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Learn about the relationship of calcium to electrical activity of the heart, how the autonomic nervous system affects heart rate, the action of cardiac drugs, the benefits of cardiac glycosides in CHF, and the usefulness of digitalis in atrial fibrillation.
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CARDIOTONICS AND CORONARY VASODILATORS NURS 1950: Pharmacology I
Objective 1: describe the relationship of calcium to electrical activity of the heart • Resting: • Preload: • Afterload:
repolarization • 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
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
Sympathetic (adrenergic) nerves also innervate the heart • Stimulation causes norepinephrine to be released. • Increases heart rate, slows refractory period
Objective 3: describe how cardiac drugs affect cardiac action
How cardiac drugs work • 1. Increase or decrease the force of myocardial action • Positive inotropics • Negative inotropics
2. Increase or decrease heart rate by altering SA node impulse conduction • Positive chronotropics • Negative chronotropics
3. Increase or decrease conduction of AV impulses • Positive dromotropics • Negative dromotropics
Cardiac glycosides • Digoxin & relatives • Come from Natural sources • Helpful in CHF • Have a positive inotropic effect
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
Action • Thought that they cause release of free calcium within the cardiac muscle cell • Also change the electrical activity of myocardium
Decrease velocity of electrical conduction, prolong refractory period in AV conduction system • Increase vagal tone
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?
Objective 6: describe the usefulness of digitalis in the treatment of atrial fibrillation
What is atrial fibrillation? • What activity of the cardiac glycosides improve this condition?
Chronotropic/dromotropic effects • Suppress impulse conduction through the AV node • This prevents excessive atrial activity from reaching ventricles
Objective 7: list the generic and brand names of the digitalis preparations • Digitalis preparations similar in pharmacological properties, toxic effects
Prototype • 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
Must take apical pulse 1 minute before administration • Hold if under 60, contact MD • Blood levels needed
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
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
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
May have vision changes, changes in color • May have halos, amblyopia and diplopia • Cardiac effects: development of arrhythmias (bradycardia, primary AV block)
Objective 10: identify factors which predispose digitalis toxicity
Contraindications • 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
Treatment • Hold the drug • Use digoxin immune fab (Digibind) • Antigen-binding fragments combine with digoxin to neutralize its action
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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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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
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
Teach client to take pulse • Teach S/S of toxicity • If hypothyroid, sensitive to digitalis • Draw blood levels periodically
Angina • Atherosclerosis narrows heart’s vessels • Blood flow impeded • Demand exceeds supply = anginal pain