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Too pooped

to pump

Managing chronic

28 Nursing made Incredibly Easy! January/February 2006


2.5
ANCC/AACN
CONTACT HOURS

heart failure The body depends


on the heart’s
ability to circulate
blood. When the heart is damaged by illness or injury, the body marshals all
of its forces to make up for the loss of function. This article examines what
happens when heart failure overcomes the body’s ability to compensate, and
offers insights on treatments that can help fix the problem.
JANET RIGGS, RN, CCRN, CCNS, MSN
Research Project Manager for Heart Failure Clinical Trials
Department of Cardiology • Penn Presbyterian Medical Center • Philadelphia, Pa.
The author has disclosed that she has no significant relationships with or financial interest in any commercial companies that pertain to this educational activity.

BEA SINGER, age 67, awakens with a gerbreadths below the lowest right rib. Her
start from a sound sleep, gasping. She sits jugular venous pressure is 8 cm above the
up, trying to catch her breath, and shakes sternal angle.
her husband awake. “Harry! Fix my pil- Mrs. Singer’s medical history is positive
lows!” Just as he has every night for the for an anterior wall myocardial infarction
past week, he fetches three pillows and (MI) 5 years before. She’s been under treat-
arranges them behind her back to prop ment for the past 2 years for New York
her up. Then he puts a finger under her Heart Association (NYHA) Class II heart
chin and looks hard into her frightened failure. Her history is negative for smoking,
eyes. “That’s it, Bea. We’re going to the reactive airway disease, cancer, renal insuffi-
hospital.” ciency, and diabetes. Her father died of an
He’d said it before, and each time she’d MI when he was 65; her mother died of
pooh-poohed the idea, but tonight it’s differ- breast cancer 20 years ago at age 66.
ent. She can’t catch her breath even sitting So what’s behind Mrs. Singer’s increasing
up, so she lets him help her into her coat and breathlessness?
out to the car. She’s so tired she just wants to
sit down. Winding down
When she’s examined at the local hospi- Mrs. Singer presented at the ED with the
tal’s emergency department (ED), Mrs. cardinal signs of heart failure: dyspnea, fa-
Singer’s oxygen saturation (SaO2) is 89% on tigue, and fluid retention. She’s among the
room air and 95% on 3 L of nasal oxygen. growing number of patients diagnosed
Vital signs include heart rate, 116 and irregu- with the condition, which is fast becoming
lar; respirations, 42; and blood pressure, one of our most important health care is-
102/74. Lung auscultation reveals bilateral sues. Hospitalizations for heart failure are
crackles halfway up. Her first and second increasing, in part due to incomplete treat-
heart sounds (S1 and S2) are soft, and she has ment during hospitalization, poor applica-
an S3 heart sound. She has 2+ pitting edema tion of chronic heart failure management
in her legs, and her liver border is two fin- guidelines, and patient nonadherence to

January/February 2006 Nursing made Incredibly Easy! 29


No matter
what you call it,
this is killing me!

treatment recommen- or even years. Inevitably, however, signs


dations. And when and symptoms will appear and worsen
you consider that mil- without treatment.
lions of baby boomers There are different types of heart failure.
are now in their 50s and In low output heart failure, the left ventricle
60s, and more people are sur- can’t eject a normal volume of blood due to
viving longer after a heart attack, it’s easy weakness of the left ventricular muscle sec-
to see why in the next decade, the number ondary to MI or cardiomyopathy, low flow
of individuals with heart failure will con- coming from an impaired right ventricle, or
tinue to grow rapidly (see Heart failure by aortic valve stenosis. Causes of impaired
the numbers). right ventricular function include MI or an
According to the National Institutes of extrinsic insult like pulmonary hyperten-
Health, about 20% of patients with heart fail- sion.
ure will die within a year of diagnosis; two- High output heart failure occurs when the
thirds will die within 5 years. The American volume of blood exceeds what the left ven-
Heart Association (AHA) says that 80% of tricle can eject. The cardiac output remains
men and 70% of women under age 65 with high for a while, until the pressure of the
heart failure will die within 8 years. Quality high blood volume causes dilatation of the
of life is adversely affected; patients with ventricle and a backup of fluid into the pul-
heart failure are at increased risk for depres- monary interstitial spaces. Mitral valve
sion. regurgitation, aortic valve insufficiency,
In this article, I’ll discuss what’s being hyperthyroidism, anemia, and hypervolemia
done to improve these outcomes. But first from an extrinsic cause (such as excess intra-
let’s see what happens to the body in heart venous [I.V.] fluid administration) are associ-
failure. ated with high-output heart failure.
Biventricular failure can occur when back-
Get me some air! up pressures from the failing left ventricle
In heart failure, the heart can’t supply suffi- result in dilatation and failure in the right
cient quantities of blood and oxygen to ventricle.
meet the metabolic needs of the body’s tis- Another important distinction in the clas-
sues. It begins with sification of heart failure involves systolic
some type of injury dysfunction versus diastolic dysfunction.
Heart failure to the myocardium Left ventricular systolic dysfunction occurs
by the numbers that impairs the when the heart muscle is too weak to con-
In the United States, there are about 5 million
ability of the ventri- tract fully. As a result, a reduced volume of
people with heart failure, and more than cles to fill with or to blood leaves the ventricles during systolic
550,000 new cases are diagnosed each year, eject blood. This in- ejection. In normal heart function, 60% to
according to the American College of jury may result in 80% of the blood contained in the left ventri-
Cardiology/American Heart Association. Heart dilatation and/or cle is ejected with each beat; this is called the
failure prompts 12 to 15 million office visits and hypertrophy of one ejection fraction.
6.5 million hospital days each year. During the or both ventricles, a Left ventricular diastolic dysfunction occurs
last 10 years, the annual number of hospitaliza- process called re- when the left ventricle has increased dias-
tions for heart failure as a primary diagnosis modeling. Remodel- tolic stiffness (reduced compliance) and can’t
has increased to over 1 million, at a cost to
ing of the ventricles fill adequately at normal diastolic pressures.
Medicare and third-party payers of about $24.3
progresses over The elevated pressures needed for filling
billion. Around 55,000 Americans are predicted
to die of heart failure in 2006.
time; the patient cause signs and symptoms of pulmonary
may remain asymp- congestion. A person with left ventricular
tomatic for months diastolic dysfunction typically has a normal

30 Nursing made Incredibly Easy! January/February 2006


All the
world’s a
stage when
your patient
has heart
failure.
or high ejection fraction. Because the contrac- structural changes and who have or have
tility of the muscle isn’t impaired, the normal had symptoms.
amount of blood is ejected from the ventricle ■ Stage D describes patients with refrac-
with each beat. Long-standing untreated sys- tory heart failure who may need mechani-
temic hypertension causes cardiac muscle cal or pharmaceutical support, a heart
hypertrophy, which can lead to this type of transplant, or end-of-life care.
diastolic dysfunction. Patients classified as Stage A, although
Coronary artery disease is responsible for asymptomatic, are treated to reduce their
about two-thirds of all cases of heart failure. risk for developing heart failure; the goal is
The remainder of cases are characterized by to help them achieve longer survival with
nonischemic cardiomyopathy. Among the better quality.
many causes of nonischemic cardiomyopa- Next, I’ll explain the NYHA functional
thy are systemic hypertension, thyroid dys- classification system.
function, valvular heart disease, and expo-
sure to cardiotoxic substances like alcohol, New York, New York
cocaine, or chemotherapeutic agents. The ACC/AHA guideline staging sys-
Frequently, the cause is unknown; this is tem was developed to complement the
referred to as idiopathic dilated cardiomy- NYHA functional classification system,
opathy. which primarily gauges the severity of
symptoms.
On stage ■ Class I: Ordinary physical activity
Heart failure is a progressive disease. A doesn’t cause undue fatigue, dyspnea, or
widely used staging system that empha- anginal pain.
sizes the development and progression of ■ Class II: The patient has slight limita-
the disease was jointly developed by the tion of physical activity but is asympto-
American College of Cardiology (ACC) matic at rest. Ordinary physical activity
and the AHA. It classifies patients as fol- causes fatigue, palpitations, dyspnea, or
lows: anginal pain.
■ Stage A identifies patients at risk of de- ■ Class III: The patient has marked limi-
veloping heart failure who don’t have any tation of physical activity but is typically
structural heart disease or symptoms of asymptomatic at rest. Less than ordinary
heart failure. Some types of patients physical activity causes fatigue, palpita-
whom you may see with Stage A heart tions, dyspnea, or anginal pain.
failure include those with diabetes, coro- ■ Class IV: The patient can’t perform any
nary artery disease, or hypertension. level of physical activity without discom-
■ Stage B describes patients with docu- fort; symptoms may be present at rest.
mented structural changes who don’t yet Discomfort increases with physical activ-
have signs or symptoms of heart failure. ity. This patient will be considered for
Some types of patients whom you may see mechanical support, continuous pharma-
with Stage B heart failure are those with a ceutical support, transplant, or end-of-life
history of MI, those with valve regurgita- care.
tion on echocardiogram, or those with left Now, let’s see how the heart tries to make
ventricular hypertrophy on a 12-lead elec- up for its inability to pump up to par in left
trocardiogram (ECG). These patients have ventricular systolic dysfunction.
a documented structural change to their
heart, but they don’t yet demonstrate Release the vasoconstrictors!
symptoms of heart failure. Compensated heart failure occurs when
■ Stage C refers to patients who have the heart is injured (such as by an MI) or

January/February 2006 Nursing made Incredibly Easy! 31


becomes diseased (such as with viral my-
ocarditis). The body launches several com- Helping hands
pensatory mechanisms to maximize the on the Web
functioning of the heart, which has begun The American Heart Association recommends
to pump less efficiently. One of these the following organizations to help caregivers
mechanisms stimulates the sympathetic and individuals cope with chronic heart failure:
nervous system to release norepinephrine • The Mended Hearts, Inc.:
and epinephrine, increasing the heart rate http://www.mendedhearts.org
and thus improving cardiac output. Usu- • Heartmates:
ally, anytime the heart rate is increased, http://www.heartmates.com
• National Family Caregivers Association:
cardiac output will also increase, accord-
http://www.nfcacares.org
ing to the equation cardiac output = stroke
• The Well Spouse Association:
volume x heart rate.
http://www.wellspouse.org.
Another compensatory mechanism is the
activation of the renin-angiotensin-aldos-
terone system that occurs when kidney
perfusion decreases. Renin converts gland to secrete aldosterone, which acts to
angiotensinogen to angiotensin I, which is retain both sodium and water. This results in
converted into angiotensin II in the lungs by compensatory changes in the structure of the
angiotensin-converting enzyme (ACE). heart. Both the ventricles and the atria begin Up to a
Angiotensin II is a powerful vasoconstrictor. to dilate in response to the excess fluid vol- point, the
This mechanism increases fluid volume and ume. According to the Frank-Starling law of body can
maintains blood pressure. The rise in blood the heart, the increased volume (increased compensate
pressure causes increased resistance (or preload) results in greater contractility and for the
increased afterload) against ventricular ejec- greater cardiac output. heart’s
tion, eventually causing ventricular hyper- A fourth mechanism to boost low cardiac failings.
trophy. Aldosterone increases the reabsorp- output is to increase the stroke volume by
tion of sodium and water in the kidneys, increasing the amount of water in the blood-
which in turn raises blood pressure. stream. Stroke volume, simply put, is the
The increase in angiotensin II also stimu- amount of blood pumped by the left ventri-
lates the release of vasopressin, or antidiuret- cle in a single contraction.
ic hormone, from the posterior pituitary The final compensatory mechanism is the
gland. Vasopressin is another powerful release of two amino acid peptides: human
vasoconstrictor, and it promotes renal atrial natriuretic peptide (hANP) and human
release of renin. It also prevents diuresis by brain natriuretic peptide (hBNP). hANP is
altering receptors in the collecting ducts of released by stretch receptors in the atria, and
the kidneys. hBNP is released by stretch receptors in the
Endothelin 1, produced in endothelial vas- ventricles, both in response to excess blood
cular smooth muscle cells in neurons and in volume. Their purpose is to cause a loss of
endometrial cells, acts as a modulator of sodium and water via the kidneys; hBNP
vasomotor tone, cell proliferation, and hor- also provides balanced vasodilatation of
mone production. Its release is stimulated by veins, arteries, and coronary arteries,
shear stress and the presence of angiotensin which reduces the blood pressure and
II, vasopressin, and epinephrine. And—you improves blood flow through the coro-
guessed it—it’s yet another potent vasocon- nary arteries. Human BNP reduces aldos-
strictor; it stimulates growth of myocytes terone levels, which helps to promote sodi-
(beating heart cells) in heart failure. um and water excretion.
Angiotensin II stimulates the adrenal When a patient is in compensated heart

January/February 2006 Nursing made Incredibly Easy! 33


failure, all of the aforementioned mecha- may cause cool or cold, pale, and possibly
nisms work together in a balanced manner cyanotic extremities.
to maximize cardiac output. They act to Right-sided heart failure is expressed as signs
prevent signs and symptoms of decom- and symptoms caused by excessive preload
pensation. on the right side of the heart: jugular venous
Let’s examine next what happens when distention, liver engorgement, ascites, and
heart failure overpowers the compensatory peripheral edema. Both left-sided and right-
mechanisms. sided heart failure are associated with an
increase in weight.
No safety net These signs and symptoms are suggestive
Decompensated heart failure is a loss of of heart failure. Now let’s see how the diag-
balance between the mechanisms of heart nosis is made.
failure and the body’s attempts to over-
come the failure process. As a result, the Hear that?
patient begins to show the signs and The most commonly used and useful diag-
symptoms of heart failure. Heart failure nostic test for heart failure is the transtho-
can be left-sided, right-sided, or both. racic echocardiogram. It provides the most
Left-sided heart failure can be recognized by information about the structure and func-
crackles in the posterior lung fields due to tion of the heart. Coupled with Doppler
excessive preload. The patient will be tachy- flow studies, it can show atrial and/or
cardic, dyspneic, and tachypneic. She may ventricular hypertrophy, valve problems,
have a low SpO2 via pulse oximetry and whether the problem is inside the heart or
complain of having to lie propped up to in the pericardium, and when the problem
sleep. She may give occurs (during systole or diastole). The
a history of waking echocardiogram can compute ejection frac-
with paroxysmal tion and determine whether any of the
Signs and cheat nocturnal dyspnea. heart walls are failing to contract normally.
symptoms
sheet

Auscultation may Other helpful tests include 12-lead ECG,


checklist reveal an S3/S4 chest X-ray, radionuclide ventriculography,
Left-sided heart failure gallop. and magnetic resonance imaging or comput-
• Crackles (posterior lung fields) Also, low blood ed tomography. The 12-lead ECG and chest
• Tachycardia flow through the X-ray alone don’t provide adequate informa-
• Dyspnea mesenteric arteries tion to make a reliable diagnosis.
• Tachypnea may cause symp- A left heart catheterization with a ven-
• Low SpO2
toms of reduced triculogram can also provide important
• Paroxysmal noctural dyspnea
blood flow to the information about the patency of the coro-
• Gastrointestinal symptoms (anorexia, nau-
sea, bloating, constipation)
gastrointestinal nary arteries, as well as structure and func-
• Reduced urinary output tract, including tion of the left ventricle. The procedure is
• Cool or cold, pale, possibly cyanotic extrem- anorexia, nausea, invasive, however, requiring injection of a
ities bloating, and con- contrast medium into the heart. The contrast
• Weight gain stipation. Low medium is excreted through the kidneys,
Right-sided heart failure blood flow through which can cause problems in certain patients
• Jugular venous distention the renal artery with impaired renal function. Some patients
• Liver engorgement causes reduced uri- may have an adverse reaction to the contrast
• Ascites nary output. medium.
• Peripheral edema
Vasoconstriction A right heart catheterization is useful for
• Weight gain
from angiotensin II measuring the pressures in the right side of
and vasopressin the heart. This test is also invasive. It’s used

34 Nursing made Incredibly Easy! January/February 2006


mainly to evaluate pressure through the renin-angiotensin-
Drug therapy cheat the degree of heart aldosterone system, afterload may become
for heart failure
sheet
failure and to guide too high. Because ACE inhibitors are vaso-
Drugs to reduce preload therapies when the dilators, they’re used to reduce both after-
• Diuretics, such as furosemide (Lasix) presence of moder- load and preload. Beta-blockers, nitrates,
• Angiotensin-converting enzyme (ACE) ate to severe heart and hydralazine may also be used to pro-
inhibitors
failure is known or mote vasodilatation.
• Nesiritide (synthetic BNP)
suspected. Nesiritide causes balanced arterial and
Drugs to reduce afterload
Once heart failure venous dilatation, thus lowering systemic
• ACE inhibitors
• Beta-blockers is diagnosed, treat- blood pressure. The left ventricle is better
• Nitrates ment begins. Let’s able to eject the blood when the blood pres-
• Hydralazine look at what’s avail- sure comes down, which increases cardiac
• Nesiritide able. output.
• Metoprolol Nesiritide has also been shown to reduce
• Carvedilol Battling back serum levels of norepinephrine and aldos-
• Spironolactone Treatment is de- terone, indicating that it can blunt activation
• Eplerenone signed to restore of the renin-angiotensin-aldosterone system
Drugs to improve contractility
the balance be- in heart failure. Metoprolol (Lopressor), a
• Digoxin (not used as often as it once was)
tween compensa- beta-blocker, and carvedilol, a combination
• Levosimendan (still experimental)
tory and decom- of alpha- and beta-blockers, also slow activa-
pensatory mecha- tion of the renin-angiotensin-aldosterone
nisms. Here’s the system.
equation again: cardiac output = stroke vol- Spironolactone (Aldactone) acts as a
ume x heart rate. Let’s look at the treatment potassium-sparing diuretic and an aldos-
options for the three components of stroke terone antagonist; it reverses sodium and
volume, one at a time. water retention. Patients given spironolac-
• Preload—Recall that preload is the tone and an ACE inhibitor have been shown
amount of fluid in the ventricles at the end to have better ventricular function and exer-
of diastole. The first line of treatment for cise tolerance than those given an ACE
heart failure, therefore, is to reduce the pre- inhibitor alone.
load, typically with a diuretic. That usually Eplerenone (Inspra), another aldosterone
means I.V. furosemide (Lasix), which pro- antagonist, is used for patients who develop
vides a relatively quick diuresis. It’s espe- heart failure following an MI.
cially useful if the patient is in respiratory ■ Contractility—If the heart’s contractility
distress from left-sided heart failure. is strengthened, cardiac output improves.
ACE inhibitors are also used to reduce Digoxin (Lanoxin), a digitalis glycoside, in-
preload. They act as vasodilators, and they creases the strength of contractions and
promote excretion of sodium and water slows the heart rate. Although once the cor-
through the kidneys. nerstone of heart failure treatment, digoxin
Nesiritide (Natrecor), a synthetic BNP, is now used less often and at lower doses.
mimics the actions of endogenous natri- Currently, research is under way to test an
uretic peptides. It promotes diuresis by implantable device to improve cardiac con-
causing the kidneys to excrete large tractility. The device delivers a small amount
amounts of sodium and water. It works of electricity, similar to a pacemaker, to open
with furosemide to cause rapid diuresis to calcium channels in the heart muscle cells.
decrease preload. The theory behind the device is that by mak-
■ Afterload—As the body tries to compen- ing extra calcium available, the myofibrils will
sate for heart failure by raising the blood improve the strength of their contractions.

36 Nursing made Incredibly Easy! January/February 2006


The ins and outs of the heart…
To better understand stroke volume, think of the heart as a balloon that’s constantly being inflated and deflated.

Preload: Inflation Contractility: It’s a stretch Afterload: Deflation


Preload is the stretching of muscle Contractility refers to the inherent abili- Afterload refers to the pressure that the
fibers in the cardiac ventricles. It ty of the myocardium to contract nor- ventricular muscles need to exert to
reflects the end-diastolic volume, mally. It’s influenced by preload: the overcome the higher pressure in the
which is influenced by diastolic pres- greater the preload, the more forceful aorta to move blood out of the heart.
sure and the composition of the the contraction of the heart muscle. Resistance is the force the heart mus-
myocardial wall. The Frank-Starling Contractility is characterized by the cle must counteract. Afterload is deter-
principle states that the degree of pre- force and velocity of contraction; it’s mined by ventricular pressure, blood
load within a physiologic range is pro- often expressed as the ejection fraction volume in the chamber, and wall thick-
portional to the systolic performance of (left ventricular stroke volume/end- ness at the time of the aortic valve
the ensuing ventricular contraction. diastolic volume). opening.
Because ventricular function is abnor-
mal in heart failure, the response is
inadequate.

Levosimendan, a calcium sensitizer, is in a signs and symptoms. Mrs. Singer, you’ll re-
Phase III clinical trial designed to study its call, came into the ED with dyspnea, tachy-
effects on patients with class III or IV heart cardia, and tachypnea. Auscultation re-
failure. Besides providing vasodilation, it vealed crackles in the posterior lung fields
improves contractility of the heart during bilaterally and an S3 gallop. These are signs
systole and allows more normal relaxation of increased left ventricular preload. Mrs.
during diastole. Singer also displayed neck vein distention,
Now, let’s see what your role is in caring liver engorgement, and pedal edema,
for patients with heart failure. which reflect an increase in right ventricu-
lar preload.
Catch your breath Once you take vital signs on a patient like
Remember, your first considerations in car- Mrs. Singer and give her supplemental oxy-
ing for a patient in heart failure are related gen, you should weigh her. This baseline
to affecting preload adjustments. You need weight is vitally important in evaluating the
to begin by assessing the patient’s clinical effectiveness of therapies.

January/February 2006 Nursing made Incredibly Easy! 37


Medical therapies that are implemented it’s important to monitor blood pressure
early on may include an I.V. bolus dose of a closely with these drugs. The best blood
diuretic, followed perhaps by a continuous pressure is one that’s as low as the patient
infusion of diuretics, along with administra- can tolerate without getting dizzy. Continue
Remind tion of an ACE inhibitor and/or a beta- giving the vasodilator, even if the systolic
your patient blocker, as prescribed. pressure is only in the 90s. Withholding the
to lose her Position the patient for comfort. Gener- vasodilator will just allow the afterload to
salt shaker ally, the semi-Fowler’s position or seated on increase, causing cardiac output to fall. If the
when she the edge of the bed with her arms resting on systolic pressure falls below 90 and the
gets home! the over-bed table works well. Advise the patient becomes dizzy, however, therapy
patient that her daily fluid intake is limited may need to be adjusted. In the case of nesir-
to 1 to 2 liters. If she has a dry mouth, she itide, for example, the infusion should be
can relieve it by brushing her teeth and rins- stopped until the systolic pressure rises over
ing her mouth with water or mouthwash. 90. Then, the infusion can be resumed at 30%
Also, tell her that it’ll be important for her of the previous rate; no bolus is given when
nurses to keep accurate records of intake and the infusion is resumed.
output to evaluate the success of her thera-
py. During her hospital stay, she’ll likely be Mrs. Singer’s progress
put on a 2 g/day sodium diet and To evaluate the effect of her therapy, Mrs.
given recommendations for dietary Singer’s nurse in the cardiac care unit
restrictions after discharge. (CCU) takes her vital signs again and does
Next, we’ll look at interventions relat- another physical assessment. Mrs. Singer’s
ed to the effect of increased afterload. heart rate is now below 100 and her respi-
ratory rate is at 22. Within about 3 hours
Take a load off of being treated with I.V. furosemide in
To increase cardiac output in heart fail- the ED, Mrs. Singer states that she’s less
ure, afterload needs to be lowered to im- short of breath. She also received a bolus
prove stroke volume of the impaired left and infusion of nesiritide in the ED before
ventricle. Remember, afterload is the being transferred to the CCU. Her blood
amount of resistance the heart has to over- pressure is now 98/56; she denies feeling
come to eject blood from the ventricle. It’s dizzy. Her diastolic pressure indicates the
influenced by the volume and mass of wonderful afterload reduction achieved by
blood ejected, the size and wall thickness the combination of therapies.
of the ventricle, and the impedance of the The crackles in Mrs. Singer’s lung fields
vasculature. have decreased to fine bibasilar crackles.
Administration of vasodilators (nesiritide, During the next couple of days, her jugular
ACE inhibitors, beta-blockers, or hydralazine venous distention and edema are reduced.
plus nitrates) is effective, and doses can be She’s producing more urine than liquid
adjusted according to the measurements taken by mouth, and her daily weights con-
from the right heart catheter. How can you firm this: Her 24-hour intake and output
tell if the drug therapy is succeeding? Here’s level is 2 L negative, and she’s 4.4 pounds
one indicator: pulse pressure, the difference lighter.
between systolic and diastolic blood pres- Now that Mrs. Singer’s feeling better, it’s
sures. The narrower the pulse pressure, the time to start teaching her about better man-
greater the afterload. A widening pulse pres- agement of heart failure. Patient teaching
sure is associated with a decrease in after- should include medications, fluid manage-
load. ment, low-sodium diet, daily weights, and
Whether you use pulse pressure or not, the importance of regular exercise. A patient

38 Nursing made Incredibly Easy! January/February 2006


who smokes should be advised to stop. Mrs. understanding of preload and afterload
take note!
Singer should also be told to avoid using can help you to make the best clinical de- Remember that ice
nonsteroidal anti-inflammatory drugs for cisions when managing your patients with or anything frozen
pain because they may cause sodium reten- heart failure. must be counted as
tion and myocardial depression. Taking Because of the prompt and effective a liquid. Usually, the
medications as prescribed and following treatment Mrs. Singer received, she and volume of ice is esti-
strict fluid-management and sodium- Harry will be able to go on that Caribbean mated to be equal
reduction plans after discharge will greatly cruise they’ve been looking forward to for to half that of liquid
reduce the number of rehospitalizations for so long! ■ volume.
recurrence of symptoms.
Stress the importance of notifying the pri- Learn more about it
mary health provider or cardiologist imme- Adams KL. Hemodynamic assessment: The physiologic
basis for turning data into clinical information. AACN
diately after a gain of 2 pounds overnight or Clinical Issues: Advanced Practice in Acute and Critical Care.
5 pounds in a week, or after awakening sud- 15(4):534-546, October/December 2004.
denly with shortness of breath. Heart Failure Society of America. Patient education mod-
ules. http://www.abouthf.org/education_modules.htm.
Accessed November 2, 2005.
Smooth sailing Hunt SA, et al. ACC/AHA 2005 Guideline Update for the
Heart failure is a major and growing Diagnosis and Management of Chronic Heart Failure in
the Adult—Summary Article. A Report of the American
health care issue due to an aging popula- College of Cardiology/American Heart Association Task
tion, improved survival after an MI, and Force on Practice Guidelines (Writing Committee to Up-
date the 2001 Guidelines for the Evaluation and Manage-
improvements in the management of ment of Heart Failure). Journal of the American College of
chronic heart failure. Nursing care is vi- Cardiology. 46(6):1116-1143, September 2005.
tally important in all health care settings. Morrison L, et al. Utility of a rapid B-natriuretic peptide
assay in differentiating congestive heart failure from lung
It’s our job as nurses to evaluate our pa- disease in patients presenting with dyspnea. Journal of the
tients’ responses to all therapies. A good American College of Cardiology. 39(2):202-209, June 2002.

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Too pooped to pump: Managing chronic heart failure
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completed form and registration fee of $19.95 to: Lippincott Williams American Nurses Credentialing Center’s Commission on
& Wilkins, CE Group, 2710 Yorktowne Blvd., Brick, NJ 08723. We will Accreditation and by the American Association of Critical-Care Nurses
mail your certificate in 4 to 6 weeks. For faster service, include a fax (AACN 00012278, CERP Category A). This activity is also provider
number and we will fax your certificate within 2 business days of approved by the California Board of Registered Nursing, Provider
receiving your enrollment form. Deadline is February 29, 2008. Number CEP 11749 for 2.5 contact hours. LWW is also an approved
• You will receive your CE certificate of earned contact hours and an provider of CNE in Alabama, Florida, and Iowa, and holds the follow-
answer key to review your results. There is no minimum passing grade. ing provider numbers: AL #ABNP0114, FL #FBN2454, IA #75. All of
its home study activities are classified for Texas nursing continuing
DISCOUNTS and CUSTOMER SERVICE education requirements as Type 1. Your certificate is valid in all
• Send two or more tests in any nursing journal published by LWW states. This means that your certificate of earned contact hours is
together and deduct $0.95 from the price of each test. valid no matter where you live.

January/February 2006 Nursing made Incredibly Easy! 39


2.5
ANCC/AACN CONTACT HOURS

Too pooped to pump: Managing chronic heart failure


GENERAL PURPOSE: To familiarize the registered professional nurse with the pathophysiology of heart failure and appropriate
treatment and nursing care for the patient. LEARNING OBJECTIVES: After reading the article and taking this test, you should
be able to: 1. Describe the pathophysiology and signs and symptoms of heart failure. 2. Discuss the diagnosis and treatment of
heart failure.

1. Which of the following are considered the cardinal signs ripheral edema most likely has which type of heart failure?
of heart failure? a. left-sided heart failure
a. shortness of breath, hypotension, and edema b. right-sided heart failure
b. anxiety, chest pain, and diaphoresis c. biventricular heart failure
c. dyspnea, fatigue, and fluid retention
11. Which of the following is the most commonly used and
2. Which of the following best describes what happens to most useful diagnostic test for heart failure?
the body in heart failure? a. 12-lead electrocardiogram
a. The heart can’t supply sufficient quantities of blood and b. cardiac catheterization with ventriculogram
oxygen to meet the metabolic needs of the body’s tissues. c. transthoracic echocardiogram
b. The lungs can’t sufficiently oxygenate the blood, resulting in
a decreased workload to the heart. 12. The amount of fluid filling the ventricles at the end of
c. The heart muscle relaxes, resulting in an enlarged heart and diastole is called
improved pumping ability. a. preload.
b. afterload.
3. Which of the following is true about remodeling? c. stroke volume.
a. It happens quickly.
b. It results in dilation of the atria only. 13. The first-line treatment for heart failure is to reduce
c. It begins with some type of injury to the myocardium. a. preload.
b. afterload.
4. Hyperthyroidism and anemia can cause c. contractility.
a. low-output heart failure
b. high-output heart failure 14. Which of the following drugs is usually the initial treat-
c. biventricular failure ment of heart failure?
a. digoxin (Lanoxin)
5. Normal ejection fraction is b. furosemide (Lasix)
a. 40% to 55%. c. metoprolol (Lopressor)
b. 60% to 80%.
c. 85% to 95%. 15. Obtaining a baseline weight for a patient with heart
failure is most important for
6. Long-standing systemic hypertension can lead to a. assessing intake and output.
a. left ventricular diastolic dysfunction. b. indicating when the patient
b. right ventricular systolic dysfunction. needs to have afterload in- Ready? Failure
c. idiopathic dilated cardiomyopathy. creased. isn’t an option!
c. evaluating the effectiveness of
7. A patient experiences fatigue, palpitations, and dyspnea therapies.
with normal activity. Which NYHA functional class would
be assigned? 16. Administration of nesiri-
a. Class II tide results in
b. Class III a. fluid retention.
c. Class IV b. an increase in preload.
c. a decrease in preload.
8. Raising the heart rate causes the cardiac output to
a. also increase. 17. Advise your patient to
b. decrease. notify her primary care
c. stay the same. provider or cardiologist if
she
9. Which of the following is a compensatory mechanism to a. awakens at night to
maximize the functioning of the heart? urinate.
a. reduction of the stroke volume by decreasing the amount of b. loses 5 pounds in
water in the bloodstream a week.
b. stimulation of the parasympathetic nervous system c. gains 2 pounds
c. activation of the renin-angiotensin-aldosterone system overnight.

10. A patient with only jugular venous distention and pe-

Turn to page 52 for the CE Enrollment Form.

January/February 2006 Nursing made Incredibly Easy! 41