CARDIAC MEDS PHAR EXAM 3 REVIEW
VOCABULARY
Preload: vol. of blood in ventricles @ end of diastole (end of diastolic pressure). Increased in:
hypervolemia & regurgitation of cardiac valves. Diuretics reduce systemic water, which helps
preload.
Afterload: resistance left ventricle must overcome to circulate blood. Increased in: HTN (artery
issues) & vasoconstriction. The more afterload you have, the more the heart has to work (^
cardiac workload). ACE & beta-blockers help to decrease afterload.
Angina pectoris: spasm—resolves w/o damage to the heart muscle.
Thrombus: starts out w/fat (cholesterol).
CHF: insufficiency or heart weakness/running low on power. Heart fails to effectively pump
blood around the body. Tx=diuretics, ACE, B-Blockers, digoxin and other inotropes and
vasodilators.
Left-sided failure (L=lungs): the left lung takes fluid in from the lungs; congestion due to
blood backing up in the lungs.
S.E.=need to sit up during sleep, pulmonary congestion behind the lining of the lungs—NOT
IN THE ALVEOLI, cyanotic fingers/toes/lips, tachycardia (heart is trying to catch up),
restlessness due to lack of O2, orthopnea—breath better sitting up.
Right-sided failure (R=rest of body):
S.E.=swelling in feet/ankles/hands/abdomen, enlarged liver/spleen, distended jugular veins,
dependent edema=the lower from the heart, the higher the risk.
Negative Chronotrope=slows down heart rate
Negative Inotrope=weakens heart rate, reduces contractility
Negative Dromotrope=slows the heart rate and lengthens it, decreases conductivity (AV
node).
Chloride: An important negatively charged ion. Helps to maintain electrical neutrality with the
movement of cations across the cell membrane
Function
Primarily reabsorbed in the loop of Henle
Promotes the movement of sodium out of the cell
CARDIAC GLYCOSIDES
DIGOXIN (the only med) is an old drug & highest toxic cardiac med.
Therapeutics

Tx of HF—positive inotrope

A Fib—negative chronotrope & negative dromotrope

Antidote—digoxin immune ?fab(Digibind)
Action

^ Contraction force—positive inotrope

Decreases heart rate—negative chronotrope (slows SA depolarization, low heart rate increases
filling time leading to SV and CO increase)

Decreases AV node conductivity—negative dromotrope

Narrow therapeutic range (0.5-2.0 ng/mL) TOXIC LEVEL IS 2.0 ng/mL
Side Effects

Dysrhythmias—bradycardia (3rd degree block); early sign of toxicity
-Take apical pulse for 60 seconds before giving

GI effects—n/v, anorexia

CNS effects—fatigue, weakness, visual changes (diplopia-double vision, yellow/gr halos)

Monitor potassium levels—hypokalemia ^ toxicity

Encourage potassium intake—potatoes/tomatoes/bananas/spinach/oranges

Teach signs of toxicity—bradycardia, anorexia (due to nausea), fatigue, weakness, visual halos
(dig level too high-changes how one perceives light so produces halos around lights)
Interactions

Thiazide or loop diuretics—lowers serum potassium.
-Monitor serum potassium. Normal rage=3.5-5.0 mEq/L

Glucocorticoids—increases sodium and decreases potassium.

ACE inhibitors or ARB’s—can increase potassium so monitor.

Sympathomimetics—increase tachy-arrhythmias

Verapamil—elevates dig levels; decreases electrical conduction

Herbals—consult w/MD
Nursing Interventions

You must take a full minute apical pulse before giving

VS=pulse & BP

Digoxin helps strengthen the heartbeat and relieves ankle edema

Take digoxin and other heart meds as prescribed

Patient will need to have periodic phy. exams

Report adverse effects to your provider

Limit salt intake and be sure to get enough potassium

Instruct patient on how to take their pulse before each dose >60bpm

Don’t crush capsules. Tabs may be crushed and can be taken w/or after meals.

Don’t skip a dose (unless pulse low), and never double up
ANTI-ANGINA DRUGS
NITRATES
“Itrate”
NITROGLYCERIN (tabs, patch, paste, spray), AMYLNITRATE (rarely used), ISOSORBIDE DINITRATE (long
lasting oral med), ISOSORBIDE MONONITRATE (long lasting oral version)
Therapeutics

Relieves acute angina

Prevent stable or variant angina

Blood pressure control
Action

Cause smooth muscle in veins (BP decreases) and arteries to relax and dilate (blood flow
increases).
-increases blood supple to ventricles (coronary vasodilation)
-decrease blood return (preload)
-decrease peripheral vascular resistance (afterload)
Side Effects

Headache (low BP in head)

Orthostatic HTN (low BP above neck)

Dizziness

Increased heart rate (reflex tachycardia—when the drug causes a side effect/produces a larger
vessel lumen so the heart speeds up)

Tolerance—should have med free periods; remove patch overnight
Interactions

Alcohol can cause severe hypotension

Viagra/Levitra/Cialis shouldn’t be taken w/in 24 hrs of nitrates

Anticholinergics delay sl. Nitroglycerin absorption

Calcium channel blockers can cause orthostatic hypotension
Nursing Interventions

Store in a cool, dark place in a tightly closed original container (light destroys the med)

Replace nitroglycerin’s after 3 months and remove the cotton from bottle (can retain the med)

Never spread the paste w/ fingers—use applicator

Carry container away from body (heat destroys the med)

Go to the ER if no relief after taking 3 nitroglycerin’s 5 min apart

Report serious/persistent adverse reactions or increased incidence of usage
ANTI-ANGINA DRUGS
ANTIHYPERTENSIVE DRUGS
A(4) B (2) C D
Nitrates
Anit-hypertensives
Beta-blockers
Calcium Channel Blockers
Angina Treatment:
1. Reduce myocardial oxygen demand to not make the muscle not work as hard
2. Increase myocardial oxygen supply
3. Alter Preload (blood volume), Afterload (BP), Heart rate, Contractility (increase
left ventricle muscle size)


A
-
Angiotensin Converting Enzyme Inhibitors (ACE-1)
-
Angiotensin II Receptor Blockers (ARB’s)
-
Alpha 1 Antagonists
-
Alpha 2 Agonists
B
-Beta Adrenergic Antagonists (Beta blockers)
-selective (Beta 1)
-non-selective (Beta 1 & Beta 2)

C
-Calcium Channel Blockers

D
-Diuretics
ANTI-ANGINA DRUGS
Angiotensin Converting Enzyme Inhibitor
ACE
“Prils”
LISINOPRIL (PRINIVIL), CAPTOPRIL /(CAPOTEN), ENALAPRIL (VASOTEC), RAMIPRIL (ALTACE)
Therapeutics

HTN

Heart Failure

Diabetic Neuropathy

MI—decrease mortality and decrease risk of heart failure
Action

Blocking the production of Angiotensin II by blocking the conversion of Angiotensin I to
Angiotensin II resulting in:
-
vasodilation (arteriole)
-
excretion of sodium and water and retention of potassium
Side Effects

Dry non-productive cough!!

Postural orthostatic hypotension—freq. 1st dose rxn

Fatigue

Renal insufficiency

Hyperkalemia—ACE retain potassium

Angioedema—swelling of tongue & oropharynx [allergic rxn]

Neutropenia—lack of WBC’s [rare]
Contraindications

Preg. Cat D

Patients with renal stenosis/impairment

Those w/a hx of angioedema following use of ACE inhibitor

Renal impairment disorders are at greater risk for developing neutropenia (low WBC’s)
Interactions

Diuretics—1st dose hypotension

Antihypertensive med (multiple doses can cause an ‘additive effect’

Potassium supplements or potassium sparing diuretics—increased risk for hyperkalemia. Too
much potassium in the blood can cause the heart to not contract!

Lithium—can increase lithium levels

NSAIDS—may decrease antihypertensive effect
Nursing Interventions

Advise clients to stop taking diuretics 2-3 days before starting ACE

Advise clients that dosage may need to be adjusted

Clients should only take if Rx’ed by PCP

Monitor lithium levels to avoid toxicity

Advise client to inform PCP of all OTC use
ANTI-ANGINA DRUGS
ANGIOTENSIN RECEPTOR BLOCKERS
ARB’S
“Sartans”
Losartan (Cozaar), Valsartan (Diovan), Irbesartan (Avapro), Candesartan (Atacand)
Therapeutics

Reduction of all HTN

Management of hear failure and prevention of mortality following MT (Valsartan)

Stroke prevention (Losartan)

Delay progression of diabetic neuropathy (Irbesartan, Losartan)
Action

Blocks the action of Angiotensin II in the body resulting in: vasodilation, excretion of sodium
and water, and retention of potassium.
Side Effects

Angioedema—swelling of the tongue and oropharynx

Fetal injury—Preg cat. D.
Nursing Interventions

Use cautiously in those who experienced angioedema w/ACE inhibitors. (Not an absolute
contraindication)

Advise client to observe for s/sx of hives/wheals, swelling of tongue.

Tell client to notify PCP immediately if sx occur

Advise women of risk during the 2 nd & 3rd trimester.
The Major Difference Between ACEs and ARBs is:
1.
Cough isn’t a side effect of ARBs
2.
Less risk of hyperkalemia w/ARBs
3.
ACEs=pril
4.
ARBs=sartan
ANTI-ANGINA DRUGS
ALPHA 1 ANTAGONISTS
DOXAZOSIN (CARDURA)—used to decrease BP, PRAZOSIN (MINIPRESS), TAMSULOSIN (FLOMAX),
TERAZOSIN (HYTRIN)
Therapeutics

Antihypertensive—resulting from arteriole and venous vasodilation

Benign prostatic hypertrophy—resulting from smooth muscle relaxation in the prostate. It
blocks Alpha1 so it relaxes the prostate.

Also lower VLDL and LDL, and increase HDL (helps w/cholesterol)
Side Effects

Orthostatic hypotension—‘first dose’ orthostatic.

Sodium and water retention (edema)

Sexual dysfunction

Nasal congestion

Reflex tachycardia
Interactions

Taking other antihypertensive meds can cause an additive effect

NSAIDS can decrease antihypertensive effects and increase edema w/Prazosin

Teach client to observe for sx of hypotension (dizzy, lightheaded, faintness)

Instruct patient to lie down if feeling faint and change positions slowly

Advise client to avoid OTC NSAIDs
Nursing Interventions

Take 1st dose at night

Instruct client to change positions slowly-sit before standing and rise slowly

Monitor BP

Avoid activities requiring mental alertness for 12-24 hrs after 1st dose (low blood flow below
neck)

Often prescribed w/a diuretic (HCTZ=potassium wasting)

Inhibits ejaculation

Obtain current drug/herbal hx—report if a drug-drug or drug-herbal (licorice) interaction are
probable

Obtain baseline vitals for future comparison

Recommend that the client take the initial dose at bedtime to decrease ‘first-dose’
hypotensive effect
ANTI-ANGINA DRUGS
CENTRAL ACTING ANTIHYPERTENSIVE
(ALPHA2 AGONIST)
CLONIDINE (CATAPRESS)-comes in oral, transdermal patch, and epidural routes.
Therapeutics

HTN—decreases systolic & diastolic BP and HR

Minimizes/eliminates s/sx of heroin/methadone/opiate withdrawal

Epidural administration for pain relief (Cancer)
Action

Stimulates Alpha2 adrenergic receptors in the CNS (brainstem)

Reduces plasma concentration of norepinephrine

Inhibits release of renin from the kidneys (renin is released to increase BP)
Side Effects

Drowsiness—give in the evening

Xerostonia (dry mouth)—diminished after 2-4 wks. Use gum/hard candy/freq. sips of H2O to
help.

Rebound HTN after stopping

Preg. Cat. C
Nursing Interventions
* Establish baseline BP and HR
ANTI-ANGINA DRUGS
BETA ADRENERGIC ANTAGONISTS
BETA BLOCKERS
DO NOT GIVE TO PATIENTS WHO HAVE ASTHMA—THIS MED CAUSES LUNG
ISSUES!!!
METOPROLOL (LOPRESSOR), ATENOLOL (TENORMIN)=Cardio-selective (Beta1)
PROPANOLOL (INDERAL), NADOLOL (CORGARD)=Nonselective (Beta1 & Beta2)
Therapeutics

Antihypertensive (BP)

Anti-angina—decrease myocardial workload/O2 demand by slowing the heart and opening
up the vessels

Antiarrhythmic—slows SA/AV conduction

MI-- decrease myocardial workload/O2 demand by slowing the heart and opening up the
vessels

CHF—weak contraction

Glaucoma (eye drops)—pupil constriction

Stage fright—slows HR

Tremors, essential

Pheochromocytoma—cancer growth on the adrenal gland

Hyperthyroid

Migraines—helps keep blood flow to brain /vasodialates
Side Effects

Bradycardia (decreased BP/AV block)

A-V block

Orthostatic hypotension

Rebound myocardium excitation

Broncho-spasm (Beta2 or nonselective effects)

Glycogenolysis is inhibited (Beta2 or non-selective effects)

Lethargy/drowsiness/depression
Action
Beta blockers block beta receptors on the heart causing:
1.
Decrease in heart rate=negative chronotrope
2.
Decrease of the force on contraction=negative inotrope
3.
Decrease in the rate of AV conduction=negative dromotrope
Nursing Interventions

Monitor pulse, hold med if <60

Obtain baseline EKG

Advise client to change positions slowly

Advise clients not to stop medication abruptly

Avoid Beta2 blockers in clients w/asthma, COPD

Avoid Beta2 blockers in diabetic clients
NON-SELECTIVE BETA BLOCKADE (B1 & B2-PROPANOLOL) INHIBITS GLYCOGENOLYSIS LEADING TO
HYPOGLYCEMIC REACTIONS IN DIABETIC PATIENTS!!!
ANTI-ANGINA DRUGS
CALCIUM CHANNEL BLOCKERS [MAIN EFFECT=VASODILATION]
BENZOTHIAZEPINES = DILTIAZEM (CARDIZEM)-in the form of a drip
DIHYDROPYRIDINES=NIFEDIPINE (PRACARDIA, ADALAT), AMLODIPINE (NORVASC), FELODIPINE
(PLENDIL), NICARDIPINE (CARDENE)
PHENYLAKYLAMINES = VERAPAMIL (CALAN)
Action

Inhibits the transport of Calcium thru the calcium channels in the blood vessels, leading to the
INHIBITION of CARDIAC MUSCLE CONTRACTION. Causing cardiac muscle relaxation

Vasodilation in the peripheral arterioles and arteries of the heart

Reduce the frequency of angina

Reduce the need for nitrates

Reduce afterload-- Decreases cardiac workload by decreasing the force of contraction

Used for its antihypertensive effect

Blocking of calcium channels in the myocardium, the SA and AV node =
-decreases force of contraction=negative inotrope
-decreases heart rate=negative chronotrope
-decreases rate of conduction thru the AV node=negative dromotrope
Side Effects

Decreases BP

Bradycardia

May precipitate A-V block

HA

Abdominal discomfort (constipation, nausea)

Peripheral edema

Constipation
Interactions

Beta blockers

Digoxin

GRAPEFRUIT JUICE

Preg. Cat. C
Nursing Interventions

Teach client to change positions slowly & have client monitor for orthostatic hypotension

Instruct client to increase fluid, fiber and exercise

Monitor heart rate/EKG due to reflex tachycardia/bradycardia

Teach client to monitor for peripheral edema (a diuretic may be Rx’ed)

Do not crush or chew extended release tabs

Advise/teach client to monitor BP and heart rate
DIURETICS
POTASSIUM WASTING
THIAZIDE & THIAZIDE-LIKE
HYDROCHLOROTHIAZIDE (HydroDIURIL)
CHLOROTHIAZIDE (DIURIL)
BENDROFLUMETHIAZIDE (NATURETIN)
BENZTHIAZIDE (EXNA)
TRICHLOMETHIAZIDE (DIURESE)
Therapeutics

Edema with CHF

Pulmonary Edema

Liver Disease

Renal Disease

Hypertension

Conditions that cause hyperkalemia
Function of Diuretics

Increase the amount of urine produced by the kidneys

Block sodium and chloride re-absorption

Increase sodium (water) excretion in urine
Side Effects

Confusion, fatigue

Muscle cramps

Dehydration
Adverse Reactions

Orthostatic hypotension

Hyponatremia (Na)

Hypokalemia (K)

Thiazide resistance
Drug Interactions

Increase blood glucose

Inhibit insulin release

Lithium levels may Increase

Increase response to skeletal muscle relaxants

NSAIDs may reduce the antihypertensive diuretic effect

Digoxin - toxicity

Cross sensitivity to sulfonamide medications
Nursing Implications
•
Monitor for adequate intake and output and potassium loss
•
Monitor the client’s weight and vitals signs
•
Monitor for signs and symptoms of hearing loss which may last for 1 to 24 hours
•
Teach mechanism and rationale for medication
•
Monitor weight daily at the same time – report gain or loss of 2 lbs/day
•
Teach client to take diuretic in the morning to prevent sleep disturbances
•
Avoid high sodium foods
•
Watch potassium intake
•
Seek your prescribers approval before taking any other drug
Implementation

Monitor urinary output

Check clients weight for loss or gain (2.2lbs = 1 liter)

Monitor vital signs (BP)

Administer IV Lasix slowly to avoid hearing loss

Monitor for signs and symptoms of hypokalemia

Monitor serum potassium

Assure access to urinal or commode
Indications for Thiazide and Thiazide-Like Diuretics
Treatment of edema associated with CHF, liver, or renal disease
Monotherapy or adjuncts for the treatment of hypertension
•
Indications: Adjunctive therapy for edema associated with CHG, cirrhosis, corticosteroid and
estrogen therapy, and renal dysfunction; treatment of hypertension
•
Actions: Inhibits reabsorption of sodium and chloride in distal renal tubules, increasing the
excretion of sodium, chloride, and water by the kidneys
•
Oral route: Onset 2 h; peak 4–6 h; duration 6–12 h
•
T½: 5.6–14 h; metabolized in the liver and excreted in urine
•
Indications for Loop Diuretics
Acute CHF
Acute pulmonary edema
Edema associated with CHF
Edema associated with renal or liver disease
Hypertension
DIURETICS
POTASSIUM WASTING
LOOP DIURETICS
FUROSEMIDE (LASIX)
BUMETANIDE (BUMEX)
TORSEMIDE (DEMADEX)
Therapeutics

Edema with CHF

Pulmonary Edema

Liver Disease

Renal Disease

Hypertension

Conditions that cause hyperkalemia

Function of Diuretics

Increase the amount of urine produced by the kidneys

Block sodium and chloride re-absorption

Increase sodium (water) excretion in urine

Indications: Treatment of edema associated with CHF, acute pulmonary edema, hypertension

Actions: Inhibits reabsorption of sodium and chloride from the proximal and distal renal
tubules and the loop of Henle, leading to a sodium-rich diuresis

Oral route: Onset 60 min; peak 60–120 min; duration 6–8 h

IV, IM route: Onset 5 min; peak 30 min; duration 2 h

T½: 120 min; metabolized in the liver and excreted in urine
Adverse Reactions

Fluid volume loss (excess)

Tinnitus (ototoxicity)

Orthostatic hypotension

Hyperglycemia

Electrolyte imbalances
K+, Cl-, Na+, Ca++, Mg+
Drug Interactions

Ototoxicity with esp w/ aminoglycosides

Reduce hypoglycemic effect of oral anti-diabetic drugs

Lithium toxicity risk

Electrolyte imbalances causing arrhythmias with cardiac glycosides
Nursing Interventions

Teach mechanism and rationale for medication

Monitor weight daily at the same time – report gain or loss of 2 lbs/day

Teach client to take diuretic in the morning to prevent sleep disturbances

Avoid high sodium foods

Watch potassium intake

Seek your prescribers approval before taking any other drug
Implementation

Monitor urinary output

Check clients weight for loss or gain (2.2lbs = 1 liter)

Monitor vital signs (BP)

Administer IV Lasix slowly to avoid hearing loss

Monitor for signs and symptoms of hypokalemia

Monitor serum potassium

Assure access to urinal or commode
LASIX IV Push give at a rate of 20mg/min
*With high doses a rate of 4mg per min is recommended to decrease risk of ototoxicity.
DIURETICS
Potassium-Sparing
SPIRONOLACTONE (ALDACTONE), TRIAMTERENE (DYRENIUM), AMILORIDE (MIDAMOR)
Therapeutics

Hypertension

Heart failure

Patients at high risk for hypokalemia associated with diuretic use

Used with Loop or Thiazide to reduce potassium loss
Side Effects

Headache

Diarrhea

Hyperkalemia

Electrolyte imbalance

Fatigue

GI disturbance
Action

Blocks the aldosterone in the kidney

Gets rids of the sodium and water, but saves the potassium
Adverse Reactions

May lead to hyperkalemia with ACE inhibitors and potassium supplements

Endocrine effects

Impotence in males

Menstrual irregularities in females
Nursing Interventions

Teach mechanism and rationale for medication

Monitor weight daily at the same time – report gain or loss of 2 lbs/day

Teach client to take diuretic in the morning to prevent sleep disturbances

Avoid high sodium foods

Watch potassium intake

Seek your prescribers approval before taking any other drug
Implementation

Monitor urinary output

Check clients weight for loss or gain (2.2lbs = 1 liter)

Monitor vital signs (BP)

Administer IV Lasix slowly to avoid hearing loss

Monitor for signs and symptoms of hypokalemia

Monitor serum potassium

Assure access to urinal or commode
DIURETICS
Osmotic Diuretics
MANNITOL (OSMITROL)
Therapeutics

To Prevent Kidney Failure
*
To Decrease Intracranial pressure
*
To Decrease intraocular pressure
Side Effects

Edema


May cause pulmonary edema or precipitate CHF
Electrolyte imbalance
Action

Creates an osmotic force to draw edematous fluid from the tissues (eye, brain, etc.)

Is not reabsorbed in the nephron so it maintains osmotic pressure to draw water into the
filtrate of the renal system
Nursing Interventions

Teach mechanism and rationale for medication

Monitor weight daily at the same time – report gain or loss of 2 lbs/day

Teach client to take diuretic in the morning to prevent sleep disturbances

Avoid high sodium foods

Watch potassium intake

Seek your prescribers approval before taking any other drug
Implementation

Monitor urinary output

Check clients weight for loss or gain (2.2lbs = 1 liter)

Monitor vital signs (BP)

Administer IV Lasix slowly to avoid hearing loss

Monitor for signs and symptoms of hypokalemia

Monitor serum potassium

Assure access to urinal or commode
Antihypertensive – Cultural
African Americans
 HTN develops earlier than in the white population
 Much higher incidence and likely to be more severe
 As a result higher risk for:
 Renal disease
 Stroke
 50% higher death from heart disease
 80% higher rate of death from stroke
 320% higher rate of HTN-related ESRD
 More responsive to diuretics, calcium channel blockers or
alpha adrenergic blockers - monotherapy
• Most responsive to single drug therapy (as opposed to
combination drug regimens)
• More responsive to diuretics, calcium channel blockers and
alpha adrenergic blockers
• Less responsive to ace inhibitors and beta blockers
• Increased adverse effects – depression, fatigue, drowsiness
Process of Coagulation
Medications Affecting Clotting

Anticoagulants

Prevent the formation of blood clots (venous)

Anti-platelets


Prevent clumping of platelets (aggregation) (arterial/venous)
Thrombolytics

Dissolve blood clots
Examples


Anticoagulants (Venous)

Heparin

Enoxaparin (Lovenox)

Warfarin (Coumadin)

Dabigatran etexilate mesylate (Pradaxa®)

Apixaban (Eliquis®)
Antiplatelets (Arterial)

Aspirin (ecotrin)

Ticlopidin (Ticlid)

Clopidogrel (Plavix)
ANTOCOAGULATION (parenteral)
HEPARIN
Therapeutics

Prevent venous thrombosis

DVT treatment

Evolving stoke treatment

DIC treatment
Action




Prevents clotting by:

Inactivation of thrombin formation.

This inhibits fibrinogen from converting to fibrin
IV or SQ

No oral or IM administration

Onset (SQ) 20-60min
Antidote

Protamine Sulfate*

Partial Thromboplastin Time*
Lab

PTT normal


11-15 sec.
PTT therapeutic

60-80sec
Heparin Side Effects/Nursing
Side Effect



Hemorrhage

Monitor – VS, Lab – PTT/aPTT

Administer antidote
Heparin induced thrombocytopenia (HIT)

Monitor clients platelet count

Stop heparin if <100,000
Hypersensitivity reactions Administer small test dose prior to administration of heparin
Nursing Interventions

Monitor for hemorrhage



Avoid aspirin
Monitor Labs

CBC (RBC, Platelets)

PTT/aPTT*
Bleeding Precautions

R.A.N.D.I

Keep Protamine Sulfate* available
Teach client signs to monitor
-Increased heart rate
-Decreased blood pressure
-Bruising, petechiae, hematomas,
The coagulation cascade of secondary hemostasis has two pathways, the
Contact Activation pathway (formerly known as the Intrinsic Pathway) and the
Tissue Factor pathway (formerly known as the Extrinsic pathway) that lead to fibrin formation.
It was previously thought that the coagulation cascade
consisted of two pathways of equal importance joined to a common pathway.
It is now known that the primary pathway for the initiation of
blood coagulation is the Tissue Factor pathway. The pathways are a series of reactions, in which a zymogen
(inactive enzyme precursor) of a serine protease and its glycoprotein
co-factor are activated to become active components that then catalyze
the next reaction in the cascade, ultimately resulting in cross-linked
fibrin. Coagulation factors are generally indicated by Roman numerals, with a lowercase a appended to indicate an
active form.
The coagulation factors are generally serine proteases (enzymes). There are some exceptions. For example, FVIII
and FV are glycoproteins and Factor XIII is a transglutaminase. Serine proteases act by cleaving other proteins at
specific sites. The coagulation factors circulate as inactive zymogens.
The coagulation cascade is classically divided into three pathways. The tissue factor and contact activation
pathways both activate the "final common pathway" of factor X, thrombin and fibrin.
ANTICOAGULANT (Oral)
WARFARIN (COUMADIN)
Therapeutics

Prevention of:

Venous thrombosis

Atrial fibrillation thrombus formation

Prosthetic heart valve thrombus formation
Action

Antagonize vitamin K



Lab:
Preventing synthesis of
-Prothrombin time (PT)

Clotting factors VII,IX, X -International Normalized Ration (INR)

Prothrombin
Normal 0.8-1.2
Oral dosing (absorbed rapidly)

Onset >2days, Peak 1-3 days

Duration 2.5-5 days, T½ 0.5-3d

Protein binding 97-9.5%
Caution
Therapeutic (1.5-3)
Antidote: Vitamin K (phytonadione)

Liver disease

Low Platelets

Surgery

Preg. Cat. X
Sources of Vit. K:
-Natural production—gut produced by
normal flora.
-Dietary
Dietary Modifications—keep vit. K intake consistent
Interactions-Highly protein meds,
OTC/Rx, Antibiotics.
Teaching:
*Supply client w/list of food high in vit. K for consistent intake
*Notify prescriber of all meds/OTC/herbals
*Need to sched. appts for INR lab draws
*Soft bristled toothbrush; monitor for s/sx of bleeding
*Need to monitor
*Bleeding precautions
Vitamin K Foods

Kale

Spinach

Turnip greens

Collards

Swiss chard

Parsley
Mustard greens

Brussels sprouts

Green leaf lettuce

Broccoli

Endive lettuce

Romaine lettuce

Liver
Anti Platelet Medication
ASPRIN (ECOTRIN, BAYER)—dose typically 81 mg (325-650 mg for pain)
TICLOPIDINE (TICLID)
CLOPIDOGREL (PLAVIX)
Therapeutics
Action

Primary prevention of Myocardial Infarction

Prevention of re-infarction

Prevention of stroke

Prevent platelets from clumping together by inhibiting enzymes and factors that
normally lead to arterial clotting
Side Effects


GI Bleeding/ulcers

Use enteric coated tablets

Take with food

May use PPI concurrently
Hemorrhagic Stroke


Advise/observe for signs of stroke

Weakness, headache

Slurred speech
Prolonged Bleeding
Interactions with other meds to enhance bleeding:


Pregnancy category D


Heparin, Warfarin, NSAIDs
In 3rd Trimester
Do not give in thrombocytopenia

Platelets less than 100,000
Blood Lipids
Lipoproteins
 VLDL
 Deliver triglycerides to nonhepatic (adipose) tissues
 LDL (bad cholesterol)
 Deliver cholesterol to nonhepatic tissues
 HDL (good cholesterol)
 Transport cholesterol from
non-hepatic tissues back to
the liver
Reducing CV Risk

Therapeutic lifestyle changes

TLC Diet

Weight control

Exercise

Smoking cessation
Medications

HMG CoA Reductase Inhibitors

Nicotinic Acid (vitamin B3)

Fibrates

Cholesterol Absorption Inhibitors

Bile Acid Sequestrants
Cholesterol has many physiologic roles.
•
It is a component of all cell membranes and membranes of intracellular organelles
•
Required for the synthesis of certain hormones
•
(estrogen, progesterone, testosterone, adrenal corticosteroids, and bile salts)
•
Deposited in the skin to reduce evaporation of water and blocks trans-dermal
absorption of water soluble compounds
Some comes from dietary sources
Some is manufactured by the cell primarily in the liver.
The liver uses saturated fats to make cholesterol
Blood Lipids
HMG-CoA Reductase Inhibitors
“The Statins”

Atorvastatin (Lipitor)

Simvastatin (Zocor)

Lovastatin (Mevacor
Therapeutics

Decrease LDL

Increase HDL

MI/CAD prevention
Adverse Effects

GI system—liver failure (Hepatotoxicity)

CNS—headache, dizziness

Rhabdomylosis (myopathy)

Cataract development
Contraindicated

Liver disease

Alcoholic

Pregnancy cat: X

Avoid grapefruit juice—CYP450 metabolism

Take with evening meal or @ h.s.
The early rate-limiting step in the synthesis of cellular cholesterol involves the enzyme HMG-CoA
reductase.
Blocks formation of cellular cholesterol.
Rhabdomylosis--and acute, sometimes fatal disease characterized by destruction of the muscles, often
associated with renal failure as myoglobin builds up in the kidney.
GI system: flatulence, abdominal pain, cramps, nausea, vomiting, and constipation
CNS- headache nausea, dizziness, blurred vision, insomnia, fatigue,
Cataract development
BLOOD LIPIDS
Nicotinic Acid
NIACIN (B3)
1.5 – 2g/day
RDA—14-16mg
Action

Inhibits release of free fatty acids (FFA) from adipose tissues

Increases rate of triglyceride removal
Adverse reactions

Flushing

Nausea, abdominal pain

Increases uric acid
Frequently used in combination with a bile sequestrant.
Nicotinic acid -Also known as vitamin B3, niacin has earned a reputation (in supplement form) as a
natural cholesterol-lowering agent that often rivals prescription drugs in mild to moderate cases.
The RDA for niacin is 14 mg for women and 16 mg for men. Specific disorders usually require higher
doses.
BLOOD LIPIDS
Fibrates
GEMFIBROZIL (LOPID)
FENOFIBRATE (TRICOR, LOFIBRA)
Therapeutics

Reduce triglyceride level

Secondarily reduce blood cholesterol
Adverse Effects

Gallstones (Cholelithiasis)

Myopathy (muscle pain)

Hepatotoxicity
Pharmacodynamics

Reduce cholesterol production

Mobilize cholesterol from the tissues

Increase cholesterol excretion

Decrease synthesis and secretion of lipoproteins

Decrease synthesis of triglycerides
Interactions

Statins—increased risk of myopathy

Warfarin—increased risk of bleeding
Take/Administer
30 minutes Before Meals
Fibric acid Derivatives (Fibrates)
Several fungi produce fibric acid
Cholesterol Absorption Inhibitors
EZETIMIBE (ZETIA)
Action

Inhibit absorption of cholesterol secreted in the bile and from food
Side/Adverse Effects

Generally well tolerated

Pregnancy Category X

Contraindication—renal dysfunction
Mediation/Food interactions

Bile sequestrants
Interfere with absorption

Statins - increase risk of
Myopathy
Hepatotoxicity

Fibrates - increase risk of
Gallstones
Myopathy
Vytorin® – Combination of Exetimibe and Simvastatin
Bile Sequestering Drugs
CHOLESTRYRAMINE (QUESTRAN)
COLESEVELAM (WELCHOL)
COLESTIPOL (COLESTID)
Bile sequestering drugs- remove excess bile acids from the fat deposits under the skin
Actions

Bind with bile acids in intestine to excrete in feces

Causes liver to use cholesterol to form bile acids

Lowers blood levels of LDL
Kinetics

Not absorbed

Remains in intestines and combines with bile acids
Take before meals

Eliminated in 5 hours
Adverse Effects
Constipation
Pregnancy Category B
Medication Interaction

Decreased absorption of fat soluble vitamins A, E, D, K

Digoxin, Warfarin, Thiazides & Tetracycline’s & fat soluble meds
As cholesterol leaves the bloodstream and other storage areas to replace the lost bile acids, blood
cholesterol levels decrease. Because the small intestine needs bile acids to emulsify lipids and form
chylomicrons, absorption of all lipids and lipid soluble drugs decreases until the bile acids are replaced.
Antiarrhythmic
AMIODARONE (CORDARONE)
Action

Used for atrial and Ventricular arrhythmias

Dynamics T½ : 25-110 days
Adverse Effects


Pulmonary Toxicity—pulmonary fibrosis

Cardio toxicity—arrhythmias, bradycardia, AV-block, CHF

Photophobia, blurred vision

Pregnancy Category D
Teaching/Monitoring

Cardiac rate/rhythm

Pulmonary Function
Chest X-ray
Pulmonary Function Tests

Monitor Liver & Thyroid function tests

Avoid Grapefruit Juice

Virtually all patient may develop corneal micro deposits, which may cause photophobia or blurred
vision.
Optic neuropathy, sometimes progressing to blindness, may also occur.
Between 2% and 5% of patients experience blue-gray discoloration of the skin.
Gastrointestinal reactions (Nausea, Vomiting, anorexia)
Possible CNS reactions include ataxia, dizziness, tremor mood alteration and hallucinations
Hepatitis and thyroid dysfunction have occurred