1. Class 11 Cardiac, renal and hematological medications
Chapter 15 & 20

2. Learning Objectives
Identify the approved way to give different forms of antianginal therapy
Discuss the uses and general actions of cardiac drugs used to treat dysrhythmias
Describe the common treatment for various types of lipoprotein disorders
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

3. Antianginals and Peripheral Vasodilators
Nitrates: “Universal Vasodilators”
Directly cause vascular smooth muscle to relax in arterial and venous circulation
Decrease myocardial oxygen use
Increase collateral-vessel circulation to the heart
Calcium Channel Blockers
Dilate coronary arteries and arterioles
Reduce response of electrical conduction system
Narrowing or constriction of smooth muscle in the coronary arteries and peripheral vascular system reduces the amount of blood flow to the heart. This lack of blood supply results in diminished oxygen and nutrient flow to the heart, causing chest pain, or “angina,” and peripheral vascular disease.
Arterial relaxation reduces the pressure the heart has to pump against. Venous relaxation causes blood pooling and decreases venous return to the heart.
Nitrates are readily absorbed under the tongue, through the skin, and orally. Nitroglycerin is a nitrate. The half-life of nitroglycerin is only 1 to 4 minutes.
Calcium is an electrolyte that helps move electrical impulses through cardiac tissue. Calcium channel blockers are drugs that help slow down the flow of calcium ions across the cell membrane, which reduces the amount of calcium available to move electrical impulses. There are many actions of these drugs.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

4. Antianginals and Peripheral Vasodilators (cont.)
Adverse Reactions
Nitrates: Flushing, postural hypotension, tachycardia, confusion, dizziness, fainting, headache, lightheadedness, vertigo, weakness, drug rash, localized pruritus, skin lesions, eye and mouth edema, local burning in mouth, nausea and vomiting
Peripheral Vasodilators: Headache, weakness, tachycardia, flushing, postural hypotension, dysrhythmias, confusion, severe rash, nervousness, tingling, and sweating
Some nitrates contain tartrazine, a chemical that may cause an asthmatic type of allergic reaction.
Peripheral vasodilating agents have a stronger action when taken with antihypertensives and alcohol. This leads to hypotension.
What are the nursing implications for the LPN/LVN regarding these drugs?
What patient teaching should be done for nitrates? (Storage? Expiration date?) For peripheral vasodilating agents?
How should patients be taught to use nitroglycerin during an acute anginal attack?
What are some drug interactions with nitrates or peripheral vasodilators?
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

5. Nitrate Products
Any drug with NITR- in the generic with cause vasodilation
Nitroglycerin**
isosorbide dinitrate
isosorbide mononitrate
These are the main drugs in this category. Nitroglycerin (NTG) can be given in multiple forms: PO pills & spray; sublingual; IV medication; ointment; & slow release topical patches.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

6. Peripheral vasodilator
Apresoline (hydralazine)
Treatment of hypertension and high afterload heart failure
Causes blood dyscrasias so monitor the CBCs

7. Question 2
Which are the best drugs for treating coronary artery disease?
Beta blockers
Calcium channel blockers
Diuretics
Nitrates
Correct Answer: 4
Rationale: Nitrates are the best drugs for treating coronary artery disease, whereas vasodilating agents (agents to open up the vessels) are used for peripheral vascular disease. The use of beta blockers in treating angina has also increased over the years, even though there is not agreement about their effectiveness. Calcium channel blockers may also play a role in treating angina, although concern about their possible role in changes in the heart (which may lead to chronic heart failure) in patients who have had a myocardial infarction (heart attack) has limited their use.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

8. Antidysrhythmics Four Classes
Class I: disopyramide, procainamide, quinidine
Lengthen the refractory period
Decrease cardiac excitability
Class II: acebutolol, esmolol, propranolol
Reduce sympathetic excitation (reduce loading)
Class III: amiodarone
Lengthen the time it takes for one cell to fire and recover
Class IV: verapamil
Blocks calcium entry into the myocardium, prolongs resting phase
**A good reference for understanding classes.
People with heart disease or other problems that affect the heart muscle are at risk of developing irregular heartbeats, or cardiac dysrhythmias. Dysrhythmias may be fast or slow, with an irregular or regular pattern.
The most common causes of dysrhythmias are an irritation to the heart tissue after a myocardial infarction, fluid and electrolyte imbalances, diet, hypoxia, and drug reactions.
Dysrhythmias vary in patients in regularity and intensity. An electrocardiogram is needed to determine the type of dysrhythmia a patient is experiencing. Halter monitors are portable ECG machines that take an ongoing tracing of the heart’s electrical function.
Antidysrhythmics act on each individual cell of the heart.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

9. Antidysrhythmics CLASS 1 A Norpace (V) Pronestyl (V,A) CLASS 1B
dysopyramide
Pronestyl (V,A)
Procainamide
(V) = ventricular action
(A) = atrial action
CLASS 1B
Xylocaine (V)
lidocaine

10. Antidysrhythmics Class 2 Beta blockers Brevibloc (V) Inderal (V)
esmolol
Inderal (V)
propranolol
Class 3
Cordarone / Pacerone (V)
Amiodarone
100 day half life !!
Betapace (V)
sotalol

11. Antidysrhythmics Class 4 Adenocard (V) Calcium channel blocker
adenosine
Given rapid IV push & flush
Causes SOB & dyspnea
Facial flushing
Calcium channel blocker
Calan / Isoptin
Verapamil
Can cause hypotension
Can not have any grapefruit while on any calcium channel blockers

12. Antidysrhythmics (cont.)
Action and Uses
Quinidine and Procainamide
Treat rapid and irregular dysrhythmias by decreasing the excitability of myocardial cells
Bretylium
Slows conduction rate in the ventricles, slows norepinephrine release in the myocardium
Disopyramide
Slows the depolarization of cardiac cells
The exact type of irregular rhythm can only be determined by taking an ECG. It is important to find the cause of the dysrhythmia.
Most dysrhythmias are caused by (1) increased sensitivity of the electrical cells in the heart, resulting in irregular or early ectopic beats and (2) electrical activity moving through abnormal conduction pathways, triggering myocardial cells to fire improperly.
Depolarization is the movement of electrolytes in and out of the cell as it gets ready to send another electrical impulse.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

13. Antidysrhythmics (cont.)
Lidocaine
Increases the strength of electrical impulses
Adenosine
Stops the heart for several seconds to allow it to convert to normal sinus rhythm
Beta-adrenergic blockers (propranolol)
Decrease the heart’s beta-receptor response to epinephrine and norepinephrine
Many patients refuse to continue taking adenosine after experiencing its effects.
Many of the antidysrhythmics are so powerful they should only be used in critical care units.
What are some of the medication-specific adverse effects of these drugs?
Antidysrhythmics often cause or worsen heart failure or urinary retention. Patients with a past history of heart failure should be watched closely.
Drug interactions: the effect of quinidine is increased by potassium and decreased by hypokalemia. The action of verapamil is stronger if the patient is taking digitalis and beta blockers. Beta blockers have many drug-specific interactions.
How can the steps of the nursing process be applied here?
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

14. Antihyperlipidemics Types of Lipoproteins
Chylomicrons (mostly triglycerides)
Formed from absorption of dietary fat in intestine
Very low-density lipoproteins (VLDLs)
Made up of large amounts of triglycerides that were made in the liver (pre-beta lipoproteins)
Low-density lipoproteins (LDLs)
Breakdown of VLDLs linked with cholesterol and protein
High-density lipoproteins (HDLs)
Clear out excess cholesterol from tissue
Lipoproteins are described by how thick or dense they are.
Chylomicrons are usually present for 1 to 8 hours in the plasma after the last meal.
Nearly all the triglycerides in plasma that are not in chylomicrons are considered to be VLDLs.
About 75% of plasma cholesterol is moved in the form of LDLs. High LDL levels indicate cholesterol levels that are higher than the body needs. Patients are at high risk for developing atherosclerosis.
HDLs block the uptake of LDL cholesterol by the vascular smooth muscle cells and may prevent atherosclerotic activity.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

15. Antihyperlipidemics Bile Acid Sequestrants (chole or cole = bile)
Cholestyramine resin
Colestid
colestipol
WelChol
colesevelam
HMG-COA reductase inhibitors (-statins)
Lipitor
atorvostatin calcium
Pravachol
pravastatin
Zocor
simvastatin

16. Antihyperlipidemics Miscellaneous Tricor Lopid Niaspan
fenofibrate
Lopid
genfribrozil
Niaspan
nicotinic acid or naicin
Make sure you check what time of day the drugs must be given.
Some are with food, others are before food.
Some do not matter.

17. Cardiotonics
Actions
Increase the contraction strength or force (positive inotropic action)
Slow the heart rate
Uses
Treatment of CHF and rapid or irregular heartbeats (atrial fibrillation, atrial flutter, frequent PVCs or paroxysmal atrial tachycardia)
Cardiotonics, often referred to as cardiac glycosides, make the heart beat slower and stronger.
The digitalis preparation digoxin is the major cardiac glycoside. It has been used for many decades.
All cardiotonic drugs have the same basic drug action. They differ only in the speed and duration of action. Chronotropic drugs affect the rate or rhythm of the heart. Dromotropic drugs influence the speed of the electrical impulse as it passes through the nerve or cardiac muscle fibers.
PVCs are premature ventricular contractions.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

18. Cardiotonics (cont.) Adverse Reactions Drug Interactions
Digitalis toxicity: serum digoxin levels verify
The amount of medication that is helpful (therapeutic) and the amount that is harmful (toxic) are not very different. This is called a narrow therapeutic window.
Don’t confuse the sound-alikes digoxin and digitoxin
Drug Interactions
Nursing Implications and Patient Teaching
Cardiotonics are powerful and can be toxic to the heart. The symptoms of digitalis toxicity may begin slowly and are easy to overlook; however, toxicity can occur quickly, especially in the elderly.
Symptoms include bradycardia, dysrhythmia, tachycardia, apathy, confusion, delirium, disorientation, drowsiness, mental depression, headache, visual changes (blurred vision, yellow/green vision, halos around dark objects), anorexia, diarrhea, nausea, vomiting, severe weakness.
Nursing implications include taking an apical pulse for a full minute prior to administering the dose of digoxin. If the apical pulse is less than 60, the medication is held (not given) and the physician immediately notified.
What patient and family teaching will the LPN/LVN be expected to give?
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

19. Cardiotonics Lanoxin / Digitek Primacor dobutamine Digoxin milrinone
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

20. Mrs. Moskaluk’s HTN Guide
A = ACE inhibitors (vasodilation and decrease plasma volume) and ARBs for vasodilation (-pril & - sartan drugs) B = Beta blockers – lowers heart rate and vasodilates (-lol) C = Calcium channel blockers (-dipine drugs) D = Diuretics (-thiazide and loop are K+ losers; aldactone is K+ sparing) E = Exercise to clean the vessels ‘F’ diet = fish, fluid, fiber, and fruit -zosin drugs are alpha 1 adrenergic blockers
Hypertension is a disorder in which the patient’s blood pressure is elevated above normal limits for age. Blood pressures above 150/90 mm Hg are associated with accelerated vascular damage of the heart, brain, and kidneys, which leads to increased risk of death.
Primary hypertension affects 80% to 90% of people with high blood pressure; the cause is unknown. The other 10% to 20% have secondary hypertension, in which elevated blood pressure is the result of another disease process or problem.
Loop diuretics block the active transport of chloride, sodium, and potassium in the thick ascending loop of Henle. These drugs work well in patients with impaired renal function.
Potassium-sparing diuretics increase the excretion of water and sodium by saving potassium. These drugs are used in patients with kidney disease or who are at risk for potassium imbalance.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

21. Urinary incontinence drugs
Antispasmotics/ anticholinergics
Ditropan (p in the pan)
oxybutynin
Pro-Banthine
propantheline
Detrol
Tolterodine
‘Gotta go right now’ TV commercial
BPH meds
Proscar (think prostate)
finasteride
Flomax
Tamulosin
‘maximize the flow’
Urinary Tract Analgesic
Pyridium
phenazopyridine

22. Hematologic Products Chapter 20 7th ed.

23. Learning Objectives
Describe the influence of anticoagulants on blood clotting
Identify drugs that act in the formation, repair, or function of red blood cells
Identify at least three adverse reactions associated with hematologic products.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

24. Anticoagulants Two Categories Coumarin and indandione derivatives
Limit the formation of blood coagulation factors II, VII, IX, and X in the liver by interfering with vitamin K
Antidote: Vitamin K injection/ infusion
Heparin sodium
Increases the action of antithrombin III (heparin cofactor) on several other coagulation factors to slow new clot development
Antidote: Protamine sulfate
Heparin and coumarin and indandione derivatives interfere with the blood clotting chain at multiple sites. Neither of these categories of medication dissolves existing clots.
Blood clots that are “fixed” in the body are called “thrombi.” Blood clots moving throughout the circulation are called “emboli.” All emboli eventually end up traveling to the lungs, heart, and brain, because that is the normal route of circulation and where major damage can occur.
Low-molecular-weight heparin is a special formulation used in special circumstances, such as prevention of deep vein thrombosis after surgery.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

25. Low Molecular Weight Heparins
Lovenox **
enoxaparin
Fragmin
dalteparin
Used to prevent clotting
Require less lab monitoring than Heparin
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

26. Anticoagulants (cont.)
Nursing Implications and Patient Teaching
Monitoring blood values
Coumadin = prothrombin time (PT); therapeutic is 1.5 to 2.5 × normal or an INR of 2.0 to 3.0
Heparin = activated partial thromboplastin time (aPPT); therapeutic is 2.5 to 3 × the control value
Many drugs alter the effect of anticoagulants. Coumarin and indandione derivatives increase the effect of heparin as do alcohol, aspirin, NSAIDs, and dextran.
Antihistamines, digitalis, nicotine, and tetracycline decrease the anticoagulant effect of heparin.
ASA, corticotropin, ethacrynic acid, glucocorticoids, and NSAIDs increase the risk of GI bleeding with heparin.
Adrenocorticosteroids, antacids, antihistamines, barbiturates, oral contraceptives, estrogens, griseofulvin, haloperidol, meprobamate, primidone, rifampin, thiazide diuretics, and vitamin K decrease the action of Coumadin.
Oral hypoglycemics taken with anticoagulants may increase the effect of either the hypoglycemic or anticoagulant.
Close monitoring and evaluation by the health care provider are essential when patients are taking these medications.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

27. Thrombolytic Agents Action
Convert plasminogen to the enzyme plasmin, which breaks down fibrin clots, fibrinogen, and other plasma proteins
Uses
Acute myocardial infarctions
Acute pulmonary emboli
Acute ischemic stroke
Acute arterial occlusion
Activase (altepase; recombinant)
Retevase (reteplase)
There is a narrow window of time for these drugs to be successful in dissolving thrombi during emergent events. Therefore, prompt initiation of the emergency system is essential.
Bleeding is the most common adverse reaction, along with dysrhythmias, hypotension, polyneuropathy, cholesterol embolism, pulmonary embolism, and drug hypersensitivity. If administered with other anticoagulants in the patient’s system, there is increased risk of bleeding.
What should the LPN/LVN consider when assisting with the administration of these drugs?
What patient and family teaching should occur?
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

28. Antiplatelet Agents Action Inhibit platelet aggregation (clumping)
Reduce thrombus formation
Uses
Salicylic acid (aspirin)
Reduces incidence of myocardial infarction-related deaths in men over 50
Drug of choice in ischemic stroke
81 mg used prophylactically
Platelet aggregation or clumping is essential for a blood clot (thrombus) to develop.
Aspirin continues to be one of the leading antiplatelet agents.
Many drugs, especially OTC preparations, contain aspirin compounds; patients should be made aware that these will increase the risk of bleeding.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

29. Antiplatelet Agents ASA Pletal Plavix Persantine Ticlid
acetylsalicyclic acid
Pletal
cilostazol
Plavix
clopridogrel
Persantine
dipyridamole
Ticlid
ticlopidine
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

30. Question 1 Cellular damage first results in the formation of:
Prothrombin.
Thrombin.
Thromboplastin.
Fibrinogen.
Correct Answer: 3
Rationale: Cellular damage results in the formation of thromboplastin, which then acts on prothrombin to form thrombin. Calcium must be present for this reaction to occur. Thrombin then acts on fibrinogen to produce fibrin, a netlike substance in the blood that traps red and white blood cells and platelets and forms the matrix, or skeleton, of the clot. Vitamin K must be present to produce prothrombin and other clotting factors that are made in the liver.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

31. Question 2 Which is true about emboli?
Emboli are not life threatening.
The function of heparin is to dissolve existing blood clots that may form emboli.
Emboli can only travel to nearby blood vessels.
An embolism can cause stroke or death.
Correct Answer: 4
Rationale: Emboli (small pieces of a blood clot) may break off from a site of thrombophlebitis (inflammation and blood clot in a vein) in the lower extremities and travel through the bloodstream to block vessels in areas of the heart, brain, or lung. This blockage can cause stroke or death. Drugs that can slow or reduce clotting, then, are very helpful.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

32. Question 3
Which is the anticoagulant of choice when an immediate effect is needed?
Warfarin
Plavix (clopidogrel bisulfate)
Heparin
Aspirin
Correct Answer: 3
Rationale: Heparin, which is only effective when given IV or subcutaneously, is the anticoagulant of choice when an immediate effect is needed. Warfarin, Plavix, and aspirin are oral agents used for long-term anticoagulant therapy.
Copyright © 2013, 2010, 2006, 2003, 2000, 1995, 1991 by Mosby, an imprint of Elsevier Inc.

33. Questions?