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Heart Failure

Heart Failure. Susan Schayes, MD, MPH Program Director Emory Family Medicine Residency Program Adapted from Dr. Joel Felner and Dr. Eddie Needham. Objectives. Define Heart Failure Know the 5 year mortality rate for heart failure

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Heart Failure

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  1. Heart Failure Susan Schayes, MD, MPH Program Director Emory Family Medicine Residency Program Adapted from Dr. Joel Felner and Dr. Eddie Needham

  2. Objectives • Define Heart Failure • Know the 5 year mortality rate for heart failure • Distinguish between New York Heart Association classes (I – IV) and the new American College of Cardiology stages (A – D) • Review and become familiar with treatment options • Know the three beta-blockers demonstrating benefit, and the two that are FDA approved

  3. Objectives • Know indications for an ICD • Know percent of patients who have diastolic dysfunction

  4. Pre-lecture Needs Assessment • What are the four NYHA classes of HF? • What are the four ACC stages of HF? • Which medication classes are routinely prescribed in heart failure? • Which three beta-blockers are approved to treat HF?

  5. DEFINITION • Clinical syndrome • Inability of the heart to produce sufficient cardiac output to meet the metabolic demands of the peripheral tissues while operating at normal filling pressure.

  6. Define Heart Failure • “Heart failure is a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.” 1 • The cardinal symptoms are dyspnea and fatigue, while the predominant clinical sign is fluid retention (rales, elevated jugular venous pulsations, and pedal edema). Given that not all patients are volume overloaded at the time of diagnosis (diastolic dysfunction), the term “heart failure” is now preferred over “congestive heart failure.” 1Hunt S, et al, ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). 2001, ACC web site, accessed November 12, 2004.

  7. CLASSIFICATION 1. Acute (pulmonary edema) 2. Chronic stable a. Systolic / Diastolic dysfunction 3. Right / Left ventricular failure 4. High output states

  8. ACUTE PULMONARY EDEMA • Definition:Sudden change: structure/function(LVFP) • Etiology: Cardiac -myocardial (ischemia / infarction) -mechanical (acute regurg; HTN urgency) -electrical (tachycardia: AF/VT) Non-cardiac -high altitude pulmonary edema (HAPE) -heroin overdose; chlorine,etc

  9. Pulmonary edema is caused by (1) imbalance of the Starling forces in the lung (cardiogenic)(2) disruption in the alveolar capillary membrane (non-cardiogenic).

  10. CARDIOGENIC PULMONARY EDEMA NON-CARDIOGENIC PULMONARY EDEMA

  11. 1. “hydrostatic APE” Acute cardiogenic or volume-overload pulmonary edema -sudden  in pulmonary venous pressure  pulmonary interstitial and alveolar fluid -pulmonary and lymphatic drainage can’t compensate acutely to remove the fluid

  12. continued Hallmark: rapid increase in hydrostatic pressure in the pulmonary capillaries causing increased transvascular fluid filtration. It is usually due to  pulmonary venous pressure from LVEDP/ LAP. As LAP rises above 25 mmHg fluid breaks thru the lung epithelium flooding the alveoli with protein poor fluid.

  13. 2. “-permeability pulmonary edema” (acute lung injury) Non-cardiogenic pulmonary edema -Lymphatic drainage cannot compensate for the  lung water caused by the disrupted alveolar capillary membrane. -Caused by  vascular permeability of the lung   flux of fluid into the interstitium and air spaces

  14. APE with NORMAL HEART SIZE*CARDIAC CAUSES • Acute MR (torn chordae / ruptured PM) • Acute AR (dissection / flail leaflet) • Mitral stenosis • Ischemic HD: AMI / stunned myocardium • Malignant HTN • Acute rapid AF (WPW) *Enlarged heart: Exacerbation of chronic HF; Myocarditis

  15. APE: NON-CARDIAC CAUSESPATHOPHYSIOLOGY • Lung injury damages alveolar-capillary membrane  “capillary leak syndrome” ie, transudation of fluid from pulmonary capillaries to alveoli •  oncotic pressure (hypoalbuminemia) • Impaired lymphatic drainage

  16. SYSTOLIC DYSFUNCTION • Defect: -myofibrils cannot shorten against a load • Various clinical presentations -asymptomatic, w/ ejection fraction -evidence of CO: fatigue/confused/BUN -evidence of congestion: DOE/leg edema -dilated LV chamber on chest x-ray • Annual mortality -NYHA II-III: 15-20% / NYHA IV: 50%

  17. DIASTOLIC DYSFUNCTION • Pathophysiology: “stiff” ventricle LV: poorly compliant;  filling/relaxation -systolic function: normal or markedly -evidence of HF: 35% • Etiology: --ischemia/LVH/fibrosis/normal aging • Symptoms: congestive (pul venous HTN) • Signs: apex-normal/ sustained+S4 • Hemodynamic abn: LVEDP / LAP • Prognosis: not as bad as systolic dysfn

  18. COMPARISON of the TYPES of MYOCARDIAL DYSFUNCTION

  19. LEFT HEART FAILURE • Etiology -CAD / HTN / Valvular HD / etc • Symptoms -fatigue/congestion (SOB / DOE) • Signs -narrow pulse pressure -hypokinetic carotid pulse -inferolaterally displaced apex -S3/S4 gallops; murmurs of MR/TR

  20. RIGHT HEART FAILURE • Etiology-lung disease: parenchymal / vascular congenital: ASD / Ebstein’s anomaly • Symptoms -fatigue / syncope / girth / edema • Signs -hypotension / parasternal lift distended neck veins / + HJ reflux -right-sided S3 / S4; murmur of TR hepatomegaly / ascites / peripheral edema

  21. HIGH OUTPUT FAILURE Non-cardiac circulatory overload • Etiology -fistula / anemia / pregnancy / hyperT4 • Pathophysiology -SV: preload (VR) + PVR(vasodilate) -CO at rest:  afterload / preload -blood volume due to xs Na/H2O • Symptoms: congestion (PCWP) • Signs:HR / SBP/DBP / wide PP / S3

  22. CLINICAL EVALUATION- HF • Risk factors for CAD • Symptoms -only weakly related to LV dysfunction • Fluid status: serum Na / weight / edema • Functional status: NYHA classification

  23. PRECIPITATING FACTORS • Diet: xs Na / H2O; alcohol • Non-compliance with medications • Arrhythmia • Infection • Anemia • Stress • Metabolic: thyroid disease / renal failure

  24. LABORATORY EVALUATION 2-D ECHO / DOPPLER • Most useful test • Determines primary abnormality • Derives Ejection Fraction (EF) -most important single measurement -but, poor correlation with symptoms • Distinguishes systolic / diastolic dysfn • Guide to prognosis (EF and ESV) • Assesses disease progression (remodels)

  25. PATHOPHYSIOLOGY • Ventricular injury / myocyte loss a. Chronic: CAD / HTN / valvular disease b. Acute: AMI / myocarditis / MR / AR • Compensation a. Ventricular remodeling -initially adaptive and benficial -eventually maladaptive and harmful b. Peripheral remodeling • Decompensation

  26. PATHOPHYSIOLOGY: THEORIES • OLD: hemodynamic disorder- ejection (EF) sx (fatigue / dyspnea) -Rx: contractility: inotropes unload periphery: dilators / diuretics • CURRENT: uncontrolled LV remodeling -chamber dilates (spherical); hypertrophy -mechanism: neurohormonal system -Rx: counteract RAAS / SNS • FUTURE: genetic abn / xs cytokines

  27. PATHOPHYSIOLOGY: EVENTS • Primary response: SNS activation (/NE) -initiates vicious circle: afterload • Secondary response: hormone constriction -RAAS: periph perfusion (Na retained) -Vasopressin: non-osmotic release • Vascular endothelial dysfunction (NO) • Result of neurohormonal compensation -adaptive / beneficial: maintains perfusion -long term: maladaptive / deleterious

  28. COMPENSATORY MECHANISMSCOUNTERACTS SV and CO • Starling effect: preload -limited role • muscle (LVH): vs myocyte loss -key • neurohumoral action:contractility-bad -SNS: EPI / NE (HR / PVR) -RAAS: Na/H2O retention;K/Mg;GFR -endothelin / vasopressin / prostacyclin • Brain natriuretic peptide (BNP) -diagnostic / prognostic • Dilatation / remodeling

  29. VENTRICULAR REMODELING • Definition -altered chamber geometry -disproportionate cavity to wall thickness • Pathophysiology-altered extracellular matrix myocfibrosis -up-regulates pro-inflam cytokines -myocyte hypertrophy/apoptosis; -inotropy -imbalance between production of O- / NO -rearranges myocardial fibers: alters length/width ratio

  30. NEUROHORMONAL RESPONSES TO CHF

  31. SYSTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION NORMAL LV Press. Left Ventricular volume LV PRESSURE-VOLUME LOOPS: SYSTOLIC DYSFUNCTION: Contractility: ejection impaired DIASTOLIC DYSFUNCTION: Chamber stiffness: filling impaired

  32. FRANK-STARLING LV FUNCTION CURVES Normal LV Review cardiac physiology to understand these curves Stroke Volume Low CO LV Failure Congestion 10 15 20 LVEDP THE RELATIONSHIP BETWEEN SV and LVEDP

  33. MYOCARDIAL DYSFUNCTION / FAILURE DIASTOLIC DYSFUNCTION SYSTOLIC DYSFUNCTION ENDOTHELIAL DYSFUNCTION LVEDP ARTERIAL BLOOD VOL CO RESERVE NO ENDO- THELIN Periph cap press PCP SNS (NE) VASO- PRESSIN RAA FATIGUE/ RENAL DYSFN Periph constrict Renal constrict ALDO- STERONE PVR ANF CONGESTION Na/H2O retention Vascular stiffness Peripheral Pulmonary EDEMA DYSPNEA PLASMA VOLUME LA cavity

  34. Epidemiology of Heart Failure • Approximately 5 million patients in the USA have HF, with a yearly incidence of close to 500,000. • It is primarily a disease of the elderly, with 6-10% patients over 65 years old being diagnosed with HF. • 80% of hospitalized patients with HF are > 65yo. • Heart failure is the most common Medicare DRG.

  35. Epidemiology of Heart Failure • “…one-year mortality of approximately 45 percent.” 2 • “Survival ranges from 80% at 2 years for patients rendered free of congestion to less than 50% at 6 months for patients with refractory symptoms.” 3 2 Jessup M, Brozena S, Medical Progress: Heart Failure, NEJM, 348(20): 2007-18, 2003. 3 Nohria A, et al, Medical Management of Advanced Heart Failure, JAMA, 287(5): 628-40, 2002.

  36. Epidemiology of Heart Failure • “Heart failure admission rates are rising, and the prognosis of heart failure has been compared with that of malignancy, with a 6-year mortality rate of 84% in men and 77% in women.” 4 • Heart failure kills people much more surely than most cancers! • Coronary artery disease is the cause of two thirds of left ventricular systolic dysfunction 4 Mair F, et al, Evaluation of suspected left ventricular systolic dysfunction, JFP, 51(5): 466-71, 2002.

  37. Diagnosing Heart FailureSymptoms • Decreased exercise tolerance • Fluid retention • Fatigue • Incidentally noted left ventricular dysfunction in an asymptomatic patient

  38. Diagnosing Heart FailureClinical Signs • Elevated jugular venous pressure • Pulmonary rales • S3 • S3 – volume overload • S4 – pressure overload • Peripheral edema

  39. Diagnosing Heart FailureClinical Signs

  40. Auscultatory Findings • S3 • S4 • http://www.egeneralmedical.com/listohearmur.html • Rales • http://www.wilkes.med.ucla.edu/intro.html

  41. Common EKG Findings

  42. CXR findings in Heart Failure

  43. Diagnosing Heart Failure • Many different terms: • Left vs right-sided failure • Backward vs forward failure • Volume vs pressure overload • Systolic vs diastolic dysfunction – there is a lot of overlap as many patients have aspects of both entities

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