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Chronic Heart Failure

Chronic Heart Failure. Dr. Apor Astrid SE Heart Center. Modern clinical definition ESC guideline. Cardiac dysfunction confirmed (ECG, imaging modalities ). Typical symptoms and signs of heart failure. Response to heart failure treatment. Neurohumoral aktivation confirmed (BNP).

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Chronic Heart Failure

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  1. ChronicHeart Failure Dr. Apor Astrid SE Heart Center

  2. Modern clinical definitionESC guideline Cardiac dysfunction confirmed (ECG, imaging modalities) Typical symptoms and signs of heart failure Response to heart failure treatment Neurohumoral aktivation confirmed (BNP)

  3. Cinical symptoms and signs fluid retention dyspnoe fatigue

  4. Pathophysiology of heart failure Heart disease valvular myocardial coronary arterial Extracardiac disease affecting the heart Pump function of the heart Long term effects: Detrimental: cardiac, Cardiovascular impairment Temporary effects: Pump function is maintained Compensatory mechanisms

  5. Adaptation in heart failure Sympathico- adrenal system Myocardial remodeling Frank-Starling mechanism RAAS vasopressin

  6. Adaptation in heart failure BP = CO x SVR BP = SV x HR x SVR Frank-Starling Remodelling SA system SA system RAAS SA system

  7. Frank-Starling mechanism • Energy of contraction is a function of the muscle fiber length • Optimal length: 2.2µm • Stretching beyond this point may diminish LV performance

  8. Myocardial hypertrophy, remodeling • 1receptor density • 1receptor coupling • Ca excitation-contraction coupling • Myocardial oxidative phosphorilation is abnormal

  9. Myocardial remodelingObjective: to maintain systolic wall stress myocyte hypertrophy (excentric/concentric) BUT This myocardium is diseased! • myocyte contraction • myocyte apoptosis, necrosis • increased collagén deposition stiff myocardium! • MMPs activity split collagen cross-links: myocyte slippage • capillary density

  10. Ventricular remodelling LV mass, size, shape is altered

  11. Ventricular remodelling Excitation-contraction coupling Electrical dyssynchrony Mechanical dyssynchrony Dysrhythmias !

  12. DCM

  13. HCM, HOCM

  14. Restrictive CMP

  15. Non-compact CMP

  16. ARVD

  17. Sympathetic nervous system is activated Heart rate Force of contraction Dilatation of coronary arteries Perif. vascular resistance Redistribution (renal blood supply) Direct cytotoxic effect Apoptosis Activation of the RAAS

  18. Activation of the RAAS Blood pressure Perfusion of the juxtaglom. apparátus SA activation Sodium and water retention Vasoconstriction Aldosterone ADH (vasopressin) Myocardial hypertrophy Myocardial fibrosis Endothel dysfunction Coagulation renin

  19. Maintenance of perfusion of the vital organs (vasoconstriction) Prevention of blood loss restoration of blood volume (salt water retention) Preparation to fight (SA) Wound healing (scarring fibrosis) Prevent wound infection (inflammation) Stop bleeding (hemostasis) Restoration of lost RBCs (erythropoesis)

  20. Counterregulation: BNP • Stress hormone of myocytes (increased wall tension) • Diuresis, natriuresis • Vasodilation, blood pressure • Sympathetic nervous system activation • RAAS activation • BNP levels correlate with the severity of heart falure

  21. Clinical symptoms of heartfailure:dyspnoe • Pulmonary capillary wedge pressure • Fluid retention lung compliance • Skeletal/respiratory muscle myopathy • Abnormal ergoreflex (muscle contraction-hyperventillation)

  22. Clinical symptoms of heart failure:fatigue • Stroke volume, cardiac output • Skeletal muscle myopathy

  23. Clinical symptoms of heart failure:edema, fluid retention • Anasarca • Hepatomegaly • Gastrointestinal congestion • Pulmonary edema

  24. Etiology of heart failure Heart failure with Low cardiac output CHD Hypertension Valve diseases Cardiomyopathies Arrhythmias Pericardial diseases Drug toxicity RV failure Heart failure with high cardiac output= circulatory failure Anaemia Thyrotoxicosis AV-fistula Cirrhosis of the liver Paget-disease Beriberi

  25. Etiology of heart failure

  26. Diagnosis of heart failure • Dyspnoe, orthopnoe, PND • Oedema, anasarca • Pulm. congestion on auscultation • S3, gallop rythm, holosystolic murmur • Jugular vein distension, hepato-jug. reflux • Pulsatility of the liver, ascites

  27. Diagnosis of heart failure • ECG 12 leads • Chest X-ray • Lab tests (hyponatraemia!) • Biomarkers of HF: BNP, proBNP, CRP, troponins… • Echocardiography (systolic/diastolic dysfunction, structural heart disease) • spiroergometry

  28. Diagnosis of heart failure

  29. NYHA classification Quality of life tests 6-minute walking test Exercise testing Other measurements of cardiac function Prognostic indices: HFSS SHFM Risk of sudden death How to judge disease severity, clinical status and prognosis

  30. Disease progression in heart failure Stable, worsening, decompensated

  31. Classification of stages of heart failure Stage A At high risk of heart failure Hypertension CHD Diabetes Metabolic sy. Cardiotoxin Stage B Structural heart disease without symptoms LV remodeling LV hypertrophy Valve disease Stage C Structural heart disease with symptoms of heart failure Stage D Refractory heart failure

  32. Forms of heart failure • Systolic (-diastolic) dysfunction • Diastolic HF with preserved systolic function HFPEF: heart failure with preserved ejection fraction: -presence of signs and symptoms of CHF -LV EF: 45-50% -evidence of diastolic dysfunction (echocardiography)

  33. Treatment of heart failure Heart transplantation Pharmacologic treatment Pozitív inotropok Digitalis Neurohumorális blokád: BB, ACEi Diureticumok Vasodilatorok Antiarrhythmiás szerek Surgical/interventional Revascularisation Valve replacement Aneurysm resection Surgical remodeling Stem-cell therapy Non-pharmacologic treatment Resynchronization (CRT) ICD IABP Assist device

  34. Treatment of heart failure Pharmacologic treatment Pozitív inotropok Digitalis Neurohumorális blokád: BB, ACEi Diureticumok Vasodilatorok Antiarrhythmiás szerek

  35. Objectives of treatment in CHF 1, Improve prognosis, reduce mortality 2, Improve morbidity: relieve symptoms - increase exercise capacity - reduce fatigue and breathlessness - eliminate oedema and fluid retention 3, Prevention - myocardial damage - remodelling - reoccurence of symptoms - hospitalisation

  36. Maintenance of perfusion of the vital organs (vasoconstriction) Prevention of blood loss restoration of blood volume (salt water retention) Preparation to fight (SA) Wound healing (scarring fibrosis) Prevent wound infection (inflammation) Stop bleeding (hemostasis) Restoration of lost RBCs (erythropoesis)

  37. Inhibition of NEURO-HUMORAL activation ACE inhibitors Betablockers Aldosterone Antagonists Digoxin Reduction of SVR Hydralazine Nitrate Ca-chanell Blockers Diuretics Elimination of oedema Diuretics

  38. Inhibition of haemostasis Treatment of precipitating factors Treatment of comorbidities Reduce risk factors Treatment of complications

  39. Symptomatic heart failure + reduced ejection fraction ACEi (or ARB)  Diuretics Betablockers Aldosterone anatgonists or ARB Digoxin, Hydralazine, Nitrate

  40. ACEi BB start with low dose titrate slowly Consider: side effects interactions renal function liver function Dosages should be adjusted to clinical state (diuretics…)

  41. ACE inhibitors • symptoms, prognosis, mortality • remodelling, myocardial fibrosis • starting dose, target dose • Hypotension • Hyperlakaemia, renal dysfunction • Cough • Angio-oedema

  42. Betablockers • symptoms, prognosis, mortality • remodelling, dyssynchrony • SCD , antiarrhythmic effect • starting dose, target dose • Hypotension • Fatigue • Bradycardia, block • Reduce dose in case of decompensation

  43. Aldosterone antagonists • symptoms, prognosis, mortality • NYHA III, EF<35% • Renal dysfunction • Hyperkalaemia

  44. Diuretics • symptoms, oedema, prognosis • only in case of fluid retention • RAAS activationadd ACEi or ARB! • Titrate, combine • Hyonatraemia, hypokalemia, volume depletion, renal dysfunction • Diuretic resistance

  45. Patients with acute heart failure frequently develop chronic heart failure. Patients with chronic heart failure frequently decompensate acutely.

  46. Thank you for your patience!

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