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CARDIOVASCULAR & HEMATOLOGIC MEDICATIONS FA20(2)

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CARDIOVASCULAR & HEMATOLOGY SYSTEM MEDICATIONS
GENERAL GUIDELINES:
Antihypertensive side effect of orthostatic hypotension is very common (particularly in older adults).
Monitor parameters of blood pressure and heart rate prior to giving many cardiovascular medications.
Multiple medication-medication interactions with cardiovascular drugs.
High risk for hemorrhage with anticoagulants & thrombolytics; bleeding with antiplatelets
Note that classifications can have multiple therapeutic uses for cardiovascular conditions.
CLASSIFICATION
THERAPEUTIC USES
MECHANISM OF ACTION
DRUG EXEMPLARS
Antihypertensives
Angiotensinconverting enzyme
(ACE) inhibitors
-
Stops conversion
Angiotensin II
receptor blockers
(ARBs)
Aldosterone
antagonists
Calcium channel
blockers (CCBs)
-
will slow down heart
-
rate
* check BP before
Hypertension
Heart failure
MI
Diabetic nephropathy
Hypertension
Heart failure
MI
Diabetic nephropathy
Heart failure post MI
Hypertension
Hypertension
Angina
Cardiac dysrhythmias
Alpha1 adrenergic
blockers
Hypertension
Centrally acting
alpha2 agonists
Hypertension
Cardioselective
Beta1 blockers
Hypertension
Angina
Heart failure
Tachydysrhythmias
MI
Non-selective Beta1
& Beta2 Blockers
Same as above +
Cardiac dysrhythmias
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giving
Blocks formation of angiotensin II causing:
a. vasodilation on quiz
b. excretion of aldosterone, Na & water
c. reduction in pathological changes to
blood vessels and heart
Blocks angiotensin II receptors leading to:
a. vasodilation
b. excretion of aldosterone, Na & water
Blocks aldosterone receptors in kidney
leading to:
a. increased excretion of Na & water
b. reduced blood volume
1) Slows movement of calcium into
smooth muscle cells leading to:
a. vasodilation
2) Slows calcium channels in myocardium
leading to:
a. decreased force of contraction
b. decreased heart rate
c. slowed conduction through AV node
Selectively blocks alpha1 adrenergic
receptors in arterioles leading to:
a. vasodilation
Stimulates alpha2 receptors in the brain,
which results in relaxation of arteries,
vasodilation, slowing of HR, and
decreased cardiac output.
Blocks beta receptors in myocardium
leading to:
a. decreased force of contraction
b. decreased heart rate
c. slowed conduction through AV node
Also blocks beta1 receptors in kidney,
reducing release of renin, angiotensin II
leading to vasodilation
Blocks beta1 receptors in myocardium and
kidney as above and also beta2 receptors
in lungs
captopril (Capoten)
lisinopril (Zestril)
enalapril (Vasotec)
fosinopril(Monopril)
losartan (Cozaar)
irbesartan (Avapro)
valsartan (Diovan)
eplerenone (Inspra)
spironolactone generic
(Aldactone)
trade
direction
Selective for blood
vessels:
nifedipine(Procardia)
amlodipine(Norvasc)
er
Non-selective for both
blood vessels & heart:
verapamil (Calan)
diltiazem(Cardizem)
doxazosin (Cardura)
prazosin (Minipress)
clonidine (Catapres)
metoprolol(Lopressor)
atenolol (Tenormin)
propranolol (Inderal)
carvedilol (Coreg)
labetalol (Trandate)
2
Vasodilators
Hypertensive
emergencies
Medications for Heart Failure
Cardiac glycosides
Heart failure
Atrial fibrillation
Centrally acting vasodilator that results in
rapid reduction of blood pressure,
preload, & afterload
nitroprusside
(Nitropress)
mon
Inhibits Na/K/ATPase (enzyme needed for digoxin
pumping Na ions out of heart cells. As Na
accumulates in the cells, calcium ions are
released producing :
a. increased force of contractions
b. improved stroke volume & CO cardiac output
Also acts to suppress SA – AV node
conduction reducing heart rate
Adrenergic agonists Emergency treatment
Stimulates Beta1 receptors in myocardium epinephrine
for cardiac arrest, heart to:
dopamine
patients dying need
failure & shock
a. increase heart rate
dobutamine
increases
b. increase myocardial contractility
c. increase cardiac output
d. increase tissue perfusion
Stimulates Beta1 receptors in kidney to
release renin leading to:
a. vasoconstriction and increased BP
+ Diuretics – See Urinary System Medication Information Sheet
Antianginal Agents
Organic nitrates
Angina
Dilates coronary arteries improving
nitroglycerin
perfusion of myocardium, reducing pain
(Nitrostat)(Nitro-Bid)
and coronary artery spasms.
isosorbide (Isordil)
Also dilates veins, reducing the amount of
blood returning to the heart and reducing
preload.
Antidysrhythmics
Class I: Sodium
V-Tachycardia
Blocks Na channels thereby slowing
procainamide
channel blockers
A-Flutter
cardiac conduction velocity
(Pronestyl)
A-Fibrillation
Class II: BetaV-Tachycardia
Prevents sympathetic nervous system
propranolol (Inderal)
adrenergic blockers A-Flutter
stimulation of the heart
See above under HTN
A-Fibrillation
Class III: Potassium
V-Tachycardia
Blocks K Channels thereby prolonging the amiodarone
channel blockers
A-Flutter
action potential & refractory period of the (Cordarone)
Which ahtidy
A-Fibrillation
cardiac cycle
Class IV: Calcium
V-Tachycardia
Prolongs cardiac conduction
verapramil (Calan)
channel blockers
A-Flutter
Decreases oxygen demand of the heart
diltiazem (Cardizem)
A-Fibrillation
See above under HTN
Antilipemics
HMG-CoA reductase Hypercholesterolemia
Interferes with hepatic enzyme HMG-CoA atorvastatin (Lipitor)
inhibitors (Statins)
Prevention of MIs
to reduce cholesterol precursors.
bacon
too much
Decreases manufacture of LDL & VLDL
Increases manufacture of HDL higher
Cholesterol
Same as above
Inhibits intestinal absorption of
ezetimibe (Zetia)
absorption inhibitor
cholesterol secreted in bile and food
Bile-acid
Same as above
Binds to bile acids in intestine, causing
colesevelam (Welchol)
sequestrants
increased excretion of cholesterol.
mom
-
to
-
-
basal dilation
=
BP
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•
•
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less than 100
then
60
high
Nicotinic acid
(Niacin)
Fibrates
Direct thrombin
inhibitors
Direct factor Xa
inhibitors
Thrombolytics
Antiplatelets
1)Salicylic
2)Glycoprotein
inhibitors
3)ADP inhibitors
3
take niacin
Same as above
Decreases LDL & triglycerides synthesis
niacin
Same as above
Decreases triglyceride production and
transport. Increases HDL precursors
gemfibrozil (Lopid)
Activates antithrombin leading to:
a. inhibition of thrombin & factor Xa
b. inhibition of fibrin formation
heparin
when
fondaparinux
(Arixtra)
enoxaparin (Lovenox)
(Low molecular weight
heparin)
warfarin (Coumadin)
Medications that affect Coagulation
Parenteral
Therapy for Deep vein
thrombosis (DVT) and
pulmonary emboli (PE)
Prevent DVT & PE and
stroke
Oral
triglycerides ?
Therapy for DVT & PE
Prevent thrombus
formation in persons
with A-fib to prevent
DVT, PE, stroke, MI
Prevent thrombus
formation in persons
with A-fib to prevent
DVT, PE, stroke, MI
Same as above
Dissolves clots in
conditions of:
CVA, MI, PE
Prevention of MI & CVA
Hematopoietic Medications
Iron Supplements
Iron-deficiency Anemia
Vitamin Supplement
B12 –
Erthyropoiesis
Growth Factors
Leukopoietic
Growth Factors
Anemia r/t kidney
disease, chemotherapy
Neutropenia
Pernicious Anemia
Folate -Folic acid Anemia
-
count too
we
give
those?
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Antagonizes vitamin K leading to:
a. prevention of synthesis of factor VII, IX,
X, and prothrombin
Directly inhibits thrombin formation
dabigatran (Pradaxa)
Directly inhibits factor Xa and fibrin
formation
Dissolves clots. Converts plasminogen to
plasmin resulting in:
a. destruction of fibrinogen
b. destruction of other clotting factors
rivaroxaban (Xarelto)
apixaban (Eliquis)
Alteplase (Activase)
(tissue plasminogen
activator tPA)
Inhibit enzymes and factors of normal
arterial clotting to:
a. prevent platelet aggregation
b. prevent platelet clumping
1)aspirin
2)abciximab (Reopro)
3)clopidogrel (Plavix)
Provides iron for hemoglobin composition
ferrous sulfate (Feosol)
Provides supplemental vitamins necessary
for normal RBC production
cyanocobalamin (B12)
folic acid (Folate)
Stimulates bone marrow to increase
production of RBCs
Stimulates bone marrow to increase
low
production of WBCs
not making
marrow
bone
-
enough production
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do
epoetin alfa (Epogen)
Filgrastim (Neupogen)
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