CARDIOVASCULAR DRUGS
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 SYTEM
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—a waste product produced by cells is
absorbed into the blood and transported to the lungs
through the venous circulation.
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.
Nutrient and Waste Product Transport
1. Delivering nutrients to the body is another critical function of
the cardiovascular system.
2. After food is digested in 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 glucose 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
metabolic waste products and toxins and transports them to
the liver, kidneys and lungs for eventual elimination from the
body.
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.
3. If an infection occurs, these cells and chemical 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.
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. And thyroid hormones affect the
metabolic rate of virtually every body organ and tissue,
thanks to their body-wide delivery via the circulatory system.
Body Temperature Regulation
1. Body temperature regulation is an important function of the
cardiovascular system.
2. If body temperature begins to rise, blood vessels close to the
body surface dilate, increasing in size. This allows the body to
clear itself excess heat through the skin.
3. If body temperature drops, surface blood vessels constrict to
conserve body heat.
4. The cardiovascular system works in concert with the body’s
sweating mechanism as the primary regulators of body
temperature.
CARDIAC DRUGS
USED IN:
 Hypertension
 Angina Pectoris
 Myocardial Infarction (heart attack )
 Shock
 Arrhytmias
 CHF ( Cognitive 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 ALL 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 vasoconstrictor and stimulus
for the release of aldosterone.
Ace Inhibitors
 Benazepril ( Lotensin, Lotensin Het)
 Captopril ( Capoten)
 Enalapril ( Vasotec)
 Fosinopril (Monopril)
 Lisinopril (Prinivil, Zestril)
 Moexipril (Univasc)
 Perindopril (Aceon)
 Quinapril ( Accupril)
Pharmacodynamics
 The mechanism of action of the ACE inhibitors prevent 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 to 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 lowering the blood pressure is attributed to the
decrease in cardiac workload and decrease peripheral
resistance and blood volume.
Pharmacotherapeutics
 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 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)B 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 ARB’s 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 Angiotensin Receptor Blockers
1. Control high blood pressure
2. Treat heart failure
3. Prevents kidney failure in people with diabetes or high blood
pressure
4. Prevents diabetes and reduce the rick of stroke in patients
with high blood pressure and an enlarged heart.
5. 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
Pharmacotherapeutics
 Calcium channel blockers are used only for long term
prevention of Angina
 CCB are particularly effective for preventing Prinz metal’s
angina, a temporary increase in coronary vascular tone (
vasospasm ) causing a marked, but transient reduction in
luminal diameter.

 Calcium-channel blockers are smooth-muscle dilators and VASODILATING DRUGS

have a negative inotropic effect on the working myocardial
cells of the atria and ventricles Actions
 When administered orally, CCB are absorbed quickly and
almost completely  Arteriolar smooth muscle, dilate arteries and decrease
 Because of the first-pass-effect, the bioavailability (active peripheral vascular resistance.
effect) of these drugs is much lower.
 CCB highly bound to plasma protein (penetrate tissues less Uses
and excreted faster.)
 Moderate to severe hypertension and hypertensive crisis

Major side Effects:

1. Headache
2. Sodium retention
3. Rebound hypertension
Pharmacodynamics 4. Increased workload of heart, tachycardia, palpitations,
nausea/vomiting, abdominal pain
 Calcium channel blockers, are a group of medications that
disrupt the movement of calcium through calcium channels.
 Also called calcium antagonist, relax and widen blood vessels  A vasodilator is a drug that causes vasodilation, a widening
by affecting the muscle cells in the arterial walls. (opening) of the diameter of the interior (lumen) of the vessel
 It prevents calcium from entering cells of the heart and blood blood vessels that results from relaxation of the smooth muscle
vessel walls, resulting in lower blood pressure. Calcium of the vessels. The opposite of vasodilation is vasoconstriction.
channel blockers are used as antihypertensives drugs, i.e., as  This type of medicine works through several mechanism. For
medications to decrease blood pressure in patients with example :
hypertension .
  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 muscles 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
 The drugs are absorbed rapidly and disturbed well. They are
metabolized in the liver and most are exerted by the kidneys.
Pharmacodynamics
 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 flow.
 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.
Pharmacotherapeutics
 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 vital signs 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 Intake and output preferably with a Foley catheter in
a critical care setting.
3. Use micro drip 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.
Common drugs
1. Sodium nitroprusside (Nipride)
2. Hydralazine hydrochloride (Apresoliine)
3. Diazoxide ( Hyperstat)
4. Guanetidine sulfate (Ismelin)
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
 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
 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
INOTROPIC Affects the force of contraction
CHRONOTROPIC Interferes with the rate of the
heart beat
DROMOTROPIC Effect of Drugs on the Heart
Pertains to contraction
parasympathetic nervous system .
CARDIAC GLYCOSIDES
 The cardiac glycosides are 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 low 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 glycosides is digoxin.
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.
A. Positive inotropic effect: increases myocardial contraction,
which may decrease heart size in clients with
cardiomyopathy, and CHF and increases renal blood flow.
B. Negative chronotropic effect: decreases heart rate
 C. Negative dromotropic effect: slows conduction through the
atrioventricular (AV) 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 hearts size in cardiomyopathy (chronic disease of
the heart muscle) clients
Uses
 Congestive heart failure (CHF)- the heart has trouble
pumping blood
 Trial 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 .
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 Congestive Heart Failure (CHF) patients, digoxin decreases
peripheral resistance
 Digitalis has a notable, effect on BP, Systolic BP may increase
and diastolic may fall in CHF patients.
 Kidney : Diuresis occurs promptly in CHF patients
 CNS: In higher doses digoxin activates CTZ (chemo receptor
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 ow
(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 congestive heart failure (systolic and
diastolic dysfunctions)
 cardiac arrhythmias (atrial fibrillation, atrial flutter and
paroxysmal supraventricular tachycardia)
Current status of Digitalis
  These drugs increases
 Before the introduction of high ceiling diuretics, ACE  Amrinone lactate (INOCOR)
stroke volume and
inhibitors and beta blockers, digitalis was considered an  Milrinone lactate (PRIMACOR)
promote vasodilation
indispensable part of anti-CHF treatment.  Severe cardiac dysrhythmias might
 They are
 However, digitalis is still the most effective drug capable result from the use of
administered via IVF
of relieving symptoms of CHF and restoring cardiac phosphodiesterase inhibitors
compensation, especially in patients with dilated heart therefore, the client’s
and low ejection fraction. electrocardiogram (ECG) and cardiac status should be
closely monitored.
Treatment options for various stages of heart failure

 ACE= angiotensin-converting enzyme

 ARBs= angiotensin receptor blockers ANTIANGINAL DRUGS
 FDC= fixed dose combination
 HYD= Hydralazine  Angina pectoris refers to a strangling or pressure-like
 ISDN= isosorbide dinitrate pam caused by cardiac ischemia.
 The pain usually located substernally but is sometimes
Antidote for overdose od Digoxin perceived in the neck, shoulder and arm, or epigastrum.
 Women develop angina at a later age than men and
 Digoxin immune fab or Digibind (digoxin-specific are less likely to have classic substernal pain.
antibody)  Antianginal drugs are those that prevent, abort or
terminate attacks of angina pectoris
PHOSPHODIESTERASE INHIBITORS

 Phosphodiesterase inhibitor are another positive

inotropic group of drugs given to treat CHF when
there is no response with the use of other agents. Types of Angina
 This drug group inhibits the enzyme
phosphodiesterase, thus promoting a positive  Atherosclerotic Angina (classic angina and a common
inotropic response and vasodilation form )

2 drugs in this group - Attacks are predictably provoked (stable angina)

by exercise, emotion, eating or coitus and subside
when the increased energy demand is
withdrawn.
 - Rest, by reducing cardiac work, usually leads to NITRATES
complete relief of the pain within 15 min.
- Constitutes about 90% cases.  Acts in the following ways:

 Vasospastic angina (rest angina, variant angina, or Prinz
metal’s angina[uncommon form])
- Attacks occur at rest or during sleep and are
unpredictable.
- Is responsible for less than 10% of angina cases.
Treatment of Angina Pectoris
 Drugs in Angina have two main categories:
Nitrates adverse effects
 Reduction of oxygen demand
 Increase of oxygen delivery to the myocardium
Classification of Antianginal Drugs
 Preload reduction: Peripheral pulling of blood
decreases venous returns ( preload reduction)
 Afterload reduction: nitrates also produce some
arteriolar dilatation slightly decreases 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
arterioles or resistance vessels.
 Headache is the most common adverse effect of
nitrates
 High dose of nitrates can cause:

 Nitrates – short acting  Postural hypotension

 Glyceryl trinitrate (GTN, Nitroglycerine)- long acting  Facial flushing
 Isosorbide dinitrate – short acting by sublingual route  Tachycardia
 B blockers
- Isosorbide, mononitrate, Erythrity tetranitrate,
Pentaerythritol tetranitrate, Propanolol,
Metoprolol, Atenolol and others.

 Calcium channel blockers

- Phenyl alkylamine: Verapamil – Benzothiazepine:
Diltiazem – Dihydropyridines: Nifedipine,
Felodipine, Amlodipine, Nitrendipine, Nimodipine,
Lacidipine, Lercanidipine, Benidipine .

ANTI ARRHYTHMIC DRUGS
 Arrythmia 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 impulses.
 Factors like myocardial hypoxia, ischemia, Electrolyte disturbance,
trauma, can cause arrhythmias.
Factors that can cause Arrhythmias
 Arrhythmias may be TACHY arrhythmias or BRADY arrhythmias
 Digitalis induced Arrhythmias
 Based on the site of impulse origin, they may be group as
supraventricular, or (SA node or AV node, atria) or ventricular
arrhythmias, VA ARE A COMMON CAUSE OF DEATH, particularly
sudden death.
Other Arrhythmics
 Adenosine
- has a 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 ( Paroxysmal
supraventricular tachycardia)
 Atropine
- Is used in sinus bradycardia. It acts by blocking M2
receptors ( muscarine 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 regulates heart rate by altering the
electrical activity of 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 DRUG
THIAZIDE AND THIAZIDE-LIKE DIURETICS
 Are sulfonamide derivatives.
  Thiazide diuretics include:
- Chlorothiazide (Diuril)
- Hydrochlorothiazide (Microzide)
 Thiazide -like diuretics include:
- Chlorthalidone
- Indapamide
 Pharmacokinetics
o Thiazides are readily absorbed and are extensively bound to
plasma proteins. They are eliminated largely by secretion
into the proximal tubule.
o Thiazides cross the placenta and are secreted in breast
milk.
 Pharmacodynamics
o Thiazides and thiazides-like diuretics work by preventing
sodium to be reabsorbed in the kidney. As sodium is
excreted, it pulls water along with it.
o Thiazides and thiazides-like diuretics also increase the
excretion of chloride, potassium and bicarbonate, which can
result in electrolyte imbalances.
 Pharmacotherapeutics
o Thiazides are used as long term treatment of hypertension
and are also used to treat edema caused by mild to
moderate heart failure, liver disease, kidney disease and
corticosteroid and estrogen therapy.
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:
- Bumentanide (Bumex)
- Ethacrynic ( Edecrin)
- Furosemide ( Lasix)
 Decreases the sodium, chloride, and potassium
reabsorption for the tubule… Dilute urine is produced
because water is retained in the tubule when it
reaches the distal tubule
 It is often called a high ceiling diuretic because it is more effective
than other diuretics.
 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
o 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,
except for furosemide, which is excreted primarily
unchanged. Loop diuretics are excreted primarily by the
kidneys.
 Pharmacodynamics
o 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.
o Bumetanide is the short- acting diuretic it is 40x more potent
than another loop diuretic, furosemide.
 Pharmacotherapeutics
o 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)
o Loop diuretics are also used to treat edema associated with
liver disease or nephrotic syndrome (kidney disease).
 Adverse reactions to loop diuretics
o Risk of ototoxicity ( damage to the organs of hearing) when
aminoglycosides are taken with loop diuretics.
o Loop diuretics reduce the hypoglycemic effect of oral
antidiabetic drugs possibly resulting in hyperglycemia
 o Loop diuretics may increase the risk of lithium toxicity.
o An increased risk of electrolytic imbalances that can trigger
arrhythmias is present when digitalis glycosides and loop
diuretics are taken together.
POTASSIUM- SPARING DIURETICS
 Have weaker diuretic and antihypertensive effects than other
diuretics, but they have the advantage of conserving potassium.
 Potassium 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
o Potassium-sparing diuretics are only available orally and are
absorbed in the GI Tract.
o Metabolized in the liver except for Amiloride (which is not
metabolized) and excreted primarily in the urine and bile.
 Pharmacodynamics
o The direct action of potassium-sparing diuretics on the distal
tubule of the kidneys produces 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.
 Pharmacotherapeutics
o Potassium-sparing diuretics are used to treat:
- Edema
- Diuretic- induced hypokalemia in patients with heart
failure
- Cirrhosis
- Nephrotic syndrome(abnormal condition of the
kidneys)
- Hypertension
- 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 increases 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 heterogenous mixtures of fatty acids and alcohol
that are present in the body.
 the major lipids in the bloodstream are cholesterol and it’s 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 as 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:  Both drugs as absorbed readily from the GI tract and are highly
protein bound. Clofibrate is hydrolyzed and Gemfibrozil
 Bile sequestering drugs (cholestyramine and colestipol undergoes extensive metabolism in the liver before BTH drugs
hydrochloride ) are excreted in the urine.
 Fibric acid derivatives (clofibrate and gemfibrozil)
 Cholesterol synthesis inhibitors (lovastatin, pravastatin sodium and  Pharmacotherapeutic
simvastatin)
 Fibric acid derivatives or fibrates are used primarily to reduce
Bile sequestering drugs triglyceride levels esp. very low density triglycerides and
secondary lower cholesterol levels
 Cholestyramine ( Questran, Prevalite)
 Colestipol ( Colestid, flavored colestid) CHOLESTEROL SYNTHESIS INHIBITORS
 Colesevelam ( Welchol)  Also known as “statins” lower lipid levels by interfering with
- They are medications for lowering LDL cholesterol cholesterol synthesis
conjunction with diet modification.
Statins include:
- Atorvastrian (lipitor)
- Simvastatin (Zocor)
- Studies show that statins lower the chance of a “cardio
FIBRIC ACID DERIVATIVES OR FIBRATES vascular event” such as a heart attack

 FIBRIC ACID DERIVATIVES OR FIBRATES are regulated as Side effects

broad-spectrum lipid lowering drugs. Their main action is to
decrease triglyceride level but they also tend to reduce low density  Side effects can include
Lipoprotein(LDL) cholesterol.  Intestinal problems
 Liver damage (rare)
 Pharmacodynamics  Muscle inflammation
 fibric acid derivatives (fibrates) are a class of medication  High blood sugar and type 2 diabetes may also be more
that lowers blood triglyceride level. Fibrates Lower blood likely. With statins, although the risk is small and the
triglyceride levels by reducing the liver’s production of VI.DL. benefits outweigh the risks, according to FDA.
(the triglyceride caring particle that circulates in the blood) and by
speeding up the removal of triglycerides from the blood. Pharmacotherapeutics

 Fibric acid derivatives or fibrates  By lowering cholesterol, levels the cholesterol synthesis
 Examples of fibrates are Gemfibrozil (lopid) and chlofibrate inhibitors reduce the risk of coronary artery disease.
(Atromid-S)
 Lipid-lowering agents used for controlling the high cholesterol and Pharmacodynamics
triglyceride level in the blood)
 Pharmacokinetic  Reduce the synthesis of LDL
  Enhance the breakdown of LDL  Anticoagulant solutions are also used for the preservation of stored
whole blood and blood fractions. These anticoagulants include
Drugs affecting blood coagulation heparin and acid citrate dextrose (commonly called ACD)
 Anticoagulants are also used to keep laboratory blood specimens
 Anticoagulant: an agent that is used to prevent the formation of from clotting. These agents include not only heparin but also
blood clots . Anticoagulant have a virus uses . Some used for the several agents that make calcium ions unavailable to the clotting
prevention or treatment of disorders characterized by abnormal
process and so prevent the formation of clots: these agents include
blood clots and emboli.
ethylenediaminetetraacetic acid (commonly called EDTA), citrate,
oxalate and fluoride.
DRUGS AFFECTING BLOOD COAGULATION
Anticoagulants

 An agent that is used to prevent the formation of blood clots.

Anticoagulants have various uses. Some are used for the
prevention and treatment of disorders characterized by abnormal
blood clots and emboli.
 Anticoagulants and antiplatelet drugs eliminate or reduced the risk
of blood clots. They’re often called blood thinners, but these
medications do not really thin the blood.
 Instead, they help or break up the dangerous blood clots that form
in your blood vessels or heart.
 Anticoagulants have various uses. Some 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, travel
through the bloodstream, and lodge in a blood vessel, such as
Pulmonary embolism.
 The anticoagulant drugs used for these clinical purposes include:
o Intravenous heparin – which acts by inactivating thrombin
and several other clotting factors required for a clot to form;
there are many newer agents, such as Enoxaparin
(Lovenox), Fondaparimux (Arixtra), and others.
o Oral anticoagulants such as Warfarin and Dieumarol –
which act by inhibiting the liver’s production of vitamin K
dependent.