1 / 94

CARDIOTONICS AND CORONARY VASODILATORS

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

lilli
Télécharger la présentation

CARDIOTONICS AND CORONARY VASODILATORS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. CARDIOTONICS AND CORONARY VASODILATORS NURS 1950: Pharmacology I

  2. Objective 1: describe the relationship of calcium to electrical activity of the heart • Resting: • Preload: • Afterload:

  3. 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

  4. Objective 2: describe how the ANS affects the heart rate

  5. 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

  6. Sympathetic (adrenergic) nerves also innervate the heart • Stimulation causes norepinephrine to be released. • Increases heart rate, slows refractory period

  7. Objective 3: describe how cardiac drugs affect cardiac action

  8. How cardiac drugs work • 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

  13. Objective 4: identify the action of cardiac glycosides

  14. Cardiac glycosides • 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. 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

  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 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. 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. 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

  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.

  35. 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

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

  37. 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

  38. 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

  39. 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

  40. 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

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

  42. 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

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

  44. Angina • Atherosclerosis narrows heart’s vessels • Blood flow impeded • Demand exceeds supply = anginal pain

  45. Objective 12: describe the actions of the antianginal drugs

More Related