CARDIOVASCULAR AGENTS
CARDIOVASCULAR AGENTS
Introduction to the Cardiovascular System
 The heart is a hollow muscle that is divided into a
right and a left side by a thick septum and into
four chambers—the two upper atria and the two
lower ventricles.
 The right side of the heart receives all of the
deoxygenated blood from the body through the
veins and directs it into the lungs. The left side of
the heart receives oxygenated blood from the
lungs and pumps it out to every cell in the body
through the arteries.
 The heart is responsible for pumping oxygenated
blood to every cell in the body and for picking up
waste products from the tissues.
 The cardiac cycle consists of a period of rest, or
diastole, when blood is returned to the heart by
veins, and a period of contraction, or systole,
when the blood is pumped out of the heart.
 The heart muscle possesses the properties of
automaticity (the ability to generate an action
potential in the absence of stimulation) and
conductivity (the ability to rapidly transmit an
action potential).
 The heart muscle is stimulated to contract by
impulses generated in the heart, not by stimuli
from the brain. The autonomic nervous system can
affect the heart to increase (sympathetic) or
decrease (parasympathetic) activity.
 In normal sinus rhythm, cells in the SA node
generate an impulse that is transmitted through the
atrial bundles and delayed slightly at the AV
node before being sent down the bundle of His
into the ventricles. When cardiac muscle cells are
stimulated, they contract.
 Alterations in the generation of conduction of
impulses in the heart cause arrhythmias
(dysrhythmias), which can upset the normal
balance in the cardiovascular system and lead to a
decrease in cardiac output, affecting all of the cells
of the body.
 Heart muscle contracts by the sliding of actin and
myosin filaments in a functioning unit called a
sarcomere. Contraction requires energy and
calcium to allow the filaments to react with each
other and slide together.
 The heart muscle needs a constant supply of blood,
which is furnished by the coronary arteries.
Increase in demand for oxygen can occur with
changes in heart rate, preload, afterload, or stretch
on the muscle.
 The cardiovascular system is a closed pressure
system that uses arteries (muscular, pressure or
resistance vessels) to carry blood from the heart,
veins (flexible, distensible capacitance vessels) to
return blood to the heart, and capillaries (which
connect arteries to veins) to keep blood flowing
from areas of high pressure to areas of low
pressure.
 Blood pressure is maintained by stimulus from
the sympathetic system and reflex control of blood
volume and pressure by the renin–angiotensin
system and the aldosterone–ADH system.
Alterations in blood pressure (hypotension or
hypertension) can upset the balance of the
cardiovascular system and lead to problems in
blood delivery.
 Fluid shifts out of the blood at the arterial ends of
capillaries to deliver oxygen and nutrients to the
tissues. It moves out due to the hydrostatic or
fluid pressure of the arterial side of the system.
Fluid returns to the system at the venous end of
the capillaries because of the oncotic pull of
proteins in the vessels. Disruptions in these
pressures can lead to edema or loss of fluid in the
tissues.
1. CARDIAC GLYCOSIDES
- were originally derived from the foxglove or
digitalis plant. These plants were once ground up
to make digitalis leaf.
- digoxin (Lanoxin) is the drug most often used to
treat HF.
Therapeutic Action
- Digoxin increases intracellular calcium and allows
more calcium to enter myocardial cells during
depolarization, causing the following effects:
 Increased force of myocardial contraction (a
positive inotropic effect).
 Increased cardiac output and renal perfusion
(which has a diuretic effect, increasing urine
output and decreasing blood volume while
decreasing renin release and activation of the
renin–angiotensin–aldosterone system).
 Slowed heart rate, owing to slowing of the rate
of cellular repolarization (a negative
chronotropic effect).
 Decreased conduction velocity through the
atrioventricular node or decreased conduction
of heart cells (Negative dromotropic
action)
- The overall effect is a decrease in the
myocardial workload and relief of HF.
Indications:
 HF
CARDIOVASCULAR AGENTS

 Atrial flutter  Digoxin may be less effective if it is combined with

 Atrial fibrillation
 Paroxysmal atrial tachycardia
Pharmacokinetics:
o Oral and parenteral administration
o Rapid onset of action and rapid absorption:
 -30 to 120 minutes when taken orally
 -5 to 30 minutes when given intravenously
o Widely distributed throughout the body
o Primarily excreted unchanged in the urine
Contraindications:
× allergy to any component of the digitalis
preparation
× ventricular tachycardia or fibrillation
× heart block or sick sinus syndrome
× idiopathic hypertrophic subaortic stenosis (IHSS)
× acute MI
× renal insufficiency
× electrolyte abnormalities (e.g., increased calcium,
Caution:
ӿ Digoxin has a very narrow margin of safety
(meaning that the therapeutic dose is very close
to the toxic dose), so extreme care must be
taken when using this drug.
ӿ Pregnant or lactating
ӿ Pediatric and geriatric patients
Adverse Effects:
X headache
X weakness
X drowsiness
X vision changes (a yellow halo around objects is
often reported)
X Gastrointestinal upset
X Anorexia
X Arrhythmias
X Digoxin toxicity (A digoxin antidote, digoxin
immune Fab, has been developed to rapidly
treat digoxin toxicity)
thyroid hormones, metoclopramide, or
penicillamine.
 Absorption of oral digoxin may be decreased if it is
taken with cholestyramine, charcoal, colestipol,
antacids, bleomycin, cyclophosphamide, or
methotrexate.
2. ANTI-ANGINAL
 Coronary Artery Disease (CAD) – aka
ischemic heart disease, is characterized
by progressive narrowing of coronary
arteries, leading to a decreased delivery
of oxygen to cardiac muscle cells. The
narrowing of the vessels is caused by the
development of atheromas (fats, blood
cells, lipids, inflammatory agents, and
platelets) or fatty tumors in the intima of
the vessels, in a process called
atherosclerosis which leads to stiffening
of the artery, and loss of distensibility and
responsiveness.
- The heart muscle then becomes
hypoxic. This imbalance between
oxygen supply and demand is
manifested as pain, or angina
pectoris, which literally means
“suffocation of the chest”
 Chronic Stable (classic)) angina
occurs when the heart muscle is
perfused adequately except during
exertion or increased demand.

Clinically Important Drug–Drug Interactions

 Risk of increased therapeutic effects and toxic

effects of digoxin if it is taken with verapamil,
amiodarone, quinidine, quinine, erythromycin,
tetracycline, or cyclosporine.
 The risk of cardiac arrhythmias could increase if
these drugs are taken with potassium-losing
diuretics.
CARDIOVASCULAR AGENTS
 Unstable or preinfarction angina
occurs when the vessels are so
narrow that the myocardial cells are
deprived of sufficient oxygen even
at rest.
 Prinzmetal angina is a spasm of a
coronary vessel that decreases the
flow of blood through the narrowed
lumen.
 Myocardial Infarction (Heart Attack) –
results when a coronary vessel is
completely occluded, the cells that
depend on that vessel for oxygen become
ischemic, then necrotic, and die.
Angina
CAD MI
Pectoris
 Antianginal drugs are used to help restore the
appropriate supply-and-demand ratio in oxygen
delivery to the myocardium when rest is not
enough. These drugs can work to improve blood
delivery to the heart muscle in one of two ways
1. by dilating blood vessels (i.e., increasing the
supply of oxygen)
2. by decreasing the work of the heart (i.e.,
decreasing the demand for oxygen)
A. Nitrates
 amyl nitrate (generic)
 isosorbide dinitrate (Isordil)
 isosorbide mononitrate (Imdur, Monoket),
nitroglycerin (NitroBid, Nitrostat, etc.)
Therapeutic Action:
- Act directly on smooth muscle to cause
relaxation and to depress muscle tone. Because
the action is direct, these drugs do not influence
any nerve or other activity, and the response is
usually quite fast.
 Relax and dilate veins, arteries, and capillaries,
allowing increased blood flow through the
vessels and lowering systemic blood pressure
because of a drop in resistance.
 main effect of nitrates, however, seems to be
related to the drop in blood pressure that
occurs. The vasodilation causes blood to pool
in veins and capillaries, decreasing preload,
while the relaxation of the vessels decreases
afterload. The combination of these effects
greatly reduces the cardiac workload and the
demand for oxygen, thus bringing the
supplyand-demand ratio back into balance.
Indication: Angina Pectoris
Pharmacokinetics:
o Available as a sublingual tablet, a translingual
spray, an intravenous solution (for bolus
injection or infusion), a transdermal patch, a
topical ointment or paste, or a transmucosal
agent
o Slow-release forms also are available for use
in preventing anginal attacks.
o Nitrates are very rapidly absorbed,
metabolized in the liver, and excreted in
urine. They cross the placenta and enter
breast milk.
Contraindications:
× presence of any allergy to nitrates
× severe anemia
× head trauma or cerebral hemorrhage
× pregnancy or lactation
Cautions:
ӿ patients with hepatic or renal disease
ӿ hypotension, hypovolemia, and conditions
that limit cardiac output
Adverse Effects:
X mainly related to vasodilation and decreased
blood flow that occurs
X Central nervous system (CNS) effects -
headache, dizziness, and weakness.
X Gastrointestinal (GI) symptoms - nausea,
vomiting, and incontinence.
X Cardiovascular problems - hypotension, reflex
tachycardia, syncope, and angina
X Skin-related effects - flushing, pallor, and
increased perspiration. risk of contact
dermatitis and local hypersensitivity reactions.
Clinically Important Drug–Drug Interactions
:
 Risk of hypertension and decreased
antianginal effects if these drugs are given
with ergot derivatives.
 Patients should not combine nitrates with
sildenafil, tadalafil, or vardenafil, drugs used
to treat erectile dysfunction, because serious
hypotension and cardiovascular events could
occur.
B. Beta Adrenergic Blockers
 metoprolol (Toprol)
 propranolol (Inderal)
CARDIOVASCULAR AGENTS
 nadolol (Corgard)
Therapeutic Action:
- Used to block the stimulatory effects of the
sympathetic nervous system.
- Competitively block beta-adrenergic receptors in
the heart and juxtaglomerular apparatus,
decreasing the influence of the sympathetic
nervous system on these tissues
 decrease in the excitability of the heart
 decrease in cardiac output
 decrease in cardiac oxygen consumption
 lowering of blood pressure
Indication:
 Propranolol and metoprolol can also be used
to prevent reinfarction in stable patients 1 to
4 weeks after an MI.
 Angina Pectoris
Pharmacokinetics:
o These drugs are absorbed from the GI tract
after oral administration and undergo hepatic
metabolism.
o They reach peak levels in 60 to 90 minutes
and have varying duration of effects, ranging
from 6 to 19 hours.
Contraindications
× Patients with bradycardia, heart block, and
cardiogenic shock
× Pregnancy and lactation
Caution:
ӿ Patients with diabetes, peripheral vascular
disease, asthma, chronic obstructive
pulmonary disease (COPD), or thyrotoxicosis.
Adverse Effects:
X Associated with the blockade of the
sympathetic nervous system
X CNS effects - dizziness, fatigue, emotional
depression, and sleep disturbances.
X GI problems - gastric pain, nausea, vomiting,
colitis, and diarrhea.
X Cardiovascular effects - heart failure,
reduced cardiac output, and arrhythmias.
X Respiratory effects - bronchospasm,
dyspnea, and cough.
X Decreased exercise tolerance and malaise
are also common complaints
Clinically Important Drug–Drug Interactions
:
 A decreased antihypertensive effect occurs
when betablockers are given with
nonsteroidal anti-inflammatory drugs.
 An initial hypertensive episode followed by
bradycardia occurs if these drugs are given
with epinephrine
 A possibility of peripheral ischemia exists if
beta-blockers are taken in combination with
ergot alkaloids.
 There also is a potential for a change in
blood glucose levels if these drugs are given
with insulin or antidiabetic agents
C. Calcium Channel Blockers
 amlodipine (Norvasc)
 diltiazem (Cardizem)
 nicardipine (Cardene)
 nifedipine (Adalat, Procardia)
 verapamil (Calan, Isoptin)
Therapeutic Action:
- Inhibit the movement of calcium ions across
the membranes of myocardial and arterial
muscle cells, altering the action potential and
blocking muscle cell contraction.
 A loss of smooth muscle tone, vasodilation,
and decreased peripheral resistance occur.
 Subsequently, preload and afterload are
decreased, which in turn decreases cardiac
workload and oxygen consumption.
Indications:
 Treatment of Prinzmetal angina
 Chronic angina
 Effort-associated angina
 Hypertension
Pharmacokinetics:
o These drugs are generally well absorbed after
oral administration, metabolized in the liver,
and excreted in urine.
o They have an onset of action of 20 minutes
and a duration of action of 2 to 4 hours.
o These drugs cross the placenta and enter
breast milk.
Contraindications:
× Presence of allergy to any of these drugs to
avoid hypersensitivity reactions
× Pregnancy or lactation
CARDIOVASCULAR AGENTS

Caution:  Increased serum levels and toxicity of

cyclosporine if they are taken with diltiazem
ӿ Heart block or sick sinus syndrome  Increased risk of heart block and digoxin
ӿ Renal or hepatic dysfunction toxicity if they are combined with verapamil
ӿ Heart failure (because verapamil increases digoxin serum
Adverse Effects: levels).
 Both verapamil and digoxin depress
X related to their effects on cardiac output and myocardial conduction.
on smooth muscle  Verapamil has also been associated with
X CNS effects - dizziness, light-headedness, serious respiratory depression when given
headache, and fatigue. with general anesthetics or as an adjunct to
X GI effects - nausea and hepatic injury related anesthesia.
to direct toxic effects on hepatic cells.
X Cardiovascular effects - hypotension, 3. ANTI-DYSRHYTHMIC/ANTIARRYTHMIC
bradycardia, peripheral edema, and heart AGENTS
block.  Antiarrhythmics affect the action potential of the
X Skin effects - flushing and rash. cardiac cells by altering their automaticity,
conductivity, or both.
Clinically Important Drug–Drug Interactions  Because of this effect, antiarrhythmic drugs can
: also produce new arrhythmias—that is, they are
proarrhythmic.
 Arrhythmias (also called dysrhythmias)  Antiarrhythmics are used in emergency situations
are disruptions in the normal rate or rhythm when the hemodynamics arising from the patient’s
of the heart. arrhythmia are severe and could potentially be
 Dysrhythmia: disturbed heart rhythm fatal.
 Arrhythmia: absence of heart rhythm
 The cardiac conduction system determines
the heart’s rate and rhythm. The property
by which the cardiac cells generate an
action potential internally to stimulate the
cardiac muscle without other stimulation is
known as automaticity.
 Electrolyte disturbances, decreases in the
oxygen delivered to the cells, structural
damage in the conduction pathway, drug
effects, acidosis, or the accumulation of
waste products can trigger arrhythmias.
 Changes in the heart rate, uncoordinated
heart muscle contractions, or blocks that
alter the movement of impulses through
the system can disrupt heart rhythm.
 Arrhythmias change the mechanics of
blood circulation (hemodynamics), which
can interrupt delivery of blood to the brain,
other tissues, and the heart.

Types of Arrhythmias:

1. Tachycardia - This fast heart rhythm

causes a heart rate of more than 100 beats
per minute.
2. Bradycardia - This slow heart rhythm
causes a heart rate of less than 60 beats
per minute.
3. Premature heartbeat - A premature, or
extra beat is a common, usually harmless
type of arrhythmia that typically does not
cause symptoms.
 4. Supraventricular arrhythmias - These
arrhythmias are tachycardias that occur in
the atria or the atrioventricular (AV) node,
CARDIOVASCULAR AGENTS
specialized tissue that conducts electrical
signals from the atria to the ventricles.
 Atrial fibrillation (AFib): Irregular, rapid
heartbeat that can be intermittent, long
lasting, or permanent
 Atrial flutter: Regular, rapid heartbeat
 Paroxysmal supraventricular
tachycardia (PSVT): Rapid, regular
heartbeat that begins and ends suddenly
 Wolff-Parkinson-White syndrome: A
type of PSVT in which the heart has an
extra electrical pathway between the
atria and ventricles, disrupting the timing
of electrical signals and causing the
ventricles to beat too fast
5. Ventricular arrhythmias - Tachycardias
that begin in the lower chambers of the
heart can be life-threatening and require
immediate medical attention.
 Ventricular tachycardia (VT): Rapid,
regular heartbeat that can last for just a
few seconds or much longer, which
increases the risk of becoming
ventricular fibrillation
 Ventricular fibrillation (VFib): Rapid,
irregular heartbeat that causes the
ventricles to quiver ineffectively instead
of pumping blood and can lead to
sudden cardiac arrest and death within
minutes, without emergency care
 Torsades de pointes: A type of VT that
develops in people with long QT
syndrome, an electrical problem that
causes the heart to take longer to
recharge after each heartbeat, which can
lead to VFib and sudden death
Types of Antidysrhythmic Drugs:
I. Class I: Sodium Channel Blockers
Therapeutic Actions:
 stabilize the cell membrane by binding to sodium
channels, depressing phase 0 of the action
potential, and generally prolong the action
potential, leading to a slowing of conduction and
automaticity.
- Class I antiarrhythmics are local anesthetics or
membrane stabilizers
 They bind more quickly to sodium channels that are
open or inactive—ones that have been stimulated
and are not yet repolarized
- A sodium channel blocker decreases sodium
influx into cardiac cells.
 decreased conduction velocity in cardiac tissues
 suppression of automaticity, which decreases the
likelihood of ectopic foci
 increased recovery time (repolarization or
refractory period).
 Class IA: slows conduction and prolongs
repolarization (quinidine, procainamide,
disopyramide).
 Class IB: slows conduction and shortens
repolarization (lidocaine, mexiletine HCl)
 Class IC: prolongs conduction with little to no
effect on repolarization (flecainide)
Indications:
 Tachycardia
 Potentially life-threatening ventricular
arrhythmias
Pharmacokinetics:
o Parenteral (IM and IV) and oral form
o These drugs are widely distributed after injection
or after rapid absorption through the
gastrointestinal (GI) tract. They undergo
extensive hepatic metabolism and are excreted in
urine. These drugs cross the placenta and are
found in breast milk
Contraindications:
× allergy to any of these drugs
× bradycardia or heart block unless an artificial
pacemaker is in place
× heart failure (HF), hypotension, or shock
× electrolyte disturbances
Caution:
ӿ renal or hepatic dysfunction
ӿ pregnancy risk Category C
Adverse Effects:
X associated with their membrane-stabilizing effects
and effects on action potentials
X Central nervous system (CNS) effects can include
dizziness, drowsiness, fatigue, twitching, mouth
numbness, slurred speech, vision changes, and
tremors that can progress to convulsions.
X GI symptoms include changes in taste, nausea, and
vomiting.
X Cardiovascular effects include the proarrhythmic
effects that lead to the development of arrhythmias
(including heart blocks), hypotension, vasodilation,
and the potential for cardiac arrest.
X Respiratory depression progressing to respiratory
arrest can also occur.
X Other adverse effects include rash, hypersensitivity
reactions, loss of hair, and potential bone marrow
depression.
 CARDIOVASCULAR AGENTS
X The CAST study found that the long-term treatment
of arrhythmias may actually cause cardiac death, so
these drugs are now indicated only for the short-
term treatment of potentially life-threatening
ventricular arrhythmias.
Clinically Important Drug–Drug and Drug-Food
Interactions:
 The risk for arrhythmia increases if these agents
are combined with other drugs that are known to
cause arrhythmias, such as digoxin and the beta-
blockers.
 The risk of bleeding effects of these drugs
increases if they are combined with oral
anticoagulants
 Quinidine requires a slightly acidic urine (normal
state) for excretion. Patients receiving quinidine
should avoid foods that alkalinize the urine [e.g.,
citrus (grapefruit) juices, vegetables, antacids, milk
products], which could lead to increased quinidine
levels and toxicity
II. Class II: Beta Blockers
 propranolol (Inderal)
 acebutolol (Sectral)
 esmolol (Brevibloc)
 sotalol (Betapace)
Therapeutic Actions:
- beta-adrenergic blockers that block beta-receptors,
causing a depression of phase 4 of the action
potential
- prevent sympathetic stimulation
- competitively block beta-receptor sites in the heart
and kidneys.
 Decrease heart rate, cardiac excitability, and
cardiac output, a slowing of conduction through the
AV node, and a decrease in the release of renin.
 These effects stabilize excitable cardiac tissue and
decrease blood pressure, which decreases the
heart’s workload and may further stabilize hypoxic
cardiac tissue.
 decrease conduction velocity, automaticity, and
recovery time (refractory period).
- more frequently prescribed for dysrhythmias than
sodium channel blockers.
Indications: supraventricular tachycardias and PVCs
Pharmacokinetics:
o Acebutolol is an oral drug. Esmolol is administered
intravenously. Propranolol may be administered
orally or intravenously.
o These drugs are absorbed from the GI tract or have
an immediate effect when given intravenously and
undergo hepatic metabolism. They are excreted in
the urine.
o Food has been found to increase the bioavailability
of propranolol
Contraindications:
× sinus bradycardia (rate less than 45 beats/min) and
AV block
× cardiogenic shock, HF, asthma, or respiratory
depression
× pregnancy and lactation
Caution:
ӿ patients with diabetes and thyroid dysfunction
ӿ renal and hepatic dysfunction
Adverse Effects:
X related to the effects of blocking beta-receptors in
the sympathetic nervous system.
X CNS effects include dizziness, insomnia, dreams,
and fatigue.
X Cardiovascular symptoms can include hypotension,
bradycardia, AV block, arrhythmias, and alterations
in peripheral perfusion.
X Respiratory effects can include bronchospasm and
dyspnea.
X GI problems frequently include nausea, vomiting,
anorexia, constipation, and diarrhea.
X Other effects to anticipate include a loss of libido,
decreased exercise tolerance, and alterations in
blood glucose levels.
Clinically Important Drug–Drug Interactions:
 The risk of adverse effects increases if these drugs
are taken with verapamil
 a possibility of increased hypoglycemia if these
drugs are combined with insulin
III. Class III: Drugs That Prolong
Repolarization
 amiodarone HCl (Cordarone), dofetilide
(Tikosyn), ibutilide (Corvert), sotalol (Betapace)
Therapeutic Actions and Indications:
- block potassium channels and slow the outward
movement of potassium during phase 3 of the
action potential, prolonging it
- prolong repolarization and are used in emergency
treatment of ventricular dysrhythmias when other
antidysrhythmics are ineffective.
CARDIOVASCULAR AGENTS
 Amiodarone (Cordarone) increases the
refractory period (recovery time) and prolongs the
action potential duration (cardiac cell activity);
 Amiodarone is the drug recommended for use
during life support measures (ventricular fibrillation
or pulseless ventricular tachycardia in cardiac arrest
situations)
Pharmacokinetics:
o Amiodarone is available in an oral or intravenous
form. Dofetilide and sotalol are administered only in
oral form. Ibutilide is given IV.
o These drugs are well absorbed after oral
administration and are immediately available after
IV administration and widely distributed.
o Absorption of sotalol is decreased by the presence
of food. They are metabolized in the liver and
excreted in urine.
Contraindications:
× When these drugs are used to treat life-threatening
arrhythmias for which no other drug has been
effective, there are no contraindications.
× Ibutilide and dofetilide should not be used in the
presence of AV block
Caution:
ӿ presence of shock, hypotension, or respiratory
depression; with a prolonged QTc interval
ӿ Renal and hepatic disorders
Adverse Effects:
X related to the changes they cause in action
potentials.
X Nausea, vomiting, and GI distress
X weakness and dizziness
X hypotension, HF, and arrhythmia are
common.
X Amiodarone has been associated with a
potentially fatal liver toxicity, ocular
abnormalities, and the development of very
serious cardiac arrhythmias.
Clinically Important Drug–Drug Interactions:
 serious toxic effects if they are combined with
digoxin or quinidine
 increased risk of proarrhythmias if they are
combined with antihistamines, phenothiazines, or
tricyclic antidepressants.
 increased risk of serious adverse effects if dofetilide
is combined with ketoconazole, cimetidine, or
verapamil, and so these combinations should be
avoided.
 Sotalol may have a loss of effectiveness if it is
combined with nonsteroidal antiinflammatory drugs,
aspirin, or antacids.
IV. Class IV: Calcium Channel Blockers
 verapamil (Calan, Isoptin)
 diltiazem (Cardizem)
Therapeutic Actions:
- block the movement of calcium ions across the cell
membrane, depressing the generation of action
potentials and delaying phases 1 and 2 of
repolarization, which slows automaticity and
conduction.
 Verapamil is a slow (calcium) channel blocker that
blocks calcium influx, thereby decreasing the
excitability and contractility (negative inotropic) of
the myocardium. It increases the refractory period
of the AV node, which decreases ventricular
response.
Indications:
 Both diltiazem and verapamil are used as
antihypertensives and to treat angina
 Diltiazem – treatment of paroxysmal
supraventricular tachycardia, atrial fibrillation, and
atrial flutter
Pharmacokinetics:
o Diltiazem is administered intravenously. When used
as an antiarrhythmic, verapamil is used
intravenously.
o These drugs are well absorbed after intravenous
administration. They are highly protein bound,
metabolized in the liver, and excreted in the urine.
They cross the placenta and enter breast milk.
Contraindications:
× allergy to any calcium channel blocker
× sick sinus syndrome or heart block (unless an
artificial pacemaker is in place)
× pregnancy or lactation
× HF or hypotension
Caution:
ӿ Caution should be used in cases of idiopathic
hypertrophic subaortic stenosis (IHSS)
ӿ impaired renal or liver function
Adverse Effects:
X related to their vasodilation of blood vessels
throughout the body.
CARDIOVASCULAR AGENTS
X CNS effects include dizziness, weakness, fatigue,
depression, and headache.
X GI upset, nausea, and vomiting can occur.
X Hypotension, HF, shock, arrhythmias, and edema
have also been reported.
Clinically Important Drug–Drug Interactions:
 Verapamil has been associated with many drug–
drug interactions, including increased risk of cardiac
depression with betablockers; additive AV slowing
with digoxin; increased serum levels and toxicity of
digoxin, carbamazepine, prazosin, and quinidine;
increased respiratory depression with atracurium,
gallamine, pancuronium, tubocurarine, and
vecuronium; and decreased effects if combined
with calcium products or rifampin.
 There is a risk of severe cardiac effects if these
drugs are given IV within 48 hours of IV beta-
adrenergic drugs
 Diltiazem can increase the serum levels and toxicity
of cyclosporine if the drugs are taken concurrently
Other Antiarhythmics:
 Adenosine
- used to convert supraventricular tachycardia to
sinus rhythm if vagal maneuvers have been
ineffective.
- It is often the drug of choice for terminating
supraventricular tachycardias, including those
associated with the use of alternative conduction
pathways around the AV node (e.g., Wolff–
Parkinson–White syndrome), for two reasons:
(1) it has a very short duration of action (about
15 seconds), after which it is picked up by
circulating red blood cells and cleared through
the liver
(2) it is associated with very few adverse effects
(headache, flushing, and dyspnea of short
duration)
- This drug slows conduction through the AV node,
prolongs the refractory period, and decreases
automaticity in the AV node.
- It is given IV with continuous monitoring of the
patient.
 Digoxin
- This drug slows calcium from leaving the cell,
prolonging the action potential and slowing
conduction and heart rate.
- effective in the treatment of atrial arrhythmias.
- The drug exerts a positive inotropic effect, leading
to increased cardiac output, which increases
perfusion of the coronary arteries and may
eliminate the cause of some arrhythmias as hypoxia
is resolved and waste products are removed more
effectively.
4. Peripheral Vascular Drugs
a.) ANTIHYPERTENSIVE DRUGS
 Essential hypertension is the most common
type, affecting 90% of persons with high
blood pressure
 Secondary hypertension - Ten percent of
hypertension cases are related to renal and
endocrine disorders
The kidneys and blood vessels strive to regulate and
maintain a “normal” blood pressure
i. SYMPATHOLYTICS (Sympathetic
Depressants)
 Beta-Adrenergic Blockers
- Beta blockers tend to be more
effective in lowering blood pressure
in patients who have an elevated
serum renin level.
Non-selective beta blockers: (n-z)
 Propanolol (Inderal)
 inhibit beta1 (heart) and beta2 (bronchial)
receptors. Heart rate slows (blood pressure
decreases secondary to the decrease in
heart rate), and bronchoconstriction occurs
because of unopposed parasympathetic
tone.
Cardioselective beta blockers: (a-m)
 Acebutolol (Sectral)
 Atenolol (tenormin)
 Metoprolol (Lopressor)
 they act mainly on the beta1 rather than the
beta2 receptors and bronchoconstriction is
less likely to occur.
Therapeutic Actions
• Beta (β+ and β−)-adrenergic blockers
reduce cardiac output by diminishing the
sympathetic nervous system response to
decrease basal sympathetic tone.
• Beta blockers reduce heart rate, contractility,
and renin release.
Pharmacokinetics
 Metoprolol is well absorbed from the
gastrointestinal tract. Its half-life is short
and its protein-binding power is low.
CARDIOVASCULAR AGENTS
Pharmacodynamics
 Cardioselective beta-adrenergic blockers
block beta1 receptors, thereby
decreasing heart rate and blood
pressure.
 The nonselective beta blockers block
beta1 and beta2 receptors, which can
result in bronchial constriction.
The onset of action of oral beta blockers is usually
30 minutes or less, and the duration of action is 6
to 12 hours. When beta blockers are administered
intravenously, the onset of action is immediate,
peak time is 20 minutes (compared with 1.5
hours orally), and duration of action is 4 to 10
hours
Side Effects and Adverse Reactions
× decreased pulse rate, markedly decreased
blood pressure
× (with noncardioselective beta1 and beta2
blockers) bronchospasm.
× should not be abruptly discontinued,
because rebound hypertension, angina,
dysrhythmias, and myocardial infarction can
result.
× dizziness, insomnia, depression, fatigue,
nightmares, and sexual dysfunction.
Caution
× Noncardioselective beta blockers inhibit the
liver’s ability to convert glycogen to glucose
in response to hypoglycemia. Because of
this side effect, beta blockers should be used
with caution in patients with diabetes
mellitus.
 Centrally Acting Alpha-2 Agonists
- Centrally acting alpha2 agonists
decrease the sympathetic response
from the brainstem to the peripheral
vessels.
 Methyldopa
 Clonidine
 Guanfacine
Therapeutic Actions
-They stimulate the alpha2 receptors, which
in turn decreases sympathetic activity; increases
vagus activity; decreases cardiac output; and
decreases serum epinephrine, norepinephrine, and
renin release
Pharmacokinetics & Pharmacodynamics
 Methyldopa was one of the first drugs
widely used to control hypertension. In high
doses, methyldopa and clonidine can cause
sodium and water retention. Frequently
methyldopa and clonidine are administered
with diuretics.
 Clonidine is available in a transdermal
preparation that provides a 7-day duration of
action. Transdermal patches are replaced
every 7 days and may be left on while
bathing; skin irritations may occur.
 Guanfacine has effects similar to clonidine.
Guanfacine has a long half-life and usually is
taken once a day
Side Effects and Adverse Reactions
× drowsiness, dry mouth, dizziness, and slow
heart rate (bradycardia).
× This group of drugs must not be abruptly
discontinued, because a rebound
hypertensive crisis can result. (If the drug
needs to be stopped immediately, another
antihypertensive drug is usually prescribed
to avoid rebound hypertensive symptoms)
× Rebound hypertension is less likely to occur
with guanfacine.
Caution
Methyldopa should not be used in patients with
impaired liver function, and serum liver enzymes
should be monitored periodically in all patients
Nursing Considerations
 The nurse should emphasize the need to
take the medication as prescribed. This
group of drugs can cause sodium and
water retention, resulting in peripheral
edema.
 A diuretic may be ordered with
methyldopa or clonidine to decrease
water and sodium retention (edema).
 Patients who are pregnant or
contemplating pregnancy should avoid
clonidine.
 Methyldopa is frequently used to treat
chronic or pregnancy induced
hypertension; however, it crosses the
placental barrier, and small amounts
CARDIOVASCULAR AGENTS
may enter the breast milk of a lactating
patient
 Alpha-Adrenergic Blockers
- Alpha blockers are useful in treating
hypertension in patients with lipid
abnormalities
- They decrease the very-low-density
lipoproteins (VLDL) and the low-
density lipoproteins (LDL) that are
responsible for the buildup of fatty
plaques in the arteries
(atherosclerosis). In addition, they
increase highdensity lipoprotein
(HDL) levels.
Non-selective alpha blockers
 Phentalamine
 Phenoxybenzomine
Selective alpha blockers
 Prazosin
 Doxazosin
 Terazosin
Therapeutic Actions
-This group of drugs blocks the alpha-adrenergic
receptors (alpha blockers), resulting in vasodilation
and decreased blood pressure
Pharmacokinetics
Selective alpha blockers: Prazosin is absorbed through
the GI tract, but a large portion of prazosin is lost
during hepatic first-pass metabolism. The half-life is
short, so the drug should be administered twice a
day. 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. With prazosin, the heart rate is
only slightly increased.
 Nonselective alpha blockers such as
phentolamine, the blood pressure is greatly
reduced, and reflex tachycardia can occur.
NOTE: Nonselective alpha blockers are more
effective for acute hypertension; selective alpha
blockers are more useful for long-term essential
hypertension.
Side Effects and Adverse Reactions.
Selective alpha blockers:
× prazosin, doxazosin, and terazosin include
orthostatic hypotension (dizziness, faintness,
lightheadedness, and increased heart rate,
which may occur with first dose), nausea,
headache, drowsiness, nasal congestion
caused by vasodilation, edema, and weight
gain.
Non-selective alpha blockers:
× Side effects of phentolamine include
hypotension, reflex tachycardia caused by
the severe decrease in blood pressure, nasal
congestion caused by vasodilation, and GI
disturbances.
Drug Interactions
- occur when alphaadrenergic blockers
are taken with antiinflammatory
drugs and nitrates (e.g., nitroglycerin
for angina). Peripheral edema is
intensified when prazosin and an
antiinflammatory drug are taken
daily.
- Nitroglycerin taken for angina lowers
blood pressure. If prazosin is taken
with nitroglycerin, syncope
(faintness) caused by a decrease in
blood pressure can occur
 Adrenergic Neuron Blockers
(Peripherally Acting Sympatholytics)
 Reserphine
Therapeutic Actions
-It is potent antihypertensive drugs that block
norepinephrine release from the sympathetic nerve
endings, causing a decrease in norepinephrine release
that results in a lowering of blood pressure.
Side Effect & Nursing Consideration
-Orthostatic hypotension is a common side effect,so
the patient should be advised to rise slowly from a
reclining or sitting position
 Alpha1- and Beta1-Adrenergic Blockers
 Labetalol (Normodyne)
- Blocking the alpha1 receptor causes
vasodilation, decreasing resistance to
blood flow. The effect on the alpha
receptor is stronger than the effect
on the beta receptor; therefore
CARDIOVASCULAR AGENTS
blood pressure is lowered and pulse
rate is moderately decreased
ii. DIRECT-ACTING ARTERIOLAR
VASODILATORS
 Vasodilator
- Direct-acting vasodilators act by
relaxing the smooth muscles of the
blood vessels, mainly the arteries,
causing vasodilation.
- With vasodilation, the blood pressure
decreases and sodium and water are
retained, resulting in peripheral
edema. Diuretics can be given with a
direct-acting vasodilator to decrease
the edema.
 Hydralazine
 Minoxidil
 Nitropusside
Indications
 Hydralazine and minoxidil used for
moderate to severe (dose-related)
hypertension.
 Nitroprusside is prescribed for acute
hypertensive emergency. This is a very
potent vasodilator that rapidly decreases
blood pressure. Nitroprusside acts on both
arterial and venous vessels.
Side Effects and Adverse Reactions
× reflex tachycardia, palpitations, edema, nasal
congestion, headache, dizziness, GI
bleeding, lupus-like symptoms, and
neurologic symptoms (tingling, numbness).
× Minoxidil has similar side effects, as well as
tachycardia, edema, and excess hair growth.
It can precipitate an anginal attack.
× Nitroprusside can cause reflex tachycardia,
palpitations, restlessness, agitation, nausea,
and confusion
iii. DIURETICS
- usually given at morning
Thiazide and Thiazide Like Diuretic
 hydrochlorothiazide
- blocks Na and K reabsorption; reabsorb Ca
- hypercalcemia
Loop Diuretics
 Furosemide (Lasix)
- blocks Na, K, and Ca reabsorption
- hypocalcemia
Carbonic Anhydrase Inhibitors
 Acetazolimide (Diamox)
- increase Na+, K+, & HCO3 secretion, along with
it is H2O
- metabolic acidosis
Osmotic Diuretic
 Mannitol
- Increase osmotic pressure of the glomerular
filtrate.
- hypotension
Potassium Sparing Diuretics
 Spironolactone (Aldactone)
- excrete Na and water but it reabsorb K
- hyperkalemia
iv. ANGIOTENSIN CONVERTING ENZYME
INHIBITORS ( Ace Inhibitors)
 captopril (Capoten),
 enalapril (Vasotec),
 quinapril,
 lisinopril
Mechanism of actions :
- prevent peripheral vasoconstriction by blocking
conversion of angiotensin I to
angiotensin II decreasing peripheral resistance.
Side Effects and Adverse Reactions
× Primary side effect – constant, irritated
cough.
× Other side effects include nausea,
vomiting, diarrhea, headache, dizziness,
fatigue, insomnia, serum potassium excess
and tachycardia.
× The major adverse effects - are first-
dose hypotension and hyperkalemia.
× Angioedema (swelling of face, tongue, lips,
mucous membranes, larynx, and extremity
edema) may occur due to hypersensitivity
and has a higher incidence in African
CARDIOVASCULAR AGENTS
Americans. This may occur within hours or
1 week after the first dose
Nursing considerations
- not to discontinue medications because it can
cause rebound hypertension.
- avoid using K+ sparing diuretics.
v. ANGIOTENSIN II RECEPTOR BLOCKERS
• Are similar to ACE inhibitors in that they
prevent the release of aldosterone (sodium-
retaining hormone). ARBs block angiotensin
II from the angiotensin I (AT1).ARBs cause
vasodilation and decrease peripheral
resistance.
• They do not cause the constant, irritated
cough ACE inhibitors can. Like ACE
inhibitors, ARBs should not be taken during
pregnancy
 Valsartan
 Losartan
 Eprosartan
Therapeutic Effects/Uses
 To treat hypertension
 Mode of Action: Potent vasodilator;
inhibits binding of angiotensin II
Side Effects Adverse Reactions
× Dizziness, drowsiness, cough (rare), blurred
vision, headache, diarrhea, insomnia,
arthralgia, fatigue
× Orthostatic hypotension, hypoglycemia,
hyperkalemia
× Life threatening: renal dysfunction
vi. CALCIUM-CHANNEL BLOCKERS
- Slow calcium channels are found in
the myocardium (heart muscle) and
vascular smooth muscle (VSM) cells.
- Free calcium increases muscle
contractility, peripheral resistance,
and blood pressure
 Nifedipine (calcibloc, adalat),
 Amlodipine (norvasc),
 Felodipine (Plendil)
 Verapramil (Isoptin)
Mechanism of action:
- decrease cardiac contractility and the workload of
the heart, thus decreasing the need for O2.
- it also promote vasodilatation of the coronary and
peripheral vessels.
Indications:
- hypertension, angina, arrhythmia
Adverse effects :
× bradycardia, hypotension, headache
× reflex tachycardia, constipation
× flushing, headache, dizziness, ankle edema,
and AV block.
Nursing consideration:
 Administer between meals to enhance
absorption.
 Take client’s pulse rate before each dose,
withhold if pulse is below 60 bpm.
 Refer for signs of congestive heart failure.
b.) ANTIHYPOTENSIVE DRUGS
- If blood pressure becomes too low, the vital
centers in the brain, as well as the rest of
the tissues of the body, may not receive
enough oxygenated blood to continue
functioning.
i. SYMPATHOMIMETICS
-used to treat shock
 dobutamine (Dobutrex)
 dopamine (Intropin),
 ephedrine (generic),
 epinephrine (Adrenalin,
EpiPen),
 isoproterenol (Isuprel),
 norepinephrine (Levophed)
 phenylephrine (Neo-
Synephrine).
Mechanisms of Action
- Sympathomimetic drugs react with
sympathetic adrenergic receptors to cause
the effects of a sympathetic stress response:
increased blood pressure, increased blood
- volume, and increased strength of cardiac
muscle contraction. These actions increase
blood pressure and may restore balance to
the cardiovascular system while the
underlying cause of the shock (e.g., volume
depletion, blood loss) is treated.
CARDIOVASCULAR AGENTS
Adverse Effect
× decreased GI activity with nausea and
constipation,
× increased respiratory rate and changes in
blood pressure,
× headache,
× changes in peripheral blood flow with
numbness, tingling, and even gangrene in
extreme cases.
ii. ALPHA-SPECIFIC ADRENERGIC
AGENTS
 Midodrine (ProAmatine)
- used to treat orthostatic hypotension—
hypotension that occurs with position
change—that interferes with a person’s
ability to function and has not responded to
any other therapy
Adverse Effects
The most common adverse effects associated with
this drug are related to the stimulation of alpha-
receptors
× piloerection, chills, and rash; hypertension
× and bradycardia; dizziness, vision changes ,
vertigo,
× headache; and problems with urination
c.) PERIPHERAL VASODILATORS
- A common problem in older adults is
peripheral arterial (vascular) disease (PAD,
PVD) - Characterized by numbness and
coolness of the extremities, intermittent
claudication and possible leg ulcers.
- Peripheral vasodilators increase blood flow to
the extremities.
- They are more effective for disorders
- resulting from vasospasm (Raynaud’s
disease) than from vessel occlusion or
arteriosclerosis (arteriosclerosis obliterans,
thromboangiitis obliterans [Buerger’s
disease]).
 Papaverine (Para-Time SR)
– direct acting vasodilator
 prazosin (Minipress) – alpha
blocker
 nifedipine (Procardia) –
peripheral vasodilators
 pentoxifylline
× Reactions to an overdose of pentoxifylline
include flushing of the skin,
faintness,sedation, and GI disturbances.
× Orthostatic hypotension is common when
taking high doses of a vasodilator.
Nursing Considerations
 The drugshould be taken with
food.
 The patient should avoid
smoking, because nicotine
increases vasoconstriction.
 Patients taking an
antihypertensive drug along
with pentoxifylline may need to
have the antihypertensive
dosage decreased to avoid side
effects.
5. Drugs for Circulatory Disorders
a. ANTICOAGULANT
 -Heparin (SQ and IV),
 Warfarin (Orally)
Mechanism of actions
a. Heparin
-prevents thrombin from converting fibrinogen
to fibrin.
b. Warfarin
-suppress coagulation by acting as an
antagonist of vitamin K after 4-5 days.
Indications
-thrombosis, pulmonary embolism, myocardial
infarction
Adverse effect
× bleeding
Nursing considerations
1. HEPARIN sodium
-if given SQ don’t aspirate or rub the injection
site (above the scapula - best site).
-therapeutic level 1.5-2.5 times normal PTT;
normal PTT is 20-35 sec. = 50-85 sec.
-antidote: (protamine sulfate)
2. WARFARIN sodium (coumadin)
-warfarin is used for long-term
-onset of action is 4-5 days.
CARDIOVASCULAR AGENTS

-therapeutic level is 1.5-2.5 times normal PT;

normal PT = 9.6 -11.8 sec. = 25 - 30 sec; INR  Cholestyramine
=2–3 (Questrant)
 • Colestipol (Colestid)
-should be taken at the same time of the day  • Colesevelam HCl
to maintain at therapeutic level.  • Gemfibrozil (Lopid)
-reduce intake of green leafy vegetables.  • Nicotinic Acid
 • Ezetimibe (Zetia)
-antidote: Vitamin K (Aquamephyton) D1. STATINS
 Statins
b. THROMBOLYTICS  -decreases the concentration of
cholesterol, decreases LDL and slightly
 Streptokinase,
increases HDL cholesterol.
 Urokinase
 -has been useful in decreasing CAD and
Mechanism of actions reducing mortality rates.
 -the present group of statins includes
-activates plasminogen to generates plasmin atorvastatin calcium (Lipitor),
(enzyme that dissolve clots). fluvastatin (Lescol), lovastatin
(Mevacor), pravastatin sodium
Indications
(Pravachol), simvastatin (Zocor) and
-use early in the course of MI (within 4-6 hours rosuvastatin calcium (Crestor)
of the onset)
D2 -Lovastatin was the first statin
Nursing considerations used to decreased cholesterol.
1. monitor bleeding  -the statin drugs can be combined with
2. antidote : Aminocarpic acid other drugs to decrease blood pressure
and blood clotting and to enhance
c. ANTIPLATELET antihyperlipidemic effect
 Aspirin
 Dipyridamole (Persantin),
 Clopidoigrel (Plavix), D3-Rosuvastatin
 Ticlopidine
Mechanism of acrion
Mechanism of action
-inhibits HMG-CoA reductase, the
-inhibit the aggregation of platelet thereby enzyme necessary for hepatic
prolonging bleeding time. production of cholesterol

Indications Indication

-used in the prophylaxis of long-term -To decrease cholesterol levels and

complication following M.I, coronary to decrease serum lipids especially LDL
revascularization, and thrombotic CVA. and triglycerides

Nursing considerations Side effects

1. Monitor bleeding time (NV = 1-9 mins) - headache, rash, constipation,

2. Take the medication with food.
D. ANTI-LIPEMIC
 Lowers lipid levels such as bile
acid, sequestamts,fibrates,
nicotine comes acid,statins and
Cholestrerol absorption
inhibitors
diarrhea,myalgia, photosensitivity,
hyperglycemia
Nursing considerations
-Monitor patient’s blood lipid levels
every 6-8 weeks for first 6 months,
then every 3-6 months. Monitor
laboratory tests for liver function.
CARDIOVASCULAR AGENTS

Observe for signs and symptoms of GI Interferes with plasminogen activator

upset. substances and blocks action of fibrinolysin
(plasmin)

ANTI FIBRONOLYTIC
Indications:
-drugs which blocks the conversion
Excessive bleeding caused by fibrinolysis
of plasminogen to plasmin & thus
inhibit fibrinolytic activity. Contraindications:
- Hypersensitivity to drug
 Tranexamic Acid
Lysteda - Disseminated intravascular coagulation
 Aminocaproic Acid
Amicar
- Neonates (injectable form)

Indications
Anti-hemophilic
 Antidote for Fibrinolytic drugs. Actions:
 In Cardio-pulmonary bypass
surgery. Replace clotting factors that are either
genetically missing or low in a particular type
 Tonsillectomy, prostatic surgery,
of hemophilia
tooth extraction
 Menorrhagia Indications:
 Recurrent epistaxis, peptic ulcer Prevent blood loss from injury or surgery
and to treat bleeding disorders
Pharmacokinetics:
Lysteda
Replace normal clotting factors and are
processed as such by the body

 Oral, i.v, topical administration

 In dentistry, tranexamic acid soaked
guaze or mouthwash is used to reduce
bleeding postoperatively in hemophiliacs
and pts on anticoagulants
 It is 7 times more potent than EACA,
more commonly used
 Treatment of cyclic heavy menstrual
bleeding.
Aminocaproic Acid (Amicar)
Pharmacologic class:
Carboxylic acid derivative
Therapeutic class:
Antihemorrhagic, antifibrinolytic
Pregnancy risk:
Category C
Action:
Antihemophilic Factor (AHF, Factor VIII)
Advate, Alphanate, Helixate FS,
Hemofil M, Humate-P, Koate-DVI,
Kogenate FS, Monoclate-P,
Recombinate, ReFacto, Wilate, Xyntha
PREGNANCY CATEGORY C
Drug class:
Antihemophilic
Therapeutic actions:
A normal plasma protein that is needed for
the transformation of prothrombin to
thrombin, the final step of the intrinsic
clotting pathway.
Indications:
●Treatment of classical hemophilia
(hemophilia A), in which there is a
demonstrated deficiency of factor VIII;
provides a temporary replacement of clotting
CARDIOVASCULAR AGENTS

factors to correct or prevent bleeding Indications:

episodes or to allow necessary surgery
Prevent or treat excess bleeding in
●Short-term prophylaxis (ReFacto) to reduce hyperfibrinolytic states
frequency of spontaneous bleeding
●Surgical and/or invasive procedures in
patients with von Willebrand disease in
whom desmopressin is ineffective or Vitamin K
contraindicated to control bleeding; not for
major surgery (Advate, Alphanate, Xyntha) Action:
Vit K acts as a cofactor at a late stage in the
●NEW INDICATION: Routine prophylaxis to
prevent or reduce the frequency of bleeding synthesis by liver of coagulation proteins -
prothrombin, factors VII, IX and X.
episodes in patients with hemophilia A
(Advate.) UsE:
The only use of vit K is in prophylaxis and treatment
Contraindications and Cautions: of bleeding due to deficiency of clotting factors.

●Contraindicated with antibodies to mouse,

hamster, or bovine proteins or to porcine or
murine factor.
●Use cautiously with pregnancy
Coagulation Factor VII A (recombinant)
 NOVOSEVEN RT
FDA BOXED WARNING:
Arterial and venous thrombotic and
thromboembolic events following
administration of NovoSeven RT
have been reported during
postmarketing surveillance.
Hemostatic Agents
Coagulants Vitamin K
●K1 (from plants fat-soluble):
Phytonadione (Phylloquinone)
●K3 (synthetic) —Fat-soluble:
Menadione, Acetomenaphthone —
Water-soluble: Menadione sod.
Bisulfite, Menadione, sod. Diphosphate
Miscellaneous
●Fibrinogen (Human), Antihemophilic
Factor, Desmopressin, Adrenochrome
monosemicarbazone, Rutin, Ethamsyl
Actions:
Stop the natural plasminogen clot-dissolving
mechanism by blocking its activation or by
directly inhibiting plasmin.
●Newborns
-All newborns have low levels of clottingfactors.
-Vit. K 1mg i.m recommended routinely.
-Menadione should not be used for this.
●Overdose of oral anticoagulants
-Most Imp. Indication of vit.K.
-Phytonadione is the drug of choice.
-Higher doses produce unresponsiveness to oral
anticoagulants for several days.
Fibrinogen
●Employed in Hemophilia,
antihemophilicglobulin(AHG) deficiency & acute
afibrinogenemicstates.
●0.5 mg i.v is infused.
Antihemophilic Factor
●Concentrated human AHG preparation.
●Indicated in Hemophilia & AHG deficiency
●Highly effective, short acting.
Fibrinogen & Antihemophilic Factor
Fibrinogen
●Employed in Hemophilia,
antihemophilicglobulin(AHG) deficiency & acute
afibrinogenemicstates.
●0.5 mg i.v is infused.
CARDIOVASCULAR AGENTS

Antihemophilic Factor
●Concentrated human AHG preparation.
●Indicated in Hemophilia & AHG deficiency
●Highly effective, short acting.

Fibrinogen & Antihemophilic Factor

Desmopressin
●Releases factor VIII & von Willebrand’s factor from
vascular endothelium.
●Checks bleeding in hemophilia & von Willebrand’s
disease.

Adrenochrome monosemicarbazone
●Reduce capillary fragility, control oozing from raw
surfaces & prevent microvessel bleeding.
●Efficacy is uncertain.
●Dose: 1-5 mg oral, i.m.

Fibrinogen & Antihemophilic Factor

Rutin
●A plant glycoside claimed to reduce
capillarybleeding.
●Used along with Vit. C, which is believed to
facilitate its action.
●Dose: 60 mg b.d/t.d.s orally.
●Efficacy is uncertain.

Ethamsylate
●Reduces capillary bleeding when platelets
areadequate.
●Used in prevention & treatment of capillary
bleeding in menorrhagia, epistaxis, malena,
etc.Dose: 250-500 mg t.d.s orally

Local Haemostatics (Styptics)

●Substances used to control bleeding from a local &
approachable site.
●Particularly effective on oozing surfaces, e.g.
toothsocket, abrasions, etc.