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Heart Failure

Heart Failure. 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

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Heart Failure

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  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

  12. 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

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

  14. Drugs Used To Treat Heart Failure

  15. 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

  16. ACE Inhibitors

  17. 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

  18. -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

  19. 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

  20. 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

  21. 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

  22. Direct Vasodilators • Isosorbide dinitrate Isordil

  23. 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

  24. Diuretics • Hydrochlorothiazide • Furosemide Lasix

  25. 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

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

  27. 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

  28. 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

  29. 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

  30. 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)

  31. 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

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

  33. Normal ECG

  34. Bradycardia

  35. Premature Ventricular Contractions

  36. Multifocal PVC’s

  37. PAT With Block

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