Transcript Heart and circulatory failure

Heart and Circulatory
Failure
Lectures from
Pathological Physiology
Study materials from Pathological
Physiology, school year 2011/2012
© Oliver Rácz
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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
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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
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Heart failure classifications
Forward and backward failure
NYHA classification I – IV
Forms:
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Left ventricle, right ventricle, both
Acute and chronic
Systolic and diastolic dysfunction
Decrease of CO and/or EF, sometimes
increase
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NYHA
I.
II.
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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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NYHA
III.
IV.
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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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Evaluation according to ejection
fraction
0,80 – 0,55
Norm
0,55 – 0,40
Mild systolic
dysfunction
0,40 – 0,30
Medium...
< 0,30
Severe...
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Young, Haas,
Starling:
American College
of Cardiology,
American Heart
Association
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General etiology of HF
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Clinical etiology of heart failure
HF, EF < 40% = systolic
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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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Clinical etiology of heart failure
HF, EF > 40% = diastolic
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Hypertrophic cardiomyopathies (genetic)
Restrictive cardiomyopathies
Hypertension (hypertrophy)
High age (?)
High output
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Thyrotoxicosis
Beri-beri, anemia, A-V shunts
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Clinical etiology of heart failure
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Pathogenesis of HF
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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
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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
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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)
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