University of San Jose-Recoletos

College of Nursing
Cebu City

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A Case Study on a Patient Diagnosed with Congestive Heart Failure

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Presented to the Faculty

In Partial Fulfillment
Of the Requirements in
Related Learning Experience
(Eversley Childs Sanitarium-Medical Ward)

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Presented by

TANGCALAGAN, Kent C.
TONZO, Hope Glysdi
TUMAMUT, Yvenette Kris
UY, Justin Earl
VILLAMIL, Molly
YBAÑEZ, Ma. Doreen
BSN-III Block 8

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Presented to
Aeda Mae Siao, RN
Clinical Instructor
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April 19-23; 26-30, 2010
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I. INTRODUCTION

a) Definition of the Disease

Heart Failure often referred to as congestive heart failure
(CHF), is the inability of the heart to pump sufficient blood to meet the
needs of the tissues for oxygen and nutrients. However, the term CHF
is misleading, because it indicates that patients must experience
pulmonary or peripheral congestion to have HF, and it implies that
patients with congestion have HF. The Agency for Health Care Policy
and Research (AHCPR) HF guidelines panel (1994) defined HF as a
clinical syndrome characterized by signs and symptoms of fluid
overload or of inadequate tissue perfusion.
These signs and symptoms result when the heart is unable to
generate a CO sufficient to meet the body’s demands. The HF
guideline panel used the term heart failure because many patients
with HF do not manifest pulmonary or systemic congestion. The term
HF is preferred and indicates myocardial heart disease in which there
is a problem with contraction of the heart (systolic dysfunction) or
filling of the heart (diastolic dysfunction) and which may or may not
cause pulmonary or systemic congestion.
Some cases of HF are reversible, depending on the cause. Most
often, HF is a life-long diagnosis that is managed with lifestyle changes
and medications to prevent acute congestive episodes. CHF is usually
an acute presentation of HF.

b) Cause or Risk Factors

1. Cause
HF may result from a number of causes like cardiac compensatory
mechanisms, other dysfunctions and other disorders of the heart.
Cardiac compensatory mechanisms (increases in heart rate,
vasoconstriction, and heart enlargement) occur to assist the struggling
heart.These mechanisms are able to compensate for the heart's
inability to pump effectively and maintain sufficient blood flow to
organs and tissue at rest. Physiologic stressors that increase the
workload of the heart (exercise, infection) may cause these
mechanisms to fail and precipitate the clinical syndrome associated
with a failing heart (elevated ventricular/atrial pressures, sodium and
water retention, decreased CO, circulatory and pulmonary congestion).
The compensatory mechanisms may hasten the onset of failure
because they increase afterload and cardiac work.
Two types of dysfunction may exist with heart failure (see Figure
13-5). Systolic failure: poor contractility of the myocardium resulting in
decreased CO and a resulting increase in the systemic vascular
resistance. The increased SVR causes an increase in the afterload (the
force the left ventricle must overcome in order to eject the volume of
blood). Diastolic failure: stiff myocardium, which impairs the ability of
the left ventricle to fill up with blood. This causes an increase in
pressure in the left atrium and pulmonary vasculature causing the
pulmonary signs of heart failure.
It may also be caused by disorders of heart muscle resulting in
decreased contractile properties of the heart.
Elevated preload can be caused by incompetent valves, renal
failure, volume overload, or a congenital left-to-right shunt. Elevated
afterload occurs when the ventricles have to generate higher pressures
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in order to overcome impedance and eject their volume. This disorder

may also be referred to as an abnormal pressure load.
An elevation in afterload also may be caused by hypertension,
valvular stenosis, or hypertrophic cardiomyopathy. Myocardial
dysfunction is most often caused by coronary artery disease,
cardiomyopathy, hypertension, or valvular disorders. Atherosclerosis of
the coronary arteries is the primary cause of HF.

Coronary artery disease is found in more than 60% of the

patients with HF (Braunwald et al., 2001). Ischemia causes myocardial
dysfunction because of resulting hypoxia and acidosis from the
accumulation of lactic acid. Myocardial infarction causes focal heart
muscle necrosis, the death of heart muscle cells, and a loss of
contractility; the extent of the infarction correlates with the severity of
HF. Revascularization of the coronary artery by a percutaneous
coronary intervention or by coronary artery bypass surgery may
correct the underlying cause so that HF is resolved.
Cardiomyopathy is a disease of the myocardium. There are three
types: dilated, hypertrophic, and restrictive Dilated cardiomyopathy,
the most common type of cardiomyopathy, causes diffuse cellular
necrosis, leading to decreased contractility (systolic failure). Dilated
cardiomyopathy can be idiopathic (unknown cause), or it can result
from an inflammatory process, such as myocarditis, from pregnancy,
or from a cytotoxic agent, such as alcohol or adriamycin. Hypertrophic
cardiomyopathy and restrictive cardiomyopathy lead to decreased
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distensibility and ventricular filling (diastolic failure). Usually, HF due to

cardiomyopathy becomes chronic. However, cardiomyopathy and HF
may resolve after the end of pregnancy or with the cessation
of alcohol ingestion.
Systemic or pulmonary hypertension increases afterload
(resistance to ejection), which increases the workload of the heart and
leads to hypertrophy of myocardial muscle fibers; this can be
considered a compensatory mechanism because it increases
contractility. However, the hypertrophy may impair the heart’s ability
to fill properly during diastole.
Valvular heart disease is also a cause of HF. The valves ensure
that blood flows in one direction. With valvular dysfunction, blood has
increasing difficulty moving forward, increasing pressure within the
heart and increasing cardiac workload, leading to diastolic HF.
Several systemic conditions contribute to the development and
severity of HF, including increased metabolic rate (eg, fever,
thyrotoxicosis), iron overload (eg, from hemochromatosis), hypoxia,
and anemia (serum hematocrit less than 25%). All of these conditions
require an increase in CO to satisfy the systemic oxygen demand.
Hypoxia or anemia also may decrease the supply of oxygen to the
myocardium. Cardiac dysrhythmias may cause HF, or they may be a
result of HF; either way, the altered electrical stimulation impairs the
myocardial contraction and decreases the overall efficiency of
myocardial function. Other factors, such as acidosis (respiratory or
metabolic), electrolyte abnormalities, and antiarrhythmic medications,
can worsen the myocardial dysfunction.
Other causes include: pulmonary embolism; chronic lung disease;
hemorrhage and anemia; anesthesia and surgery; transfusions or
infusions; increased body demands (fever, infection, pregnancy,
arteriovenous fistula); drug-induced; physical and emotional stress;
and, excessive sodium intake.

2. Risk Factors

GENETIC CONSIDERATIONS
HF is a complex disease combining the actions of several genes
with environmental factors. Many HF risk factors have genetic causes
or are associated with genetic predispositions. These include
hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy
(DCM), coronary artery disease, myocardial infarction, and
hypertension. Genetic polymorphisms of the reninangiotensin-
aldosterone system (RAAS) and sympathetic system have also been
associated with susceptibility to and/or mitigation of HF. Gene variants
in the alpha-2c adrenoceptor and the alpha-1 adrenoceptor have been
associated with a higher risk of HF among African Americans.

GENDER, ETHNIC/RACIAL, AND LIFE SPAN CONSIDERATIONS

HF may occur at any age and in both genders as a result of
congenital defects, hypertension, valve disease, coronary artery
disease, or autoimmune disorders. Elderly people, however, are much
more prone to the condition because of chronic hypertension, coronary
artery disease, myocardial infarction, chronic ischemia, or valve
disease, all of which occur more frequently in the elderly population.
As compared with whites, the incidence and prevalence of HF are
higher in African Americans, Hispanic/Latinos, and Native Americans.
Compared with the general U.S. population, recent immigrants from
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nonindustrialized nations and the former Soviet republics have a

higher prevalence of HF as well. Although men and women have
similar rates of HF, women tend to have the condition later in life than
men.

OTHER RISK FACTORS

Other risk factors include: hypertension; hyperlipidemia.;
diabetes; CAD; family history; smoking; alcohol consumption; and, use
of cardiotoxic drugs.

c) Signs and Symptoms

The clinical manifestations produced by the different types of HF
(systolic, diastolic, or both) are similar (Chart 30-2) and therefore do
not assist in differentiating the types of HF. The signs and symptoms of
HF are most often described in terms of the effect on the ventricles.
Left-sided heart failure (left ventricular failure) causes different
manifestations than right-sided heart failure (right ventricular failure).
Chronic HF produces signs and symptoms of failure of both ventricles.
Although dysrhythmias (especially tachycardias, ventricular ectopic
beats, or atrioventricular [AV] and ventricular conduction defects) are
common in HF, they may also be a result of treatments used in HF (eg,
side effect of digitalis).

LEFT-SIDED HEART FAILURE

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Pulmonary congestion occurs when the left ventricle cannot

pump the blood out of the ventricle to the body. 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 rise,
forcing fluid from the pulmonary capillaries into the pulmonary tissues
and alveoli, which impairs gas exchange.
These effects of left ventricular failure have been referred to as
backward failure. The clinical manifestations of pulmonary venous
congestion include dyspnea, cough, pulmonary crackles, and lower-
than-normal oxygen saturation levels. An extra heart sound, S3, may
be detected on auscultation.
Dyspnea, or shortness of breath, may be precipitated by minimal
to moderate activity (dyspnea on exertion [DOE]); dyspnea also can
occur at rest. The patient may report orthopnea, difficulty in breathing
when lying flat. Patients with orthopnea usually prefer not to lie flat.
They may need pillows to prop themselves up in bed, or they may sit in
a chair and even sleep sitting up. Some patients have sudden attacks
of orthopnea at night, a condition known as paroxysmal nocturnal
dyspnea (PND).
Fluid that accumulated in the dependent extremities during the
day begins to be reabsorbed into the circulating blood volume when
the person lies down. Because the impaired left ventricle cannot eject
the increased circulating blood volume, the pressure in the pulmonary
circulation increases, causing further shifting of fluid into the alveoli.
The fluid filled alveoli cannot exchange oxygen and carbon dioxide.
Without sufficient oxygen, the patient experiences dyspnea and has
difficulty getting an adequate amount of sleep.
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. Large
quantities of frothy sputum, which is sometimes pink (blood tinged),
may be produced, usually indicating severe pulmonary congestion
(pulmonary edema).
Adventitious breath sounds may be heard in various lobes of the
lungs. Usually, bi-basilar 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, a decrease in
oxygen saturation may occur.
In addition to increased pulmonary pressures that cause
decreased oxygenation, the amount of blood ejected from the left
ventricle may decrease, sometimes called forward failure. 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.
Blood flow to the kidneys decreases, causing decreased
perfusion and reduced urine output (oliguria). Renal perfusion pressure
falls, which results in the release of renin from the kidney. Release of
renin leads to aldosterone secretion. Aldosterone secretion causes
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sodium and fluid retention, which further increases intravascular

volume. However, when the patient is sleeping, the cardiac workload is
decreased, improving renal perfusion, which then leads to frequent
urination at night (nocturia).
Decreased CO causes 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, enhancing 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.
The decrease in the ejected ventricular volume causes the
sympathetic nervous system to increase the heart rate (tachycardia),
often causing the patient to complain of palpitations. The pulses
become weak and thready. Without adequate CO, the body cannot
respond to increased energy demands, and the patient is easily
fatigued and has decreased activity tolerance. Fatigue also results
from the increased energy expended in breathing and the insomnia
that results from respiratory distress, coughing, and nocturia.

RIGHT-SIDED HEART FAILURE

When the right ventricle fails, congestion of the viscera and the
peripheral tissues 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. The increase in
venous pressure leads to jugular vein distention (JVD).
The clinical manifestations that ensue include edema of the
lower extremities (dependent edema), hepatomegaly (enlargement of
the liver), distended jugular veins, ascites (accumulation of fluid in the
peritoneal cavity), weakness, anorexia and nausea, and paradoxically,
weight gain due to retention of fluid.
Edema usually affects the feet and ankles, worsening when the
patient stands or dangles the legs. The swelling 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 not uncommon
for 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 (Fig. 30-2), is obvious only after
retention of at least 4.5 kg (10 lb) of fluid (4.5 liters).
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 perform (secondary
liver dysfunction). As hepatic dysfunction progresses, pressure within
the portal vessels may rise enough to force fluid into the abdominal
cavity, a condition known as ascites. This collection of fluid in the
abdominal cavity 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 results
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.
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d) Epidemiology or Statistics
UNITED STATES
As with coronary artery disease, the incidence of HF increases with
age. However, the rate of coronary artery disease is decreasing and
just the opposite is true for HF. Nearly 5 million people in the United
States have HF, with more than one-half million new cases diagnosed
each year (American Heart Association, 2001). The prevalence rate of
HF among non-Hispanic whites 20 years of age or older is 2.3% for
men and 1.5% for women; for non-Hispanic blacks, the rates are 3.5%
and 3.1%, respectively (American Heart Association, 2001). HF is the
most common reason for hospitalization of people older than age 65
and the second most common reason for visits to a physician’s office.
The rate of readmission to the hospital remains staggeringly high. The
rise in the incidence of HF reflects the increased number of elderly and
improvements in treatment of HF resulting in increased survival rates.
However, the economic burden caused by HF is estimated to be more
than 23 billion dollars in direct and indirect costs and is expected to
increase (American Heart Association, 2001). Many hospitalizations
could be prevented by improved and appropriate outpatient care.
PHILIPPINES
In the Philippines, HF is the fastest-growing cardiac disorder and it
affects 2% of the population. Almost 1 million hospital admissions
occur each year for acute decompensated HF, and the rehospitalization
rates during the 6 months following discharge are as much as 50%. In
spite of recent advances in the treatment of HF, the 5-year estimated
mortality rate is almost 50% (Department of Health, 2005).

e) Assessment Highlights
HISTORY
Patients with HF typically have a history of a precipitating factor
such as myocardial infarction, recent open heart surgery,
dysrhythmias, or hypertension. Symptoms vary based on the type and
severity of failure. Ask patients if they have experienced any of the
following: anxiety, irritability, fatigue, weakness, lethargy, mild
shortness of breath with exertion or at rest, orthopnea that requires
two or more pillows to sleep, nocturnal dyspnea, cough with frothy
sputum, nocturia, weight gain, anorexia, or nausea and vomiting. Take
a complete medication history, and determine if the patient has been
on any dietary restrictions. Determine if the patient regularly
participates in a planned exercise program.
The New York Heart Association has developed a commonly used
classification system that links the relationship between symptoms and
the amount of effort required to provoke the symptoms.
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PHYSICAL EXAMINATION
Observe the patient for mental confusion, anxiety, or irritability
caused by hypoxia. Pale or cyanotic, cool, clammy skin is a result of
poor perfusion. In rightsided HF, the jugular veins may become
engorged and distended. If the pulsations in the jugular veins are
visible 4.5 cm or more above the sternal notch with the patient at a 45-
degree angle, jugular venous distension is present. The liver may also
become engorged, and pressure on the abdomen increases pressure in
the jugular veins, causing a rise in the top of the blood column.
This positive finding for HF is known as hepatojugular reflux
(HJR). The patient may also have peripheral edema in the ankles and
feet, in the sacral area, or throughout the body. Ascites may occur as a
result of passive liver congestion.
With auscultation, inspiratory crackles or expiratory wheezes (a
result of pulmonary edema in left-sided failure) are heard in the
patient’s lungs. The patient’s vital signs may demonstrate tachypnea
or tachycardia, which occur in an attempt to compensate for the
hypoxia and decreased CO. Gallop rhythms such as an S3 or an S4,
while considered a normal finding in children and young adults, are
considered pathological in the presence of HF and occur as a result of
early rapid ventricular filling and increased resistance to ventricular
filling after atrial contraction, respectively. Murmurs may also be
present if the origin of the failure is a stenotic or incompetent valve.

PSYCHOSOCIAL
Note that experts have found that the physiological measures of HF
(such as ejection fraction) do not always predict how active, vigorous,
or positive a patient feels about his or her health; rather, a person’s
view of health is based on many factors such as social support, level of
activity, and outlook on life.

f) Diagnostic Procedures
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g) Management
The basic objectives in treating patients with HF are the
following: eliminate or reduce any etiologic contributory factors,
especially those that may be reversible, such as atrial fibrillation or
excessive alcohol ingestion; and, reduce the workload on the heart by
reducing afterload and preload.

MEDICAL MANAGEMENT
Managing the patient with HF includes providing general
counseling and education about sodium restriction, monitoring daily
weights and other signs of fluid retention, encouraging regular
exercise, and recommending avoidance of excessive fluid intake,
alcohol, and smoking. Medications are prescribed based on the
patient’s type and severity of HF. Oxygen therapy is based on the
degree of pulmonary congestion and resulting hypoxia. Some patients
may need supplemental oxygen therapy only during activity.
Others may require hospitalization and endotracheal intubation.
If the patient has underlying coronary artery disease, coronary artery
revascularization with percutaneous transluminal coronary angioplasty
(PTCA) or bypass surgery may be considered. If the patient’s condition
is unresponsive to advanced aggressive medical therapy, innovative
therapies, including mechanical assist devices and transplantation,
may be considered.
Cardiac resynchronization, involving the use of left ventricular
and biventricular pacing, is a treatment for HF with electrical
conduction defects. Left bundle branch block (LBBB) is frequently
found in patients with systolic dysfunction. LBBB occurs when the
electrical impulse, which normally depolarizes the right and left bundle
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branches at the same time, depolarizes the right bundle branch but not
the left bundle branch. The dyssynchronous electrical stimulation of
the ventricles causes the right ventricle to contract before the left
ventricle, which can lead to further decreased ejection fraction (Gerber
et al., 2001). Use of a pacing device (eg, Medtronic InSync), with leads
placed on the inner wall of the right atrium and right ventricle and on
the outer wall of the left ventricle, provides synchronized electrical
stimulation to the heart. In one study, 63% of the patients who had
received these devices showed improvement in clinical status,
including NYHA functional class and global assessment, compared with
38% of placebo patients (Abraham, 2002).

PHARMACOLOGICAL MANAGEMENT
Several medications are indicated for systolic HF. Medications for
diastolic failure depend on the underlying condition, such as
hypertension (see Chap. 32) or valvular dysfunction (see Chap. 29).
If the patient is in mild systolic failure, an ACE inhibitor usually is
prescribed. If the patient is unable to continue an ACE inhibitor (eg,
because of development of renal impairment as evidenced by elevated
serum creatinine or persistent serum potassium levels of 5.5 mEq/L or
above), an angiotensin II receptor blocker (ARB) or hydralazine and
isosorbide dinitrate are considered as part of the treatment plan. A
diuretic is added if signs of fluid overload develop. Digitalis is added to
ACE inhibitors if the symptoms continue. Although previously
contraindicated in HF, specific beta-blockers decrease mortality and
morbidity if added to the initial medications. Spironolactone, a weak
diuretic may also be added for persistent symptoms.

ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. ACE inhibitors (ACE-

Is) have a pivotal role in the management of HF due to systolic
dysfunction. They have been found to relieve the signs and symptoms
of HF and significantly decrease mortality and morbidity (when used to
treat a symptomatic patient) by inhibiting neurohormonal activation
(CONSENSUS Trial Study Group, 1987; SOLVD Investigators, 1992).
Available as oral and intravenous medications, ACE-Is promote
vasodilation and dieresis by decreasing afterload and preload. By doing
so, they decrease the workload of the heart.
Vasodilation reduces resistance to left ventricular ejection of
blood, diminishing the heart’s workload and improving ventricular
emptying. In promoting diuresis, ACE-Is decrease the secretion of
aldosterone, a hormone that causes the kidneys to retain sodium. ACE-
Is stimulate the kidneys to excrete sodium and fluid (while retaining
potassium), thereby reducing left ventricular filling pressure and
decreasing pulmonary congestion.
ACE-Is may be the first medication prescribed for patients in mild
failure—patients with fatigue or dyspnea on exertion but without signs
of fluid overload and pulmonary congestion. Results from studies
(Clement et al., 2000; NETWORK Investigators, 1998) to identify the
specific dose to achieve this effect are equivocal, although one large
study showed significant reductions in death and hospitalization with
higher doses (Packer et al., 1999). However, it is recommended to start
at a low dose and increase 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, renal status, and degree of cardiac failure.
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Patients receiving ACE-I therapy are monitored for hypotension,

hypovolemia, hyponatremia, and alterations in renal function,
especially if they are also receiving diuretics. When to observe for
these effects and for how long depends on the onset, peak, and
duration of the medication. Table 30-3 identifies several types of ACE-
Is and their pharmacokinetics. Hypotension is most likely to develop
from ACE-I therapy in patients older than age 75 and in those with a
systolic blood pressure of 100 mm Hg or less, a serum sodium level of
less than 135 mEq/L, or severe cardiac failure.
Adjusting the dose or type of diuretic in response to the patient’s
blood pressure and renal function may allow for continued increases in
the dosage of ACE-Is. Because ACE-Is cause the kidneys to retain
potassium, the patient who is also receiving a diuretic may not need to
take oral potassium supplements. However, patients receiving
potassiumsparing diuretics (which do not cause potassium loss with
diuresis) must be carefully monitored for hyperkalemia, an increased
level of potassium in the blood. Before the initiation of the ACE-I,
hyperkalemic and hypovolemic states must be corrected. ACE-Is may
be discontinued if the potassium remains above 5.0 mEq/L or if the
serum creatinine is 3.0 mg/dL and continues to increase. Other side
effects of ACE-Is include a dry, persistent cough that may not respond
to cough suppressants. However, the cough could also indicate a
worsening of ventricular function and failure. Rarely, the cough
indicates angioedema. If angioedema affects the oropharyngeal area
and impairs breathing, the ACE-I must be stopped immediately.

ANGIOTENSIN II RECEPTOR BLOCKERS (ARBS). Although their action is

different than that of ACE-Is, ARBs (eg, losartan [Cozaar]) have a
similar hemodynamic effect as ACE-Is: lowered blood pressure and
lowered systemic vascular resistance. Whereas ACE-Is block the
conversion of angiotensin I to angiotensin II, ARBs block the effects of
angiotensin II at the angiotensin II receptor. ACE-Is and ARBs also have
similar side effects: hyperkalemia, hypotension, and renal dysfunction.
ARBs are usually prescribed when patients are not able to tolerate
ACE-Is.

HYDRALAZINE AND ISOSORBIDE DINITRATE. A combination of

hydralazine (Apresoline) and isosorbide dinitrate (Dilatrate-SR, Isordil,
Sorbitrate) may be another alternative for patients who cannot take
ACE-Is. 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. It has also been shown to help avoid the development of
nitrate tolerance. As with ARBs, this combination of medications is
usually used when patients are not able to tolerate ACE-Is.

BETA-BLOCKERS. When used with ACE-Is, beta-blockers, such as

carvedilol (Coreg), metoprolol (Lopressor, Toprol), or bisoprolol
(Zebeta), have been found to reduce mortality and morbidity in NYHA
class II or III HF patients by reducing the cytotoxic effects from the
constant stimulation of the sympathetic nervous system (Beta-Blocker
Evaluation of Survival Trial [BEST] Investigators, 2001; CIBIS-II
Investigators and Committees, 1999; MERIT, 1999; Packer et al., 1996;
Packer et al., 2001). These agents have also been recommended for
patients with asymptomatic systolic dysfunction, such as after acute
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myocardial infarction or revascularization to prevent the onset of

symptoms of HF.
However, beta-blockers may also produce many side effects,
including exacerbation of HF. The side effects are most common in the
initial few weeks of treatment. The most frequent side effects are
dizziness, hypotension, and bradycardia. To minimize these side
effects, staggering the administration of the beta-blocker with the ACE-
I is recommended. Because of the side effects, betablockers are
initiated only after stabilizing the patient and ensuring a euvolemic
(normal volume) state. They are titrated slowly (every 2 weeks), with
close monitoring at each increase in dose. If the patient develops
symptoms during the titration phase, treatment options include
increasing the diuretic, reducing the dose of ACE-I, or decreasing the
dose of the beta-blocker.
An important nursing role during titration is educating the patient
about the potential worsening of symptoms during the early phase of
treatment, and that improvement may take several weeks. It is very
important that nurses provide support to patients going through this
symptom-provoking phase of treatment. Because beta-blockade can
cause bronchiole constriction, a beta1-selective beta-blocker (ie, one
that primarily blocks the beta-adrenergic receptor sites in the heart),
such as metoprolol (Lopressor, Toprol), is recommended for patients
with well-controlled, mild to moderate asthma. However, these
patients need to be monitored closely for increased asthma symptoms.
Any type of beta-blocker is contraindicated in patients with severe or
uncontrolled asthma.

DIURETICS. Diuretics are medications used to increase the rate of urine

production and the removal of excess extracellular fluid from the body.
Of the types of diuretics prescribed for patients with edema from HF,
three are most common: thiazide, loop, and 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. Thiazide diuretics, such as metolazone (Mykrox,
Zaroxolyn), inhibit sodium and chloride reabsorption mainly in the
early distal tubules. They also increase potassium and bicarbonate
excretion. Loop diuretics, such as furosemide (Lasix), inhibit sodium
and chloride reabsorption mainly in the ascending loop of Henle.
Patients with signs and symptoms of fluid overload should be started
on a diuretic, a thiazide for those with mild symptoms or a loop diuretic
for patients with more severe symptoms or with renal insufficiency
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(Brater, 1998). Both types of diuretics may be used for those in severe
HF and unresponsive to a single diuretic. These medications may not
be necessary if the patient responds to activity recommendations,
avoidance of excessive fluid intake (<2 quarts/day), and a lowsodium
diet (eg, <2 g/day).
Spironolactone (Aldactone) is a potassium-sparing diuretic that
inhibits sodium reabsorption in the late distal tubule and collecting
duct. It has been found to be effective in reducing mortality and
morbidity in NYHA class III and IV HF patients when added to ACE-Is,
loop diuretics, and digoxin. Serum creatinine and potassium levels are
monitored frequently (eg, within the first week and then every 4
weeks) when this medication is first administered. Side effects of
diuretics include electrolyte imbalances, symptomatic hypotension
(especially with overdiuresis), hyperuricemia (causing gout), and
ototoxicity. Dosages depend on the indications, patient age, clinical
signs and symptoms, and renal function. Table 30-4 lists commonly
used diuretics, dosages, and pharma cokinetic properties. Careful
patient monitoring and dose adjustments are necessary to balance the
effectiveness with the side effects of therapy. Diuretics greatly
improve the patient’s symptoms, but they do not prolong life.

DIGITALIS. The most commonly prescribed form of digitalis for patients

with HF is digoxin (Lanoxin). The medication increases the force of
myocardial contraction and slows conduction through the AV node. It
improves contractility, increasing left ventricular output. The
medication also enhances diuresis, which removes fluid and relieves
edema. The effect of a given dose of medication depends on the state
of the myocardium, electrolyte and fluid balance, and renal and
hepatic function. Although digitalis does not decrease the mortality
rate, it is effective in decreasing the symptoms of systolic HF and in
increasing the patient’s ability to perform activities of daily living
(Digitalis Investigation Group, 1997). It also has been shown to
significantly decrease hospitalization rates and emergency room visits
for NYHA class II and III HF patients (Uretsky et al., 1993).
A key concern associated with digitalis therapy is digitalis
toxicity. Chart 30-3 summarizes the actions and uses of digitalis along
with the nursing surveillance required when it is administered. The
patient is observed for the effectiveness of digitalis therapy: lessening
dyspnea and orthopnea, decrease in pulmonary crackles on
auscultation, relief of peripheral edema, weight loss, and increase in
activity tolerance. The serum potassium level is measured at intervals
because diuresis may have caused hypokalemia. The effect of digitalis
is enhanced in the presence of hypokalemia, so digitalis toxicity may
occur. Serum digoxin levels are obtained once each year or more
frequently if there have been changes in the patient’s medications,
renal function, or symptoms.

CALCIUM CHANNEL BLOCKERS. First-generation calcium channel

blockers, such as verapamil (Calan, Isoptin, Verelan), nifedipine
(Adalat, Procardia), and diltiazem (Cardizem, Dilacor, Tiazac), are
contraindicated in patients with systolic dysfunction, although they
may be used in patients with diastolic dysfunction. Amlodipine
(Norvasc) and felodipine (Plendil), dihydropyridine calcium channel
blockers, cause vasodilation, reducing systemic vascular resistance.
They may be used to improve symptoms especially in patients with
 P a g e | 15

nonischemic cardiomyopathy, although they have no effect on

mortality.

OTHER MEDICATIONS. Anticoagulants may be prescribed, especially if

the patient has a history of an embolic event or atrial fibrillation or
mural thrombus is present. Other medications such as antianginal
medications may be given to treat the underlying cause of HF.
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprophen
(Aleve, Advil, Motrin) should be avoided (Page & Henry, 2000). They
can increase systemic vascular resistance and decrease renal
perfusion, especially in the elderly. For similar reasons, use of
decongestants should be avoided.

NUTRITIONAL MANAGEMENT
 P a g e | 16

A low-sodium (≤2 to 3 g/day) diet and avoidance of excessive

amounts of fluid are usually recommended. Although it has not been
shown to affect the mortality rate, this recommendation reduces fluid
retention and the symptoms of peripheral and pulmonary congestion.
The purpose of sodium restriction is to decrease the amount of
circulating volume, which would decrease the need for the heart to
pump that volume. A balance needs to be achieved between the ability
of the patient to alter the diet and the amount of medications that are
prescribed. Any change in diet needs to be done with consideration of
good nutrition as well as the patient’s likes, dislikes, and cultural food
patterns.

SURGICAL MANAGEMENT
If the elevated preload is caused by valvular regurgitation, the
patient may require corrective surgery. Corrective surgery may also be
warranted if the elevated afterload is caused by a stenotic valve.
Another measure that may be taken to reduce afterload is an intra-
aortic balloon pump (IABP). This is generally used as a bridge to
surgery or in cardiogenic shock after acute myocardial infarction. It
involves a balloon catheter placed in the descending aorta that inflates
during diastole and deflates during systole. The balloon augments
filling of the coronary arteries during diastole and decreases afterload
during systole. IABP is used with caution because there are several
possible complications, including dissection of the aortoiliac arteries,
ischemic changes in the legs, and migration of the balloon up or down
the aorta.

OTHER MEASURES
Other measures the physician may use include supplemental
oxygen, thrombolytic therapy, percutaneous transluminal coronary
angioplasty, directional coronary atherectomy, placement of a
coronary stent, or coronary artery bypass surgery to improve oxygen
flow to the myocardium. Finally, a cardiac transplant may be
considered if other measures fail, if all other organ systems are viable,
if there is no history of other pulmonary diseases, and if the patient
does not smoke or use alcohol, is generally under 60 years of age, and
is psychologically stable.

h) Nursing Responsibilities and Preventive Measures

The nurse is responsible for administering the medications and for
assessing their beneficial and detrimental effects to the patient. It is
the balance of these effects that determines the type and dosage of
pharmacologic therapy. Nursing actions to evaluate therapeutic
effectiveness include the following:
• Keeping an intake and output record to identify a
negative balance (more output than input)
• Weighing the patient daily at the same time and on the
same scale, usually in the morning after urination; monitoring for
a 2- to 3-lb gain in a day or 5-lb gain in week
• Auscultating lung sounds at least daily to detect an
increase or decrease in pulmonary crackles
• Determining the degree of JVD
• Identifying and evaluating the severity of dependent
edema
 P a g e | 17

• Monitoring pulse rate and blood pressure, as well as

monitoring for postural hypotension and making sure that the
patient does not become hypotensive from dehydration
• Examining skin turgor and mucous membranes for signs
of dehydration
• Assessing symptoms of fluid overload (eg, orthopnea,
paroxysmal nocturnal dyspnea, and dyspnea on exertion) and
evaluating changes

MAINTAINING ADEQUATE CARDIAC OUTPUT

Place patient at physical and emotional rest to reduce work of
heart. Provide rest in semi-recumbent position or in armchair in air-
conditioned environment that reduces work of heart, increases heart
reserve, reduces BP, decreases work of respiratory muscles and
oxygen utilization, improves efficiency of heart contraction;
recumbency promotes diuresis by improving renal perfusion. Provide
bedside commode to reduce work of getting to bathroom and for
defecation. Provide for psychological rest since emotional stress
produces vasoconstriction, elevates arterial pressure, and speeds the
heart. Promote physical comfort. Avoid situations that tend to promote
anxiety and agitation. Offer careful explanations and answers to the
patient's questions.
Evaluate frequently for progression of left-sided heart failure.
Take frequent BP readings. Observe for lowering of systolic pressure.
Note narrowing of pulse pressure. Note alternating strong and weak
pulsations (pulsus alternans). Auscultate heart sounds frequently and
monitor cardiac rhythm. Note presence of S3 or S4 gallop (S3 gallop is a
significant indicator of heart failure). Monitor for premature ventricular
beats.
Observe for signs and symptoms of reduced peripheral tissue
perfusion: cool temperature of skin, facial pallor, and poor capillary
refill of nail beds. Monitor clinical response of patient with respect to
relief of symptoms (lessening dyspnea and orthopnea, decrease in
crackles, relief of peripheral edema). Watch for sudden unexpected
hypotension, which can cause myocardial ischemia and decrease
perfusion to vital organs.

IMPROVING OXYGENATION
Raise head of bed 8 to 10 inches (20 to 30 cm) reduces venous
return to heart and lungs; alleviates pulmonary congestion. Support
lower arms with pillows to eliminate pull of their weight on shoulder
muscles. Sit orthopneic patient on side of bed with feet supported by a
chair, head and arms resting on an over-the-bed table, and
lumbosacral area supported with pillows.
Auscultate lung fields at least every 4 hours for crackles and
wheezes in dependent lung fields (fluid accumulates in areas affected
by gravity). Mark with ink that does not easily rub off, the level on the
patient's back where adventitious breath sounds are heard. Use
markings for comparative assessment over time and among different
care providers. Observe for increased rate of respirations (could be
indicative of falling arterial pH). Observe for Cheyne-Stokes
respirations (may occur in elderly patients because of a decrease in
cerebral perfusion stimulating a neurogenic response). Position the
patient every 2 hours (or encourage the patient to change position
frequently) to help prevent atelectasis and pneumonia. Encourage
deep-breathing exercises every 1 to 2 hours to avoid atelectasis.
 P a g e | 18

Offer small, frequent feedings to avoid excessive gastric filling

and abdominal distention with subsequent elevation of diaphragm that
causes decrease in lung capacity. Administer oxygen as directed.

PROMOTING ACTIVITY TOLERANCE

Although prolonged bed rest and even short periods of
recumbency promote diuresis by improving renal perfusion, they also
promote decreased activity tolerance. Prolonged bed rest, which may
be selfimposed, should be avoided because of the deconditioning
effects and hazards, such as pressure ulcers (especially in edematous
patients), phlebothrombosis, and pulmonary embolism. An acute event
that causes severe symptoms or that requires hospitalization indicates
the need for initial bed rest. Otherwise, a total of 30 minutes of
physical activity three to five times each week should be encouraged
(Georgiou et al., 2001). The nurse and patient can 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 are unable to 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 perform physical activities only 3 to 5 minutes at a time, one
to four times per day. The patient then should be advised to increase
the duration of the activity, then the frequency, before increasing the
intensity of the activity (Meyer, 2001).
Barriers to performing an activity are identified, and methods of
adjusting an activity to ensure pacing but still accomplish the task are
discussed. For example, objects that need to be taken upstairs can be
put in a basket at the bottom of the stairs throughout the day. At the
end of the day, the person can carry the objects up the stairs all at
once. Likewise, the person can carry cleaning supplies around in a
basket or backpack rather than walk back and forth to obtain the
items. Vegetables can be chopped or peeled while sitting at the
kitchen table rather than standing at the kitchen counter. Small,
frequent meals decrease the amount of energy needed for digestion
while providing adequate nutrition.
The nurse helps the patient to identify peak and low periods of
energy and plan energy-consuming activities for peak periods. For
example, the person may prepare the meals for the entire day in the
morning. Pacing and prioritizing activities help maintain the patient’s
energy to allow participation in regular physical 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 are within the desired range. Heart rate should return to
 P a g e | 19

baseline within 3 minutes. If the patient is at home, the degree of

fatigue felt after the activity can be used as assessment of the
response. If the patient tolerates the activity, short-term and long-term
goals can be developed to gradually increase the intensity, duration,
and frequency of activity.
Referral to a cardiac rehabilitation program may be needed,
especially for HF patients with recent myocardial infarction, recent
open-heart surgery, or increased anxiety. A supervised program may
also benefit those who need the structured environment, significant
educational support, regular encouragement, and interpersonal
contact.

MANAGING FLUID VOLUME

Patients with severe HF may receive intravenous diuretic
therapy, but patients with less severe symptoms may receive oral
diuretic medication (see Table 30-4 for a summary of common
diuretics). Oral diuretics should be administered early in the morning
so that diuresis does not interfere with the patient’s nighttime rest.
Discussing the timing of medication administration is especially
important for patients, such as elderly people, who may have urinary
urgency or incontinence. A single dose of a diuretic may cause the
patient to excrete a large volume of fluid shortly after administration.
The nurse monitors the patient’s fluid status closely—
auscultating the lungs, monitoring daily body weights, 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 (Chart 30-4). If the diet includes fluid restriction, the
nurse can assist the patient to plan the fluid intake throughout the day
while respecting the patient’s dietary preferences. If the patient is
receiving intravenous 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
amount of intravenous fluid (eg, double-concentrating to decrease the
fluid volume administered).
The nurse positions the patient or teaches the patient how to
assume a position that shifts fluid away from the heart. The number of
pillows may be increased, the head of the bed may be elevated (20- to
30-cm [8- to 10-inch] blocks may be used), or the patient may sit in a
comfortable armchair. In this position, the venous return to the heart
(preload) is reduced, pulmonary congestion is alleviated, and
impingement of the liver on the diaphragm is minimized. The lower
arms are supported with pillows to eliminate the fatigue caused by the
constant pull of their weight on the shoulder muscles.
The patient who can breathe only in the upright position may sit
on the side of the bed with the feet supported on a chair, the head and
arms resting on an overbed table, and the lumbosacral spine
supported by a pillow. If pulmonary congestion is present, positioning
the patient in an armchair is advantageous, because this position
favors the shift of fluid away from the lungs.
Because decreased circulation in edematous areas increases the
risk of skin injury, the nurse assesses for skin breakdown and institutes
preventive measures. Frequent changes of position, positioning to
avoid pressure, the use of elastic compression stockings, and leg
exercises may help to prevent skin injury.

CONTROLLING ANXIETY
 P a g e | 20

Because patients in HF have difficulty maintaining adequate

oxygenation, they are likely to be restless and anxious and feel
overwhelmed by breathlessness. These symptoms tend to intensify at
night. Emotional stress stimulates the sympathetic nervous system,
which causes vasoconstriction, elevated arterial pressure, and
increased heart rate. This sympathetic response increases the amount
of work that the heart has to do. By decreasing anxiety, the patient’s
cardiac work also is decreased. Oxygen may be administered during an
acute event to diminish the work of breathing and to increase the
patient’s comfort.
When the patient exhibits anxiety, the nurse takes steps to
promote physical comfort and psychological support. In many cases, a
family member’s presence provides reassurance. To help decrease the
patient’s anxiety, the nurse should speak in a slow, calm, and
confident manner and maintain eye contact. When necessary, the
nurse should also state specific, brief directions for an activity.
After the patient is comfortable, the nurse can begin teaching
ways to control anxiety and to avoid anxiety-provoking situations. The
nurse explains how to use relaxation techniques and assists the patient
to identify factors that contribute to anxiety. Lack of sleep may
increase anxiety, which may prevent adequate rest. Other contributing
factors may include misinformation, lack of information, or poor
nutritional status. Promoting physical comfort, providing accurate
information, and teaching the patient to perform relaxation techniques
and to avoid anxietytriggering situations may relax the patient.
Cerebral hypoxia with superimposed carbon dioxide retention
may be a problem in HF, causing the patient to react to sedative-
hypnotic medications with confusion and increased anxiety. Hepatic
congestion may slow the liver’s metabolism of medication, leading to
toxicity. Sedative-hypnotic medications must be administered with
caution.
In cases of confusion and anxiety reactions that affect the
patient’s safety, the use of restraints should be avoided. Restraints are
likely to be resisted, and resistance inevitably increases the cardiac
workload. The patient who insists on getting out of bed at night can be
seated comfortably in an armchair. As cerebral and systemic
circulation improves, the degree of anxiety decreases, and the quality
of sleep improves.

MINIMIZING POWERLESSNESS
Patients need to recognize that they are not helpless and that
they can influence the direction of their lives and the outcomes of
treatment. The nurse assesses for factors contributing to a sense of
powerlessness and intervenes accordingly. Contributing factors may
include lack of knowledge and lack of opportunities to make decisions,
particularly if health care providers and family members behave in
maternalistic or paternalistic ways. If the patient is hospitalized,
hospital policies may promote standardization and limit the patient’s
ability to make decisions (eg, what time to have meals, take
medications, prepare for bed).
Taking time to listen actively to patients often encourages them
to express their concerns and ask questions. Other strategies include
providing the patient with decision-making opportunities, such as when
activities are to occur or where objects are to be placed, and
increasing the frequency and significance of those opportunities over
time; providing encouragement while identifying the patient’s
 P a g e | 21

progress; and assisting the patient to differentiate between factors

that can be controlled and those that cannot. In some cases, the nurse
may want to review hospital policies and standards that tend to
promote powerlessness and advocate for their elimination or change
(eg, limited visiting hours, prohibition of food from home, required
wearing of hospital gowns).

MONITORING AND MANAGING POTENTIAL COMPLICATIONS

Profuse and repeated diuresis can lead to hypokalemia (ie,
potassium depletion). Signs are weak pulse, faint heart sounds,
hypotension, muscle flabbiness, diminished deep tendon reflexes, and
generalized weakness. Hypokalemia poses new problems for the
patient with HF because it markedly weakens cardiac contractions. In
patients receiving digoxin, hypokalemia can lead to digitalis toxicity.
Digitalis toxicity and hypokalemia increase the likelihood of dangerous
dysrhythmias (see Chart 30-3). Low levels of potassium may also
indicate a low level of magnesium, which can add to the risk for
dysrhythmias. Hyperkalemia may also occur, especially with the use of
ACE-Is or ARBs and spironolactone.
The sources of sodium should be specified in describing the
regimen, rather than simply saying “low-salt” or “saltfree,” and the
quantity should be indicated in milligrams. Salt is not 100% sodium;
there are 393 mg of sodium in 1 g (1000 mg) of salt.
To reduce the risk for hypokalemia, the nurse advises patients to
increase their dietary intake of potassium. Dried apricots, bananas,
beets, figs, orange or tomato juice, peaches, and prunes (dried plums),
potatoes, raisins, spinach, squash, and watermelon are good dietary
sources of potassium. An oral potassium supplement (potassium
chloride) may also be prescribed for patients receiving diuretic
medications. If the patient is at risk for hyperkalemia, the nurse
advises the patient to avoid the above products, including salt
substitutes.
Grapefruit (fresh and juice) is a good dietary source of potassium
but has serious drug–food interactions. Patients are advised to consult
their physician or pharmacist before including grapefruit in their diet.
Periodic assessment of the patient’s electrolyte levels will alert
health team members to hypokalemia, hypomagnesemia, and
hyponatremia. Serum levels are assessed frequently when the patient
starts diuretic therapy and then usually every 3 to 12 months. It is
important to remember that serum potassium levels do not always
indicate the total amount of potassium within the body.
Prolonged diuretic therapy may also produce hyponatremia
(deficiency of sodium in the blood), which results in apprehension,
weakness, fatigue, malaise, muscle cramps and twitching, and a rapid,
thready pulse.
Other problems associated with diuretic administration are
hyperuricemia (excessive uric acid in the blood), volume depletion
from excessive urination, and hyperglycemia.

PROMOTING HOME AND COMMUNITY-BASED CARE

The nurse provides patient education and involves the patient in
implementing the therapeutic regimen to promote understanding and
adherence to the plan. When the patient understands or believes that
the diagnosis of HF can be successfully managed with lifestyle changes
and medications, recurrences of acute HF lessen, unnecessary
hospitalizations decrease, and life expectancy increases. Patients and
 P a g e | 22

their families need to be taught to follow the medication regimen as

prescribed, maintain a low-sodium diet, perform and record daily
weights, engage in routine physical activity, and recognize symptoms
that indicate worsening HF.
Although noncompliance is not well understood, interventions
that may promote adherence include teaching to ensure accurate
understanding. A summary of teaching points for the patient with HF is
presented in Chart 30-5.
The patient and family members are supported and encouraged
to ask questions so that information can be clarified and understanding
enhanced. The nurse should be aware of cultural factors and adapt the
teaching plan accordingly. Patients and their families need to be
informed that the progression of the disease is influenced in part by
choices made about health care and the decisions about following the
treatment plan. They also need to be informed that health care
providers are there to assist them in reaching their health care goals.
Patients and family members need to make the decisions about the
treatment plan, but they also need to understand the possible
outcomes of those decisions. The treatment plan then will be based on
what the patient wants, not just what the physician or other health
care team members think is needed. Ultimately, the nurse needs to
convey that monitoring symptoms and daily weights, restricting
sodium intake, avoiding excess fluids, preventing infection with
influenza and pneumococcal immunizations, avoiding noxious agents
(eg, alcohol, tobacco), and participating in regular exercise all aid in
preventing exacerbations of HF.
 P a g e | 23

II. OBJECTIVES
a) General
After 1-3 hours of case presentation in the medical ward, the
students will be able to develop and apply specific knowledge,
skills and attitude on the disease process of Congestive Heart
Failure generally on the body; anticipate and provide effective
nursing care; and, deliver specific interventions needed to treat the
disease.

b) Specific
1. Nurse-Centered Objectives

Upon completion of this case study, the student nurse should be able to:
a) Make a thorough assessment about the patient’s personal history,
family background and lifestyle
b) Cite factors that contribute to the patient’s condition.
c) Review the anatomy and physiology of the integumentary system.
d) Explain the histopathology and pathogenesis of Congestive Heart
Failure.
e) Make a comprehensive nursing care plan and its intervention.
f) Impart knowledge to the patient regarding on his condition
g) Evaluate patient’s response towards rendered care given by the
student nurse.

2.Patient-Centered Objectives

Upon completion of this case study, the Guest should be able to:
a) Establish rapport and trusting relationship with the student nurse.
b) Give information about self, family and past experiences.
c) Cooperate on management prepared by the student nurse.
d) Verbalize feelings and thoughts of his present condition.
e) Understand awareness of his disorder.
f) Know the possible causes of the disorder.
g) Learn and understand why such laboratory examinations are being
done.
h) Apply the learned self-care measures to improve well-being.
 P a g e | 24

III. Health History

a) Client Profile
A case of Patient MR, 33 years old, female, married, Filipino
citizen, a Roman Catholic, housewife and presently living in Paknaan,
Mandaue City was assessed last April 23, 2010 by 4:30am at the
Evvesley Childs Sanitarium (Female Medical ward). Client was admitted
last April 19, 2010 at around 12:00 a.m via Taxi accompanied by her
eldest son with admitting complaints of shortness of breath, dizziness
and fatigue. Admitting V/S is as follows: T-37.9; PR-92; RR-25; BP-
200/160. She's under the care of Dr. Lagora. Patient was transferred to
the Female Medical Ward at 4:10 am of the same day. Patient claimed
to be hypertensive but not diabetic or asthmatic. Patient is neither a
smoker nor an alcoholic beverage drinker. She has no known allergies
to drug as well as to foods; but, since she has a heart problem, she ate
less on restricted foods high in cholesterol.

b) Past Medical History

Patient disclosed that she has received the following
immunizations: BCG 1 and 2, DPT 1, 2 and 3, OPV 1, 2 and 3, Anti
Hepa-B 1, 2 and 3, TT1, 2, 3, 4 and 5. Patient is currently having 3
children. Upon her 2nd child, she was admitted to the hospital last year
2001 for 4 days in Eversley Child's Sanitarium under unrecalled doctor
and was diagnosed with Pre-eclampsia. She was also unable to recall
the specific medications she took that time. Patient MR was then
adviced by the doctor not to have another child but then was not
followed since she had her 3rd child in the year 2007 and was confined
for 3 consecutive days in Vicente Sotto Memorial Medical Center under
the Service of unrecalled Doctor. The patient was diagnosed with
Eclampsia with a BP of 180/120mmHg which was her usual BP
measurement for her current illness. She was only able to remember
Nefidipine as her medication.

c) History of Present Illness

Prior to admission the patient was experiencing dizziness, headache
and fatigue. She then sought for medical assistance in Mandaue
District and had a BP of 200/160mmHg. Due to lack of financial
support, the patient was unable to comply the necessary medications
and decided to stay at home for care. Two days prior to admission, the
patient experienced symptoms of shortness of breath. On April 17,
2010, Patient MR manifested symptoms of on and off moderate grade
fever, and gradually coughing episodes were noted.

d) Developmental History
According to Sigmund Freud Psychosexual Stage, Patient MR is in
the Genital phase. This stage represents the major portion of life, and
the basic task for the individual is the detachment from the parents.
Patient is already living with her own family. In this stage the focus on
the genitals, the energy is expressed with adult sexuality. Patient
claimed to be sexually active. The ego in the genital stage is well-
 P a g e | 25

developed, and so uses secondary process thinking, which allows

symbolic gratification. Patient MR expressed symbolic gratification that
includes the formation of love relationships and families, or acceptance
of responsibilities associated with adulthood.
In Erik Erikson's psychosocial Stages of development, Patient MR
belongs to Generativity vs. Stagnation wherein it concerns of
establishing and guiding the next generation. Socially-valued work and
disciplines are expressions of generativity as well as contributing to
society and helping future generations. Patient is already raising a
family and verbalized her hopes on working towards the betterment of
society, a sense of generativity- a sense of productivity and
accomplishment.
According to kohlberg's Theory of Moral Development, Patient
MR is in the Postconventional Morality wherein people begin to account
for the differing values, opinions, and beliefs of other people. Rules of
law are important for maintaining a society, but members of the
society should agree upon these standards. Patient considers values of
honesty, hardwork and nurturing as important values on being a
mother and a wife to her family.
In Fowler's stages of faith development, patient belongs to the
4th stage of "Individuative-Reflective" faith (usually mid-twenties to
late thirties) a stage of angst and struggle. The patient took personal
responsibility for her beliefs and feelings. She expressed her faith to
God that despite her situation and that she still believes that God will
heal her from her illness.

e) Environmental History
Patient MR is currently residing in Paknaan Mandaue City Cebu.
She together with her family with three children are living in a rented
house and lot nearby the street side which is made out of mixed
materials. They have two bedrooms, a dining area and a living room.
Their toilet is a manual flush type, they have electricity and have their
own water source. Patient MR disposes their garbage through garbage
trucks which collects their trash during Mondays and Thursdays. They
use plastic bags and old barrels for garbage containers. They have one
dog and a cat as their pet. The patient claimed that there is no
difficulty in seeking healthcare because of the distance from the health
center is not that far approximately 5km. Patient MR also has no
problems with going to Church and to the market which is only 2km
away from their house. Patient MR has a quiet type of personality but
though such, she can still manage to talk to some friends and mingle
with her neighbors from time to time.
 P a g e | 26

IV. Marjorie Gordon’s Functional Health Patterns

1. Health Perception/ Health Management

Patient MR defines health as “panglawas”. She scaled her health 6 out
of 10. Her perception of her health was in sync with reality. She was
aware of the fact that she was “pretty sick” when she came in to the
hospital. She was very independent and did not like to be waited on. Her
past medical history was concise as presented previously. She wanted to
see a health care provider each time she feels ill but not realized due to
financial restraints. She exercised by walking or swimming daily and was
very careful about what she ate. She was visibly weak, and was unable
to perform all of her ADL’s without assistance. She was not well oriented
with knowledgeable and medications of her disease. She once practiced
drinking “mangagaw” when she experience fever. She was not well
educated about her CHF and the dietary restrictions it imposed.

2. Nutritional/ Metabolic
PTA, the patient’s usual diet from breakfast, lunch and dinner is
composed of rice, side dish of fish in varied preparation, vegetables and
meat. She can consume 7-9 glasses a day.
During admission, Patient’s current dietary status is DAT. She reported
during on her 24-hour diet recall that she had been eating a cup of
coffee and bread for breakfast, a cup of rice and fish for lunch, and a cup
of rice and a vegetable soup for dinner. She was not aware of the effects
of an increase in sodium and fat intake to her CHF. She stated that she
did not take vitamin supplements because they are expensive. She
reported adequate fluid intake, drinking 1-2 cups of coffee daily and
along with two 5-7 glasses of water. She had recently experienced a 5-8
lb weight gain as a result of her CHF. She did not report any changes in
appetite or difficulty chewing but have difficulty swallowing. Her diet
restrictions were low sodium and low fat because of her CHF and cardiac
history. She reported experiencing occasional nausea and loose stools.
She was 5’6” and 165 pounds. Her prescribed diet was a cardiac diet.
She had no enteral feeding or NG tube, and her IV was 500mL D5W
running at 10ggts/min.

3. Elimination
Prior to admission, patient experiences 1-2 bowel movements per day
and usually voids 4-5 times a day with estimates 200ml per urination.
During admission, the patient was fully functional in the elimination
pattern. She reported urinating three to four times daily with no
difficulty and no recent change in her urinary pattern. She had a bowel
movement the day of our interview, and reported moving her bowels
daily, sometimes twice. She denied changes in this pattern. Her fluid
balance was improving, with an intake total of 200 mL and an output
total of 500 mL in the entire shift. Her urine was clear and yellow, and
her abdomen was soft with active bowel sounds in all four quadrants.
She was fully continent with experience profuse sweating.
 P a g e | 27

4. Activity/ Exercise
Prior to admission, patient complains about her low stamina. She can’t
tolerate strenuous activities. Her ADL includes washing clothes, doing
household chores and cleaning the backyard. As a past time she
watches television with her children during late afternoon.
During admission, Patient was weak and needs assistive devices. She
reported don’t have sufficient energy to perform activities due to
fatigue. She reported feeling shortness of breath, fatigue, and
palpitations related to her CHF. She reported exercising daily by walking
or swimming, and doing her household chores. She needed assistance
with her ADL’s and to keep herself well groomed. She had a limited
range of motion and her tone and strength were symmetrical in all
extremities. She had a steady gait. Her respiratory rate was 28 with
normal, symmetrical breaths. O2 was placed through nasal cannula
regulated at 4 L. She had fine inspiratory and expiratory crackles
posteriorly througout. Her apical pulse was 70 and irregular due to a-fib,
and her BP was 119/59. She had +2 strength radial pulses and +1
strength pedal pulses. Her capillary refill was less than 3 seconds and
her extremities were warm and pink. Risk for falls is the main nursing
diagnosis in this health pattern due to fatigue.

5. Sleep/ Rest
PTA, patient has an approximately 3-4 hours of sleep. Client usually
wakes at 6am. Client’s problemof the very small number of hours of
sleep is due to nocturnal paroxysmal dyspnea. Patient sometimes have
short naps in the afternoon.
During admission, she reported sleeping about 4 hours per night and
feeling well rested during the day. She reported having occasional
difficulty falling asleep for which she sometimes used milk as sleeping
aid. She took occasional naps after her walk or during soap operas in the
afternoon. She did exhibit lethargy and irritability and during night times
due to SOB and nocturnal paroxysmal dyspnea. Her diagnosis in this
area is risk for disturbed sleep pattern related to difficulty falling asleep
at night.

6. Cognitive/ Perceptual
Patient can decode simple instructions such as advising her to change
her position or clothes. She was functional in this health pattern. She
had no real visual difficulties other than wearing glasses and no hearing
problems. She reported occasional difficulty with her short term
memory; things like word and name recall. She said that the easiest way
for her to learn things is to do them herself and she did not like being
waited on. She did not report any numbness, tingling or pain in her
extremities. She was at some risk for impaired short term memory
related to her age.
Client is not able to read the text of the calendar and writings from
chart half a meter away. The client has difficulty to follow the pen placed
 P a g e | 28

in the six cardinal gazes and sometimes have involuntary movements.

Client is unable to hear and comprehend sentences during the test,
whispered pectoriloquy. Client can’t hear whispers a foot away and
can’t hear distinct conversation 2 meters away. Client has difficulty
distinguishing smell (perfume, alcohol). Client can distinguish blunt and
sharp areas at the bottom of the pen; hot (rubbed hand) or cold (mineral
water bottle) objects and location of touch in the distinct parts of the
body. Client is able to taste familiar flavors (sugar, salt, iced tea,
vinegar) as verbalized.
She can read and write as verbalized by SO. She can reply
appropriately to questions during conversation. Client is dependent in
the decision-making process. Client has a clear but weak speech. Client
expresses that she can learn better through visual aids and experience.
Client demonstrates nonverbal communication congruent to verbal
communication. Client relays messages with consistency and exhibit
agreement and disagreement of statements. Her primary language was
“Bisaya” and she had a high school degree.

7. Sexuality/ Reproductive
Client has an obstetric history of G3P3. Client has an irregular
menstrual cycle with menses appearing once in two-three months. She
was noted menarche at the age of 13. The client speaks of single
partner sexual contact to date. Client experienced sexual contact with
husband at the age of 22 y.o. with her husband. She stated that her
sexual relationship with her husband was satisfying, and that sexual
intercourse had been limited for a while due to dypnea during strenuous
activity. The client uses contraceptives such as pills from 2005-2008.
She verbalizes that sexual activity should be in the context of marriage.
Client expresses no concern, abuse or problems regarding illness and
sexual patterns. She uses 3-4 napkin pads per day. Thelarche began at
10 years of age. Menarche was experienced during 13 years of age.
Client verbalizes no history of sexually related illnesses or problems is
currently in UTI. The client is not aware of the importance of self breast
examination; and, consents that she never performed it.

8. Self-Perception/ Self-Concept
Her recent job is a factory worker. She currently was retired. She
described herself as determined and stubborn and said she liked to do
things herself and ask for help if she needed it. She stated the feeling of
emptiness sometimes. She said that her recent illness had not changed
her self image and that it had only motivated her to get better. She said
she felt angry/annoyed when she was not in control and experienced
occasional heart palpitations when she felt anxious or fearful. Her
children and grandchildren had been challenging for her recently, and
she reported feeling depressed when she couldn’t help them out with
their various issues in life. She said that she sometimes feels weak; she
was powerless or had lost hope. She had excellent eye contact and
conversational skills.
 P a g e | 29

9. Role-Relationship Pattern
She was fully functional in this pattern. She was married and lived with
her husband, and they had three daughters. She reported that they had
no financial concerns. She said that she turns to her older daughter for
support. She was very assertive and noticed everything that went on
during her hospital stay. She was not afraid to point out when she felt
something was not right or could be improved.
 P a g e | 30

Three Generation Genogram

 P a g e | 31

10. Coping and Stress Tolerance

Her family situation and illness was the major stressor in her life. She
said that she just tries “to get through it.” She reported relieving stress
by going for a walk or talking to her daughter and friends. She said that
she felt relaxed when she have someone to share to. In this area, her
diagnosis is readiness for enhanced family coping related to the
situation with her mother and children as evidenced by desire to solve
their problems.

11. Values and Belief

Patient was fully functional in this health pattern as well. She said
that in general, she gets the things she wants from life. She was Catholic
and stated that her religion was important to her. She practiced by
praying and reading the bible. When I asked her about her beliefs about
health and illness, she said, “magkasakit ang tanang taw”. Patient sees
respect as the most important value in life. Her source of strength is her
family and God. Every time she experiences decision making process,
she consults her husband as her second opinion.
 P a g e | 32

V. Physical Assessment

GENERAL APPEARANCE:
Patient seen lying on bed, awake, alert, responsive, coherent, afebrile,
with venoclysis of # 3 D5 Water, infusing well at right hand with the
following vital signs: T- 38 C, BP – 180/90, PR – 98 bpm, RR – 28 cpm

Head
Head is rounded with smooth skull contour. Nodules and masses
are absent. Hair is evenly distributed, black in color, and with smooth
texture. Facial feature is symmetric, palpebral fissures equal in size
and symmetric nasolabial folds. Facial movements are symmetric.

Eyes
Hair in eyebrow is evenly distributed, skin is intact,
symmetrically aligned, moves equally. Eyelashes are equally
distributed, curled slightly outward. Skin are intact on eyelids, absence
of discharge, and no discoloration. Lids close symmetrically. When lids
open, no visible sclera above corneas, and upper and lower borders of
cornea are slightly covered. Conjunctiva is transparent, capillaries are
evident, and sclera is white. Palpebral conjunctiva is shiny, smooth and
pink in color. Lacrimal gland has no edema and no tenderness. Cornea
is transparent, shiny and smooth. Patient blinks when the cornea is
touched. Pupils are black in color, equal in size, round, and smooth. Iris
is flat and round. Patient can see objects in the periphery. Both eyes
are coordinated, moves in unison with parallel alignment. Light
reflection appears at symmetric spots in both eyes.

Ears
Color is the same as the face. Position is symmetric. Auricles are
mobile, firm and not tender. Pinna recoils after it is folded. Tympanic
membrane is pearly gray in color and semitransparent. Cerumen is wet
and brown in color. Both ears can hear normal voice tones.

Nose
Symmetric and straight, no discharge or flaring. No tenderness
noted and lesions are absent. Air moves freely as the patient breath
through the nares. The mucosa of the nasal cavities is pink with clear
watery discharge. Lesions are absent. Nasal septum is intact and in
midline. Facial sinuses are not tender, well outlined, contain air and
light up equally.

Mouth and Oropharynx

Lips are uniform in pink color, soft, moist, smooth texture;
contour is symmetrical and has the ability to purse lips. Buccal mucosa
is uniform in pink color, moist, smooth, soft, glistening and elastic
texture. The patient has 25 teeth with smooth, yellowish and shiny
tooth enamel. Gums have no retractions, firm, moist and pink in color.
Tongue is centrally located, pink in color, moist, slightly rough and with
 P a g e | 33

thin whitish coating. Tongue moves freely without tenderness. Bse of

the tongue is smooth with prominent veins. Salivary glands has the
same color with the buccal mucosa and floor of the mouth. Uvula is
light pink and smooth. Hard palate is lighter pink and has more
irregular texture. Oropharynx is pink and has a smooth posterior wall.
Tonsils are pink and smooth, no discharge.

Neck
Neck muscles are equal in size and head is centered. Head
movement is coordinated with smooth motion without discomfort.
Nodes are not palpable on the entire neck. Trachea is centrally placed
in midline of the neck with space equal on both sides. Thyroid gland is
not visible upon inspection. Gland ascends upon telling the patient to
swallow but is not visible. Gag reflex is present.

Thorax and Lungs

Patient has barrel chest. Spinal alignment is vertical. Posterior
thorax has intact skin and has uniform temperature. Chest wall is
intact, no tenderness and masses are absent. Expansion on posterior
chest is evident. Crackles and wheezing heard upon auscultation on
the chest. Cough is productive. Rapid breathing is noted and use of
accessory muscles when breathing.

Heart
Pulsations are absent on the aortic and pulmonic areas.
Pulsations are present on the tricuspid area. Upon auscultation of the
heart on the aortic, pulmonic, tricuspid and apical, intensity is
increased. S3 is present.

Peripheral Vascular System

Pulse volumes on periphery are symmetric. Carotid arteries have
also symmetric pulse volumes. Pulsations are decreased. Jugular veins
are absent. When limbs were elevated, veins collapse. Limbs are not
tender and symmetric in size. Skin color is pink. Skin temperature is
not excessively warm or cold. No edema was noted. Skin texture is
resilient and moist.

Abdomen
Skin is unblemished on the abdomen, uniform in color, rounded,
and no evidence of enlargement of liver or spleen. The contour of
abdomen with reference to the foot is symmetric. Movement of the
abdomen while breathing is symmetric. Upon palpation, no tenderness
was noted with consistent tension. Liver is not palpable and border
feels smooth. Bladder is not palpable.

Musculoskeletal System
Muscle size is equal on both sides of the body. No contractures
were noted on the tendons and muscles. Upon palpation, muscles at
rest are atonic (lacking firm). Patient has slow, coordinated
 P a g e | 34

movements. Upon palpation of the bone, tenderness or swelling was

not noted. Bones have no deformities. Joints have no swelling, no
tenderness, swelling or nodules upon palpation.

MENTAL STATUS

Level of Consciousness
Patient is awake, alert and responds to verbal stimuli. She can
respond to questions simultaneously. Speaks clearly and uses
appropriate words. Patient can able to comprehend questions and
directions.

Awareness
Patient is oriented to time, place, and person by tactful
questioning. Patient was asked of the time of the day, the date and
names of family members.

Thought Process
Patient can recall three digit numbers that was asked to repeat.
She can still recall the things she has done within the day. Patient can
still recall information given earlier such as the name of the student
nurse. Patient is able to answer questions that need simple abstract
thinking. She can be able to perform simple mathematical calculations
and problem solving. Patient has sound judgment and can be able to
express her decisions and interests.

Communicating Process
Patient is able to use verbal and nonverbal communication such
as facial expression and hand gestures. She is able to use appropriate
affect and mood and able to use appropriate words when
communicating. Patient communicates in a an average page with
proper choice of words.

CRANIAL NERVE FUNCTION

Cranial Nerve I
Patient is able to identify the smell of alcohol and perfume.

Cranial Nerve II
Patient can see the periphery when one eye is covered. Snellen chart
was not used in the assessment.

Cranial Nerve III

Patient can follow the six ocular movements and pupil reaction when
light has been used in testing for PERRLA.

Cranial Nerve IV
 P a g e | 35

Patient is positive to six ocular movements.

Cranial Nerve V
Patient’s blink reflex is positive through the use of cotton in touching
the sclera. Alternating blunt and sharp ends over client’s forehead
showed positive result.

Cranial Nerve VI
Eyes equally move, eyeballs move laterally.

Cranial Nerve VII

Patient is able to perform facial expression as assessed. She can also
identify sweet and sour taste.

Cranial Nerve VIII

Patient is able to hear words that were spoken to her and can hear
audible sounds through the use of alternative device in assessing
hearing of the patient.

Cranial Nerve IX
Swallowing ability is present and gag reflex. Patient is able to move her
tongue freely side to side and up to down.

Cranial Nerve X
Client’s speech has no hoarseness. Vibration on vocal chord is felt
upon palpation. Swallowing is also present.

Cranial Nerve XI
Head can extend to front, back and sides. Patient can shrug shoulder
against resistance from hand.

Cranial Nerve XII

Patient can move tongue from side to side and can protrude it.

CEREBELLAR / MOTOR FUNCTION

Assessment on gross motor function is deferred. Patient was able to
squeeze fingers, make fist, able to perform finger to nose test, alternating
supine and pronation of hand on lap, finger to nose and to nurse’s fingers,
finger to fingers and fingers to thumb.

SENSORY FUNCTION
Patient is able to react on light and touch sensation. Patient is able to
discriminate between sharp and dull sensation. She can able to determine
one poin and two point objects being used. Patient can also discriminate
between hot and cold temperature. Patient can recognize objects being
placed on hands. She can also identify numbers and letters written on palm.
P a g e | 36
 P a g e | 37

VI. Significant Laboratory Findings and Diagnostic

Procedures

Date Normal Range

Ordered
Diagnostic or
and Date Patient’s Analysis and Interpretation
Laboratory
Results Results of Results
Procedure
were Male Female
released

HEMATOLOGY
Hemoglobin 04-20- 140- 120- 117 g/L A decrease implies
10 180 160 anemia, recent
g/L g/L hemorrhage and fluid
retention
Hematocrit 04-20- 0.42- 0.37- 0.35 g/L A decrease implies
10 0.52 0.47 anemia and
g/L g/L hemodilution
RBC 04-20- 4.7- 4.2- 4.4 /L A decreaseimplies
10 6.1 5.4 anemia and fluid
/L /L overload of >24 hours
WBC 04-20- 5-10 x /L 8.8 x /L Within normal range
10
Differential Count
Neutrophils 04-20- 40-74 % 84 % An increase implies
10 asthma, hay fever,
parasitic infections,
chronic myelocytic
leukemia, Hodgkin’s
disease and metastasis
Lymphocyt 04-20- 19-48 % 12 % A decrease implies no
es 10 significant
interpretation
Monocyte 04-20- 3-9 % 2% A decrease implies no
10 significant
interpretation
Eosinophil 04-20- 0-7 % 2% Within normal range
10
Basophil 04-20- 0-2 % 0% Withn normal range
10
URINE CHEMISTRY
Color 04-20- Straw to dark Dark Normal Result
10 yellow Yellow
Appearance 04-20- Clear Cloudy Turbity implies kidney
10 infection
Specific 04-20- Newborns: 1- 1.030 An increase implies
Gravity 10 1.02 nephritic syndrome
Infants: 1.002-
1.006
Adults: 1.016-
 P a g e | 38

1.022
pH 04-20- 4.6-6.5 5.0 Within normal range
10
Protein 04-20- None (++) Presence implies
10 proteinuria, renal failure
or myeloma
Glucose 04-20- Negative Negative Normal result
10
RBC 04-20- 0 /hpf 0-2 2-4 /hpf Within maximum
10 /hpf normal range.
WBC 04-20- 0-2 0-5 10-12 /hpf An increase implies
10 /hpf /hpf trauma or tumors
Casts 04-20- Hyaline, Coarsely Normal result
10 coarse. granular.
Fine granular. 1-2 /hpf
RBC, WBC.
Waxy casts
Amorphous 04-20- Small amounts Few Normal result
Materials 10
Epithelial 04-20- Small amounts Few Normal result
Cells 10
Bacteria 04-20- None Many Presence implies GUT
10 infection or
contamination of
external genitalia

Other Procedures:

X-ray 04/20/10
Conclusion: Bilateral Pleural Effusion predominantly at the left.

Electrocardiograph 04/20/10
10 mm/ mV 25 mm/s
HF:DF HR=112 bpm
 P a g e | 39

VII. Summary of Significant Findings

FINDINGS ACTUAL NURSING POTENTIAL/ RISK

DIAGNOSES NURSING DIAGNOSES
a. Marjorie Activity intolerance
Gordon’s related to imbalance
Functional between oxygen supply
health Patterns and demand

Anxiety related to
breathlessness and
restlessness from
inadequate oxygenation

Powerlessness related to
inability to perform role
responsibilities secondary
to chronic illness and
hospitalization.
b. Physical Ineffective airway
Assessment clearance related to
presence of
tracheobronchial
obstruction

Decreased Cardiac
Output related to
impaired contractility
and increased preload
and afterload.

Excess fluid volume

related to excess fluid or
sodium intake and
retention of fluid
secondary to heart
failure and its medical
therapy
c. Laboratory and Impaired gas
Diagnostic Tests exchange related to
alveolar edema due to
elevated ventricular
pressure secondary to
pleural effusion
 P a g e | 40

VIII. Anatomy and Physiology

THE HEART

THE HEART WALLS

 P a g e | 41

THE HEART CHAMBERS AND VALVES

THE CONDUCTION SYSTEM OF THE HEART

 P a g e | 42

THE CIRCULATORY SYSTEM

The Heart
The heart is located in the thoracic cavity in the mediastinum, between the
lungs and deep to the sternum.
• Base – broad superior portion of the heart which is the point of
attachment for the great vessels
• Apex – inferior end that tapers to a blunt point immediately above the
diaphragm
The adult heart is about 9 cm wide at the base, 13 cm from base
to apex and 6 cm from anterior to posterior at its thickest point –
roughly size of one’s fist. Its weight is 300 g.
• Pericardium – a double-walled sac that encloses the heart
Parts:
- Parietal Pericardium – outer wall with thick superficial fibrous
layer and thin serous layer.
 P a g e | 43

- Visceral Pericardium – covers the heart surface.

The Heart Wall

• Epicardium – serous membrane on the heart surface consisting of
squamous epithelium overlying a thin layer of adipose tissue. It is
where the largest branch of coronary blood vessel travel
through.
• Endocardium – lines the interior of the heart chambers. It is a simple
squamous endothelium overlying a thin areolar tissue layer. It
covers the valve surfaces and is continuous with the endothelium
of the blood vessels.
• Myocardium – the layer between the epicardium and the endocardium.
It is the thickest and performs the work of the heart.

The Chambers
• Right and Left Atria – the thin- walled receiving chambers for blood
returning to the heart by way of the great veins. Each atrium has
a small earlike extension called auricle that slightly increases its
volume.
• Right and Left Ventricles – the pumps that eject blood into the arteries
And keep it flowing around the body. The right ventricle
constitutes most of the anterior aspect of the heart, while the left
ventricle forms the apex and inferoposterior aspect.

Sulci (grooves) – boundaries on the surface of the four chambers of the heart
Namely:
 Coronary Sulcus – encircles the heart near the base and
separates the atria above the ventricles below.
 Anterior Intraventricular Sulcus – extends obliquely down the
heart from the coronary sulcus toward the apex at the front
 Posterior Intraventricular Sulcus - extends obliquely down the
heart from the coronary sulcus toward the apex at the back

Thin flaccid walls that are exhibited by the atria:

 Interatrial Septum – separates both atria
 Intraventricular Septum – much more vesicular

The Valves
 Atrioventricular (AV) Valves – regulate the openings between the atria
and the ventricles
 Semilunar Valves – regulate the flow of blood from the ventricles into
the great arteries
 Pulmonary Valve – controls the opening from the right ventricle into
the pulmonary trunk
 Aortic Valve - controls the opening from the left ventricle into the
aorta

Blood Flow through the Chambers

 P a g e | 44

Blood returns to the heart through the two large veins, the superior
vena cava draining the head, neck, upper limbs and thoracic cavity, and the
inferior vena cava draining the abdominal cavity and lower limbs. Blood in
the right atrium flows through the right AV valve and into the right ventricle.
When the right ventricle contracts, the AV valve closes and blood is
forced through the pulmonary valve into the pulmonary trunk. This artery
ascends from the heart front of the heart and branches into the right and left
pulmonary arteries, which lead to the respective lungs. In the lungs, this
blood unloads its carbon dioxide and picks up a load of oxygen.
The oxygen-enriched blood returns by way of several veins which
converge to form four pulmonary veins by the time they reach heart. These
four empty into the left atrium. Blood flows from there past the left valve into
the left ventricle. The left ventricle contracts at the same time as the right,
and expels blood through the aortic valve into the ascending aorta. Blood in
the aorta flows to every organ in the body, unloading some of its O2 from the
tissues, and returning to the heart via the vena cavae.

The Conduction System

1. Sinoatrial Node – the pacemaker of the heart that initiates each
heartbeat and determines the heart rate.
2. Atrioventricular Node – acts as an electrical gateway to the
ventricles;the fibrous skeleton acts as an insulator to prevent currents
from getting to the ventricle by another route.
3. Atrioventricular Bundle – forks into the right and left bundle branches,
which enter the interventricular septum and descend toward the apex.
4. Purkinje Fibers – distribute the electrical excitation to the myocytes of
the ventricles. They form more elaborate networks in the left ventricle
than in the right.

Cardiac cycle is the term referring to all or any of the events related to the
flow or blood pressure that occurs from the beginning of one heartbeat to
the beginning of the next.
Heart Rate - the frequency of the cardiac cycle
Five Stages of 'beat' of the heart:
1. "Late diastole" which is when the semilunar valves close, the AV Valves
open and the whole heart is relaxed. Second,
2. "Atrial systole" when atria is contracting, AV valves open and blood
flows from atrium to the ventricle.
3. "Isovolumic ventricular contraction" it is when the ventricles begin to
contract, AV valves close, as well as the semilunar valves and there is
no change in volume.
4. "ventricular ejection", Ventricles are empty, they are still contracting
and the semilunar valves are open.
5. "Isovolumic ventricular relaxation", Pressure decreases, no blood is
entering the ventricles, ventricles stop contracting and begin to relax,
semilunars are shut because blood in the aorta is pushing them shut.
 P a g e | 45

Throughout the cardiac cycle, the blood pressure increases and

decreases. The cardiac cycle is coordinated by a series of electrical
impulses that are produced by specialized heart cells found within the
sino-atrial node and the atrioventricular node. The cardiac muscle is
composed of myocytes which initiate their own contraction without help of
external nerves (with the exception of modifying the heart rate due to
metabolic demand). Under normal circumstances, each cycle takes
approximately one second.

Myocyte (also known as a muscle cell) is the type of cell found in muscles.
They arise from myoblasts. Each myocyte contains myofibrils, which are
long chains of sarcomeres, the contractile units of the cell.

Stroke volume (SV) is the volume of blood pumped from one ventricle of
the heart with each beat. It is calculated by subtracting the volume of
blood in the ventricle at the end of a beat (called end-systolic volume)
from the volume of blood just prior to the beat (called end-diastolic
volume). This applies equally to both left and right ventricles of the heart.
These two stroke volumes are generally equal, both approximately 70 ml
in a healthy 70-kg man.

Stroke volume is an important determinant of cardiac output, which is the

product of stroke volume and heart rate. Because stroke volume
decreases in certain conditions and disease states, stroke volume itself
correlates with cardiac function.
 P a g e | 46

IX. Pathophsiology (Left Sided Heart Failure)

AGENT
HOST
GENES
Inappropriate Restricted Decreased
*Genetic methods placed filling on myocyte
Myocyte
predisposition on on the heart the heart loss contractility
hypertrophic
cardiomyopathy
(HCM) and dilated Decreased Decreased Increased
Systolic WHEN SLEEPING
relaxation elastic stiffness of the
cardiomyopathy dysfunction
Reduced Nocturnal recoil ventricle
(DCM), coronary Decreased adrenergic depression of
artery disease, stroke volume support of the respiratory Diastolic
myocardial ventricular center dysfunction
Decreased
function
infarction, and cardiac output
Increased left Rapid filling in
hypertension ventricular end- early diastole
* Genetic diastolic pressure S3, apical impulse is
hypertrophy Increased Increased
polymorphisms of catecholamine preload S4 displaced laterally
Paroxysmal
the release nocturnal Increased pulmonary
reninangiotensin- breathing
capillary pressure
Increased Increased Increased
aldosterone system
ventricular heart rate contraction of
(RAAS) and volume sarcomeres Air in lungs Pulmonary
edema
sympathetic system replaced by blood/
Increased strokeinterstitial fluid
have also been Small airway Rales
volume Stimulates
associated with juxta- obstruction
susceptibility to Increased end- capillary I
wheezing

and/or mitigation of diastolic pressure receptors

Reflex shallow
HF
and rapid
* Gene variants in Left-sided HF
breathing
the alpha-2c
adrenoceptor and Reduction in vital capacity Restrictive physiology Air trapping
the alpha-1
adrenoceptor Work of breathing increases
RACE
Respiratory Dyspnea
* African Americans muscle fatigue
* Hispanic/Latinos
* Native Americans Ventilation/ Perfusion mismatch
*Soviet Republics
AGE Peripheral Decreased Underper-Reduced blood Inability of the Reduced renal
vascons- perfusion of fusion of pooling in the heart to supply perfusion
*Elderly people
triction the heart the extremities appropriate during the day
OTHERS cerebrum and abdomen amounts of blood to
*hypertension Ischemia Confusion skeletal muscles
*hyperlipidemia Shortness of breath, Fatigue
orthopnea
* diabetes Decreased Sweating Fluid retention Normal
O2 in during the day
perfusion at
*CAD
venous night
LIFESTYLE
blood Nocturia
*smoking Skin appears
*alcohol dusky

consumption
*Use of cardiotoxic Right-sided HF
drugs
ENVIRONMENT
 P a g e | 47

Pathophsiology (Right Sided Heart Failure)

AGENT
HOST
GENES Pulmonary HTN Cor Pulmonale
*Genetic
predisposition on Right Ventricular Pressure > Left Ventricular Pressure
hypertrophic Interventricular septum bows to the left
cardiomyopathy
Prevent efficient filling of the left ventricle
(HCM) and dilated
Pulmonary congestion
cardiomyopathy
(DCM), coronary Partial obstruction of the left ventricular outflow
artery disease, Left-Sided HF
myocardial
infarction, and Increased Destruction of Hypoxia-induced Sequela to Right
hypertension afterload on the pulmonary vasoconstriction of thepulmonary ventricular
* Genetic right ventricle capillary bed pulmonary arteries disease ischemia

polymorphisms of
the Systolic Decreased Decreased Decreased Increased
reninangiotensin- dysfunction ventricular relaxation elastic stiffness of the
function recoil ventricle
aldosterone system Decreased
(RAAS) and stroke volume
Diastolic
sympathetic system Decreased dysfunction
have also been cardiac output
Increased right
associated with
ventricular end-
susceptibility to hypertrophy Increased Increased Increased diastole pressure
and/or mitigation of catecholamine preload right-sided
Congestion of
HF release Increased atrial pressure
pressure hepatic veins
* Gene variants in
the alpha-2c Increased Increased Increased
Accumulation Expansion of Impinge
ventricular heart rate contraction of
adrenoceptor and of fluid in the the liver normal
volume sarcomeres diaphragm-
the alpha-1 systemic
matic
adrenoceptor Increased stroke venous
circulation function
RACE volume
dyspnea
* African Americans Venous Distention of
liver capsule
* Hispanic/Latinos congestion
Anasarca, ascites,
* Native Americans RUQ pain
dependent edema
*Soviet Republics
AGE
*Elderly people Right-Sided HF
OTHERS
*hypertension
*hyperlipidemia
* diabetes
*CAD
LIFESTYLE
*smoking
*alcohol
consumption
*Use of cardiotoxic
drugs
ENVIRONMENT

X. Nursing Care Plans
DATE ACTIVE PROBLEM
April 22, 2010 Impaired gas exchange related to
alveolar edema due to elevated
ventricular pressures
Subjective cue:
“Maglisod jud ko'g ginhawa”,as
verbalized by the patient
Objective cue:
>restlessness
>irritability
>diaphoresis
>bilateral crackles that do not
clear with cough
>pale skin color
Scientific Analysis:
Dyspnea, or shortness of
breath, may be precipitated by
minimal to moderate activity
(dyspnea on exertion [DOE]);
dyspnea also can occur at rest.
The patient may report
orthopnea, difficulty in breathing
when lying flat. Patients with
NURSING INTERVENTIONS
Independent:
1. R: Monitor vital signs and cardiac
rhythm
I: for baseline data and monitoring
2. R: Auscultate breath sounds,
I: notes areas of
decreased/adventitious breath
sounds
3. R:Note character and
effectiveness of cough mechanism
I: ability to clear airways of
secretions
4. R: Elevate head of bed, provide
adjuncts and suction, as indicated
I: to maintain airway
5. R: Encourage frequent position
changes and deep-
breathing/coughing exercises. Use
incentive spirometer, chest
physiotherapy, as indicated
I: promotes chest expansion and
drainage of secretions
6. R: Maintain adequate I/O
I: for mobilization of secretions
7. R: Encourage adequate rest and
P a g e | 48
EVALUATION
Desired Outcome:
After 8 hours of nursing
intervention, the patient was
able to demonstrate improved
ventilation and adequate
oxygenation of tissues by ABGs
within patient's normal limits
and absence of symptoms of
respiratory distress
Actual Outcome:
After 8 hours of nursing
intervention, the objectives
were partially met. The patient
was able to improved
ventilation and
oxygenation of tissues as
evidenced by patient breathing
without using much of the
accessory muscle

orthopnea usually prefer not to
lie flat. They may need pillows to
prop themselves up in bed, or
they may sit in a chair and even
sleep sitting up. Some patients
have sudden attacks of
orthopnea at night, a condition
known as paroxysmal nocturnal
dyspnea (PND).
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. Large quantities of frothy
sputum, which is sometimes pink
(blood tinged), may be produced,
usually indicating severe
pulmonary congestion
(pulmonary edema).
Adventitious breath sounds
may be heard in various lobes of
the lungs. Usually, bi-basilar
crackles that do not clear with
coughing are detected in the
early phase of left ventricular
P a g e | 49
limit activities to within client
tolerance.
I: Promote calm/restful environment
helps limit oxygen need/consumption
8. R: Keep environment
allergen/pollutant free
I: to reduce irritant effect of dust and
chemicals on airway
9. R: Provide psychological support,
active-listen questions/concerns
I: to reduce anxiety
Dependent:
1. R: Administer medications, as
indicated
I: to treat underlying conditions
Source: Source: Sparks, S and
Taylor, C, Nursing Diagnosis
Reference Manual 3rd edition;
Springhouse Corporation,
Pennsylvannia

failure. As the failure worsens and
pulmonary congestion increases,
crackles may be auscultated
throughout all lung fields. At this
point, a decrease in oxygen
saturation may occur
(Wolkenstein, 2000).
April 22, 2010 Decreased Cardiac Output
related to impaired contractility
and increased preload and
afterload.
Subjective cue:
“Sige ra jud kog pangluspad”,as
verbalized by the patient
Objective cue:
>restlessness
>irritability
>diaphoresis
>pale skin color
Scientific Analysis:
In addition to increased
pulmonary pressures that cause
decreased oxygenation, the
amount of blood ejected from the
left ventricle may decrease,
Independent:
1. R: Place patient at physical and
emotional rest
I: to reduce work of heart.
2. R: Provide rest in semi-recumbent
position or in armchair in air-
conditioned environment
I: that reduces work of heart,
increases heart reserve, reduces BP,
decreases work of respiratory
muscles and oxygen utilization,
improves efficiency of heart
contraction; recumbency promotes
diuresis by improving renal perfusion
3. R:Provide bedside commode
I: to reduce work of getting to
bathroom and for defecation.
4. R: Provide for psychological rest
since emotional stress produces
vasoconstriction.
I:elevates arterial pressure, and
P a g e | 50
Desired Outcome:
After 8 hours of nursing
intervention, the patient was
able to demonstrate improved
cardiac output within normal
levels of preload and afterload.
Actual Outcome:
After 8 hours of nursing
intervention, the objectives
were partially met. The patient
was able to initiate actions to
increase cardiac output but
symptoms persisted.

sometimes called forward failure.
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.
Blood flow to the kidneys
decreases, causing decreased
perfusion and reduced urine
output (oliguria). Renal perfusion
pressure falls, which results in
the release of renin from the
kidney. Release of renin leads to
aldosterone secretion.
Aldosterone secretion causes
sodium and fluid retention, which
further increases intravascular
volume. However, when the
patient is sleeping, the cardiac
workload is decreased, improving
renal perfusion, which then leads
to frequent urination at night
(nocturia).
Decreased CO causes other
P a g e | 51
speeds the heart.
5. R: Promote physical comfort. Avoid
situations that tend to promote
anxiety and agitation. Offer careful
explanations and answers to the
patient's questions.
I: Decreases anxiety
6. R: Take frequent BP readings.
Observe for lowering of systolic
pressure. Note narrowing of pulse
pressure. Note alternating strong and
weak pulsations (pulsus alternans).
Auscultate heart sounds frequently
and monitor cardiac rhythm. Note
presence of S3 or S4 gallop (S3 gallop
is a significant indicator of heart
failure). Monitor for premature
ventricular beats.
I: Evaluates for progression of left-
sided heart failure.
Source: Source: Sparks, S and
Taylor, C, Nursing Diagnosis
Reference Manual 3rd edition;
Springhouse Corporation,
Pennsylvannia
 P a g e | 52

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, enhancing 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.(Wolkenstein, 2000).

April 22, 2010 Excess fluid volume related to
excess fluid or NA intake and
retention of fluid secondary to
Heart failure and its medical
therapy
Subjective cue:
“puno kaayo akong gibati,”, as
verbalized by the patient
Objective cue:
>Adventitious breath
Independent:
1. R: Compare current weight
admission and/or previously stated
weight
I: provides a comparative baseline
2. R: Auscultate breath sounds
I: for presence of crackles and
congestion
3. R: Measure abdominal girth
for changes that
I: may indicate increasing fluid
retention/edema
Desired Outcome:
After 8 hours of nursing
intervention, the patient was
able to stabilize fluid volume as
evidenced by balance I/O, vital
signs within patient's normal
limits, stable weight, and free
signs of edema
Actual Outcome:
After 8 hours of nursing
intervention, the objectives

sounds(crackles)
>changes in respiratory pattern
>Dyspnea
>Restless
>Pulmonary congestion
Scientific Analysis:
Fluid that accumulated in the
dependent extremities during the
day begins to be reabsorbed into
the circulating blood volume
when the person lies down.
Because the impaired left
ventricle cannot eject the
increased circulating blood
volume, the pressure in the
pulmonary circulation increases,
causing further shifting of fluid
into the alveoli. The fluid filled
alveoli cannot exchange oxygen
and carbon dioxide. Without
sufficient oxygen, the patient
experiences dyspnea and has
difficulty getting an adequate
amount of sleep. (Wolkenstein,
2000).
P a g e | 53
4. R: Assess neuromuscular reflexes were partially met. The patient
I: to evaluate for presence of was able to have a normal vital
electrolyte imbalances such as signs of
hypernatremia T-37.1 c, P-77 bpm
5. R: Observe skin and mucous R-19 cpm, BP- 110/70 mmHG
membranes
I: for presence of
decubitus/ulceration
6. R: Elevate edematous extremities,
change position frequently
I: to reduce tissue pressure and risk
for skin breakdown
7. R: Place in semi-Fowler's position,
as appropriate
I: to facilitate movement of
diaphragm, thus improving
respiratory effort
Dependent:
1. R: Administer medications
(e.g.diuretics)
I: To treat underlying conditions
Collaborative:
1. R: Restrict sodium and fluid intake,
as indicated
I: for nutritional therapy
Source: Source: Sparks, S and

April 23, 2010 Activity intolerance related to
imbalance between oxygen
supply and demand
Cues and Objectives
Subjective:
“dali ra ko makutasan, dili ko
kasugakod ug dugay ug bug-at
nga trabaho,” as verbalized by
the patient.
Objective:
- generalized weakness
- limited range of motion
- short term performance of an
activity
Scientific Analysis:
As heart failure becomes more
severe, the heart is unable to
pump the amount of blood
required to meet all of the body’s
needs. To compensate, blood is
Taylor, C, Nursing Diagnosis
Reference Manual 3rd edition;
Springhouse Corporation,
Pennsylvannia
Independent:
1. I: Discuss with the patient the
need for activity.
R: Improves physical and
psychosocial well-being.
2. I: Identify activities the patient
considers desirable and meaningful.
R: To enhance their positive impact.
3. I: Encourage patient to help plan
activity progression, being sure to
include activities the patient
considers essential.
R: Participation in planning helps
ensure patient compliance.
4. I: Instruct and help patient to
alternative periods of rest and
activity.
R: To reduce the body’s organ
demand and prevent fatigue.
5. I: Identify and minimize factors
that decrease the patient’s exercise
tolerance.
R: To help increase the activity level.
6. I: Monitor physiological responses
to increased activity.
P a g e | 54
Desired Outcomes:
After 8 hours of nursing
interventions,
* Patient states desire to
increase activity level.
* Patient states understanding
of the need to increase activity
level gradually.
* Blood pressure and pulse and
respiratory rates remain within
prescribed limits during
activity.
* Patient states satisfaction
with each new level of activity
attained.
* Patient demonstrates skill in
conserving energy while
carrying out daily activities to
tolerance level.
* Patient explains illness and
connects symptoms of activity
intolerance with deficit in
oxygen supply or use.
Actual Outcome:

diverted away from less-crucial
areas, including the arms and
legs, to supply the heart and
brain. As a result, people with
heart failure often feel weak
(especially in their arms and
legs), tired and have difficulty
performing ordinary activities
such as walking, climbing stairs
or carrying groceries
P a g e | 55
R: To ensure return to normal a few Afer 8 hours of nursing
minutes after exercising. intervenions, the objectives
7. I: Teach patient how to conserve were partially met. The:
energy while performing activities of *Patient stated understanding
daily living. of the need to perform daily
R: These measures reduce cellular activities.
metabolism and oxygen demand. *Patient demonstrated
8. I: Teach patient exercises for conservation of energy while
increasing strength and endurance. performing activities.
R: Improves breathing and gradually
increase activity level.
9. I: Support and encourage activity
to patient’s level of tolerance.
R: Helps patient develop level of
tolerance.
10. I: Before discharge, formulate a
plan with the patient and caregivers
that will enable the patient either to
continue functioning at maximum
activity intolerance or to gradually
increase the tolerance.
R: Participation in planning
encourages patient satisfaction and
compliance.
Source: Source: Sparks, S and
Taylor, C, Nursing Diagnosis
Reference Manual 3rd edition;
Springhouse Corporation,

April 23, 2010 Ineffective airway clearance
related to presence of
tracheobronchial obstruction
Cues and Evidences:
Subjective:
“maglisod ko ug ginhawa nya
huot ako dughan,” as verbalized
by the patient.
Objective:
- shortness of breath
- dyspnea
- use of accessory muscles when
breathing
- tachypnea with RR of 28
Scientific Analysis:
Mucus is produced at all times by
the membranes lining the air
passages. When the membranes
are irritated or inflamed, excess
mucus is produced and it will
retain in tracheobronchial tree.
The inflammation and increased
in secretions block the airways
making it difficult for the person
Pennsylvannia
Independent:
1. I: Assess respiratory status at
least every for hours or according to
establishment standards.
R: To detect early signs of
compromise.
2. I: Place patient in Fowler’s position
and support upper extremities.
R: To aid breathing and chest
expansion, and to ventilate basilar
lung fields.
3. I: Help patient turn, cough, and
deep breath every 2 to 4 hours.
R: To help prevent pooling of
secretions and to maintain airway
patency.
4. I: Suction as needed. Be alert for
progression of airway clearance.
R: To stimulate cough and airways.
5. I: Encourage fluids (atleast 3,000
mL daily).
R: To ensure adequate hydration and
loosen secretions, unless
contraindicated.
6. I: Mobilize patient to full
capabilities.
R: To facilitate chest expansion and
P a g e | 56
Desired Outcome:
After 8 hours of nursing
interventions,
* Patient clears airway using
controlled coughing
techniques.
* Patient expectorates sputum.
* Patient drinks 3 to 4 liters of
fluid daily.
*Patient’s arterial blood gas
values are within normal limits.
*Patient performs chest
physiotherapy, especially
postural drainage.
*Patient understands necessity
of adequate hydration
Actual Outcome:
After 8 hours of nursing
interventions, the objectives
were partially met. The:
*Patient verbalized
understanding on coughing
techniques
* Patient increased fluid
volume to 3 to 4 liters per day.

to maintain a patent airway. In
order to expel excessive
secretions, cough reflex will be
stimulated. An increased in RR
will also be expected as a
compensatory mechanism of the
body due to obstructed airways
(Wolkenstein, 2000).
P a g e | 57
ventilation.
7. I: Perform postural drainage,
percussion, and vibration every 4
hours or as ordered.
R: To enhance mobilization of of
secretions that interferes with
oxygenation.
8. I: Avoid supine position for
extended periods. Encourage lateral,
sitting, prone, and upright positions
as much as possible.
R: To enhance lung expansion and
ventilation.
9. I: Provide tissues and paper bags
for hygienic sputum disposal.
R: To prevent spreading infection.
10. I: Monitor and document sputum
characteristics every shift.
R: To gauge therapy’s effectiveness.
Source: Sparks, S and Taylor, C,
Nursing Diagnosis Reference Manual
3rd edition; Springhouse Corporation,
Pennsylvannia
 P a g e | 58

XI. Drug Study

Side effects,
Name of
indications/reasons for adverse
medication or Nursing Interventions
administrating the drugs reactions a
drugs
nurse note for

Cefuroxime CNS: headache,

750mg IVTT It is effective for the treatment dizziness,letharg • Determine history of hypersensitivity reactions to
of penicillinase-producing y, paresthesias cephalosporins, penicillins, and history of allergies,
Neisseria gonorrhoea (PPNG). particularly to drugs, before therapy is initiated.
Effectively treats bone and joint GI: • Inspect IM and IV injection sites frequently for signs
infections, bronchitis, nausea,vomiting of phlebitis.
meningitis, gonorrhea, otitis , • Report onset of loose stools or diarrhea. Although
media, pharyngitis/tonsillitis, diarrhea,anorexi pseudomembranous colitis.
sinusitis, lower respiratory tract a, abdominal • Monitor I&O rates and pattern: Especially important
infections, skin and soft tissue pain, flatulence, in severely ill patients receiving high doses. Report
infections, urinary tract any significant changes.
infections, and is used for GU:
surgical prophylaxis, reducing nephrotoxicity
or eliminating infection.
Hematologic:
bone marrow
depression

Hypersensitivi
ty: ranging from
rash to fever to
anaphylaxis,
serum sickness
reaction
 P a g e | 59

To relieve mild to moderate Side effects are

Paracetamol pain due to things such as rare with Assessment & Drug Effects
500mg 1 tab q 8h headache, muscle and joint paracetamol • Monitor for S&S of: hepatotoxicity, even with
for fever pain, backache and period when it is taken moderate acetaminophen doses, especially in
pains. It is also used to bring at the individuals with poor nutrition.
down a high temperature. For recommended
this reason, paracetamol can doses. Skin Patient & Family Education
be given to children after rashes, blood • Do not take other medications (e.g., cold
vaccinations to prevent post- disorders and preparations) containing acetaminophen without
immunisation pyrexia (high acute medical advice; overdosing and chronic use can
temperature). Paracetamol is inflammation of cause liver damage and other toxic effects.
often included in cough, cold the pancreas • Do not self-medicate children for pain more than 5 d
and flu remedies. have without consulting a physician.
occasionally • Do not use for fever persisting longer than 3 d,
occurred in fever over 39.5° C (103° F), or recurrent fever.
people taking • Do not give children more than 5 doses in 24 h
the drug on a unless prescribed by physician.
regular basis for
a long time. One
advantage of
paracetamol
over aspirin and
NSAIDs is that it
doesn't irritate
the stomach or
causing it to
bleed, potential
Side effects of
aspirin and
 P a g e | 60

NSAIDs.

Furosemide 80mg CV: Postural

IVTT Treatment of edema associated hypotension,
with CHF, cirrhosis of liver, and dizziness with Assessment & Drug Effects
kidney disease, including excessive diuresis,
nephrotic syndrome. May be acute hypotensive • Observe patients receiving parenteral drug carefully; closely
actions: used for management of episodes, circulatory monitor BP and vital signs. Sudden death from cardiac arrest has
hypertension, alone or in collapse. Metabolic: been reported.
Rapid-acting combination with other Hypovolemia, • Monitor BP during periods of diuresis and through period of
potent antihypertensive agents, and dehydration, dosage adjustment.
sulfonamide for treatment of hypercalcemia. hyponatremia • Observe older adults closely during period of brisk diuresis.
"loop" diuretic and Has been used concomitantly hypokalemia, Sudden alteration in fluid and electrolyte balance may precipitate
antihypertensive with mannitol for treatment of hypochloremia significant adverse reactions. Report symptoms to physician.
with severe cerebral edema, metabolic alkalosis, • Lab tests: Obtain frequent blood count, serum and urine
pharmacologic particularly in meningitis. hypomagnesemia, electrolytes, CO2, BUN, blood sugar, and uric acid values during
effects and uses hypocalcemia first few months of therapy and periodically thereafter.
almost identical to (tetany), • Monitor for S&S of hypokalemia.
those of hyperglycemia, • Monitor I&O ratio and pattern. Report decrease or unusual
ethacrynic acid. glycosuria, elevated increase in output. Excessive diuresis can result in dehydration
Exact mode of BUN, and hypovolemia, circulatory collapse, and hypotension. Weigh
action not clearly hyperuricemia. GI: patient daily under standard conditions.
defined; decreases Nausea, vomiting, • Monitor urine and blood glucose & HbA1C closely in diabetics
renal vascular oral and gastric
and patients with decompensated hepatic cirrhosis. Drug may
resistance and burning, anorexia,
cause hyperglycemia.
may increase diarrhea,
renal blood flow constipation,
 P a g e | 61

abdominal cramping,
acute pancreatitis,
jaundice.
Urogenital: Allergic
interstitial nephritis,
irreversible renal
failure, urinary
frequency.
Hematologic:
Anemia, leukopenia,
thrombocytopenic
purpura; aplastic
anemia,
agranulocytosis
(rare). Special
Senses: Tinnitus,
vertigo, feeling of
fullness in ears,
hearing loss (rarely
permanent), blurred
vision. Skin:
Pruritus, urticaria,
exfoliative
dermatitis, purpura,
photosensitivity,
porphyria cutanea
tarde, necrotizing
angiitis (vasculitis).
Body as a Whole:
Increased
perspiration;
paresthesias;
activation of SLE,
 P a g e | 62

muscle spasms,
weakness;
thrombophlebitis,
pain at IM injection
site.

Salbutamol 1 neb
q6 To relieve bronchospasm Assessment & Drug Effects
associated with acute or Body as a Whole:
 P a g e | 63

Hypersensitivity
chronic asthma, bronchitis, or reaction. CNS: • Monitor therapeutic effectiveness which is indicated
actions: other reversible obstructive Tremor, anxiety, by significant subjective improvement in pulmonary
airway diseases. Also used to nervousness, function within 60–90 min after drug administration.
Synthetic prevent exercise-induced restlessness, • Monitor for: S&S of fine tremor in fingers, which
sympathomimetic bronchospasm. convulsions, may interfere with precision handwork; CNS
amine and weakness, headache, stimulation, particularly in children 2–6 y,
moderately hallucinations. (hyperactivity, excitement, nervousness, insomnia),
selective beta2- CV: Palpitation, tachycardia, GI symptoms. Report promptly to
adrenergic agonist hypertension, physician.
hypotension, • Lab tests: Periodic ABGs, pulmonary functions, and
with
bradycardia, reflex pulse oximetry.
comparatively
tachycardia. Special • Consult physician about giving last albuterol dose
long action. Acts
Senses: Blurred several hours before bedtime, if drug-induced
more prominently
vision, dilated insomnia is a problem.
on beta2
pupils.
receptors GI: Nausea,
(particularly vomiting. Other:
smooth muscles of Muscle cramps,
bronchi, uterus, hoarseness.
and vascular
supply to skeletal
muscles) than on
beta1 (heart)
receptors. Minimal
or no effect on
alpha-adrenergic
receptors. Inhibits
histamine release
by mast cells.

Aldozide 1 tab BID Essential hypertension, Gynecoma • ducate patient to avoid hazardous activity such as
edema and ascites of stia, GI driving until response to drug is known.
 P a g e | 64

CHF, liver cirrhosis, symptoms • Take with meals or milk; avoid excessive ingestion
nephritic syndrome, , lethargy, of food high in potassium or use of salt substitutes
Mechanism idiopathic edema headache • Diuretic effect may be delayed 2-3 days and
of Action: : and maximum hypertensive may be delayed 2-3weeks;
competes thrombocy monitor I and O ratios and daily weight, BP, serum
with topenia, electrolytes (K, Na) and renal function
aldosterone leukopeni
for receptor a,
sites in the agranuloc
distal renal ytosis,
tubules, cutaneous
increasing eruptions,
sodium pruritus,
chloride and mental
water confusion,
excretion paresthesi
while a, acute
conserving pancreatiti
potassium s,
and jaundice,
hydrogen orthostati
ions, may c
block the hypertensi
effect of on,
aldosterone muscle
on arteriolar spasm,
smooth weakness,
muscle as fever,
well ataxia
 P a g e | 65

XII. Discharge Plan

METHODS Outcome Identification Nursing Interventions

Medication Patients need to understand the purpose, A - Assess patient and SO’s ability to understand regarding home
dosage, route, and possible side effects of all medication orders and instructions to be given
prescribed medications.
I - Remind and instruct the parent on home medication instructions

- Refer to drug instructions for each.

E - Evaluate the patient’s level of understanding on the instructions

given about the medications

Exercise Regularly scheduled, moderate exercise
and performed for at least 30 minutes most days
Environme of the week promotes the utilization of
nt carbohydrates, assists with weight control,
enhances the action of insulin, and improves
cardiovascular fitness.
A - Assess patient’s understanding of exercise regimen.
I - Explain the importance of exercise:
• Caloric expenditure for energy in exercise
• Carryover of enhanced metabolic rate and efficient food
utilization
- Advise patient to assess blood glucose level before and after
strenuous exercise.

- Instruct patient to plan exercises on a regular basis each day.

- Encourage patient to eat a carbohydrate snack before exercising

to avoid hypoglycemia.

- Advice patient that prolonged strenuous exercise may require

increased food at bedtime to avoid nocturnal hypoglycemia.

− Instruct patient to avoid exercise whenever blood glucose


Treatment Teach patients the appropriate technique for
testing blood and urine and how to interpret
the results.
Stress the importance of close attention to
even minor skin injuries.
Because of the atherosclerotic changes that
occur, encourage patients to stop smoking.
Health If the patient continues to smoke, provide A - Assess for the patient’s ability to do self-care
Teaching the name of a smoking cessation program or
and a support group. You follow the same
P a g e | 66
levels exceed 250 mg/day and urine ketones are present.
Patient should contact health care provider if levels remain
elevated.
− Encouraged so to maintain quiet environment
− Encouraged so to maintain patient surrounding clean
− Encouraged so to provide patient proper hygiene
E - Evaluate patient’s level of understanding on the information
given and degree of awareness on the importance of good sanitation
and proper exercise.
A - Assess if the patient is continually sticking to V/S monitoring
schedules and treatment regimen.
I - Patients need to know when to notify the physician and increase
testing during times of illness.
− In addition, teach patients to avoid crossing their legs when
sitting and to begin a regular exercise program.
− Instructed the patient to right information or advice by the
physician
− Instructed the patient to follow right time & medication
E - Check the response to the interventions and actions performed
- Assess patient’s will or degree to decrease/ cease smoking.
 P a g e | 67

Hygiene protocol for drinking to avoid other diseases. I - Discuss concerns with parent to identify underlying issues

− Identify health behaviors/habits that may interfere to improve

patient’s health status

− Instructed patient to do other way of personal hygiene like proper

hand washing, tooth brushing after eating and taking a bath
everyday

E - Evaluate responses to wellness plan and action performed

- Evaluate progress of health condition.

Out Patient Note any referrals to social services. Remind A - Assess for signs and symptoms
follow-up for follow-up schedule. Call if appropriate.
- Assess the understanding of the parent as to the possible reason
and
for follow-up visit
Observatio
n I - Instruct patient/ SO to refer immediately to physician if health
condition worsens

− Instructed the patient to express every time of discomfort

− Encourage patient to side to side position

E - Evaluate patient’s level of understanding on the instructions

given and information open to her.

Diet Emphasize the importance of adjusting diet
during illness, growth periods, stress, and
pregnancy.
A - Assess foods in compliance to given diet
-Assess patient’s preference of food
I - Instruct patient to watch for timing of food and not to eat more
 P a g e | 68

than necessary.

Encourage patients to avoid alcohol - Teach how to calculate caloric intake.

- Each meal should consist of a balance of carbohydrates, proteins,

and fats.

• Carbohydrates should be varied to include fruits, starches, and

vegetables.
• Protein selections that are lean will help reduce fat and
cholesterol intake.
• Fats should be used sparingly with <10% of total calories
derived from saturated fats. High in calories, fats contribute to
weight gain in type 2 diabetes mellitus (DM).
- Avoid salt whenever possible.

• Do not season foods with salt or salt-containing spices.

• Limit use of foods with hidden sodium content (eg, crackers,
pickled foods, cheese, processed meats).
• Use salt-containing condiments sparingly (ketchup, soy sauce,
gravies, bouillon).
- Prepare foods to retain vitamins and minerals and reduce fats.

• Do not fry foods.

• Bake, broil, or boil foods and discard fat.
• Eat raw fruits and vegetables or steam vegetables to retain
fiber.
• Avoid adding calories with butter or cream sauces, fat back,
and bacon.
• Trim all visible fat from meat; skim off fat from stews or other
prepared dishes.
- Use alcohol only in moderation.
 P a g e | 69

• Do not omit food from meal plan in exchange for alcohol.

• Limit intake to 1-2 drinks per week (4 oz dry wine, 12 oz beer,
or 1.5 oz distilled liquor = 1 alcohol serving).
- Use alternative nonnutritive, noncaloric sweeteners in
moderation.

• Limit diet: soda intake to 2 L/day.

• Avoid frequent use of foods and beverages with concentrated
sucrose.
E - Evaluate patient’s level of understanding and degree of
awareness about strict implementation of the diet.

Spiritual Provide emotional and spiritual support. A - Assess patient’s readiness to be involved in such activities

- Assess for barriers to practice religious beliefs

I - Encourage patient to attend Sunday Masses if Catholic

- Strengthen patient’s relationship with God by letting him

participate religious activities: Sunday Mass, Rosary, Prayer
Meetings, etc.

E – Evaluate patient’s desire for spiritual growth

- Evaluate emotional, psychosocial and spiritual progress.

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XIII. Bibliography

Amnesi, Sandra M, and et. al. Brunner& Suddarth's Medical-Surgical

Nursing 10th Edition. Chicago: Lippincott Williams & Wilkins, 2009.

Doenges, Marilynn, Mary Frances Moorhouse, and Alice Murr. Nurse's

Pocket Guide, 11th edition. Pennsylvania: F.A. Davis Company, 2008.

McPhee, Stephen J, Vishwanath R Linggapa, William F Ganong, and Jack D

Lange. Pathophysiology of Disease: An Introduction to Clinical Medicine.
Stamford, Connecticut: Appleton & Lange, 1997.

Nettina, Sandra M., and Elizabeth Jacqueline Mills. Lippincott Manual of

Nursing Practice, 8th Edition. Lippincott Williams & Wilkins, 2006.

PPD's Nursing Drug Guide, 2nd Edition. Pasig: Medicomm Pacific, Inc.,
2008.

Sommers, Marilyn S, Susan A Johnson, and Theresa A Beery. Diseases

and Disorders: A Nurses; Therapeutic Manual 3rd Edition. Philadelphia:
F.A. Davis Company, 2007.
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XIV. Learning Insights

Upon conducting the case study on congestive heart failure, I have

learned another aspect in the field of Medical Surgical Nursing. Studying
about the disease process itself from factors affecting it, the symptoms,
pathophysiology, diagnostic procedures on identifying the disease, its
treatment procedures including medical regimen and developing nursing
care plans has helped me understood the details and necessary
information about the disease.
Through this case study, I was able to learn to identify the problems
being encountered by patients and therefore, being able to prioritize
them and address then accordingly. Appropriate nursing interventions
are needed to be carried on in order to help the patient alleviate
symptoms and regain the health status.

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