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1. Cardiovascular diseases Chronic Heart Failure

2. Definition Current AHA defn of HF HF is a complex clinical syndrome that results from structural or functional impairment of ventricular filling or ejection of blood, which in turn leads to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF, namely edema and rales

3. Epidemiology > 20 million people affected worldwide prevalence of HF in the adult population in developed countries is 2% . In developing countries the prevalence of HF is not known but itn isd The prevalence of HF is on the rise T he prevalence and incidence of HF increases steeply with age W omen constitute at least half of the cases of HF A approximately one-half of patients who develop HF have a normal or preserved E (EF>50%)

4. PREVALENCE OF HF

5. Etiology HF broadly classified in to HF with depressed EF (systolic HF) HF with preserved EF (Diastolic HF) Industrialized countries CAD is the predominant cause , responsible for 60-70% HTN contributes to the development of HF in 75% of patients, including most patients with CAD Developing countries RHD is the commonest cause HTN is also an important cause CAD incidence is rising

6. Etiology cont

7. Etiology

8. P ATHOGENESIS

9. HF AS A PROGRESSIVE MODEL

10. PATHOGENESIS Neurohormonal Mechanisms Remodeling: is a process by which mechanical, neurohormonal and possibly genetic factors alter ventricular size, shape and function

11. NEUROHORMONAL MECHANISM

12. NEUROHORMONAL MECHANISM Maintenance of systemic pressure by vasoconstriction, resulting in redistribution of blood flow to vital organs Restoration of C/O by increasing myocardial contractility and heart rate and by expansion of ECF volume

13. Neurohormonal activation and compensatory mechanisms in HF

14. MALADAPTIVE CONSEQUENCES OF THE NEUROHORMONAL SYSTEM elevation in diastolic BP is transmitted to the atria and to the pulmonary and systemic venous circulations  the ensuing elevation in capillary pressures promotes the development of pulmonary congestion and peripheral edema increase in LV afterload induced by the rise in peripheral resistance can both directly depress cardiac function and enhance the rate of deterioration of myocardial function Catecholamine-stimulated contractility and increased heart rate can worsen coronary ischemia Catecholamines and angiotensin II may promote the loss of myocytes by apoptosis, the induction of maladaptive fetal isoforms of proteins involved in contraction, and hypertrophy

15. LEFT VENTRICULAR REMODELING

16. CONSEQUENCES OF LV REMODELING

17. SUMMARY OF THE MALADAPTIVE MECHANISMS

18. Diastolic dysfunction Reduced ATPase concentration( eg in ischemia)  reduced relaxation of myocites Reduced LV compliance ( e.g., from hypertrophy or fibrosis)  decreased vent filling Increased HR reduce time for vent filling

19. SYMPTOMS OF HEART FAILURE

20. PHYSICAL FINDINGS IN HF

21. P/E

22. C/F

23. Sensitivity, Specificity, and Predictive Accuracy of Symptoms and Signs for Diagnosing Heart Failure

24. Stage A High Risk for developing Heart failure Stage B Asymptomatic LV dysfunction Stage C Past or current Symptoms of HF Stage D End-stage HF Stages of HF: ACC/AHA Class I symptoms at activity levels that would limit normal individuals Class II symptoms of HF with ordinary exertion Class III symptoms of HF with less than ordinary exertion Class IV Symptoms of HF at rest NYHA Functional Class

25. INVESTIGATION MODALITIES

26. BNP IN THE DIAGNOSIS OF HF

27. CHEST X-RAY Findings suggestive of HF include : C ardiomegaly (cardiac-to-thoracic width ratio above 50 percent) C ephalization of the pulmonary vessels K erley B-lines P leural effusions

28. CHEST X-RAY

29. SUMM A RY OF THE WORK UP OF A PATIENT WITH HF

30. CHRONIC HEART FAILURE MANAGEMENT OF HF WITH DEPRESSED LV FUNCTION(EF<40%)

31. GENERAL PRINCIPLES IN THE MANAGEMENT OF HF Treatment of underlying disease Correction of precepitating factors General measures Treatment of the congestive state(management of fluid status) Increase myocardial contractility Preventing disease progression

32. GENERAL MEASURES screen for and treat comorbidities advise to stop smoking and to stop or limit alcohol consumption Avoid extremes of temperature and heavy physical exertion Certain drugs are known to make HF worse and should also be avoided immunization with influenza and pneumococcal vaccines to prevent respiratory infections

33. GENERAL MEASURES R outine and modest exercise is beneficial in patients with NYHA Class I to III HF Dietary restriction of sodium Fluid restriction is generally unnecessary unless the patient has H yponatremic (sodium less than 130 mEq /liter ) F luid retention that difficult to control despite high doses of diuretics and sodium restriction educate the patient and family about HF, the importance of proper diet, as well the importance of compliance with the medical regimen

34. Management of Underlying cause Arterial hypertension hypertensive therapy Coronary heart disease revascularisation (CABG, PCI) VHD reconstruction of the valve Congenital heart disease sugery, ballon valvuloplasty Pericardial construction surgery Tachycardia pharmacological therapy, cardioversion, ablation Bradycardia pacemaker therapy Thyroid gland dysfunction euthyreosis Alcoholic cardiomyopathy stopping the misuse Chronic anemia diagnosis and correction Hypertrophic cardiomyopathy resection of LVOT LBBB (desyncronisation) resynchronisation therapy

35. Identification and treatment of precipitants

36. Management based on Stages for (systolic failure

37. Management based on Stages

38. Management based on Stages

39. Management based on Stages( in depressssed EF

40. MANAGEMENT OF CHRONIC HF MANAGEMENT OF THE CONGESTIVE STATE

41. USE OF DIURETICS IN HF

42. USE OF DIURETICS IN HF Diuretics differ in their potency and pharmacologic properties F ractional excretion of Na Loop diuretics:  by 20–25% T hiazide diuretics :  by only 5–10% Thiazide s tend to lose their effectiveness in patients with moderate or severe renal insufficiency ( creatinine >2.5 mg/ dL )

43. USE OF DIURETICS IN HF In patients who are volume overloaded, a reasonable goal is weight reduction of 1.0 kg/day Duration of therapy: o nce begun, diuretic therapy is generally continued indefinitely unless cardiac function improves subpopulation of stable patients with less severe disease who can be withdrawn from diuretics N o history of hypertension L eft ventricular ejection fraction (LVEF) above 27 percent H ave been controlled on a furosemide dose of 40 mg/day or less Follow up: subjective complaint,signs of congestion,daily weight measurement,input and output,RFT and serum electrolyte

44. USE OF DIURETICS IN HF

45. SIDE EFFECTS OF DIURETICS Electrolyte and metabolic disturbances Neurohormonal activation Hypotension and azothemia Ototoxicity Hyperuricemia Hypersensitivity reactions

46. PREVENTING DISEASE PROGRESSION

47. Prevention of disease progression

48. ACE INHIBITORS

49. ACEI should be used in symptomatic and asymptomatic patients with a depressed EF (<40%) . are corner stones in the management of HF All ACEIs are equaly effective stabilize LV remodeling, improve symptoms, reduce hospitalization, and prolong life Start with low dose and titrate to the target dose used in the clinical trials or the MAXIMUM TOLERATE D DOSE Dose adjustement is every 1or 2wks Serum K, RFT 2wks after initiation thenafter periodically

50. ADVERSE EFFECTS OF ACEIs Hypotension Azothemia Hyperkalemia N onproductive cough (10–15% of patients) and angioedema (1% of patients ) Adverse effects during pregnancy

51. ANGIOTENSIN II RECEPTOR BLOCKERS IN HF appear to be as or possibly slightly less effective than ACEI when compared directly ARB should be used in symptomatic and asymptomatic patients with an EF <40% who are ACE-intolerant for reasons other than hyperkalemia or renal insufficiency Have the same side effect profile as that of ACEIs except for cough Dosage can be uptitrated every 3 to 5 days As with ACEIs, BP, RFT, and K levels should be reassessed within 1 - 2 wks after initiation and followed closely after changes in dose

52. BETA-ADRENERGIC RECEPTOR BLOCKERS ßB ( carvedilol, metoprolol, or bisoprolol ) reverse the process of LV remodeling, improve patient symptoms, prevent hospitalization, and prolong life are indicated for patients with symptomatic or asymptomatic HF and a depressed EF <40% unless contraindicated Prior to initiation of therapy, the patient should have no or minimal evidence of fluid retention and should not have required recent intravenous inotropic therapy may lead to an increase in symptoms for 4 to 10 wks before any improvement is noted

53. USE OF BETA-ADRENERGIC RECEPTOR BLOCKERS IN HF should be initiated in low doses followed by gradual increments in the dose if lower doses have been well tolerated to max tolerated doses If worsening fluid retention does occur, it is likely to do so within 3–5 days of initiating therapy can usually be managed by increasing the dose of diuretics In some patients the dose of the beta blocker may have to be reduced Duration of therapy: life long

54. RELATIVE CONTRAINDICATIONS FOR USE OF BB Heart rate <60 bpm Symptomatic hypotension Greater than minimal evidence of fluid retention Signs of peripheral hypoperfusion PR interval >0.24 sec Second- or third-degree AV block History of asthma or reactive airways PAD with resting limb ischemia

55. ADVERSE EFFECTS OF BB Worsening of HF symptoms Negative chronotropic effect Beta blocker withdrawal Increased air way resistance Exacerebation of PAD Facilitation of hypoglycemia Hyperkalemia Depression, fatigue, sexulal dysfunction Weight gain

56. DRUGS USED FOR THE TREATMENT AND PREVENTION OF HF

57. ALDOSTERONE ANTAGONISTS recommended for patients with NYHA class IV or class III (previously class IV) HF who have a depressed EF (<35%) and are receiving standard therapy, including diuretics, ACE inhibitors, and beta blockers in patients who had an MI within the preceding two weeks and who had an LVEF <= 40%

58. ADVERSE EFFECTS Hyperkalemia ( Aldosterone antagonists are not recommended when the serum creatinine is >2.5 mg/dL (or creatinine clearance is <30 mL/min) or when the serum potassium is >5.0 mmol/L ) Risk factors for hyperkalmeia Painful gynecomastia may develop in 10–15% of patients who use spironolactone

59. Management of Heart failure Management of Patients Who Remain Symptomatic

60. Hydralazine & Isosorbid dinitrate recommended as part of standard therapy in addition to beta blockers and ACE inhibitors for African Americans with NYHA class II–IV HF Considered in patients with refractory symptoms despite standard therapy

61. Rate controlling agents Ivabradin , inhibitor of I f (funny current) can be used inpatients with class II or III HFrEF , a heart rate >70 beats/min, and history of hospitalization for heart failure during the previous year Reduced hospitalization and cardiovascular related deaths

62. Digoxin : Improvement in symptoms but not survival recommended for patients with symptomatic LV systolic dysfunction who have concomitant atrial fibrillation, should be considered for patients who have signs or symptoms of HF while receiving standard therapy, including ACE inhibitors and beta blockers NEJM 1997;336:525. All-cause mortality Death or hospitalization for worsening HF

63. CARDIAC RESYNCHRONIZATION THERAPY ( CRT)

64. CRT When CRT is added to optimal medical therapy in patients in sinus rhythm, there is a significant decrease in mortality and hospitalization, a reversal of LV remodeling, as well as improved quality of life and exercise capacity CRT is recommended for patients in sinus rhythm with an EF <35% and a QRS >120 ms and those who remain symptomatic (NYHA III–IV) despite optimal medical therapy

65. IMPLANTABLE CARDIAC DEFIBIRILLATORS prophylactic ICDs in patients with mild to moderate HF (NYHA class II–III) has been shown to reduce the incidence of sudden cardiac death in patients with ischemic or nonischemic cardiomyopathy ICD should be considered for patients in NYHA class II–III HF with EF of <30–35% who are already on optimal background therapy, including an ACEI (ARB), ßB , and aldosterone antagonist

66. ICD

67. MANAGEMENT OF REFRACTORY HF Intravenous inotrops and vasodilators Hemofiltration Mechanical circulatory support Surgery Cardiac transplantation

68. Beta Blocker Diuretics for fluid retention Aldosterone antagonists in select patient Digoxin to reduce hospitalizations Hydralazine/nitrate or ARB if BP allows + sxs Bi-v pacing if sxs ACE-I (or ARB if ACE intolerant) Regular exercise program Sodium restriction Summary of management systolic failure

69. Management of HF with preserved Ejection fraction Despite the wealth of information with respect to the evaluation and management of HFrEF , there are no proven therapies for the management of patients with HFpEF it is recommended that initial treatment efforts should be focused, wherever possible, on the underlying disease process

70. DIASTOLIC HEART FAILURE Precipitating factors, such as tachycardia or atrial fibrillation, should be treated as quickly as possible Dyspnea may be treated by reducing total blood volume (dietary sodium restriction and diuretics), decreasing central blood volume (nitrates), Treatment with diuretics and nitrates should be initiated at low doses to avoid hypotension and fatigue