1. Heart and Circulatory Failure
Lectures from Pathological Physiology
Study materials from Pathological Physiology, school year 2011/2012
© Oliver Rácz
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2. 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
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3. 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
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4. 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
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5. 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
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6. 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
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7. 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...
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8. American College of Cardiology,
Young, Haas, Starling:
American College of Cardiology,
American Heart Association
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9. General etiology of HF
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10. 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 (!)
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11. 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
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12. Clinical etiology of heart failure
Overlap
Combination
Genetic background
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13. Pathogenesis of HF
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15. 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
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16. 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
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18. 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)
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