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HEART FAILURE
by Nancy Jenkins
The most common reason for
hospitalization in adults >65
years old.
Heart Failure- Clinical syndrome
that can result from any structural
or functional cardiac disorder that
impairs ability of ventricle to fill
with or eject blood
Heart Failure
Click here!
5 million Americans have heart
failure
•500,000 new cases every year
• 25-50 billion dollars a year to
care for people with Heart Failure
•6,500,000 hospital days / year
•300,000 deaths/year
Heart Failure
Mild
Mild
Cardiogenic shock
Cardiomyopathy
Uncompensated Heart Failure
Pulmonary Edema-ADHF
Severe End Stage
Irreversible
Control With
Drugs
Diet
Fluid
Restriction
/Same as Mild with
Morphine Sulfate
Needs new ventricle
VAD
IABP
Heart Transplant
Heart Failure Pneumonic
U
Upright Position
N
Nitrates
L
Lasix
O
Oxygen
A
Amiodorone, ACE, ARBs
D
Dig, Dobutamine
M
Morphine Sulfate
E
Extremities Up or Down
Definition
• CO=SVxHR is insufficient to meet the
metabolic needs of the body
• SV is determined by preload, afterload and
myocardial contractility
• Systolic failure- dec. contractility
• Diastolic failure- dec. filling
• EF< 40%
Heart Failure
Etiology and Pathophysiology
• Systolic failure is the most common cause
– **Hallmark finding: Decrease in the left ventricular
ejection fraction (EF)
• Caused by
– Impaired contractile function (e.g., MI)
– Increased afterload (e.g., hypertension)
– Cardiomyopathy
– Mechanical abnormalities (e.g., valve disease)
http://coursewareobjects.elsevier.com/objects/mccance5e_v1/McCance/Module15/Part02/M15L04S41a.html??hostType=undefined&
authorName=Mccance&prodType=undefined
hypokinesis
90/140= 64% EF- 55-65 normal
Heart Failure
Etiology and Pathophysiology
• Diastolic failure
– Impaired ability of the ventricles to relax and fill
during diastole resulting in decreased stroke
volume and CO
– Diagnosis based on the presence of pulmonary
congestion, pulmonary hypertension, ventricular
hypertrophy, normal ejection fraction (EF)
diastolic failure
Heart Failure
Etiology and Pathophysiology
• 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)
Your patient has a normal EF but
shows signs of heart failure. Your
patient most likely has:
1. Decreased cardiac
output
2. Systolic failure
3. Diastolic failure
4. LV hyypertrophy
Preload
• Volume of blood in ventricles at end
diastole.
• Depends on venous return
• Depends on compliance
Afterload
• Force needed to eject the blood into the
circulation
• Arterial B/P, pulmonary artery pressure
• Valvular disease increases afterload
CHF
• Pathophysiology
• A. Cardiac compensatory mechanisms
– 1.tachycardia
– 2.ventricular dilation-Starling’s law
– 3.myocardial hypertrophy
• Hypoxia leads to dec. contractility
http://www.heartsite.CHF/
html/chf_3.html
cont.
• B.Homeostatic compensatory mechanisms(medications block these)
• Sympathetic Nervous System-(beta blockers block this)
– 1.vascular system- norepinephrine- vasoconstriction(What
effect on afterload?) (ACE) (ARB)
– 2.kidneys•
•
•
•
A. dec. CO and B/P cause renin angiotensin release.(ACE)
B. Aldosterone release causes Na and H2O retention(aldactone)
Inc. Na causes release of ADH(diuretics)
Release of atrial natriuretic factor- promotes Na and H20 excretion
and prevents severe cardiac decompensation (Natrecor)
– 3.liver- stores venous volume(ascites, +HJR),
– Hepatamegaly- can store 10 L. check enzymes
Heart Failure
Etiology and Pathophysiology
• Compensatory mechanisms are activated to
maintain adequate CO
– Neurohormonal responses: Endothelin is
stimulated by ADH, catecholamines, and
angiotensin II and causes
• Arterial vasoconstriction
• Increase in cardiac contractility
• Hypertrophy
Heart Failure
Etiology and Pathophysiology
Contiinued:
Neurohormonal responses: Proinflammatory cytokines
(e.g., tumor necrosis factor)
• Released by cardiac myocytes in response to cardiac
injury
• Depress cardiac function by causing cardiac
hypertrophy, contractile dysfunction, and myocyte cell
death
Heart Failure
Etiology and Pathophysiology
– Neurohormonal responses: Over time, a systemic
inflammatory response is mounted resulting in
• Cardiac wasting
• Muscle myopathy
• Fatigue
Heart Failure
Etiology and Pathophysiology
• Counter regulatory processes- these help protect the heart
– Natriuretic peptides: atrial natriuretic peptide (ANP)
released with cardiac muscle stretch and b-type natriuretic
peptide (BNP) released with increased pressure of LV
• Released in response to increases in atrial volume and
ventricular pressure
• Promote venous and arterial vasodilation, reducing
preload and afterload
• Prolonged HF leads to a depletion of these factors
Which of the following are
compensatory mechanisms for HF?
1.
2.
3.
4.
Tachycardia
Hypotension
RAAS
LV hypertrophy
Heart Failure
– Natriuretic peptides (ANP and BNP) are endothelin
and aldosterone antagonists so they:
• Enhance diuresis
• Block effects of the RAAS
– Natriuretic peptides inhibit the development of
cardiac hypertrophy and may have antiinflammatory effects
– **Natrecor or Neseritide has same effects
Result of Compensatory
Mechanisms
Heart Failure
Pathophysiology
Structural Changes
•
•
•
•
Decreased contractility
Increased preload (volume)
Increased afterload (resistance)
Ventricular remodeling(ACE inhibitors can
prevent this)
– Ventricular hypertrophy
– Ventricular dilation
Ventricular remodeling
(from football to basketball)
END RESULT
FLUID OVERLOAD AND EDEMA
Heart Failure
Classification Systems
• New York Heart Association Functional
Classification of HF
– Classes I to IV
• ACC/AHA Stages of HF
– Stages A to D
AHA Newer Classifications of
Heart Failure- Staging
Stage A
Stage B
Stage C
Those at high risk for
developing heart failure.
Includes people with:
•Hypertension
•Diabetes mellitus
•Coronary artery disease
(including heart attack)
•History of cardiotoxic
drug therapy
•History of alcohol abuse
•History of rheumatic
fever
•Family history of CMP
Those diagnosed with “systolic”
heart failure but have never had
symptoms of heart failure
(usually by finding an ejection
fraction of less than 40% on
echocardiogram).
Patients with known heart failure
with current or prior symptoms.
Symptoms include:
•Shortness of breath
•Fatigue
•Reduced exercise
intolerance.
•Exercise regularly
•Quit smoking
•Treat hypertension
•Treat lipid disorders
•Discourage alcohol or illicit drug use
•If previous heart attack or current
diabetes mellitus or hypertension 
angiotensin converting enzyme
inhibitor (ACE-I)
•Care measures in Stage A +
•All patients should be on ACE-I
•Beta-blockers should be added
•Surgical consultation for coronary
artery revascularization and valve
repair/replacement (as appropriate)
In this group, care measures from Stage A
apply, ACE-I and beta-blockers should be
used +
•Diuretics (water pills)
•Digoxin
•Dietary sodium (salt) restriction
•Weight monitoring
•Fluid restriction (as appropriate)
•Withdrawal of drugs that worsen the
condition
•Spironolactone when symptoms
remain severe with other therapies
Stage D
Presence of advanced symptoms, after
assuring optimized medical care
All therapies under Stages A, B and C + evaluation
for:
•Cardiac transplantation
•Ventricular assist devices
•Surgical options
•Research therapies
•Continuous intravenous inotropic infusions
•End-of-life care
A patient has an EF of 15% and is a
candidate for a heart transplant.
Which AHA stage would he be
considered to be?
1.
2.
3.
4.
Stage C
Stage A
Stage D
Stage B
Heart Failure
Risk Factors
• Primary risk factors
– Coronary artery disease (CAD)
– Advancing age
• Contributing risk factors
–
–
–
–
–
–
–
–
Hypertension
Diabetes
Tobacco use
Obesity
High serum cholesterol
African American descent
Valvular heart disease
Hypervolemia
Which of the following are risk
factors for Heart Failure
1. Hypertension
2. Myocardial
Infarction
3. Diabetes
4. Valvular Disease
Classifications
• Systolic versus diastolic
– Systolic- loss of contractility get dec. CO
– Diastolic- decreased filling or preload
• Left-sided versus right –sided
– Left- lungs
– Right-peripheral
• High output- hypermetabolic state- pregnancy
• Acute versus chronic
– Acute- MI
– Chronic-cardiomyopathy
Symptoms
Left Ventricular Failure
• Signs and symptoms
–
–
–
–
–
–
dyspnea
orthopnea PND
Cheyne Stokes
fatigue
Anxiety
rales
– NOTE L FOR LEFT AND L FOR LUNGS
CXR before and after treatment
Before treatment
After treatment
Which of the following is associated
with left sided failure?
1.
2.
3.
4.
crackles
hypoxemia
tachypnea
Peripheral edema
???????
• WHY DOES THIS OCCUR?
Heart Failure
Clinical Manifestations
• Acute decompensated heart failure (ADHF)
– Pulmonary edema, often life-threatening
• Early
– Increase in the respiratory rate
– Decrease in PaO2
• Later
– Tachypnea
– Respiratory acidemia
Heart Failure
Clinical Manifestations
• Acute decompensated heart failure (ADHF)
• Physical findings (like ARDS)
• Orthopnea
• Dyspnea, tachypnea
• Use of accessory muscles
• Cyanosis
• Cool and clammy skin
Acute decompensated heart failure
(ADHF) Clinical Manifestations
• Physical findings
• *Cough with frothy, blood-tinged sputumwhy???
• Breath sounds: Crackles, wheezes, rhonchi
• Tachycardia
• Hypotension or hypertension
• 4 groups base on hemodynamics and clinical
status
– Dry -warm
– Dry-cold
– Wet-warm- most common (adequate perfusion but fluid
overload)
– Wet -cold
QuickTime™ and a
YUV420 codec decompressor
are needed to see this picture.
Case study of Heart Failure in Lewis
online resources
Pulmonary Edema
(advanced L side HF)
• When PA WEDGE pressure is approx 30mmHg
– Signs and symptoms
• 1.wheezing
• 2.pallor, cyanosis
• 3.Inc. HR and BP
• 4.s3 gallopThe Auscultation Assistant - Rubs
and Gallops
• 5.rales,copious pink, frothy sputum
An S3 or ventricular gallop is
associated with heart failure.
1. True
2. False
Person literally drowning in
secretions
Immediate Action Needed
Goals of Treatment
• MAD DOG
• Improve gas exchange (much like ARDS)
–
–
–
–
O2
intubate
elevate HOB
BIPAP
Right Heart Failure
• Signs and Symptoms
– fatigue, weakness, lethargy
– wt. gain, inc. abd. girth, anorexia,RUQ
pain
– elevated neck veins
– Hepatomegaly +HJR
– may not see signs of LVF- why??
Images of Congestive Heart failure
Can Have RVF Without LVF
• What is this called and what causes it?
COR PULMONALE
Blue bloater
This results from pulmonary
hypertension.How does
this affect afterload?
Pulmonary hypertension is to Cor
Pulmonale as Arterial hypertension
is to:
1. Decreased cardiac
output
2. Left sided heart failure
3. Right sided heart
failure
4. Myocardial infarction
Heart Failure
Complications
• Pleural effusion
• Atrial fibrillation (most common
dysrhythmia)
– Loss of the atrial contraction (kick) can reduce
CO by 20%
– Promotes thrombus/embolus formation
increasing risk for stroke
– Treatment may include cardioversion,
antidysrhythmics, and/or anticoagulants
Heart Failure
Complications
• High risk of fatal dysrhythmias (e.g., sudden
cardiac death, ventricular tachycardia) with HF and
an EF <35% (Use of ICDs and CRT)
– HF can lead to severe hepatomegaly, especially
with RV failure
• Fibrosis and cirrhosis can develop over time
– Renal insufficiency or failure
Ventricular tachycardia is the most
common arrhythmia with heart
failure
1. True
2. False
Heart Failure
Diagnostic Studies
• Primary goal is to determine underlying
cause
–
–
–
–
History and physical examination( dyspnea)
Chest x-ray
ECG
Lab studies (e.g., cardiac enzymes, BNP)
electrolytes
– EF
One of the first signs of Heart failure
is:
1. Decreased cardiac
output
2. Edema
3. Shortness of breath
4. Atrial fibrillation
Heart Failure
Diagnostic Studies
– Hemodynamic assessment-Hemodynamic
Monitoring-CVP- (right side) and SG(left and
right side)
– Echocardiogram-TEE best (EF)
– Stress testing- exercise or medicine
– Cardiac catheterization- determine heart
pressures ( inc.PAW )
CVP is to right side preload as
_____is to left side preload
1.
2.
3.
4.
PAD
PAW
Cardiac output
Arterial B/P
Transesophageal
echocardiogram
TEE
Nursing Assessment
•
•
•
•
•
•
•
Vital signs
PA readings
Urine output
---------------------------------------------------------------
Nursing Diagnosis
– Activity intolerance
– Decreased cardiac output
– Fluid volume excess
– Impaired gas exchange
– Anxiety
– Deficient knowledge
Decreased cardiac output
•
•
•
•
Plan frequent rest periods
Monitor VS and O2 sat at rest and during activity
Take apical pulse
Review lab results and hemodynamic monitoring
results
• Fluid restriction- keep accurate I and O
• Elevate legs when sitting
• Teach relaxation and ROM exercises
Activity Intolerance
•
•
•
•
•
•
Provide O2 as needed
practice deep breathing exercises
teach energy saving techniques
prevent interruptions at night
monitor progression of activity
offer 4-6 meals a day
Fluid Volume Excess
•
•
•
•
•
•
•
Give diuretics and provide BSC
Teach side effects of meds
Teach fluid restriction
Teach low sodium diet
Monitor I and O and daily weights
Position in semi or high fowlers
Listen to BS frequently
Knowledge deficit
•
•
•
•
•
Low Na diet
Fluid restriction
Daily weight
When to call Dr.
Medications
3 Main Goals- in acute as well as
chronic HF
• Decrease preload
• Decrease afterload
• Increase contractility
How to Achieve Goals
• Decrease preload
– Dec. intravascular volume-diuretics, natrecor
– Dec venous return
• Fowlers
• MSO4 and Ntg
• Decrease afterload–
–
–
–
–
ACE (pril or ril),
ARB (sartans),
Vasodilators,
beta blockers (al or ol)
BiDil (combination drug containing isosorbide dinitrate
and hydralazine) approved only for the treatment of HF
in African Americans
Increase Contractility
• Improve cardiac function
– For patients who do not respond to conventional
pharmacotherapy (e.g., diuretics, vasodilators,
morphine sulfate)
• Inotropic therapy
– Digitalis
– -Adrenergic agonists (e.g., dopamine)
– Phosphodiesterase inhibitors (e.g., milrinone)
– Question use of calcium channel blockers
– New calcium sensitizer
– CRT
Other
• Balance supply and demand of oxygen
– Inc. O2- O2, intubate, HOB up,Legs down,
mech vent with PEEP
– Dec. demand-beta blockers, rest, dec B/P
Manage symptoms
Chronic Heart Failure
Manifestations
• FACES
–
–
–
–
–
Fatigue
Activity-limitations
Chest congestion, cough
Edema
Shortness of breath
Heart Failure- Chronic
• Overall long term goals of therapy for
ADHF and chronic HF
– Decrease patient symptoms
– Improve LV function
– Reverse ventricular remodeling
– Improve quality of life
– Decrease mortality and morbidity
PATIENT TEACHING
Joint Commission has mandated 6
areas of discharge teaching
Discharge Teaching
6 areas
•
•
•
•
•
•
Weight Monitoring
Medications
Activity
Diet
What to do if symptoms worsen
Follow-up
Weight Monitoring
• Weight reduction recommendations must be
individualized and culturally sensitive
• Same scale every day at same time
• Preferably in the morning after voiding
• Report weight gain of 3 or more pounds in
two days or 3-5 or more in 1 week.
Activity
• Instruct patient in energy-conserving and energyefficient behaviors
• Improves symptoms but often not prescribed
• Cardiac Rehab program
• Goal is 150 minutes per week
• Walking, biking, swimming or a combo is
recommended
• Nutritional therapy
Diet
– Diet and weight reduction recommendations must be
individualized and culturally sensitive
– Dietary Approaches to Stop Hypertension (DASH) diet
is recommended
• Avoid fats such as butter and margarine
• Avoid fried foods
• Read labels for hidden sodium
– Sodium is usually restricted to 2.5 g per day
• Avoid any food with more than 400mg of sodium
– Alcohol- limit women 1 drink, men 2 drinks
– Fluid restriction may or may not be required
Medications
– Medications (lifelong) diuretics, vasodilators, positive
inotropics
• Diuretics- loop, thiazides, spirinolactone (aldactone)
• Vasodilators- Ntg,
• Postive inotropics- digoxin
– Taking pulse rate
• Know when drugs (e.g., digitalis, -adrenergic
blockers) should be withheld and reported to health
care provider
• Home BP monitoring
– Signs of hypo- and hyperkalemia if taking diuretics that
deplete or spare potassium
When to call Dr.
• Symptoms worsen
–
–
–
–
–
Shortness of breath
Edema
Weight gain
Side effects of medications
Chest pain
4 Core Measures for Heart
Failure
• Discharge instructions- weight, activity,
medications, follow up and when to call dr.
• LV function is documented (EF)
• If EF less than 40% on ACE or ARB
• Smoking Cessation
Follow-up
• Frequent follow-up with physician
• Home health care may be needed
– Monitor symptoms
– Effects of medications and side effects
– Blood draws for potassium
• Other
– Stop smoking
– Flu and pneumonia vaccines
– Refer to local support group
Chronic HF
• Ways to achieve goals:
–
–
–
–
CRT
Intraaortic balloon pump (IABP) therapy
Ventricular assist devices (VADs)
Destination therapy—permanent, implantable
VAD
CRT-Cardiac Resynchronization
Therapy
HOW IT WORKS:
Standard implanted pacemakers are
equipped with two wires (or "leads")
that conduct pacing signals to specific
regions of the heart (usually at positions
A and C). The biventricular pacing
devices have added a third lead (to
position B) that is designed to conduct
signals directly into the left ventricle.
The combination of all three leads
creates a synchronized pumping of the
ventricles, increasing the efficiency of
each beat and pumping more blood on
the whole.
Non-pharmocological Therapies
cont.
• Intraaortic balloon pump (IABP)
• Ventricular assist device (VAD)
– Takes over pumping for the ventricles
– Used as a bridge to transplant
Artificial Heart
Cardiomyoplasty-wrap latissimus dorsi around heart
Ventricular reduction surgery-ventricular wall is resected
Intraaortic Balloon Pump (IABP)
• Provides temporary circulatory assistance
– Used for cardiac shock
– Allows heart fo rest
– ↓ Afterload
– Augments aortic diastolic pressure
• Outcomes
– Improved coronary blood flow
– Improved perfusion of vital organs
YouTube - IABP Intraaortic Ballon Pump
IABP
Fig. 66-14
Ventricular Assist Devices (VADs)
• Indications for VAD therapy
– Patients with New York Heart Association
Classification IV who have failed medical
therapy
LVAD
Heart Mate
http://www.clevelandclinic.org/heartcenter/
pub/guide/disease/heartfailure/lvad_devices.
htm
Cardiomyoplasty technique: the left latissimus dorsi muscle
(LDM) is transposed into the chest through a window created by
resecting the anterior segment of the 2nd rib (5 cm). The LDM is
then wrapped arround both ventricles. Sensing and pacing
electrodes are connected to an implantable cardiomyostimulator
heartnet ventricular support system
Cardiac Transplantation
Nursing Management
• Treatment of choice for patients with refractory
end-stage HF, inoperable CAD and
cardiomyopathy
– Goal of the transplant evaluation process is to
identify patients who would most benefit from a
new heart
Cardiac Transplantation
Nursing Management
• Transplant candidates are placed on a list
– Stable patients wait at home and receive
ongoing medical care
– Unstable patients may require hospitalization
for more intensive therapy
– The overall waiting period for a transplant is
long, and many patients die while waiting for a
transplant
Cardiac Transplantation
Nursing Management
• Surgery involves removing the recipient’s heart,
except for the posterior right and left atrial walls
and their venous connections
• Recipient’s heart is replaced with the donor heart
• Donor sinoatrial (SA) node is preserved so that a
sinus rhythm may be achieved postoperatively
• Immunosuppressive therapy usually begins in the
operating room
Cardiac Transplantation
Nursing Management
• Infection is the primary complication followed by
acute rejection in the first year after transplantation
• Beyond the first year, malignancy (especially
lymphoma) and coronary artery vasculopathy are
major causes of death
Cardiac Transplantation
Nursing Management
• Endomyocardial biopsies are obtained from the
right ventricle weekly for the first month, monthly
for the following 6 months, and yearly thereafter to
detect rejection
Cardiac Transplantation
Nursing Management
• Peripheral blood T lymphocyte monitoring to
assess the recipient’s immune status
• Care focuses on
–
–
–
–
Promoting patient adaptation to the transplant process
Monitoring cardiac function
Managing lifestyle changes
Providing relevant teaching
Blackboard Learning System™ (Release 6)
What’s New in Heart Failure?
(myoblasts)
Myoblasts for the Heart - Watch WebMD Video
CHF case 4
Congestive Heart Failure:
Overview
Heart failure case study
http://www.austincc.edu/adnlev4/r
nsg2331online/module04/heart_fail
ure_case_study.htm
Practice Game
http://www.quia.com/cb/107511.html
Angiotensin-converting enzyme inhibitors ,
such as captopril and enalapril, block the
conversion of angiotensin I to angiotensin II, a
vasoconstrictor that can raise BP. These drugs
alleviate heart failure symptoms by causing
vasodilation and decreasing myocardial workload.
Beta-adrenergic blockers , such as bisoprolol,
metoprolol, and carvedilol, reduce heart rate,
peripheral vasoconstriction, and myocardial
ischemia.
Diuretics prompt the kidneys to excrete sodium,
chloride, and water, reducing fluid volume. Loop
diuretics such as furosemide, bumetanide, and
torsemide are the preferred first-line diuretics
because of their efficacy in patients with and
without renal impairment. Low-dose
spironolactone may be added to a patient's
regimen if he has recent or recurrent symptoms
at rest despite therapy with ACE inhibitors, betablockers, digoxin, and diuretics.
Digoxin increases the heart's ability to contract
and improves heart failure symptoms and
exercise tolerance in patients with mild to
moderate heart failure.
Other drug options include nesiritide
(Natrecor), a preparation of human BNP that
mimics the action of endogenous BNP, causing
diuresis and vasodilation, reducing BP, and
improving cardiac output.
Intravenous (I.V.) positive inotropes such
as dobutamine, dopamine, and milrinone, as
well as vasodilators such as nitroglycerin or
nitroprusside, are used for patients who
continue to have heart failure symptoms
despite oral medications. Although these drugs
act in different ways, all are given to try to
improve cardiac function and promote diuresis
and clinical stability.
#24
• As the charge nurse in a long-term facility that has
RN,LPN and nursing assistant staff members, a plan for
ongoing assessment of all residents with a diagnosis of
heart failure has been developed. Which activity is most
appropriate to delegate to an LVN team leader?
• A. Weigh all residents with heart failure each morning
• B. Listen to lung sounds and check for edema weekly.
• C. Review all heart failure medications with residents
every month.
• D. Update activity plans for residents with heart failure
every quarter.
Please make your selection...
1.
2.
3.
4.
Choice One
Choice Two
Choice Three
Choice Four
#26
• A cardiac surgery client is being ambulated when another
staff member tells them that the client has developed a
supraventricular tachycardia with a rate of 146 beats per
minute. In what order will the nurse take these actions?
• A. Call the client’s physician.
• B. Have the client sit down.
• C. Check the client’s blood pressure.
• D. Administer oxygen by nasal cannula
#27
• The echocardiagram indicates a large thrombus in the left
atrium of a client admitted with heart failure. During the
night, the client complains of severe, sudden onset left foot
pain. It is noted that no pulse is palpable in the left foot and
that it is cold and pale. Which action should be taken next?
• A. Lower his left foot below heart level.
• B. Administer oxygen at 4L per nasal cannula.
• C. Notify the physician about the assessment data.
• D. Check the vital signs and pulse oximeter.
Please make your selection...
1.
2.
3.
4.
Choice One
Choice Two
Choice Three
Choice Four
#14
• The nurse is caring for a hospitalized client with
heart failure who is receiving captopril (Capoten)
and spironolactone (aldactone). Which lab value
will be most important to monitor?
• A. Sodium
• B. Blood urea nitrogen (BUN)
• C. Potassium
• D. Alkaline phosphatase (ALP)
Please make your selection...
1.
2.
3.
4.
Choice One
Choice Two
Choice Three
Choice Four