Physiology, Pathology and Treatment of Heart Failure

1. DON’T FAIL MY HEART Physiology, Pathology and Treatment of Heart Failure

2. Objectives • To understand how a normal heart develops heart failure, learning the physiologic compensatory mechanisms that play roles in preventing and/or delaying progression to a failing heart. • To learn the different symptoms and signs that signal heart failure and understanding how these develop in the course of the disease; and • To acquire knowledge on how to approach treatment of heart failure addressing the different pathologic insults that lead to the development and progression of the failing heart.

3. Definition Heart Failure is a clinical syndrome that occurs in patient who, because of an INHERITED or acquired abnormality of cardiac structure and/or function, develop a constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales) that lead to frequent hospitalizations, a poor quality of life, and a shortened life expectancy.

4. Burden of the disease • Prevalence in the adult population in developed countries is 2%. • Prevalence rises with age and affects 6-10% of people over the age of 65. • Categorized into 2 groups: • HF with a depressed EF (systolic failure) • HF with preserved EF (diastolic failure)

5. Take – off case • ZA • 75 years old • Female • Widow • Roman Catholic • From Tondo • Known hypertensive for 50 years • Known Diabetic for 15 years

6. History of Present Illness 9 days PTA • Started to complain DOB on excertion described as drowning. • Difficulty climbing 1 flight of stairs • 2-3 pillow orthopnea • Intermittent chest heaviness radiating to the upper back. • Decreased urine output from almost 5 glasses/day to 2 cups/day. • Bipedal edema non-pitting noted • Facial edema noted • Decreased appetite

7. Day of Admission • Bipedal edema, pitting persisted • Facial edema also persisted • 2-3 pillow orthopnea still noted • Intermittent chest heaviness radiating to the upper back • Decreased urine output still approx. 1-2 cups per day. • Bloatedness which resulted to decreased appetite • Prompted consult to a DM physician in this institution • Noticed by the physician to have abdominal enlargement • Patient was then advised for admission

10. Past Medical History • 1958 - HTN (UBP= 120-130/90; Highest BP= 160) • Combizar 100mg/25mg/tab, 1 tab OD • Atenolol 100mg/tab, 1 tab OD • Clopidogrel 75mg/tab, 1 tab OD • 1997 – DM type II • HUM 70/30 = 28 ‘u’ AM; 14 ‘u’ PM • 1990 – S/p TAB for myoma Uteri

11. 1995 – S/P cholecystectomy for cholecystitis • 2004 – Mass excision on popliteal area • 2006 – Bronchitis • Hyperurecemia – allopurinol 100mg/tab, 1 tab OD • Dyslipidemia – Simvastatin 40mg/tab, 1 tab qHS

12. Family History • (+) HTN – mother • (+) Kidney disease – sister • (+) Stroke – sister • (+) TB – mother • (+) DM – mother

13. Physical Exam on Admission • VS: • Anictericsclerae, pink palpebral conjunctivae, (+) Prominent neck veins, (-) CLADS, (-) TPC • ECE, (+) bibasal crackles, (-) wheezing • AP, distinct S1 and S2, NRRR, (-) murmur • Globular, (+) fluid wave, (-) caput medusae, (-) Bruits • FEP, (+) bipedal edema, pitting

14. Laboratories Done

17. ECG • NSR • Freq. PVCs in singles • Left atrial abnormality • HBa1c: 7.5% • CBG: 52

18. Chest X-ray – mild bilateral pulmonary congestion – biventricular cardiomegaly – atherosclerotic aorta • 2D Echom

19. The Normal Heart

21. Pathogenesis

22. Underlying Cause • Ischemic Heart Disease • Cardiomyopathies • Congenital, Valvular Hypertensive Heart Disease

23. Precipitating Cause • Infection • Arrhytmia • Physical, Dietary, Fluid, Environment • Myocardial Infarction • Pulmonary Embolism • Anemia • Thyrotoxicosis and Pregnancy • Aggravation of Hypertension • Rheumatic, Viral and other forms of Myocarditis • Infective Endocarditis

24. Heart Failure • Systolic Dysfunction – Depressed EF • Diastolic Dysfunction – EF Preserved

25. Hemodynamic Derangement in HF • Reduction in Cardiac Reserve • Increased ventricular diastolic pressure

26. Systolic Dysfunction • Main Pathology: Decreased Cardiac Output

27. 4 Major Determinants of the Systolic Function of the Heart and the Cardiac Output • Contractile State of the Myocardium • Preload • Afterload • Heart Rate

28. Representative Causes

33. Diastolic Dysfunction • Main Pathology: Impaired Ventricular Filling

34. Representative Causes

44. Contractility Preload Afterload Myocardial Fiber Shortening LV Size Heart Rate Stroke Volume Cardiac Output TPR Arterial Pressure

45. Compensatory Mechanisms to a Decreased Cardiac Output • Increased Sympathetic Activity • Increased Heart Rate • Increased Myocardial Contractility • Increased Venous Tone

46. Compensatory Mechanisms to a Decreased Cardiac Output • Activation of the RAA System

47. Compensatory Mechanisms to a Decreased Cardiac Output • Secretion of AVP