2. Congestive heart failure by Dawit.pptx

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1. Congestive Heart Failure

2. Objectives Definition Epidemiology Forms of HF Causes Pathophysiology C/F, evaluation, severity classification Investigation Management Prognosis Heart Failure(Dr. Dawit)

3. DEFINITION —  Heart failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder ( of an inherited or acquired) that impairs the ability of the ventricle (heart) to fill with or eject blood. The final pathway for myriad (many) disease that affect the heart. It is characterized by specific symptoms , such as dyspnoea and fatigue , and signs , such as those related to fluid retention (edema and rales) . There are many ways to assess cardiac function. However, there is no diagnostic test for HF, since it is largely a clinical dx that is based upon a careful hx & P/E. Heart Failure(Dr. Dawit)

4. Heart Failure ~ is a clinical syndrome which develops and progresses with time resulting in failure of the heart to function adequately. Could be acute or chronic (with 2 phases Sx & Asx) The development and disease progression of HF has 4 different stages ( Risk ----- Refractory HF )( Stage A, B,C D) The disease progression Could be fast or slow can be slowed or stopped by Rx may reverse spontaneously Heart Failure(Dr. Dawit)

5. Epidemiology HF is Common costly disabling fatal (potentially) Eg. In USA Prevalence 5 million pt Incidence 0.55 mill/yr Death 0.05 mill/yr 1-3 mill admissions /yr $ 28 bill /yr Heart Failure(Dr. Dawit)

6. Epidemiology A major public health problem in industrialized nations. US – ~ 5 million have HF & >55,000 Dxed for 1 st time each year - HF is responsible for ~1 million hospital admissions & 50,000 deaths annually. More in elderly (incidence ~1% of popn, 20% of all hospital admissions in >65yrs of age, ~ 80% of hospitalizn for HF) ; likely to increase as Pop n . ages. Heart Failure(Dr. Dawit)

7. Epidem. Cont. 5 years survival rate of less than 40% from the time of diagnosis Higher mortality in the African-American population, people over 65 yrs Once symptomatic at rest, 1-yr mortality of 50% In those with symptoms at rest and CAD, 1 and 3 yrs survival of 43% and 18% Ethiopia : 3.7% of MICU admission and 3.6% of total deaths (case fatality ratio of 30.5% [ 40 of 131 CHF admissions] ) Heart Failure(Dr. Dawit )

8. Nearly any form of heart disease may ultimately lead to the HF syndrome The clinical syndrome may result from disorders of the pericardium, myocardium, endocardium, valves or great vessels , but many of the symptoms are caused by LV dysfunction. LV dysfunction is wide in spectrum EF reduction Dilated LV size Systolic/diastolic dysfunction Heart Failure(Dr. Dawit)

9. Heart Failure as a Symptomatic Disorder The degree of functional limitation imposed by HF is quantified (graded) 1 to 4 functional classes, first by NYHA -depending on the degree of effort needed to elicit symptoms: Class I - Sxs on ‘ vigorous’ exertion as normal person Class II - Sxs on ordinary activities Class III - Sxs on < ordinary activities Class IV - Sxs a rest be associated with a wide spectrum of LV functional abnormalities, Heart Failure(Dr. Dawit)

10. Left Ventricular Dysfunction Begins with injury to or stress on the myocardium Is generally a progressive process The progression is mainly manifestation by a change in the geometry and structure of the LV, such that the chamber dilates and/or hypertrophies and becomes more spherical—a process referred to as Cardiac Remodeling . ↓ ↑ Hemodynamic stresses on the walls of the failing heart Depresses its mechanical performance and Regurgitant flow through the mitral valve. ↓ Sustain and exacerbate the remodeling process. ↓ Appearance and worsening of Symptoms (HF) Heart Failure(Dr. Dawit )

11. Factors affecting Cardiac Remodeling Activation of endogenous neuro-hormonal systems ( nor epinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines) increase the hemodynamic stresses on the ventricle by causing sodium retention and peripheral vasoconstriction Exert direct toxic effects on cardiac cells and Stimulate myocardial fibrosis, ↓ Alter the architecture and impair the performance of the failing heart. Alters the performance and phenotype of myocytes Heart Failure(Dr. Dawit)

12. Heart Failure(Dr. Dawit) Forms of heart failure Systolic/Diastolic/ *combined High output/low output Forward/backward Right sided/left sided Acute/chronic

13. Systolic Heart Failure Impaired contractility , weak systolic contraction Increased ventricular volume and pressure Cardiac dilatation Inadequate ventricular emptying Examples – DCMP, IHD , Valvular regurgitant lesions, cardiogenic shock secondary to AMI. Heart Failure(Dr. Dawit)

14. Diastolic Heart Failure Typical SSxs of HF in pt with Normal LVEF & no valvular abnormalities on Echo . At least 1/3 rd of CHF pts Impaired diastolic(filling phase) function regardless of EF (increased resistance to inflow, impaired relaxation, myocardial fibrosis). Elevated diastolic P o at any volume Preserved systolic func. with small LV cavity In aging population, mostly female Heart Failure(Dr. Dawit)

15. Etiologic Risk Factors for HF CAD or history of MI Valvular heart disease Congenital heart defects Hypertension Diabetes Alcoholism Anemia Thyrotoxicosis Other: Obesity Age Smoking High or low hematocrit level Reduced or falling vital capacity Heart Failure(Dr. Dawit) CAD=coronary artery disease; LVH=left ventricular hypertrophy.

16. Other Etiologic Risk Factors for CHF Valvular cardiomyopathy Mostly regurgitation and not stenosis Idiopathic dilated cardiomyopathy Various genetic variants Idiopathic myocardial fibrosis Endomyocardial fibrosis Tropical eosinophilic endomyocardial fibrosis Commonly in South/Central America and Tropical/Subtropical Africa Inflammatory (Autoimmune and infectious - HIV) Tachycardia Induced Metabolic, peripartum, and toxin exposure  cardiomyopathy Heart Failure(Dr. Dawit)

17. Precipitating causes Aggravation of H TN A nemia T hyrotoxicosis A rrhythmias P ulmonary embolism M I I nfection (Rheumatic fever, Endocarditis, Myocarditis P regnancy A lcohol consumption D rug discontinuation (of HF) S tress (Physical, Dietary, Env’tal, and Emotional) Heart Failure(Dr. Dawit) HATA PMI PADS

18. Heart Failure(Dr. Dawit) Pathophysiology of CHF CHF begins with an injury and a daptive response it induces Myocardial infarction, genetic mutation, valvular lesion with volume or pressure overload … Index event may result in failure with decreased cardiac efficiency and reduced blood pressure Mechanisms Causes Hemodynamic burden Valvulopathy, cong HD, HTN (P o or volume overload) Sustained myocardial loss (structural, functional) MI, infectious, cardiomyopathy , inflammatory, infiltrative, genetic mutation (HCM) Depressed contractility Metabolic, drugs Tachycardia induced depression Arrhythmias

19. Heart Failure(Dr. Dawit) Frank-Starling curves in HF

20. Pathophysiology cont. Adaptive mechanism An increase in diastolic volume ( Frank- Starling mechanism) Hypertrophy Redistribution of blood to the brain, heart and away from muscle, skin, kidney and VC due to neurohumoral adjustment: to maintain arterial perfusion in face of a sudden reduction of COP Adaptive mechanisms well suited for acute CHF As adaptive response fails : The process to the index event becomes maladaptive perpetuating the heart failure The need for protection of BP and flow to vital organs activates baroreceptors that control RAAS,SNS Elevation of endothelin and fibrotic cytokines (TNF- α) Heart Failure(Dr. Dawit)

21. Pathoph. Cont. Chronic elevation of renin, angiotensin, aldosterone and NE have harmful effect on heart & other organs Maladaptive mechanism Excessive dilation Remodeling (the process by which mechanical, neurohormonal, and possibly genetic factors alter ventricular size, shape [spherical-decreases effectiveness of ejection], and function. Its hallmarks are hypertrophy, loss of myocytes, and increased interstitial fibrosis). Remodeling occurs in MI, CMP, HTN, VHD,… Persistent remodeling : decline in LV function Excess hypertrophy causing impaired filling Excess and prolonged neurohumoral effect causing increased after load and myocyte death Heart Failure(Dr. Dawit)

22. Biochemical abnormality of CHF Reduced myocardial energy reserve Reduction of myosin ATPase activity Reduced delivery of Ca++ to the contractile site Abnormal neurohumoral and cytokine adjustment Increase hemodynamic burden and oxygen consumption (maladaptive) Heart Failure(Dr. Dawit)

23. Biochemical abn. of CHF cont . Adrenergic nervous system Raise vascular resistance May cause myocyte damage through Ca++ overload Cardiac arrhythmias 2. RAAS Vasoconstriction Water retention and volume overload Cardiac fibrosis 3. Endothelin excess : VC 4. Over expression of TNF- α myocardial reduced contractility, CHF, increased mortality Proinflammatory cytokines and oxidative stresses are cytotoxic to myocardium. Heart Failure(Dr. Dawit )

24. Heart Failure Pathophysiology Heart Failure(Dr. Dawit) Index Event (MI, Valve Lesion, Mutation) Fall in LV Performance Activation of RAAS, SNS, ET, and Others Myocardial Toxicity Peripheral Vasoconstriction Hemodynamic Alterations Remodeling and Progressive Worsening of LV Function Heart Failure Symptoms Morbidity and Mortality Shah M et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2 –S 6. Adaptive Response

25. Heart Failure(Dr. Dawit)  CNS sympathetic outflow  Cardiac sympathetic activity  Renal sympathetic activity Activation of RAS Sodium retention Myocyte hypertrophy Myocyte injury Increased arrhythmias Disease progression  1 b 1 How Sympathetic Activation Promotes the CV Disease Continuum b 1 b 2  1  Vascular sympathetic activity Vasoconstriction  1

26. RAS Pathophysiology Heart Failure(Dr. Dawit) Angiotensin I Angiotensin II Increased Cellular Growth & Hypertrophy Increased Sympathetic Activity Apoptosis Sodium Retension Increased Aldosterone Release Vasoconstriction AT1 Receptor ACE

27. Heart Failure Pathophysiology Heart Failure(Dr. Dawit) Myocardial Injury Fall in LV Performance Activation of RAAS, SNS, ET, and Others Myocardial Toxicity Peripheral Vasoconstriction Hemodynamic Alterations Remodeling and Progressive Worsening of LV Function Heart Failure Symptoms Morbidity and Mortality ANP BNP Shah M et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2 –S 6.

28. The NPS Is Overwhelmed in Decompensated Heart Failure Heart Failure(Dr. Dawit) Adapted from Shah M et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2 –S6. ANP BNP Endothelin Aldosterone Vasopressin Angiotensin II Norepinephrine Excess vasoconstriction Compensation Excess vasodilation

29. Physiologic Effects of the RAAS and NPS RAAS (Renin-Angiotensin-Aldosterone System) Activation of AT 1 receptors Vasoconstriction by angiotensin II Sodium retention Increased aldosterone release Increased cellular growth Increased sympathetic nervous activity NPS (Natriuretic Peptide System) ANP, BNP Vasodilation Sodium excretion Decreased aldosterone levels Inhibition of RAAS Inhibition of SNS Antiprolif . of vasc.smooth ms cells Heart Failure(Dr. Dawit) AT 1 = angiotensin I; ANP = atrial natriuretic peptide; BNP = B-type natriuretic peptide. Burnett JC Jr. J Hypertens. 1999;17(suppl 1):S37 – S43.

30. to Dx Pt. Evaluation/ Approach Initial Evaluation of pts with HF: 1. Pts . Identification : Pt. can present with (a) syndrome of decreased exercise tolerance (b) syndrome of fluid retention (c) no SSx ( evid.of cardiac enlarg . or dysfunction) 2. Identification of a structural & functional abnormality Hx , P/E, Dxic tool 3. Evaluation of cause Hx , P/E, Lab. Test Ongoing evaluation : assessment of functional capacity, volume status, lab, prognosis Discordance b/n EF & degree of functional impairement Outcomes of Dev’t of structural abnormalities: 1. Sxs controlled by Rx 2. Death from progressive HF 3. Death before dev’t of Sxs Heart Failure(Dr. Dawit)

31. Clinical Manifestation The cardinal Sxs of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary congestion and peripheral edema Both abnormalities can impair the functional capacity and quality of life Dyspnea and fatigue ≠ Fluid retention CHF X HF √ Heart Failure(Dr. Dawit)

32. Modified Framingham clinical criteria for the dx of HF Major PND Orthopnoea Pulmonary rales Elevated JVP Third heart sound Cardiomegaly on CXR Pulm. edema on CXR Wt loss ≥4.5 kg in 5 days in response to Rx of presumed HF Minor Nocturnal cough Dyspnea on ordinary exertion Tachycardia ( ≥120 bpm) Pleural effusion Hepatomegaly Bilateral leg edema Wt loss ≥4.5 kg in 5 days Heart Failure(Dr. Dawit) Diagnosis 2 major or 1 major + 2 minor criteria cannot be attributed to another medical condition.

33. New York Heart Association Functional Class Class I No limitations. No symptoms with ordinary activities. Class II Slight limitations. Symptoms with ordinary activities. Class III Marked limitations. Symptoms with < ordinary activities. Class IV Symptoms at rest. Heart Failure(Dr. Dawit) Subjective assessment; doesn’t consider natural progression; can change frequently over short periods of time .

34. New Approach to the Classification of Heart Failure (ACC/AHA Staging) Heart Failure(Dr. Dawit) Stage Patient Description A High risk for developing heart failure (HF) Hypertension, CAD Diabetes mellitus Family Hx of cardiomyopathy B Asymptomatic HF Previous MI LV systolic dysfunction Asymptomatic valvular disease C Symptomatic HF Known structural heart disease Shortness of breath and fatigue Reduced exercise tolerance D Refractory end-stage HF Marked Sxs at rest despite maximal medical therapy ( eg , those who are recurrently hospitalized or cannot be safely discharged from the hospital without specialized interven .)

35. Classification of HF: Comparison Between ACC/AHA HF Stage and NYHA Functional Class Heart Failure(Dr. Dawit) ACC/AHA HF Stage NYHA Functional Class A At high risk for heart failure but without structural heart disease or symptoms of heart failure (e.g. patients with hypertension or coronary artery disease) B Structural heart disease but without symptoms of heart failure C Structural heart disease with prior or current symptoms of heart failure D Refractory heart failure requiring specialized interventions I Asymptomatic II Symptomatic with moderate exertion IV Symptomatic at rest III Symptomatic with minimal exertion None

36. INVETIGATIONS CBC → anemia ,leukocytosis SERUM ELECTROLYTE RFT → Normal in pt with mild to moderate HF IN pt with sever HF those on large dose of diuretics may have ↑BUN &Cr because of chronic reduction of renal blood flow from ↓CO LFT→ impaired in pt with congestive hepatomegally & cardiac cirrhosis Heart Failure(Dr. Dawit)

37. Cont… B type Natriutric peptide ~ is a 32 amino acid polypeptide containing a 17 amino acid ring structure Secreted from cardiomyocytes in response to ventricular wall stretch. Major source are the cardiac ventricles Have a fundamental role in CVS remodeling, volume homeostasis & the response to ischemia Guide to treatment of HF Predict the response to therapeutics interventions & Predict prognosis. Heart Failure(Dr. Dawit)

38. Cont… CXR ECHO reliable in the dx of the cause or causes of HF Determine LV function , wall thickness , chamber size Regional wall motion abnormality Presence of VHD, pericardial disease Heart Failure(Dr. Dawit)

39. Cont… ECG ABG PULSE oximetriy Heart Failure(Dr. Dawit)

40. Medical Therapy

41. Goals of Heart Failure Therapy in the Symptomatic Patient Relieve HF symptoms i.e., make patients feel better Improve overall clinical status Stabilize acute episodes of decompensation Decrease morbidity and mortality Slow and/or reverse disease progression Identify and treat reversible causes of LV dysfunction

42. How Do We Make Heart Failure Patients Feel Better? With hemodynamic interventions Diuretics Digoxin Vasodilators Positive inotropic agents Mechanical interventions that improve hemodynamics (e.g., CRT, LVADs)

43. How Do We Make HF Pts Live Longer? With neurohormonal interventions ACE inhibitors Angiotensin receptor antagonists (in ACE-inhibitor intolerant patients) Aldosterone antagonists Beta-Blockers And with Mechanical interventions that improve LV remodeling (e.g., CRT, LVADs)

44. ACEI All patients at all classes will benefit from ACEI Improved symptoms, decrease risk of death and combined risk of death and hospitalization Prevent disease progression Should be used even in patients with structural heart disease but no symptoms

45. ACEI All ACEI are equally effective Optimal dosage is controversial Ideally started at a low dose( Captopril 6.25, enalapril 2.5, lisinopril 2.5-5 ) and titrated up every 3 to 7 days with a goal daily dose ( Captopril 150mg, enalapril 20mg and lisiniopril 20-40mg ) If ACEI not tolerated Hydralazine/ isosorbide dinitrate combination ARB

46. ACEI Contraindications Symptomatic hypotension Renal failure Cautious use with renal insufficiency Renal artery stenosis Hyperkalemia Past Angioedema Persistent dry cough can affect compliance

47. ALDOSTERONE ANTAGONISTS SPIRNOLACTONE EPLRENONE MECANISM OF BENEFIT Reduce urinary K loss maintaining a higher plasma K conc. & block deleterious effect of aldosterone on the heart. 30% ↓ in overall mortality 35%↓ in hospitalization

48. RECOMMENDED In pts with moderately severe or severe HF Recent de-compensation or LV dysfunction after MI Check baseline K and RFT with follow up monitoring Spironolactone 12.5 -25 mg /day Eplerenone 25-50 mg/day ALDOSTERONE ANTAGONISTS

49. Beta-blockers Most exciting advance in the last 15 years Reduce total mortality Slow left ventricular remodeling Reduce the size of the heart Improve ejection fraction by up to 8-10% Mild initial decline in EF and fatigue might be seen Patients feel better 3-12 wks after initiating therapy

50. Beta-blockers Unlike ACEI, NOT all beta-blockers are equally effective Metoprolol and Carvedilol are the two commonly used drugs Carvedilol is ideal since it is nonselective vasodilator with antioxidant and anti-endothelin properties Metoprolol better in those with lower blood pressure

51. Beta-blockers Best candidates for beta-blockers are stable patients with mild to moderate heart failure and optimal fluid status Drugs initiated at a low dose (Carvedilol 3.125mg, Toprol 12.5-25mg) and slowly and carefully up-titrated every 2-4 weeks (Carvedilol 50-100mg and Metoprol 100-200 mg/day)

52. Indications and Contraindications of Beta-blockers Indications CHF To improve survival and, also, to reduce hospitalizations in mild to severe CHF Ischemic or cardiomyopathic origin Hypertension Can be used alone or in combination with other antihypertensive agents, especially thiazide-type diuretics Contraindications Bronchial asthma Severe bradycardia, 2° or 3° AV block, sick sinus syndrome (unless a permanent pacemaker is in place) Cardiogenic shock Decompensated HF requiring use of IV inotropic therapy Hypersensitivity to the drug Clinically manifest hepatic impairment

53. Diuretics Pivotal in reliving the volume-overload states in CHF If no overt congestion, no need for chronic use Often volume overload can be due to inadequate sodium and fluid restriction Generally the least toxic drug ( HCTZ or chlorthalidone ) at the lowest dose is used If congestion worsens, long-acting loop diuretics ( furosemide, bumetanide, or torsemide ) are prescribed For refractory edematous states, combination diuretics may be tried

54. Diuretics Reduction in plasma volume might adversely activate the RAAS & SNS. This paradoxically promotes fluid and sodium retention and eventually contribute to the progression of heart failure and remodeling . Therefore diuretics should not be used without ACEI and beta-blockers +/- aldactone

55. Digoxin Has no significant mortality benefit Substantially improved heart failure symptoms and reduced recurrent hospitalization Very beneficial in those with persistent symptoms and atrial arrhythmias Lower doses( 0.125-0.25mg ) used with drug combinations

56. Calcium Channel Antagonists Generally have negative inotropic effects To date, no symptomatic or mortality benefit At best, neutral effect for few drugs ( amlodipine and felodipine ) However in ischemic heart failure, greater chance of adverse effects seen with nifedipine and diltiazem NO ROLE IN CHF MANAGMENT

57. Use of CHF drugs based on the NYHA Functional Class Class I ACEI Class II ACEI , Beta-blocker, Diuretic Class III ACEI , BB, Diuretic , Digoxin, Aldactone(1) Class IV ACEI , BB, Diuretic , Digoxin , Aldactone(1) Aldactone reserved for those with severe CHF who have remained symptomatic despite conventional therapy of ABDD or those with hypokalemia who don’t tolerate potassium supplements

58. General Non-Pharmacologic Therapy 3 gm ( mild CHF ) or 2 gm ( moderate to advanced CHF ) sodium diet Fluid restriction Avoidance of alcohol/nicotine Regular aerobic physical activity( 3x/wk for 30min ) Avoid NSAIDs and decongestants Weight control and low animal fat diet Education, compliance monitoring, self-management

59. Surgical and Mechanical Interventions Contemporary medical therapy should be given before and after surgical interventions Beta-blockers and ACEI can independently promote reverse remodeling All new onset cardiomyopathy should be optimally medically treated and the patient observed before considering other interventions

60. Prognosis Depends on the nature of underlying heart disease presence or absence of precipitating factor that can be treated Factors associated with poor prognosis: Severely depressed EF (< 15%) Reduced maximal O 2 uptake ( 10 ml/Kg/min ) Inability to walk on a level and at a normal pace for more than 3 minutes Reduced serum Na conc.(< 133 mEq/L) Reduced serum K (< 3 mEq/L) Markedly elevated BNP (> 500 pg/ml) Frequent ventricular extra systole

61. Mortality Main cause of death in patient with HF are: Sudden or arrhythmic death Progressive pump failure Annual mortality - Asymptomatic < 5% - Mild 10% - Moderate 20-30% - Severe 30- 80%