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Heart Failure (Introduction)

heart failure powerpoint

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0% found this document useful (0 votes)
15 views

Heart Failure (Introduction)

heart failure powerpoint

Uploaded by

Leyla Johnson
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
You are on page 1/ 22

Chapter 34

Heart Failure

Copyright © 2020 by Elsevier, Inc. All rights reserved.


Heart Failure
• Complex clinical syndrome resulting in insufficient blood supply/oxygen to
tissues and organs
• Decreased cardiac output leads to:
• decreased tissue perfusion
• Impaired gas exchange
• Fluid volume imbalance
• Activity intolerance

Copyright © 2020 by Elsevier, Inc. All rights reserved. 2


Cardiac output
• Preload
• Afterload
• Contractility
• Heart rate
• Any process that affects CO can cause HF

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.


Ejection fraction
• Ejection fraction divides the
amount of blood pumped out of
the left ventricle by the amount
of blood that was in the left
ventricle.

• Normal EF=55-65%
• https://www.youtube.com/
watch?v=1-BDMXOWMD8
Risk Factors
• Primary risk factors
• Hypertension
• Modifiable risk factor
• If aggressively treated and managed, incidence of HF can be reduced by 50%
• CAD
• Co-morbidities contribute to development of HF
• Diabetes
• metabolic syndrome
• advanced age
• tobacco use
• vascular disease

Copyright © 2020 by Elsevier, Inc. All rights reserved. 5


Etiology of Heart Failure
• Any interference with mechanisms regulating cardiac output (CO)
• Primary causes
• Conditions that directly damage the heart (heart attack)
• Precipitating causes
• Conditions that increase workload of the heart (hypertension)

Copyright © 2020 by Elsevier, Inc. All rights reserved. 6


Classification of Heart Failure
• Left-sided versus right-sided
• Most common form of HF
• Results from inability of LV to
• Empty adequately during systole, or
• Fill adequately during diastole
• Systolic versus diastolic
• Systolic-reduced ejection fraction
• Problem with LV contraction or emptying
• Diastolic-preserved ejection fraction
• Problem with filling
Left-Sided Heart Failure
• Most common form
• Results from left ventricular dysfunction
• Blood backs up into left atrium and pulmonary veins
• Increased pulmonary pressure causes fluid leakage →→ pulmonary
congestion and edema

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.


Pathophysiology of Systolic HF
• Inability to pump blood forward
• Caused by
• Impaired contractile function
• Increased afterload
• Cardiomyopathy
• Mechanical abnormalities
• Decreased left ventricular ejection fraction (EF) ↓ EF as low as
10%, normal is 55-60

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.


Pathophysiology Diastolic HF
• Impaired ability of the ventricles to relax and fill
during diastole, resulting in decreased stroke
volume and CO
• Heart failure with normal EF
• Result of left ventricular hypertrophy from
hypertension, MI, valve disease, or
cardiomyopathy

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.


Pathophysiology
Mixed Heart Failure
• Mixed systolic and diastolic failure
• Seen in disease states such as dilated cardiomyopathy (DCM)
• Poor EFs (<35%)
• High pulmonary pressures
• Biventricular failure
• Both ventricles may be dilated and have poor filling and emptying capacity

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.


Right-Sided Heart Failure
• Right ventricular dysfunction
• Blood backs up into the right atrium and venous circulation
• Jugular venous distention
• Hepatomegaly, splenomegaly
• Vascular congestion of GI tract
• Peripheral edema
• Most commonly caused by left-sided HF

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.


Pathophysiology
Biventricular Failure
• Both right and left ventricular dysfunction
• Inability of both ventricles to pump effectively
• Fluid build-up and venous engorgement
• Decreased perfusion to vital organs

Copyright © 2020 by Elsevier, Inc. All rights reserved. 15


Compensatory Mechanisms
• Renin-Angiotensin-Aldosterone-System (RAAS)
• Cardiac output decreases—renal perfusion is decreased
• Kidneys release renin causing Angiotensin I to be converted to angiotensin II causing
vasoconstriction
• Aldosterone is released—causes sodium and water retention
• Peripheral vasoconstriction caused increased BP

Copyright © 2020 by Elsevier, Inc. All rights reserved. 16


Compensatory Mechanisms
• Sympathetic nervous system
• Baroreceptors sense low arterial pressure
• Catecholamines are released
• Stimulation of β-adrenergic receptors increases HR and ventricular
contractility

Copyright © 2020 by Elsevier, Inc. All rights reserved. 17


Compensatory Mechanisms
• Dilation
• Enlargement of the heart
chambers that occurs when
pressure in left ventricle is
elevated over time
• Initially effective (Frank-Starling
Law)
• Increased preload causes a more
forceful ventricular contraction
• Eventually this mechanism
becomes inadequate and CO
decreases

Copyright © 2020 by Elsevier, Inc. All rights reserved. 18


Compensatory Mechanisms
• Hypertrophy
• Adaptive increase in muscle mass
and heart wall thickness
• Initially effective
• Over time leads to poor
contractility, increased O2 needs,
poor coronary artery circulation,
and risk for dysrhythmias

Copyright © 2020 by Elsevier, Inc. All rights reserved. 19


Compensatory Mechanisms
• Remodeling
• Continuous activation of neuro-hormonal responses (RAAS and SNS)
• Hypertrophy of ventricular myocytes
• Ventricles larger but less effective in pumping
• Can cause life-threatening dysrhythmias and sudden cardiac death (SCD)

Copyright © 2020 by Elsevier, Inc. All rights reserved. 20


Beneficial Counterregulatory
Mechanisms
• Natriuretic peptides
• Atrial natriuretic peptide (ANP),
Brain (b-type) natriuretic peptide (BNP)
• Released in response to increased blood volume and ventricular wall
stretching
• Improved GFR, improved excretion of water and sodium
• Causes vasodilation, and lowered BP
• Counteracts effects of SNS and RAAS
• High BNP=more fluid retention and increased severity of HF

Copyright © 2020 by Elsevier, Inc. All rights reserved. 21


Counterregulatory Mechanisms
• Nitric oxide (NO) and prostaglandin
• Released from vascular endothelium in response to compensatory
mechanisms
• Cause relaxation of arterial smooth muscle, resulting in vasodilation and
decreased afterload

Copyright © 2020 by Elsevier, Inc. All rights reserved. 22

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