to inhibit clot

❖

formation. Unlike thrombolytics, they do not

dissolve clots that have already formed, but
rather act prophylactically to prevent new
clots from forming.
Anticoagulants are used in patients with
❖

venous and arterial disorders that put

them at high risk for clot formation.
Venous problems include deep vein
thrombosis (DVT) and pulmonary
embolism, and arterial problems include
coronary thrombosis, or myocardial
infarction;
presence of artificial heart valves; and
cerebrovascular accidents (CVAs, or
stroke). Anticoagulants are administered
orally or parenterally.
 ❑ HEPARIN
Heparin, introduced in 1938, is a natural
❖

substance in the liver that prevents clot

formation. It was first used in blood transfusions
to prevent clotting. Heparin is indicated for rapid
anticoagulant effect when a thrombosis occurs
because of a deep vein thrombosis (DVT),
pulmonary embolism (PE), or an evolving
stroke.
Heparin is also used in open-heart
surgery to prevent blood from clotting
and in the critically ill patient with
disseminated intravascular coagulation
(DIC).
Heparin combines with antithrombin III,
which accelerates the anticoagulant cascade
of reactions that prevents thrombosis
formation. By inhibiting the action of
thrombin, conversion of fibrinogen to fibrin
does not occur and the formation of a fibrin
clot is prevented.
❖ Because heparin is poorly absorbed
orally, it is given subQ for prophylaxis or
IV to treat acute thrombosis. It can be
administered as an IV bolus or in IV fluid
for continuous infusion.
Heparin prolongs clotting time. Partial
❖

thromboplastin time (PTT) and activated

partial thromboplastin time (aPTT) are
laboratory tests used to detect deficiencies
of certain clotting factors, and these tests
are used to monitor heparin therapy.
Heparin can decrease the platelet count,
causing thrombocytopenia. If hemorrhage
occurs during heparin therapy, the
anticoagulant antagonist protamine sulfate
is given IV.
Protamine sulfate can be an anticoagulant,
but in the presence of heparin, it is an
antagonist to reverse the action of heparin.
Before discontinuing heparin, oral therapy
with warfarin therapy is begun.
 ❑ LOW MOLECULAR WEIGHT
HEPARIN

These derivatives of standard heparin were

❖

introduced to prevent venous

thromboembolism.
Studies have shown that by extracting only
the low–molecular-weight fractions of
standard heparin through depolymerization,
the equivalent of anticoagulation can be
achieved with a lower risk of bleeding.
Low–molecular-weight heparins (LMWHs)
produce more stable responses at
recommended doses.As a result, frequent
laboratory monitoring of aPTT is not
required, because LMWH does not have the
standard effect of heparin.
Heparin prevents coagulation by combining
with Antithrombin III to inactivate factor Xa
and thrombin. Low–molecular-weight
heparin inactivates the Xa factor, but it is
less able to inactivate thrombin.
❑ There are examples of LMWHs
include enoxaparin sodium
(Lovenox) and dalteparin sodium
(Fragmin).
The anticoagulant fondaparinux
❖

(Arixtra)is a synthetically engineered

antithromboticdesigned to be effective as a
once-daily subcutaneous injection.
Categorized as a selective Factor Xa
inhibitor, fondaparinux is closely related in
structure to heparin and LMW heparins and
is used for the same purposes.
❖ These agents are most commonly
prescribed to prevent DVT and acute
pulmonary embolism after orthopedic or
abdominal surgery. Hip- and knee-
replacement anticoagulant therapy often
includes enoxaparin, and abdominal
surgery includes dalteparin.
The drugs can be administered at home,
because aPTT monitoring is not
necessary, whereas heparin must be given
in the hospital. LMWHs are administered
subQ once or twice a day, depending on
the drug or drug regimen, and are
available in prefilled syringes with attached
needles.
The patient or family member is taught how
to administer the subQ injection, which is
usually given in the abdomen. The average
treatment period lasts 7 to 10 days.
The LMWH is usually started in the
❖

hospital within 24 hours after surgery.

The half-life of LMWHs is two to four
times longer than that of heparin.
Patients should be instructed not to take
antiplatelet drugs such as aspirin while
taking LMWHs or
heparin.
Bleeding because of LMWH use is less
likely to occur than when heparin is given.
LMWH overdose is rare; if bleeding
occurs, protamine sulfate is the
anticoagulant antagonist used.
The dosage is 1 mg of protamine sulfate
for every 100 units of unfractionated
heparin or LMWH given.
 ❑ Contraindications
The LMWHs are contraindicated for
❖

patients with strokes, peptic ulcers, and

blood anomalies. These drugs should not
be given to patients having eye, brain, or
spinal surgery.
❑ Direct Thrombin Inhibitors:
Parenteral Anticoagulants II
❖Parenteral anticoagulants directly inhibit
thrombin from converting fibrinogen to fibrin.
These drugs differ from heparin-like
anticoagulants. Three of these drugs are
given intravenously: argatroban (Acova),
bivalirudin (Angiomax), and lepirudin
(Refludan).
Bivalirudin binds with and inhibits free-
❖

flowing thrombin. The fourth drug,

desirudin (Iprivask), is administered
subcutaneously. Dabigatran (Pradaxa) is an
oral anticoagulant that does not require
routine coagulation monitoring. These drugs
are more expensive than the other
anticoagulants.
❑ ANTICOAGULANTS ORAL
ANTICOAGULANTS
Warfarin (Coumadin) is an oral
❖

anticoagulant from the coumarin drug

family. Oral anticoagulants inhibit hepatic
synthesis of vitamin K, thus affecting the
clotting factors II, VII, IX, and X.
Warfarin is used mainly to prevent
thromboembolic conditions such as
thrombophlebitis, pulmonary embolism, and
embolism
formation caused by atrial fibrillation, which
can lead to stroke (CVA).
Oral anticoagulants prolong clotting time
and are monitored by the prothrombin time
(PT), a laboratory test that measures the
time it takes blood to clot in the presence of
certain clotting factors, which warfarin
affects.
This laboratory test is usually performed
immediately before administering the
next drug dose until the therapeutic level
has been reached.
❖ Warfarin (Coumadin) half-life and very
long duration. Drug accumulation can
occur and lead to external or internal
bleeding, so the nurse must observe for
petechiae, ecchymosis, tarry stools, and
hematemesis and teach the patient to do
the same at home.
❖ The Antidote for warfarin overdose is
Vitamin K, but it takes 24 to 48 hours to
be effective. Usually a low dose of oral
Vitamin K may be recommended for
patients with an INR of 5.5.
If excessive Vitamin K is given, it may take
warfarin 1 to 2 weeks before it can be
effective again. For acute bleeding, fresh
frozen plasma is.
 ❑ Side Effects and Adverse Reactions.

❖ Bleeding (hemorrhage) is the major

adverse effect of warfarin. Patients should
be monitored closely for signs of bleeding
(e.g., petechiae, ecchymosis,
hematemesis). Laboratory testing of PT or
INR should be scheduled at recommended
intervals.
 ❑ Interactions
Aspirin, nonsteroidal anti-inflammatory drugs
❖

(NSAIDs), other types of anti-inflammatory

drugs, sulfonamides, phenytoin (Dilantin),
cimetidine (Tagamet), allopurinol (Zyloprim),
and oral hypoglycemic drugs for diabetes
can displace warfarin from the protein-
bound site, causing more free circulating
anticoagulant.
Numerous other drugs also increase the
action of warfarin, and bleeding is likely to
occur. Acetaminophen (Tylenol) should be
used instead of aspirin by patients taking
warfarin.
For frank bleeding resulting from excess free
drug, parenteral vitamin K is given as a
coagulant to decrease bleeding and promote
clotting. However, caution must be used with
this approach, because the prothrombin can
remain depressed for prolonged periods.
Xa Inhibitor: Oral Anticoagulants. Two new
oral anticoagulants form a new anticoagulant
category called Xa inhibitors. Rivaroxaban
(Xarelto) was FDA approved in July 2011, and
apixaban (Eliquis) was FDA approved in
December 2012.
These drugs do not require routine
coagulation monitoring and are given
once or twice daily.
 ❑ Nursing Process
Patient-Centered Collaborative Care
Anticoagulants: Warfarin and Heparin
❖ Assessment

Obtain a history of abnormal clotting or health

problems that affect clotting, such as severe
alcoholism or severe liver or renal disease.
Warfarin is contraindicated for patients with
blood dyscrasias, peptic ulcer,
cerebrovascular accident (CVA), hemophilia,
or severe hypertension. Use with caution in
patients with acute traumatic injury.
Gather a drug and herbal history of current
❖

drugs and herbs patient takes. Report if drug-

drug or drug-herbal interaction is probable.
Warfarin is highly protein-bound and can
displace other highly protein-bound drugs, or
warfarin could be displaced, which may result
in bleeding.
❖Develop a flowchart that lists prothrombin
time (PT) or international normalized ratio
(INR) and warfarin dosages. A baseline PT
or INR should be obtained before warfarin
is administered.
 ❑ Nursing Diagnoses

❖Risk for injury related to bleeding due to

adverse effect of heparin or warfarin
❖ Deficient knowledge related to lack of

previous exposure to side effects of

anticoagulants and their action.
 ❑ Nursing Interventions

Monitor vital signs. An increased pulse rate

❖

followed by a decreased systolic pressure

can indicate a fluid volume deficit resulting
from external or internal bleeding.
Monitor PT or INR for warfarin (Coumadin)
❖

and a PTT for heparin before administering

anticoagulant. PT should be 1.25 to 2.5
times control level or INR 2 to 3, except for
prosthetic heart valves (up to INR 3.5).
Monitor platelet count (anticoagulants can
decrease platelet count).
Examine patient’s mouth, nose (epistaxis),
❖

urine (hematuria), and skin (petechiae,

purpura) for bleeding. Watch older adults
closely for bleeding; their skin is thin, and
capillary beds are fragile.
❖ Check stools periodically for occult blood.
❖ Keep anticoagulant antagonists (protamine

sulfate for heparin and vitamin K for warfarin)

available when drug dose is increased or
there are indications of frank bleeding. Fresh-
frozen plasma may be needed for
transfusion.
 ❑ Patient Teaching
General
❖ Teach patient to inform dentist when taking
anticoagulant. Contacting health care
provider may be necessary.
❖ Advise patient to use a soft toothbrush to
prevent gums from bleeding.
❖Warn patient to shave with an electric razor.
Bleeding from shaving cuts may be difficult to
control.
❖ Advise patient to have laboratory tests such

as PT or INR performed as ordered by health

care provider. Warfarin dose is regulated
according to INR derived from PT.
Suggest that patient carry medical
❖

identification card or wear MedicAlert

bracelet that lists name, telephone number,
and drug taken.
Encourage patient not to smoke. Smoking
❖

increases drug metabolism, so warfarin

dose may need to be increased. If patient
insists on smoking, notify health care
provider.
Tell patient to check with health care
❖

provider before taking OTC drugs. Aspirin

should not be taken with warfarin, because
aspirin intensifies its action and bleeding is
apt to occur. Suggest that patient use
acetaminophen.
Inform patient that many herbal products
❖

interact with anticoagulants and may

increase bleeding (Herbal Alert 45-1).
Closely monitor international normalized
ratio (INR) or prothrombin time (PT).
Teach patient to control external
❖

hemorrhage (bleeding) from accidents or

injuries by applying firm, direct pressure for
at least 5 to 10 minutes with a clean, dry,
absorbent material.
 ❑ Diet
Advise patient to avoid large amounts of
❖

green, leafy vegetables; broccoli; legumes;

soybean oil (rich in vitamin K); coffee, tea,
cola (caffeine); excessive alcohol; and
certain herbs and nutritional supplements
(coenzyme Q10) or to be very consistent with
their intake.
Coenzyme Q10, fish oils, items high in vitamin
K, St. John’s wort, ginseng, and vitamin C may
decrease effectiveness of warfarin. Garlic,
ginger, kava kava, green tea, chamomile tea,
ginkgo biloba, and acute alcohol intoxication
decrease warfarin effectiveness.
 ❑ ANTIPLATELETS

Antiplatelets are used to prevent

❖

thrombosis in the arteries by suppressing

platelet aggregation. Heparin and warfarin
prevent thrombosis in the veins.
Antiplatelet drug therapy is mainly for
❖

prophylactic use in (1) prevention of

myocardial infarction or stroke for patients
with familial history, (2) prevention of repeat
myocardial infarction or stroke, and (3)
prevention of stroke for patients having
transient ischemic attacks (TIAs).
Long-term, low-dose aspirin therapy has
❖

been found to be both an effective and

inexpensive treatment for suppressing
platelet aggregation. Aspirin inhibits
cyclooxygenase, an enzyme needed by
platelets to synthesize thromboxane A2
(TxA2).
For patients with familial history of stroke or
❖

myocardial infarction, the recommended

aspirin dose is 81, 162, or 325 mg/d.
Because aspirin has prolonged antiplatelet
activity, it should be discontinued at least 7
days before surgery.
Other antiplatelet drugs include dipyridamole
❖

(Persantine), ticlopidine (Ticlid),

clopidogrel (Plavix), anagrelide HCl
(Agrylin), abciximab (ReoPro), eptifibatide
(Integrilin), tirofiban (Aggrastat), and
ticagrelor (Brilinta).
Clopidogrel, dipyridamole, and ticlopidine
❖

have similar effects as aspirin, but they are

known as Adenosine Diphosphate (ADP)
antagonists affecting platelet aggregation.
Cilostazol (Pletal) inhibits platelet aggregation
and is a vasodilator that may be used for
intermittent claudication.
Ticagrelor is taken in conjunction with
aspirin 75 to 100 mg in a maintenance
regime. Doses greater than 100 mg
should be avoided.
Clopidogrel (Plavix) is an antiplatelet drug
❖

frequently used after myocardial infarction or

stroke to prevent a second event. It may be
prescribed singly or with aspirin.
It has been stated that Plavix and aspirin are
more effective in inhibiting platelet
aggregation if used together than if used as
separate antiplatelet therapies.
 ❑ Pharmacokinetics
Clopidogrel (Plavix) is rapidly absorbed
❖

and has a high protein-binding power.

Studies have not established a relationship
between the concentration of the main
metabolite and platelet aggregation.
. The half-life is 8 hours; it is usually
prescribed once a day. Excretion of the
drug metabolite occurs equally in the urine
and feces.
 ❑ Pharmacodynamics
Clopidogrel (Plavix) prevents platelet
❖

aggregation by blocking the binding of

adenosine diphosphate (ADP) to the
platelet ADP receptor. ADP-mediated
activation of the glycoprotein (GP) IIb/IIIa
complex inhibits platelet aggregation.
Plavix prolongs bleeding time; therefore, it
should be discontinued for 7 days preceding
surgery. The onset of action of Plavix is 1 to 2
hours, and its peak time is 2 to 3 hours. The
drug should not be taken if the patient has a
bleeding peptic ulcer, any active bleeding, or
intracranial hemorrhage.
Abciximab, eptifibatide, and tirofiban are
❖

used primarily for acute coronary syndromes

(unstable angina or non–Q-wave myocardial
infarction) and for preventing re-occlusion of
coronary arteries following percutaneous
transluminal coronary angioplasty (PTCA).
❖ These drugs are usually given before and
after PTCA. The drug of choice for
angioplasty is abciximab. Abciximab,
eptifibatide, and tirofiban block the
binding of fibrinogen to the glycoprotein
IIb/IIIa receptor on the platelet surface. They
are called platelet glycoprotein (GP) IIb/IIIa
receptor antagonists.
Following IV infusion, the antiplatelet effects
for abciximab persist for 24 to 48 hours; for
eptifibatide and tirofiban, the antiplatelet
effects last for 4 hours. Herbal products can
interact with antiplatelet drugs (Herbal Alert).
 ❑ THROMBOLYTICS

Thromboembolism (occlusion of an artery or

❖

vein caused by a thrombus or embolus)

results in ischemia (deficient blood flow) that
causes necrosis (death) of the tissue distal to
the obstructed area.
It takes approximately 1 to 2 weeks for
the blood clot to disintegrate by natural
fibrinolytic mechanisms .
If a new thrombus or embolus can be
❖

dissolved more quickly, tissue necrosis is

minimized, and blood flow to the area is
reestablished faster. This is the basis for
thrombolytic therapy.
Thrombolytics have been used since the
❖

early 1980s to promote the fibrinolytic

mechanism (converting plasminogen to
plasmin, which destroys the fibrin in the
blood clot).
The thrombus, or blood clot, disintegrates
when a thrombolytic drug is administered
within 4 hours after an acute myocardial
infarction (AMI) (acute heart attack).
Necrosis resulting from the blocked artery is
prevented or minimized, and hospitalization
time may be decreased.
The need for cardiac bypass or coronary
angioplasty can be evaluated soon after
thrombolytic treatment. A thrombolytic drug
should be administered within 3 hours of a
thrombolytic stroke. These drugs are also
used for pulmonary embolism, DVT,
noncoronary arterial occlusion from an acute
thromboembolism, and thrombolytic stroke.
❖ Commonly used thrombolytics include
urokinase (Abbokinase), alteplase tPA
(Activase),reteplase rPA (Retavase), and
tenecteplase TNK-tPA (TNKase).
Streptokinase and urokinase are enzymes
that act systemically to promote the
conversion of plasminogen to plasmin.
Alteplase, also known as tissue
Plasminogen Activator (tPA), is clot-specific
and binds to the fibrin surface of a clot,
promoting the conversion of plasminogen to
plasmin. Plasmin, an enzyme, digests the
fibrin in the clot.
Plasmin also degrades fibrinogen,
prothrombin, and other clotting factors.
These five drugs all induce fibrinolysis (fibrin
breakdown).
Prototype Drug Reteplase (Retavase) is a
❖

derivative of tPA. Anticoagulants and

antiplatelet drugs increase the risk of
hemorrhage; therefore, they should be
avoided until the thrombolytic effect has
passed.
The health care provider needs to
determine whether the patient has taken
any of these drugs before seeking
treatment.
 5

ANTIHYPERLIPIDEMIC &
PERIPHERAL
VASODILATORS
 ❑OBJECTIVES

❖Describe the action of the two main drug

groups: Antihyperlipidemic and peripheral
vasodilators.
❖Compare the side effects and adverse

reactions of Antihyperlipidemic.
❖Differentiate the side effects and
adverse reactions of Peripheral
vasodilators.
❖Apply the nursing process, including

patient teaching, For antihyperlipidemic

and peripheral vasodilators.
❖ VARIOUS DRUGS are used to
maintain or decrease blood lipid
concentrations and promote dilation of
vessels. Drugs that lower blood lipids
are called antihyperlipidemic,
antilipidemic, antilipemic, and
hypolipidemic.
In this chapter, drugs used to lower
❖

lipoproteins are called antihyperlipidemic.

Peripheral vasodilators are drugs that
dilate vessels that have been narrowed by
vasospasm.
 ❑ LIPOPROTEINS
Lipids (cholesterol, triglycerides, and
❖

phospholipids)-are bound in the inner

shell of protein, which is a carrier that
transports lipids in the bloodstream. The
four major Categories of lipoprotein:
1.High-density lipoprotein (HDL)-also
known a “friendly” or “good” lipoprotein,
is the smallest, most dense lipoprotein,
meaning that it contains more protein and
less fat than the others.
2. Low-density lipoprotein (LDL)-the
“bad” lipoprotein, contains 50% to 60% of
cholesterol in the bloodstream.
3.Very low-density lipoprotein -carries
mostly triglycerides and less Cholesterol.
4. Chylomicrons -are large particles that
transport fatty acids and cholesterol to
the liver.
❖ Serum cholesterol and triglyceride
measurements are frequently part of a
regular physical examination or
readmission evaluation.
❖ If levels are high, a 12- to 14-hour
fasting lipid profile may be ordered.
❖ When cholesterol, triglycerides, and
LDL are elevated, the patient is at
increased risk for coronary artery
disease(CAD).
 ❑ APOLIPOPROTEINS
❖Apolipoproteins are within the
lipoprotein shell and contain
apolipoprotein (apo) A-1, apoB, and
apoE.
❖The major component of apoA1 is HDL.
❖The major component of apoB isLDL,
which exists in two forms, apoB-100
and apoB-48.
❖ApoB-100 has VLDL as well as LDL

and is a better indicator of risk for

coronary artery disease (CAD) than LDL
alone.
 ❑ NONPHARMACOLOGIC METHODS
FOR CHOLESTEROL REDUCTION
❖Before drugs to lower LDL and raise HDL

are prescribed, nondrug therapy should be

initiated for decreasing cholesterol.
❖Saturated fats and cholesterol in the diet

should be reduced.
❖In many cases, diet alone will not lower
blood lipid levels.
❖This and the fact that adherence to dietary

restrictions is often short-lived explains why

many patients do not respond to diet
modification alone.
❖ Exercise is an important aspect of the no
pharmacologic method to reduce
cholesterol and increase HDL.
❖ It must be emphasized to the patient that
dietary changes need to be made and an
exercise program followed even after drug
therapy is initiated.
 ❑ ANTIHYPERLIPIDEMICS

Drugs that lower lipid levels include bile-

❖

acid sequestrants, fibrates (fibric acid),

nicotinic acid, cholesterol absorption
inhibitor, and hepatic 3-hydroxy-
3methylglutaryl-coenzyme A (HMG-
CoA)reductase inhibitors (statins).
❖ One of the first antihyperlipidemic,
cholestyramine (Questran), is a bile-acid
sequestrant that reduces LDL cholesterol
(LDL-C) levels by binding with bile acids in
the intestine.
Colestipol (Colestid)-is another resin
❖

antihyperlipidemic similar to
cholestyramine. Both are effective in
lowering cholesterol. Colesevelam HCl,
another bile acid sequestrant similar to
cholestyramine and colestipol.
❖ Colesevelam also has less effect on the
absorption of Fat-soluble vitamins than the
older agents and is usually the First-choice
bile-acid sequestrant drug.
.
Gemfibrozil (Lopid)-is a fibric acid
❖

derivative that is more effective at reducing

triglyceride and VLDL levels than reducing
LDL.Fenofibrate has similar actions and
some of the same side effects as
gemfibrozil. If taken with warfarin, bleeding
might occur
❖Nicotinic acid-is actually very effective at
lowering cholesterol levels, and its effect on
the lipid profile is highly desirable.
❖Ezetimibe (Zetia)-is a cholesterol

absorption inhibitor that acts on the cells in

the small intestine to inhibit cholesterol
absorption.
 ❑ STATINS
The statin drugs inhibit the enzyme
❖

HMG CoA reductase in cholesterol

biosynthesis; thus the statins are called
HMG CoA reductase inhibitors
❖By inhibiting cholesterol synthesis in the
liver, this group of antihyperlipidemic
decreases the concentration of cholesterol,
decreases LDL, and slightly increases HDL
cholesterol.
❖Atorvastatin and simvastatin are at the top of

the list of most prescribed drugs in the

United States.
The statin drugs can be combined with
❖

other drugs to decrease blood pressure

and blood clotting and to enhance the
antihyperlipidemic effect.
 ❑ LABORATORY TEST
❖A high level of homocysteine has been
linked to cardiovascular disease, stroke, and
the possibility of Alzheimer’s disease.
❖High-sensitivity C-reactive protein (hsCRP)

reference values are <0.175 mg/L; low risk

are <1 mg/L; moderate risk are 1 to 3 mg/L;
and high risk are >3 mg/L.
The standard C-Reactive Protein (CP)
is produced in the liver in response to
tissue injury and inflammation.
❖The hsCRP is a highly sensitive test for
detecting the inflammatory protein that can
be associated with cardiovascular and
peripheral vascular disease.
A positive hsCRP test can indicate that
❖

the patient is at high risk for coronary

artery disease (CAD), making it a
valuable test for predicting CAD.
 ❑ Pharmacokinetics:
Rosuvastatin (Crestor) decreases LDL by
❖

46% at a dose of 10 mg. It is highly protein-

bound, so it usually is prescribed as a once-
daily dose. Rosuvastatin has a half-life of 20
hours.
❖ Pharmacodynamics: The positive
effect of lowering lipids with
rosuvastatin is seen in about 2 weeks.
The peak time after a dose of
rosuvastatin is 3 to 5 hours.
 ❑ SIDEEFFECTS AND ADVERSE

REACTION:
❖ Side effects and adverse reactions of
cholestyramine include constipation and
peptic ulcer.
However, as mentioned, aspirin and
❖

careful drug titration can reduce side

effects to a manageable level in most
patients.
❖The statin drugs can cause a dose-
related increase in liver enzyme levels.
❖Baseline liver enzyme studies should

be obtained before initiating statin drug

therapy.
❖Patients with acute hepatic disorder should
not take a statin drug.
❖The serious skeletal muscle adverse effect

known as rhabdomyolysis has been

reported with use of the statin drug class.
 ❑ PERIPHERAL VASODILATORS

A common problem in older adults is

❖

peripheral arterial (vascular) disease (PAD,

PVD).
❖It is characterized by numbness and
coolness of the extremities, intermittent
claudication (pain and weakness of limb
when walking but no symptoms at rest),
and possible leg ulcers.
❖ Peripheral vasodilators increase blood
flow to the extremities.
❖ They are used in peripheral vascular

disorders of venous andarterial vessels.

Patients with diabetes mellitus are more
❖

likely to have PAD by two to four times the

usual rate and are at risk of intermittent
claudication.
with PAD who are treated with HMG-
❖

CoAreductase inhibitors (statins) for

dyslipidemia may get improvement for
intermittent claudication symptoms as
well as a decrease in serum lipids.
Cilostazol is an antiplatelet that has a
❖

dual purpose of inhibiting platelet

aggregation as well as causing
vasodilation to treat intermittent
claudication.
 ❑ CILOSTAZOL

Pharmacokinetics Cilostazol is a direct-

❖

acting vasodilator that is absorbed from GI

tract. Cilostazol is usually taken two times a
day.
Pharmacodynamics Cilostazol causes
❖

vasodilation of arteries, especially within the

femoral vasculature. Common adverse
effects include headache, diarrhea, and
abnormal stools. This drug has an onset of
action with 2 to 12 weeks.
 ❑ SIDE EFFECTS AND ADVERSE
REACTIONS
The effectiveness of peripheral vasodilators
❖

in increasing blood flow by vasodilation is

questionable in the presence of
arteriosclerosis. These drugs may decrease
some of the symptoms of cerebrovascular
insufficiency.
 ❑ PENTOXIFYLLINE
❖ Pentoxifylline (Trental), classified as a
hemorrheologic agent, improves
microcirculation and tissue perfusion by
decreasing blood viscosity and improving the
flexibility of erythrocytes, thus increasing
tissue oxygenation.
Pentoxifylline has been approved by the
❖

FDA for patients with intermittent

claudication and has been prescribed for
those with Buerger’s disease resulting from
arterial occlusions.
However, in one research study,
❖

pentoxifylline was not determined to be

more effective than a placebo.
Reactions to an overdose of
❖

pentoxifylline include flushing of the skin,

faintness, sedation, and GI
disturbances. The drug should be
taken with food.
THANKS YOU!
 Group 1 Members:
Aplacador, Kristle G.
Arayan, Alexa Aline M.
Arones, Chelizza C.
Badilla, Farrah O.
Baydal, Mary Jean B.
Corage, Mark Justine C.