Republic of the Philippines

Tarlac State University

College of Science
Department of Nursing
Lucinda Campus, Brgy. Ungot, Tarlac City Philippines 2300
Accredited Level 2 Status by the Accrediting Agency of Chartered College and
Universities in the Philippines (AACCUP). Inc.

A Case Study Presented to the

Faculty of the Department of Nursing, Tarlac State University
Villa Lucinda Campus, Brgy. Ungot, Tarlac City Philippines
In Partial Fulfillment of the Requirements of the Subject

NURSING CARE MANAGEMENT 104

Congestive Heart Failure

Submitted by:
Agustin, Anthony Elijah P.
Dionisio, Jay Ann
Juliano, Joan
Lumibao, Krisha Ann
Olama, Hamila C.
Oladipupo, Emmanuel I.
Rojo, Vincent Luis M.
Salunga, Merlene
Sugala, Rhajeeb Aennas A.
Valloyas, Gwen Stefanie L.

Submitted to:
Mr. Jomer V. Manalang RN, MAN
Clinical Instructor

March 7, 2019
 TABLE OF CONTENTS
I. INTRODUCTION..........................................................................................................3
II. OBJECTIVES...............................................................................................................7
III. NURSING PROCESS.................................................................................................8
A. ASSESSMENT..................................................................................................8
1. Personal Data.....................................................................................................8
2. Genogram..........................................................................................................10
3. History of Past Illness.......................................................................................11
4. History of Present Illness.................................................................................11
5. 13 Areas of Assessment....................................................................................11
6. Laboratory and Diagnostic Status.................................................................23
7. Pathophysiology...............................................................................................29
a. Book-Based...........................................................................................29
b. Client-Based..........................................................................................30
B. PLANNING (NCP)..........................................................................................32
C. IMPLEMENTATION.....................................................................................36
1. Drug Study........................................................................................................36
2. Medical Treatment...........................................................................................41
3. Activity and exercise.........................................................................................42
D. EVALUATION................................................................................................44
1. Discharge Planning...........................................................................................44
IV. CONCLUSION..........................................................................................................45
V. RECOMMENDATION..............................................................................................45
VI. REVIEW OF RELATED LITERATURE...............................................................46
VII. BIBLIOGRAPHY....................................................................................................52
 3

I. Introduction
A. Brief Discussion

Congestive heart failure (CHF) is a chronic progressive condition that affects the
pumping power of the heart muscles. While often referred to simply as “heart failure,” CHF
specifically refers to the stage in which fluid builds up around the heart and causes it to
pump inefficiently.

There are four heart chambers. The upper half of the heart has two atria, and the lower half
of the heart has two ventricles. The ventricles pump blood to the body’s organs and tissues,
and the atria receive blood from the body as it circulates back from the rest of your body.
CHF develops when the ventricles can’t pump enough blood volume to the body.
Eventually, blood and other fluids can back up inside the: lungs, abdomen, liver and lower
body. CHF can be life-threatening.

Types of CHF

 Left-sided CHF - is the most common type of CHF. It occurs when the left ventricle
doesn’t properly pump blood out to the body. As the condition progresses, fluid can
build up in the lungs, which makes breathing difficult.

There are two kinds of left-sided heart failure:

o Systolic heart failure occurs when the left ventricle fails to contract normally.
This reduces the level of force available to push blood into circulation. Without
this force, the heart can’t pump properly.
o Diastolic failure or diastolic dysfunction, happens when the muscle in the left
ventricle becomes stiff. Because it can no longer relax, the heart can’t quite fill
with blood between beats.
 Right-sided CHF - occurs when the right ventricle has difficulty pumping blood to the
lungs. Blood backs up in the blood vessels, which causes fluid retention in the lower
extremities, abdomen, and other vital organs.

It’s possible to have left-sided and right-sided CHF at the same time. Usually, the
disease starts in the left side and then travels to the right when left untreated.

Congestive heart failure stages

Stage Main symptoms Outlook

Class I Patient don’t experience CHF at this stage can be

any symptoms during managed through lifestyle
typical physical activity.
 4

changes, heart medications,

and monitoring.

Class II Patient are likely CHF at this stage can be

comfortable at rest, but
normal physical activity
may cause fatigue,
palpitations, and shortness
of breath.
managed through lifestyle
changes, heart medications,
and careful monitoring.

Class III Patient are likely Treatment can be

comfortable at rest, but complicated. Talk with
there’s a noticeable your doctor about what
limitation of physical heart failure at this stage
activity. Even mild may mean for you.
exercise may cause fatigue,
palpitations, or shortness of
breath.

Class IV Patient are likely unable to There’s no cure for CHF at

carry on any amount of
physical activity without
symptoms, which are
present even at rest.
this stage, but there are still
quality-of-life and
palliative care options.
You’ll want to discuss the
potential benefits and risks
of each with your doctor.

Risk Factors

 Hypertension - blood pressure is higher than normal; it may lead to CHF.

Hypertension has many different causes. Among them is the narrowing of the arteries,
which makes it harder for the blood to flow through them.

 Coronary artery disease - Cholesterol and other types of fatty substances can block
the coronary arteries, which are the small arteries that supply blood to the heart. This
causes the arteries to become narrow. Narrower coronary arteries restrict the blood flow
and can lead to damage in the arteries.

 Valve conditions - The heart valves regulate blood flow through the heart by opening
and closing to let blood in and out of the chambers. Valves that don’t open and close
correctly may force your ventricles to work harder to pump blood. This can be a result
of a heart infection or defect.

 Other Conditions - These include diabetes, thyroid disease, and obesity.

 5

Sign and Symptoms

Symptoms that may Symptoms that indicate Symptoms that indicate a

notice first the condition has severe heart condition
worsened

chest pain that radiates

irregular heartbeat
fatigue through the upper body

swelling in the ankles, feet, a cough that develops from

rapid breathing
and legs congested lungs

skin that appears blue,

weight gain wheezing which is due to lack of
oxygen in the lungs

shortness of breath, which

increased need to urinate,
may indicate pulmonary fainting
especially at night
edema

B. Current Trends

Statistic

Worldwide

WHO (2017) CVDs are the number 1 cause of death globally: more people die
annually from CVDs than from any other cause. An estimated 17.9 million people died
from CVDs in 2016, representing 31% of all global deaths. Of these deaths, 85% are due
to heart attack and stroke. Over three quarters of CVD deaths take place in low- and middle-
income countries. Out of the 17 million premature deaths (under the age of 70) due to non-
communicable diseases in 2015, 82% are in low- and middle-income countries, and 37%
are caused by CVDs.

Most cardiovascular diseases can be prevented by addressing behavioural risk

factors such as tobacco use, unhealthy diet and obesity, physical inactivity and harmful use
of alcohol using population-wide strategies. People with cardiovascular disease or who are
at high cardiovascular risk (due to the presence of one or more risk factors such as
hypertension, diabetes, hyperlipidaemia or already established disease) need early
detection and management using counselling and medicines, as appropriate.

National

NCBI (2017) The study determined the prevalence of hospitalisation due to

congestive heart failure (CHF) among adult patients aged 19 years and above in the
Philippines and its 17 regions in 2014. It also determined the demographic profile of these
 6

patients, aetiology and type of CHF, comorbidities, duration of hospitalisation and the
overall in-hospital mortality rate. The prevalence rate was 1.6% or 1648 cases of CHF for
every 100 000 patient claims for medical conditions in 2014. The mean age was 52.6±15.1
years.

There was no sex predilection. Only 22.67% of the hospitalisation claims for CHF
listed possible specific aetiologies, the most common of which was hypertensive heart
disease (86.7%). There were more cases of systolic compared to diastolic heart failure. The
mean length of hospital stay was 5.9 days (+8.2) days (median 4 days), with an overall in-
hospital mortality rate of 8.2%. There were 16 cases of heart failure for every 1000 Filipino
patients admitted due to a medical condition in 2014. Hypertension was possibly the most
common etiologic factor. Compared to western and Asia-Pacific countries, the local
mortality rate was relatively higher.

Local

According to the report published by the PMC of the National center for
biotechnology information using the prospect of the incidence from 2010-2014;
Congestive heart failure (CHF) is an important public health problem, with prevalence
reported to range from 1% to 12% in western countries, and 0.5% to 6.7% in Southeast
Asian countries. It is defined as a clinical syndrome resulting from any structural or
functional cardiac disorder that leads to an impaired ventricular filling or incomplete
ejection of blood. The current three types of heart failure based on the recent revisions of
the European Society of Cardiology are: (1) reduced with ejection fraction (EF) <40%
(HFrEF); (2) preserved with EF ≥50% (HFrEF); and (3) mid-range with EF 40–49%.
Although their clinical presentations are mostly the same, patients with HFrEF are more
likely to be male and have coronary artery disease (CAD), while HFpEF are more likely to
be female, elderly, and have hypertension. Patients with HFrEF have increased mortality
and recurrent hospitalizations. (HFrEF(heart failure with low ejection fraction) and
(HFPEF(Failure with a Preserved. Ejection Fraction) and can be further described as acute
or chronic).

The prevalence of CHF was determined through a review of all records for
hospitalization for CHF for adult patients aged 19 years and above who were admitted to
PhilHealth-accredited hospitals from 1 January 2014 to 31 December 2014. The data were
retrieved from the anonymized records in the PhilHealth database which consisted of
healthcare data from 87% of the population of approximately 99.6 million Filipinos

There was a total of 6 914 410 PhilHealth claims for hospitalization for either
medical or surgical causes during the time period of the study. Of these, 2 673 546 were
claims for hospitalization due to medical causes.
 7

Of the claims for medical causes, 44 046 were due to heart failure. This represented
a prevalence rate of 1.6% or 1648 cases of CHF for every 100 000 patient claims for
medical causes. The majority of these came from Region IV-A (13.5%), National Capital
Region (NCR) (10.7%), and Region III (10.3%). Patient claims without assigned regions
(0.9%) were attributed to those who were admitted in non-PhilHealth accredited hospitals
who were probably subsequently reimbursed in the local PhilHealth offices that may or
may not have been the region where they were confined.

As a whole, there was no sex predilection in the occurrence of heart failure (49.9%
males vs. 50.1% females). There were more males than females with systolic (51.3% vs.
48.7%) and diastolic (53.8% vs. 46.1%) heart failure, but among those with combined
systolic and diastolic heart failure the number of males and females were equal. Differences
from the worldwide trend might be because the majority of patient claims were encoded as
plain heart failure (I50) or heart failure, unspecified (I50.9). Other reasons might include
an increasing number of risk factors brought about by negative lifestyle changes on both
sexes, such as smoking and a sedentary lifestyle.

The prevalence rate was 1.6% or 1648 cases of CHF for every 100 000 patient
claims for medical conditions in 2014. The mean age was 52.6±15.1 years. There was no
sex predilection. Only 22.67% of the hospitalization claims for CHF listed possible specific
aetiology, the most common of which was hypertensive heart disease (86.7%). There were
more cases of systolic compared to diastolic heart failure. The mean length of hospital stay
was 5.9 days (+8.2) days (median 4 days), with an overall in-hospital mortality rate of
8.2%.

C. Reason for Choosing the Case

The main reason why we choose this study is for the readers and future researchers
to have a broader/additional knowledge about Congestive Heart Failure
incidence/prevalence in Philippines. As well as we the researchers will benefit from this
study as a student nurse enhancing our skills and acquiring knowledge on how to deal with
this kind of disorder.

D. Objectives
General Objectives:

 At the end of the rotation we the BSN- 3A, Group 1 will enhance our knowledge,
skills and attitude in the care and management of patient who had Congestive Heart
 8

Failure utilizing the nursing process and will improve the health status of the
patient.

Specific Objectives:

At the end of this case, the group will able to:

1. Assess the general health condition, routines of daily living as well as health
lifestyle factors affecting the health status of the client.
2. Recognize and prioritize nursing problems and create nursing diagnoses based
on assessment findings
3. Plan efficient nursing care to solve identified problems based from patient’s
condition and health needs.
4. Carry out proper nursing intervention based from the patient’s condition and
health needs.
5. Evaluate the effectiveness of nursing interventions rendered to be able to
improve patient’s condition for possible discharge.

II. Nursing Process

A. Personal Data
1. Demographic Data

Name: Patient X

Age: 40 years old

Address: Cubcub Mayantoc

Gender: Male

Date of birth: 06/29/1978

Nationality: Filipino

Religion: Roman Catholic

Diagnosis: Congestive Heart Failure Reduced Ejection Fraction Secondary to

Community Acquired Pneumonia

Date admitted: 02/18/2019

Time admitted: 7:41:00 P.M.

 9

2. Environmental Data

Resides in a rural area. Their house is located beside the farm at their backyard
they have Eggplant and lady’s finger. The family do not participate in any activities in their
community. Tricycle is their means of transportation in their place.

3. Lifestyle (Habits, Recreation, Hobbies)

He is a tricycle driver, car agency and a farmer, he plants corn and “palay” before
he got sick. His hobby is to watch television and water his plants at the backyard. He is
fond of sleeping and he doesn’t exert some physical activities such as exercise. He seldom
go outside their house. His wife was the one who clean and cook for their meals as stated
by the patient.
 10

Family history of health and illness

GENOGRAM

GRANDFATHER GRANDMOTHER GRANDFATHER GRANDMOTHER

FATHER
MOTHER

PATIENT
LEGEND:

CHF DM DECEASED

ASTHMA HYPERTENSION MALE FEMALE

 11

4. History of Past Illness

Patient X completed his immunization and no serious injuries and accident. She
experienced childhood disease such chicken pox, measles, mumps, cough and cold. He had
no identified allergies. Patient X experienced chest pain, difficulty of breathing and edema
in his both lower and upper extremities. He was admitted at Tarlac Provincial Hospital for
5 days last 2017 with admitting case of poor ejection fraction.

5. History of Present Illness

On February 02, 2019 patient was schedule for follow up check-up and on the same
day he was also admitted because of chest pain, cough and edema on both lower
extremities, and was discharged on February 04, 2019 and was advice to come back for his
follow up check-up after 1 week. 1 week has passed patient doesn’t go for his follow up
check-up.

6 days prior to admission he experienced body weakness, chest pain and cough and
was admitted at Tarlac Provicial Hospital on February 18, 2019 at 7:41 pm with admitting
diagnosis of Congestive Heart Failure Reduced Ejection Fraction Secondary to Community
acquired pneumonia. He stated that he experienced dizziness and difficulty in breathing
when he was transferred to his room in Medicine ward. Ordered medications were given
and diagnostic procedures such as blood exam and chest ultrasound were performed.

6. 13 areas of assessment
I. Social Status

The patient lives with his mother, they are 7 in their house and he has 2 daughters.
His friends often visit him in their house because he can’t walk too far because of his
condition, and in their house they play some cards and board games or just chat with each
other. He socializes with his neighbours well. He speaks Ilocano, tagalog and English as
his way of communicating. They are very open in their family whenever there’s a problem
they will talked about it and solved it in a nice way.

Norms

Social status includes family relationships that state the patient’s support system in

time of stress and in the time of stress and in the time of need. It means a fundamental

human need for socialites making life less stressful and social support buffers the negative
 12

effects of stress, thus indicating indirectly contributing to good health outcomes.

(Fundamentals of Nursing Barbara E. Kozier, Seventh Edition)

Analysis

Based on the norms his social status is normal.

II. Mental Status

He was alert and was able to answer accordingly to the questions we have asked

him and responds appropriately. He is conscious and cooperative during the assessment

but complains of pain and difficulty of breathing when he is talking so there’s a little bit of

delay when answering the questions being asked. He is aware of the time, date and place

where he is. He also finished vocational course in TESDA.

Norms

The client must be alert and awake with eyes open and looking at the examiner with

eyes open and looking at the examiner and responds appropriately. (Fundamentals of

Nursing Barbara E. Kozier, Seventh Edition)

Analysis

Based on the norms he has normal mental status but slightly delay because of his

condition.

III. Emotional Status

He is calm to approach us throughout the assessment but he is slightly distorted

because of the pain he is enduring. According to him at first he is very sad about his

situation because it’s really painful when he can’t work for the family but for he already

accepted it because his family supported him all throughout and they never make him feel

that he is useless.

Norms
 13

A human’s emotional status depends on the ability to cope up and be ready for

whatever happens in their life. They may or may not be ready to be emotionally stable of

unfortunate happenings in life. Emotional information guide thinking and behavior to

manage and adjust emotions to adapt an environment. Stages of grief and mourning are

expected by people in response to death of valued being. (Health Assessment and Physical

Examination, Mary Ellen Zator Estes)

Analysis

Based on the norms the patient’s emotional status is not normal

IV. Sensory Perception

Sense of Sight

The patient’s eye placement and alignment, pupils, sclera, orbital bruit, and

conjunctiva was assessed. We asked him to read a couple of phrases in the notebook and

I.D since there is no Snellen’s Chart available and the patient was able to read the written

phrases and words on the notebook and I.D. There is no assessed eye discharges and

redness on both eyes.

Norms

The normal version of an average person is 20/20 in distance of 20 feet away and

doesn’t wear any corrective graded lenses. Health Assessment and Physical Examination,

Mary Ellen Zator Estes

Analysis

Based on the norms the patient’s sense of sight is normal.

Sense of Smell
 14

Before assessing, we checked the nasal passages of the patient if he has colds or

any nasal secretions, we did not see any colds or any nasal secretions. We then instructed

the patient to close his eyes and let him identify what kind of aroma he smells using the

cotton balls with alcohol and perfume that we prepared. The patient was able to identify

the difference between the two aromas.

Norms

The normal person can smell and identify the aroma of a given object like perfume

or any other. The person should be able to distinguish the foul to a good smelling things

but it can be deviated if the person has colds or a problem in his nasal sinuses. Health

Assessment and Physical Examination, Mary Ellen Zator Estes

Analysis

Based on the norms the patient’s sense of smell is normal.

Sense of Hearing

We assessed the patient’s sense of hearing by instructing the patient to cover his

ear with his fingers and stood 2 feet behind him and whispered his name and the patient

was able to repeat what we were whispering. There is no tinnitus or any problem assessed.

Norms:

The auditory of the person is normal if the patient do not have a tinnitus or any ear

problem. He should be able to hear in the minimum of 2 feet away. Health Assessment and

Physical Examination, Mary Ellen Zator Estes

Analysis

Based on the norms and our findings the patient’s sense of hearing is normal

Sense of Touch
 15

We assessed the sense of touch of the patient by using two cotton balls soaked in

warm and cold water and we applied in his hands, the patient was able to differentiate the

two. We also assed his pain receptor using a sharp pencil and the eraser for dull to prick

his skin and asked whether he can feel a sharp or dull sensation and can still feel the two

receptor.

Norms

The Tactile sensitivity or hypersensitivity is an unusual or increased sensitivity to

touch that makes the person feel peculiar, or even in pain. It is also called tactile

defensiveness or tactile over-sensitivity. Like other sensory processing issues, tactile

sensitivity can run from mild to severe. Health Assessment and Physical Examination,

Mary Ellen Zator Estes.

Analysis:

Based on the norms the patient’s sense of touch is normal

Sense of Taste:

We assessed the sense of taste of the patient by asking him if he can differentiate

the taste of rice, fish and bread that was in his food tray. The patient was able to identify

the different taste of the food served.

Norms

A person usually identifies the taste of bitter, sweet and sour. By the use of our

sense of taste, we can fix or adjust the taste of our cooked food base on our tasting capacity.

Health Assessment and Physical Examination, Mary Ellen Zator Estes

Analysis

Based on the norms the patient’s sense of taste is normal.

 16

Motor Stability

We instructed the patient to flex and extend both of his arms and legs, rotate his

head and hyperextend the neck. He can do it with ease and the gait is normal but there’s a

little complains of tiredness. There are no involuntary movement assessed and the size of

the muscle is appropriate to his body.

Norms

Normal motor stability includes the ability to perform different steps in doing range

of motions. It should be firm and coordinated movements. Health Assessment and Physical

Examination, Mary Ellen Zator Estes

Analysis

The patient’s motor stability is slightly impaired because of his condition.

Body Temperature

Temperature was taken by using an axillary thermometer at the right axilla, the

temperature reading was:

DATE TIME TEMPERATURE ANALYSIS

02/21/19 9:25 AM 36.5 °C Normal

02/21/19 10:25 AM 36.8 °C Normal

02/22/19 9:00 AM 36.7 °C Normal

Norms

Normal axillary temperature is within 36.4 °C to 37.4 °C. Health Assessment and

Physical Examination, Mary Ellen Zator Estes

 17

Analysis

Based on the norms the patient’s body temperature is normal

Respiratory Status

The respiratory rate, pattern and sounds was assessed, and the results was:

DATE TIME RATE PATTERN SOUNDS ANALYSIS

02/21/19 9:27 AM 24 irregular Fine Above

Crackles Normal

02/21/19 10: 30 AM 26 irregular Fine Above

Crackles Normal

02/22/19 9:35 AM 25 irregular Fine Above

Crackles Normal

Breathes effortly and the rhythm is irregular.

Norms

Normal respiratory rate for adult is 12-20 cpm. Average is 18. In terms of pattern,

normal respirations must be regular and even in rhythm (Eupnea). The normal depth of

respirations is non-exaggerated and effortless. Health Assessment and Physical

Examination 3rd edition Mary Ellen Zator Estes

Analysis

Based on the norms the patient’s respiratory status is above normal because the

patient’s respiratory rate is higher than the normal values and he has a pleural effusion that

causes him to breathe hard and we also noted abnormal breath sound.

Circulatory Status

Blood Pressure was taken at his left brachial pulse, and the results were:
 18

DATE TIME BLOOD ANALYSIS

PRESSURE

02/21/19 9:27 AM 110/70 mmHg Below Normal

02/21/19 10:35 AM 110/80 mmHg Below Normal

02/22/19 9:00 AM 100/80 mmHg Below Normal

Pulse rate was taken at his left peripheral pulse, and the results were:

DATE TIME PULSE RATE ANALYSIS

02/21/19 9:00AM 66 bpm Normal

02/21/19 10:28 AM 64 bpm Normal

02/22/19 8:35 AM 70 bpm Normal

Norms

Normal cardiac rate for an adult is 60-100 beats per minute while the normal blood

pressure is 120/80 mmHg. The working capacity of the heart diminishes with aging. The

heart rate of older people is slow to respond to stress and slow to return to normal after

stress. Reduced arterial elasticity results in diminished blood supply to the parts of the body

especially the extremities. Health assessment and physical examination 3rd Edition Mary

Ellen Estes

Analysis

His blood pressure monitoring was below the normal range. Pulse rates recorded

are normal.
 19

Nutritional Status

The patient is eating three times a day mainly fruits and vegetables, fish and meat

in the diet. He drinks very limited, only 1 liter per day.

Height:5’4”

Weight:50kg

BMI = 18.9 kg/m2 (Normal)

Norms

Nutritional status represents the balance between the nutritional and energy needs

of the body for carbohydrates, proteins, fats, vitamins, and minerals, and the consumption

of these nutrients. Malnutrition, or an altered nutritional status, results from either under

nutrition or over nutrition (nutritional deprivation or excess). Knowledge of an individual’s

nutritional status is essential to the assessment of the person’s general health. Water

consumption per day is 8-10 glasses. Health assessment and physical examination 3rd

edition Mary Ellen Zator Estes

Category BMI range - kg/m2

Severe Thinness < 16

Moderate Thinness 16 – 17

Mild Thinness 17 - 18.5

Normal 18.5 – 25

Overweight 25 – 30

Obese Class I 30 – 35

Obese Class II 35 – 40
 20

Obese Class III > 40

Analysis

Based on the norms is normal, his fluid intake is low but he eats nutritious foods.

Elimination Status

He usually defecates 2-3 times a day, he urinates only 15-20cc per hour. He drinks

1 liter of water per day.

Norms

An individual usually defecate one to two times a day or every 2 days and urinates

30cc/hr. Nutrition by Alex Abelos

Analysis

Based on the norms the patient’s elimination status is not normal because he

urinates less than 30cc of urine per hour.

Reproductive Status

He was circumcised at the age of 11 years old. He had his first sexual intercourse

at 22 years old. He is currently inactive at any sexual activity for 7 years already.

Norms

Males usually begins puberty between the ages on 9 and a half, and 13 and a half.

The average male proceeds through puberty in about 3 years, with a possible range of 2 to

5 years. (Health assessment and physical examination 3rd edition Mary Ellen Zator Estes).

Analysis

The patient’s reproductive system is normal

 21

State of Rest and Sleep

The patient told us that he usually sleeps at 10 pm and wakes up at 6-7am the day

after. During his stay in the hospital the patient has trouble sleeping because of the noise

and people who goes in and out of the room he usually sleeps around 4 am and wakes up

at 6 am.

Norms

A person usually sleeps for about 7 to 9 hours a day and takes a rest using some of

activities that will help you to relax including reading, watching television and others.

Sleep refers to altered consciousness with general slowing of physiologic process while

rest refers to relaxation and calmness, both mental and physical. Health assessment and

physical examination 3rd edition Mary Ellen Zator Estes

Analysis

Abnormal sleeping pattern is observed because of environmental factors such as

noise, temperature and people who goes in and out of the room.

State of Skin and Appendages

When we assessed the patient, there is a hep lock inserted at the right metacarpal

vein. His hair is smooth and the colour is black, there are no lesions, rashes or wounds

seen. Skin is smooth. There is oedema on both legs and hands. There is no dehydration

observed.

Norms

When the skin is pinched, then released, it should return to its original contour

rapidly. Hair varies from dark to pale blonde based on the amount of melanin present. Skin

is dry with minimum perspiration. Skin surfaces should be non-tender, normally feel
 22

smooth, even, and firm. Health assessment and physical examination 3rd edition Mary

Ellen Zator Estes

Analysis

Based on the norms the state of skin and appendages is not normal due to edema

on both hands and legs.

 23

Laboratory and Diagnostic Procedure

LABORAT INDICA FINDIN REFERE INTERPRET NURSING

ORY AND TON GS NCE ATION RESPONSIBI
DIAGNOS VALUE LITIES
TIC
PROCEDU
RE

HEMATOL Indicated Hemoglo Hemoglo NORMAL -Explain the

OGY for bin bin procedure, why
laborator it is done and its
y 128 (135-170) purpose
Date: assessme
nts of the NORMAL
Feb 18, blood Hematoc Hematocr -Monitor vital
2019 formation rit it sign
and to
0.418 (0.390-
detect
0.500%) NORMAL
any blood
-monitor and
associate
RBC regulate the
d
RBC intravenous
disorders.
4.43 fluid
(3.9-5.7 NORMAL
L)
MCV

94.4
MCV
NORMAL
(80-96 L)
MCHC

306 MCHC
NORMAL
(334-355
MCH g/L)

28.9 NORMAL

WBC MCH

9.0 (27.5-32.2
pg )
NORMAL
WBC
POLYS
(4.5-10.5
0.638 L)
NORMAL

POLYS
 24

Lympho (0.55-0.63 NORMAL

cytes )

0.266

Platelet Lymphoc
ytes
206,000
(0.23-
0.35)

Platelet

(150,000-
450,000)

LABORAT INDICA FINDIN REFERE INTERPRET NURSING

ORY AND TON GS NCE ATION RESPONSIBI
DIAGNOS VALUE LITIES
TIC
PROCEDU
RE

BLOOD Analysis Creatini Creatinin ABOVE -Explain the

CHEMIST of blood ne e NORMAL procedure, why
RY chemistry it is done and its
is used to 140.55 (53.0- High level of purpose
measure 106.0 creatine thus
levels of mmol/L ) warn of
important possible
malfunction or -Monitor vital
DATE: electrolyt sign
es such as failure of the
FEB 19 kidney.
sodium,
2019
potassium Kidneys are not -Monitor and
and other doing a good regulate the
chemicals job of clearing intravenous
. waste products fluid
and toxins from
the blood.

-Report any
Electroly Electrolyt
complication
ctes es

Sodium Sodium NORMAL

138.8 (135-
148.0
mmol/L )
 25

Potassiu Potassiu NORMAL

m m

4.15 (3.50-5.30
mmol/L)

LABORATORY INDICATION/ DATE FINDINGS INTERPRETATIONS

AND PURPOSE
DIAGNOSTIC
PROCEDURE

CHEST A noninvasive FEB Chest There is a fluid at the

ULTRASOUND diagnostic exam 19 , sonography right lungs.
that produces 2019 reveals a
images, which right pleural
used to assess effusion w/
the organs and an
structures approximate
within the chest volume of
such as lung, 431 cc.
mediastinum
and pleural
space.
 26

7. Anatomy and Physiology

The cardiovascular system circulates blood and helps in the transport of nutrients,
oxygen, and hormones, and removal of carbon dioxide and cellular wastes from all over
the body. It functions to sustain life by nourishing, protecting, and stabilizing the organ
systems of the body.

Structure of the Cardiovascular System

The cardiovascular system comprises the heart, the blood vessels, and blood are the
components of the cardiovascular system. In an average human, the heart pumps about 5
liters of blood through an approximate distance of 60,000 miles every day.

The Heart

The heart forms the center of the circulatory system, which pumps blood throughout
the body. The heart is about 350 grams and is slightly larger than the fist. It contains 4
chambers: 2 atria (left and right) on the top and 2 ventricles (left and right) at the bottom.
The atria receive blood from all over the body, and the ventricles pump blood into the
system. The right ventricle receives deoxygenated blood and sends it to the lungs for
oxygenation, while the left ventricle receives oxygenated blood from the lungs and sends
it into the system for circulation across the body. Valves between the atria and ventricles
ensure unidirectional flow of blood. The heart beats about 100,000 times, and circulates
about 2,000 gallons of blood every day.

The Blood

An average adult has 4.5 – 5 liters of blood. Blood is made of plasma that is 90%
water, and blood cells. Blood cells are of three types: red blood cells, white blood cells,
and platelets. In addition, it contains secretions such as hormones, nutrients, oxygen,
proteins, and so on. Main functions are supply of oxygen and nutrients, removal of carbon
dioxide and wastes, immune protection, and regulation of body temperature and pH
(homeostasis).

The Blood Vessels

In vertebrates, the circulatory system is of closed type since it never leaves the
network of blood vessels. Arteries, veins, and capillaries, along with coronary vessels and
portal veins, form the network that circulates blood throughout the body. Oxygenated blood
from the heart is carried by arteries for circulation to other parts of the body. Aorta, a
massive thick-walled artery, forms the first part of systemic circulation. Arteries branch
into arterioles and then to capillaries, where nutrients and wastes are exchanged, forming
 27

the microcirculation part. Capillaries reunite to form venules that in turn converge to form
veins. Veins carry the deoxygenated blood back to the heart. All the veins converge to form
superior and inferior vena cava, the two major veins that empty into the right atrium.

Circulatory System

The main organ of the circulatory system is the Human Heart. The other main parts
of the circulatory system include the Arteries, Arterioles, Capillaries, Venules, Veins, and
Blood. The lungs also play a major part in the pulmonary circulation system.

Functions of the circulatory system

The function of a human’s circulatory system is to transport blood around the body.
The blood itself also carries numerous other substances which the body requires to
function.

The main substance being Oxygen, carried by a protein called haemoglobin, found
inside red blood cells. White blood cells are also vital in their role of fighting disease and
infection. Blood contains platelets which are essential for clotting the blood, which occurs
following an injury to stop blood loss. Blood also carries waste products, such as Carbon
Dioxide away from muscles and organs in order to be dispelled by the lungs.
 28

Systemic & pulmonary circulation

There are three circulatory processes occurring simultaneously within the body.
Firstly, systemic circulation carries blood around the body, pulmonary circulation carries
blood to the lungs and coronary circulation provides the heart with its own supply of blood.

At the start of the blood circulatory cycle, the heart pumps oxygenated blood out of
the left ventricle, through the Aorta (the largest artery in the body). The aorta divides into
smaller arteries, then arterioles and finally into microscopic capillaries found deep within
muscles and organs. Here the Oxygen (and other nutrients) passes through the thin capillary
walls, into the tissues where it can be used to produce the energy muscles require to
contract.

A waste product of energy production (metabolism) is Carbon dioxide and in order

to be removed, it too passes across the walls of the capillaries, into the bloodstream. The
blood continues back towards the heart, through venules and then veins, into the right
atrium.

Once blood returns to the heart it is then pumped from the right ventricle through
the Pulmonary arteries to the lungs, where the waste carbon dioxide can be expelled and
more Oxygen collected. The Pulmonary vein carries oxygenated blood back to the left
atrium of the heart, where the cycle starts again.
 29

9. Pathophysiology
Book Based
Left Ventricle Failure Right Ventricle Failure
 Ischemic heart disease  Cor pulmonale
 Myocarditis  Right-sided valvular disease
 Valvular heart disease  Right-sided myocardial disease
 Restrictive pericarditis  Pulmonary hypertension

Compensatory Mechanism

Activation of non- Activation of renin- Myocardial contractility

epinephrine atrial angiotensin aldosterone
natriuretic peptide mechanism
Cardiac workload
Tachycardia
Na and water retention
Cell stretching

Further stress on myocardium Compensatory

Hypertrophy and dilation

Congestive Heart Failure

 30

Client Based:

Modifiable Factors Non-Modifiable Factors

Drinks Alcohol (1-2 bottles) Age: 40

Sedentary Lifestyle Race: Filipino

Fond of eating salty food Gender: Male

Decreased elasticity and formation of plaques on

blood vessels

Narrowing of the blood vessels

Scarring of the vascular endothelium

Impediment of blood flow to the body

Reduced myocardial contractility

Increased cardiac workload

Dilation of the ventricles

Decrease diastolic filling

 31

Contraction of the right sided atrial filling

Increased stretching of the myocardial muscles

Increased in preload

Increased stretching of myocardial muscle

Blood drains back from RV to the RA

Obstruction of right atrial emptying

Ineffective cardiac muscle contraction and increased O2 demand of cardiac muscles cells

Chest pain, difficulty

Decreased contraction of cardiac muscles
breathing and easy
fatigability
Decreased cardiac output and systemic perfusion

Peripheral Edema Congestive Heart Failure

 32

B. PLANNING
VI. Nursing Care Plan

Assessmen Nursing Planning Intervention Rationale Nursing

t Diagnosi Outcomes
s

Subjective Acute After 30 - Provide - To provide non After 30

: Pain minutes to comfort pharmacologic minutes to
1 hour of measures al pain 1 hour of
“Masakit proper
such as management.
proper
yung providing
nursing bed making nursing
dibdib ko” interventio interventio
and
as n patient n patient
hygiene,
verbalized pain will emotional verbalized
be and spiritual relieve of
Objectives
decreased support, pain as
: breathing
and evidence
techniques,
Vital demonstrat by absence
etc.
Signs: e lively - Elevate of chest
aura. head of bed. pain,
BP: 110/70
doesn’t
mmhg - Elevation look
improves chest restless
PR: 66
expansion and
bpm - Monitor and pale
oxygenation.
vital signs, - Tachycardia and pain
RR: 24 especially scale is
and elevated
cpm pulse and blood pressure 1/10.
blood usually occur
Pallor pressure, with angina
every 5 and reflect
Restless minutes compensatory
until pain mechanisms
Chest pain subsides. secondary to
Pain Scale: sympathetic
6/10 nervous system
stimulation.
- Anginal pain is
often
- Teach precipitated by
patient emotional
relaxation stress that can
techniques be relieved
and how to non-
use them to pharmacologic
reduce al measures
stress such such as
as praying, relaxation.
deep
breathing,
thinking of
 33

peaceful - Helps in
scenery etc. relieving pain
Dependent:

- Administere
d pain
reliever as
ordered

Assessment Nursing Planning Intervention Rationale Nursing

Diagnosis Outcomes

Subjective: Ineffectiv After 30 - Position the - Facilitates After 30

e minutes of client in a respiratory minutes of
“Nahihirapa breathing proper semi-fowler function by proper
n ako position use of
pattern nursing nursing
huminga” as gravity.
related to interventio Also to interventio
verbalized fluid in n patient n patient
improve
Objectives: the lungs experience chest experience
lessen expansion d relieve of
Vital Signs: difficulty and shortness
breathing decreases of breath,
BP: 110/80 pressure on
doesn’t
mmhg the
abdomen. look
- Instruct not
PR: 64 bpm - For the exhausted
to wear
fitted patient to or restless
RR: 26 cpm breath and there is
clothes
easily no sign of
Pallor without using
compressin
Restless accessory
g the
diaphragm muscle to
Chest pain breathe.
and for
Dyspnea comfort
purposes
Fine also
Crackles on - Promote
- Encouraged chest
right lung deep expansion
breathing
Use of exercises
accessory - Monitor - Assess the
muscle: respiratory condition of
trapezius pattern the client
including:
rate, depth - To avoid
and effort further
- Teach problem
patient with
about breathing
relaxation
techniques
 34

to reduce
stress and/or - Helps in
anxiety giving
Dependent: adequate
oxygen to
- Give the patient
supplementa
l oxygen as
ordered - To
Collaborative: measures
the acidity,
- Obtain or pH, and
blood the levels of
specimen oxygen
for ABG (O2) and
study carbon
dioxide
(CO2) from
an artery.
And to
know the
function of
the lungs in
receiving
and
excreting
carbon
dioxide

Assessme Nursing Planning Intervention Rationale Nursing

nt Diagnosis Outcomes

Subjective Activity After - Assess for - Fatigue is a After

: intolerance series of other causes side effect series of
related to proper of fatigue of some proper
“Hindi ako imbalance nursing
(treatments, medication
nursing
masyado pain, s (beta-
between interventio medications) blockers, interventio
gumagala oxygen n patient n patient
. tranquilizer
w kasi supply/deman achieve achieved
s, and
mabilis d measurabl sedatives). measurabl
ako e increase Pain and e increased
mapagod” in activity stressful in activity
as regimens
tolerance, tolerance,
verbalized also extract
evidence energy and evidenced
Objectives by reduced produce by
: fatigue and fatigue. weakness
weakness and vital
Vital and by - Conserves signs
Signs: vital signs energy and within
within promote acceptable
safety
acceptable limits
 35

BP: 100/80 limits - Instruct during

mmhg during client in activity.
activity unfamiliar
PR: 70 activities
- Relaxes the
bpm and in
body and
alternate
promotes
RR: 25 ways of
comfort
cpm conserve
energy
Pallor - Prevents
risk for
Restless - Encourage
falls that
patient to
could lead
Dyspnea have
to injury
adequate
Limited bed rest and
range of sleep - Prevents
injuries
motion
- Assist the
client in
ambulation

- Assist the
- Meets
client in
patient’s
learning and
personal
demonstrati
care needs
ng
without
appropriate
undue
safety
myocardial
measures
stress and
excessive
- Provide oxygen
assistance demand.
with self-
care
activities as - To prevent
indicated. deep vein
Intersperse thrombosis
activity due to
periods with vascular
rest periods. congestion.

- Assist
patient with
ROM
exercises.
Check
regularly for
calf pain and
tenderness.
 36

C. IMPLEMENTATION
1. DRUG STUDY

Dosage and Route Nursing

Responsibilities
Name of Drug Action Indications Contra-indications Side Effects

Generic Name:  750 mg IVP Second generation  Pharyngitis  Hyper- Body as a Whole:  Observe 10
q8 cephalosporin  Tonsillitis sensitivity to rights
Cefuroxime  Infection of drug  Thrombo-  Monitor Vital
that inhibits cell Phlebitis Signs
the urinary and  Hyper-
wall synthesis , lower sensitivity to (IV site)  Determine
Brand Name: promoting osmotic respiratory penicillin  Pain history of
instability : usually tracts
because of  Burning Hypersensitivity
Zoltax bactericidal  Skin and skin  Cellulitis to
structure possibility of cephalosphorins
(IM site)
infections cross
 Super  History of
caused by sensitivity Allergies
Infection
Classification: streptococcus with other  (+)Coombs  Report onset of
pneumoniae betalactam loose stools
Test
Antibiotic and antibiotics  Absorption of
S.pyogenes , cefuroxime is
haemophillus  Breast
GI: enchanced by
influenzae , feeding
food
women
staphylococcus   Notify
aureus ,  History of Diarrhea
 Nausea prescriber about
escherichia colitis or
 Antibiotic rashes or
coli. renal
associated superinfections
sufficiency
colitis
 37

Skin:

 Rash
 Pruritus
 Urticaria

Name of Drug Dosage and Route Action Indications Contra-indications Side Effects Nurssing
Responsibilities

Generic Name:  10 mg / OD A fungal metabolite  Adjunct to  Allergy to any CNS:  Observe 10

that inhibits the diet in component of rights
Rosuvastatin enzyme (HMG- treatment of the product ,  Headache  Monitor Vital
Calcium elevated total active liver  Dizziness Signs
CoA) that catalyzes
cholesterol disease or  Insomnia  Establish
the first step in
and LDL persistent  Hypertonia baseline serum
cholesterol synthesis cholesterol elevated serum  Paresthesia lipid levels and
Brand Name: pathway , resulting and transaminase ,  Depression liver functio n
Torus
in a decrease in triglyceride pregnancy ,  Anxiety test results
serum cholesterol , levels in lactation  Vertigo before
serum LDLs and patients with  Used  Neuralgia beginning
primary cautiously with therapy
either increase or no
Classification: hyperchole impaired  Consult
sterolemia hepatic dietician about
function ,
 38

Anti-hyperlipidemic change in serum  Adjunct to alcoholism , CV: low cholesterol

drug HDLs slow renal diets
atherosclerosis impairment ,  Hypertension  Administter
progression in advanced age ,  Angina drug at
patients with hypothyroidism pectoris bedtime(highest
elevated  Vasodilation  Rate of
cholesterol  Palpitation cholesterol
 Adjunct to  Peripheral synthesis occur
diet for edema between
treatment of midnight and
patients with 5am)
elevated GI:  Monitor
serum patients for
triglyceride  Nausea closely signs of
levels  Vomiting injury
  Dyspepsia
 Diarrhea
 Constipation
 Gastroenteritis
 Flatulence
 Peridontal
abscess
 Gastritis
 Liver failure
 39

Name of Drug Dosage and Route Action Indications Contra-indications Side effects Nursing
Responsibilities

Generic Name:  Mg IV q8 Inhibits sodium and  Edema due  Anuria: CNS:  Observe 10
with strict chloride to cardiac Hepatic right
Furosemide bp reabsorption in the  Hepatic and Coma and  Dizziness  Monitor
precaution renal disease precoma  Encephalo- Vital Signs
ascending loop of
 Burns : mild  Severe pathy  Assess fluid
henle , thus
to moderate hypokalemia  Headache status during
Brand Name: increasing renal
 Hypertension or Hypo  Insomnia therapy
excretion of sodium 
Lasix Crisis natremia  Nervousness Monitor
, chloride and water  Acute heart  Hypovolemia Daily weight
failure or Intake and
 Chronic hypotension EENT: output ratios
Classification: renal failure  Hyper  Amount and
 Hearing loss
 Nephritic sensitivity to location of
Loop Diuretics
syndrome fursemide or  Tinnitus edema
 Latent or sulfonamides  Assess lung
manifest sounds , skin
CV:
diabetes turgor , and
mellitus  Hypo mucous
 Gout tension membranes
 Obstruction  Monitor
of passages electrolytes ,
GI: renal and
hepatic
 Constipation function ,
 Diarrhea serum
glucose and
 40

 Dry mouth uric acid

 Dyspepsia levels befre
 Nausea and
 Vomiting periodically
throughout
therapy

Derm:

 Photosensitivity
 Rashes

Endo:

 hyperglycemia
 41

2.MEDICAL MANAGEMENT

Treatment Date Indication Client Nursing

performed reaction responsibilities

Administration Feb 18, Inhibits Client was  Assess

of furosemide 2019 sodium and relieved from fluid
chloride edema due to status
reabsorption congestive during
therapy
in the heart failure
 Monitor
ascending Daily
loop of weight
henle , thus Intake
increasing and
renal output
excretion of ratios
sodium ,  Amount
chloride and and
water location
of
edema

3. DIET

TYPE OF DIET DATE INDICATION/S

Feb 18, 2019 Eating too much salt causes

the body to keep or retain too
much water, worsening the
Low sodium fluid buildup that happens
with heart failure.

Feb 18, 2019 A low-fat diet is one that

restricts fat and often
Low fat saturated fat and cholesterol
as well.
 42

Feb 18, 2019 Low cholesterol diet that

restricts foods containing
Low Cholesterol
animal fats and saturated fatty
acids. The diet is indicated for
persons with high serum
cholesterol levels,
cardiovascular disorders and
obesity.

4. ACTIVITY AND EXERCISE

ACTIVITY AND EXERCISE INDICATION PURPOSE

-This type of exercise involves slow movement to

Flexibility/Stretching
lengthen the muscles. Flexibility exercises include
stretching, tai chi and yoga. They are also used
before and after exercising to prevent injury and
strain. Benefits include better balance, range of
motion and better movement in your joints.
 43

-Walking improves muscle tone and strength

Walking -Walking keeps you from losing endurance and

getting weak muscles

-This exercise is one of the main gaits of

locomotion. The body vaults over the stiff limb.
This exercise is used to increase body mobility and
functionality. It also helps to promote muscle
function and increase tolerance for body capacity in
exerting effort and activity.

-This exercise is used to improve pulmonary gas to

exchange and maintain respiratory functions
Deep Breathing Exercise
especially after generalized/ minimal
immobilization. This is also use as a relaxation
technique.
 44

D. EVALUATION

Assessment:

Subjective: “Nahihirapan ako huminga” as verbalized

Objectives:

Vital Signs:

BP: 110/80 mmhg

PR: 64 bpm

RR: 26 cpm

Pallor

Restless

Chest pain

Dyspnea

Fine Crackles on right lung

Use of accessory muscle: trapezius

Nursing Diagnosis: Ineffective breathing pattern related to fluid in the lungs

Planning: After 30 minutes of proper nursing intervention patient experience lessen difficulty
breathing

Intervention: Position the client in a semi-fowler position, instruct not to wear fitted clothes,
encouraged deep breathing exercises, monitor respiratory pattern including: rate, depth and
effort, teach patient about relaxation techniques to reduce stress and/or anxiety
Dependent: Give supplemental oxygen as ordered

Collaborative: Obtain blood specimen for ABG study

Evaluation: After 30 minutes of proper nursing intervention patient experienced relieve of

shortness of breath, doesn’t look exhausted or restless and there is no sign of using accessory
muscle to breathe.
 45

V. Conclusion

After our exposure in the medicine ward, we as student nurses of Tarlac State University
had gain more skills and had acquired knowledge with regards to handling patients who are
suffering from Congestive Heart Failure. We learned a lot about the symptoms, manifestations,
risk factors, complications, etiology, pathophysiology, proper management and treatment. The
group established good rapport to the patients and good teamwork and collaboration within the
group. We were able to maximize our skills, behaviour and knowledge and have delivered the
best possible care that our patients need based on the nursing process. The group has
emphasized and able to provide proper health educations that could help improve the health of
our patients. Based on the data that has been gathered in this case study, we therefore conclude
that all the objectives and goals were achieved.
VI. RECOMMENDATION

A. Student Nurse

To our fellow student nurses, to enhance our knowledge, attitude and skills in having a proper
nursing care management, we will use this case as a guide and will serve as an educational
companion to have a better understanding about specific cases including Congestive Heart Failure.
Case studies will help us to be more aware of different causes, risk factors, pathophysiology
therapies and treatments on different cases. To establish a good rapport to the patient is also like
building an effective collaboration with your groupmates. Unity, teamwork, patience, trust,
prioritization, and focus are necessary things to accomplish a good case study.

B. Patient

Patient must keep in mind the diet changes of decreased fat intake is prudent. Patient should
eat more foods that low in cholesterol, sodium and fats, food that rich in vitamins and minerals
such as whole grains, poultry eggs, fish and nuts. Drinking plenty of water to maintain the
hydration of the body and a healthy lifestyle is important. Patient must continue the treatment and
take the medications as prescribed by the physician. Daily exercise is also essential. Walking daily
should be performed. Following the regimen of discharge medications is also important.
 46

VII. REVIEW OF RELATED LITERATURE

Introduction
Acute heart failure (AHF) is a relevant public health problem causing the majority of
unplanned hospital admissions in patients aged of 65 years or more. Despite major
achievements in the treatment of chronic heart failure (HF) over the last decades, which led to
marked improvement in long-term survival, outcomes of AHF remain poor with 90-day
rehospitalization and 1-year mortality rates reaching 10–30%. Persistence of poor outcomes in
AHF might be related to the paucity of improvements in the acute management of those
patients. Despite lacking evidence of beneficial effects on outcome, acute treatment of AHF
still mainly consists of non-invasive ventilation in case of pulmonary oedema, intravenous
diuretics and/or vasodilators. These interventions are tailored according to the initial
haemodynamic status with little regard to the underlying pathophysiological particularities.
Acute heart failure was historically described as a pump failure causing downstream
hypoperfusion and upstream congestion. During the last decades a more complex network of
interactions has been added to the simplistic haemodynamic model for explaining the
pathophysiology of AHF. In addition, AHF is not a specific disease but the shared clinical
presentation of different, heterogeneous cardiac abnormalities. Therefore, there is an unmet
need for increased individualization of AHF treatment according to the predominant
underlying pathophysiological mechanisms to, hopefully, improve patient’s outcome.

Pathophysiology of acute heart failure

Acute heart failure is defined as new-onset or worsening of symptoms and signs of HF, often
requiring rapid escalation of therapy and hospital admission. The clinical presentation of AHF
typically includes symptoms or signs related to congestion and volume overload rather than to
hypo perfusion. Since congestion plays a central role for the vast majority of AHF cases,
understanding of the underlying pathophysiological mechanisms related to congestion is
essential for treating AHF patients. More importantly, the level of congestion and the number
of congested organs have prognostic relevance in HF patients.

Mechanisms of congestion: fluid accumulation and fluid redistribution

In presence of cardiac dysfunction, several neuro-humoral pathways, including the
sympathetic nervous system, the renin-angiotensin-aldosterone system and the arginine-
vasopressin system, are activated to counter the negative effects of HF on oxygen delivery to
the peripheral tissues. Neuro-humoral activation in HF leads to impaired regulation of sodium
excretion through the kidneys which results in sodium and, secondarily, fluid accumulation .
Indeed, significantly increased cardiac filling pressures and venous congestion are frequently
observed days or weeks before the overt clinical decompensation.

Congestion in heart failure.

Tissue oedema occurs when the transudation from capillaries into the interstitium exceeds the
maximal drainage of the lymphatic system. Transudation of plasma fluid into the interstitium
results from the relation between hydrostatic and oncotic pressures in the capillaries and in the
interstitium as well as interstitial compliance. Increased transcapillary hydrostatic pressure
gradient, decreased transcapillary oncotic pressure gradient and increased interstitial
compliance promote oedema formation.
 47

In healthy individuals, increased total body sodium is usually not accompanied by oedema
formation since a large quantity of sodium may be buffered by interstitial glycosaminoglycan
networks without compensatory water retention. Moreover, the interstitial glycosaminoglycan
networks display low compliance which prevents fluid accumulation in the interstitium.
In HF, when sodium accumulation persists, the glycosaminoglycan networks may become
dysfunctional resulting in reduced buffering capacity and increased compliance. In AHF the
presence of pulmonary or peripheral oedema correlates poorly with left- and right-sided filling
pressures, but in patients with dysfunctional glycosaminoglycan networks even mildly
elevated venous pressures might lead to pulmonary and peripheral oedemas. In addition, since
a large amount of sodium is stored in the interstitial glycosaminoglycan networks and does not
reach the kidneys, it escapes renal clearance and is particularly difficult to remove from the
body.
Moreover, persistent neuro-humoral activation induces maladaptive processes resulting in
detrimental ventricular remodelling and organ dysfunction. Based on that, pharmacological
therapies that inhibit the sympathetic and renin-angiotensin-aldosterone systems, including
beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers,
aldosterone antagonists and more recently the angiotensin receptor neprilysin inhibitor
LCZ696 have become the mainstays of chronic HF therapy.
Fluid accumulation alone cannot explain the whole pathophysiology of AHF. Indeed, the
majority of AHF patients display only a minor increase in body weight (<1 kg) before hospital
admission.
In those patients, congestion is precipitated by fluid redistribution, rather than accumulation.
Sympathetic stimulation has been shown to induce a transient vasoconstriction leading to a
sudden displacement of volume from the splanchnic and peripheral venous system to the
pulmonary circulation, without exogenous fluid retention. Nonetheless, the prerequisite for
fluid redistribution is the presence of a certain amount of peripheral and splanchnic congestion.
In physiological states, capacitance veins contain one fourth of the total blood volume and
stabilize cardiac preload, buffering volume overload. In hypertensive AHF, the primary
alteration is a mismatch in the ventricular-vascular coupling relationship with increased
afterload and decreased venous capacitance (increased preload).
Fluid accumulation and fluid redistribution both produce an increase in cardiac load and
congestion in AHF, but their relevance is likely to vary according to different clinical
scenarios. While fluid accumulation might be more common in decompensations of congestive
heart failure (CHF) with reduced ejection fraction, fluid redistribution might be the
predominant pathophysiological mechanism in AHF with preserved ejection fraction.
Accordingly, the decongestive therapy should be tailored. While diuretics might be useful in
presence of fluid accumulation, vasodilators might be more appropriate in presence of fluid
redistribution to modulate ventricular-vascular coupling.
Furthermore, recent experimental data from human models suggest that venous congestion is
not simply an epiphenomenon secondary to cardiac dysfunction but rather plays an active
detrimental role in the pathophysiology of AHF inducing pro-oxidant, pro-inflammatory and
haemodynamic stimuli that contribute to acute decompensation. How these pathophysiological
changes are induced remains incompletely understood but the biomechanical forces generated
by congestion significantly contribute to endothelial and neuro-humoral activation. Indeed,
endothelial stretch triggers an intracellular signalling cascade and causes endothelial cells to
undergo a phenotypic switch to a pro-oxidant, pro-inflammatory vasoconstricted state.
 48

Congestion-induced organ dysfunction

Venous congestion significantly contributes to organ dysfunction in both chronic and acute HF
(see Table 1).
Table 1
Overview of congestion-induced organ dysfunction and clinical manifestations

Congested
Clinical manifestation References
organ
Third heart sound, jugular vein distension, positive hepato-jugular
reflux
83–85
Heart Functional mitral and tricuspid regurgitation
Elevated NPs: BNP >100 pg/mL, NT-proBNP >300 pg/mL, MR-
proANP >120 pmol/L
Dyspnoea, orthopnoea, bendopnoea, paroxysmal nocturnal
dyspnoea
Auscultatory rales, crackles, wheezing; tachypnoea and hypoxia 8,66
Lung
Pathological chest radiography (interstitial/alveolar oedema,
pleural effusion)
B-lines (‘comets’) on lung ultrasound
Decreased urine output 44,45
Kidney
Elevated creatinine levels, hyponatraemia
Right-sided upper abdominal discomfort, hepatomegaly, icterus 47,48
Liver
Elevated parameters of cholestasis
Nausea, vomiting, abdominal pain
46,51
Bowel Ascites, increased abdominal pressure
Cachexia

The close interaction between cardiac and renal dysfunction is known as the cardio-renal
syndrome. Historically, renal dysfunction in HF was described as consequence of reduced
cardiac index and arterial underfilling both causing renal hypoperfusion. More recent data
showed that venous congestion (assessed as increased central venous pressure) was the
strongest haemodynamic determinant for the development of renal dysfunction and low cardiac
index alone in AHF has minor effects on renal function. However, the combination of elevated
central venous pressure and low cardiac index is particularly unfavourable for renal function.
Visceral congestion may increase intra-abdominal pressure in HF, which further negatively
affects renal function in HF. Recent data showed that reducing central venous and intra-
abdominal pressures by decongestive therapy may ameliorate serum creatinine, presumably by
alleviating renal and abdominal congestion.
Cardiac dysfunction is frequently associated with liver abnormalities (cardio-hepatic
syndrome) and negatively influences prognosis in AHF. Cholestatic liver dysfunction is
common in HF and is mainly related to right-sided congestion, while rapid and marked
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elevation in transaminases in AHF indicates hypoxic hepatitis related to hypoperfusion.

Finally, bowel congestion may contribute to development of cachexia in patients with
advanced HF.

Assessment of congestion
Detection of congestion at an early (asymptomatic) stage is still an unmet need. Improved
diagnostic methods would be highly valuable to enable early initiation of appropriate therapy
following the ‘time to therapy’ approach recently introduced into HF guidelines. The
guidelines emphasize the potentially greater benefit of early treatment in the setting of AHF,
as has long been the case for acute coronary syndromes. Indeed, the congestive cascade often
begins several days or weeks before symptom onset and includes a sub-clinical increase of
cardiac filling and venous pressures (‘haemodynamic congestion’) which may further lead to
redistribution of fluids within the lungs and visceral organs (‘organ congestion’) and finally to
overt signs and symptoms of volume overload (‘clinical congestion’). Clinical congestion may
be the ‘tip of the iceberg’ of the congestive cascade. Although organ congestion is usually
related to haemodynamic congestion, this might not be always true: indeed, several
mechanisms might prevent oedema formation despite increased venous pressures and
conversely, oedema might develop even in absence of increased hydrostatic pressure.
To achieve early detection of congestion, several strategies including cardiac biomarkers,
intrathoracic impedance monitoring and implantable haemodynamic monitoring have been
proposed. However, the use of classical biomarkers, in particular natriuretic peptides (NPs),
which are released by the failing heart, reflect the severity of myocardial dysfunction and only
indirectly haemodynamic congestion. Novel vascular biomarkers (e.g. soluble CD146,
CA125) might better correlate with congestion than NPs.

Diagnosis of acute heart failure

The early management of AHF should consist of three parts: triage, diagnosis and initiation of
treatment, and reassessment Since AHF is a life threatening condition, current guidelines for
the management of AHF recommend that diagnosis and initiation of treatment should occur as
early as possible, optimally during the first 30–60 min after hospital admission.

Clinical evaluation
The initial clinical evaluation of dyspnoeic patients should help to (i) assess severity of AHF
(ii) confirm the diagnosis of AHF and (iii) identify precipitating factors of AHF.
Since congestion is a typical feature of AHF, patient history and physical examination should
primarily focus on the presence of congestion which would support the diagnosis of AHF.
Left-sided congestion may cause dyspnoea, orthopnoea, bendopnoea, paroxysmal nocturnal
dyspnoea, cough, tachypnoea, pathological lung auscultation (rales, crackles, wheezing) and
hypoxia. The absence of rales and a normal chest radiography do not exclude the presence of
left-sided congestion. Indeed, 40–50% of patients with elevated pulmonary-artery wedge
pressure may have a normal chest radiography. Right-sided congestion may cause increased
body weight, bilateral peripheral oedema, decreased urine output, abdominal pain, nausea and
vomiting, jugular vein distension or positive hepato-jugular reflux, ascites, hepatomegaly,
icterus.
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Symptoms and signs of hypoperfusion indicate severity and may include hypotension,
tachycardia, weak pulse, mental confusion, anxiety, fatigue, cold sweated extremities,
decreased urine output and angina due to myocardial ischaemia. The presence of inappropriate
stroke volume and clinical and biological signs of hypoperfusion in AHF defines cardiogenic
shock, the most severe form of cardiac dysfunction. Cardiogenic shock is most frequently
related to acute myocardial infarction and accounts for less than 10% of AHF cases but is
associated with in-hospital mortality rates of 40–50%.
However, given the limited sensitivity and specificity of symptoms and signs of AHF, the
clinical evaluation should integrate information from additional tests.
According to the presence of clinical symptoms or signs of organ congestion (‘wet’ vs. ‘dry’)
and/or peripheral hypoperfusion (‘cold’ vs. ‘warm’), patients may be classified in four groups.
About two of three AHF patients are classified ‘wet-warm’ (congested but well perfused),
about one of four are ‘wet-cold’ (congested and hypoperfused) and only a minority are ‘dry-
cold’ (not congested and hypoperfused). The fourth group ‘dry-warm’ represent the
compensated (decongested, well-perfused) status. This classification may help to guide initial
therapy (mostly vasodilators and/or diuretics) and carries prognostic information. Patients with
cardiopulmonary distress should be managed in intensive cardiac care units.
Notably, the use of inotropes should be restricted to patients with cardiogenic shock or AHF
resulting in hypotension and hypoperfusion to maintain end-organ function, since their often
inappropriate use is associated with increased morbidity and mortality.
Acute heart failure usually consists of acute decompensation of chronic HF (ADHF) or, less
frequently, may arise in patients without previous history of symptomatic HF (de novo AHF).
The distinction of these two scenarios is important because the underlying mechanisms leading
to AHF are significantly different. Indeed, while pre-existing pathophysiological
derangements predispose CHF patients to ADHF, de novo AHF is typically induced by severe
haemodynamic alterations secondary to the initial insult. Common causes of de novo AHF
include acute myocardial infarction, severe myocarditis, acute valve regurgitation and
pericardial tamponade. On the other hand, ADHF may be precipitated by several clinical
conditions, while in some patients, no precipitant can be identified.
Rapid identification of precipitants of AHF is crucial to optimize patient management. The
most common precipitants are myocardial ischaemia, arrhythmias (in particular paroxysmal
atrial fibrillation), sepsis and/or pulmonary disease, uncontrolled hypertension, non-
compliance with medical prescriptions, renal dysfunction and iatrogenic causes. The
identification of precipitants of AHF aims at detecting reversible or treatable causes and at
assisting prognostication. Indeed, the initial management should include, in addition to
vasodilators and/or diuretics, also specific treatments directed towards the underlying causes
of AHF. In particular, early coronary angiography with revascularization is recommended in
AHF precipitated by acute coronary syndrome, antiarrhythmic treatment and/or electrical
cardioversion are recommended in AHF precipitated by arrhythmia, rapid initiation of
antimicrobial therapy is recommended for AHF precipitated by sepsis. Furthermore,
identification of precipitants of AHF may allow risk stratification of patients with AHF.
Indeed, AHF precipitated by acute coronary syndrome or infection is associated with poorer
outcomes whereas outcomes tend to be better in AHF precipitated by atrial fibrillation or
uncontrolled hypertension.
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Additional tests
Additional laboratory tests are helpful in the evaluation of patients with AHF. Natriuretic
peptides, including B-type NP (BNP), amino-terminal pro-B-type NP (NT-proBNP) and mid-
regional pro-atrial NPs (MR-proANP) show high accuracy and excellent negative predictive
value in differentiating AHF from non-cardiac causes of acute dyspnoea. Natriuretic peptide
levels in HFpEF are lower than in HFrEF. Low circulating NPs (thresholds: BNP <100 pg/mL,
NT-proBNP <300 pg/mL, MR-proANP <120 pmol/L) make the diagnosis of AHF unlikely.
This is true for both HFrEF and HFpEF. A recent meta-analysis indicated that at these
thresholds BNP and NT-proBNP have sensitivities of 0.95 and 0.99 and negative predictive
values of 0.94 and 0.98, respectively, for a diagnosis of AHF. MRproANP had a sensitivity
ranging from 0.95 to 0.97 and a negative predictive value ranging from 0.90 to 0.97.
However, elevated levels of NPs do not automatically confirm the diagnosis of AHF, as they
may also be associated with a wide variety of cardiac and non-cardiac causes. Among them,
atrial fibrillation, age, and renal failure are the most important factors impeding the
interpretation of NP measurements. On the other hand, NP levels may be disproportionally low
in obese patients and in those with flash pulmonary oedema. Natriuretic peptides should be
measured in all patients with suspected AHF upon presentation to the emergency department
or intensive cardiac care units.
Cardiac troponin may be helpful to exclude myocardial ischaemia as precipitating factor of
AHF. However, cardiac troponin, in particular when measured with high-sensitive assays, is
frequently elevated in patients with AHF, often without obvious myocardial ischaemia or an
acute coronary event. Indeed, AHF is characterized by accelerated myocardial necrosis and
remodelling. Troponin measurement may be considered for prognostication as elevated levels
are associated with poorer outcomes. Numerous clinical variables and biomarkers are
independent predictors of in-hospital complications and longer-term outcomes in AHF
syndromes, but their impact on management has not been adequately established. The easy-to
perform AHEAD score based on the analysis of co-morbidities has been shown to provide
relevant information on short and long term prognosis of patients hospitalized for AHF.
An electrocardiography (ECG) may be helpful to identify potential precipitants of AHF (e.g.
arrhythmia, ischaemia) and to exclude ST-elevation myocardial infarction requiring immediate
revascularization. However, ECG is rarely normal in AHF patients. Current guidelines do not
recommend immediate echocardiography in all patients presenting with AHF. However, all
patients presenting with cardiogenic shock or suspicion of acute life-threatening structural or
functional cardiac abnormalities (mechanical complications, acute valve regurgitation, aortic
dissection) should receive immediate echocardiography. Early echocardiography should be
considered in all patients with de novo AHF and in those with unknown cardiac function,
however, the optimal timing is unknown (preferably within 24–48 h from admission).
Thoracic ultrasound and chest X-ray may both be useful to assess the presence of interstitial
pulmonary oedema. While chest X-ray may also be helpful to rule-out alternative causes of
dyspnoea (e.g. pneumothorax, pneumonia), both techniques provide complementary
information about the presence of pulmonary oedema or pleural effusion. Abdominal
ultrasound may be useful to measure inferior vena cava diameter and collapsibility and exclude
the presence of ascites.
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Reassessment and allocation

Most of the patients presenting with AHF require hospital admission. The level of care
(discharge, observation, ward, telemetry and intensive cardiac care unit) should be based on
history (including symptom severity, precipitating factors), physical examination
(haemodynamic and respiratory status, degree of congestion) and biomarkers (NPs, cardiac
troponin, renal function, serum lactate). Forty to 50% of AHF patients require admission to
intensive cardiac care units. Low risk AHF patients (those with slightly elevated NP levels,
normal blood pressure, stable renal failure, normal troponin) and with good response to initial
therapy may be considered for early discharge. Follow-up plans must be in place prior to
discharge and clearly communicated to the primary care team.

Pathophysiology-based management
According to current knowledge on the pathophysiology of AHF, the initial treatment of AHF
patients should include decongestive therapy (e.g. vasodilators and/or diuretics) and specific
therapy directed towards the underlying causes of AHF (e.g. revascularization, antiarrhythmic
treatments, antimicrobial drugs). Moreover, early administration of oral disease-modifying HF
therapy (beta-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor
blockers and mineralocorticoid receptor antagonists), before hospital discharge is
recommended in all patients with AHF.

Conflict of interest: MA is recipient of a fellowship of the Collège de Médecine des Hôpitaux

de Paris. JP has received honoraria for lectures from Novartis, Orion Pharma and Roche
Diagnostics. AM has received speaker honoraria from Abbott, Novartis, Orion, Roche and
Servier and fee as member of advisory board and/or steering committee from Cardiorentis,
Adrenomed, MyCartis, ZS Pharma and Critical Diagnostics. The other authors declare no
conflict of interest.

BIBLIOGRAPHY

a. Reference books:
-Health assessment and physical examination 3rd edition Mary Ellen Zator Estes
-Brunner and Suddarth textbook of Medical and Surgical Volume 1 twelfth edition
-Brunner and Suddarth textbook of medical and Surgical Volume 2 10th edition
-Nursing 92 drug handbook
-Lynda Juall Carpenito-Moyet, Hand of Nursing Diagnosis 12th edition
- Wolters Kluwer Nursing Drug hand Book 2017

b. Websites:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2813829/