A CASE PRESENTATION ON ACUTE CORONARY SYNDROME AND

MYOCARDIAL INFARCTION

Presented to the Faculty of the School of Nursing

Adventist Medical Center College
Brgy. San Miguel, Iligan City

In Partial Fulfillment
of the Requirements for the Degree
BACHELOR OF SCIENCE IN NURSING

Abdullah, Asniah
Amano, Amirah
Chinchuntic, Joan
Cornell, Nur Muhammad
Etulle, Earl Juffeny
Borres, Mary Rucile
Bughaw, Alvin Miko
Largo, Ditchen

OCTOBER 2018
 TABLE OF CONTENTS

I. TITLE PAGE

II. TABLE OF CONTENTS

III. LIST OF TABLES

IV. LIST OF FIGURES

V. OBJECTIVES 1

General Objective

Specific Objectives

VI. DEFINITION OF TERMS 2

VII. INTRODUCTION 3-5

VIII. NURSING HEALTH HISTORY

Vital information 6

History of present health concern 7

Past history 8

Genogram 9

Physical assessment and review of systems 10-15

Gordons assessment 16-17

Diagnostic tests 18-20

IX. NORMAL ANATOMY AND PHYSIOLOGY 21-24

X. PATHOPHYSIOLOGY 25-26

XI. NURSING CARE PLANS 27-33

XII. DISCHARGE PLAN 34-46

XIII. REFERENCES 47
 LIST OF TABLES

1 PHYSICAL ASSESSMENT AND REVIEW OF SYSTEMS 10-15

2 GORDONS ASSESSMENT 16-17

3 NORMAL ANATOMY AND PHYSIOLOGY 21-24

4 NURSING CARE PLAN 27-33

 LIST OF FIGURES

1 GENOGRAM 9

2 PATHOPHYSIOLOGY 25-26
 OBJECTIVES

General Objectives:

At the end of one and a half hour of case presentation, the participants will be able to
learn about the disease process of Acute Coronary Syndrome and Myocardial
Infarction.

Specific Objectives:

At the end of one and a half hour of case presentation, the participants will be able to:

1. Relate the health history of the patient to Acute Coronary Syndrome and
Myocardial Infarction;
2. Categorize the physical assessment and review of system involved Acute
Coronary Syndrome and Myocardial Infarction.
3. Numerate at least 5 diagnostic tests related to Acute Coronary Syndrome and
Myocardial Infarction.
4. Discuss the anatomical structure and functions involved in Acute Coronary
Syndrome and Myocardial Infarction.
5. Summarize the pathophysiology, risk factors and manifestations of Acute
Coronary Syndrome and Myocardial Infarction.
6. Formulate appropriate nursing process for the client with Acute Coronary
Syndrome and Myocardial Infarction.
7. Organize a health education and discharge plan.

1
 DEFINITION OF TERMS

Acidosis- an acid-base imbalance characterized by an increase in H concentration

(decreased blood pH). (Tortora,2011)

Atherosclerosis- Progressive disease characterized by the formation in the walls of

large and medium sized arteries of lesions called artherosclerotic plaques.

(Tortora,2011)

Automaticity- ability of cardiac cells to initiate an electrical impulse. (Hinke, 2014)

Contractility- The ability of cells or parts of cells to actively generate force to

undergo shortening for movements. Muscle fibers exhibit a high degree

of contractility. (Tortora,2011)

Collateral circulation- re-routing of blood circulation around a blocked artery or

vein via nearby minor vessels. (Hinke, 2014)

Hypoxia- lack of adequate tissue oxygen at the tissue level. (Hinke, 2014)

Ischemia- lack of sufficient blood to a part due to obstruction or constriction of a

blood vessel. (Hinke, 2014)

Necrosis- a pathological type of cell death that results from disease, injury, or lack of

blood supply in which many adjacent cells swell, burst, and spill their contents into

the interstitial fluid, triggering an inflammatory response. (Tortora,2011)

Thrombosis- formation of clot in an unbroken blood vessel, usually a vein.

(Tortora,2011)

Transmural- existing or occurring across the entire wall of an organ or blood vessel.

(Tortora,2011)

2
 INTRODUCTION

A heart beat signifies life, from the day it starts to beat in the worm, till it
stops, and where death conquers us. The heart beats not only to one tune but it also
responds to the tune of emotions and physical stress. As some of us may have also
experience moments of joy or sorrow and the heart may feel pain or pleasure. In
medicine, an acute disease is a disease with a rapid onset or a short course. The term
“Acute” may often be confused by the general public to mean “severe”, however, this
has a different meaning. Coronary, may refer to as “heart” or “relating to the heart”.
While syndrome is define as a set of signs and symptoms that tend to occur together
and which reflect the presence of a particular disease or an increased chance of
developing a particular disease.

Acute coronary syndrome (ACS) is an enlargement situation characterized by

an acute onset of myocardial ischemia that results in myocardial death. In acute
coronary syndrome, it is believed that the atherosclerotic plaque in the coronary
artery rupture, resulting in platelet aggregation (“clumping”), thrombus (“clot”)
formation, and vasoconstriction. The amount of disruption of the atherosclerotic
plaque determines the degree of obstruction of the coronary artery and the specific
disease process (unstable angine or myocardial infarction, MI). Because between 10%
and 30% of clients with unstable angina progress to having MI in 1 year, and 29% die
in MI in 5 years (AHA,2013).

The most serious acute coronary syndrome is MI, often referred to as a “heart
attack”. Undiagnosed or untreated angina can lead to this very serious health
problems.

Myocardial Infarction (MI) occurs when myocardial tissue is abruptly and

severely deprived of oxygen. When blood flow acutely reduced by 80% to 90%,
ischemia develops. Ischemia can lead to injury and necrosis (infarction) of
myocardial tissue if blood flow is not restored. Most of MIs are the result of
atherosclerosis of coronary artery, rupture of the plaque, subsequent thrombosis, and
occlusion of blood flow. Other factors may be implicated, however, such as artery
spasm, platelet aggregation, and emboli from mural thrombi (thrombi lining the walls
of the cardiac chambers). Often MIs begin with infarction (necrosis) of the
subendocarcial layer of the cardiac muscle. This layer has the longest myofibrils in
the heart, the greatest oxygen demand, and the poorest oxygen supply. Around the
initial area of infarction (zone of necrosis) in the subendocardium are two other

3
zones: (1) the zone of injury, tissue that is injured but nit necrotic, and (2) the zone of
ischemia, tissue that is oxygen deprived.

Infarction is a dynamic process that does not occur instantly; rather, it evolves
over a period of several hours. Hypoxia (decreased oxygen) from ischemia may lead
to local vasodilation of blood vessels and acidosis. Potassium, calcium, and
magnesium imbalances, as well as acidosis at the cellular level, may lead to
suppression of normal conduction and contractile functions. Automaticity and ectopy
are enhanced. Catecholamines (epinephrine and norepinephrine) released in response
to hypoxia and pain increase the heart’s rate and contractility and afterload. These
factors increase oxygen requirements in tissue that is already oxygen deprived. The
area of infarction may extend into the zones of injury and ischemia. The actual extent
of the zone of infarction depends on three factors; collateral circulation, anaerobic
metabolism, and workload demands on the myocardium.

The infarction may involve only the subendocardium (called a subendocardial

MI), or it may spread to the epicardium or to all three layers of cardiac muscle. When
all three layers involved, the MI is termed transmural. Subendocardial MIs have less
effect on wall motion and cardiac output than do transmural infarctions.

Obvious physical changes do not occur in the heart until 6 hours after the
infarction, when the infarcted region appears blue and swollen. After 48 hours, the
infarct turns gray with yellow streaks as neutrophils invade the tissue and begin to
remove the necrotic cells. By 8 to 10 hours days after infarction, granulation tissue
forms at the edges of necrotic tissue. Over a 2 to 3-month period, the necrotic area
eventually develops into shrunken, thin, firm scar. Scar tissue permanently changes
the size and shape of the entire left ventricle (ventricle remodelling). Remodelling
may decrease left ventricle function, cause heart failure, and increase morbidity and
mortality.

The client’s response to an MI also depends on which coronary artery or

arteries were obstructed and which part of left ventricle wall was damage; anterior,
lateral, septal, inferior, or posterior.

Obstruction of the left anterior descending (LAD) artery causes anterior or

septal MIs because the LAD artery perfuses the anterior wall and most of the septum
of the left ventricle. Anterior wall MIs (AWMIs) account for 25% of all MIs and have
the highest mortality rate. Clients with anterior MIs are most likely to experience left

4
ventricular heart failure a d ventricular dysrhythmias because a large segment of the
left ventricle wall may have been damaged.

The circumflex supplies the lateral wall of the left ventricle and possibly
portions of the posterior wall or the sinoatrial (SA) and atrioventricular nodes. Clients
with obstruction of the circumflex artery may experience a posterior wall MI
(PWMIs) or a lateral wall MI (LWMIs) and sinus dysrhythmias.

In most people, the right coronary artery perfuses the SA and AV nodes as well as the
right ventricle and inferior or diaphragmatic portion of the left ventricle. Clients with
obstruction of the right coronary artery often have inferior wall MIs. Inferior wall MIs
(IWMIs) account for about 17% of all MIs and have a mortality rate of about 10%.
Up to50% of all inferior wall MIs are associated with an occlusion of the right
coronary artery causing significant damage to the right ventricle (Litton, 2015).

Many people die from coronary heart disease without being hospitalized.
Most of these are sudden deaths caused by cardiac arrest, usually resulting from
ventricular fibrillation. On the basis of data from NHANES 2011 to 2014, an
estimated 16.5 million Americans ≥20 years of age have CHD.This year, ≈720 000
Americans will have a new coronary event (defined as first hospitalized myocardial
infarction [MI] or CHD death), and ≈335 000 will have a recurrent event.Whites had
a higher rate of recognized MI than blacks (5.04 versus 3.24 per 1000 person-years)
in the Atherosclerosis Risk in Communities Study.In individual’s ≥45 years of age,
median survival (in years) after a first MI is 8.4 for white males, 5.6 for white
females, 7.0 for black males, and 5.5 for black females. Individuals self-reporting low
income and low education have twice the incidence of CHD as those reporting high
income and high education (10.1 per 1000 person-years versus 5.2 per 1000 person-
years, respectively).

The purpose of this case presentation is to have knowledge about Myocardial

Infarction and how to take care patient in a systematic approach. This would help
nursing student to enhance assessment and management skills in caring of patients
with this type of disease

5
 VITAL INFORMATION
Code Name: Mr. X
Age: 45
Gender: Male
Civil status: Married
Date of birth: March 5, 1973
Place of birth: Sta. Filomena Iligan City
Race: Filipino
Cultural or ethnic background: Cebuano
Primary language: Bisaya
Secondary language: English, English
Religion: Roman Catholic
Highest educational attainment: College Graduate
Occupation: Welder/Installment
Usual health care provider: Attending Physician
Date of admission: October 2, 2018 11pm
Date of discharge: Transported in ward on October 04, 2018
Source of history: Patient 50%, Nurse 3%, Chart 47%

Reasons for seeking health care: Chest Pain

Primary attending physician: Jill Irene Capistrano- M.D
Initial impression/diagnosis: Acute Coronary Syndrome, ST elevation Myocardial Infarction,
Antiseptal Wall Hypertensive Cardiovascular Disease
Final diagnosis:Acute Coronary Syndrome, ST elevation Myocardial Infarction, Antiseptal
Wall Hypertensive Cardiovascular Disease

6
HISTORY OF PRESENT ILLNESS

Mr. Q was admitted last August 19, 2018 in Intensive Care Unit for 1 week. He
manifested squeezing chest pain with the pain scale of 9/10, duration of 5 seconds
with the interval of 5 minutes. He described that the pain will radiate to left
shoulder, to back portion, going back to his chest. The pain was associated with cool,
clammy skin, diaphoresis and pale appearance. He also felt nauseated, body
weakness, and restlessness. The symptoms worsened, hence prompted for admission.
He was diagnosed with Myocardial infarction ST elevation and Hypertension. He
was given maintenance medication: Enalapril 50mg I tab OD, Atorvastatin 80 mg
OD, Carvedilol, 6.25 mg, 1 tab, BID, Isosorbidemononitrate 30 mg, 1 tab BID. He
stated that he is compliant with his medications religiously.

After a month, he was admitted again in Northern Mindanao Medical Hospital

with the same complaints. He was diagnosed with Acute Coronary syndrome;
Myocardial Infarction ST elevation, Hypertension, and Cardiomegaly. He
undergone Angiogram for confirmatory with the result of blockage in right and left
artery of his heart. He was admitted there for 5 days in ICU and was given the take
home medications.

7 hours prior to admission, Mr. X drinks a half cup of soda and minutes after, he
experienced chest pain, described as tight, squeezing, pain scale of 6/10, with the
duration of 3 seconds and interval of 5 minutes. It radiates on his left shoulder, to
back portion, going back to his chest. It was associated with cold and clammy
extremities and accompanied by weakness of both extremities. He took his
maintenance medication but was not relived. He complained of nausea and dizziness.
Persistence of symptoms, prompted for admission.

October 02, 2018, @ 11 pm, he was brought to Emergency Room and was given
Aspirin 4 tabs and supplemental oxygen @ 2L/ min. His vital signs were checked:
T:36 degreecelcius, P: 63 bpm, R: 20 bpm, BP:120/80 mmHg.

At 11:15 pm, he was admitted in Intensive Care Unit, bed4, under Dr. Capistrano.
The Dr. ordered the following: 02 inhalation @ 2 L/min via nasal cannula continous ,
low salt, low fat diet, CBR without toilet privilege, medications: Aspirin 80mg 1 tab
OD, Isosorbidemononitrate 30 mg 1 tab OD, Enalapril 5 mg, I tab BID, Carvedilol
6,25 mg BID, Atorvastatin, 80mg 1 tab OD.

7
HISTORY OF PAST ILLNESS

Mr. X was delivered via normal spontaneous vaginal delivery at hospital. He

forgot if he had immunizations and vitamins. He experienced measles and chickenpox
in his childhood years. He stated he had frequent hospitalization because of fever,
cold, and flu. He had hypertension with no previous consultation and maintenance.

Mr. X was fond of eating foods high in fat and cholesterol like “ginataang
manok”, lechon, and meat products .He drinks 1 bottle of soda 3x a day and 1 cup
every day. He eats fast food most of the time because of his work (OFW). He
started started to smoke at the age of 22 consuming 1 and half pack of cigarettes a
day. He also drinks alcohol beverages occasionally. He experienced emotional stress
since he worked throughout his life as OFW.

8
Maternal Paternal

PATIENT

LEGEND:

(FEMALE) (HYPERTENSION) (ALIVE) (UNKNOWN) HEART PROBLEM

(MALE) (HEART ATTACK) ( DECEASED) (LOWER GASTROINTESTINAL PROBLEM)

9
 PHYSICAL ASSESSMENT AND REVIEW OF SYSTEMS

AREAS PROBLEM
ASSESSE NOC SHIFT AM SHIFT IDENTIFIED
D (October 02,2018) (October 3, 2018)

General  Subjective Subjective findings:

health findings:
survey (Not assessed)  Have you been feeling
well? “Okay naman
koron Ma’am, dili
pareha atong gahapon”
Objective findings: “
-Vital signs:  Have you lost or gained
T: 36.0 C weight recently?
BP: 90/70 mmHg “wala man maora gihapon.”
PR: 50-60 bpm
RR: 13-17 bpm
O2sat: 98% Objective findings:
GCS:15 -Vital signs
T: 36.0 C
 O2 inhalation via BP: 120/80 mmHg
nasal cannula at 2L/ PR: 55-65 bpm
min RR: 14-18 bpm Decreased
 Body weakness O2sat: 98-99% cardiac tissue
 Afebrile GCS: 15 perfusion related
 Sinus Bradycardia to reduced
on ECG tracing coronary blood
long lead II  O2 inhalation @2L/min flow.
 Patient able to  Venoclysis of the left
urinate w/o urinary vein with IVF@
catheter, refuse to 10cc/hr via IV infusion
wear diaper need pump
assistance during  Palpable peripheral
urination. pulses
 Venoclysis on Left  Abdomen round, soft,
vein with IVF bottle slighter distended, non-
tender, with hematomas Risk for
no. 1 PNSS 1L @
noted all around navel. Impaired gas
10 cc/hour via IV
exchange related
infusion pump. no  Conversant and able to
to left
signs of infiltration. follow commands.
ventricular
 Cold clammy  Not in respiratory
failure
extremeties distress
 Diaphoretic  no complains at chest
 Body weakness pain -Anxiety related
 Chest pain, pain  Still on continues to cardiac event
scale of 6/10, cardiac monitoring via and possible
described as tight 5 chest leads depicting death.
that radiates on the sinus bradycardia.
left shoulder , to his  Well rested the whole
back portion, back shift.
to his chest.
Duration of 3

10
 seconds with the
interval of 5
minutes.

Integument Subjective findings: Subjective findings:

ary system (Not assessed)  Do you have skin
rashes or lesions?
“wala man.” Ineffective
 Do you have excessive tissue perfusion
itching?
Objective findings: “wala man pod.”
 Hematoma noted all  Do you sweat a lot?
around the navel Any odor problems?
 Poor skin turgor “dili man perupaningtonko.”
 Delayed CRT, less  Are you exposed to
than 2 seconds sun?
 Diaphoretic “Oo”
 Do you use sunblock?
“Dili”

Objective findings:
 Pale skin, dry and
warm to touch.
(Temp 36.0 Celcius)
 Hematoma around right
navel because of
Angiogram
 Fingernails and toenails
were pale in color and
cool to touch

HEENT Subjective findings: Subjective findings: Ineffective

a) Hea (Not assessed)  Eyes -Do you have any tissue perfusion
d visual problem?
and “Oohanapakongpanan-aw.
face Objective findings:  Ears -Do you have any
b) Eye (-) lumps hearing problem? Risk for
s (-) earache “wala man. Makadungog man decreased
c) Ear (-) difficulty of swallowing kogsakto.” cardiac output
s
d) Nos Objective findings:
e  Pupillary reflex: 4mm
e) Ora  Anicteric sclerae,
l pinkish conjunctivae.
Cav  No nasal discharges
ity  Lips were dry and
slightly pale.
 Warm, clammy,
diaphoretic, and pale
appearance

Neck Subjective findings: Subjective findings: No problem

(Not Applicable)  Do you experience stiff Identified

11
 neck? How often?
“oousahay
pagmakaunlankogtaas.”

Objective findings:
-Supple, no lymphadenopathy
Objective findings:
(-) stillness
(-) lumps
(-) vein engorgement

Respirator Subjective findings: Subjective findings:

y system  Not assessed  Do you ever have
trouble breathing?
Objective findings: “dilinakaayo”.
RR: 15-22 bpm  Do you feel any Risk for
 7 hours PTA as an discomforts or pain decreased
onset of chest pain, when breathing? cardiac output
described as tight, “sakarun, walana.”
pain scale 6/10 on  Do you have asthma?
and off with the “walara pod bya”
duration of 5  Do you ever have
minutes. trouble breathing?
 Cracking sounds “Maglisodkogginhawa,
noted  Are you exposed to air
 Grasping breathing pollutants, smoke, or
noted second hand smoke?
 DOB “Manigarilyoko sauna
(-) Asthma peruniundangnako.”
(start at age of 22 - Aug 2018)
 Do you feel any
discomforts or pain
when breathing?
“oo, sakitjud kayo
akongdughan.”

Objective:

 No complaints of DOB
anymore
 PR: 50-65 bpm
 RR: 15-22bpm
 Nasal flaring is not
observed.

Cardiovasc Subjective findings: Subjective findings: Acute pain

ular system  Do you have any  Do you have any chest related to
chest pain? pain? increased
“muraggikumotakongdugha “walana kayo myocardial
nsakasakit.” diliparehakagahapon. ” oxygen demand
and decreased
Objective findings: myocardial
oxygen supply.

12
 RR: 13-17 bpm Objective findings:
HR: 50-65 RR: 14-18 bpm
BP: 90/70-130/80 HR: 55-65bpm
O2sat: 98 % BP: 120/80 mmHg
O2sat: 98-99%
 Chest pain scale of  chest pain scale of 1
6/10,, described as out of 10
tight, with the
duration of 3 radiates on left
seconds and interval shoulder, to his back
of 5 minutes, portion, and back to his -Risk for
radiates on the left chest impaired gas
shoulder,back exchange related
portion, going back to left
to his chest ventricular
 ECG LEAD II- ST failure
segment elevation
-

Breast and Not assessed Not assessed

Axilla
Gastrointes Subjective findings: Subjective findings: No problem
tinal Not assessed  Do you have any Identified
system and stomach problems?
the Vomiting?
abdomen “walara man sad.”
 How often do you have
a bowel movement?
‘wala pa sad kokalibang.”
 Do you feel any
pulsations in your
Objective findings: abdomen?
(-) Abdominal pain “Oo”
(-) Vomiting
(-) LBM Objective findings:
-Abdominal respiratory
 Hematoma noted all movement is seen. (RR: 15-22
around his navel bpm)
-Abdomen is free of lesions or
rashes.
-Umbilicus is midline at lateral
line
-Abdomen is non tender and
soft
-Hypoactive bowel sounds

Genitourin Subjective findings: Subjective findings:

ary/ (Not assessed)  Do you have bladder
Reproducti control?
ve system “okay man Maam.”

Objective findings:
Objective findings:  Urinates thrice the

13
 -no urine output for the whole shift -Risk for
whole shift (NOC-II)  no urinary catheter imbalance fluid
-complained of weakness attached volume
of both extremities  refuse to use diaper
-no urinary catheter  need assistance during
attached urination
-refuse to use diaper
-need assistance during
urination
Musculosk Subjective findings: Subjective findings: Activity
eletal (Not assessed)  Do you have any back intolerance
system problems?
“wala pod. Kato rang
Objective findings: hawoyakongmgatiilngadilinak
 Venoclyis on the omalihok.”
left vein 1L PNSS
@ 10cc/hr via Objective findings:
infusion pump  Good posture.
 (+) muscle pains of  Neck muscle is
both lower legs. symmetry
 Numbness on both  no joint deformities
extremeties  motor response scale :6
obeys commands
 hematomas noted
around navel.
 No complaints of
weakness anymore
Neurologic Subjective findings: Subjective findings:
system (Not assessed)  How would you
describe your mood?
“usahaykaydilikoganahanugdis
turbo.”
 Do you feel any Anxiety related
numbness? to cardiac event
“katoraakongduhakatiilngadili and possible
nakomalihok.” death.

Objective findings:
 eyes move in a smooth,
coordinated motion in
Objective findings: all directions
 Anxiety  Pupillary reflex: 4mm
 Restlessness and (open spontaneously)
lightheadedness.  eyelids blink bilaterally
 client smiles, shows
teeth when he talk and
closes eyes against
resistance.
 client swallows without
difficulty (soft, low
salt, low fat)
Lymphatic/ Subjective findings: Subjective findings: Risk for
Hematologi (Not assessed)  Have you been tired? decreased

14
c system “gahaponkapoyjud kayo cardiac output
akonglawas.”
 Do you have any lumps
in your neck,
underarms or groin? Ineffective
“wala” tissue perfusion
Objective findings:
 pale lips
 pinkishconjunctiva
Objective findings:  cool, pale fingernails
(Not assessed) and toenails
 no bowel movement for
the whole shift
 no bruising, petechial
rashes and ecchymosis
on the skin.
 no lymph nodes.
LABS RESULTS:
RBC: 4.90
Hemoglobin: 144.0
Hematocrit: 0.41
Uric Acid:141.8
Endocrine Subjective findings: Subjective findings:
system (Not assessed)  How is your tolerance
to heat and cold
temperatures?
“dalira kayo kopanognawon,
maongakonggipapalongangairc
on.”
 Do you have excessive
thirst, hunger, and
excessive urination?
“maskinunsa man akongkan
on.?

Objective findings:
-no presence of buffalo lumps -Deficient
-No wounds knowledge
-No abnormal pigmentation about post-MI
Objective findings: -No excessive sweating or self-care
(Not Applicable) flushing
-Body weakness noted

15
 GORDONS ASSESSMENT

BEFORE HOSPITALIZATION DURING HOSPITALIZATION

NUTRITIONAL/ METABOLIC PATTERN
Before diagnosed with
M.I
 Mr. X was fond of eating foods high in fat and
cholesterol like “ginataang manok”, lechon,
and meat products .He drinks soda 3x a day and
coffee OD. He eats fast food most of the time
because of his work (OFW) before he was
diagnosed with M.I
 He tried to modify his lifestyle after knowing
his condition. He preferred eating fruits and
vegetable, he stopped drinking soda, coffee, and
he tried not to eat in fast food area. He drinks 4-5
glasses a day
ELIMINATION PATTERN
 The client states he defecates once a day usually
every morning with the characteristic of sem
formed stool without difficulty and use of
laxatives.
 iThe client urinate 3x a day or more varying in
his fluid, he verbalizes no difficulty in voiding.
 Low sodium and Low fat diet
 He has a good appetite and always
consumed all the foods served at him.
 Drinks 1000 mL of water noted on our shift
last October 03, 2018.
 The patient has no dental problems, no foul
odor and excess perspiration.
 Presently, the client has urinal bag in his
bedside. He urinates 3 x which 300cc
already during our shift
 He refuse to wear diapers or to catheter
him.
 The nurse instructed the patient to inform
them when defecating because he is
advised to avoid straining due to his
condition.
 No BM within shift

EXERCISE AND ACTIVITY PATTERN

 He is fond of playing outdoor games such as  Complete bed rest without toilet privilege
basketball before he was diagnosed with his
current condition.
 After diagnosing his condition, he was instructed
to avoid doing strenuous activities, and things
that can make him exert efforts and can trigger
his condition.
 He stayed in his house 24 hours a day. He
watched TV most often .

SLEEP/ REST PATTERN

 He usually sleeps early around 8-9 in the evening  Mr. X sleeps most of the time. He is anxious
and wakes 6 am in the morning. The client has 9 and irritated. He doesn’t want to be
hours of sleep every day without the any use disturbed by anyone.
sleeping aids.
ALCOHOL AND STREET DRUGS
 Confine to bed
 Mr. X started to smoke at the age of 22. He can
consumes 5 sticks a day
 At the age of 30, he can already consumed 1 and
half pack of cigarettes a day
 At the age of 37, he tried to stop gradually
consuming 3-4 sticks a day

16
  He is back with smoking in the year 2004
because of loneliness in work (OFW)
 He drinks alcoholic beverages occasionally
 He officially stopped his vices when he was
diagnosed with his current condition

ENVIRONMENTAL HAZARDS
 They lives in subdivision, 1km away from the  Confine to bed
highwayThe patient stated that their  He is irritated and anxious and does not
surroundings are well sanitized and safe. want to be disturbed by anyone.
INTIMATE PARTNER VIOLENCE
 He never mistreated his wife or forced to do  His wife takes good care of him
something that does not satisfy them both. In  They are so sweet, with the endearment of
fact he takes good care of him so much. “Babe, Bebe”
OCCUPATIONAL HEALTH
 He started to work in Taiwan in year 1997 as
welder and installer
 He was transferred by his agency in Saudi  Confine to bed
Arabia in the year 2004- 2018 with the same
job

COGNITIVE AND PERCEPTUAL PATTERN  Conscious

 Patient wears glasses.  Conversant
 He had his eye examined with a grade of 100.  GCS of 15
SELF- RELATIONSHIP PATTERN  Fears
 He sees himself able to do things according to  Anxiety
the manner he wants it but with extra careful
of his health condition.
COPING STRESS MANAGEMENT PATTERN
 He was emotionally stress when he worked
abroad  Anxiety
 The client states that he felt so down when his
mother died recently
 Whenever he encounters difficult situation, he
yould think about it several times or ask his
wife’s opinion prior to decision making, as
verbalized by the patient.
VALUES AND BELIEF
 The patient is a Roman Catholic.  He always prays to God for his
 He stated that he barely attends to church. condition.
SPIRITUAL RESOURCES
Patient seek help and guidance to God for his condition.

17
 DIAGNOSTIC TEST

CBC RESULT NORMAL INTERPETATI IMPLICATIONS

VALUE ON
Red Blood Cells 6.3 4-6 x 10 12/L NORMAL Implications for high levels:
Primary polycythemia (eg.
polycythemia vera), secondary
polycythemia, or
erythrocytosis-usually caused
by oxygen need (eg. chronic
lung disease, congenital heart
disease)

Implications for low levels:

abnormal loss or destruction of
erythrocytes, lack of needed
elements or hormones for
erythrocyte production, bone
marrow suppression, lead
poisoning, thalasemia
Hematocrit 0.55 0.37-0.47 INCREASED Implications for high levels:
dehydration, burns,
hypovolemia

Implications for low levels:

blood loss, overhydration,
dietary deficiency, anemia
Hemoglobin 150 110-180 g/L NORMAL Implications for high levels:
dehydration, burns,
hypovolemia
Implications for low levels:
blood loss, overhydration,
dietary deficiency, anemia
Implications for high levels:
WBC 15.5 5-10 x 10 g/L INCREASED leukocytosis, infection

Implications for low levels:

leukopenia, autoimmune

18
 disease

Segmenters 0.96 0.50-0.65 High levels usually represent

INCREASED
and ongoing infection, an

inflammation, malignancy,

cause by some drugs, etc. Low

levels could be seen in patients

with viral infection,

autoimmune diseases, some

medications and malignancy.

Lymphocytes 0.3 NORMAL An increased in lymphocyte

0.25-0.35 count usually represents an
acute infection especially viral
infections, leukemia, smoking,
etc. Low lymphocyte count is
usually not significant.
An increase in band neutrophils
Stabs 0 0.05-0.10 DECREASED typically means that the bone
marrow has been signaled to
release more WBCs
and increase production of
WBCs. Low stab means
increased risk for infection
Monocytes 0.01 0.03-0.07 DECREASED An increase in monocyte could
signify a chronic infection like
your tuberculosis or a chronic
inflammation condition like
your inflammatory bowel
disease and malignancy. Low
levels of monocytes are usually
none significant if other cells
are normal.
Eosinophils 0.05 0.01-0.03 INCREASED They are usually increase in

19
 cases of allergy, asthma and in
parasitic infections. Low levels
are usually not significant.
Basophils 0 0.01 DECREASED This type could produce
histamine. Increased numbers
could represent a
myeloproliferative disorder.
Plaletet Count 195 140-450 x 10 NORMAL Implications for high levels:
g/L malignant tumors, polycythemia
vera

Implications for low levels:

idiopathic (unknown cause),
thrombocytopenic purpura, viral
infections, AIDS, systemic
lupus erythematosus,
chemotherapy drugs, some
types of anemia

BLOOD CHEMISTRY
TEST NORMAL RANGE RESULT IMPLICATION

Creatinine 7-12 1.3mg/dL MYOCARDIAL

INFFARCTION
Na 134-145 132mmol/L HYPONATREMIA
K+ 3.5-5 3.4 mmol/L HYPOKALEMIA
ALT 9-52 3.0u/L LIVER
FUNCTIONING
DECREASES

TROPONIN T <0.03 2.0 ng/dL MASIVE

MYOCADIAL

20
 DAMAGE

TROPONIN I <0.01 <0.01

CK-MB 0-18 7u/L

FASTING BLOOD SUGAR LIPID PROFILE

TEST NORMAL RESULT IMPLICATION
RANGE
GLUCOSE 74-106 88 mg/dL NORMAL
URIC ACID 2.5-.6.2 8.4mg/dL Hyperuricemia
CHOLESTEROL 0-200 187mg/dL NORMAL
TRIGLYCERIDES 0-150 60mg/dL Athersclerosis
Direct HCL 40-60 38mg/dL NORMAL
LDL 60-180 137mg/Dl NORMAL
VDRL 25-50 12mg/Dl
ALT 8-52 27u/L NORMAL

ECG
Result Pre Nursing Responsibilities
Elevated ST segment -explain procedure
-tell pt to relax
-shave area of the placement if body hair is present
-remove any jewelries in the body
-tell pt not to move while procedure is ongoing

ANGIOGRAM
Result Pre Nursing Responsibilities
Blockage in left and right -instruct pt to fast usually for 8-12 hours before procedure
coronary artery -explain procedure to the pt
-reassure pt that IV medications are given to maintain comfort
-explain that sensations will be felt during procedure
-encourage pt to express fears and anxiety

21
 NORMAL ANATOMY AND PHYSIOLOGY

Anatomy of Heart Function of Heart

HEART  Is located in the  Arterial blood (red,

mediastrium; about two oxygen-rich blood)
thirsds of its mass is to flows from the heart to
the left of the midline. each part of the body to
 It is shaped like a cone provide oxygen and
lying on its side. nutrients. The venous
 Its apex is the pointed, blood (blue, oxygen-
inferior parts its base is poor blood) returns
from the body to the
the broad, superior
heart. The blood then
part.
travels through the
 The pericardium is the lungs to exchange
membrane that carbon dioxide for new
surrounds and protects oxygen. The heart is a
the heart. pump, which moves the
 It consists of an outer blood. The arteries and
fibrous layer and inner veins are the pipes
serous pericardium, through which the
which is composed of blood flows. The lungs
parietal and a visceral provide a place to
layer. Between the exchange carbon
parietal and visceral dioxide for oxygen.
layers of the serous
pericardium is the
pericardial cavity, a
potential space filled
with a few milliliters of
lubricating pericardial
fluid that reduces
friction between the
two membranes
 Three layers make up
the wall of the
heart;Epicardium
(visceral layer of the
serous pericardium),
myocardium, and
endocardium.
 The epicardium
consists of
mesothelium and
connective tissue.
 Themyocardium is

22
 composed of cardiac
muscle tissue.
 The endocardium
consists of endothelium
and connective tissue.
 The chambers include
two superior chambers,
the right and left atria,
and two inferior
chambers, the right and
left ventricles. External
features of the heart
include the auricles
(flaps of each atrium
that slightly increase
their volume), the
coronary sulcus
between the atria and
ventricles, and the
anterior and posterior
sulci between the
ventricles on the
anterior and posterior
surfaces of the heart,
respectively.
 The right atrium
receives blood from the
superior vena cava, and
coronary sinus.
 It is separated
internally from the left
atrium by the interatrial
septum, which contains
the fossa ovalis.
 Blood exits the right
atrium through the
tricuspid valve.
 The right ventricle
receives blood from the
right atrium.
 It is separated
internally from the left
ventricle by the
interventricular septum
and pumps blood
through the pulmonary
valve into the
pulmonary trunk.
 Oxygenated blood
enters the left atrium

23
 from the pulmonary
veins and exits through
the bicuspid (mitral)
valve.
 The left ventricle
pumps oxygenated
blood through the
aortic valve into aorta.
 The thickness of the
myocardium of the four
chambers varies
according to the
chamber’s function.
 The left ventricle, with
the highest workload,
has the thickest wall.
 The fibrous skeleton of
the heart is dense
connective tissue that
surrounds and supports
the valves of the heart.
 Chamber of the Heart
is a hollow, muscular
organ, which functions
as a pump for the
movement of blood
through the body. The
flow of blood through
the four chambers of the
heart is regulated by
valves. The heart valves
function like one-way
doors which allow blood
flow through in the
forward direction but
prevent the backward
flow of blood.
 Venous blood returns
from the body to the
right side of the heart
which pumps the blood
to the lungs.
 The oxygen-rich blood
returns from the lungs to
the left side of the heart.
 The left side of the heart
pumps blood to the
entire body. As you
would expect, the left
side of the heart must
generate a much greater

24
 pressure to pump the
blood to the body.
 On the left side the
valves are called mitral
and aortic valves.
 The mitral valve
connects the receiving
chamber from the lungs,
the left atrium, with the
pumping chamber, the
left ventricle.
 The aortic valve
controls the flow of
blood out of the heart
into the aorta, the largest
artery of the body which
then gives rise to all the
other arteries.
 Coronary arteries first
branches of the aorta are
arteries to the heart
muscle itself.
 There are two main
coronary arteries:
 The left main coronary
artery divides into two
main branches:
 The left anterior
descending (LAD),
which runs down the
front of the heart, and
the circumflex artery
(CX) which runs behind
the heart. Branches of
the LAD are called
diagonalarteries and
branches of the
circumflex are called
obtuse marginal arteries
(OM).
 The right main
coronary artery travels
on the right side of the
heart and gives off the
posterior descending
artery (PD).

25
 MODIFIABLE FACTOR NON- MODIFIABLE
 HYPERTENSION  AGE
 DIET( HIGH FAT, HIGH CARBS,  GENDER (MALE)
DRINKING SODA, OCCASIONAL  FAMILY HISTORY (
ALCOHOL DRINKING) PATERNAL AND MATERNAL
 SEDENTARY LIFESTYLE( INACTIVE) SIDE)
 CIGARETTE SMOKING (1 & half pack of
cigarette a day)
 STRESS (OFW)
PATHOPHYSIOLOGY

Endothelial lining of
the arteries are injured

Permeability of the blood Platelets, WBC, and fibrin

vessels to lipoprotein increases converge at the injured site

T- lymphocyte and monocyte(

that becomes macrophages)
infiltrate the area lipids and die

Formation of
dead fatty core

Formation of fibrous cap over

dead fatty core (plaque)

Plaque protrudes in
lumen of vessel

Narrowed blood vessel Plaque ruptures and causes

obstruct blood flow thrombus formation

Occlusion of the artery

Decreased myocardial perfusion

Myocardial ischemia

Partially ischemic cells Total ischemic cells

(+) chest pain radiating to
the left shoulder)
No ATP
Anaerobic metabolism
DOB
Reduced ATP
production Noncontractile Los of cell
Hypocontractile 26 membran
Accumulation of f lactate
e integrity

Altered cell membrane integrity

  Unrelieved chest pain
Ion leak
radiating to the left
Myocyte death/ necrosis shoulder
 Severe anxiety
 Troponin T. elevation
Myocardial infarction  ST segment elevation
 Angiogram: Blockage

Heart muscle loses

Disrupt conduction system of
optimal strength
the heart
 Decreased
contractility
Baroreceptor  Stroke volume Decreased tissue
activation  Cardiac output perfusion

Sympathetic nervous Renin-angiotensin-

system activation Aldosterone system activation

 Increased action Fluid retention

potential Vasocontriction
 Increased
contractility
speed
 Increased vascular  Increased venous
resistance return
 Increased mean  Increased ventricular
arterial pressure filling

 Increased stroke
volume
 Increased Blood
pressure
 Increased cardiac
output

Sens Integumenta Urinary Cardiovascul Respiratory Digestive CNS

ory ry system system ar system system system
Eyes Increased
Increased
Peripheral mean arterial Decreased
myocardial
vasocontriction Increased pressure Decreased cerebral
workload
Dilatati fluid secretions perfusion
on of retention
the Decreased
Possible
pupil peripheral tissue Peripheral  Nausea  Disorientati
pulmonary
perfusion Decrease vasocontriction  Vomiting on
congestion
 Cool clammy skin d urine  Abdominal  Confusion
 Diaphoresis output  Restlessness
discomfort
 Skin pallor  DOB  Anxiety
 Poor capillary
 Chest pain  Tachypnea
refill
 Palpitations  Crackles sound
 Tachycardia  Dyspnea

27
 NURSING CARE PLANS

ASSESSMENTS NURSING PLANNING INTERVENTIONS RATIONALE EVALUATION

DIAGNOSIS
Acute pain related to STO: Independent:
Subjective: “Sakit kayo myocardial ischemia The client was able to:
akongdughanatonggabii, as evidenced by severe After 3-4 hours nursing  Assess and evaluate the patient  Assist in determining the
murasiyaggikumotogayo, pain and tightness, intervention the patient status , description of pain, cause and effect of chest  Beginning relief of
karon kay 1/10 nalang) radiation of pain to with relieve from chest intensity, and location discomfort chest discomfort
the armpit (L) and ® pain and discomfort  Obtain ECG  Can diagnose the ongoing  Appears
Objective: arms  Vital signs assessed frequently ischemia comfortable and is
 Pain scale of 7/10  Physical rest in bed with the head  Baseline data free of pain
 Squeezing pain that LTO: of the bed elevated  Skin warm and dry
radiate on axillary and Within 12 hours of  Instruct the patient to avoid  Helps decrease chest  Adequate cardiac
arm brought by nursing intervention the straining discomfort and dyspnea output as
drinking half cup of patient will balance  Provide a quiet environment  Prevent increase oxygen evidenced by:
soda and ameal myocardial oxygen demand - Stable or
 Associated with nausea, with demand  Position the patient in semi-  This allows for rest and improving
indigestion , pallor fowler’s position adequate chest exurcion, ECG
diaphoresis , to increase available - HR and
palpitations and Dependent: oxygen Rhythm
dyspnea  Administer oxygen as prescribed - BP
(flow rate of 2-4 L/ min) via - Mentation
ECG FINDINGS: nasal cannula  Adequate to achieve - Urine output
 ST Segment elevation  Administer medications as oxygen demand - Skin color and
ANGIOGRAM:  First line defense in temp
 BLOCKAGE IN o Aspirin 50 mg 1 preserving myocardial
RIGHT AND LEFT prescribed 1 TAB BID tissue
VENTRICLE  Inhibits platelet aggregation
o Norplat 75mg 1 tab OD by blocking binding of

28
Creatinine adenosine diphosphate to
 1.3mg/Dl(7-12)  Atorvastatin platelets, thereby preventing
TRIGLYCERIDES thrombus formation
 60mg/Dl( 0-150)  Increases hepatic LDL
recapture sites, enhances
reuptake and catabolism of
TROPONIN 1 LDL; lowers triglyceride
2ng/dL(<0.3) levels.

TROPONIN T
0.1ng/dL
Collaborative:

Nutrition diet ( Low fat, low salt)

29
 ASSESSMENTS NURSING DIAGNOSIS PLANNING INT5ERVENTIONS RATIONALE EVALUATION
Activity intolerance related STO: INDEPENDENT The patient was able to
Subjective: to decreased cardiac  Determine factors maintain:
“ Dali ra kayo ko kapoyon” output and poor lung and After 3-4 hours of contributing to fatigue  Provide comparative
tissue perfusion as nursing intervention  Evaluate client’s perceived baseline data  No complaints of
Objective: evidenced by fatigue the client will limitations by asking past DOB and fatigue
participate willingly activities and present  Warm skin
 DOB in necessary and factors  To reduce oxygen  Limit activities
 Body weakness desired activities  Encourage to limit demand
 Pallor activities  To prevent orthostatic
 Diaphoretic LTO:  Encourage to slowly wake hypotension
 Cool clammy skin up in morning
 Pale nail beds After or within 12  Encourage complete bed  Provide an increase
 Delayed CRT less than 2 sec hours of nursing rest without TP oxygen supply
 RR of 14-18 interventions the
client will emphasize DEPENDENT:  Reduces myocardial
workload
the importance of
desired activation  Provide and monitor
Hematocrit response to
supplemental oxygen
 0.55 (0.37-0.47)
 Administer prescribed
RBC
meds
 6.3 (4-6 x 10 12/L)
Hemoglobin Isosorbidemononitrate30mg/tab, 2tab
 144( 110-180g/L)  Relaxes vascular smooth
BID
muscle with a resultant
ECG FINDINGS:
decrease in venous return
 ST Segment elevation Collaborative: and decrease in arterial
ANGIOGRAM: BP, which reduces left
 BLOCKAGE IN RIGHT Nutrition diet ( Low fat, low ventricular workload and
AND LEFT VENTRICLE carbs ) decrease myocardial of
oxygen consumption.

30
 ASSESSMENTS NURSING PLANNING INT5ERVENTIONS RATIONALE EVALUATION
DIAGNOSIS
Anxiety related to STO: INDEPENDENT The patient was able
Subjective: perceived or actual  Assess the patient’s level anxiety to maintain:
“ Bag o pa death, pain, and After 3-4 and coping mechanisms  To determine appropriate
ganinamatayakong Mama possible lifestyle hours of  Assess the need for spiritual intervention to the problem  Reduction of
unyaakonapudnaadiri ICU” changes as evidenced nursing counseling  Find support in religion that may help anxiety
by restlessness intervention  Observe verbal and nonverbal signs in reducing fear and anxiety  Patient and wife
Objective: the client will of anxiety  It may help the client to feel discuss the
display  Less calm, and reassuring comforted and supported anxieties and
 Irritable reduction of environement  Associated with increase sympathetic illness and
 Anxious anxiety activity, which increases cardiac death
 Verbal expression of  Offer prayer workload  Appears restful
worry LTO:  Consistency of routine and staff  Practice stress
 Stares blankly for  Observe for autonomic signs and promotes trust and confidence reduction
about a minute After or symptoms for anxiety  Help to divert his attentionfor time technique
being
within 12
hours of  Maintain continuity of care
nursing
 Provide sufficient oxygen
interventions  Divert client’s attention through
 Relaxes vascular smooth muscle with
the client will guided imagery and soothing music a resultant decrease in venous return
emphasize the and decrease in arterial BP, which
ECG FINDINGS: importance of reduces left ventricular workload and
 ST Segment elevation desired DEPENDENT: decrease myocardial of oxygen
ANGIOGRAM: activation consumption.
 BLOCKAGE IN  Provide and monitor response to  Reduces gastric acid secretion and
RIGHT AND LEFT supplemental oxygen @2L/min increases gastric mucus and
VENTRICLE  Administer prescribed meds bicarbonate production, creating
protective coating on gastric mucosa
o Isosorbidemononitrate
30mg/tab, 2tab BID
o Pantoprazole+Domperidine

31
32
33
 ASSESSMENTS NURSING PLANNING INT5ERVENTIONS RATIONALE EVALUATION
DIAGNOSIS
Ineffective tissue STO: INDEPENDENT The patient was able
Subjective: perfusion related to  Assist the client to ambulate but to maintain:
“ Bag o pa ganinamatayakong Mama myocardial injury After 3-4 hours of within his tolerance  Prevent thrombus
unyaakonapudnaadiri ICU” as evidenced by nursing formation, thus, improving  Reduction of
dysrhythmias intervention the  Monitor and recorded intake and blood circulation anxiety
Objective: client will display output  May be a sign of decreased  Patient and wife
increased tissue renal perfusion discuss the
 Cool, clammy skin perfusion  Instructed the significant of others  Prevent impairement of anxieties and
 Diaphoresis not to wear tight clothing blood flow illness and
 Body weakness LTO:  To prevent orthostatic death
 Nausea  Encourage to slowly wake up in hypotension  Appears restful
 Dizziness After or within 12 morning   Practice stress
 Pale lips hours of nursing reduction
 Cool to touch skin interventions the  Bed rest, with head slightly technique
client will maintain elevated
 Provide increase oxygen
peripheral
concentration
perfusion
 Inhibits platelet
DEPENDENT:
aggregation by blocking
binding of adenosine
 Provide and monitor response to diphosphate to platelets,
Hematocrit supplemental oxygen @2L/min thereby preventing
 0.55 (0.37-0.47)  Administer prescribed meds thrombus formation
o Norplat 75mg 1 tab OD  mucosal protective agent
RBC
o Mucosta 1 tab 3x/day and is postulated to
 6.3 (4-6 x 10 12/L)
increase gastric blood
Hemoglobin flow,prostaglandin
144( 110-180g/L) biosynthesis and decrease
free oxygen radicals.

34
 NURSING PLANNING INT5ERVENTIONS RATIONALE EVALUATION
DIAGNOSIS
ASSESSMENTS

Risk for decreased STO: Independent:

Subjective: cardiac output  Closely monitoring of the  Baseline data The client was able to
“Dali rakokapoyon kung related to After 3-4 hours patient every hour maintain:
ibakod or ilakawlakaw” degeneration of nursing interventions  Keep the client on complete  Decreased oxygen
cardiac muscle the patient will bed rest consumption  BP within
Objective: maintain or  Decrease stimuli , provide  Promote adequate rest normal range
attainment of quiet environment  Appears
 HR: 64 adequate tissue  Encourage changing position comfortable
 Generalized weakness perfusion slowly  To reduce risk for  Extremities
 Cool, clammy skin  Instruct to avoid straining orthostatic hypotension warm and dry
 Diaphoretic After 12 hours  To reduce oxygen within normal
 Nauseaous nursing intervention  Provide comfort measures, demand color
the patient will e.g back and neck massage,  Decrease discomfort and  Remains alert
display hemodynamic elevation of head may reduce sympathetic and oriented
stability stimulation and without
 Can reduce stressful
 Instruct in relaxation cognitive or
stimuli, promotes
Hematocrit techniques, guided imagery, behavioral
relaxation
distractions change
 0.55 (0.37-0.47)
RBC Dependent:
 6.3 (4-6 x 10 12/L)  Administer oxygen as
Hemoglobin  Achieve sufficient
prescribed (2-4 L/min) oxygen demand
144( 110-180g/L)  Administer IVF as ordered  Maybe necessary to
 Administer medications as compensate for the
prescribed decreased venous return
Carvedilol 6.25 mg, I tab OD  Inhibits conversion of
ECG FINDINGS:
Enalapril 5 mg 1 tab, BID angiotensin I to
 ST Segment elevation
angiotensin II, a potent
ANGIOGRAM:
Collaborative: vasoconstrictor;
 BLOCKAGE IN RIGHT Nutritional diet ( low fat, low salt)  Foods high in fat nad
AND LEFT sodium contributes to
VENTRICLE plaque formation

35
 NURSING PLANNING INT5ERVENTIONS RATIONALE EVALUATION
ASSESSMENTS DIAGNOSIS
Risk for impaired STO: INDEPENDENT The patient was able
Subjective: gas exchange  Encourage frequent positioning to maintain:
“ Usahay maglisod ko ginahawa’ related to alveolar- After 3-4 hours of  Helps prevent atelactasis
capillary membrane nursing  Maintain bed rest wih head and pneumonia  Reduction of
Objective: changes intervention the elevated 20-30 degrees, semi  Reduces oxygen anxiety
client will display fowler’s position. Support arms consumption  Patient and wife
reduction of anxiety with pillosws  Helps to relax the resp discuss the
 DOB  Deep breathing technique mucles anxieties and
 Pallor LTO:  Instruct to avoid straining  To reduce myocardial illness and
 Appears weak demand death
After or within 12  Appears restful
hours of nursing  Practice stress
PR range- 50-65 interventions the reduction
RR- 16-22 client will technique
BP: 90/70- 130-80 emphasize the DEPENDENT:
importance of  Administer oxygen as indicated, 2L/ min
desired activation via nasal cannula
 Administer meds as prescribed  Increases alveolar oxygen
ECG FINDINGS:
concentration which may
 ST Segment elevation Isosorbidemononitrate
reduce hyposemia
ANGIOGRAM: 30mg/tab, 2tab BID
 Relaxes vascular smooth
 BLOCKAGE IN RIGHT muscle with a resultant
AND LEFT VENTRICLE decrease in venous return
and decrease in arterial BP,
which reduces left
ventricular workload and
decrease myocardial of
oxygen consumption

36
DISCHARGE PLAN
A. OBJECTIVE
1. Summarize a simple and productive health education plan;
2. Adhere prescribed medications for health maintenance and resistance;
3. Promote a health lifestyle, maximize the level of health ;
4. Gains knowledge in managing the condition; and
5. Maintain and ensure adequate intake for nourishment

B. METHOD
Medications
DRUG STUDY

Generic Classifica Indication Mechanism of Route/F Adverse Reaction Drug to Drug Interaction Patient teaching
Name tion Action requenc
y/Dosag
e
Aspirin Analgesic  mild to Analgesics and 80mg/ta  Acute aspirin toxicity:  increased risk of  take extra
moderate antirheumatic b, 1tab respiratory alkalosis, bleeding with oral precautions to
pain effects are PO OD hyperpnea, anticougulants, keep this drug out
 fever attributable to tachycardia,hemorrhage,exci heparin of the reach of
 inflammatory aspirin’s to inhibit tement,confusion,asterixis,p  increased risk of GI children; this
conditions- the synthesis of ulmunoryedema,seizurers,tet ulceration with drug can be very
rheumatic prostaglandins, any,metabolic acidosis, steroids, dangerous for
fever, important fever, coma ,CV collapse, phenylbutazone, children
rheumatic mediators of renal and respiratory failure alcohol, NSAIDS  use the drug only
arthritis, inflammation.  Aspirin intolerance:  increased serum as suggested;
osteoarthritis, exacerbation of salicylate levels due avoid over dose.

37
 juvenile bronchospasm, rhinitis (with to decreased Avoid the use of
rheumatoid nasal polyps, asthma, salicylate excretion other over-the-
arthritis, rhinitis) with urine acidifies counter drugs
spondyloarthr  GI: nausea, dyspepsia, (ammonium contain aspirin,
opathies hearburn, chloride, ascorbic and serious
epigastricdiscomfort, acid, methionine) overdose can
anorexia, hepatoxicity occur.
 Hematologic: occult blood  Take the
loss, hemostatic defects drug with
 Hypersensitivity: food or
anaphylactoid reaction to after
anaphylactic shock meals if
GI upset
occurs.
Isosorbidem Antiangin  Dinitrate: Relaxes vascular 30mg/ta  CNS: headache,  Increased systolic  Place
ononitrate al treatment and smooth muscle b, 2tab apprehension, restlessness, BP and decreased sublingua
prevention of with a resultant BID weakness, vertigo, antianginal effects if l tablets
angina decrease in venous dezziness, faintness taken concurrently under
pectoris return and  CV: tachycardia, retrosternal with ergot alkalosis your
 Mononitrate: decrease in arterial discomfort, palpitations, tongue or
prevention of BP, which reduces hypotension, syncope, in your
angina left ventricular collapse cheek; do
pectoris; workload and  GI: nausea, vomiting, not chew,
treatment of decrease incontinence of feces, swallow,
angina myocardial of abdominal pain, diarrhea, or crush
pectoris oxygen ulcer the tablet.
(mmonoket) consumption.  GU: dysuria, impotence, Take the
 Unlabeled urinary frequency isosorbide
use before
(dinitrate); chest pain
use with begins,
hydralazine when
in black activities

38
 patients with or
advanced situationa
heart failure; l may
acute angle- precipitat
closure e an
glaucoma in attack.
emergent  Keep life-
situations; support
achalasia equipmen
t readily
available
if
overdose
occurs or
cardiac
condition
s
worsens.
Atorvastatin Antihyperl  Adjunct to Inhibits HMG- 80mg/ta  CNS: headache, asthenia  Increased digoxin  Take this drug once
ipidemic diet in CoA reductase, b, 1tab  GI: flatulence, dyspepsia, levels with possible a day, at about the
treatment of the enzyme that OD q heartburn, liver failure toxicity if taken same time each
elevated total catalyzes the first HS  Respiratory: sinusitis, together, monitor day, preferably in
cholesterol, step in the pharyngitis digoxin level the evening; may
serem cholesterol  Increased estrogen be taken with food.
triglycerides, synthesis pathway, levels with Do not drink
and LDL resulting in a hormonal grapefruit juice
cholesterol decrease in serum contraceptives; while taking this
and to cholesterol, serum monitor patients on drug
increase LDLs (associated this combination.  Institute
HDL-C in with increased risk appropriate dietary
patients with of CAD), and changes
primary increased serum  Arrange to have
hypercholeste HDLs (associated periodic blood test

39
 rol (types II with deceased risk while you are
and IIb) and of CAD); taking this drug.
mixed increases hepatic
dyslipidemia LDL recapture
and primary sites, enhances
dysbetalipopr reuptake and
oteinemia, catabolism of
whose LDL; lowers
response to triglyceride levels.
dietary
restriction of
saturated fat
and
cholesterol
and other non
pharmacologi
c measure
has not been
adequate.
Enalapril Ace  Hypertension Inhibits 5mg/tab  CNS: dizziness, fatigue,  Allopurinol:  Assess for rapid
inihibitor conversion of , 1 tab headache, insomnia, increased risk of blood pressure drop
angiotensin I to BID drowsiness, vertigo, hypersensitivity leading to
angiotensin II, a asthenia, paresthesia, ataxia, reaction cardiovascular
potent confusion, depression,  Antacids: decreased collapse, especially
vasoconstrictor; nervousness, enalapril absorption when giving with
inactivates cerebrovascular accident Cyclosporine, diuretics
bradykinin and  CV: orthostatic hypotension, indomethacin,  In patient with
prostaglandins. palpitations, angina pectoris, potassiumsparing renal insufficiency
Also increases tachycardia, peripheral diuretics, potassium or renal artery
plasma renin and edema, arrhythmias, cardiac supplements: stenosis, monitor
potassium levels arrest hyperkalemia for worsening renal
and reduces  EENT: sinusitis Digoxin, lithium: function.
aldosterone levels,  GI: nausea, vomiting, increased blood  After initial dose,
resulting in

40
 systemic constipation, dyspepsia, levels of these observe patient
vasodilation. abdominal pain, dry mouth, drugs, possible closely for at least
pancreatitis toxicity Diuretics, 2 hours until blood
nitrates, other pressure has
antihypertensives, stabilized. Then
phenothiazines: continue to observe
additive hypotension for additional hour.
Nonsteroidal anti-
inflammatory drugs:
decreased
antihypertensive
response Rifampin:
decreased enalapril
efficacy
Carvedilol Antihypert Hypertension Blocks stimulation 6-  CNS: dizziness, fatigue,  Antihypertensives:  Watch for signs
ensive of cardiac beta1- 25mg/ta anxiety, depression, additive hypotension and symptoms of
adrenergic b, 1tab insomnia, memory loss, Calcium channel hypersensitivity
receptor sites and OD q nightmares, headache, pain blockers, general reaction.
pulmonary beta2- HS  CV: orthostatic hypotension, anesthetics, I.V.  Assess baseline
adrenergic peripheral vasoconstriction, phenytoin: additive CBC and kidney
receptor sites. angina pectoris, chest pain, myocardial and liver function
Shows intrinsic hypertension, bradycardia, depression test results.
sympathomimetic heart failure, atrioventricular  Cimetidine:  Monitor vital signs
activity, causing block increased carvedilol (especially blood
slowing of heart  EENT: blurred or abnormal toxicity pressure), ECG,
rate, decreased vision, dry eyes, stuffy nose,  Clonidine: increased and exercise
myocardial rhinitis, sinusitis, pharyngitis hypotension and tolerance. Drug
excitability,  GI: nausea, diarrhea, bradycardia, may alter cardiac
reduced cardiac constipation GU: urinary exaggerated output and cause
output, and tract infection, hematuria, withdrawal ineffective airway
decreased renin albuminuria, decreased phenomenon clearance.
release from libido, erectile  Weigh patient
kidney dysfunction,renal daily and measure

41
 dysfunction fluid intake and
output to detect
fluid retention.
 Measure blood
glucose regularly if
patient has diabetes
mellitus. Drug may
mask signs and
symptoms of
hypoglycemia.
 ●Instruct patient to
take drug with food
exactly as
prescribed.
 Tell patient to take
extended-release
capsule in the
morning with food,
to swallow capsule
whole, and not to
chew, crush, or
divide its contents.
Mucosta Antacid  Peptic ulcer Rebamipide is a 1 tab  CNS: dizziness, headache,  Ampicillin,  Assess vital signs.
 Gastritis mucosal protective 3x/day asthenia cyanocobalamin,  Check for
agent and is  GI: nausea, vomiting, iron salts, abdominal pain,
postulated to diarrhea, constipation, ketoconazole: emesis, diarrhea, or
increase gastric abdominal pain reduced absorption constipation.
blood  Metabolic: hypomagnesemia of these drugs  Evaluate fluid
flow,prostaglandin  Musculoskeletal: back pain; Clarithromycin: intake and output.
biosynthesis and fractures of hip, wrist, spine increased  Watch for elevated
decrease free (with long-term daily use) omeprazole blood liver function test
oxygen radicals.  Respiratory: cough, upper level results (rare).
respiratory tract infection  Clopidogrel:  Monitor

42
  Skin:rash diminished magnesium level
antiplatelet activity before starting drug
Diazepam, and periodically
phenytoin, warfarin: thereafter in
prolonged patients expected to
elimination and be on long-term
increased effects of treatment or who
these drugs take proton pump
 Digoxin: increased inhibitors with
digoxin absorption other drugs such as
and blood level, digoxin or drugs
possible digoxin that may cause
toxicity Drugs hypomagnesemia.
metabolized by
CYP450 system:
competitive
metabolism
Methotrexate:
increased
methotrexate serum
level
 Penicillins: serious
and occasionally
fatal hypersensitivity
reactions including
anaphylaxis
 Rifampin:
substantially
decreased
omeprazole
concentrations
Pantoprazole Anti- For the treatment of Reduces gastric 40/30m  CNS: dizziness, headache  Ampicillin,  Assess for
+Domperidi Ulcerant gastroesophageal acid secretion and g 1 tab  CV: chest pain cyanocobalamin, symptomatic

43
ne reflux disease; non- increases gastric once a  EENT: rhinitis digoxin, iron salts, improvement.
ulcer dyspepsia, mucus and day  GI: vomiting, ketoconazole:  Monitor blood
gastric or duodenal bicarbonate diarrhea, abdominal pain, delayed absorption glucose level in
ulcer, dyspepsia, production, dyspepsia Metabolic: of these drugs diabetic patient.
bloating, fullness, creating protective hyperglycemia  Atazanavir,  Tell patient to
belching, NSAID coating on gastric  Musculoskeletal: hip, wrist, nelfinavir: swallow
induced dyspepsia. mucosa spine fractures (with long- substantially delayedrelease
term daily use) decreased atazanavir tablets whole
 Skin: rash, pruritus or nelfinavir plasma without crushing,
 Other: injection site reaction concentration with chewing, or
loss of therapeutic splitting.
effect and
development of drug
resistance

Norplat Antiplatelet  Recent Inhibits 75mg 1 tab OD  CNS: depression, Abciximab, aspirin,  Monitor
myocardial platelet dizziness, fatigue, eptifibatide, hemoglobin
infarction aggregation headache heparin, and
(MI) or by blocking  CV: chest pain, heparinoids, hematocrit
stroke or binding of hypertension nonsteroidal anti- periodically.
established adenosine EENT: epistaxis, inflammatory drugs  Monitor
peripheral diphosphate rhinitis (NSAIDs), patient for
arterial to platelets,  GI: diarrhea, thrombolytics, unusual
disease thereby abdominal pain, ticlopidine, bleeding or
preventing dyspepsia, gastritis, tirofiban, warfarin: bruising; drug
thrombus GI bleeding increased risk of significantly
formation  Hematologic: bleeding increases risk
bleeding, CYP2C19 of bleeding.
neutropenia, inhibitors (such as  Assess for
thrombotic esomeprazole, occult GI
thrombocytopenic omeprazole): blood loss if
purpura significantly patient is
reduced clopidogrel receiving

44
 Metabolic: antiplatelet activity naproxen
hypercholesterolem Fluvastatin, many concurrently
ia, gout NSAIDs, with
Musculoskeletal: phenytoin, clopidogrel.
joint pain, back tamoxifen,  Advise patient
pain Respiratory: tolbutamide, to
cough, dyspnea, torsemide: immediately
bronchitis, upper interference with report unusual
respiratory tract metabolism of these or acute chest
infection, drugs pain,
bronchospasm respiratory
Skin: pruritus, rash, difficulty,
angioedema rash, purplish
bruises on
skin or in
mouth, purple
skin patches,
unusual
fatigue, fast
heart rate,
confusion,
signs and
symptoms of
stroke
(including
weakness on
oneside,
speech
changes), low
urine output,
unresolved
bleeding,
diarrhea, GI
distress,

45
 nosebleed, or
acute
headache.

2. EXERCISE/ACTIVITY and HOME ENIVRONMENT

1. Depending on the status, the patient is encouraged to return to usual activities gradually.
a) Encourage the patient and instructed the significant others to control activities for daily living
b) Encourage the patient and instructed the significant others to participate in passive active range of motion as tolerated
c) Instructed the significant others to provide safety precautions to the patient, especially when ambulating or using a bathroom
d) Instructed the significant others to include 30 minutes of walking as tolerated
a) Encourage patient to include atleats 30 minutes of walking
e) or jogging or perform tolerated and preferred activities as a means of exerci

RESTRICTIONS:
1. Strenuous activities
2. Heavy lifting greater than 5kg
3. Prolonged exposure to sunlighrt

HOME ENVIRONMENTAL HAZARDS:

a) Restrict smoker
b) Crowded area

46
 3. TREATMENTS/THERAPIES
a) Attending the follow up check up :
 Educate client by adhering maintenance therapy, appropriate diet and having exercise will reduce likelihood

of occurrence and aggravation of disease.

4. HEALTH TEACHING/EDUCATION
PREVENTION/PROMOTION
Health teaching about the disease, exercise and diet
 Instructs the patient about home-made interventions in reducing blood such as:
a.) Pineapple or calamansi juice to reduce blood pressure
b) chewing of raw or fried garlic after meals
c.) refrain from consumption of caffeinated beverages, such as coffee and chocolate

5. OPD Visit
Instruct that they need to have a health check up
 Emphasize the importance of adhering to medications and attending follow-up check.
 Encourage patient to adhere to weakly blood pressure monitoring.

6. DIET
 Low calories- calorie restriction in individuals with hypertension
 Low fat- Advisable to reduce the fat consumption since hypertension has greater risk of atherosclerotic. Foods rich in cholesterol are liver, meat organ, egg
yolk,lobster, crabs, and prawns. Recommended: vegetable oil like sunflower and olive oil

47
  High protein: Most high protein foods are extremely low in carbs and extremely low in saturated fat. Therefore, by eating a high protein diet loaded with high
protein foods, at the same time you’d end up eating low carbs and low saturated foods
 Low sodium and High in potassium: Help to lower blood pressure
Foods rich in potassium: tomato, watermelon, banana, apple, raw carrots, leafy vegetables and potato
r
7. SPIRITUAL CARE AND PSYCHOLOGICAL OR SEXUAL NEEDS
(/) Spiritual counseling
(/) Grief work
(/) Anger Management
(/) Confession
(/) Family therapy
(/) Reconciliation of conflicted Relationships
(/) Supportive Counseling
(/) Join church Organizations/Activities
(/) Prayer
(/) Meditation, Reflection, and Spiritual Devotion
(/) Religious rituals
(/) Religious/ Spiritual Materials

48
SEXUAL NEEDS
(/) Marriage counseling
(/) Sex Therapy
(/) Sexual Therapy
(/s) Referral to appropriate Agencies

49
References:

1. Taylor (2008) Nursing Diagnosis Pocket Guide (2th ed.).Philadelphia: Wolters

Kluwer Health/Lippincott Williams & Wilkins.

2. Lewis, Heitkemper ,Dirksen ,O'Brien,Bucher (2007): Assessment and

Management of Clinical Problems, liver, Pancreas and Biliary Tract problems,
Medical Surgical Nursing, MOSBY.1st Edition, 1101:15.

3. Ignatavicius & Workman (2006) Medical Surgical Nursing: Critical Thinking for
Collaborative Care. USA. Elsevier.

4. Smeltzer & Bare (2004). Medical- Surgical Nursing. Philadelphia. Lippincott

Williams & Wilkins.

5. Tortora (2011). Principles of Anatomy and Physiology , 14th Edition John Wiley
& Sons, 2008.

6. Weber & Kelley (2014). Health Assessment In Nursing. Philadelphia. Lippincott

Williams & Wilkins.

7. Goldman and Schafer (2016).Goldman-Cecil Medicine. 25th ed. Philadelphia,

PA: Elsevier Saunders.

8. Cecil, Goldman,Bennett (2000).Cecil Textbook of Medicine . 21st ed.

Philadelphia, PA: WB Saunders Company.

50
51