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HEART FAILURE Heart Failure (HF) Definition A complex clinical syndrome in which the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return. HEART FAILURE • Prevalence 1-2% • Incidence 1-3 new cases annually per 1000 inhabitants • Causes – IHD 70% – Other myocardial diseases incl. cardiomyopathy 10-15% – Valvular heart disease 10% – Hypertension 6-10% Prevalence of HF by Age and Gender United States: 1988-94 10 8 Percent of Population Males Females 6 4 2 0 20-24 25-34 35-44 45-54 55-64 65-74 Source: NHANES III (1988-94), CDC/NCHS and the American Heart Association 75+ Diagnosis of heart failure Typical symptoms and signs of HF Less typical signs and symptoms of HF Cardiac Output • Cardiac output is the amount of blood that the ventricle ejects per minute Cardiac Output = HR x SV Determinants of Ventricular Function Contractility Afterload Preload Stroke Volume • Synergistic LV Contraction • Wall Integrity • Valvular Competence Heart Rate Cardiac Output Left Ventricular Dysfunction Volume Overload Pressure Overload Loss of Myocardium Impaired Contractility LV Dysfunction EF < 40% End Systolic Volume Cardiac Output Hypoperfusion End Diastolic Volume Pulmonary Congestion Hemodynamic Basis for Heart Failure Symptoms LVEDP Left Atrial Pressure Pulmonary Capillary Pressure Pulmonary Congestion Hemodynamic Basis for Heart Failure Symptoms Compensatory Mechanisms • Frank-Starling Mechanism • Neurohormonal Activation • Ventricular Remodeling Compensatory Mechanisms Frank-Starling Mechanism a. At rest, no HF b. HF due to LV systolic dysfunction c. Advanced HF Compensatory Mechanisms Neurohormonal Activation • Sympathetic nervous system (SNS) • Renin-angiotensin-aldosterone system (RAAS) • Vasopressin (a.k.a. antidiuretic hormone, ADH) Compensatory Mechanisms: Sympathetic Nervous System Decreased MAP Sympathetic Nervous System Contractility Tachycardia Vasoconstriction MAP = SV x HR x TPR Compensatory Mechanisms: Renin-Angiotensin-Aldosterone (RAAS) Angiotensinogen Renin Angiotensin I Angiotensin Converting Enzyme Angiotensin II AT I receptor Vasoconstriction Oxidative Stress Cell Growth Vascular remodeling LV remodeling Proteinuria Compensatory Mechanisms: Renin-Angiotensin-Aldosterone (RAAS) Renin-Angiotensin-Aldosterone ( renal perfusion) Salt-water retention Thirst Sympathetic augmentation Vasoconstriction MAP = SV x HR x TPR Compensatory Mechanisms: Vasopressin Decreased systemic blood pressure Central baroreceptors - Increased systemic blood pressure Vasoconstriction Stimulation of hypothalamus, which produces vasopressin for release by pituitary gland Release of vasopressin by pituitary gland Concentric remodelation Excentric remodelation Other Neurohormones • Natriuretic Peptides – Atrial Natriuretic Peptide (ANP) • Predominantly found in the atria • Diuretic and vasodilatory properties – Brain Natriuretic Peptide (hBNP) • Predominantly found in the cardiac ventricles • Diuretic and vasodilatory properties Endothelium-Derived Vasoactive Substances Endothelium-derived relaxing factors (EDRF) – Vasodilators: • Nitric Oxide (NO) • Bradykinin • Prostacyclin Endothelium-derived constricting factors (EDCF) – Vasoconstrictors: • Endothelin I Cytokines • Negative inotropes • Elevated levels associated with worse clinical outcomes • Examples: – Tumor necrosis factor (TNF)-alpha – Interleukin 1-alpha – Interleukin-2 – Interleukin-6 – Interferon-alpha Neurohormonal Responses to Impaired Cardiac Performance Initially Adaptive, Deleterious if Sustained Response Short-Term Effects Long-Term Effects Salt and Water Retention Augments Preload Pulmonary Congestion, Anasarca Vasoconstriction Maintains BP for perfusion of vital organs Exacerbates pump dysfunction (excessive afterload), increases cardiac energy expenditure Sympathetic Stimulation Increases HR and ejection Increases energy expenditure Jaski, B, MD: Basics of Heart Failure: A Problem Solving Approach Sympathetic Activation in Heart Failure CNS sympathetic outflow Cardiac sympathetic activity 1receptors 2receptors Sympathetic activity to kidneys + peripheral vasculature 1receptors Myocardial toxicity Increased arrhythmias 1- Activation of RAS Vasoconstriction Sodium retention Disease progression Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52. 1- Vicious Cycle of Heart Failure LV Dysfunction Increased cardiac workload (increased preload and afterload) Increased cardiac output (via increased contractility and heart rate) Increased blood pressure (via vasoconstriction and increased blood volume) Decreased cardiac output and Decreased blood pressure Frank-Starling Mechanism Remodeling Neurohormonal activation CHRONIC HEART FAILURE etiology • Decreased contractility – IHD, DCMP, infection, toxic agents… • Pressure overload – hypertension, aortic stenosis… • Volume overload – aortic or mitral regurgitation… CHRONIC HEART FAILURE symptoms • Dyspnoe – on exertion, paroxysmal nocturnal, at rest • Fatigue, muscular weakness, oliguria, cardiac cachexia New York Heart Association Functional Classification Class I: No symptoms with ordinary activity Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnea, or angina Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain Class IV: Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency may be present even at rest CHRONIC HEART FAILURE prognosis Mortality • NYHA II • NYHA III • NYHA IV 5-15% 20-25% 30-70% CHRONIC HEART FAILURE initial work-up • • • • • Patient history Physical examination BP, ECG, chest X-ray, ECHO, SpO2 minerals, creatinin, BNP, blood count (Coronary angiography, stress test...) CHRONIC HEART FAILURE General Measures LifestyleModifications: • Weight reduction • Discontinue smoking • Avoid alcohol and other cardiotoxic substances • Exercise CHRONIC HEART FAILURE General Measures Medical Considerations: • Treat HTN, hyperlipidemia, diabetes, arrhythmias • Coronary revascularization • Anticoagulation • Immunization • Sodium restriction • Daily weights • Close outpatient monitoring CHRONIC HEART FAILURE Pharmacologic Management ACE Inhibitors • Blocks the conversion of angiotensin I to angiotensin II; prevents functional deterioration • Recommended for all heart failure patients • Relieves symptoms and improves exercise tolerance • Reduces risk of death and decreases disease progression • Captopril (Capoten), enalapril (Enap), perindopril (Prestarium), ramipril (Tritace), trandolapril (Gopten)… CHRONIC HEART FAILURE Pharmacologic Management Diuretics • Used to relieve fluid retention • Improve exercise tolerance • Patients can be taught to adjust their diuretic dose based on changes in body weight • Electrolyte depletion a frequent complication The Vicious Cycle of Heart Failure Management Chronic HF Diurese & Home Hospitalization IV Lasix or Admit Emergency Room SOB Weight MD’s Office PO Lasix CHRONIC HEART FAILURE Pharmacologic Management Beta-Blockers • Cardioprotective effects due to blockade of excessive SNS stimulation • In the short-term, beta blocker decreases myocardial contractility; increase in EF after 1-3 months of use • Reduce the combined risk of morbidity and mortality, or disease progression • Metoprolol SR (Betaloc ZOK), bisoprolol (Concor COR), carvedilol (Dilatrend) CHRONIC HEART FAILURE Pharmacologic Management Digoxin • Slightly enhances inotropy of cardiac muscle • Reduces activation of SNS and RAAS • Reduces symptoms, Increases exercise tolerance • Reduces hospitalization rates for decompensated HF • Does not improve survival CHRONIC HEART FAILURE Pharmacologic Management Aldosterone Antagonists • Shown to reduce heart failure-related morbidity and mortality • Generally reserved for patients with NYHA Class III-IV HF • Side effects include hyperkalemia and gynecomastia. Potassium and creatinine levels should be closely monitored • spironolacton (Verospiron), eplerenon CHRONIC HEART FAILURE Pharmacologic Management Angiotensin Receptor Blockers (ARBs) • Block AT1 receptors, which bind circulating angiotensin II • In clinical practice, ARBs should be used to treat patients who are ACE intolerant due to intractable cough or who develop angioedema • valsartan, telmisartan, candesartan, losartan CHRONIC HEART FAILURE Pharmacologic Management Inotropic agents • Digoxin • Catecholamines (dopamin - Tensamin, noradrenalin, dobutamin - Dobuject, adrenalin) • Phosphodiesterase inhibitors (amrinonWincoram, milrinon - Corotrop) • Ca-sensitizers (levosimendan - Simdax) – improve symptoms, decrease mortality? CHRONIC HEART FAILURE Pharmacologic Management Other drugs • Statins • Antiarrhythmics • Drugs under clinical investigation – neutral endopeptidase inhibitors – natriuretic peptides agonists – endothelin receptor inhibitors – vasopressin antagonists (tolvaptan) – renin inhibitors (aliskiren) – cytokin modulators CHRONIC HEART FAILURE Pharmacologic Management Therapeutic strategy • Asympt. LV dysfunction non-ischemic etiol. – ACEI • Asympt. LV dysfunction ischem. etiol. – ACEI, BB, ASA • NYHA II-III, EF 20-40% – ACEI, BB, diuretics, (ASA, digoxin, AC) • NYHA II-III, EF < 20% – ACEI, BB, diuretics, digoxin, spironolacton, (ASA, AC) • NYHA IV – ACEI, BB, diuretics, digoxin, spironolacton, (ASA, AK, nitrates, inotrops?) CHRONIC HEART FAILURE Non-pharmacologic management Cardiac resynchronization therapy – Standard pacing lead in RA and RV – Specially designed left heart lead placed in a left ventricular cardiac vein via the coronary sinus Right Atrial Lead Right Ventricular Lead Left Ventricular Lead CHRONIC HEART FAILURE Non-pharmacologic management Cardiac resynchronization therapy • Abnormal interventricular septal wall motion1 • Reduced dP/dt3,4 • Reduced pulse pressure4 • Reduced EF and CO4 • Reduced diastolic filling time1,2,4 • Prolonged MR duration1,2,4 CHRONIC HEART FAILURE Non-pharmacologic management • Left-ventricle assisst devices (LVAD) • Implantable cardioverter-defibrilator (ICD) • Cellular therapy?? • Heart transplantation CHRONIC HEART FAILURE Non-pharmacologic management – cell Tx Ideally, „stem cell therapy“ should: • enhance the number of functional (cardio)myocytes • enhance systolic and diastolic function of the heart • reduce LV dilatation and remodeling • be safely administered First clinical experiences are, however, rather unconvincing CHRONIC HEART FAILURE Modes of Death NYHA II NYHA III CHF CHF 12% Other 26% 59% Sudden Death 24% 64% Other 15% n = 103 Sudden Death n = 103 NYHA IV CHF Other 33% 56% 11% Sudden Death n = 27 MERIT-HF Study Group. Effect of Metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomized intervention trial in congestive heart failure (MERIT-HF). LANCET. 1999;353:2001-07. ACUTE HEART FAILURE definition, causes • Definition: rapid onset of symptoms and signs, caused by abnormal cardiac performance • New onset: acute MI, mechanical complication of AMI, acute valvular regurgitation, acute arrhythmias, acute myocarditis, hypertensive crisis, severe aortic stenosis, cardiac tamponade, aortic dissection • Decompensation of chronic HF ACUTE HEART FAILURE • Asthma cardiale • Pulmonary oedema – Intersticial (> 25 mmHg) – Alveolar (> 35 mmHg) • Cardiogenic shock ACUTE HEART FAILURE pulmonary oedema symptoms, signs, test • Dyspnoe, ortopnoe, cough, anxiety, paleness, sweating • Physical examination: pulmonary crackles, whistles, tachycardia, gallop • BP, ECG, chest X-ray, ECHO, SpO2 • CRP, electrolytes, creatinin, BNP, blood count, troponin, blood gases ACUTE HEART FAILURE pulmonary oedema - therapy • Oxygen – mask, CPAP, non-invasive ventilation support, ventilation support • Diuretics – i.v. furosemide • Vasodilatation – i.v. nitrates, nitroprusside, (nesiritid) • Levosimendan • Causal therapy of acute HF • Morphin, syntophyllin, antiarrhythmics, pacing, cardioversion… RIGHT HEART FAILURE causes • Pressure overload – Precapillar pulmonary hypertension (PH) – Primary right HF – Postcapillar PH • Volume overload (L-R shunt) • Decreased contractility RIGHT HEART FAILURE cor pulmonale hypertrophy and dilatation of right ventricle, caused by pre-capillar PH in diseases of lungs, pleura, thoracic wall or pulmunary vasculature RIGHT HEART FAILURE forms • Hypoxic (COPD) • Restrictive (pulmonary fibrosis, pneumoconiosis, resection of lungs) • Vascular (pulmonary embolism, primary pulmonary hypertension, ARDS) RIGHT HEART FAILURE symptoms, signs • Dyspnoe • Systemic venous congestion – Increased jugular vein filling – Hepato-jugular reflux – Hepatomegaly – Cardiac swelling (according to the highest hydrostatic pressure) – Anasarca PRIMARY RIGHT HEART FAILURE hypoxic form - COPD • Chronic bronchitis (with obstruction), emphysema • Respiratory insuficiency hypoxia PH right HF (cor pulmonale chronicum) • Therapy – therapy of COPD – oxygen therapy PRIMARY RIGHT HEART FAILURE restrictive form • Vital capacity 80-50% latent PH • Vital capacity below 50% rest PH • Therapy – management of primary disease PRIMARY RIGHT HEART FAILURE vascular form • Pulmonary embolism – Dg.: history, physical exam., ECG, angioCT, ventilatory-perfusion scan, pulmonary angiography, ECHO – Therapy: anticoagulation, thrombolysis PRIMARY RIGHT HEART FAILURE vascular form • Primary PH – Rare disease, mid-age women – Therapy: • • • • Ca-antagonists Prostacyklin Bosentan (antagonist ET-1 R) Sildenafil SHOCK SHOCK definition • acute circulatory failure with inadequate perfusion of vital tissues systemically, leading to generalized tissue hypoxia. SHOCK basic signs • • • • • • Hypotension Increased heart rate Decreased diuresis Pale, cool skin Metabolic acidosis Cerebral dysfunction SHOCK classification • Cardiogenic shock • Complication of acute myocardial infarction • Obstructive shock • Pulmonary embolism • Cardiac tamponade • Hypovolemic shock • Blood loss (hemorrhage, burns) • Distributive shock • Septic shock Modulators of shock • Sympathetic stimulation (catecholamines) • Neuroendocrine stimulation (cortisol) • Inflammatory mediators (cytokines, complement, arachidonic acid metabolites, lysosomal enzymes, vasoactive mediators) • Toxic agents SHOCK therapeutic targets • (i) basic life function support • (ii) assessment and therapy of the cause of shock • (iii) prevention of damage extension – Multiple organ dysfunction syndrome Hemodynamic monitoring Swan-Ganz catheter Hemodynamic parameters • CVP (central venous pressure) 0-7 mmHg • PCWP (pulmonary capillary wedge pressure) 6-12 mmHg • CO (cardiac output, SVxHR) 4-8 L/min • CI (cardiac index, CO/body surface) 2.5-4.2 L/min/m2 • MAP (mean arterial pressure) optimum at least 75-80 mmHg • SVR (systemic vascular resistance) • PVR (pulmonary vascular resistance) SHOCK therapy • Aim: restoration of tissue oxygen supply with simultaneous effort to eliminate cause of shock • Intravenous administration of drugs !!! (intramuscular medication should be avoided) SHOCK therapy - circulatory support • Optimum - MAP 75-80 mmHg • Volume replacement – Blood (red blood cells, plasma) – Crystaloides (saline, solution Ringer) – Colloides (HAES - hydroxy aethyl starch), polygelatines (Haemaccel), dextranes (Rheodextran), human albumin SHOCK therapy - circulatory support • Positive inotropic drugs – catecholamines (dopamin, noradrenalinnorepinephrin, dobutamin, adrenalin-epinephrin) – phosphodiesterase inhibitors (amrinon, milrinon) – digoxin – Ca-sensitizers (levosimendan) ? • Non-pharmacological circulatory support – IABP – intraaortic baloon counterpulsation – LVAD, Impella SHOCK therapy - other methods • • • • • Surgery (abscess drainage, stop bleeding) Catheterization, endoscopy Antibiotics Hemodialysis Correction of mineral and acidobasis dysbalances • Ventilatory support – Intubation – Artefitial pulmonary ventilation Cardiogenic shock Pulmonary embolism • PAP, CVP, PCWP • Diagnosis: history, physical examination, ECG, ECHO, laboratory investigation (CT angio, pulmonary angiography, perfusion scan) • Therapy – Thrombolysis – Catheterization or surgical intervention – Anticoagulation Hypovolemic shock • Hemorrhage, burns, trauma to major vessels • CVP, PCWP, MAP, HR, SVR • Therapy – Prevention of volume loss progression – Volume replacement Distribuive shock septic shock • SIRS, sepsis, inflammation mediated damage • SVR, HR, CO (CI) • Mikrobiological examination (blood, sputum, urine, skin, abscess, etc.) • Therapy – Antibiotics, therapy of the source of infection – Increase of SVR (catecholamines - noradrenalin, volume replacement) – Hemodialysis Cardiogenic shock • Myocardial (acute myocardial infarction, myocarditis, cardiomyopathy) • Mechanical (acute valvular dysfunction) • Arrhythmogenic • Obstructive (pulmonary embolism, cardiac tamponade) Cardiogenic shock pathogenesis • Stage I – Vasoconstriction (skin) – Preserve perfusion of vital organs • Stage II – Decreased organ perfusion – Marked deterioration of tissue metabolism – Organ failure • Stage III – Irreversible microcirculation failure – Severe tissue hypoxia, acidosis – Cell death Cardiogenic shock monitoring • Clinical monitoring (mental functions, pulse, BP, respiration, diuresis, fluid balance, skin perfusion) • ECG • Arterial catheter (invasive BP measurement, blood gases) • Swan-Ganz catheter • Chest X-rays • Biochemical and haematological tests Cardiogenic shock Acute myocardial infarction (AMI) • • • • • • 5-8% of patients with AMI Damage > 40% of left ventricle Mortality 50-90% Myocardial Arrhythmogenic „Mechanical complications“ of AMI (acute mitral regurgitation, free-wall rupture of LV, interventricular septal defect) Cardiogenic shock Acute myocardial infarction • MAP, CO (CI), PCWP • Diagnosis – History – Physical examination – ECG, ECHO Cardiogenic shock AMI - therapy • SHOCK trial early invasive x early conservative management early invasive approach superior • Percutaneous coronary intervention – Open closed coronary artery (coronary angioplasty/stent implantation) Cardiogenic shock AMI - therapy Cardiogenic shock AMI - therapy • Positive inotropic drugs – catecholamines (dopamin, dobutamin, noradrenalin, adrenalin) – (phosphodiesterase inhibitors) – (levosimendan) • Mechanical circulatory support – IABP, LVAD, Impella Cardiogenic shock AMI - therapy • Surgical intervention of mechanical complications – Valvuloplasty or valve replacement (mitral regurgitation caused by papillary muscle rupture) – Resection and/or patch of LV (LV rupture, septal defect) Intra-Aortic Balloon Pulsation (IABP) Impella Impella Impella TandemHeart • Inflow Oxygenated blood from the left atrium – transseptal cannulation. • Pump – Magnetically driven, six-bladed impeller • Outflow - One or both femoral arteries via arterial •cannulas. Extra-Corporeal Membrane Oxygenator Cardiogenic shock Arrhythmogenic • Causal therapy (AMI, poisoning) • Symptomatic therapy – Antiarrhythmic drugs – DC cardioversion – Temporary pacemaker Cardiogenic shock Cardiac tamponade • Diagnosis: history, physical examination, ECG, ECHO • Therapy – Pericardiocentesis – Surgical drainage – Causal therapy