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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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ChronicHeart Failure Dr. Apor Astrid SE Heart Center
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)
Cinical symptoms and signs fluid retention dyspnoe fatigue
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
Adaptation in heart failure Sympathico- adrenal system Myocardial remodeling Frank-Starling mechanism RAAS vasopressin
Adaptation in heart failure BP = CO x SVR BP = SV x HR x SVR Frank-Starling Remodelling SA system SA system RAAS SA system
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
Myocardial hypertrophy, remodeling • 1receptor density • 1receptor coupling • Ca excitation-contraction coupling • Myocardial oxidative phosphorilation is abnormal
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
Ventricular remodelling LV mass, size, shape is altered
Ventricular remodelling Excitation-contraction coupling Electrical dyssynchrony Mechanical dyssynchrony Dysrhythmias !
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
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
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)
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
Clinical symptoms of heartfailure:dyspnoe • Pulmonary capillary wedge pressure • Fluid retention lung compliance • Skeletal/respiratory muscle myopathy • Abnormal ergoreflex (muscle contraction-hyperventillation)
Clinical symptoms of heart failure:fatigue • Stroke volume, cardiac output • Skeletal muscle myopathy
Clinical symptoms of heart failure:edema, fluid retention • Anasarca • Hepatomegaly • Gastrointestinal congestion • Pulmonary edema
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
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
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
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
Disease progression in heart failure Stable, worsening, decompensated
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
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)
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
Treatment of heart failure Pharmacologic treatment Pozitív inotropok Digitalis Neurohumorális blokád: BB, ACEi Diureticumok Vasodilatorok Antiarrhythmiás szerek
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
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)
Inhibition of NEURO-HUMORAL activation ACE inhibitors Betablockers Aldosterone Antagonists Digoxin Reduction of SVR Hydralazine Nitrate Ca-chanell Blockers Diuretics Elimination of oedema Diuretics
Inhibition of haemostasis Treatment of precipitating factors Treatment of comorbidities Reduce risk factors Treatment of complications
Symptomatic heart failure + reduced ejection fraction ACEi (or ARB) Diuretics Betablockers Aldosterone anatgonists or ARB Digoxin, Hydralazine, Nitrate
ACEi BB start with low dose titrate slowly Consider: side effects interactions renal function liver function Dosages should be adjusted to clinical state (diuretics…)
ACE inhibitors • symptoms, prognosis, mortality • remodelling, myocardial fibrosis • starting dose, target dose • Hypotension • Hyperlakaemia, renal dysfunction • Cough • Angio-oedema
Betablockers • symptoms, prognosis, mortality • remodelling, dyssynchrony • SCD , antiarrhythmic effect • starting dose, target dose • Hypotension • Fatigue • Bradycardia, block • Reduce dose in case of decompensation
Aldosterone antagonists • symptoms, prognosis, mortality • NYHA III, EF<35% • Renal dysfunction • Hyperkalaemia
Diuretics • symptoms, oedema, prognosis • only in case of fluid retention • RAAS activationadd ACEi or ARB! • Titrate, combine • Hyonatraemia, hypokalemia, volume depletion, renal dysfunction • Diuretic resistance
Patients with acute heart failure frequently develop chronic heart failure. Patients with chronic heart failure frequently decompensate acutely.