NURS 1950: Pharmacology I 1
Objective 1: describe the relationship of calcium to electrical activity of the heart Resting: Preload: Afterload: 2
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
Objective 2: describe how the ANS affects the heart rate 4
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
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
1. Increase or decrease the force of myocardial action Positive inotropics Negative inotropics 9
2. Increase or decrease heart rate by altering SA node impulse conduction Positive chronotropics Negative chronotropics 10
3. Increase or decrease conduction of AV impulses Positive dromotropics Negative dromotropics 11
Diuretics to decrease blood volume 12
Objective 4: identify the action of cardiac glycosides 13
Digoxin & relatives come from Natural sources Helpful in CHF Have a positive inotropic effect 14
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 15
Action Thought that they cause release of free calcium within the cardiac muscle cell Also change the electrical activity of myocardium 16
Decrease velocity of electrical conduction, prolong refractory period in AV conduction system Increase vagal tone 17
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? 18
Objective 6: describe the usefulness of digitalis in the treatment of atrial fibrillation 19
What is atrial fibrillation? What activity of the cardiac glycosides improve this condition? 20
Chronotropic/dromotropic effects ◦ Suppress impulse conduction through the AV node ◦ This prevents excessive atrial activity from reaching ventricles 21
Objective 7: list the generic and brand names of the digitalis preparations Digitalis preparations similar in pharmacological properties, toxic effects 22
Digoxin (Lanoxin, Lanoxicaps): oral or IV Onset minutes oral Peaks 2-6 hrs Duration 2-4 days Eliminated by kidney ◦ Used most often as rapid onset, short duration 23
Must take apical pulse 1 minute before administration Hold if under 60, contact MD Blood levels needed 24
Objective 8: define digitalization 25
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 26
Example ◦ Oral dose of digoxin mg ◦ mg then given every 6-8 hours until desired blood level reached ◦ Then maintenance dose: mg daily 27
Objective 9: list symptoms of digitalis toxicity 28
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 29
May have vision changes, changes in color ◦ May have halos, amblyopia and diplopia ◦ Cardiac effects: development of arrhythmias (bradycardia, primary AV block) 30
Objective 10: identify factors which predispose digitalis toxicity 31
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 32
Treatment ◦ Hold the drug ◦ Use digoxin immune fab (Digibind) Antigen-binding fragments combine with digoxin to neutralize its action 33
Objective 11: describe the nursing responsibilities associated with administering cardiac glycosides preparations 34
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 35
Teach client to take pulse Teach S/S of toxicity If hypothyroid, sensitive to digitalis Draw blood levels periodically 36
Atherosclerosis narrows heart’s vessels Blood flow impeded Demand exceeds supply = anginal pain 37
Objective 12: describe the actions of the antianginal drugs 38
Drugs are used to dilate coronary arteries This brings in oxygen and nutrients Supply = demand so no pain 39
Objective 13: identify the drugs used to treat angina pectoris 40
Nitroglycerin Calcium channel blockers Beta blockers ACE inhibitors 41
Nitroglycerin drugs Works by relaxing arterial and venous smooth muscle Dilate coronary arteries 42
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 43
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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) 45
Nitroglycerin patches: worn hours “Patch-off” period of 6-12 hours Prevents tolerance (Transderm-Nitro, Nitro-Dur) 46
IV nitroglycerin in early treatment, then another form 47
Long acting forms for prophylaxis ◦ Erythrityl tetranitrate (Cardilate) ◦ Pentaerythritol tetranitrate (PETN) 48
Objective 14: list the side effects of nitroglycerin 49
Tolerance Headache Postural hypotension Dizziness Weakness Syncope ◦ Don’t use alcohol with nitros 50
Nitrates can increase intraocular and/or intracranial pressure 51
Objective 15: identify the nursing responsibilities associated with administering the nitroglycerin preparations 52
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 53
Shelf-life is 6 months. If burning/stinging sensation under tongue, drug still potent Replace 3 months after opening bottle 54
Objective 16: identify the beta-adrenergic blocker used to treat angina 55
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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 57
When used with nitrates, hypotensive episodes more likely to occur Drugs used ◦ Atenolol (Tenormin)--prototype ◦ Metoprolol (Lopressor) ◦ Nadolol (Corgard) ◦ Propranolol (Inderal) 58
Objective 17: identify the calcium channel blockers used to treat angina 59
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Nifedipine (Adalat, Procardia) Diltiazem HCl (Cardizem, Dilacor SR)-- prototype Verapamil (Calan, Isoptin) Bepridil (Vascor) Nicardipine HCl (Cardene) 61
These drugs create coronary vasodilation, increased coronary blood flow, lowered blood pressure, increased cardiac output, and relax coronary artery spasms 62
Objective 18: identify the ACE inhibitors used to treat angina 63
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The angiotensin-converting enzyme inhibitors decrease myocardial oxygen demands 65
Captopril (Capoten) Lisinopril (Prinivil)--prototype Ramipril (Altace) 66
Objective 19: nursing care 67
Frequency, nature, precipitants of angina attack Lifestyle changes made Effectiveness of coronary vasodilators in relief of pain Monitor VS, esp. BP 68
Ineffective tissue perfusion, cardiac function RT angina Risk for injury RT side effects of coronary vasodilators Deficient knowledge RT health alteration and medication regimen 69
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? 70