CARDIOVASCULAR DRUGS 3.
If an infection occurs, these cells send chemical
Cardiovascular System
 The cardiovascular system, also known as the
circulatory system, includes the heart, arteries, veins,
capillaries and blood.
 The heart functions as the pump that moves blood
through the body.
 The arterial circulation delivers blood from the heart to
the body, and the venous circulation carries it back to
the heart.
 Capillaries are tiny blood vessels at the interface of the
arterial and venous circulation where exchange of
substances between the blood and body tissues occurs.
Major Functions of the Cardiovascular System:
a. Oxygen and Carbon Dioxide Transport
1. Supplying oxygen to the body is the most essential
function of the cardiovascular system.
2. All cells require oxygen, especially the brain cells
which is the most sensitive and begin to die in as
little as 3 minutes if deprived of oxygen.
3. During inhalation, air enters the lungs and oxygen
is absorbed through the air sacs into the
bloodstream.
4. This oxygen-rich blood is pumped through the
heart into the arterial circulation.
5. In the capillaries, oxygen diffuses out of the blood
and into the cells of the body’s organs and tissues.
At the same time, carbon dioxide – waste product
produced by cells is absorbed into the blood and
transported to the lungs through the venous
circulations.
6. When this oxygen-poor blood reaches the lungs,
carbon dioxide diffuses through the air sacs and is
then exhaled. This cycle occurs with every breath.
b. Nutrient and Waste Product Transport
1. Delivering nutrients to the body is another critical
function of the cardiovascular system.
2. After food is digested into the stomach and
intestines, its component nutrients are absorbed
into the bloodstream.
3. These nutrients include sugars, fats, vitamins,
minerals, and protein building blocks called amino
acids.
4. Each of these nutrients is vital to healthy body
function. For example, the sugar glucoses is the
body’s primary fuel to generate energy, and amino
acids enable the body to manufacture new cells.
5. Like oxygen, nutrients diffuse from the
bloodstream into body cells via the capillaries.
6. In addition to carbon dioxide, the circulatory
system picks up the metabolic waste products and
toxins and transports them to the liver, kidneys,
and lungs for eventual elimination from the body.
c. Disease Protection and Healing
1. The circulatory system serves as the path for
disease-fighting cells and proteins, and messengers
of the immune system.
2. Immune system cells called white blood cells
patrol the body in search of invading germs.
alarm signals that travel through the bloodstream,
which subsequently transports infection-fighting
cells to the site of the infection.
4. The circulatory system also carries chemical
messengers that attract cells to heal tissues that
have been damaged due to injury or disease.
d. Hormone Delivery
1. Hormones are chemical messengers produced by
endocrine glands that affect distant organs.
2. The cardiovascular system serves as the
transportation connection between the endocrine
glands and the organs or tissues they control via
hormones.
3. For example, hormones produced in the pituitary
gland in the brain control other endocrine glands –
such as the thyroid, ovaries and testes – as well as
directing childhood growth.
4. Similarly, the blood-sugar-lowering hormone
insulin produced in the pancreas affects the uptake
and use of blood sugar throughout the body.
Thyroid hormones affect the metabolic rate of
virtually every body organ and tissue, thanks to
their body-wide delivery via the circulatory system.
e. Body Temperature Regulation
1. Body temperature regulation is an important
function of the cardiovascular system.
2. If body temperature drops, surface blood vessels
constrict to conserve body heat.
3. The cardiovascular system works in concert with
the body’s sweating mechanism as the primary
regulators of body temperature.
Cardiac Drugs are used in:
a. Hypertension
b. Angina Pectoris (chest pain)
c. Myocardial Infarction (heart attack)
d. Shock
e. Arrhythmias
f. CHF (Congestive Heart Failure) – a weakness of the
heart that leads to a buildup of fluid in the lungs and
surrounding body tissues.
Angiotensin Converting Enzyme Inhibitors:
 These are commonly called ACE inhibitors because the
agents BLOCK the conversion of AI to AII in the LUNGS.
 These agents alter one of the mechanisms of blood
pressure control – the RAAS or renin-angiotensin-
aldosterone system.
 Angiotensin II is a very powerful vasoconstriction and
stimulus for the release of aldosterone.
ACE Inhibitors:
 benazepril (Lotensin, Lotensin Het)
 captopril (Capoten)
 enalapril (Vasotec)
 fosinopril (Monopril)
 lisinopril (Prinivil, Zestril)
 moexipril (Univase)
 perindopril (Aceon)
 quinapril (Accupril)
Pharmacodynamics of ACE Inhibitors:
 The mechanism of action of the ACE Inhibitors prevents
the conversion of angiotensin I to angiotensin II by
inhibiting the enzyme in the lungs – the angiotensin
converting enzyme.
 Angiotensin, a potent vasoconstrictor, increases
peripheral resistance and promotes the release of
aldosterone.
 Aldosterone in turn, promotes the retention of sodium
and water, increasing the volume of blood in the
causing the heart pump.
 ACE Inhibitors work by preventing the conversion of
Angiotensin I to Angiotensin II. As Angiotensin II is
reduced, arterioles dilate, thus reducing peripheral
vascular resistance.
 The action leads to decreased AII and decreased
aldosterone level leading to a decrease in blood
pressure.
 The effect of lowering the blood pressure is attributed
to the decrease in cardiac workload and decrease
peripheral resistance and blood volume.
Pharmacokinetics of ACE Inhibitors:
 ACE Inhibitors may be used alone or in combination
with another drug such as thiazide diuretic to treat
hypertension.
 ACE Inhibitors are commonly used when beta blockers
or diuretics are ineffective.
 ACE Inhibitors are also used to manage heart failure.
Drug Interactions:
 ACE Inhibitors can cause several different types of
interactions with other cardiovascular drugs. All ACE
Inhibitors enhance the hypotensive effects of diuretics
and other hypertensives such as beta blockers. They
can also increase serum lithium levels possibly resulting
in lithium toxicity.
Angiotensin II Receptor Blocker:
 Angiotensin II is a very potent chemical formed in the
blood that causes muscles surrounding the blood
vessels to contract, thereby, narrowing the vessels. This
narrowing increases the pressure within the vessels and
can cause high blood pressure (hypertension).
 Angiotensin II receptor blockers (ARBs) are medications
that block the action of angiotensin II by preventing
angiotensin II from binding to angiotensin II receptors
on the muscles surrounding blood vessels. As a result,
blood vessels enlarge (dilate) and blood pressure is
reduced. Reduced blood pressure makes it easier for
the heart to pump blood and can improve heart failure.
 In addition, the progression of kidney disease caused by
the high blood pressure or diabetes is slowed. ARBs
have effects that are similar to angiotensin converting
enzyme (ACE) inhibitors, but ACE inhibitors act by
preventing the formation of angiotensin II rather than
by blocking the binding of angiotensin II to muscles on
blood vessels.
Uses of ARB:
a. Control high blood pressure
b. Treat heart failure
c. Prevents kidney failure in people with diabetes or high
blood pressure
d. Prevents diabetes and reduce the risk of stroke in
patients with high blood pressure and an enlarged
heart.
e. Prevents the recurrence of atrial fibrillation.
Examples of Angiotensin II Receptor Blockers include:
 Azilsartan (Edarbi)
 Candesartan (Atacand)
 Eprosartan
 Irbesartan (Avapro)
 Losartan (Cozaar)
 Olmesartan (Benicar)
 Telmisartan (Micardis)
 Valsartan (Diovan)
Calcium channel blockers
 Calcium channel blockers are prescription medications
that relax blood vessels and increase the supply of
blood and oxygen to the heart while also reducing the
heart’s workload. Examples of calcium channel blockers
include: Amlodipine besylate (Norvase), Bepridil
(Vascor), Verapamil hydrochloride (Isoptin)
Pharmacokinetics of Calcium channel blockers:
 Calcium channel blockers are smooth muscle dilators
and have a negative inotropic effect on the working
myocardial cells of the atria and ventricles.
 When administered orally, CCB are absorbed quickly
and almost completely.
 Because of the first-pass effect, the bioavailability
(active effect) of this drug is much lower.
 CCB highly bound to plasma protein (penetrate tissues
less and excreted faster)
Pharmacodynamics of Calcium channel blockers:
 Calcium channel blockers are a group of medications
that disrupt the movement of calcium through calcium
channels.
 Also called calcium antagonists, relax and widen blood
vessels by affecting the muscle cells in the arterial
walls.
 It prevents calcium from entering cells of the heart and
blood vessel walls, resulting in lower blood pressure.
Channel calcium blockers are used as antihypertensive
drugs i.e., as medications to decrease blood pressure in
patients with hypertension.
Pharmacotherapeutics of Calcium channel blockers:
 Calcium channel blockers are used only for long term
prevention of Angina.
 CCB are particularly effective for preventing
Prinzmetal’s angina, a temporary increase in coronary
vascular tone (vasospasm) causing a marked, but
transient reduction in luminal diameter.
Vasodilating drugs:
 A vasodilator is a drug that causes vasodilation, a
widening (opening) of diameter of the interior (lumen)
of the blood vessels that results from relaxation of the
smooth muscle of the vessels. The opposite of
vasodilation is vasoconstriction.
A. Actions: arteriolar smooth muscle, dilate arteries
and decrease peripheral vascular resistance.
B. Uses: moderate to severe hypertension and
hypertensive crisis (extreme increase in blood
pressure)
C. Major side effects:
1. Headache
2. Sodium retention
3. Rebound hpn
4. Increased workload of heart; tachycardia,
palpitations, n/v, abdominal pain
 This type of medicine works through several
mechanisms. For example:
 ACE (angiotensin converting enzyme)
inhibitors: ACE inhibitors slows (inhibits) the
activity of the enzyme ACE, which decreases
the production of a chemical (angiotensin)
that causes the blood vessels to narrow. As a
result, blood pressure reduces (lowers)
because of the enlarged (dilated) blood
vessels.
 ARB’s (angiotensin receptor blockers): ARBs is
another type of medicine that enlarges blood
vessels. They work by blocking angiotensin
from attaching to the smooth muscle of blood
vessels. This causes vasodilation.
 CCB’s (calcium channel blockers): the smooth
muscle cells of the arteries use calcium for
muscle contraction. CCBs block calcium from
entering into the smooth cells, which relax the
artery muscles. This leads to dilation (opening)
of the artery.
 Nitrites: Nitrates are converted to nitric
oxide, which activates another chemical that
causes the veins and arteries to open. Doctors
prescribe nitrates to treat angina (heart or
cardiac pain).
Pharmacokinetics of Vasodilating drugs:
 The drugs are absorbed rapidly and distributed well.
They are metabolized in the liver and most are excreted
by the kidneys
Pharmacodynamics of Vasodilating drugs:
 A blood vessel carries blood. They also help the body
regulate blood pressure and blood low to organs. When
a blood vessel dilates (opens), it allows more blood
flows.
 Widening of arteries (a type of blood vessel) reduces
blood pressure because dilation of the arteries makes it
easier for the heart to pump blood to the rest of the
body.
 When arteries open, it increases the blood flow and
oxygen supply to the heart.
 When veins open, it reduces the amount of blood
returned to the heart chambers.
Pharmacotherapuetics of Vasodilating drugs:
 Vasodilating drugs are rarely used alone to treat
hypertension. Instead they are usually used in
combination with other drugs to treat the patient with
moderate to severe hypertension (hypertensive crisis).
Nursing Implications:
1. Monitor VS every 5 to 15 minutes, titrate dose to BP
and do not leave patient unmonitored. (Titrate means
the process of adjusting the dose of a medication for
the maximum benefit without adverse effects)
2. Monitor I&O preferably with a foley catheter in a
critical care setting.
3. Use microdrip tubing and have IVF on a controller
pump.
4. Do not mix this drug with any other drugs.
5. Since sodium nitroprusside (Nipride) must be protected
from light, wrap IV bag and tubing with foil.
Vasodilating drugs: Common drugs
 Sodium nitropusside (Nipride)
 Hydralazine hydrochloride (Apresoline)
 Diazoxide (Hyperstat)
 Guanetidine sulfate (Ismelin)
5. Ganglionic blockers:
 Ganglionic blockers inhibit autonomic activity by
interfering with neurotransmission within autonomic
ganglia.
 This reduces sympathetic outflow to the heart thereby
decreasing cardiac output by decreasing heart rate and
contractility.
 Reduced sympathetic output to the vasculature
decreases sympathetic vascular tone, which causes
vasodilation and reduced systemic vascular resistance,
which decreases arterial pressure.
 Parasympathetic outflow is also reduced by ganglionic
blockers.
Therapeutic Indications of Ganglionic blockers:
 Ganglionic blockers are not used in the treatment of
chronic hypertension in large part because of their side
effects, and because there are numerous, more
effective, and safer antihypertensive drugs that can be
used. They are, however, occasionally used for
hypertensive emergencies.
Specific Drug:
 Several different ganglionic blockers are available for
clinical use; however, only one (trimethaphan
camsylate) is sometimes used in hypertensive
emergencies or for producing controlled hypotension
during surgery.
Side Effects and Contraindications of Ganglionic blockers:
 It can produce excessive hypotension and impotence
due to its sympatholytic effect, and constipation,
urinary retention, dry mouth due to its
 parasympatholytic effect. It also stimulates histamine
release.
 Sympatholytic effect: inhibit the transmission
of nerve impulses in the sympathetic nervous
system.
 Parasympatholytic effect: reduces the activity
of the parasympathetic nervous system.
Cardiac Glycosides:
A. Actions: a positive inotropic, negative chronotropic,
and negative dromotropic, effect produced by
inhibiting the adenosine triphosphatase (ATPase)
enzyme and increasing calcium into the myocardial
cytoplasm.
Effects of Drugs on the Heart
Inotropic Affects the force of contraction
Chronotropic Interferes with the rate of the heart
beat
Dromotropic Pertains to contraction
 Positive inotropic – increases myocardial
contraction, which may decrease heart size in
clients in cardiomyopathy and CHS, and increases
renal blood flow.
 Negative chronotropic effect – decreases heart
rate
 Negative dromotropic effect – slows conduction
through the atrioventricular node.
Overall Effects:
1. Increased cardiac output without increased oxygen
demand in non-myocardial infarction situations.
2. Decreased workload from the effect of decreased heart
rate
3. Mild diuretic effect
4. Decreased heart size in cardiomyopathy (chronic
disease of the heart muscle) clients
Uses of Cardiac glycosides:
 Congestive heart failure (CHF) – the heart has trouble
pumping blood
 Atrial dysrhythmias – irregular heartbeat
 Atrial flutter – abnormal heart rhythm associated with a
fast heart rate
 Supraventricular tachycardia – an abnormally fast heart
rhythm arising from improper electrical activity in the
upper part of the heart
Cardiac glycosides:
 Often called digitalis or digitalis glycosides
 They are a group of chemically similar compounds that
can increase the contractility of the heart muscle, and
therefore, are used in treating heart failure.
 The digitalis glycosides have a low therapeutic index,
with only a small difference between a therapeutic
dose and doses that are toxic or even fatal. The most
widely used cardiac glycoside is digoxin.
Cardiac glycosides Digoxin:
 Mechanism of action: Increased contractility of the
cardiac muscle.
 Digoxin increases the force of cardiac contraction,
causing cardiac output to more closely resemble that of
the normal heart.
Other effects of Digoxin:
 Blood vessels: Digitalis has mild direct vasoconstrictor
action and increases peripheral resistance in normal
individuals.
 In CHF patients, digoxin decreases peripheral
resistance.
 Digitalis has no notable effect on BP. Systolic BP may
increase and diastolic may fall in CHF patients.
 Kidney: Diuresis occurs promptly in CHS patients.
 CNS: in higher doses digoxin activates CTZ
(chemoreceptors trigger zone).
Pharmacokinetics of Digoxin:
 Absorbed orally. Absorption varies from zero to nearly
100%.
 Distributed widely to tissues, including the central
nervous system. Digoxin is not extensively metabolized
in humans.
 Almost two thirds is excreted unchanged by the
kidneys. Its renal clearance is proportional to creatinine
clearance, and the half-life is 36-40 hours in patients
with normal renal function.
Adverse effects of Digoxin:
 Toxicity of digitalis is high, margin of safety is low
(therapeutic index 1.5 – 3)
 Higher cardiac mortality has been reported among
patients with steady-state plasma digoxin levels >1.1
ng/ml but still within the therapeutic range during
maintenance therapy.
Uses of Digoxin:
 Treatment of CHF (systolic and diastolic dysfunctions)
 Cardiac arrhythmias (atrial fibrillation, atrial flutter, and
paroxysmal supraventricular tachycardia)
Current Status of Digitalis:
 Before the introduction og high ceiling diuretics, ACE
inhibitors and B blockers, digitalis was considered an
indispensable part of anti-CHF treatment.
 However, digitalis is still the most effective drug
capable of reliving symptoms of CHF and restoring
cardiac compensation, especially in patients with
dilated heart and low ejection fraction.
Treatment Options for Various Stages of Heart Failure:
 ACE – angiotensin converting enzyme
 ARBs – angiotensin receptor blockers
 FDC – fixed dose combination;
 HYD – hydralazine
 ISDN – isosorbide dinitrate
Phosphodiesterase Inhibitors:
 Phosphodiesterase inhibitors are another positive
inotropic group of drugs given to treat CHF when there
is no response with the use of other agents.
  This drug group inhibits the enzyme
phosphodiesterase, thus promoting a positive inotropic
response and vasodilation.
2 Drugs in this group:
 Amrinone lactate (INOCOR)
 Milrinone lactate (PRIMACOR)
 These drugs increase stroke volume and promote
vasodilation.
 They are administered IV.
 Severe cardiac – dysrhythmias might result from the
use of phosphodiesterase inhibitors therefore, the
client’s electrocardiogram (ECG) and cardiac status
should be closely monitored.
 Digoxin immune fab or Digoxin-specific antibody
(Digiband) – antidote for overdose of digoxin.
Antianginal Drugs:
 Angina pectoris refers to a strangling or pressure-like
pain caused by cardiac ischemia (inadequate blood
supply).
 The pain is usually located substernally but it
sometimes perceived in the neck, shoulder and arm, or
epigastrium.
 Women develop angina at a later age than men and are
less likely to have classic substernal pain.
 Antianginal drugs are those that prevent, abort, or
terminate attacks of angina pectoris.
Types of Angina:
a. Atherosclerotic angina (classic angina and a common
form)
o Attacks are predictably provoked (stable
angina) by exercise, emotion, eating, or coitus
and subside when the increased energy
demand is withdrawn.
o Rest, by reducing cardiac work, usually leads
to complete relief of the pain within 15 mins.
Atherosclerotic angina constitutes about 90%
of angina cases.
b. Vasospastic angina (rest angina, variant angina, or
Prinzmetal’s angina (uncommon form)
o Attacks occur at rest or during sleep and are
unpredictable
o Vasospastic angina is responsible for less than
10% of angina cases.
Treatment of Angina Pectoris:
 Drugs used in angina have to main strategies:
- Reduction of oxygen demand
- Increase of oxygen delivery to the myocardium.
Classification of Antianginal drugs:
 Nitrates – short acting
 Glyceryl trinitrate (GTN, Nitroglycerine) – long acting
 Isosorbide dinitrate – short acting by sublingual route
Beta Blockers:
 Isosorbide, monoitrate, Erythrityl tetranitrate,
Pentaerythritol tetranite, Propanolol, Metaprolol,
Atenolol, and others.
Calcium channel blockers:
 Phenyl alkylamine, Verapamil – Benzothiazepine:
Diltiazem – Dihydropyridines: Nifedipine,
Felodipine, Amlodipine, Nitrendipine, Nimodipine,
Lacidipine, Lercanidipine, Benidipine
Nitrates:
Nitrates act in the following ways:
 Preload reduction: Peripheral pooling of blood
decreased venous return (preload reduction).
 Afterload reduction: Nitrates also produce some
arteriolar dilation slightly decrease total
peripheral resistance or afterload on heart.
 Redistribution of coronary flow: In the arterial tree,
nitrates preferentially relax bigger conducting
(angiographically visible) coronary arteries than arteries
than arterioles or resistance vessels.
Adverse Effects of Nitrates:
 Headache is the most common adverse effects of
nitrates.
 High doses of nitrates can also cause:
o Postural hypotension
o Facial flushing
o Tachycardia
Anti-arrhythmic drugs:
 Arrhythmia is an abnormality of the rate, rhythm, or
site of origin of the cardiac impulse or an abnormality in
the impulse conduction.
 Cardiac arrhythmia may be due to abnormal generation
or conduction of impulses.
 Factors like myocardial hypoxia, ischemia, electrolyte
disturbances, trauma, can cause arrhythmias.
Factors that can cause Arrhythmias:
 Tachycardia arrhythmias.
 Brady arrhythmias
 Digitalis-Induced Arrhythmias
 Based on the site of impulse origin, they may be
grouped as supraventricular or (SA node, AV node,
atria) or ventricular arrhythmias. VA is a common cause
of death, particularly sudden death.
Other arrhythmic:
 Adenosine – has rapid and short antiarrhythmic
action. Given orally suppress automaticity, AV
conduction (electrical continuity between the atria
and ventricles) and dilate the coronary arteries. It is
the drug of choice for PSVT
 Atropine – is used in sinus bradycardia. It acts by
blocking M2 receptors (muscarinic receptors) found
in the SA and AV nodes that have a large amount of
vagal innervation.
 - The heart is innervated by vagal and sympathetic
fibers. The right vagus nerve primarily innervates
the SA node, whereas the left vagus innervates the
AV node
- Muscarinic receptors regulate heart rate by
altering the electrical activity of the sinoatrial
node.
- Activation of M2 receptors can affect conduction
of electrical impulses through the atrioventricular
node.
 Digoxin – depress the AV conduction, reduce heart
rate and increase the force of contraction of the
myocardium
 Magnesium sulfate – is used to treat digitalis
induced arrhythmias.
Diuretic Drugs:
 Diuretics are used to promote the excretion of water
and electrolytes by the kidneys. By doing so, diuretics
play a major role in the treatment of hypertension as
well as other cardiovascular conditions.
The Major Diuretics Used as Cardiovascular Drugs:
 Thiazide and Thiazide-like Diuretics
 Loop Diuretics
 Potassium- Sparing Diuretics
a. Thiazide and Thiazide-like Diuretics –sulfonamide
derivatives.
Thiazide diuretics include:
 Chlorothiazide (Diuril)
 Hydrochlorothiazide (Microzide)
Thiazide-like Diuretics include:
 Chlorthalidone
 Indapamide
Pharmacokinetics of Diuretic Drugs:
 Thiazides are readily absorbed and are extensively
bound to plasma proteins (hard to excrete). They are
eliminated largely by secretion into the proximal
tubule.
 Thiazide cross the placenta and are secreted in breast
milk.
Pharmacodynamics of Diuretics Drugs:
 Thiazide and Thiazide-like Diuretics work by preventing
sodium to be reabsorbed in the kidney. As sodium is
excreted, it pulls water alone with it.
 Thiazide and Thiazide-like diuretics also increase the
excretion of chloride, potassium and bicarbonate,
which can result in electrolyte imbalances.
Pharmacotherapeutics of Diuretic Drugs:
 Thiazides are used as long term treatment of
hypertension and are also used to treat edema by mild
to moderate heart failure, liver disease, kidney disease
and corticosteroid and estrogen therapy.
Types of Diuretics:
a. Loop Diuretics
- are diuretics that act at the ascending limb of the
loop of Henle in the kidney. They are primarily
used in medicine to treat hypertension and edema
often due to congestive heart failure or renal
insufficiency. Examples of loop diuretics include:
Bumetanide (Bumex), Ethacrynic acid (Edecrin),
Furosemide (Lasix)
- it is often called a high-ceiling diuretic because it is
more effective than other diuretics. Flurosemide
decreases the sodium, chloride, and potassium
reabsorption from the tubule… Dilute urine is
produced because water is retained in the tubule
when it reaches the distal tubule.
- Act primarily on the thick ascending loop of Henle
(part of the nephron responsible for concentrating
urine) to increase the secretion of sodium,
chloride, and water.
- These drugs also inhibit sodium, chloride and
water reabsorption.
Pharmacokinetics of Loop Diuretics:
 Loop diuretics usually are absorbed well and
distributed rapidly. These diuretics are highly
protein bound. Loop diuretics undergo partial
or complete metabolism in the liver, exceot
for furosemide, which is excreted primarily
unchanged. Loop diuretics are excreted
primarily by the kidneys.
Pharmacodynamics of Loop Diuretics:
 Loop diuretics are the most potent diuretics
available, producing the greatest volume of
diuresis (urine production). They also have a
high potential for causing severe adverse
reactions.
 Bumetanide is the short-acting diuretic it is
40x more potent than another loop diuretic,
furosemide.
Pharmacotherapeutics of Loop Diuretics:
 Loop diuretics are used to treat edema
associated with heart failure as well as
hypertension (usually with a potassium-
sparing diuretic or a potassium supplement to
prevent hypokalemia.
 Loop diuretics are also used to treat edema
associated with liver disease or nephrotic
syndrome (kidney disease).
Adverse Reactions to Loop Diuretics:
 Risk of ototoxicity (damage to the organs of
hearing) when aminoglycosides are taken with
loop diuretics.
 Loop diuretics reduce the hypoglycemic effect
of oral antidiabetic drugs possibly resulting in
the hyperglycemia.
 Loop diuretics may increase the risk of lithium
toxicity.
  An increased risk of electrolyte imbalances
that can trigger arrhythmias is present when
digitalis glycosides and loop diuretics are
taken together.
b. Potassium-sparing Diuretics
- Have weaker diuretic and antihypertensive effects
than other diuretics but they have the advantage
of conserving potassium.
- Potassium-sparing diuretics include:
 Amiloride
 Spironolactone
 Triamterene
- Potassium sparing refers to a special group of
diuretics which helps the body eliminate excess
water, while preventing the loss of potassium,
which is why it is called potassium-sparing
diuretics.
Pharmacokinetics of Potassium-sparing Diuretics:
 Potassium-sparing diuretics are only available
orally and are absorbed in the GI tract.
 Metabolized in the liver except for Amiloride
(which is not metabolized) and excreted
primarily in the urine and bile.
Pharmacodynamics of Potassium-sparing Diuretics:
 The direct action of potassium-sparing
diuretics on the distal tubule of the kidneys
produces in the following effects:
o Urinary excretion of sodium and water
increases, as does excretion of chloride
and calcium ions.
o The excretion of potassium and
hydrogen ions decreases.
o These effects lead to reduced blood
pressure and increased serum
potassium levels.
Pharmacotherapuetics of Potassium-sparing Diuretics:
 Potassium-sparing diuretics are used to treat:
o Edema
o Diuretic-induced hypokalemia in patients
with heart failure
o Cirrhosis
o Nephrotic syndrome (abnormal condition
of kidneys)
o Hypertension
o Spironolactone is also used to treat
hyperaldosteronism (excessive secretion
of aldosterone including hirsutism
associated with Stein-Leventhal
(polycystic ovary syndrome)
Antilipemic Drugs:
 Antilipemic drugs are used to lower abnormally high
levels of lipids, such as cholesterol, triglycerides, and
phospholipids. The risk of developing coronary artery
disease increased when serum lipid levels are elevated.
Drugs are used when lifestyle changes such as proper
diet, weight loss, exercise and treatment of an
underlying disorder causing the lipid abnormality, fail to
lower lipid levels.
Causes of Hyperlipidemia:
 The biochemistry of Plasma Lipids
 Lipids are the heterogeneous mixtures of fatty acids
and alcohol that are present in the body
 The major lipids in the bloodstream are cholesterol
and its esters, triglycerides, and phospholipids.
Normal Functions of Cholesterol in the Body:
 It is necessary for new cells to form and for older cells
to repair themselves after injury.
 Cholesterol is also used by the adrenal glands to form
hormones such as cortisol, by the testicles to form
testosterone, and by the ovaries to form estrogen and
progesterone.
Normal Functions of Triglycerides and Phospholipids in the Body:
 Triglycerides supply energy for the body.
 Triglycerides either meet immediate energy needs in
muscles or stored ass fat for future energy
requirements.
 Phospholipids are compounds that are used to make
cell membranes, generate second messengers, and
store fatty acids for the use in generation of
prostaglandins.
Antilipemic Drug Classes include:
 Bile sequestering drugs (cholestyramine and colestipol
hydrochloride)
 Fibric acid derivatives (clofibrate and gemfibrozil)
 Cholesterol synthesis inhibitors (lovastatin, pravastatin
sodium and simvastatin)
a. Bile sequestering drugs
- They are medications for lowering LDL cholesterol
in conjunction with diet modification.
 Cholestyramine (Questran, Prevalite)
 Colestipol (Colestid, Flavored Colestid)
 Colesevelam (Welchol)
b. Fibric acid derivatives or fibrates
- Are regarded as broad-spectrum lipid lowering
drugs. Their main action is to decrease triglyceride
levels but they are also tend to reduce low density
lipoprotein (LDL) chloresterol levels and help to
raise high density lipoprotein (HDL) cholesterol
 Gemfibrozil (Lopid)
 Clofibrate (Antromid-S)
Pharmacodynamics of Fibric acid derivatives:
 Fibrates are a class of medication that lowers
blood triglyceride levels. Fibrates lower blood
triglyceride levels by reducing the liver’s
production of VLDL (the triglyceride-carrying
particle that circulates in the blood) and by
speeding up the removal of trigylcerides from
the blood.
 Lipid-lowering agents are used for controlling
the high cholesterol and triglyceride level in
the blood.
 Pharmacokinetics of Fibric acid derivatives:
 Both drugs are absorbed readily from the GI
tract and are highly protein bound. Clofibrate
is hydrolyzed and Gemifibrozil undergoes
extensive metabolism in the liver before both
drugs are excreted in the urine
Pharmacotherapeutics of Fibric Acid derivatives:
 Fibric acid derivatives or fibrates are used
primarily to reduce triglyceride levels
especially very low density triglycerides and
secondary to lower cholesterol levels.
Cholesterol Synthesis inhibitors:
 Also known as statins lower lipid levels by interfering
with cholesterol synthesis.
 Statins include:
 Atorvastatin (Lipitor)
 Simvastatin (Zocor)
clotting factors required for a clot to form;
there are many newer agents, such as
Enoxaparin (brand name Lovenox),
Fondaparinux (brand name Arixtra), and
others.
o Oral anticoagulants such as Warfarin and
Dicumarol – which act by inhibiting the liver’s
production of vitamin K dependent
 Anticoagulant solutions are also used for the
preservation of stored whole blood and blood
fractions. These anticoagulants include heparin
and acid citrate dextrose (commonly called ACD).
 Anticoagulants are also used to keep laboratory
blood specimens from clotting. These agents
include not only heparin but also several agents
that make calcium ions unavailable to the clotting
process and so prevent the formation of clots,
these agents include etylenediaminetetraacetic
acid (commonly called EDTA), citrate, oxalate and
fluoride.

 Statins lower the chance of a “cardiovascular event”

such as a heart attack

Side Effects of Cholesterol Synthesis Inhibitors:

 Intestinal problems
 Liver damage (rare)
 Muscle inflammation
 High blood sugar and type 2 diabetes may also be more
likely with statins, although the risk is “small” and the
benefits outweigh the risks, according to the FDA

Pharmacodynamics of Cholesterol Synthesis Inhibitors:

 Reduce the synthesis of LDL

 Enhance the breakdown of LDL

Pharmacotherapeutics of Cholesterol Synthesis Inhibitors:

 By lowering cholesterol levels, the cholesterol synthesis

inhibitors reduce the risk of coronary artery disease.

Drugs Affecting Blood Coagulation:

 Anticoagulant – an agent that is used to prevent the

formation of blood clots. Some anticoagulants are used
for prevention on treatment of disorders characterized
by abnormal blood clots and emboli.
 Anticoagulants and antiplatelet drugs eliminate or
reduce the risk of blood clots. They’re often called
blood thinners, but these medications do not really
thin the blood. Instead, they help prevent or break up
dangerous blood cloths that form in your blood vessels
or heart.
 Anticoagulants are used for the prophylaxis
(prevention), and treatment of thromboembolic
disorders, such as stroke, heart attack (myocardial
infarction) and deep venous thrombosis (DVT). Emboli
are clots that break free, travel through the
bloodstream, and lodge in a blood vessel, such as
pulmonary embolism. The anticoagulant drugs are sued
for these clinical purposes include:
o Intravenous heparin – which acts by
inactivating thrombin and several other