Tina Munzu, RN
Alverno College
munzutt@alverno.edu
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Outcomes
By the end of this tutorial the audience will be able to:
- Comprehend the basic anatomy and physiology of the heart
- Understand and articulate the pathophysiology behind heart failure
-Articulate the role of genetics, aging, inflammation and stress on
heart failure
- Identify the significance of diet, activity, and exercise
recommendations and medication therapy in the treatment and
management of heart failure
- Promote patient adherence to self management of heart failure
- Summarize the role of nursing in heart failure management
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Before we begin ….
This is an interactive Powerpoint. You will with be asked questions and
receive feedback with each answer.
With the multiple choice questions, select an answer on click on the letter
choice for feedback.
For the open ended questions click of the slide for the answer.
Enjoy learning!!!!!
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TABLE OF CONTENTS
• Background
•Role of aging
•The Heart: Anatomy & Physiology
•Role of stress
• Heart Failure: Definition
•Role of inflammation
•Left and Right Sided heart failure
• Heart Failure Self Management
Recommendation:
•Medication
•Fluid Restriction
•Diet
•Weight management and
exercise
•Action plan
•Case study
•Role of genetics
• References
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Background
-According to the American Heart Association (AHA 2006), nearly 5 million Americans
are living with Heart Failure (HF), with 550,000 new cases are diagnosed each year.
-HF is the final common pathway for several common illnesses especially
hypertension and coronary artery disease.
-HF is currently the leading diagnosis and cause of hospitalizations among patients 65
years and older. The costs of healthcare associated with the illness are excessive.
(AHA, 2006)
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Background: role of nursing …
“Stop telling us what to do and teach us how to do it”
(anonymous woman with chronic heart failure)
Microsoft clip art 2007
-As nurses we have the privilege of being patient educators
-Nurses assess a patient’s cognitive function and knowledge of heart failure
to help them develop essential skills to manage their disease.
-Our goal is to partner with patients for better outcomes.
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The Heart: Anatomy and Physiology
Blood from
lungs
Pulmonary
Artery
Pulmonary Vein
Left side of the
heart (atrium
ventricle)
Right side of the
heart (atrium 
ventricle)
Aorta
Vena Cava
Rest of the
body (organs
and tissues)
Retrieved 4/12/10 from
http://www.biomaterials.org/SIGS/Cardiovascular/images/cv_anatomy
_heart.jpg
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PHYSIOLOGY OF THE HEART
Microsoft clip art 2007
To increase cardiac output in response to body needs the heart depends on 4 factors:
(i) Preload (ventricular filling),
(ii) afterload (degree of resistance of blood ejection from the heart),
(iii) cardiac contractility,
(iv) the heart rate
Preload: represents the blood volume in the heart chambers just before a contraction. In
ventricular diastolic dysfunction often seen in heart failure, the heart is stiff and thickened
from ventricular hypertrophy and cannot relax completely. This reduces preload as the
ventricles do not fill adequately with blood volume.
Afterload: represents the pressure/tension that the left side of the heart, primarily the left
ventricle, must generate in order to contract and force blood into the aorta and the rest of the
body. Elevated systemic blood pressure and aortic valve disease increase afterload as the left
ventricle must generate a greater tension to pump blood out of its chamber which can lead to
heart hypertrophy. All else being equal as afterload increases, cardiac output decreases.
(Porth, 2005)
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PHYSIOLOGY OF THE HEART
Microsoft clip art 2007
Cardiac contractility: refers to the ability of the heart to change its force of contraction. It
is heavily determined by factors that mediate actin and myosin interactions in myocardial
cells. The concentration of calcium in the cell is one of the most significant biochemicals that
affect this interaction. The higher the intracellular calcium, the higher the contractility force.
The sympathetic nervous system with the release of epinephrine and norephinephrine
promotes increased intracellular calcium and thus increased cardiac contractility.
Heart rate: refers to the frequency with which the heart beats/contracts to force blood out to
the rest of the body’s tissues. As the heart rate increases, generally so does cardiac output
because more blood is being pumped out in a minute. However, if the heart were to continue
beating at these higher rates, as seen in ventricular tachycardia, it translates into lesser
volume to pump out since the ventricles are not allowed enough time to fill up before they
contract again. This could then result in a decreased cardiac output.
(Porth, 2005)
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Question:
Identify the factors that affect the heart’s ability to meet the body’s needs for
oxygen and nutrients.
1. Preload
Correct! Volume work imposed on
the heart before it contracts
2. Afterload
Right! The pressure the left
ventricle must overcome to force
blood into aorta
3. Cardiac contractility
Correct! Ability of the heart muscle
cells to contract.
4. Heart rate
Correct! The frequency with which the
heart ejects blood. Affects preload as
faster heart rates means less filing time
for the ventricles
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Question:
True or false:
Everything else equal there is an inverse relationship between afterload and cardiac output.
TRUE
FALSE
Correct! The higher the afterload, the lower
the cardiac output overtime as the heart is
overworked and cannot meet body needs.
Try again. With increased afterload the heart
must work harder to meet body needs.
The higher the heart rate the higher the preload.
TRUE
FALSE
Correct! Preload corresponds to the filling time
of the heart chambers. The faster the heart
beats the less time it has for the ventricle to fill
with blood.
Wrong! Remember that preload
corresponds to the filling time of the heart
chambers.
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What is Heart Failure?
Definition: Heart failure is the inability of the heart to pump blood adequately to the tissues
2 main categories:
1) Systolic dysfunction: Experienced during the pumping/contraction phase, it involves
a decrease in cardiac contractility and ejection fraction. Diseases that affect the
contractile performance of the heart (MI and cardiomyopathy) or that cause
increase pressure overload (hypertension and Valvular stenosis) are most
responsible for systolic dysfuntion
2) Diastolic dysfunction: Long standing hypertension is usually the cause of diastolic
dysfunction. Over time, the heart muscles stiffen and become less flexible. The
heart is no longer able to stretch effectively and fill with blood.
(Porth, 2005)
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www.med.uc.edu/kranias/heart_failure.htm
Systolic and Diastolic Heart Failure
Retrieved from www.med.uc.edu/kranias/heart_failure.htm
* Evaluated by echocardiogram. Normal ejection fraction is ≥
50%
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Signs and Symptoms of HF
Left heart failure
Right heart failure
Congestion of
peripheral tissues
Edema and
ascites
Liver congestion
 impaired liver
function
GI tract
congestion
Pulmonary
congestion
Cardiac output
Activity
intolerance
Impaired
digestion
Impaired gas
exchange
Pulmonary
edema
Dyspnea 
cyanosis
Cough (w/
frothy sputum)
orthopnea
Anorexia, Weight loss,
cachexia
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Question
The primary most significant contributing factor to heart failure is:
A) Infection
Try again!
B) Uncontrolled
hypertension
Correct
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C) Mental illness
Try again!
Question – Click on the screen below each question for answers
Take a guess! What percentage of blood is pumped out of the heart
with each heart beat?
60%
What is the cardiologic diagnostic test used to estimate a patient’s EF?
An ECHOCARDIOGRAM
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Common Factors that Precipitate HF
Hospitalization
- Noncompliance with medical regimen, sodium and/or fluid
restriction,
- Acute myocardial ischemia
- Uncorrected high blood pressure
- Atrial fibrillation and other arrhythmias
- NSAIDS (Nonsteroidal anti-inflammatory drugs)
- Excessive alcohol, drug use
- Infections (e.g., pneumonia, viral illnesses)
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Case Study
Ms. M is an 80year woman with a history of hypertension and
occasional angina. She presents to the ER with shortness of
breath that has gotten worse over the last three days
especially with activity. Ms. M reports an inability to sleep at
night due to a non productive cough and constantly having to
urinate. She sleeps with 2-3 pillows and lately finds herself
waking up gasping for air. She presents with severe swelling in
her legs. Her admission vitals were: blood pressure 175/75,
heart rate 102bpm, respiratory rate 22, temperature 98.5 and
pulse oximetry 91% on 2L nasal cannula. Her EKG and chest xray show left ventricular hypertrophy.
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Question
Identify her significant risk factors plus signs and symptoms of HF
-Age (80yrs old)
-History of hypertension and angina
- Shortness of breath
- Activity intolerance
- Constant urination (probable side effect of medication)
- lower extremity edema
-Tachypneic and tachycardia
- Cardiac remodeling (left ventricular hypertrophy)
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Role of genetics in HF
-Researchers are beginning to trace the etiology of HF partly to
genetics
-The fundamental basis for heart cells are 1) the generation of a
contractile force, 2) transmission of this force throughout.
-Mutations in the sarcomere proteins of muscle cells have been
linked to HF. These mutations
- cause uncoordinated heart contractions  increased
energy consumption
- cause changes in calcium homeostasis  apoptosis
and fiber formation  inflammation
- However, more research is still on the way to identify exactly the
direct role genetics has to play.
(Morita et al, 2005)
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Modified from Google page
http://www.scq.ubc.ca/wpcontent/dna.gif
Effects of Aging
-HF is a progressive disease and develops over time; hence it is most common with aging. It
affects an individual’s quality of life and promotes early mortality.
- Aging causes changes in the heart and in the blood vessels:
- thickening of the heart’s walls
- increased deposits of lipofuscin: heart valves thicken and become stiffer  increased
workload of the heart
- the aorta becomes thicker, stiffer and less flexible  increased blood pressure which
makes the heart work even harder  muscle hypertrophy
(Medline Plus, 2008)
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Stress Response
The body’s systemic response to stress involves baroreceptor reflexes and the reninangiotensin-aldosterone (RAAS) mechanism.
Heart failure  Decrease cardiac output ( the heart is less capable to pump blood (volume)
around to the tissues)
HF = Decreased CO
Angiotensin II =
vasoconstrictor and
aldosterone
production
Sodium and water
retention 
Increased BP
Decreased Blood
volume to kidneys
Converted in the
lungs to Angiotensin
II by ACE
Increased CO and
coronary perfusion
Kidneys release renin
in response to low BP
Converts
Angiotensinogen 
Angiotensin I
Long term 
increased workload
by the heart 
worsening EF  HF
Start here
(Angerio, 2005)
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stress response cont’d
Stress (Decreased Cardiac Output)
“Fight-flight” hormones (epinephrine &
norepinephrine) are released into bloodstream
Increase heart rate. Heart contracts and pumps more
forcefully to compensate for low cardiac output
Temporary solution. Overtime, if this is sustained, it
puts more demand on an already weak heart.
Leads to further deterioration of the heart 
worsening heart failure
(Angerio, 2005)
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STRESS CONTINUED
Prolonged compensatory mechanisms by the RAAS and norepinephrine
system lead to deterioration and remodeling of heart muscles
Normal Heart
MI, HTN
etc
Compensatory
mechanisms
Overtime

permanent
heart
remodeling
Decreased
CO and
increased
mortality
(Angerio, 2005)
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Role of Inflammation in HF
- One belief is that the progression of HF is heavily influenced by inflammation.
-Proinflammatory cytokines ( CRP, TNF, interleukin 6) produce toxins that
directly affect the heart and peripheral vasculature.
- In response to cardiac stress such as a myocardial infarction (MI), increased
pressure or volume overload, myocardial cells produce cytokines especially TNF
Secretes
more
cytokines
Tissue
Release of
Attract monocytes ->
Releases
damage,
cytokines
mature into macrophages
toxins
infection
(TNF, IL 6)
Decreased CO
- HF
Increased
workload on heart
to meet body
needs
Remodeling
(hypertrophy,
dilation)
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Kills
cardiomyocytes
TUMOR NECROSIS FACTOR (tnf)
-TNF is the most known pro-inflammatory cytokine that contributes to HF:
-Elevated levels of TNF in the blood are a good indicator of HF prognosis:
- instigates cardiomyocyte hypertrophy  thickening and stiffening of heart vessels
-triggers apoptosis (cell death) of myocytes  less contractile force of the heart 
decreased cardiac output
- blunts adrenergic (epinephrine and norepinephrine) responsiveness  prevents
initial activation of compensatory mechanism
-induces left ventricular dilation  cardiac muscle stiffening
-promotes progression towards muscle wasting (cachexia)
Alcohol and smoking release toxins that induce inflammation!!!!!
Copied from
http://z.about.com/d/chemistry/1
/0/r/d/flamingdrinks.jpg
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The Nursing Impact
Focus on Self- Management Education
“Stop telling us what to do and teach us how to do it”
(anonymous woman with chronic heart failure)
- Self care maintenance involves taking all medications as prescribed, following a low salt
diet, exercising, watching out for any signs and symptoms such as increased swelling,
cognition changes or shortness of breath.
-Although knowledge of illness is the basis for self management, it is not sufficient.
Patients must develop skill to apply the knowledge.
-Our education goal is to transition from an authoritative/prescriptive model of teaching
towards a more collaborative skill building model that will promote better selfmanagement by patients
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Medication Education and Compliance
Microsoft clip art 2007
- Common reasons for medication noncompliance include:
- cost
- lack of understanding of discharge instructions
- not being convinced of the effects and usefulness of the medication.
-At discharge only 80% of patients with a prescription for an ACE inhibitor filled
their prescription during the 30days after discharge
** NSAIDS: Discourage NSAID use in HF patients
(Butler ,2004).
Microsoft clip art 2007
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Medication Education and Compliance
-Educate on the usefulness of ACE/ARBs and beta blockers in HF management.
-For the most part these medications work best when combined with one another.
Patients may sometimes be on up to 4 different combinations and must understand
their usefulness and mechanism as related to their particular condition to ensure
compliance
-Encourage patient to use system, such as pill boxes and alarms, to help remind
patients when to take their medications
Microsoft clip art
2007
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COMMON HEART FAILURE MEDICATIONS
Drugs
Effects
Examples
ACE (angiotensin-converting
enzyme) Inhibitors
Primary drug of choice: block
angiotensin II and aldosterone
production, dilate vessels, prolong life
*cough*
Lisinopril, enalapril, captopril
Angiotensin II receptor blockers
(ARBs)
Similar to ACE inhibitors. More tolerable
for most patients because has no cough
side effects. Usually used together with
ACE inhibitors
Valsartan, losartan
Diuretics
Helps kidneys eliminate salt and water
 decreased fluid volume to relieve the
heart’s workload
Furosemide, HCTZ
Beta-blockers
Slows heart rate and blocks excessive
heart stimulation such as seen in heart
arrhythmias. Usually works well with
ACE inhibitors for added benefits
Metoprolol , coreg
Anticoagulants
Helps prevent formation of blood clots
especially if blood is pulling in heart
chambers such as seen in atrial
fibrillation
Lovenox, heparin
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Question
What are the 2 most common drug groups used to manage HF
A) ACE inhibitors
& NSAIDS
B) ACE inhibitors
and ARBs
Wrong. NSAIDs are
contraindicated in HF
patients
Correct!
C) ARBs and
nitroglycerin
D) Oxygen and
diuretics
Nitroglycerin is not 1st
drug of choice
Wrong. Try again
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Question
On review of Ms M’s (case study) home medications you discover that she was
recently started on 5mg lisinopril daily by her primary care physician. She has also
been taking 160mg of diovan daily and 40mg of lasix daily. Which medication might
be responsible for her cough?
A) Lisinopril
Correct. Side
effect of most
ACE inhibitors
B) Valsartan
Wrong! Pts usually
tolerate ARBs
better due to lack of
coughing side
effects
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C) Furosemide
Try again!
Fluid Restriction
- General advice to the elderly and public is to maintain hydration especially
when ill; thus HF patients often think it helpful to drink loads of fluid.
- Some patients on diuretics believe they have to drink to replenish the fluids
being lost as urine.
- Fluid overload results in increased edema, which increases the workload of
an already compensating heart and may lead to difficulty breathing.
- United States HF guidelines currently restrict fluid intake to 1.5-2L per day in
patients with severe symptoms and hyponatremia.
- Encourage patients to weigh themselves daily for early detection of fluid
retention.
-1 cup = 8 ounces = 240 ml
Microsoft clip
art 2007
*Importance of daily weight is not for monitoring change in adipose (fat) tissue
but instead fluid status*
(Riegel et al, 2009)
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Question
When are HF patients most encouraged to weigh themselves?
A) In the Am after
breakfast
B) At bedtime after
taking lasix
Try again!
Lasix that late will keep
them up all night
C) On rising in the AM
after urinating
Correct!
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!
Diet
- In HF, diet and weight management are very important.
Microsoft clip art
- HF guidelines recommend 2-3g of sodium per day. Due to its water retaining
capabilities excess sodium consumption contributes significantly to HF exacerbation
and hospitalization.
-Partner up with the nutrition/dietary departments to create learning opportunities
for patients where they can learn and understand how to read food labels.
- Discourage foods believed to be proinflammatory such as simple sugars, saturated
fats and alcohol.
- Encourage foods that counteract inflammation such as walnuts, fruits and
vegetables, garlic, ginger and sunflower seeds according to patient preferences.
(Riegel et al, 2009)
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Exercise and Weight Management
-The benefits of exercise are extensive.
- Exercise is a great way to improve circulation and decrease inflammation. Following an
exercise regimen to help maintain ideal body weight helps reduce the workload on the heart.
- Exercise:
• improves appetite and mood
• helps to obtain a more restful sleep
• reduces stress
• controls blood pressure and cholesterol
Microsoft clip art 2007
• eases shortness of breath
- The goal is to partner with the patient to develop an exercise plan that fits well into their
daily life, budget and their environment.
* Weight loss is encouraged if BMI is >40kg/m2. If <30kg/m2 discourage. Encourage patient
instead to monitor for loss of appetite, unexpected weight loss and muscle wasting (=
symptoms of cachexia).
(Riegel et al, 2009)
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Question:
Ms. M’s echo results come back. She has an EF of 20% and is afraid that her heart will “stop
pumping well” and she will get short of breath again. What advice can you give her as to how to
manage her heart failure?
Weigh yourself daily in the AM
Yes. This will help her identify if
she is retaining any fluids and how
much. Encourage her to keep a
journal
Raise feet on pillows and wear
ted stockings
Yes. To help manage any swelling
Limit your salt intake. Use
spices for food seasoning
Take your medications as
prescribed.
Yes. Salt makes her retain water
which increases the workload of the
heart
Yes. To help manage and prevent
exacerbation
Drink loads of fluids
No. Too much fluids put more
pressure on an already struggling
heart  exacerbation
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Stay current on your seasonal
vaccines. Follow up with
doctor regularly.
Yes. Prevents infection which triggers
the inflammation process.
Action Plan and MD follow up – Use this to help guide you to what action to take!
Green
• No change in symptoms
• No cough or wheeze
• Breathing is good
• Usual strength and activity
• Weight is stable
Yellow
• Weight gain of more than 3 pounds in 1-2 days
• Weight gain of more than 5 pounds in 1 week
• Have to sleep sitting up
• Start coughing at night
• Notice swelling in your ankles or any part of your body
• Have pain or bloating in your stomach and lose your appetite
• Become tired faster or feel yourself losing energy
• Wheezing (noisy breathing)
• Have side effects from your pills
• Weight loss of more than 5 pounds in 2 days
Red
• Trouble breathing
• Pain or tightness in chest
• Dizzy spells or feel faint
• Feel anxious or like something
bad will happen
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Green means GO –
You’re doing fine stay
on treatment and active
2. Yellow means Caution –
Be alert to changes
Call your MD within 24
hours
Red means Stop – Call for
help right away – 911 if
emergency
* Modified with permission from Aurora HF discharge
education packet (2010)
References:
Riegel B, Moser D, Anker S, et al. AHA state of the science: Promoting self-care in persons with
heart failure. Circulation. 2009;120:1141-1163
Dickson, V. V., Riegel B. Are we teaching what patients need to know? Building skills in heart
failure self-care. Heart & Lung. 2009;38:253-262
Albert N., Fonarrow G, Abraham W, et al. (2007) Predictors of delivery of hospital-based heart
failure patient education: A report from optimize-hf. J Cardiac Failure 13(3) 189-198.
Freeman. G, Murray D. Proinflammatory cytokines; predictors of a failing heart? Circulation.
2003;107:1460-1462
Libera L, Vescovo G. (2004) Muscle wastage in chronic heart failure, between apoptosis,
catabolism and altered anabolism: a chimaeric view of inflammation? Clinical nutrition and
Metabolic Care. 7:435-441
Mueller C, Kilian K, Christ A, et al. (2006) Inflammation and long-term mortality in acute
congestive heart failure. American Heart Journal 151:845-850
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References:
Angerio A. (2005) The role of endothelin in heart failure. Critical Care Nurse 28(4)335-359
Medical News Today. The genetic background of heart failure and the role of hypertension.
Retrieved April 4, 2010 from
http://www.medicalnewstoday.com/printerfriendlynews.php?newsid=105716
Medline Plus. Aging changes in the heart and blood vessels. Retrieved April 7, 2010 from
http://www.nlm.nih.gov/medlineplus/ency/article/004006.htm
Chantier P, Clements R et al. (2006) Congestive heart failure: extent of cardiac functional
changes caused by aging and organ dysfunction. Heart 92:686-688
Alexander J, Alexander K, Kong D et al. (1998) Session highlights from the AHA scientific
session: november 7-12, 1997. American Heart Journal 135(1) 169-170
Berra K, Miller N. (2009) Inhibiting the renin-angiotensin system: why and in which patients.
American Academy of Nurse Practitioners 21:66-75
Morita H, Seidman J, & Seidman C. Genetic causes of human heart failure. Journal of Clinical
Investigation. 115:518-526 (2005).
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Contact Information
Tina Munzu
MSN Alverno College Student
munzutt@alverno.edu
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