12.2.2008 kvs1ed.ppt 1 Heart and Circulatory Failure Lectures from Pathological Physiology Dental Medicine Study materials from Pathological Physiology,

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HEART FAILURE (HF) Heart failure is the pathophysiological state in which an abnormality of cardiac function is responsible for failure of the heart to.

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Presentation transcript:

kvs1ed.ppt 1 Heart and Circulatory Failure Lectures from Pathological Physiology Dental Medicine Study materials from Pathological Physiology, school year 2007/2008 © Oliver Rácz 2008

kvs1ed.ppt The concept of heart failure 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. A syndrome which develops after different diseases/conditions producing cardiac/circulatory injury. Failure = the system is not able to meet proper performance For clinicians: Earlier identification, intervention, better therapy Dropsy = hydrops, stasis

kvs1ed.ppt Young, Haas, Starling: American College of Cardiology, American Heart Association

kvs1ed.ppt General etiology of HF

kvs1ed.ppt Clinical etiology of heart failure Coronary artery disease Hypertension Valvular dysfunction Congenital defects Cardiomyopathies Myocarditis, endocarditis, pericarditis Arrhytmias

kvs1ed.ppt Heart failure – basic terms Forward and backward failure NYHA classification I – IV Forms: Left ventricle, right ventricle, both Left ventricle, right ventricle, both Acute and chronic Acute and chronic Systolic and diastolic dysfunction Systolic and diastolic dysfunction Decrease of CO, sometimes increase Decrease of CO, sometimes increase

kvs1ed.ppt Pathogenesis of HF

kvs1ed.ppt

kvs1ed.ppt Cellular adaptation - maladaptation Myocytes do not divide Contractile proteins regenerate (30 – 90 d) Stimuli: GH, ATII, Noradrenaline, TNF- , Interleukins, ADH, NO, ANP… Growth of cells – hypertrophy, back to fetal phenotype Apoptosis and necrosis

kvs1ed.ppt

kvs1ed.ppt 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- α)

kvs1ed.ppt