NURS 1950: Pharmacology I 1.  Objective 1: describe the relationship of calcium to electrical activity of the heart  Resting:  Preload:  Afterload:

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Presentation transcript:

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

7

 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

Figure 24.1 Pathophysiology of heart failure

 Objective 4: identify the action of cardiac glycosides 14

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

 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

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

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

 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

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

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

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

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

 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 24

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

 Objective 8: define digitalization 26

 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

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

 Objective 9: list symptoms of digitalis toxicity 29

 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

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

 Objective 10: identify factors which predispose digitalis toxicity 32

 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

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

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

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

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

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

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

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

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

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

 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

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

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

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

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

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

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

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

 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

56

 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

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

 IV nitroglycerin in early treatment, then another form 59

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

 Objective 14: list the side effects of nitroglycerin 61

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

 Nitrates can increase intraocular and/or intracranial pressure 63

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

 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

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

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

68

 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

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

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

72

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

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

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

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

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

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

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

85

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

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

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

 Objective 19: nursing care 90

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

 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

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

 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