CARDIOTONICS AND CORONARY VASODILATORS

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CARDIOTONICS AND CORONARY VASODILATORS

NURS 1950: Pharmacology I

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Objective 1: describe the relationship of calcium to electrical activity of the heart

Resting: Preload: Afterload:

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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

repolarization

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Objective 2: describe how the ANS affects the heart rate

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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

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Sympathetic (adrenergic) nerves also innervate the heart

Stimulation causes norepinephrine to be released.

Increases heart rate, slows refractory period

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Objective 3: describe how cardiac drugs affect cardiac action

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1. Increase or decrease the force of myocardial action

Positive inotropics Negative inotropics

How cardiac drugs work

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2. Increase or decrease heart rate by altering SA node impulse conduction

Positive chronotropics Negative chronotropics

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3. Increase or decrease conduction of AV impulses

Positive dromotropics Negative dromotropics

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Diuretics to decrease blood volume

Figure 24.1 Pathophysiology of heart failure

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Objective 4: identify the action of cardiac glycosides

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Digoxin & relatives

Come from Natural sources Helpful in CHF Have a positive inotropic effect

Cardiac glycosides

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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

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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

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Decrease velocity of electrical conduction, prolong refractory period in AV conduction system

Increase vagal tone

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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?

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

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What is atrial fibrillation? What activity of the cardiac glycosides

improve this condition?

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

reaching ventricles

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Objective 7: list the generic and brand names of the digitalis preparations

Digitalis preparations similar in pharmacological properties, toxic effects

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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

Prototype

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Must take apical pulse 1 minute before administration

Hold if under 60, contact MD Blood levels needed

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Objective 8: define digitalization

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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

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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

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Objective 9: list symptoms of digitalis toxicity

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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

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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)

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Objective 10: identify factors which predispose digitalis toxicity

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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

Contraindications

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

Lisinopril Animation

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

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.

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

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

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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

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

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

Angina

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Objective 12: describe the actions of the antianginal drugs

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

Goals

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Objective 13: identify the drugs used to treat angina pectoris

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Nitroglycerin Calcium channel blockers Beta blockers ACE inhibitors

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Nitroglycerin drugs Works by relaxing arterial and venous

smooth muscle Dilate coronary arteries

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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

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Transdermal

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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)

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

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IV nitroglycerin in early treatment, then another form

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

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Objective 14: list the side effects of nitroglycerin

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Tolerance Headache Postural hypotension Dizziness Weakness Syncope

◦ Don’t use alcohol with nitros

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Nitrates can increase intraocular and/or intracranial pressure

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

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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

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Shelf-life is 6 months. If burning/stinging sensation under tongue, drug still potent

Replace 3 months after opening bottle

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

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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

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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)

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

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Nifedipine (Adalat, Procardia) Diltiazem HCl (Cardizem, Dilacor SR)--

prototype Verapamil (Calan, Isoptin) Bepridil (Vascor) Nicardipine HCl (Cardene)

Examples: calcium channel blockers

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

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

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Objective 18: identify the ACE inhibitors used to treat angina

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The angiotensin-converting enzyme inhibitors decrease myocardial oxygen demands

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

Examples: ACE inhibitors

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

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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

Assessment

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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

Nursing diagnoses

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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

Goals

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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?

Implementation