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The Cardiovascular System:
CORONARY ARTERY DISEASE (CAD)
AND
CARDIAC ARRHYTHMIAS
Physiology
• The heart requires oxygen to be delivered to its
own cells.
• Coronary arteries deliver this oxygenated blood
to the heart.
• Oxygen requirements of the heart increase as
the heart pumps faster and works harder.
• Oxygen demands of the heart also increase if the
heart has to overcome peripheral resistance in
the vessels (high afterload).
Cardiac Glycosides
The cardiac glycosides also are
known as digitalis preparations
Digoxin is used to maintain clinical
stability and improve symptoms, quality
of life, and exercise tolerance in patients
with all phases of heart disease.
Digoxin does not decrease mortality.
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The Foxglove
Plant (Digitalis
purpurea)
Cardiac Glycosides (cont.)
• Digoxin increases the force of cardiac
contraction, increasing cardiac output and
slowing heart rate.
• Digoxin is used for patients with chronic heart
disease and heart failure.
Prototype drug: digoxin (Lanoxin)
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Digoxin: Core Drug Knowledge
• Pharmacotherapeutics
– Used in the treatment of CHF and atrial fibrillation
• Pharmacodynamics
– Exerts an indirect effect on the heart from stimulation of
the autonomic nervous system (cholinergic agonist).
• Side effects
– Anorexia, N/V, diarrhea, headache, weakness, apathy,
drowsiness, visual disturbances
• Adverse effects
– Dysrhythmias,, confusion, restlessness, disorientation,
seizures, delirium, hallucinations, neuralgia, and psychosis
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Digoxin: Core Drug Knowledge (cont.)
• Minimizing adverse effects
– Digoxin has a narrow therapeutic index. It is
important to monitor the serum levels of digoxin.
– Check pulse rate and hold dose if <60
• Patient and family education
– Explain the reason for taking digoxin and the
adverse effects of the drug. Teach patient how to
monitor pulse at home.
– Discuss that many OTC drugs can interact with
digoxin.
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Pathophysiology: Ischemia
• When the oxygen requirements of the heart are
greater than the supply of oxygen it is getting,
the heart muscle becomes ischemic.
• Oxygen imbalance may be from:
– reduced coronary blood flow
– need for increased oxygen
• Chest pain that results from ischemia is termed
angina.
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Pathophysiology: Coronary Artery
Disease
Major Risk Factors for CAD
• Cigarette smoking
• Diabetes
• Elevated blood lipid
levels
• Hypertension.
There are four types of
angina:
– Stable angina
– Unstable angina
– Variant angina
– Microvascular angina
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Antianginal Agents
•
•
•
•
Nitrates
Beta adrenergic antagonists (Beta Blockers)
Calcium Channel Blockers
Other Drugs
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Nitrates
• Nitrates dilate vascular smooth muscle in both venous
and arterial vessels.
• Venous dilation decreases the returning flow of blood
to the heart (preload).
• Arterial dilation reduces systemic vascular resistance
and arterial pressure (afterload).
These effects decrease the total workload on the
heart and its oxygen needs – both preload and
afterload.
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Beta Blockers
• Beta blockers prevent the beta-adrenergic
(sympathetic nervous system) receptors from
being stimulated.
• These drugs have multiple effects on the heart
and cardiovascular system.
• These effects decrease the oxygen demands of
the heart and thereby decrease angina.
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Calcium Channel Blockers
• Calcium is needed in the conducting cells of the heart to help
create an electric action potential.
• Calcium-channel blockers inhibit calcium from moving across cell
membranes.
• The effects are a decrease in contraction, depression of impulse
formation (automaticity), and slowing of conduction.
• These have the effect of decreasing the oxygen needs of the
heart.
• Calcium channel blockers also cause arteriolar dilation, decreasing
afterload.
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Adjunctive (Additional) Drug Therapies
• Oher drugs are used as adjuncts to the main drug
therapies for treating angina.
• They are used to:
– Slow down the progression of coronary artery disease,
– Prevent complications that may arise with angina, or
– Minimize symptoms.
• Thrombus formation is an important concern with
unstable angina, and some of these therapies
specifically target this problem.
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Adjunct Drug Therapies (cont.)
• Lipid-lowering agents often are often used in conjunction to
slow the progression of coronary heart disease.
• An ACE inhibitor can be used in patients with coronary artery
disease if they also have diabetes, systolic dysfunction, or
both.
• If the pain of unstable acute angina is not controlled by
nitrates, morphine can be used to treat the pain.
• Oxygen, although not a drug, is commonly used to provide an
additional 02 supply to cardiac muscle tissue.
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Question
Nitrates dilate the vascular smooth muscle
resulting in what effect?
A. Increased systemic vascular resistance
B. Decreased preload & afterload
C. Increased afterload
D. Increased ejection fraction
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Question
Nitrates dilate the vascular smooth muscle
resulting in what effect?
B. Decreased preload & afterload
Answer: Nitrates dilate vascular smooth
muscle. Venous dilation decreases the
returning flow of blood to the heart
(preload) & arterial dilation decreases
peripheral resistance (afterload)
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Nitrates
Nitrates improve the circulation to the heart by
redistributing blood flow to the collateral vessels
and dilating both veins and arteries.
Prototype drug: nitroglycerin (Nitrostat,
Nitrodur)
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Nitroglycerin: Core Drug Knowledge
• Pharmacokinetics
– Administered: IV, topical, oral, sublingual,
nasal. Pharmacokinetics vary with route of
administration
• Pharmacodynamics
– Relaxes vascular smooth muscle and dilates
both arterial and venous vessels
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Nitroglycerin: Core Drug Knowledge
• Side effects
– Headache, hypotension, postural hypotension,
tachycardia, vertigo, anxiety, and weakness
• Adverse effects
– Syncope (fainting)
• Minimizing adverse effects
– Assess pulse and blood pressure before administering
– Monitor for orthostatic hypotension and assist the
patient to a standing position gradually when arising.
– Treat any headache that develops with aspirin or
acetaminophen.
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Nitroglycerin: Teaching, Assessment,
and Evaluations
• Patient and family education
– Explain the purpose and adverse effects of
nitroglycerin.
– Instruct patients to sit or lie down when experiencing
angina.
– Explain that postural hypotension may occur.
– Keep PRN tablets in a dark and relatively cool place.
Advise patient to not keep PRN tablets in a warm
place, e.g. a pants pocket
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Question
Which statement by the patient would indicate the
need for additional teaching about proper
administration of nitroglycerin?
A. I will keep the sublingual tablets out of the sun or
heat.
C. I will apply the transdermal patch on my lower arm
to prevent a headache.
D. If the chest pain is not relieved after three
sublingual nitroglycerin’s I will call EMS.
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Question
Which statement by the patient would indicate the
need for additional teaching about proper
administration of nitroglycerin?
C. I will apply the transdermal patch on my lower arm
to prevent a headache.
Rationale: Transdermal nitro should be applied to an area of the
body that does not have excessive hair, to promote absorption.
Apply to the chest, upper arm, or upper thigh to promote
absorption and increase onset of systemic action. Do not apply to
distal parts of extremities.
Headaches are a common side effect possible because of the
vasodilation effects and are not related to administration route.
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Cardiac Rhythm: Physiology
• Contractions of the heart depend on the electrical
conduction system of the cardiac muscle.
• The conduction system connects to highly specialized
cardiac cells that allow the heart to beat predictably
and rhythmically.
• The electrical system is composed of the:
– Sinoatrial (SA) node
– Atrioventricular (AV) node
– Bundle of HIS
– Bundle branches
– Purkinje fibers
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Travel of Electrical Current
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Physiology (cont.)
• The SA node, influenced by both the
sympathetic and the parasympathetic nervous
systems, is known as the pacemaker of the
heart.
• It is important to understand how potassium,
sodium, and calcium ions bring about
electrical changes in the cardiac cells that
stimulate contraction of the cardiac cells.
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Movement of Electrolytes – Cause of
Depolarization of Cells
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Electrolytes
• Alterations in potassium (K), sodium (Na) or
calcium (Ca) levels - either too high or too low
- will result in cardiac electrical abnormalities
called cardiac arrthymias.
• Some of these arrthymias are life-threatening
and all can interfere with normal cardiac
output.
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Damage to the Myocardium
• Any damage to the myocardium (muscles of
the heart) causes scar tissue to form.
• Scar tissue cannot transmit electrical activity,
therefore the electrical impulses have to take
a circuitous route.
• This can be detected on an Electrocardiogram
(ECG, EKG) tracing.
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Electrocardiogram
SA Node Fires >
Depolarization
Impulse
travels to
Atrium then
Ventricles
causing
contraction
Muscle cells return to
a resting state >
Repolarization
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Electrocardiogram
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Question
It is possible to have electrical activity reflected
on an EKG tracing but not to have a beating
heart.
1. True
2. False
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Question
It is possible to have electrical activity reflected
on an EKG tracing but not to have a beating
heart.
This is True!
Electrical activity is an indirect measure of
cardiac health. The SA node will continue to fire
for a while even if the heart muscle is too
damaged to respond.
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Pathophysiology
• Arrhythmias, also called dysrhythmias, are a
disturbance in the electrical activity of the
heart.
• Some are insignificant and do not create any
problems for the patient.
• Others disrupt the function of the heart,
increase the oxygen demand of the heart,
and/or interfere with cardiac output.
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Examples of Arrhythmias
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Examples of Arrhythmias
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Examples of Arrhythmias
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Examples of Arrhythmias
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Drugs and Other Therapies to Treat
Arrhythmias
• Drug therapy previously was the mainstay for treating
arrhythmias; now Implanted Cardiac Defibrillators (ICDs)
are equally important in preventing sudden cardiac
death.
• Arrhythmias can
also be treated by
ablation (cauterizing).
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Class I Antiarrhythmic Drugs
Prototype drug:
Lidocaine (Xylocaine)
• Pharmacotherapeutics
– Treat all acute ventricular arrhythmias.
• Pharmacokinetics
– Administered: IV. Metabolism: liver. Excreted:
kidneys. T1/2: 1.5 to 2 hours
• Pharmacodynamics
– Decreases automaticity, excitability and membrane
responsiveness. Decreases action potential duration
and effective refractory period of Purkinje fibers and
ventricular muscle
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Lidocaine: Core Drug Knowledge (cont.)
• Side effects
– Hypotension, dizziness, lightheadedness, fatigue,
drowsiness
• Adverse effects
– Cardiac arrhythmias
• Drug interactions
– Many classes of drugs
• Environment
– Should be given in hospital or emergency setting
with continuous ECG monitoring
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Class II Antiarrhythmic Drugs
• Antiarrhythmic class II drugs (beta blockers)
depress depolarization.
• Beta blockers slow heart rate by suppressing the
SA node, slow the speed of conduction through
the AV node, and decrease the force of
contraction.
• They effectively reduce mortality in patients who
have had a recent MI, those with symptomatic
heart failure, and those with congenital long QT
syndrome.
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Class III Antiarrhythmic Drugs
• Class III antiarrhythmics produce a
prolongation of repolarization.
• Action potential duration and refractory
periods are prolonged, leading to reduction in
membrane excitability of all myocardial tissue.
Prototype drug:
amiodarone (Cordarone)
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Amiodarone: Core Drug Knowledge
• Pharmacotherapeutics
– Approved for use only in life-threatening
arrhythmias
• Pharmacodynamics
– Prolongation of the refractory period, and
noncompetitive alpha- and beta-adrenergic
inhibition
• Significant Drug interactions
– Digoxin and warfarin
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Amiodarone: Core Drug Knowledge
(cont.)
• Adverse effects
– Pulmonary toxicity, exacerbation of the arrhythmia,
and liver disease
– Occasionally causes an ocular symptom of colored
rings around lights and gradually decreased vision.
– Occasionally causes a cutaneous photosensitivity
reaction that may be associated with a peculiar bluegray discoloration of the skin
• Minimizing adverse effects
– Correct electrolyte disturbances before beginning
therapy.
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Pulmonary Toxicity w/ Amiodarone
• Amiodarone is an iodine-containing compound that
tends to accumulate in several organs including lungs.
• It can occasionally cause either hypo or hyperthyroidism
• It has high lipid solubility & tends to accumulate
extensively in adipose (fat) tissue and highly perfused
organs such as the liver, lungs and spleen
• It can produce lung damage directly by a cytotoxic effect
and indirectly by an immunological reaction (2%-15%)
• Most patients respond well to the withdrawal of the
drug and the administration of corticosteroids, which are
usually given for four to 12 months.
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Amiodarone: Teaching, Assessment, and
Evaluations
• Patient and family education
– Explain the purpose of the drug and possible adverse
effects of the drug.
– Emphasize the importance of returning for follow-up
blood work and ECGs.
– Teach patients to use appropriate protection when
out in the sun and to limit sun exposure.
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Class IV Antiarrhythmic Drugs
• Class IV antiarrhythmics depress depolarization and
lengthen phases 1 and 2 of repolarization.
Prototype drug: verapamil (Calan)
• Pharmacotherapeutics
– Antiarrhythmic for chronic atrial flutter or fibrillation
• Pharmacodynamics
– Inhibits the movement of calcium ions across the cardiac
and arterial muscle cell membrane
• Side effects
– Constipation, dizziness, headache, nausea, hypotension
• Adverse effects
– Peripheral edema
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Verapamil: Teaching, Assessment, and
Evaluations
• Patient and family education
– Stress the importance of adequate fluid intake
and dietary fruit and fiber to help prevent
constipation.
• Ongoing assessment and evaluation
– It is important to monitor liver function
periodically to detect elevated serum drug
levels.
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Physiology: Lipid Management
• Serum lipids are fats found in
the bloodstream.
• These lipids include
cholesterol, phospholipids,
and triglycerides.
• They are transported in the
blood as part of large
molecules called lipoproteins.
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Physiology (cont.)
• Cholesterol is a soft, waxy substance found among
the lipids in the bloodstream and in all of the body’s
cells.
• The body, mostly in the liver, produces essentially all
of the cholesterol needed for normal functioning—
about 1,000 mg a day.
• Cholesterol plays a role in forming cell membranes,
some hormones, and other needed tissues.
• Low Density Lipoprotein (LDL) is the major
cholesterol carrier in the blood.
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Pathophysiology
• Hyperlipidemia is an elevation of blood lipid
levels.
• Hyperlipidemia is considered a risk factor for the
following disorders:
– Atherosclerosis
– Coronary artery disease
– Thrombosis (clotting)
• When the amount of cholesterol within cells
builds up, the number of these receptors on cell
surfaces is reduced, preventing all of the lipids
from entering the cells.
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Pathophysiology (cont.)
• Patients with narrowed arteries from
atherosclerotic cardiovascular disease are more
likely to have hypertension.
• Ideal cholesterol levels:
– Total cholesterol: less than 200 mg/dL
– Low-density Lipoproteins = LDL: <100 mg/dL
– High-density Lipoproteins = HDL: >40 to 59
mg/dL
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Lifestyle and Reduction of Low-Density
Lipoprotein Levels
Therapeutic Lifestyle Changes.
• Lifestyle changes include:
– Diet
– Weight loss
– Increased physical activity
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Antihyperlipidemics
• Anti-hyperlipidemics are a group of
medications that reduce cholesterol, reduce
triglycerides or both.
• Some non-prescription agents are now
included in this grouping:
– Fish oil (Omega 6 Fatty Acid) at 3000 mg/day has
been shown to reduce triglyceride levels
• Prescription formulation: Lovaza
– Nicotinic acid (Niacin, Vitamin B3)
• Prescription formulation: Niaspan
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Statins
• Statins lower blood cholesterol levels.
• Statin therapy can:
– Lower LDL cholesterol by 20% to 55%
– Raise HDL levels between 5% and 15%
– Lower triglycerides between 7% and 33%.
• Evidence suggests that statins work in other
ways beside lowering cholesterol levels to
decrease the occurrence of cardiovascular
events, e.g. reducing inflammation.
Prototype drug: atorvastatin (Lipitor)
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Atorvastatin: Core Drug Knowledge
• Pharmacotherapeutics
– Used for primary hypercholesterolemia and
combined hyperlipidemia
• Pharmacokinetics
– High first-pass effect. Highly protein bound. Excreted
primarily through the GI tract
• Pharmacodynamics
– Competitively inhibits an enzyme important in
cholesterol biosynthesis (making cholesterol).
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Atorvastatin: Core Drug Knowledge
• Contraindications and precautions
– Active liver disease and pregnancy
• Side effects
– Muscle and joint aches, weakness, muscle cramps
• Adverse effects
– Muscle damage, liver damage, and rhabdomyolysis*
*Potentially lethal muscle destruction
• Drug interactions
– Anti-fungal drugs, erythromycin, and grapefruit juice
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Atorvastatin: Planning and Interventions
• Maximizing therapeutic effects
– Most effective when administered in the evening
– Immediate-release administered after evening meal
– Extended-release administered at bedtime
• Minimizing adverse effects
– Liver function test (AST and ALT) results should be
monitored before starting therapy.
– Evaluate the patient carefully for muscle soreness,
tenderness, or pain and CK levels.
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Statins: Teaching, Assessment, and
Evaluations
• Patient and family education
– Stress the importance of following a low-cholesterol
and low-saturated-fat diet.
– Instruct patients to report any unexplained muscle
pain, tenderness, or weakness.
– Photosensitivity may occur.
• Ongoing assessment and evaluation
– The patient should have liver function tests and CK
measurement performed periodically throughout
drug therapy.
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Drugs Closely Related to Atorvastatin
- Lovastatin (Mevacor)
- Fluvastatin (Lescol)
- Pravastatin (Pravachol)
- Rosuvastatin (Crestor)
- Simvastatin (Zocor)
____________________________________________
• All work similarly to lower LDL cholesterol and have
similar adverse effects.
• Pravastatin differs from the prototype lovastatin
because it is not metabolized via the P-450 system
and thus does not produce the drug interactions of
lovastatin (best with liver disease)
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Drugs Significantly Different from the
Statins: Fibric Acid Derivatives
• These drugs lower triglyceride levels and
increase HDL cholesterol.
• These drugs can reduce triglyceride levels
between 35% and 53%.
• Effects on LDL cholesterol may be either to lower
it between 6% and 20% or to raise it slightly.
• Although in certain patients these drugs may be
used alone, most frequently they are used in
combination with statins.
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Fibric Acid Derivatives (cont.)
• The combined used of a fibrate and a moderatedose statin carries a somewhat increased risk of
myopathy.
• Contraindications include hepatic or severe renal
dysfunction, including primary biliary cirrhosis,
preexisting gallbladder disease, or hypersensitivity.
• Serious adverse effects include abnormal liver
function tests, rhabdomyolysis, and
hyperglycemia.
Prototype: fenofibrate (Tricor)
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Cholesterol Absorption Inhibitors
• These drugs act in the small intestine, where
they inhibit the absorption of cholesterol.
• It is given orally once daily either as
monotherapy or in combination therapy with a
statin.
• This drug decreases LDL about 17% but has no
effect on HDL or triglycerides.
Prototype: Ezetimibe (Zetia)
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Ezetimibe: Core Drug Knowledge
• Pharmacotherapeutics
– Used to reduce cholesterol, particularly LDL
– Used in combination with statins
• Pharmacokinetics
– 90% protein bound, increased absorption with a
high-fat meal, once daily oral dosing
• Pharmacodynamics
- Decreases cholesterol absorption in the small
intestine
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Ezetimibe: Core Drug Knowledge
• Contraindications
– Severe liver disease
• Side effects
– Headache, Diarrhea
• Adverse effects
– Elevated liver enzymes, myopathy, angioedema
• Drug Interactions
– Minimal
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Nicotinic Acid (Niacin, Vitamin B3)
• Nicotinic acid (niacin or vitamin B3) is used to treat
hyperlipidemia.
• Nicotinic acid reduces levels of triglycerides and LDL
cholesterol levels and raises levels of HDL
cholesterol.
• Triglycerides and VLDL levels are reduced by 25% to
30% in 1 to 4 days.
• LDL level reductions may be seen in 5 to 7 days, with
the maximal effect seen in 3 to 5 weeks.
Prototype: nicotinic acid (Niaspan)
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Adverse Reaction to Nicotinic Acid
Although all B Vitamins are water
soluble and safe in people with
normal renal function, some people
experience flushing (vasodilation),
and a tingling, itching or the sensation
of being pricked by cactus needles
(paresthesia) and cannot tolerate this
product.
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Homework
• Review your ATI Modules
• Do Quiz #7: The Cardiovascular System (10 points)
• Do Shadow Health DCE: Patient John Larsen
(10 points)
– This activity will take approximately one-hour to complete.
– You will be asked to administer medications to Mr. Larsen
including anti-hypertensive drugs.
– Don’t forget to communicate with the patient and do patient
education!
– Do the questions at the end for my review.
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