1. NURS 1950: Pharmacology I 1

2.  Objective 1: describe the relationship of calcium to electrical activity of the heart  Resting:  Preload:  Afterload: 2

3.  Heart dependent upon influx of calcium  Ca+ enters channels in the cardiac cell membrane and go into the cell along with Na  K+ comes out  Cardiac cells contract 3

4.  Objective 2: describe how the ANS affects the heart rate 4

5.  The ANS is the primary controller of heart rate  Cholinergic (parasympathetic) vagal fibers are close to the SA node  Stimulation with acetylcholine slows the heart rate 5

6.  Sympathetic (adrenergic) nerves also innervate the heart  Stimulation causes norepinephrine to be released.  Increases heart rate, slows refractory period 6

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8.  Objective 3: describe how cardiac drugs affect cardiac action 8

9.  1. Increase or decrease the force of myocardial action  Positive inotropics  Negative inotropics 9

10.  2. Increase or decrease heart rate by altering SA node impulse conduction  Positive chronotropics  Negative chronotropics 10

11.  3. Increase or decrease conduction of AV impulses  Positive dromotropics  Negative dromotropics 11

12.  Diuretics to decrease blood volume 12

13. Figure 24.1 Pathophysiology of heart failure

14.  Objective 4: identify the action of cardiac glycosides 14

15.  Digoxin & relatives  Come from Natural sources  Helpful in CHF  Have a positive inotropic effect 15

16.  Increases mechanical efficiency of heart  This pumps more blood  With increased blood to kidneys, diuresis occurs, edema reduced  Cardiac glycosides also have negative chronotropic effect,  Negative dromotropic effect 16

17.  Action ◦ Thought that they cause release of free calcium within the cardiac muscle cell ◦ Also change the electrical activity of myocardium 17

18.  Decrease velocity of electrical conduction, prolong refractory period in AV conduction system  Increase vagal tone 18

19.  Objective 5: relate how the effects of digitalis are beneficial to the client with CHF  Recall the signs/symptoms of CHF  How do you think cardiac glycosides improve this condition? 19

20.  Objective 6: describe the usefulness of digitalis in the treatment of atrial fibrillation 20

21.  What is atrial fibrillation?  What activity of the cardiac glycosides improve this condition? 21

22.  Chronotropic/dromotropic effects ◦ Suppress impulse conduction through the AV node ◦ This prevents excessive atrial activity from reaching ventricles 22

23.  Objective 7: list the generic and brand names of the digitalis preparations  Digitalis preparations similar in pharmacological properties, toxic effects 23

24.  Digoxin (Lanoxin, Lanoxicaps): oral or IV  Onset 30-120 minutes oral  Peaks 2-6 hrs  Duration 2-4 days  Eliminated by kidney ◦ Used most often as rapid onset, short duration 24

25.  Must take apical pulse 1 minute before administration  Hold if under 60, contact MD  Blood levels needed 25

26.  Objective 8: define digitalization 26

27.  Digitalization is the administration of digitalis that is more than the maintenance dose  This raises the blood level quickly to therapeutic range ◦ May also be called a loading dose 27

28.  Example ◦ Oral dose of digoxin 0.5-0.75 mg ◦ 0.25-0.5 mg then given every 6-8 hours until desired blood level reached ◦ Then maintenance dose: 0.125-0.5 mg daily 28

29.  Objective 9: list symptoms of digitalis toxicity 29

30.  Digitalis toxicity: ◦ GI distress: N/V, anorexia, and/or diarrhea (flu like symptoms) ◦ May have excessive salivation and abdominal pain ◦ Neurological: restless, irritable, lethargy, drowsiness, and/or confusion 30

31.  May have vision changes, changes in color ◦ May have halos, amblyopia and diplopia ◦ Cardiac effects: development of arrhythmias (bradycardia, primary AV block) 31

32.  Objective 10: identify factors which predispose digitalis toxicity 32

33.  Toxicity predisposition: hypokalemia as cardiac muscles more sensitive to the glycosides  Renal impairment as 60-90% excreted by kidney  IV administration: rapid accumulation can occur 33

34.  Treatment ◦ Hold the drug ◦ Use digoxin immune fab (Digibind)  Antigen-binding fragments combine with digoxin to neutralize its action 34

35. Lisinopril Animation Click here to view an animation on the topic of lisinopril.here

36. Diuretics  Prototype drug: furosemide (Lasix)  Mechanism of action: to increase urine flow, reducing blood volume and cardiac workload  Primary use: to reduce edema and pulmonary congestion  Adverse effects: dehydration, electrolyte imbalance, hypotension, ototoxicity

38. Furosemide Animation Click here to view an animation on the topic of furosemide.here

39. Cardiac Glycosides  Prototype drug: digoxin (Lanoxin)  Mechanism of action: to cause more forceful heartbeat, slower heart rate  Primary use: to increase contractility or strength of myocardial contraction  Adverse effects: neutropenia, dysrhythmias, digitalis toxicity

41. Beta-Adrenergic Blockers  Prototype drug: Metoprolol (Lopressor, Troprol XL)  Mechanism of action: block cardiac action of sympathetic nervous system to slow heart rate and B/P, reducing workload of heart  Primary use: to reduce symptoms of heart failure and slow progression of disease  Adverse effects: fluid retention, worsening of heart failure, fatigue, hypotension, bradycardia, heart block

43. Vasodilators  Drugs: hydralazine (Apresoline); (isosorbide dinitrate (Isordil)  Mechanism of action: to relax blood vessels  Primary use: to lower blood pressure  Used for clients who cannot take ACE inhibitors  Adverse reactions: reflex tachycardia, orthostatic hypotension

44. Phosphodiesterase Inhibitors  Prototype drug: milrinone (Primacor)  Mechanism of action: to block enzyme phosphodiesterase in cardiac and smooth muscle  Primary use: as short-term therapy for heart failure  Adverse effects: hypokalemia, hypotension, ventricular dysrhythmias

46.  Objective 11: describe the nursing responsibilities associated with administering cardiac glycosides preparations 46

47.  Take apical pulse 1 full minute  Hold if under 60, over 100 in adults  Report any evidence of irregular rhythm  Observe for toxicity S/S  Monitor K+ if on diuretics  Encourage K+ rich foods 47

48.  Teach client to take pulse  Teach S/S of toxicity  If hypothyroid, sensitive to digitalis  Draw blood levels periodically 48

49.  Atherosclerosis narrows heart’s vessels  Blood flow impeded  Demand exceeds supply = anginal pain 49

50.  Objective 12: describe the actions of the antianginal drugs 50

51.  Drugs are used to dilate coronary arteries  This brings in oxygen and nutrients  Supply = demand so no pain 51

52.  Objective 13: identify the drugs used to treat angina pectoris 52

53.  Nitroglycerin  Calcium channel blockers  Beta blockers  ACE inhibitors 53

54.  Nitroglycerin drugs  Works by relaxing arterial and venous smooth muscle  Dilate coronary arteries 54

55.  Liquid nitroglycerin unstable, highly volatile  Oral tablets stable, non-explosive  Can be given sublingual for rapid, predictable action  Can be transmucosal, aerosol translingual spray, IV, transdermal 55

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57.  Ointment: placed on paper with inches marked off  Amount prescribed placed on the paper, taped into place  4-8 hours of action  (Nitro-bid, Nitrol) 57

58.  Nitroglycerin patches: worn 12-14 hours  “Patch-off” period of 6-12 hours  Prevents tolerance  (Transderm-Nitro, Nitro-Dur) 58

59.  IV nitroglycerin in early treatment, then another form 59

60.  Long acting forms for prophylaxis ◦ Erythrityl tetranitrate (Cardilate) ◦ Pentaerythritol tetranitrate (PETN) 60

61.  Objective 14: list the side effects of nitroglycerin 61

62.  Tolerance  Headache  Postural hypotension  Dizziness  Weakness  Syncope ◦ Don’t use alcohol with nitros 62

63.  Nitrates can increase intraocular and/or intracranial pressure 63

64.  Objective 15: identify the nursing responsibilities associated with administering the nitroglycerin preparations 64

65.  Teach: when angina occurs, take 3 tabs in 15 min; if no pain relief, call 911  Keep nitro in original container, cap tightly closed  Store in cool, dry place  Rotate sites of topical applications  Monitor BP during therapy 65

66.  Shelf-life is 6 months. If burning/stinging sensation under tongue, drug still potent  Replace 3 months after opening bottle 66

67.  Objective 16: identify the beta-adrenergic blocker used to treat angina 67

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69.  Examples: propranolol, Atenolol  Decrease heart rate, contractility ◦ Results in reduction of myocardial oxygen consumption ◦ Better if used with nitrates  Can not use in COPD, CHF, heart block, bradycardia, DM 69

70.  When used with nitrates, hypotensive episodes more likely to occur  Drugs used ◦ Atenolol (Tenormin)--prototype ◦ Metoprolol (Lopressor) ◦ Nadolol (Corgard) ◦ Propranolol (Inderal) 70

71.  Objective 17: identify the calcium channel blockers used to treat angina 71

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73.  Nifedipine (Adalat, Procardia)  Diltiazem HCl (Cardizem, Dilacor SR)-- prototype  Verapamil (Calan, Isoptin)  Bepridil (Vascor)  Nicardipine HCl (Cardene) 73

74.  These drugs create coronary vasodilation, increased coronary blood flow, lowered blood pressure, increased cardiac output, and relax coronary artery spasms 74

75. Nitrates  Prototype drug: nitroglycerin (Nitrostat)  Mechanism of action: relax both arterial and venous smooth muscle; dilate coronary arteries ◦ Short acting-terminate acute angina episode ◦ Long-acting-decrease severity and frequency of episodes

76. Nitrates (continued)  Primary use: for lowering myocardial oxygen demand  Adverse effects: hypotension, dizziness, headache, flushing of face, rash

78. Beta-Adrenergic Blockers  Prototype drug: atenolol (Tenormin)  Mechanism of action: to reduce the cardiac workload by slowing heart rate and reducing contractility  Primary use: for prophylaxis of stable angina  Adverse effects: fatigue, insomnia, drowsiness, impotence, bradycardia, confusion

80. Calcium Channel Blockers  Prototype drug: diltiazem (Cardizem)  Mechanism of action: to reduce cardiac workload by relaxing arteriolar smooth muscle; dilate coronary arteries  Primary use: for lowering blood pressure; bring more oxygen into myocardium  Adverse effects: hypotension, bradycardia, heart failure, constipation, headaches, dizziness, edema

84.  Objective 18: identify the ACE inhibitors used to treat angina 84

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86.  The angiotensin-converting enzyme inhibitors decrease myocardial oxygen demands 86

87.  Captopril (Capoten)  Lisinopril (Prinivil)--prototype  Ramipril (Altace) 87

88. ACE Inhibitors  Prototype drug: lisinopril (Prinivil, Zestril)  Mechanism of action: to enhance excretion of sodium and water  Primary use: to decrease blood pressure and reduce blood volume; dilate veins  Adverse effects: first-dose hypotension, cough, hyperkalemia, renal failure

90.  Objective 19: nursing care 90

91.  Frequency, nature, precipitants of angina attack  Lifestyle changes made  Effectiveness of coronary vasodilators in relief of pain  Monitor VS, esp. BP 91

92.  Ineffective tissue perfusion, cardiac function RT angina  Risk for injury RT side effects of coronary vasodilators  Deficient knowledge RT health alteration and medication regimen 92

93.  Client will ◦ Verbalize decrease in attacks ◦ Not experience injury due to coronary vasodilitation ◦ Verbalize s/s of drug toxicity and report to MD 93

94.  What teaching is done for clients taking nitroglycerin?  What teaching is done for clients taking calcium channel blockers, ACE inhibitors, beta blockers?  What will the nurse monitor when clients are on these medications? 94