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Heart Failure
Heart Failure
• Heart failure (HF) is a progressive clinical syndrome caused by
inability of the heart to pump sufficient blood to meet the body’s
metabolic needs.
• HF can result from any disorder that reduces
 ventricular filling (diastolic dysfunction) and/or
 myocardial contractility (systolic dysfunction).
Heart Failure
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY
• Causes of systolic dysfunction (decreased contractility) are reduced
 muscle mass (eg, myocardial infarction [MI]),
 dilated cardiomyopathies, and
 ventricular hypertrophy.
• Ventricular hypertrophy can be caused by
 pressure overload (eg, systemic or pulmonary hypertension and aortic or
pulmonic valve stenosis) or
 volume overload (eg, valvular regurgitation, shunts, high-output states).
Preload
• Preload is the initial stretching of the cardiac myocytes (muscle cells)
prior to contraction. It is related to ventricular filling.
• Preload is a measure of the degree of the ventricular stretch when the
heart is at the end of diastole.
Afterload
• Afterload is the force or load against which the heart has to contract to
eject the blood.
Shunt
• A shunt is a passage by which blood moves from one area (blood
vessel or heart chamber) to another in a pattern that isn't normal.
• Cardiomyopathy is a disease of the heart muscle that makes it harder for the
heart to pump blood to the rest of the body.
• Fibrosis is the thickening and scarring of connective tissue, usually as a result of
injury.
• Stenosis narrowing of a passage in the body.
• Concentric hypertrophy is associated with increased left ventricular wall
thickness.
• Eccentric hypertrophy is associated with dilatation of the left ventricular
chamber.
• ECM degradation – extracellular matrix degradation.
• Ejection fraction means the % of blood leaving left ventricle in 1
heartbeat.
• Stroke volume is the amount of blood pumped by left ventricle in 1 heart
beat. (normal stroke volume 70 ml)
• A healthy left ventricle with a total blood volume of 100 ml will try to pump
60 ml to the aorta has a ejection fraction of 60%.
• A heart with an enlarged left ventricle (ventricular hypertrophy) that has a
total blood volume of 140 ml will try to pump the same amount (60 ml), to
the aorta has an ejection fraction of 43%.
PATHOPHYSIOLOGY
• Causes of diastolic dysfunction (restriction in ventricular filling) are
increased ventricular stiffness, ventricular hypertrophy, infiltrative
myocardial diseases, myocardial ischemia and MI, mitral or tricuspid
valve stenosis, and pericardial disease (eg, pericarditis and pericardial
tamponade).
• The leading causes of HF are coronary artery disease and
hypertension.
PATHOPHYSIOLOGY
• As cardiac function decreases after myocardial injury, the heart relies on
compensatory mechanisms:
 (1) tachycardia and increased contractility through sympathetic nervous
system activation;
 (2) the Frank–Starling mechanism, whereby increased preload increases
stroke volume;
 (3) vasoconstriction; and
 (4) ventricular hypertrophy and remodeling.
Frank–Starling mechanism
• The Frank- starling law was named to honor two physiologists, Otto
Frank and Ernest Henry Starling who found the relationship between
stroke volume and end diastolic volume.
• The Frank-Starling law states that the more the ventricular muscle are
stretched, the more forcefully they contract.
PATHOPHYSIOLOGY
• Although these compensatory mechanisms initially maintain cardiac
function, they are responsible for the symptoms of HF and contribute to
disease progression.
• In the neurohormonal model of HF, an initiating event (eg, acute MI) leads
to decreased cardiac output; the HF state then becomes a systemic disease
whose progression is mediated largely by neurohormones and
autocrine/paracrine factors.
Autocrine / Paracrine factors
• Paracrine – a cell targets a nearby
cell by signaling.
• Autocrine – a cell targets itself,
releasing a signal that can bind to
itss own receptors on its surface.
PATHOPHYSIOLOGY
• These substances include angiotensin II, norepinephrine, aldosterone,
natriuretic peptides, arginine vasopressin, endothelin peptides, and other
circulating biomarkers (eg, C-reactive protein).
• Common precipitating factors that may cause a previously compensated HF
patient to decompensate include myocardial ischemia and MI, atrial
fibrillation, pulmonary infections, nonadherence with diet or drug therapy,
and inappropriate medication use.
• Drugs may precipitate or exacerbate HF because of their negative inotropic,
cardiotoxic, or sodium- and water-retaining properties.
 Norepinephrine (Noradrenaline) –
• Norepinephrine, also called noradrenaline, is both
a neurotransmitter and a hormone.
• As a neurotransmitter, it’s a chemical messenger that helps transmit
nerve signals across nerve endings to another nerve cell, muscle cell or
gland cell.
• As a hormone, it’s released by our adrenal glands.
 Aldosterone
• Aldosterone is a mineralocorticoid hormone produced in the zona
glomerulosa of the adrenal cortex that influences water and salt
regulation in the body.

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Heart Failure-1.pptx

  • 2. Heart Failure • Heart failure (HF) is a progressive clinical syndrome caused by inability of the heart to pump sufficient blood to meet the body’s metabolic needs. • HF can result from any disorder that reduces  ventricular filling (diastolic dysfunction) and/or  myocardial contractility (systolic dysfunction).
  • 4. PATHOPHYSIOLOGY • Causes of systolic dysfunction (decreased contractility) are reduced  muscle mass (eg, myocardial infarction [MI]),  dilated cardiomyopathies, and  ventricular hypertrophy. • Ventricular hypertrophy can be caused by  pressure overload (eg, systemic or pulmonary hypertension and aortic or pulmonic valve stenosis) or  volume overload (eg, valvular regurgitation, shunts, high-output states).
  • 5. Preload • Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling. • Preload is a measure of the degree of the ventricular stretch when the heart is at the end of diastole.
  • 6. Afterload • Afterload is the force or load against which the heart has to contract to eject the blood.
  • 7. Shunt • A shunt is a passage by which blood moves from one area (blood vessel or heart chamber) to another in a pattern that isn't normal.
  • 8.
  • 9. • Cardiomyopathy is a disease of the heart muscle that makes it harder for the heart to pump blood to the rest of the body. • Fibrosis is the thickening and scarring of connective tissue, usually as a result of injury. • Stenosis narrowing of a passage in the body. • Concentric hypertrophy is associated with increased left ventricular wall thickness. • Eccentric hypertrophy is associated with dilatation of the left ventricular chamber. • ECM degradation – extracellular matrix degradation.
  • 10. • Ejection fraction means the % of blood leaving left ventricle in 1 heartbeat. • Stroke volume is the amount of blood pumped by left ventricle in 1 heart beat. (normal stroke volume 70 ml) • A healthy left ventricle with a total blood volume of 100 ml will try to pump 60 ml to the aorta has a ejection fraction of 60%. • A heart with an enlarged left ventricle (ventricular hypertrophy) that has a total blood volume of 140 ml will try to pump the same amount (60 ml), to the aorta has an ejection fraction of 43%.
  • 11. PATHOPHYSIOLOGY • Causes of diastolic dysfunction (restriction in ventricular filling) are increased ventricular stiffness, ventricular hypertrophy, infiltrative myocardial diseases, myocardial ischemia and MI, mitral or tricuspid valve stenosis, and pericardial disease (eg, pericarditis and pericardial tamponade). • The leading causes of HF are coronary artery disease and hypertension.
  • 12. PATHOPHYSIOLOGY • As cardiac function decreases after myocardial injury, the heart relies on compensatory mechanisms:  (1) tachycardia and increased contractility through sympathetic nervous system activation;  (2) the Frank–Starling mechanism, whereby increased preload increases stroke volume;  (3) vasoconstriction; and  (4) ventricular hypertrophy and remodeling.
  • 13. Frank–Starling mechanism • The Frank- starling law was named to honor two physiologists, Otto Frank and Ernest Henry Starling who found the relationship between stroke volume and end diastolic volume. • The Frank-Starling law states that the more the ventricular muscle are stretched, the more forcefully they contract.
  • 14. PATHOPHYSIOLOGY • Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression. • In the neurohormonal model of HF, an initiating event (eg, acute MI) leads to decreased cardiac output; the HF state then becomes a systemic disease whose progression is mediated largely by neurohormones and autocrine/paracrine factors.
  • 15. Autocrine / Paracrine factors • Paracrine – a cell targets a nearby cell by signaling. • Autocrine – a cell targets itself, releasing a signal that can bind to itss own receptors on its surface.
  • 16. PATHOPHYSIOLOGY • These substances include angiotensin II, norepinephrine, aldosterone, natriuretic peptides, arginine vasopressin, endothelin peptides, and other circulating biomarkers (eg, C-reactive protein). • Common precipitating factors that may cause a previously compensated HF patient to decompensate include myocardial ischemia and MI, atrial fibrillation, pulmonary infections, nonadherence with diet or drug therapy, and inappropriate medication use. • Drugs may precipitate or exacerbate HF because of their negative inotropic, cardiotoxic, or sodium- and water-retaining properties.
  • 17.  Norepinephrine (Noradrenaline) – • Norepinephrine, also called noradrenaline, is both a neurotransmitter and a hormone. • As a neurotransmitter, it’s a chemical messenger that helps transmit nerve signals across nerve endings to another nerve cell, muscle cell or gland cell. • As a hormone, it’s released by our adrenal glands.
  • 18.  Aldosterone • Aldosterone is a mineralocorticoid hormone produced in the zona glomerulosa of the adrenal cortex that influences water and salt regulation in the body.