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C HRONIC H EART F AILURE

C HRONIC H EART F AILURE. Pathophysiology. Toni M. Aprami Department of Cardiology and Vascular Medicine Cardiovascular Subdivision, Department of Internal Medicine Hasan Sadikin Hospital/Medical School, Padjadjaran University. Pulmonary veins. Definition : Heart Failure .

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C HRONIC H EART F AILURE

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  1. CHRONIC HEART FAILURE Pathophysiology Toni M. Aprami Department of Cardiology and Vascular Medicine Cardiovascular Subdivision, Department of Internal Medicine HasanSadikin Hospital/Medical School, Padjadjaran University

  2. Pulmonary veins

  3. Definition : Heart Failure “The situation when the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return.“ Braunwald’s Heart Disease, 8th Ed, 2008 “Pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues.” Euro Heart J; 2001. 22: 1527-1560

  4. CAUSES OF HEART FAILURE *Indicates conditions that can also lead to HF with a preserved ejection fraction

  5. Block diagram of left ventricular pump performance PULMONARY VENOUS PRESSURE Input Filling Emptying ED volume x EFeffective = Stroke volume LV Distensibility Relaxation Left atrium Mitral valve Pericardium Contractility Afterload Preload Structure x Heart rate Diastolic function Systolic function Output (Little, 2001) CARDIAC OUTPUT

  6. Aorta Lung Left atrium Pulmonal vein SVC Pump Container Pulmonal artery Right Atrium Systemic Vascular Resistance (SVR) Left ventricle Right ventricle IVC organ Volume (blood within circulatory system)

  7. - Synergistic LV contraction - LV wall integrity - Valvular competence DETERMINANTS OF VENTRICULAR FUNCTION CONTRACTILITY PRELOAD AFTERLOAD STROKEVOLUME HEART RATE Determinants of heart rate: -balance of parasympathetic and sympathetic tone -sinus node function -presence of an ectopic focus -conduction system CARDIAC OUTPUT

  8. COMPENSATORY MECHANISM Frank - Starling mechanism Neurohormonal stimulation Myocardial hypertrophy with or without chamber dilatation

  9. Myocardial Failure or Valvular Insufficiency Reduced cardiac output Decreased tissue perfusion Reduced blood pressure Activation of compensatory mechanisms: -Sympathetic Nervous System (SNS) -Frank-Starling Mechanism -Renin-Angiotensin-System (RAS) -Aldosterone -Ventricular hypertrophy -others… (anti-diuretic hormone, atrialnatriuretic factor) An effort to normalize tissue perfusion and blood pressure

  10. Myocardial Failure or Valvular Insufficiency Activates Compensatory Mechanisms SNS Anti-diuretic Hormone RAS Aldosterone Angiotensin II Vasoconstriction Sodium and water retention Increased Venous Return and Increased Blood Pressure Heart Rate F-S Mech. Contractility Augmentation of cardiac performance

  11. CONCENTRIC HYPERTROPHY PRESSURE OVERLOAD Thickened Ventricular Walls Altered ventricular geometry Myocardial Failure Valvular Insufficiency Ischemia and Fibrosis Elevated Cardiac Filling Pressures Diastolic Dysfunction CONGESTIVE HEART FAILURE

  12. - Thick and Stiff Ventricular Walls • - Abnormal Ventricular Relaxation • - Ventricular Fibrosis • Pericardial Disease - Myocardial Failure - Valvular Insufficiency • Moderate to large • L -> R shunt VOLUME OVERLOAD DIASTOLIC DYSFUNCTION Elevated Cardiac Filling Pressures CONGESTIVE HEART FAILURE

  13. MECHANISM OF HEART FAILURE Pressure overload Normal pumping function adequate Compensatory mechanism Volume overload failed Heart failure • Myocardial • contractility

  14. Classical Pathophysiology of HF Primary disease state Release of Renin / angiotensin aldosteron Decreased aortic pressure SNS stimulation Decreased cardiac output Vasoconstriction Increased vascular volume Ventricular dilatation Increased afterload Heart Failure symptoms Increased Preload

  15. MI-INDUCED HEART FAILURE Myocardial Damage Contractility Pump Performance  Systolic Work Load  SAS Drive Vasoconstriction RAAS SYSTEM FLUID RETENTION

  16. EVOLUTION OF CLINICAL STAGES Normal Asymptomatic LV Dysfunction No symptoms Normal exercise Normal LV fxn No symptoms Normal exercise Abnormal LV fxn Compensated CHF Decompensated CHF No symptoms  Exercise Abnormal LV fxn Refractory CHF Symptoms  Exercise Abnormal LV fxn Symptoms not controlled with treatment

  17. Stages in the evolution of HF and recommended therapy by stage Stage A Stage B Stage C Stage D • Pts with : • Struct. HD • Shortness of breath and fatigue, reduce exercise tolerance • Pts with : • Hypertension • CAD • DM • Cardiotoxins • FHx CM • Pts with : • Previous MI • LV systolic • dysfunction • Asymptomatic • Valvular disease Pts who have marked symptoms at rest despite maximal medical therapy. Refract. Symp.of HF at rest Struct. Heart Disease Develop Symp.of HF • THERAPY • All measures under stage A • ACE inhibitor • Beta-blockers • THERAPY • Treat Hypertension • Stop smoking • Treat lipid disorders • Encourage regular exercise • Stop alcohol & drug use • ACE inhibition • THERAPY • All measures under stage A • Drugs for routine use: • diuretic • ACE inhibitor • Beta-blockers • digitalis • THERAPY • All measures under stage A,B and C • Mechanical assist device • Heart transplantation • Continuous IV inotrphic infusions for palliation ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult 2005

  18. Pregnancy Arrhythmias (AF) Infections Hyperthyroidism Thromboembolism Endocarditis Obesity Hypertension Physical activity Dietary excess

  19. Diagnosis of C H F

  20. IDENTIFICATIONS OF HEART FAILURE PATIENTS • Criteria 1 and 2 should be fulfilled in all cases 1. Symptoms of heart failure (at rest or during exercise) And 2. Objective evidence of cardiac dysfunction (at rest) And (in cases where the diagnosis is in doubt) 3. Response to treatment directed towards heart failure Task Force Report. Guidelines for the diagnosis and treatment of chronic heart failure. European Society of Cardiology.2005

  21. SYMPTOMS AND SIGN • Breathlessness, Ankle Swelling, Fatique → Characteristic Symptoms • Peripheral Oedema, JVP ↑, Hepatomegaly → Signs of Congestion of Systemic Veins • S3 , Pulmonary Rales , Cardiac Murmur 

  22. Vital Signs • Positional blood pressure • Pulse rate, rhythm, pulse pressure • Respiratory rate and pattern • Temperature • Abdominal • Ascites • Hepatosplenomegaly • Pulsatile liver • Decreased bowel sounds • Obesity • Neurologic • Mental status abnormalities • Pulmonary • Rales • Rhonchi • Prolonged expiration • wheezes • dullness to chest percussion • Friction rubs • Cardiovascular • Neck vein distention • Abdominal-jugular neck vein reflux • Cardiomegaly • Displaced, sustained, or hyperkinetic apical impulse • Chest wall pulsatile activity (Right ventricular lift) • Gallop rhythms • Heart murmurs (especially aortic, mitral, tricuspid, • and pulmonic insufficiency or stenosis murmurs) • Diminished S1 or S2 • Friction rub • Peripheral venous insufficiency • Systemic • Acrocyanosis • Edema • Temporal muscle wasting • Cachexia Physical Examinations of Heart Failure patient

  23. CHEST X-RAY • A Part of Initial Diagnosis of HF → Cardiomegaly, Pulmonary Congestion, pulmonary disease • In pts CHF, CTR > 0.50 and pulmonary congestion → indicators of abnormal cardiac func. with ↓ EF • Relationship Between Radiological Signs and Haemodynamic Findings may Depend on the Duration and Severity HF

  24. E C G • A normal ECG suggests that the diagnosis of CHF should be carefully reviewed • LAH and LVH May Be Associated wit LV Dysfunction • Anterior Q-wave and LBBB a good predictors of EF ↓↓ • Detecting Arrhytmias as Causative of HF Value of electrocardiography* in identifying heart failure Resulting from left ventricular systolic dysfunction Sensitivity 94% Specificity 61% Positive predictive value 35% Negative predictive value 98% *Electrocardiographic abnormalities are defined as atrial fibrillation, evidence of Previous myocardial infarction, left ventricular hypertrophy, bundle branch block, and left axis deviation.

  25. HAEMATOLOGY & BIOCHEMISTRY A Part of Routine Diagnostic • Hb, Leucocyte, Platelets • Electrolytes, Creatinine, Glucose, Hepatic Enzyme, Urinalysis • TSH, hs-CRP, Uric Acid ECHOCARDIOGRAPHY • The Preferred Methods • Helpful in Determining the Aetiology • Follow Up of Patients Heart Failure

  26. NATRIURETIC PEPTIDES • Cardiac Function ↓↓ (LV Function ↓↓) → ↑↑ Plasma Natriuretic Peptide Concentration (Diagnostic Blood Use for HF) • Natriuretic Peptide ↑↑ : Greatest Risk of CV Events Natriuretic Peptide ↓↓ : Improve Outcome in Patients with Treatment • Identify Pts. With Asymptomatic LV Dysfunction (MI, CAD)

  27. PULMONARY FUNCTIONS • A Little Value in Diagnosis Heart Failure • Usefull in Excluding Respiratory Diseases EXERCISE TESTING • Focused on Functional, Treatment Assessment and Prognostic

  28. STRESS ECHOCARDIOGRAPHY • For Detecting Ischaemia • Viability Study NUCLEAR CARDIOLOGY • Not Recommended as a Routine Use CMR ( CARDIAC MAGNETIC RESONANCE IMAGING) • Recommended if Other Imaging Techniques not Provided Diagnostic Answer

  29. INVASIVEINVESTIGATION Elucidating the Cause and Prognostic Informations • Coronary Angiography : in CAD’s Patients • Haemodynamic Monitoring : To Assess Diagnostic and Treatment of HF • Endomyocardial Biopsy : in Patients with Unexplained HF

  30. TerimaKasih

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