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Heart and Circulatory Failure
Lectures from Pathological Physiology Study materials from Pathological Physiology, school year 2011/2012 © Oliver Rácz 2/25/2017 kvs1701e
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Heart failure – basics Clinical syndrome (not a disease)
Acquired/inherited abnormality of cardiac function/structure Constellation of symptoms – dyspnea, fatigue, edema, rales… Frequent hospitalization, poor QOL, shortened life expectancy (30/40% in 1 y, 60/70% in 5 y) Despite (or due to!) better treatments increasing prevalence 2/25/2017 kvs1701e
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New concept Old: Cardiac dropsy* due to decompensation of ventricular hypertrophy. Recent: Neuroendocrine, hormonal and inflammatory factors, molecular mechanism of adaptation and deadaptation – not only the contractile elements. Ventricular remodeling, Both systole and diastole impaired For clinicians: Earlier identification, intervention, better therapy Dropsy = hydrops, stasis 2/25/2017 kvs1701e
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Heart failure classifications
Forward and backward failure NYHA classification I – IV Forms: Left ventricle, right ventricle, both Acute and chronic Systolic and diastolic dysfunction Decrease of CO and/or EF, sometimes increase 2/25/2017 kvs1701e
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NYHA Patient with cardiac disease but without resulting limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, dyspnea or anginal pain Patient with cardiac disease resulting in slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitations, dyspnea or anginal pain 2/25/2017 kvs1701e
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NYHA Patient with cardiac disease resulting in marked limitation of physical activity. Less than ordinary physical activity results in fatigue, palpitations, dyspnea or anginal pain Patient with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of heart failure or anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased 2/25/2017 kvs1701e
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Evaluation according to ejection fraction
0,80 – 0,55 0,55 – 0,40 0,40 – 0,30 < 0,30 Norm Mild systolic dysfunction Medium... Severe... 2/25/2017 kvs1701e
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American College of Cardiology,
Young, Haas, Starling: American College of Cardiology, American Heart Association 2/25/2017 kvs1701e
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General etiology of HF 2/25/2017 kvs1701e
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Clinical etiology of heart failure
HF, EF < 40% = systolic Coronary artery disease (different forms) Pressure overload (hypertension, obstructive valvular conditions) Volume overload (regurgitant valvular diseases, congenital conditions with shunts, extracardiac shunts) Dilated cardiomyopathies (genetic, metabolic, toxic, viral, m. Chagas) Arrhytmias (!) 2/25/2017 kvs1701e
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Clinical etiology of heart failure
HF, EF > 40% = diastolic Hypertrophic cardiomyopathies (genetic) Restrictive cardiomyopathies Hypertension (hypertrophy) High age (?) High output Thyrotoxicosis Beri-beri, anemia, A-V shunts 2/25/2017 kvs1701e
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Clinical etiology of heart failure
Overlap Combination Genetic background 2/25/2017 kvs1701e
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Pathogenesis of HF 2/25/2017 kvs1701e
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Cellular adaptation - maladaptation
Myocytes do not divide Contractile proteins regenerate (30 – 90 d) Stimuli: GH, ATII, Noradrenaline, TNF-a, Interleukins, ADH, NO, ANP… Growth of cells – hypertrophy, back to fetal phenotype Apoptosis and necrosis 2/25/2017 kvs1701e
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Maladaptation Myocyte hypertrophy Alterations of contractile proteins
Loss of myocytes through apoptosis/necrosis Beta-adrenergic desensitation Reorganization of extracellular matrix – dissolution of the collagen weave and replacement by a matrix NOT supporting myocytes 2/25/2017 kvs1701e
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Neurohumoral (mal)adaptation
Fixed reaction to decrease of cardiac output in shock Adrenergic stimulation (afferentation through baro- & chemoreceptors – CNS) Renin – angiotensin – aldosteron system (RAAS) – renal & local Erytropoetin Subclinical inflammation (TNF-alfa) 2/25/2017 kvs1701e
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