HEART FAILURE

a case analysis

BRIX ALVIN L. VALDRIZ

BSN 4C – GROUP 1

2021

HEART FAILURE
Definition of Heart Failure
Heart failure is the inability of the heart to pump sufficient blood to meet the needs
of the tissues for oxygen and nutrients. In the past, HF was often referred to as congestive
heart failure (CHF), because many patients experience pulmonary or peripheral congestion.
The term HF indicates myocardial disease in which there is a problem with
contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction)
that may or may not cause pulmonary or systemic congestion. The current American College
of Cardiology Foundation (ACCF)/American Heart Association (AHA) guidelines define HF as
a complex clinical syndrome that results from structural or functional impairment of
ventricular filling or ejection of blood, which in turn leads to the cardinal clinical symptoms
of dyspnea and fatigue and signs of HF, namely edema and rales.
Because many patients present without signs or symptoms of volume overload, the
term “heart failure” is preferred over the older term “congestive heart failure.”
Some cases of HF are reversible, depending on the cause. Most often, HF is a
progressive, life-long condition that is managed with lifestyle changes and medications to
prevent episodes of acute decompensated heart failure. These episodes are characterized
by an increase in symptoms, decreased CO, and low perfusion (Varughese, 2007).

Types of Heart Failure

ACUTE OR CHRONIC HEART FAILURE
Acute Heart Failure
Acute heart failure develops suddenly and symptoms are initially severe.
Acute heart failure may follow a heart attack, which has caused damage to an area
of your heart. It may also be caused by a sudden lack of ability by the body to
compensate for chronic heart failure. If you develop acute heart failure, it may be
severe initially, but may only last for a short period of time and improve rapidly. It
usually requires treatment and medication to be administered by injection
(intravenously).
Chronic Heart Failure
Chronic heart failure is very common. Symptoms appear slowly over time and
gradually get worse.

LEFT-SIDE & RIGHT SIDE HEART FAILURE

Left-Sided Heart Failure
Left-sided heart failure means that the power of the left heart chamber,
which pumps blood throughout the body, is reduced; thus, the left chamber must
work harder to pump the same amount of blood.
There are two types of left-sided heart failure:

Systolic Dysfunction

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 Systolic dysfunction (or systolic heart failure) happens when the heart muscle
doesn't contract with enough force, so there is less oxygen-rich blood pumped
throughout the body.

Diastolic Dysfunction
Diastolic dysfunction (or diastolic heart failure) happens when the heart
contracts normally, but the ventricles don’t relax properly or are stiff, and less blood
enters the heart during normal filling.

Right-Sided Heart Failure

In right-sided heart failure, the right pumping chamber or ventricle, which
pumps blood to the lungs, is compromised. This may be due to muscle injury, such as
a heart attack localized to the right ventricle, damage to the valves in the right side
of the heart or elevated pressure in the lungs.

Risk Factors
Certain conditions can predispose a patient to heart failure, especially if he has
underlying heart disease. These include:
o Arrhythmias, such as tachyarrhythmias, which can reduce ventricular filling
time; arrhythmias that disrupt the normal atrial and ventricular filling
synchrony; and bradycardia, which can reduce cardiac output
o Pregnancy and Thyrotoxicosis, which increase cardiac output
o Pulmonary Embolism, which elevates PAP, causing right-sided heart failure
o Infections, which increase metabolic demands and further burden the heart
o Anemia, which leads to increased cardiac output to meet the oxygen needs
of the tissues
o Increased physical activity, increased salt or water intake, emotional stress,
or failure to comply with the prescribed treatment regimen for the
underlying heart disease.

Pathophysiology
 HF results from a variety of cardiovascular conditions, including chronic
hypertension, coronary artery disease, and valvular disease. These conditions can
result in systolic failure, diastolic failure, or both.
 As HF develops, the body activates neurohormonal compensatory mechanisms.
These mechanisms represent the body’s attempt to cope with the HF and are
responsible for the signs and symptoms that eventually develop.
 Systolic HF results in decreased blood volume being ejected from the ventricle. The
decreased ventricular stretch is sensed by baroreceptors in the aortic and carotid
bodies. The sympathetic nervous system is then stimulated to release epinephrine
and norepinephrine. The purpose of this initial response is to increase heart rate and
contractility and support the failing myocardium, but the continued response has
multiple negative effects. Sympathetic stimulation causes vasoconstriction in the
skin, gastrointestinal tract, and kidneys.

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  A decrease in renal perfusion due to low CO and vasoconstriction then causes the
release of renin by the kidneys. Renin promotes the formation of angiotensin I, a
benign, inactive substance. Angiotensin-converting enzyme (ACE) in the lumen of
pulmonary blood vessels converts angiotensin I to angiotensin II, a potent
vasoconstrictor, which then increases the blood pressure and afterload. Angiotensin
II also stimulates the release of aldosterone from the adrenal cortex, resulting in
sodium and fluid retention by the renal tubules and stimulation of antidiuretic
hormone. These mechanisms lead to the fluid volume overload commonly seen in
HF. Angiotensin, aldosterone, and other neurohormones (eg, endothelin,
prostacyclin) lead to an increase in preload and afterload, which increases stress on
the ventricular wall, causing an increase in the workload of the heart.
 A counterregulatory mechanism is attempted through the release of natriuretic
peptides. Atrial natriuretic peptide (ANP) and B-type (ie, brain type) natriuretic
peptide (BNP) are released from the overdistended cardiac chambers. These
substances promote vasodilation and diuresis. However, their effect is usually not
strong enough to overcome the negative effects of the other mechanisms.
 As the heart’s workload increases, contractility of the myocardial muscle fibers
decreases. Decreased contractility results in an increase in end-diastolic blood
volume in the ventricle, stretching the myocardial muscle fibers and increasing the
size of the ventricle (ventricular dilation). The increased size of the ventricle further
increases the stress on the ventricular wall, adding to the workload of the heart. One
way the heart compensates for the increased workload is to increase the thickness
of the heart muscle (ventricular hypertrophy). However, hypertrophy results in an
abnormal proliferation of myocardial cells, a process known as ventricular
remodeling. Under the influence of neurohormones (eg, angiotensin II), large
myocardial cells are produced that are dysfunctional and die early, leaving the other
normal myocardial cells to struggle to maintain CO. The compensatory mechanisms
of HF have been called the “vicious cycle of HF” because the heart does not pump
sufficient blood to the body, which causes the body to stimulate the heart to work
harder; thus, the heart cannot respond and failure becomes worse.
 Diastolic HF develops because of continued increased workload on the heart, which
responds by increasing the number and size of myocardial cells (ie, ventricular
hypertrophy and altered cellular functioning). These responses cause resistance to
ventricular filling, which increases ventricular filling pressures despite a normal or
reduced blood volume. Less blood in the ventricles causes decreased CO. The low CO
and high ventricular filling pressures can cause the same neurohormonal responses
as described for systolic HF.

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Signs and Symptoms
The clinical manifestations produced by the different types of HF (systolic, diastolic,
or both) are similar and therefore do not assist in differentiating the types of HF. The signs
and symptoms of HF can be related to which ventricle is affected. Left-sided heart failure
(left ventricular failure) causes different manifestations than right-sided heart failure (right
ventricular failure). In chronic HF, patients may have signs and symptoms of both left and
right ventricular failure.
Left-Sided Heart Failure
Pulmonary congestion occurs when the left ventricle cannot effectively pump blood
out of the ventricle into the aorta and the systemic circulation. The increased left ventricular
end-diastolic blood volume increases the left ventricular end-diastolic pressure, which
decreases blood flow from the left atrium into the left ventricle during diastole. The blood
volume and pressure in the left atrium increases, which decreases blood flow from the
pulmonary vessels. Pulmonary venous blood volume and pressure increase, forcing fluid
from the pulmonary capillaries into the pulmonary tissues and alveoli, causing pulmonary
interstitial edema and impaired gas exchange.
The clinical manifestations of pulmonary congestion include dyspnea (Dyspnea, or
shortness of breath, may be precipitated by

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minimal to moderate activity (dyspnea on exertion [DOE], dyspnea also can occur at rest.),
cough (The cough associated with left ventricular failure is initially dry and nonproductive.
Most often, patients complain of a dry hacking cough that may be mislabeled as asthma or
chronic obstructive pulmonary disease (COPD). The cough may become moist over time.
Large quantities of frothy sputum, which is sometimes pink (blood-tinged), may be
produced, usually indicating severe pulmonary congestion (pulmonary edema)), pulmonary
crackles, and low oxygen saturation levels. An extra heart sound, the S3, or “ventricular
gallop,” may be detected on auscultation. It is caused by a large volume of fluid entering the
ventricle at the beginning of diastole.
Adventitious breath sounds may be heard in various areas of the lungs. Usually,
bibasilar crackles that do not clear with coughing are detected in the early phase of left
ventricular failure. As the failure worsens and pulmonary congestion increases, crackles may
be auscultated throughout all lung fields. At this point, oxygen saturation may decrease.
In addition to increased pulmonary pressures that cause decreased oxygenation, the
amount of blood ejected from the left ventricle decreases. The dominant feature in HF is
inadequate tissue perfusion. The diminished CO has widespread manifestations because not
enough blood reaches all the tissues and organs (low perfusion) to provide the necessary
oxygen. The decrease in SV can also lead to stimulation of the sympathetic nervous system,
which further impedes perfusion to many organs. A reduction in CO decreases blood flow to
the kidneys, reducing urine output (oliguria). Renal perfusion pressure falls, which results in
the release of renin from the kidney. Release of renin leads to aldosterone secretion and
increased intravascular volume. However, when the patient is sleeping, the cardiac
workload is decreased, improving renal perfusion, which in some patients leads to frequent
urination at night (nocturia). As HF progresses, decreased CO may cause other symptoms.
Decreased gastrointestinal perfusion causes altered digestion. Decreased brain perfusion
causes dizziness, lightheadedness, confusion, restlessness, and anxiety due to decreased
oxygenation and blood flow. As anxiety increases, so does dyspnea, increasing anxiety and
creating a vicious cycle. Stimulation of the sympathetic system also causes the peripheral
blood vessels to constrict, so the skin appears pale or ashen and feels cool and clammy.

Right-Sided Heart Failure

When the right ventricle fails, congestion in the peripheral tissues and the viscera
predominates. This occurs because the right side of the heart cannot eject blood and cannot
accommodate all the blood that normally returns to it from the venous circulation.
Increased venous pressure leads to JVD and increased capillary hydrostatic pressure
throughout the venous system.
The systemic clinical manifestations include edema of the lower extremities
(dependent edema), hepatomegaly (enlargement of the liver), ascites (accumulation of fluid
in the peritoneal cavity), anorexia and nausea, and weakness and weight gain due to
retention of fluid. Edema usually affects the feet and ankles and worsens when the patient
stands or sits for a long period. The edema decreases when the patient elevates the legs.
The edema can gradually progress up the legs and thighs and eventually into the external
genitalia and lower trunk. Edema in the abdomen, as evidenced by increased abdominal
girth, may be the only edema present. Sacral edema is common in patients who are on bed
rest, because the sacral area is dependent. Pitting edema, in which indentations in the skin
remain after even slight compression with the fingertips, is obvious only after retention of at
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least 4.5 kg (10 lb) of fluid (4.5 L). Hepatomegaly and tenderness in the right upper
quadrant of the abdomen result from venous engorgement of the liver. The increased
pressure may interfere with the liver’s ability to function (secondary liver dysfunction). As
hepatic dysfunction progresses, increased pressure within the portal vessels may force fluid
into the abdominal cavity, causing ascites. Ascites may increase pressure on the stomach
and intestines and cause gastrointestinal distress. Hepatomegaly may also increase pressure
on the diaphragm, causing respiratory distress. Anorexia (loss of appetite) and nausea or
abdominal pain result from the venous engorgement and venous stasis within the
abdominal organs. The weakness that accompanies right-sided HF results from reduced CO,
impaired circulation, and inadequate removal of catabolic waste products from the tissues.

Diagnostic Procedures
In ABG, it provides valuable information in assessing and managing a patient’s
respiratory (ventilation) and metabolic (renal) acid–base and electrolyte homeostasis. It is
also used to assess the adequacy of oxygenation; in chronic heart failure, respiratory
alkalosis would be present (normal: pH = 7.35 – 7.45; PCO2 = 35 – 45 mmHg; HCO3 = 22 – 26
mEq/L ; R.Alkalosis = Increased pH, Decreased PaCO2, Normal HCO3). Creatinine Clearance
is performed to measure the GFR of the kidney. With heart failure, there would be
decreased levels (Adult <40 y.o. = Male: 107–139 mL/min ; Female: 87–107 mL/min).
Galectin is a test that is helpful in determining the prognosis of congestive heart
failure. Galectin-3 (GAL-3) is a biomarker that appears to be actively involved in both the
inflammatory and fibrotic pathways involved in remodeling. Increased levels indicates heart
failure (normal: ≤22.1 ng/mL). Troponins is a test that is performed on patients with chest
pain to determine if the pain is caused by cardiac ischemia. It is a specific indicator of
cardiac muscle injury. It is also helpful in predicting the possibility of future cardiac events.
Increased levels indicates myocardial injury such as in the case of myocardial infarction
(normal: Cardiac troponin T: <0.1 ng/mL ; Cardiac troponin I: <0.03 ng/mL).
Pericardiocentesis is performed to determine the cause of an unexplained
pericardial effusion. It is also performed to relieve the intrapericardial pressure that
accumulates with a large volume of fluid and inhibits diastolic filling. In heart failure,
normally, a small amount of fluid exists within the pericardial space. Fluid is constantly
secreted and reabsorbed by the pericardium. If venous pressure of the pericardium is
increased as a result of passive congestion of the pericardium associated with congestive
heart failure, fluid will accumulate (normal: Less than 50 mL of clear, straw-colored luid
without evidence of any bacteria, blood, or malignant cells). Cardiac Nuclear Scan is used
for the evaluation of: coronary vascular disease, coronary surgery or angioplasty, chest pain.
Normally, the following results should be retrieved:
 Heterogeneous uptake radionuclide throughout the myocardium of the left ventricle
 Left ventricular end diastolic volume ≤70 mL
 Left ventricular end systolic volume ≤25 mL
 Left ventricular ejection fraction >50%
 Right ventricular ejection fraction >40%
 Normal cardiac wall motion
 No muscle wall thickening

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 But in heart failure, hypokinesia of the cardiac wall. Infarcted areas have little or no
wall motion. Paradoxical motion may be noted.

Medical Managements
The overall goals of management of HF are to relieve patient symptoms, to improve
functional status and quality of life, and to extend survival. Medical management is based
on the type, severity, and cause of HF.

Pharmacologic Managements
Angiotensin-Converting Enzyme Inhibitors
ACE inhibitors play a pivotal role in the management of systolic HF. They have been
found to relieve the signs and symptoms of HF and significantly decrease mortality and
morbidity. ACE inhibitors (eg, lisinopril [Prinivil, Zestril]) slow the progression of HF, improve
exercise tolerance, and decrease the number of hospitalizations for HF (Institute for Clinical
Systems Improvement [ICSI], 2006). ACE inhibitors are started at a low dose that is
increased
every 2 weeks until the optimal dose is achieved and the patient is hemodynamically stable.
The final maintenance dose depends on the patient’s blood pressure, fluid status, and renal
status, as well as the severity of the HF.
Angiotensin II Receptor Blockers
Although the action of ARBs is different from that of ACE inhibitors, ARBs (eg,
valsartan [Diovan]) have similar hemodynamic effects: decreased blood pressure, decreased
systemic vascular resistance, and improved cardiac output (ICSI, 2006). Whereas ACE
inhibitors block the conversion of angiotensin I to angiotensin II, ARBs block the effects of
angiotensin II at the angiotensin II receptor. ACE inhibitors and ARBs also have similar side
effects: hyperkalemia, hypotension, and renal dysfunction. ARBs are prescribed as an
alternative to ACE inhibitors, especially when patients cannot tolerate ACE inhibitors
because of cough.
Hydralazine and Isosorbide Dinitrate
A combination of hydralazine and isosorbide dinitrate may be another alternative for
patients who cannot take ACE inhibitors (Hunt, et al., 2005). Nitrates (eg, isosorbide
dinitrate) cause venous dilation, which reduces the amount of blood return to the heart and
lowers preload. Hydralazine lowers systemic vascular resistance and left ventricular
afterload. This combination of medications is also recommended in heart failure guidelines.
Beta-Blockers
Beta-blockers, such as carvedilol (Coreg) and metoprolol (Lopressor, Toprol), have
been found to reduce mortality and morbidity in patients with HF by reducing the adverse
effects from the constant stimulation of the sympathetic nervous system. Beta-blockers are
routinely prescribed in addition to ACE inhibitors, diuretics, and digitalis (ICSI, 2006). In
addition, they have been recommended for patients with asymptomatic systolic
dysfunction, such as those with a decreased EF, to prevent the onset of symptoms of HF.
Diuretics

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 Diuretics are prescribed to remove excess extracellular fluid by increasing the rate of
urine produced in patients with signs and symptoms of fluid overload. Of the types of
diuretics prescribed for patients with edema from HF, three are most common: loop,
thiazide, and aldosterone blocking (potassium-sparing) diuretics. These medications are
classified according to their site of action in the kidney and their effects on renal electrolyte
excretion and reabsorption. Loop diuretics, such as furosemide (Lasix), inhibit sodium and
chloride reabsorption mainly in the ascending loop of Henle. Patients are generally treated
with a loop diuretic first (HFSA, 2006). Thiazide diuretics, such as metolazone (Zaroxolyn),
inhibit sodium and chloride reabsorption in the early distal tubules. Both of these classes of
diuretics increase the excretion of potassium; therefore, patients treated with these
medications must have their serum potassium levels closely scrutinized. A medication from
each of these classes may be used for patients in severe HF who are unresponsive to a single
diuretic. Diuretics may be most effective if the patient assumes a supine position for 1 or 2
hours after taking them. The need for diuretics can be decreased if the patient avoids
excessive fluid intake (eg, more than 2 qt/day) and adheres to a low-sodium diet (eg, less
than 2 g/day).
Digitalis
The most commonly prescribed form of digitalis for patients with HF is digoxin
(Lanoxin). Until recently, this medication was considered an essential agent for the
treatment of HF, but with the advent of new medications, it may or may not be prescribed.
Digoxin increases the force of myocardial contraction and slows conduction through the
atrioventricular node. It improves contractility, increasing left ventricular output, which also
enhances diuresis. Although the use of digitalis does not result in decreased mortality rates
among patients with HF, it is effective in decreasing the symptoms of systolic HF and may
help prevent hospitalization (ICSI, 2006).
Calcium Channel Blockers
First-generation calcium channel blockers, such as verapamil (Calan), nifedipine
(Procardia), and diltiazem (Cardizem), are contraindicated in patients with systolic HF,
although they may be used in patients with diastolic HF (ICSI, 2006). Amlodipine (Norvasc)
and felodipine (Plendil), which are dihydropyridine calcium channel blockers, cause
vasodilation, reducing systemic vascular resistance. They may be used to improve
symptoms, especially in patients with nonischemic cardiomyopathy.
Intravenous Infusion
Nesiritide. Nesiritide (Natrecor), a BNP that is made using recombinant technology,
is indicated for patients with acute decompensated HF. BNPs are produced by the failing
myocardium to mount a compensatory response in the presence of the myocardial
demands, including increased ventricular end-diastolic pressure, myocardial wall stress, and
increased release of neurohormones (eg, norepinephrine, renin, aldosterone) that occur
with HF. Specifically, BNP binds to vascular smooth muscle and endothelial cells, causing
dilation of arteries and veins. It also suppresses the neurohormones responsible for fluid
retention, thus promoting diuresis. The result is reduced preload and afterload and
increased SV (Fontana, 2006)
Milrinone. Milrinone (Primacor) is a phosphodiesterase inhibitor that delays the
release of calcium from intracellular reservoirs and prevents the uptake of extracellular
calcium by the cells. This promotes vasodilation, resulting in decreased preload and

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afterload and reduced cardiac workload. Milrinone is administered intravenously if the
patient has not responded to other therapies. The major side effects are hypotension,
gastrointestinal dysfunction, increased ventricular dysrhythmias, and, rarely, decreased
platelet counts. Blood pressure is monitored closely during and following infusions of
milrinone.
Dobutamine. Dobutamine (Dobutrex) is an IV medication administered to patients
with significant left ventricular dysfunction and hypoperfusion. A catecholamine,
dobutamine stimulates the beta-1–adrenergic receptors. Its major action is to increase
cardiac contractility. However, at high doses, it also increases the heart rate and can
precipitate ectopic beats and tachydysrhythmias. Because it also increases atrioventricular
conduction, care must be taken in patients who have underlying atrial fibrillation. IV
inotropes such as dobutamine and milrinone are reserved for patients with severe
ventricular dysfunction, who must be monitored continuously via ECG. Some patients
require admission to the intensive care unit and hemodynamic monitoring with a pulmonary
artery catheter or impedance cardiography. A form of noninvasive monitoring, impedance
cardiography uses external electrodes placed on the chest that generate a small current
between the electrodes to assess fluid status and cardiac output (Folan & Funk, 2008).
Hemodynamic data guide therapy and assess patient response (Varughese, 2007).
Other Medical Therapies
Nutritional Therapy
A low-sodium (2 to 3 g/day) diet and avoidance of drinking excessive amounts of
fluid are usually recommended. Dietary restriction of sodium reduces fluid retention and the
symptoms of peripheral and pulmonary congestion. The purpose of sodium restriction is to
decrease the amount of circulating blood volume, which decreases myocardial work. A
balance needs to be achieved between the ability of the patient to comply with the diet and
the recommended dietary restriction. Any change in diet needs to be made with
consideration of good nutrition as well as the patient’s likes, dislikes, and cultural food
patterns. Patient compliance is important because dietary indiscretions may result in severe
exacerbations of HF requiring hospitalization (Albert, 2005). However, behavioral changes in
this area are difficult for many patients.
Oxygen Therapy
Oxygen therapy may become necessary as HF progresses. The need is based on the
degree of pulmonary congestion and resulting hypoxia. Some patients require supplemental
oxygen only during periods of activity.

Nursing Managements
Assessment
The nursing assessment for the patient with HF focuses on observing for
effectiveness of therapy and for the patient’s ability to understand and implement self-
management strategies. Signs and symptoms of pulmonary and systemic fluid overload are
recorded and reported immediately so that adjustments can be made in therapy. The nurse
also explores the patient’s emotional response to the diagnosis of HF because it is a chronic
and often progressive condition.

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 1. Health History
The health history focuses on the signs and symptoms of HF, such as dyspnea,
shortness of breath, fatigue, and edema. Sleep disturbances, particularly sleep
suddenly interrupted by shortness of breath, may be reported. Patients are
asked about the number of pillows needed for sleep, edema, abdominal
symptoms, altered mental status, activities of daily living, and the activities that
cause fatigue. The nurse explores each patient’s understanding of HF, self-
management strategies, and the ability and willingness to adhere to those
strategies. Patients are asked to identify the impact that HF has had on their
quality of life and successful coping skills that they have used. Family and
significant others are often included in these discussions.

2. Physical Examination
The lungs are auscultated to detect crackles and wheezes. Crackles are produced
by the sudden opening of edematous small airways and alveoli. They may be
heard at the end of inspiration and are not cleared with coughing. Wheezing may
also be heard in some patients. The rate and depth of respirations are also
documented. The heart is auscultated for an S3 heart sound, a sign that the heart
is beginning to fail and that increased blood volume fills the ventricle with each
beat. HR and rhythm are also documented. When the heart rate is rapid, the SV
decreases because the ventricle has less time to fill. This in turn produces
increased pressure in the atria and eventually in the pulmonary vascular bed. JVD
is also assessed; distention greater than 3 cm above the sternal angle is
considered abnormal. This is an estimate, not a precise measurement, of central
venous pressure. Sensorium and level of consciousness must be evaluated. As
the volume of blood ejected by the heart decreases, so does the amount of
oxygen transport to the brain. The nurse assesses dependent parts of the
patient’s body for perfusion and edema. With significant decreases in SV, there is
a decrease in perfusion to the periphery, causing the skin to feel cool and appear
pale or cyanotic. The feet and lower legs are examined for edema; if the patient
is supine in bed, the sacrum and back are also assessed for edema. Fingers and
hands may also become edematous. The liver is assessed for hepatojugular
reflux. The patient is asked to breathe normally while manual pressure is applied
over the right upper quadrant of the abdomen for 30 to 60 seconds. If neck vein
distention increases more than 1 cm, the finding is positive for increased venous
pressure. If the patient is hospitalized, the nurse measures urinary output
carefully to establish a baseline against which to assess the effectiveness of
diuretic therapy. Intake and output records are rigorously maintained. It is
important to know whether the patient has ingested more fluid than he or she
has excreted (positive fluid balance), which is then compared with any gain in
weight. The patient must be monitored for oliguria (diminished urine output, less
than 500 mL/24 h) or anuria (urine output less than 50 mL/24 h). The patient is
weighed daily in the hospital or at home, at the same time of day, with the same
type of clothing, and on the same scale. If there is a significant change in weight
(ie, 2- to 3-lb increase in a day or 5-lb increase in a week), the physician is
notified and medications are adjusted (eg, the diuretic dose is increased).

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 Nursing Diagnosis
 Activity intolerance and fatigue related to decreased CO
 Excess fluid volume related to the HF syndrome
 Anxiety related to breathlessness from inadequate oxygenation
 Powerlessness related to chronic illness and hospitalizations
 Ineffective therapeutic regimen management related to lack of
knowledge

Nursing Interventions
1. Promoting Activity Tolerance
Reduced physical activity caused by HF symptoms leads to physical
deconditioning that worsens the patient’s symptoms and exercise tolerance.
Prolonged bed rest, which may be self-imposed, should be avoided because of its
deconditioning effects and risks such as pressure ulcers (especially in edematous
patients), venous thrombosis, and pulmonary embolism. An acute illness that
exacerbates HF symptoms or that requires hospitalization may be an indication
for temporary bed rest. Otherwise, a total of 30 minutes of physical activity every
day should be encouraged (HFSA, 2006). Exercise training has many favorable
effects for HF, including increasing functional capacity and decreasing dyspnea.
The exercise regimen should include 5 minutes of warm-up activities followed by
about 30 minutes of exercise at the prescribed intensity level. A typical program
for a patient with HF might include a daily walking regimen, with duration
increased over a 6-week period. The physician, nurse, and patient collaborate to
develop a schedule that promotes pacing and prioritization of activities. The
schedule should alternate activities with periods of rest and avoid having two
significant energy-consuming activities occur on the same day or in immediate
succession. Before undertaking physical activity, the patient should be given the
following safety guidelines:
 Begin with a few minutes of warm-up activities.
 Avoid performing physical activities outside in extreme hot, cold, or
humid weather.
 Ensure that you are able to talk during the physical activity; if you
cannot do so, decrease the intensity of activity.
 Wait 2 hours after eating a meal before performing the physical
activity.
 Stop the activity if severe shortness of breath, pain, or dizziness
develops.
 End with cool-down activities and a cool-down period.
 Because some patients may be severely debilitated, they may need to
limit physical activities to only 3 to 5 minutes at a time, one to four times
per day. The patient should increase the duration of the activity, then the
frequency, before increasing the intensity of the activity.
 The patient’s response to activities needs to be monitored. If the patient
is hospitalized, vital signs and oxygen saturation level are monitored
before, during, and immediately after an activity to identify whether they

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 are within the desired range. HR should return to baseline within 3
minutes following the activity
2. Managing Fluid Volume
 Patients with severe HF may receive IV diuretic therapy, but patients with
less severe symptoms may receive oral diuretic medication. Oral diuretics
should be administered early in the morning so that diuresis does not
interfere with the patient’s nighttime rest.
 The patient’s fluid status is monitored closely, auscultating the lungs,
monitoring daily body weight, and assisting the patient to adhere to a
low-sodium diet by reading food labels and avoiding high-sodium foods
such as canned, processed, and convenience foods
 If the diet includes fluid restriction, the nurse can assist the patient to
plan fluid intake throughout the day while respecting the patient’s dietary
preferences.
 If the patient is receiving IV fluids, the amount of fluid needs to be
monitored closely, and the physician or pharmacist can be consulted
about the possibility of maximizing the amount of medication in the same
volume of IV fluid (eg, double concentrating to decrease the fluid volume
administered).
 The patient is positioned or taught how to assume a position that
facilitates breathing. The number of pillows may be increased, the head
of the bed may be elevated, or the patient may sit in a comfortable
armchair. In these positions, the venous return to the heart (preload) is
reduced, pulmonary congestion is alleviated, and pressure on the
diaphragm is minimized. The lower arms are supported with pillows to
eliminate the fatigue caused by the pull of the patient’s weight on the
shoulder muscles.
 Because decreased circulation in edematous areas increases the risk of
pressure ulcers, the nurse assesses for skin breakdown and institutes
preventive measures. Frequent changes of position, positioning to avoid
pressure, and leg exercises may help prevent pressure ulcers.

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