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NURS 1950: Pharmacology I 1
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Objective 1: describe the relationship of calcium to electrical activity of the heart Resting: Preload: Afterload: 2
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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
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Objective 2: describe how the ANS affects the heart rate 4
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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
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Sympathetic (adrenergic) nerves also innervate the heart Stimulation causes norepinephrine to be released. Increases heart rate, slows refractory period 6
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Objective 3: describe how cardiac drugs affect cardiac action 8
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1. Increase or decrease the force of myocardial action Positive inotropics Negative inotropics 9
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2. Increase or decrease heart rate by altering SA node impulse conduction Positive chronotropics Negative chronotropics 10
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3. Increase or decrease conduction of AV impulses Positive dromotropics Negative dromotropics 11
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Diuretics to decrease blood volume 12
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Figure 24.1 Pathophysiology of heart failure
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Objective 4: identify the action of cardiac glycosides 14
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Digoxin & relatives Come from Natural sources Helpful in CHF Have a positive inotropic effect 15
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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
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Action ◦ Thought that they cause release of free calcium within the cardiac muscle cell ◦ Also change the electrical activity of myocardium 17
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Decrease velocity of electrical conduction, prolong refractory period in AV conduction system Increase vagal tone 18
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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
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Objective 6: describe the usefulness of digitalis in the treatment of atrial fibrillation 20
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What is atrial fibrillation? What activity of the cardiac glycosides improve this condition? 21
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Chronotropic/dromotropic effects ◦ Suppress impulse conduction through the AV node ◦ This prevents excessive atrial activity from reaching ventricles 22
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Objective 7: list the generic and brand names of the digitalis preparations Digitalis preparations similar in pharmacological properties, toxic effects 23
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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
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Must take apical pulse 1 minute before administration Hold if under 60, contact MD Blood levels needed 25
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Objective 8: define digitalization 26
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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
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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
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Objective 9: list symptoms of digitalis toxicity 29
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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
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May have vision changes, changes in color ◦ May have halos, amblyopia and diplopia ◦ Cardiac effects: development of arrhythmias (bradycardia, primary AV block) 31
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Objective 10: identify factors which predispose digitalis toxicity 32
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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
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Treatment ◦ Hold the drug ◦ Use digoxin immune fab (Digibind) Antigen-binding fragments combine with digoxin to neutralize its action 34
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Lisinopril Animation Click here to view an animation on the topic of lisinopril.here
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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
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Furosemide Animation Click here to view an animation on the topic of furosemide.here
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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
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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
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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
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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
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Objective 11: describe the nursing responsibilities associated with administering cardiac glycosides preparations 46
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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
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Teach client to take pulse Teach S/S of toxicity If hypothyroid, sensitive to digitalis Draw blood levels periodically 48
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Atherosclerosis narrows heart’s vessels Blood flow impeded Demand exceeds supply = anginal pain 49
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Objective 12: describe the actions of the antianginal drugs 50
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Drugs are used to dilate coronary arteries This brings in oxygen and nutrients Supply = demand so no pain 51
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Objective 13: identify the drugs used to treat angina pectoris 52
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Nitroglycerin Calcium channel blockers Beta blockers ACE inhibitors 53
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Nitroglycerin drugs Works by relaxing arterial and venous smooth muscle Dilate coronary arteries 54
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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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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
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Nitroglycerin patches: worn 12-14 hours “Patch-off” period of 6-12 hours Prevents tolerance (Transderm-Nitro, Nitro-Dur) 58
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IV nitroglycerin in early treatment, then another form 59
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Long acting forms for prophylaxis ◦ Erythrityl tetranitrate (Cardilate) ◦ Pentaerythritol tetranitrate (PETN) 60
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Objective 14: list the side effects of nitroglycerin 61
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Tolerance Headache Postural hypotension Dizziness Weakness Syncope ◦ Don’t use alcohol with nitros 62
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Nitrates can increase intraocular and/or intracranial pressure 63
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Objective 15: identify the nursing responsibilities associated with administering the nitroglycerin preparations 64
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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
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Shelf-life is 6 months. If burning/stinging sensation under tongue, drug still potent Replace 3 months after opening bottle 66
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Objective 16: identify the beta-adrenergic blocker used to treat angina 67
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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
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When used with nitrates, hypotensive episodes more likely to occur Drugs used ◦ Atenolol (Tenormin)--prototype ◦ Metoprolol (Lopressor) ◦ Nadolol (Corgard) ◦ Propranolol (Inderal) 70
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Objective 17: identify the calcium channel blockers used to treat angina 71
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Nifedipine (Adalat, Procardia) Diltiazem HCl (Cardizem, Dilacor SR)-- prototype Verapamil (Calan, Isoptin) Bepridil (Vascor) Nicardipine HCl (Cardene) 73
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These drugs create coronary vasodilation, increased coronary blood flow, lowered blood pressure, increased cardiac output, and relax coronary artery spasms 74
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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
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Nitrates (continued) Primary use: for lowering myocardial oxygen demand Adverse effects: hypotension, dizziness, headache, flushing of face, rash
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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
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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
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Objective 18: identify the ACE inhibitors used to treat angina 84
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The angiotensin-converting enzyme inhibitors decrease myocardial oxygen demands 86
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Captopril (Capoten) Lisinopril (Prinivil)--prototype Ramipril (Altace) 87
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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
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Objective 19: nursing care 90
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Frequency, nature, precipitants of angina attack Lifestyle changes made Effectiveness of coronary vasodilators in relief of pain Monitor VS, esp. BP 91
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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
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Client will ◦ Verbalize decrease in attacks ◦ Not experience injury due to coronary vasodilitation ◦ Verbalize s/s of drug toxicity and report to MD 93
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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
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