Maintaining Fluid Balance
In Patients with Heart
Failure
Sarah Carek, RN, MSN Student
Alverno College
Spring 2010
What should I know by the
end of this tutorial?
• Understand the basic physiology of the heart.
• Develop a clear picture as to how Heart Failure is a
pathological process.
• Recognize how excess fluid volume can result from Heart
Failure.
• Apply nursing interventions to patients with Heart Failure.
• Examine how aging, stress, inflammation and genetics play
in the development of Heart Failure.
Tutorial Navigation
•
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•
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• All buttons will be on the bottom of each page.
• Begin the tutorial by clicking on the first topic on
the home page.
Slides with Animation
• FYI..many slides contain animation. Keep clicking
the mouse to advance through the entire
animation. If you hover your cursor over areas and
it changes from an arrow to a hand…click and
animation will occur.
• Any underlined words have definitions available.
Hover your cursor over the word and the definition
will appear.
Home Page
Cardiac Physiology
Pathophysiology of Heart Failure
Causes of Heart Failure
Important Nursing Interventions
Fresh and New: Aging, Stress, Inflammation & Genetics
References
Contact Information
CARDIAC
PHYSIOLOGY
Microsoft Clipart (manually altered)
Let’s see what you
know already!
Hover your mouse
cursor over each
section of the heart
until the cursor turns
from an arrow to a
hand. Then click to
reveal its label.
**If the mouse has not
turned from an arrow
to a hand..Do Not
Click***
Aorta
Pulmonary
Arteries Pulmonary
Veins
Superior
Vena
Cava
Left
Atrium
Right
Atrium
Left
Ventricle
Right Ventricle
Inferior
Vena
Cava
Microsoft Clipart (manually altered)
What do the areas of the heart do?
Click on the boxes to the left to find their function.
Right Atrium
Pumps deoxygenated blood from the
body into the right ventricle.
Right Ventricle
Pumps deoxygenated blood to the
lungs to get oxygenated.
Left Atrium
Receives oxygenated blood from the
lungs and pumps it to the left
ventricle.
Left Ventricle
Pumps oxygenated blood to the body
to get used for energy
Normal
Blood
Flow
Microsoft Clipart (manually altered)
What about the valves?
The valves of the
heart assure that
blood flows in the
right direction.
Click on the diagram to find
the four valves. They are
half-moon shaped. Again
when the cursor turns into a
hand, it means you can click
on it.
Pulmonic
Valve
Aortic
Valve Mitral
Tricuspid
(Bicuspid)
Valve
Valve
Microsoft Clipart (manually altered)
The Cardiac Cycle
Click on the
boxes on the
left to find their
definition.
Microsoft Clipart
Microsoft Clipart (manually altered)
Systole
The period during the cardiac cycle where the ventricles
are contracting and moving the blood forward.
Diastole
The period during the cardiac cycle where the ventricles
are relaxed and filling with new blood.
(Porth & Matfin, 2009)
The Heart as a Pump
Cardiac
Ouput
Stroke
Volume
Heart
Rate
• Cardiac output measures how well the heart is doing its job of
pumping blood to the body.
• The heart has the ability to adjust cardiac output based on the
body’s needs (i.e. exercise, sleep, illness). This depends on
preload, afterload, cardiac contractility and heart rate.
• Average cardiac output = 3.5 – 8 Liters/minute
(Porth & Matfin, 2009)
Keep clicking to
advance through
the animation of the
slide.
End-Diastolic
Volume
Starling’s Law
Stretching of
Cardiac Muscle
Force of
Contraction
FYI: The fibers only stretch so far. There
is a maximum force of contraction that
can be achieved.
The more
blood in the
heart at the
end of
diastole…
The more the
cardiac muscle
fibers stretch…
The greater
the force of
the
contraction.
(Porth & Matfin, 2009)
Let’s Review
Right
Try Again!
Atrium
Left
Excellent!
Ventricle
Left
Close!
Atrium
No…but you are
Right Ventricle
on the right track.
To prevent blood
from
Try Again!
moving
forward.
To let air escape
preventing
Nope.an air
embolus.
To keep blood
You’re Right!
moving forward.
To prevent blood
from
Keep
leaking
Trying!
out
of the heart.
A. CO = HR x AV
Incorrect
B. CO = SV x HR
Good Job!
C. CO = AV x SV
Try Again!
D. CO = HR x EF
Nope
A.
Blood Viscosity does not help the heart increase
Blood Viscosity
cardiac output.
In order to increase cardiac output the heart
B. Correct!
Cardiac
Contractility
must be able
to change the force of contraction.
C.
Yes! The heart can change its rate in order to
Heart
Rateor decrease cardiac output.
increase
Good Job! According to Starling’s Law, if End-Diastolic Volume
D. Preload
(preload) increases, the force of contraction will as well.
E.
Excellent! Cardiac output can be adjusted based
Afterload
on systemic arterial pressure (afterload).
PATHOPHYSIOLOGY OF
HEART FAILURE
Microsoft Clipart (manually altered)
Cardiac Function is Impaired
Heart the
Failure
when there is
Remember
hearthappens
is a pump…
one or more alterations in preload,
SV
COcardiac contractility
HR leading
afterload or
to decreased Cardiac Output.
• Cardiac Output is a reflection of how well the
heart is doing its jobAFTERLOAD
of being a pump. CONTRACTILITY
Decreased ATP
Preload
If
vascular
resistance
is
• HR either speeds up or slows down depending
production and
A stiffer heart will
elevated, the heart has
availability of Calcium
of what
the sympathetic
or parasympathetic
decrease
the amount
to pump harder
to
causes the heart to
of blood
at the end
of
overcome
putting whations
nervous
system
tells theit, heart
to do.
become less able to
diastole
stress
on
it
which
can
• SV is determined by our friends preload,
contract effectively
wear it out
afterload and cardiac contractility.
(Porth & Matfin, 2009)
These Malfunctions can be
Classified into Systolic and
Diastolic Dysfunction
Click on each box to find
the definition. Remember
the arrow should turn to a
hand before you click.
Impaired contractility leads to
a decrease in Ejection Fraction
SYSTOLIC
and Cardiac
Output. Preload,
ventricular wall dilation and
DYSFUNCTION
pressure subsequently
increase.
The ventricles are unable to
DIASTOLIC
relax and
expand, leading to a
decrease in preload, stroke
DYSFUNCTION
volume and cardiac output.
(Porth & Matfin, 2009)
Heart Failure can also be classified
as either Left Sided Heart Failure
or Right Sided Heart failure.
Right Heart Failure
Left Heart Failure
Are you starting to
see how excess fluid
balance contributes
to heart failure?
Blood cannot reach the
lungs to get oxygenated.
Blood begins to pool in the
venous system and tissues.
Dependent Edema
Jugular Vein Distension
Ascites
Pooling of Blood in GI Tract
Pooling of Blood in Hepatic Veins
Oxygenized blood from the
lungs cannot get to the body.
Cardiac Output decreases
and blood pools in the lungs.
Decrease in Tissue Perfusion
Activity Intolerance
Cough, Orthopnea
Hypoxia, PND
Pumonary Edema
(Porth & Matfin, 2009)
Before learning about what causes these
malfunctions to occur….Let’s Review
Yes!
Good Job.
Afterload
Excellent!
Preload
Cardiac
That’s Right!
Contractility
Try Again.
This is
Blood
the thickness of
Viscosity
the blood.
Diastolic
Try Again!
Dysfunction
Priastolic
Sorry
 I made
this one up!
Dysfunction
No. Right
We didn’t
talk
about this
Ventricular
one.
Dysfunction
Systolic
Great!
Dysfuction
CAUSES OF
HEART FAILURE
***Remember to place
your cursor over the
underline words to get
the definition***
Microsoft Clipart (manually altered)
Acute Coronary Syndrome
Myocardial Infarction and Unstable Angina
Decreased blood flow to the myocardium caused by
a clot in the coronary arteries.
Blood begins to pool
leading to fluid volume
overload!!!
Myocardial Damage (Infarction): evidenced by
serum cardiac markers (CK-MB, Troponin).
Ventricular Remodeling: the area of the ventricle
that is damaged undergoes changes in size, shape
and thickness (hypertrophy and dilation).
Damage to the ventricle can lead to alterations in
preload, afterload and cardiac contractility leading
to a decrease in cardiac output.
(Porth & Matfin, 2009)
Ischemic Heart Disease
Coronary Artery Disease
Decreased blood flow to the myocardium from the
coronary arteries caused by plaque buildup.
Blood begins to pool
leading to fluid volume
overload!!!
Myocardial Damage (Infarction): evidenced by
serum cardiac markers (CK-MB, Troponin).
Ventricular Remodeling: the area of the ventricle
that is damaged undergoes changes in size, shape
and thickness (hypertrophy and dilation).
Damage to the ventricle can lead to alterations in
preload, afterload and cardiac contractility leading
to a decrease in cardiac output.
(Porth & Matfin, 2009)
Cardiomyopathy
Hypertrophic Cardiomyopathy
Left Ventricle thickens through genetic predisposition.
Blood begins to pool
leading to fluid volume
overload!!!
The heart is unable to fill properly during diastole –
Altered Preload.
Stroke volume is decreased.
Cardiac Output is decreased.
(Porth & Matfin, 2009)
Cardiomyopathy cont…
Dilated Cardiomyopathy
The ventricle is enlarged and wall thickness is
decreased due to genetic predisposition, infection,
alcohol or unknown cause.
Blood begins to pool
leading to fluid volume
overload!!!
Preload and pressure increase.
Cardiac Output decreases.
(Porth & Matfin, 2009)
Valvular Heart Disease
Mitral Valve Disorders
Stenosis
Regurgitation
Because the valve is
unable to open
fully, the left atrium
becomes distended
leading to impaired
filling during
diastole. This leads
to decreased
cardiac output.
Because the valve
does not open and
close completely, it
becomes leaky.
Stroke volume is
reduced leading to
decreased cardiac
output.
Blood begins to pool
leading to fluid volume
overload!!!
(Porth & Matfin, 2009)
Valvular Heart Disease Cont…
Aortic Valve Disorder
Stenosis
Regurgitation
Because the valve is
unable to open
fully, blood is
unable to exit the
left ventricle
properly and begins
to pool. This
decreases cardiac
output.
Because the valve
allows blood to
flow back into the
left ventricle during
diastole, cardiac
output is
decreased.
Blood begins to pool
leading to fluid volume
overload!!!
(Porth & Matfin, 2009)
Let’s see if you understand causes of
heart failure…
Try Again! This is
Dilated
a cause of chronic
Cardiomyopathy
heart failure.
Excellent! Ischemia to the
Myocardial
heart
can cause it to not
pumpInfarction
blood like it should
resulting in heart failure.
Nope. Keep
thinking!
This is a
Aortic Stenosis
chronic cause of HF.
This is a cause of
Mitral Valve
chronic heart
Prolapse
failure.
Blood cannot fill
Now you’re
properly during
thinking!
diastole.
Cardiac Output is
Yay!
decreased.
Blood will spill out
Now that’s just
of the heart
crazy talk.
everywhere.
Blood pools
Good Job!
creating edema.
Microsoft Clipart
Nursing Interventions
Let’s take a look at how you fit
into taking care of heart failure
patients…
Take a minute to think of nursing
interventions you do on a daily basis
that might apply to a patient with
heart failure.
Remember the nursing process…?
Assess
Evaluate
Implement
Diagnose
Plan
Keep clicking
to advance the
animation.
Fluid Volume Excess
(Ackley & Ladwig, 2006)
Things You Would Find On Assessment
• Assessment
–
–
–
–
–
–
Lung sounds
Daily weights
Vital signs
I & O’s
Behavior
Drug side effects
• Interventions
–
–
–
–
Restricted sodium diet
Fluid restrictions
Diuretics
Turning patients with
edema
– Promoting positive self
image
– Consult with physician
Microsoft Clipart
Heart Failure and Aging
The Stats
• ¾ of the 5 million Americans suffering with heart
failure are over the age of 65 and ½ are over the age
of You
75. can see that older adults with heart
failure
are
a
huge
population
for
us
as
• Heart failure is the leading cause of hospitalization
healthcare
providers. As America ages, the
among
the elderly.
population
will
grow larger.
• 1 million
older adults
areonly
hospitalized
annually with
heart failure.
(AHA, 2010)
Changes Related to Aging
(Thomas & Rich, 2006)
• Arteries stiffen creating resistance against which the
heart has to pump.
• Heart muscle stiffens, creating filling difficulty.
• Cardiac Output declines due to a decline in the
maximum rate the heart can reach.
• The aged are less able to increase the force of their
contractions as is needed during stress, illness and
exercise.
Remember Starling’s Law…
End-Diastolic
Volume
Stretching of
Cardiac Muscle
Force of
Contraction
With age the heart muscles stiffens,
limiting the amount of blood that can fill
during diastole. Thus the fibers cannot
stretch
as
far,
creating
a
decreased
force
The more
The greater
blood in the
The
more
the
of
contraction.
the force of
heart at the
cardiac muscle
end of
diastole…
fibers stretch…
the
contraction.
(Thomas & Rich, 2006)
Microsoft Clipart
Heart Failure and Stress
Remember the equation for
cardiac output…
SV
CO
HR
In a diseased heart,
cardiac
output would
not increase as it should during the
If the heart rate is under sympathetic nervous system (SNS) and
parasympathetic
nervous
system (PSNS)
control….think
about
normal
stress
response.
The
heart
would
what chronic stress would do to the heart rate and subsequently
cardiacof
output….
not be capable
pumping blood
Stress
efficiently. Therefore
a prolonged stress
Release of
Increased
Activation
Epinephrine
responseof SNS
would onlyandexacerbate
signs
heartthe
rate and
blood pressure
Norepinephrine
and symptoms of heart failure.
(Porth & Matfin, 2009)
Heart Failure and Inflammation
• Inflammatory mediators (such as nitric oxide) are activated in
a patient with heart failure in an effort to improve cardiac
function.
• These mediators can damage the endothelium in blood
vessels supplying the heart with blood.
• Ventricular and vascular remodeling of the myocardium may
be a result of this damage.
• Ventricular remodeling of the myocardium can result in heart
failure because the ventricular cannot pump blood efficiently.
Blood begins to pool leading
to fluid volume overload!!!
(Brunini, et.al., 2009)
Genetics and Heart Failure
• Some patients are believed to be at high risk for heart failure
due to their genetic make-up.
• In a small population, mutations have been found in single genes
that trigger the development of heart failure.
• Gene mutations have been found in the people with ventricular
remodeling and cardiomyopathies
• Some mutation examples are
– Genes encoding for protein components of the sarcomere
which leads to hypertrophy of the myocardium.
– Gene mutations resulting in altered dystrophin which
normally gives stability to the sarcomere.
Blood begins to pool leading
to fluid volume overload!!!
(Morita, Seidman & Seidman, 2005)
References
Ackley, B.J. & Ladwig, G.B (2006). Nursing diagnosis handbook: a guide to planning care (7th Ed.).
St. Louis, MO: Mosby Elsevier.
American Heart Association (2010). Statistics retrieved from
http://www.americanheart.org/presenter.jhtml?identifier=1200026.
Brunini, T.M., Mann, G.E., Matsuura, C., Meirelles, L.R., Menden-Ribeiro,A.C., & Moss, M.B.
(2009). The role of exercise on l-arginine nitric oxide pathway in chronic heart failure. The
Open Biochemistry Journal, 3, 55-65.
Morita, H., Seidman, C.E., & Seidman, J. (2005). Genetic causes of human heart failure. The
Journal of Clinical Investigation, 115(3), 518-526.
Porth, C.M. & Matfin, G. (2009). Pathophysiology: concepts of altered health status (8th Ed.).
Philadelphia, PA: Lippincott Williams & Wilkins.
Thomas, S. & Rich, M.W. (2006). Heart failure in older people. Generations (Fall 2006), pp. 25-32.
Contact Information
Questions, Comments, Concerns?
Sarah Carek, RN, MSN student
careksl@yahoo.com
(608) 577-7866