Understanding Heart Failure: Causes, Complications, and Treatments

1. Heart Failure

2. Overview • Heart failure is a complex progressive disorder in which the heart is unable to pump sufficient blood to meet the needs of the body • 1) Due to an impaired ability of the heart to adequately fill with blood and/or • 2) An impaired ability of the heart to eject blood

3. Overview • Heart failure is often accompanied by abnormal increases in blood volume that leads to edema • Results in pulmonary congestion (lungs) • Results in peripheral edema • Often called congestive heart failure (CHF) • Due to accumulation of fluid

4. Symptoms of Heart Failure • Dyspnea from pulmonary congestion • Dyspnea: difficulty breathing • Peripheral edema or pitting edema • Fluid retention, swelling, pitting with applied pressure • Fatigue

5. Underlying Causes • Arteriosclerotic cardiovascular disease (ASCVD) • Also known as Coronary Artery Disease (CAD) • *main thing that causes heart failure • Myocardial Infarction (heart attack) • Heart attack  part of the heart dies, if severe enough  you get inability of heart to function normally • Less likely: • Severe hypertension • Disease of the valves of the heart • Dilated cardiomyopathy • Congenital heart disease

6. Underlying Causes • Left ventricular failure secondary to coronary artery disease is most common cause of heart failure • 70% of all cases of heart failure are caused by CAD

7. Compensatory Changes

8. Compensatory Changes • Failing heart activates 3 major compensatory changes • Increased sympathetic activity w/hope of raising BP • (1st thing that happens w/heart failure  BP goes down) • Activation of renin-angiotensin-aldosterone system • Retention of sodium and water to increase fluid • If sxs of heart failure is fluid retention, THIS WILL MAKE IT WORSE • Myocardial hypertrophy • Cardiac pneumonally • Initially beneficial, these alternations ultimately cause deterioration of cardiac function

9. Increased Sympathetic Activity • Decrease in BP causes activation of sympathetic nervous system • Results in increased HR, force of contraction, vasoconstriction, and increased in preload and afterload • Afterload • Preload:return of blood back to heart (superior vena cava) • When you get return to heart, heart stretches, L ventricular diastolic pressure goes up • But if heart isn’t pumping efficiently, can’t get extra blood out • If heart isn’t pumping efficiently, can’t get extra blood out, blood has hard time pumping against pressure of vena cava  everything backs up…into lungs, periphery • Compensatory changes increase work of the heart and eventually make HF worse

10. Activation of RAA System • Increased afterload • Fall in CO decreases blood flow to kidney • RAA system is activated • Results in increased peripheral resistance and retention of sodium and water • Blood volume increases and more blood is returned to heart(more preload) • If heart is unable to pump extra volume, edema results • Compensatory changes increase work of heart and eventually make HF worse

11. Myocardial Hypertrophy • Heart increases in size stretching the heart muscle and leading to stronger contraction • Eventually causes elongation of heart fibers resulting in weakercontraction • Force of contraction goes down • Results in inability of heart to pump blood eventually making heart failure worse • Hypertrophic changes can become permanent • Called cardiac remodeling

14. Compensated Heart Failure • If compensatory changes restore cardiac function(GOOD), HF is said to be compensated • if the compensatory mechs end up helping patient • This isn’t normal, doesn’t occur much, if it does occur it doesn’t last long • If compensatory changes fail to restore cardiac function, HF is said to be decompensate • Patient is worse

15. Goals of Therapy • Alleviate symptoms • Slow progression of disease • Improve patient survival

16. Drugs Used To Treat Heart Failure

17. Effects of Drug Therapy • Reduce load on the heart • Decreased extracellular fluid volume • Ex: w/diuretics • Improved cardiac contractility • By decreasing afterload and preload • Slow rate of cardiac remodeling • BB and digoxin do this the most

18. ACE Inhibitors

19. ARBs • Similar effect as ACE inhibitors but are not therapeutically identical • Used as substitute for ACE inhibitors in patients who have developed angioedema or in patients who have developed severe cough

20. -Blockers • Seems counterintuitive to administer a drug whose major therapeutic effect is to lower cardiac output to a patient with heart failure • Block chronic activation of sympathetic nervous system • Decreases sympathetic tone, decreased comepnsatory mechs • Improved left ventricular functioning • Reverses cardiac remodeling

21. Consultation (β-blockers) • Consultation for β-blocking drugs used to treat patients with CHF should include warnings about increasing symptoms of heart failure early in the course of treatment • Pt: can get mild worsening initially, BUT if it stays for a long time  contact PCP

22. Approved -Blockers for HF • Carvedilol Coreg • Non-selective -blocker that also blocks - receptors • Metoprolol Toprol • Selective 1-blocker • Recommended for nearly all patients with mild to moderate HF in combination with diuretics, ACEinhibitors, and digoxin

23. Vasodilators (nitrates) • Direct vasodilator, works directly on smooth muscle of the vasculature • Causes dilation of venous blood vessels • Causes some pooling of blood in periphery • Leads to a decrease in cardiac preload • Less venous return to heart • Less LVEDP • Reductioninsymptoms of congestion • Heart pumps more efficiently

24. Direct Vasodilators • Isosorbide dinitrate Isordil

25. Thiazide Diuretics • Promote sodium and water elimination, reduce plasma volume • Relieve pulmonary and peripheral congestion • Relieve symptoms of nocturnal dyspnea and orthopnea • orthopnea: Sxs of pulmonary congestion when u lie flat • In order to breathe, have to prop up w/a few pillows • Diagnostic feature of heart failure (ex: pt has “2-pillow orthopnea”) • Decrease plasma volume and decrease preload (reduced amt of return to heart, reduces pulmonary congestion) • Decrease cardiac work and myocardial oxygen demand

26. Diuretics • Hydrochlorothiazide • Furosemide Lasix

27. Potassium Sparing Diuretics • Patient with advanced heart disease have elevated levels of aldosterone • Aldosterone causes sodium and fluid retention • Spironolactone is direct antagonist of aldosterone and prevents salt and water retention • Reserved for most advanced cases of heart failure

28. Inotropic Agents • Inamrinone • Milrinone Primacore • Dobutamine Dobutrex • Digoxin Lanoxin, Digitek

29. Digoxin • Alkaloid from foxglove • Has a positive inotropic effect by increasing contraction of atrial and ventricular myocardium • Problem: Show small differences between therapeutic and toxic or even fatal levels

30. Therapeutic Digoxin Levels • 0.8-2.0ng/ml • 30% of patients develop signs of toxicity below a blood level of 2.0ng/ml • Drug MUST be monitored closely

33. Clinical Effects • Increases contractility of the heart and increases cardiac output • Decreases LVEDP thus increasing efficiency of heart • Improved circulation reduces sympathetic tone and peripheral resistance. • Reduces heart rate by slowing conduction through the AV node • Reduction in myocardial oxygen demand

34. Consultation for Digoxin • Take this medicine by mouth with a glass of water. • it is best to take this medicine on an empty stomach. • ***Visit your doctor or health care professional for regular checks on your progress. • ***Do not stop taking this medicine without the advice of your doctor or health care professional • Do not change the brand you are taking, other brands may affect you differently. • Check your heart rate and blood pressure regularly while you are taking this medicine. • Less digoxin may be absorbed if you consume a diet high in bran fiber • Do not treat yourself for coughs, colds or allergies without asking your doctor or health care professional for advice • Cold meds or antihistamines, ESP NO PSEUDOEPHEDRINE (increases heart rate, BP) • Antihistamines: those w/significant anticholinergicproerpties- -> block vagus nerve, increase heart rate , and dries you out, stops secretions  SHOULD RECOMMEND 2ND GENERATION (loratidine, fexofenadine)

35. Side Effects • Blood levels must be kept in a very narrow range • 0.8—2.0 ng/ml • Side effects are associated with higher blood levels

37. Cardiac Arrhythmias • Bradycardia • Premature atrial contraction • Premature ventricular contractions • Atrial tachycardia • Atrial tachycardia with block • Atrial fibrillation • Ventricular tachycardia

39. Normal ECG

40. Bradycardia

43. Premature Ventricular Contractions

44. Multifocal PVC’s

50. PAT With Block