PRELIMINARY REPORT AND NURSING CARE

PATIENT Mrs H WITH MEDICAL DIAGNOSIS OF ACUTE CORONARY

SYNDROME AT NOTRE DAME DE CHARTRES HOSPITAL BAGUIO CITY
PHILIPPINES

Member of Group
Chumaira Anindayudina 14.IK.381
Erwin Setiawan 14.IK.386
Muhammad Syaud Faisal 14.IK.405

COURSE OF NURSING PROGRAM

SARI MULIA SCHOOL AND HEALTH SCIENCE
BANJARMASIN
2018
 SHEET APPROVAL

Title case : Acute Coronary Syndrome

Case taking : Intensive Care Unit
Member of group : Chumaira Anindayudina
Erwin Setiawan
Muhammad Syaud Faisal

Baguio City, January 15 2018

Clinical Instructor (CI)

CORY C. MANUEL, MSN

ii
 FOREWORDS

Thanks God Almighty, we can complete this preliminary report and

nursing care. We sincerely hope this preliminary report and nursing care can be
useful in order to increase our insight and knowledge. We are also fully aware
that in this paper there is a shortage and is far from perfect. Therefore, we expect
criticism, suggestions and suggestions for the improvement of this preliminary
report and nursing care we have made in the future, given that nothing is perfect
without constructive suggestions.
Hopefully this simple introductory report and nursing care can be
understood for anyone who reads it. If this report has been prepared, it can be
useful for both ourselves and the people who read it. Previously we apologize if
there are any errors of words that are less favorable and we ask for constructive
criticism and suggestions for future improvement.

Banjarmasin, January 15 2018

Authors

iii
 CONTENTS

Cover ............................................................................................................ i
Sheet Approval ............................................................................................. ii
Forewords..................................................................................................... iii
Contents ....................................................................................................... iv
Chapter l Introduction ................................................................................... 1
A. Background ....................................................................................... 1
B. Problem Formulation ......................................................................... 2
C. Purpose............................................................................................. 2
D. Benefits ............................................................................................. 2
Chapter ll Concept ........................................................................................ 4
A. Anatomy of heart ............................................................................... 4
B. Physiology of heart ............................................................................ 7
C. Definition ........................................................................................... 8
D. Etiology ............................................................................................. 8
E. Pathophysiology ................................................................................ 11
F. Signs and symtomps ......................................................................... 12
G. Complications ................................................................................... 14
H. Diagnostic Procedures ...................................................................... 14
I. Medical treatment.............................................................................. 16
J. Nursing assestment .......................................................................... 18
K. Nursing diagnosis.............................................................................. 22
L. Nursing planning ............................................................................... 22
Chapter lll Critical assessment in ICU ..................................................................... 30
References .................................................................................................. 52

iv
 CHAPTER l
INTRODUCTION

A. Background
Acute Coronary Syndrome (ACS) is a term or terminology used to
describe the state spectrum or collection of disease processes including
unstable angina (UA), myocardial infarction without ST (non-STelevation
myocardial infarction / NSTEMI) and myocardial infarction with ST-segment
elevation myocardial infarction (STEMI). Acute Coronary Syndrome (ACS) is
used to describe patients who come with Unstable Angina Pectoris (UAP) or
with Acute Myocard Infarction (AMI) with either ST (STEMI) or ST (NSTEMI)
ST-segment elevation. A 2009 study in the United States concluded that the
number of inpatients due to ACS was 1,190,000 patients; 694,000 were men
and 496,000 were women (Overbaugh, 2009)..
Which describes any condition characterized by signs and symptoms
of sudden myocardial ischemia—a sudden reduction in blood flow to the
heart. The term ACS was adopted because it was believed to more clearly
reflect the disease progression associated with myocardial ischemia.
Unstable angina and myocardial infarction (MI) both come under the ACS
umbrella.The signs and symptoms of ACS constitute a continuum of intensity
from unstable angina to non STsegment elevation MI (NSTEMI) to ST-
segment elevation MI (STEMI). Unstable angina and NSTEMI normally result
from a partially or intermittently occluded coronary artery, whereas STEMI
results from a fully occluded coronary artery (Overbaugh, 2009).
According to World Health Organization (WHO) data in 2013, ACS is
the leading cause of death by reaching 7 million deaths annually worldwide,
especially in developing countries The 2016 Heart Disease and Stroke
Statistics update of the American Heart Association (AHA) has recently
reported that 15.5 million persons ≥ 20 years of age in the USA have CHD
(16), whilst the reported prevalence increases with age for both women and
men and it has been estimated that approximately every 42 seconds, an
American will suffer for an MI (Fabian, et all, 2016).
Every year, more than one million Americans suffer from Acute
Coronary Syndrome (ACS). Risk factors for Acute Coronary Syndrome
(ACS) include sex (men slightly higher risk), age (men > 45 years and

5
 women > 55 years), family history of cardiovascular disease, and modifiable
risk factors. Modifiable risk factors include hypertension, hyperlipidemia,
diabetes mellitus, sedentary lifestyle, and smoking (Fabian, et all, 2016).

B. Problem Formulation
Based on of the cases and the importance of disease handling with
the formulation of the problem is "How is nursing care in patients with acute
coronary syndrome?"

C. Purpose
1. General Purpose
Able to know and apply nursing care to patients with acute
coronary syndrome according to nursing standard.

2. Specific Purpose
a. Able the assessment of patients with acute coronary syndrome and
their families.
b. Able to determine nursing diagnoses in acute coronary syndrome
patients
c. Able to know the preparation of nursing planning in patients acute
coronary syndrome
d. Able to implement the implementation in patients with acute coronary
syndrome
e. Able the evaluation in patients with acute coronary syndrome.

D. Benefits
1. Authors
It is expected that the authors have additional insight and knowledge
in management in patients with Osteosarcoma disease and in
providing nursing care to clients with acute coronary syndrome.
2. Patient and Family
In order for patients and families to have knowledge about treatment
in acute coronary syndrome patients.

6
3. Service Institutions
Provide assistance that affects the client's development to achieve
nursing care level and follow-up for the quality care of patients with
acute coronary syndrome.
4. Educational Institutions
As a source of reading or reference to improve the quality of nursing
education and as an input in the improvement of acute coronary
syndrome patients, especially in the field of documentation of nursing
care

7
 CHAPTER ll
CONCEPT

A. Anatomy of heart
The heart itself is made up of 4 chambers, 2 atria and 2 ventricles.
Deoxygenated blood returns to the right side of the heart via the venous
circulation. It is pumped into the right ventricle and then to the lungs where
carbon dioxide is released and oxygen is absorbed. The oxygenated blood
then travels back to the left side of the heart into the left atria, then into the
left ventricle from where it is pumped into the aorta and arterial circulation
(Belleza, 2017).
The pressure created in the arteries by the contraction of the left
ventricle is the systolic blood pressure. Once the left ventricle has fully
contracted it begins to relax and refill with blood from the left atria. The
pressure in the arteries falls whilst the ventricle refills. This is the diastolic
blood pressure (Belleza, 2017).
The atrio-ventricular septum completely separates the 2 sides of the
heart. Unless there is a septal defect, the 2 sides of the heart never directly
communicate. Blood travels from right side to left side via the lungs only.
However the chambers themselves work together. The 2 atria contract
simultaneously, and the 2 ventricles contract simultaneously (Belleza, 2017).

8
1. Heart Structure and Functions

a. Weight. Approximately the size of a person’s fist, the hollow, cone-

shaped heart weighs less than a pound.
b. Mediastinum. Snugly enclosed within the inferior mediastinum, the
medial cavity of the thorax, the heart is flanked on each side by the
lungs.
c. Apex. It’s more pointed apex is directed toward the left hip and rests
on the diaphragm, approximately at the level of the fifth intercostal
space.
d. Base. Its broad posterosuperior aspect, or base, from which the great
vessels of the body emerge, points toward the right shoulder and lies
beneath the second rib.
e. Pericardium. The heart is enclosed in a double-walled sac called the
pericardium and is the outermost layer of the heart.
f. Fibrous pericardium. The loosely fitting superficial part of this sac is
referred to as the fibrous pericardium, which helps protect the heart

9
 and anchors it to surrounding structures such as the diaphragm and
sternum.
g. Serous pericardium. Deep to the fibrous pericardium is the slippery,
two-layer serous pericardium, where its parietal layer lines the interior
of the fibrous pericardium.
2. Layers of the Heart
The heart muscle has three layers and they are as follows :
a. Epicardium. The epicardium or the visceral and outermost layer is
actually a part of the heart wall.
b. Myocardium. The myocardium consists of thick bundles of cardiac
muscle twisted and whirled into ringlike arrangements and it is the
layer that actually contracts.
c. Endocardium. The endocardium is the innermost layer of the heart
and is a thin, glistening sheet of endothelium hat lines the heart
chambers
3. Associated great vessels
The great blood vessels provide a pathway for the entire cardiac
circulation to proceed :
a. Superior and inferior vena cava. The heart receives relatively oxygen-
poor blood from the veins of the body through the large superior and
inferior vena cava and pumps it through the pulmonary trunk.
b. Pulmonary arteries. The pulmonary trunk splits into the right and left
pulmonary arteries, which carry blood to the lungs, where oxygen is
picked up and carbon dioxide is unloaded.
c. Pulmonary veins. Oxygen-rich blood drains from the lungs and is
returned to the left side of the heart through the four pulmonary veins.
d. Aorta. Blood returned to the left side of the heart is pumped out of the
heart into the aorta from which the systemic arteries branch to supply
essentially all body tissues.
4. Heart velves
The heart is equipped with four valves, which allow blood to flow in only
one direction through the heart chambers
a. Atrioventricular valves. Atrioventricular or AV valves are located
between the atrial and ventricular chambers on each side, and they
prevent backflow into the atria when the ventricles contract.

10
 b. Bicuspid valves. The left AV valve- the bicuspid or mitral valve,
consists of two flaps, or cusps, of endocardium.
c. Tricuspid valve. The right AV valve, the tricuspid valve, has three
flaps.
d. Semilunar valve. The second set of valves, the semilunar valves,
guards the bases of the two large arteries leaving the ventricular
chambers, thus they are known as the pulmonary and aortic
semilunar valves.

B. Physiology of heart
As the heart beats or contracts, the blood makes continuous round
trips into and out of the heart, through the rest of the body, and then back to
the heart- only to be sent out again (Belleza, 2017).
1. Intrinsic Conduction System of the Heart
The spontaneous contractions of the cardiac muscle cells occurs in a regular
and continuous way, giving rhythm to the heart.

11
 a. Cardiac muscle cells. Cardiac muscle cells can and do contract
spontaneously and independently, even if all nervous connections
are severed.
b. Rhythms. Although cardiac muscles can beat independently, the
muscle cells in the different areas of the heart have different
rhythms.
c. Intrinsic conduction system. The intrinsic conduction system, or the
nodal system, that is built into the heart tissue sets the basic rhythm.
d. Composition. The intrinsic conduction system is composed of a
special tissue found nowhere else in the body; it is much like a cross
between a muscle and nervous tissue.
e. Function. This system causes heart muscle depolarization in only
one direction- from the atria to the ventricles; it enforces a
contraction rate of approximately 75 beats per minute on the heart,
thus the heart beats as a coordinated unit.
f. Sinoatrial (SA) node. The SA node has the highest rate of
depolarization in the whole system, so it can start the beat and set
the pace for the whole heart; thus the term “pacemaker“.
g. Atrial contraction. From the SA node, the impulse spread through
the atria to the AV node, and then the atria contract.
h. Ventricular contraction. It then passes through the AV bundle, the
bundle branches, and the Purkinje fibers, resulting in a “wringing”
contraction of the ventricles that begins at the heart apex and
moves toward the atria.
i. Ejection. This contraction effectively ejects blood superiorly into the
large arteries leaving the heart.

2. The pathway of the conduction system

The conduction system occurs systematically through :
a. SA node. The depolarization wave is initiated by the sinoatrial
node.
b. Atrial myocardium. The wave then successively passes through
the atrial myocardium.
c. Atrioventricular node. The depolarization wave then spreads to the
AV node, and then the atria contract.
d. AV bundle. It then passes rapidly through the AV bundle.

12
 e. Bundle branches and Purkinje fibers. The wave then continues on
through the right and left bundle branches, and then to the
Purkinje fibers in the ventricular walls, resulting in a contraction
that ejects blood, leaving the heart.
3. Cardiac cycle and hearth sound
In a healthy heart, the atria contract simultaneously, then, as they start
to relax, contraction of the ventricles begin.
a. Systole. Systole means heart contraction.
b. Diastole. Diastole means heart relaxation.
c. Cardiac cycle. The term cardiac cycle refers to the events of one
complete heart beat, during which both atria and ventricles
contract and then relax.
d. Length. The average heart beats approximately 75 times per
minute, so the length of the cardiac cycle is normally about 0.8
second.
e. Mid-to-late diastole. The cycle starts with the heart in complete
relaxation; the pressure in the heart is low, and blood is flowing
passively into and through the atria into the ventricles from the
pulmonary and systemic circulations; the semilunar valves are
closed, and the AV valves are open; then the atria contract and
force the blood remaining in their chambers into the ventricles.
f. Ventricular systole. Shortly after, the ventricular contraction
begins, and the pressure within the ventricles increases rapidly,
closing the AV valves; when the intraventricular pressure is higher
than the pressure in the large arteries leaving the heart, the
semilunar valves are forced open, and blood rushes through them
out of the ventricles; the atria are relaxed, and their chambers are
again filling with blood.
g. Early diastole. At the end of systole, the ventricles relax, the
semilunar valves snap shut, and for a moment the ventricles are
completely closed chambers; the intraventricular pressure drops
and the AV valves are forced open; the ventricles again begin
refilling rapidly with blood, completing the cycle.
h. First heart sound. The first heart sound, “lub”, is caused by the
closing of the AV valves.

13
 i. Second heart sound. The second heart sound, “dub”, occurs
when the semilunar valves close at the end of systole.

C. Definition
Acute coronary syndrome (ACS) is the umbrella term for the clinical
signs and symptoms of myocardial ischemia: unstable angina, non–ST-
segment elevation myocardial infarction, and ST-segment elevation
myocardial infarction (Overbaugh, 2009).
Acute coronary syndrome (ACS) refers to a spectrum of clinical
presentations ranging from those for ST-segment elevation myocardial
infarction (STEMI) to presentations found in non–ST-segment elevation
myocardial infarction (NSTEMI) or in unstable angina. It is almost always
associated with rupture of an atherosclerotic plaque and partial or complete
thrombosis of the infarct-related artery (David, 2016).

D. Etiology
Acute coronary syndrome (ACS) is caused primarily by
atherosclerosis. Most cases of ACS occur from disruption of a previously
nonsevere lesion (an atherosclerotic lesion that was previously
hemodynamically insignificant yet vulnerable to rupture). The vulnerable
plaque is typified by a large lipid pool, numerous inflammatory cells, and a
thin, fibrous cap.
Elevated demand can produce ACS in the presence of a high-grade
fixed coronary obstruction, due to increased myocardial oxygen and nutrition
requirements, such as those resulting from exertion, emotional stress, or
physiologic stress (eg, from dehydration, blood loss, hypotension, infection,
thyrotoxicosis, or surgery). ACS without elevation in demand requires a new
impairment in supply, typically due to thrombosis and/or plaque hemorrhage.
The major trigger for coronary thrombosis is considered to be plaque
rupture caused by the dissolution of the fibrous cap, the dissolution itself
being the result of the release of metalloproteinases (collagenases) from
activated inflammatory cells. This event is followed by platelet activation and
aggregation, activation of the coagulation pathway, and vasoconstriction.
This process culminates in coronary intraluminal thrombosis and variable
degrees of vascular occlusion. Distal embolization may occur. The severity
and duration of coronary arterial obstruction, the volume of myocardium

14
 affected, the level of demand on the heart, and the ability of the rest of the
heart to compensate are major determinants of a patient's clinical
presentation and outcome. Anemia and hypoxemia can precipitate
myocardial ischemia in the absence of severe reduction in coronary artery
blood flow (Overbaugh, 2009).

E. Pathophysiology
Acute coronary syndrome (ACS) begins when a disrupted
atherosclerotic plaque in a coronary artery stimulates platelet aggregation
and thrombus formation. It’s the thrombus occluding the vessel that prevents
myocardial perfusion . In the past, researchers supposed that the narrowing
of the coronary artery in response to thickening plaque was primarily
responsible for the decreased blood flow that leads to ischemia, but more
recent data suggest that it’s the rupture of an unstable, vulnerable plaque
with its associated.
Myocardial cells require oxygen and adenosine 5b-triphosphate
(ATP) to maintain the contractility and electrical stability needed for normal
conduction. As myocardial cells are deprived of oxygen and anaerobic
metabolism of glycogen takes over, less ATP is produced, leading to failure
of the sodium–potassium and calcium pumps and an accumulation of
hydrogen ions and lactate, resulting in acidosis. At this point, infarction—cell
death—will occur unless interventions are begun that limit or reverse the
ischemia and injury. During the ischemic phase, cells exhibit both aerobic
and anaerobic metabolism. If myocardial perfusion continues to decrease,
aerobic metabolism ceases and eventually anaerobic metabolism will be
significantly reduced. This period is known as the injury phase. If perfusion is
not restored within about 20 minutes, myocardial necrosis results and the
damage is irreversible. Impaired myocardial contractility, the result of scar
tissue replacing healthy tissue in the damaged area, decreases cardiac
output, limiting perfusion to vital organs and peripheral tissue and ultimately
contributing to signs and symptoms of shock. Clinical manifestations include
changes in level of consciousness; cyanosis; cool, clammy skin;
hypotension; tachycardia; and decreased urine output (Overbaugh, 2009).

15
F. Signs and symtomps
Signs and symtomps of acute coronary syndrome is the degree to
which a coronary artery is occluded typically correlates with presenting
symptoms and with variations in cardiac markers and electrocardiographic
findings. Angina, or chest pain, continues to be recognized as the classic
symptom of ACS. In unstable angina, chest pain normally occurs either at
rest or with exertion and results in limited activity. Chest pain associated with
NSTEMI is normally longer in duration and more severe than chest pain
associated with unstable angina. In both conditions, the frequency and
intensity of pain can increase if not resolved with rest, nitroglycerin, or both
and may last longer than 15 minutes. Pain may occur with or without
radiation to the arm, neck, back, or epigastric area. In addition to angina,
patients with ACS also present with shortness of breath, diaphoresis,
nausea, and lightheadedness. Changes in vital signs, such as tachycardia,
tachypnea, hypertension, or hypotension, and decreased oxygen saturation
(SaO2) or cardiac rhythm abnormalities may also be present.:

16
Other symptoms :
1. Chest or abdominal pain, Pressure
2. Any discomfort above the nevel
3. Jaw pain
4. Alterations in mental status, confusion, dizziness
5. Palpitations
6. Profuse sweating
7. Shortness of breath
8. Unexplained excessive fatique

17
G. Complications
Numerous complications can occur and increase morbidity and
mortality. They can be roughly categorized as
1. Electrical dysfunction (conduction disturbance, arrhythmias)
2. Mechanical dysfunction (heart failure, myocardial rupture or aneurysm,
papillary muscle dysfunction)
3. Thrombotic complications (recurrent coronary ischemia, mural
thrombosis)
4. Inflammatory complications (pericarditis, Dressler syndrome)
If the artery supplying the sinus node is affected by an acute coronary
syndrome, sinus node disturbances can occur; they are more likely if there is
a preexisting sinus node disorder (sinus bradycardia and sinus tachycardia).

H. Diagnostic Prosedures
1. Laboratorium Prosedure
a. CBC
b. Blood Chemistry (HDL, LDL, Triglceride, Cholesterol)
c. Serum cardiac markers
Serum cardiac marker determinations play a vital role in the
diagnosis of acute coronary syndrome. Serum markers such as
aspartate transaminase, lactate dehydrogenase, and lactate
dehydrogenase subforms are no longer used as early as possible.
Cardiac specificity and their delayed elevation precludes early
diagnosis.
1) Creatine Kinase
Creatine kinase (CK) is an enzyme that is found in striated
muscle and tissues of the brain, kidney, lung, and gastrointestinal
tract. This widely available marker has low sensitivity and
specificity for cardiac damage. Furthermore, CK levels may be
elevated in a number of noncardiac conditions, including trauma,
seizures, renal insufficiency, hyperthermia, and hyperthyroidism.
The serum CK level rises within three to eight hours after
myocardial injury, peaks by 12 to 24 hours, and returns to
baseline within three to four days. A serum CK level may be used
as a screening test to determine the need for more specific

18
 testing. Although CK commonly was measured serially (along
with CK-MB) at the time of hospital admission and six to 12 hours
after admission, this marker largely has been replaced by cardiac
troponins and CK-MB.
2) CK-MB Isoenzyme
CK-MB is much more cardiac specific than CK alone, and
is useful for the early diagnosis of acute myocardial infarction.
CK-MB typically is detectable in the serum four to six hours after
the onset of ischemia, peaks in 12 to 24 hours, and normalizes in
two to three days. The CK-MB mass assay is more sensitive than
the CK-MB activity assay.
Like the CK level, the peak CK-MB level does not predict
infarct size; however, it can be used to detect early reinfarction.
Serial CK-MB levels commonly are obtained at admission to the
emergency department and are repeated in six to 12 hours,
depending on the assay that is used.
3) CK-MB Subforms
CK-MB may be further characterized into subforms (or
isoforms). CK-MB2 is found in myocardial tissue, and CK-MB1 is
found in plasma. The CK-MB subform assay takes about 25
minutes to perform. A CK-MB2 level greater than 1 U per L in
combination with a subform ratio greater than 1.5 suggests
myocardial injury. One large study23 involving 1,110 patients
with chest pain found that CK-MB subform analysis is 96 percent
sensitive and 94 percent specific when the marker is measured
six hours after symptom onset. However, the CK-MB subform
assay is not yet widely available.
4) Cardiac Troponins
Troponins (T,I,C) are found in striated and cardiac muscle.
Because the cardiac and skeletal muscle isoforms of troponin T
and I differ, they are known as the “cardiac troponins.” They are
the preferred markers for the diagnosis of myocardial injury.
Troponin T and I generally have similar sensitivity and specificity
for the detection of myocardial injury. Unlike troponin I levels,

19
 troponin T levels may be elevated in patients with renal disease,
polymyositis, or dermatomyositis.
2. Chest X-ray
3. Electrocardiogram (ECG)
a. STEMI: Changes in patients with acute Myocardial Infarction include:
hyperacute T, ST segment elevation followed by Q pathological, the
formation of bundle branch block / which is considered new.
ECG changes are ST segment elevation ≥ 1 mm in 2 leads adjacent
to the limb lead and / or elevation segment ≥2 mm at 2 lead chest
leads.
b. NSTEMI: ECG change in the form of depression segment ST ≥ 1 mm
at 2 adjacent leads on the limb lead and / or depressive segment ≥ 2
mm on 2 lead chest leads.
4. Coronary angiography
Describes narrowing or blockage of the coronary arteries. Usually
carried out in relation to the measurement of the porch pressure and
review left ventricular function (ejection fraction). Procedures are not
always done in phase AMI except near angioplasty or emergency heart
surgery.

I. Medical Treatment
The purpose of therapy in patients with AKS, namely to stabilize
angina (on APTS) and eliminate further damage to infarction. The critical
times are on infarction sufferer is the first 2 hours after the attack, where the
complication fatal heart failure VT-VF is the most frequent thingas the cause
of Suddent's death. Management is divided into 2 parts:
1. General
Patients are recommended total rest
Fasting patients 4-6 hours, after the patient no complaints of chest pain
can liquid diit
Immediately plug IV line, Oxygen
Nitral (cedocard) sublingual
Oral nitroglycerin or infusion (drip)
Aspirin 160 mg chewed
Pain killer (Morphine / Petidine)

20
 Patients treated in CVCU / ICCU, require a tight monitor
2. Specific
a. B Blocker
Reduce oxygen consumption. Options on B Block non ISA.
KI on AV block, Bronchial Asthma, Severe LHF. Giving B blockers
can
reducing progressive AKS by about 13%.
b. ACE Inhibitor
The first day of attack, can reduce mortality of fasca infarction.
c. Thrombolytic Therapy
Giving thrombolytic therapy only to Infrak with Q Waves (ST
elevation), while in non-Q infarction and APTS there is no benefit of
administration
trombolitk.
d. Heparin
UFH (unfractional heparin), the risk of bleeding requires a monitor
APTTT, dose of 5000 IU bolus, followed by 1000 IU / hour infusion
(2-2.5 x values APTT baseline). Low Molucle Weight Heparin
(LMWH) is safer, riskier small bleeding and does not require
monitoring of APTT. Dosage accordingly with weight, 1 mg / kgBB.

21
J. Nursing Assessment
In conducting assesment patient with cardiovascular system
disorders nurses still view the client as a holistic beings. Therefore in review
always pay attention to the biological, psychological, social and spiritual
aspects of kilen. Changes in biological aspect disorders may affect other
aspects, which will also have an impact on the development of client
diseases. Aspects that need to be studied in clients with cardiovascular
system disorders include:

22
1. Identity
A. Patient Identity: includes name, age, sex, occupation, religion,
education, address, medical diagnosis, date / time of MRS and date /
time of assessment.
B. Chift complaint: is the most perceived complaint by the patient and is
the main reason of the MRS client (the main complaint during MRS).
C. Another major complaint is a major complaint during an assessment
(some time or day after the client's MRS).
D. Current Disease History which contains the circumstances and
complaints of the client during the onset of the attack, the timing and
the frequency of the attack, the spread, the quality (severity of the
attack), the actions taken by the client / family to resolve the client's
complaints.
E. The guidelines used in finding the course of the client's illness are P
(Provocative / palliative), Q (Quality / Quantity), R (Regio / Radiation),
S (Severe l severity), and T (Time / time).
F. History of LaIu Disease: includes a history of illnesses that have been
suffered by clients, especially diseases that can support the
emergence of current diseases (predisposing and precipitation
factors), such as hypertension, vascular disease, diabetes mellitus,
impaired function of tyroid, RHD, heart disease, blood and others.
G. Family Disease History: includes history of diseases that have been
suffered by families, especially those associated with disorders of the
cardiovascular system or on other systems that have hereditary
properties and affect the functioning of the cardiovascular system.
H. Psychosocial history includes the patient's psychological history
relating to the condition of his illness as well as its impact on the
patient's social life.
I. Patterns of daily activity: includes nutritional and fluid patterns (eating
and drinking), pattern of elimination (urine / bowel), rest-sleep,
personal hygiene and other activities / habits that can aggravate the
client's condition
J. General Impression: includes the client's condition visible to the
nurse.

23
 K. Vital signs: Meilputi Blood Pressure (hypertension, normal,
hypotension), Pulse Rate, Respiration rate, Temperature, Height,
Weight.
L. Head and neck examination:
2. Physical examination
A. Face may get pale, cyanosis (impact and decrease oxygen
distribution to peripheral tissue), periorbital edema (impact and
decrease of glomerular filtration rate and water and salt
retention), grimace / signs of illness, and others.
B. Nasal nostril nose, cyanosis.
C. Eyes: pale conjunctiva, ptechieae; sclera icterus / normal; arcus
senilis on the cornea; state of retinal vessels (fundus of the eye).
D. Neck: Jugular venous distention (Jugularis Venous Pressure > 5,
2 cm or > 3 cm), the presence of a pulse indicates CHF.
E. Carotid Artery:
Palpation: to assess the presence of atherosclerosis in either the
left / right carotid artery; when throbbing like dancing suggests
aortic insufficiency The thyroid gland with auscultation when
sound is noisy shows increased vascularization due to thyroid
hyperfunction.
F. Trachea: palpation when any palpable tracheal heartbeat pulled
down (Oliver Sign) shows aortic aneurysm; observe symmetry.
G. Thorax (Lung and Heart)
1. Inspection Assessing symmetry and thorax form (Cekung:
chronic pericarditis, pulmonary fibrosis Convex to intercosta
showing signs of effusion pericardial / pleura. Convex in Os.
costae indicates a congenital heart abnormality); respiratory
movement; the pattern of the breath; widening of the veins in
the chest; heart apex pulse; chest / back pulse; localized
throbbing of the chest: retraction in precordium (in tune with
systole indicating pericarditis, Insufficiency). Tricuspidalis and
aorta); muscle retraction intercostae and suprasternal.
2. Palpation rate Vocal fremitus to assess the vibration of sound
on the chest wall. Apex pulse (normal: ICS V MidClavicula
Line. Sinistra width I. cm), apex pulse increased in aortic /

24
 mitral Insufficiency, slightly increased in hypertension and
aortic stenosis, when the apex pulse obtained on the sternal
line of the sinus indicates the presence right ventricular
hypertrophy.
Vibration / Thrill: shows heart noisy with location at:
lCS II LSS is a thrill due to pulmonary stenosis
lCS IV LSS is a thrill due to ventricular septum defect noise
lCS II LSD is a thrill due to aortic stenosis
Apex in the diastolic phase indicates Mitral stenosis, occurring
in the sistole phase indicating Mitral Insufficiency Arterial
pulse at location: Clavicula and / or lCS II LSD show aortic
aneurysm. lCS II LSS shows Patent ductus arteriosus,
Pulmonary arterial aneurysm, aortic descending aneurisms.
3. Percussion: Assess the limits of the lungs and heart, as well
as the lung condition (normal resonant / sonor).
4. Auscultation Breath sounds and additional breath sounds
such as ronchi, rales, wheezing, friction rub pleura Heart
sounds I, II, lIl / IV or Gallops rithme. Heart noisy: mitral, aorta,
tricuspidalis, pulmonalis, septal defect, friction rub / pericardic
friction.
H. Abdomen
1. Auscultate Assess intestinal peristalsis, systolic bleeding
(abdominal aortic aneurysm)
2. Inspection Assessing the form; abdominal surface state;
movement of abdominal wall; widening of the abdominal vein;
pulsation in the abdominal wall in the epigastrium (the right
ventricle), other sites (abdominal aortic aneurysm), in the right
hypochondrium (hepatic venous pulse due to hypertension
and right cord decompensation)
3. Palpation Assessing the presence of hepatomegaly,
splenomegaly, ascites (on right cord decompensation and
CHF)
4. Percussion: Shifthing dullness indicates the presence of fluid
in the abdomen (ascites).

25
 I. Extremities
1. Inspection:
Cyanosis in the nail and fingertip skin shows signs of
peripheral tissue hypoxia. Pale white on nails and fingertips,
Purpura / ptechiae between fingers, palms / legs (signs of
endocarditis / SBE, viral infections) Erytema nodusum of the
skin in the tibia area (endocarditis causa streptococcus)
Haemorragic splinter on nails (Endocarditis / SBE) Oedema
Clubbing fingers (causa hipoxia chronic)
2. Palpation
Pulse rate (See pulse assessment Extremely cold
temperatures Muscle tone Pitting oedema Integumentary pain
Pale yellow (impact of metabolic acidosis) or jaundice /
jaundice (impact of hepatic hepatic impairment) Neurologic
changes / decreased levels of consciousness and sensory
changes due to brain hypoxia.

I. Nursing Diagnosis
1. Ineffective breathing pattern related by respiratory muscle weakness /
fatigue
2. Ineffective tissue perfusion related by ineffectiveness between ventilation
and blood flow
3. Acute pain related by biological injury agent
4. Activity intolerance related by generalized weakness
5. Risk infection

J. Nursing Planning
Nursing
No NOC NIC
Diagnosis
Ineffective  Respiratory status :  Airway
1. breathing Management
Ventilation
pattern related 1. Monitor vital
by respiratory  Respiratory status : signs
muscle Airway patency 2. Observe for
weakness / After nursing care done for breathing
fatigue 3 x 8 hours is expected patterns
patient showed the 3. Assess the
effectiveness of the breath position that the
patternwith result criteria: patient assumes

26
 1. breath sounds clean, no for breathing.
cyanosis and dyspnea 4. Ask if they are
(able to remove sputum, “short of breath”
able to breathe easily, and note any
no pursed lips) dyspnea
2. Show the airway that is 5. Assess ability to
patent mobilize
3. Vital signs in the normal secretions.
range 6. Monitor for
BP: 110-140 / 70- diaphragmatic
90mmhg muscle fatigue or
RR: 12-20x / min weakness
F: 60-90 x / m 7. Collaboration
T: 36.5-37.5oC with doctor and
pulmonary
therapist
Ineffective  Circulation Status  Circulation
2. tissue perfusion  Cardiac pump : Management
related by Effectiveness 1. Monitor vital
ineffectiveness signs
between After nursing care done for 2. Assess
ventilation and 3 x 8 hours is expected neurogical status
blood flow patient showed the 3. Check
effectiveness tissue respirations and
perfusion with result criteria absence of work
: of breathing.
1. Patient identifies factors 4. Check for pallor,
that improve circulation. cyanosis,
2. Patient exhibits growing mottling, cool or
tolerance to activity clammy skin.
3. Patient shows no further Assess quality of
worsening/repetition of every pulse.
deficits. 5. Monitor intake,
4. Patient maintains observe changes
maximum tissue in urine output.
perfusion to vital organs, Record urine
as evidenced by warm specific gravity
and dry skin, present as necessary.
and strong peripheral
pulses, vitals within
patient’s normal range,
balanced I&O, absence
edema, normal ABGs,
alert LOC, and absence
of chest pain.
5. Vital signs in the normal
range
BP: 110-140 / 70-
90mmhg
RR: 12-20x / min
F: 60-90 x / m
T: 36.5-37.5oC

27
 Acute pain  Pain level  Pain
3. related by  Pain control management
biological injury After treatment for 1 x 30 1. Monitor vital
agent minutes is expected to signs
reduce pain with the results 2. Observe non-
criteria: verbal discomfort
3. Perform pain
1. Able to control pain assessment
2. Reported that pain is (including
reduced by using pain location,
management characteristics,
3. Declares a sense of duration,
comfort after the pain is frequency.
reduced 4. Teach non-
4. Vital signs in the normal pharmacological
range techniques such
BP: 110-140 / 70- as relaxation,
90mmhg disturbance,
RR: 12-20x / min deep breath
F: 60-90 x / m 5. Collaboration
T: 36.5-37.5oC with medical
personnel for
administration of
analgesics
Activity  Energy conservation  Activity
4. intolerance  Activity Tolerance Tolerance
related by After nursing care done for
generalized 3 x 8 hours is expected 1. Monitor vital signs
weakness client can increase 2. Assess weakness
ambulation or activity with of patient
result criterion: 3. Monitor the
cardiovascular
1. Able to increase daily response
activities independently (tachycardia,
2. Able to move with or shortness of
without tools breath)
3. Vital signs within the 4. Monitor adequate
normal range nutrition and
BP: 110-140 / 60- energy sources
70mmhg 5. Involve families to
RR: 12-20x / min help clients
F: 60-90 x / m activities
T: 36.5-37.5oC
Risk Infection  Immune status  Infection control
5.  Knowledge: infection
control 1. Monitor the signs
and symptoms of
After treatment for 3x8 systemic and local
hours expected risk of infection
infection does not occur 2. Use an
with the criteria of results antimicrobial soap
to wash your

28
1. Clients are free of signs hands
and infections 3. Monitor
2. Demonstrate ability to laboratorium
prevent infection result
3. Show healthy behaviors 4. Increase
4. Number of leukocytes adequate
within normal limits nutritional intake
5. Use antiseptic
techniques when
performing actions
to patient

29
 CHAPTER III
CRITICAL ASSESSMENT IN ICU

PATIENT IDENTITY

Name : Mrs. H
Date & Birth : July, 07 1956, Banko
Gender : Female
Address : Benguet, Phillipines
Religion : Roman Chatolic
Civil Status : Married
Medical Diagnostik : Acute Coronary Syndrom (ACS)
No. Reg : 12xxx
Addimted in ICU : December 30, 2017
Date of Asessment : January 1, 2018

IDENTITY OF PERSON IN CHARGE

Name : Mr. T
Date & Birth : August, 19 1980, Banko
Gender : Male
Address : Benguet, Phillipines
Relationship with the patient : Daughter

ASSESSMENT

1. History of disease
a. History of the disease now
On December 29, 2017 morning, the patient had complalin discomfort
on lung and this afternoon patient had complains of pain from lung to neck.
Desember 30, 2017, family of the patient brought to Emergency Room.
When she in the Emergency Room the nurses did the assessment and an
ECG record. After that, the physician gave an advice to admitted at Notre
Dame de Chartes Hospital in Baguio, Philippines.

30
 b. Past medical history
Patient is known case of CKD, since May 2017 nearssent
unhydronephrosis, 2 days the patient complained epigastric pain, burning in
chest. Patient had 5 episodes of vomiting, all of body weakness and
epigastric pain.

c. Family history of disease

Patient had family history of disease such as Diabetes Mellitus, HTN
and CKD.

d. Medical diagnosis
Acute Coronary Syndorm (ACS)

2. Primary survey
a. Airway
Patient has clear airway, no noted airway obstruction, no noted secretion.

b. Breathing
Vesicular breath sound, respiration rate 24x/m, reguler, fast, and shallow,
no noted cough, no noted abnormal breating sounds, balanced chest wall
expansions

c. Circulation
BP : 130/80 mmHg, PR : 87x/m, with intact and patent nassal canule @ 2
LPM, IV line PNSS 1000ml on the right arm, CRT < 2 second with no
noted sign of cyanosis, dry lips

d. Dissability
Patient not paralyzed.

31
3. Secondry survey
a. B1 (Breathing)
Patient has breath fast, respiration rate 24x/m, reguler, shallow, and
vesicular breath sound, no noted cough, no noted abnormal breating
sounds, balanced chest wall expansions

b. B2 (Blood)
Patient has not noted abnormal heart sound, reguler rytme, CRT < 2
seconds, and no noted increase JVP.

c. B3 (Brain)
No noted headache, pupil reaction 2 mm, and GCS E4 V5 M6 (15).

d. B4 (Bowel)
Patient has dry lips mucosa, normal bowel sound 8x/minute, no complain
on stomach.

e. B5 (Bladder)
Patient has intact and patent IFC connected with urinal bag,
,color of urine is yellow and no complain with elimination

4. Physical assessment of the head to toe

a. Vital Sign
BP : 130/80 mmHg
PR : 87x /minute
RR : 24x /minute
T : 36,1 ºC
SPO2 : 96 %

b. Head
Patient has black hair, no bumps on the head, no tenderness on the
head.

c. Neck

32
 Patient has no jugular venous enlargement, no motion barrier, no
tenderness on the neck.

d. Eye
Patient has eye symmetric, no nystagmus, reaction to light, pupil shrink
2 mm when in doing assessment, conjunctiva no anemis, white clera, not
use visual aids.

e. Ear
Patient has symmetrical ears, no secretions, no hearing aids.

f. Nose
Patient has no secretions, no tenderness, use oxygen nasal canule 2
@Lpm.

g. Mouth
Patient has cough, teeth look yellow, no sprue, no dentures, lips look
dry.
h. Wound
Turgor skin < 2 second, no signs of dehydration, brown skin, a cold
sweet.
i. Thorax (Respiration and Circulation)
Assessment Pain
P : Movement
Q : Stabbing
R : Right chest
S : 3 (1 – 5)
T : Staying

- Inspection : Patient has additional breath muscles, fast to breath,

shallow breath, normal chest, no noted barrel chest and pigeon chest,
no chest retraction, no noted of ictus cordis
- Palpation : Patient has symmetrical chest wall expantion, has a fibration
on both of chest wall (tactil fremitus).

33
 - Percution : Sonor on both lung fields often percution, dull sound on the
heart often percution.
- Auscultation : Vesicular breath sound on both lung fields.

j. Abdomen
- Inspection : no noted distention on abdomen, with tenderness on
abdomen, no enlarged on stomach.
- Auscultation : Peristalcis  8x/minutes
- Percution : tympanic sound on 9 quadrants of the stomach often
percution.
- Palpation : Patient with tenderness on 4 quadrants of the stomach
(liver, 2 kidneys and stomach) often palpation.

k. Extremities
4444 4444
(right arm) (left arm)
3333 3333
(right lower) (left lower)

Note :
5 : Against gravity, against full resistance
4 : Against gravity, against minimal resistance
3 : Against gravity
2 : Against gravity if with support at joines
1 : With visible / palpable muscle contraction
0 : Complete paralysis

Patient received ongoing IVF PNSS 0.9% 1000 ml/8 hours, with no signs
of inflamation.

l. Genetalia
Patient has intact and patent IFC connected with urinal bag.

34
 m. Supporting investigation

LAB PROCEDURE

1. CLINICAL CHEMISTRY
Result
Normal
Analyte Result (S.I. Units) Normal Range (Conventional
Range
Units)
Cholestrole 184.23 mg/dL <200.00 5 µmol/L <5.18
Trigleserida 64.66 mg/dL <200.00 1 µmol/L <2.28
HDL 68.54 mg/dL >65.00 2 µmol/L >1.68
LDL H 102.76 mg/dL <100.00 H 3 µmol/L <2.59
Potassium 4.37 mmol/L 3.50-5.30 17 mg/dL 13.69-20.32

HEMATOLOGY SECTION
Test Result Unit References
RBC 5.31 X10^6/uL 3.50-5.00
Hemoglobin 143 g/L 110-150
Hematocrit 0.441 L/L 0.370-0.480

BLOOD INDICES
MCV 83.1 um^3 82.0-95.0
RBC 26.9 Pcg 27.0-31.0
MCHC 324 g/L 320-360
WBC Count 10.0 X10^3/uL 4.0-10.0

CLINICAL CHEMISTRY
Reference
Analyte Result Unit
Interprelation
Troponin I 0.003 ng/mL <0.02
CK-MB 2.73 ng/mL 0.34-4.99

Result
Normal
Analyte Result Unit Normal Range (Conventional
Range
Units)
Blood Urea H 51.93 mg/dL 6.00-20.00 H 19 mmol/L 2.14-7.14

35
 Nitrogen
Creatinine H 1.76 mg/dL 0.70-1.20 H 155 mmol/L 61.08-106.08
mmol/ 310.50-
Sodium H 157.20 135.00-148.00 H 362 mg/dL
L 340.40
mmol/
Potassium 3.57 3.80-5.30 14 mg/dL
L

2. Psychosocial and spiritual data

Patient talks to the nurses when she is awake when she went home and
patient always pray to God for the healing of her illness.

36
 Side Nursing
No Generic Brand Classification Dose MoA Indication Contraindication
Effect Responsibility
1 Trimetazidine Belongs to the 95 mg Description : Angina Parkinson’s Dizzine 1. Ensure that
class of other (TID) Trimetazidine pectoris disease, ss, giving
cardiac inhibits β- parkinsonian headac paracetamol
preparations. oxidation of fatty symptoms, he, to : the
acids through tremors, restless abdomi correct
inhibition of long- leg syndrome and nal patient, the
chain 3-ketoacyl- other movement pain, correct dose,
CoA thiolase, related disorders. dyspep the correct
which enhances Severe renal sia, time, the
glucose oxidation. impairment. nausea, correct route.
It ensures proper vomitin 2. Ensure that
functioning of g, rash, there is a
ionic pumps and urticaria written order
transmembrane l. from the
Na-K flow by doctor
preventing 3. Ensure that
decrease in patient is not
intracellular ATP allergic

37
 levels 4. Know
Absorption : the drug-drug
Well absorbed interactions

2 Paracetamol 500 Description : Mild to Thromb 1. Ensure that

mg Paracetamol moderate ocytope giving
exhibits analgesic pain and nia, paracetamol
action by fever leucope to : the
peripheral nia, correct
blockage of pain neutrop patient, the
impulse enia, correct dose,
generation. It burning the correct
produces sensati time, the
antipyresis by on at inj correct route.
inhibiting the site 2. Ensure that
hypothalamic there is a
heat-regulating written order
centre. from the
Absorption : doctor
Readily absorbed 3. Ensure that

38
from the GI tract. patient is not
Time to peak allergic to
plasma paracetamol
concertration 4. Know the
drug-drug
interactions
5. Assessed the
patient score
of pain after
giving the
medication
taking in
consideration
in which
route the
paracetamol
was given
6. Assessed the
patient after
giving the

39
 medication
for any
reaction
7. Document all
the above
3 Ketoanalogue Amino acids Believed to Preventio Known to be Hyperc
s and derivatives involve in the n and hypersensitive or alcemia
; used in prevention and therapy of who have ,
treatment of therapy of damage previously had a generali
alimentary damages due to due to hypersensitivity to zed
tract and faulty or deficient faulty or one or more flushing
metabolism metabolism in deficient amino acids or ,
problems chronic renal protein idiosyncratic bdomin
insufficiency metabolis reaction to al pain,
m in Ketoanalogues of fever
chronic a\essential amino and
renal acids, nausea
insufficien hypercalcemia have
cy in disturbed amino been
connectio acid metabolism reporte

40
 n with d in the
limited literatur
protein in e the
food of adminis
40g per tration
day and of
less in amino
patients acids
with
patients
with
glomerular
filtration
rate
(GFR)
below 25
mL/min.
4 Eperisone Myonal Eperisone ; Eperisone acts by Spastic Patients with Shock
belongs to the relaxing both paralysis known and
class of other skeletal muscles in hypersensitivity to anaphyl

41
centrally-acting and vascular conditions the drug actoid
muscle smooth muscles, such as reaction
relaxants and demonstrates cerebrova s : in
a variety of scular the
effects such as disease, event of
reduction of spastic sympto
myotonia, spinal ms
improvement of paralysis, such as
circulation, and cervical redness
suppression of syndrome, ,
the pain reflex. periarthriti itching,
s of the urticaria
shoulder l,
oedema
of the
face
and
other
parts of
the

42
 body.
5. Nicardipine Nicardex Antianginals, 50 ml Nicardipine is a HTN, Patients with Pedal 1. Ensure that
antihypertensiv (10 dihydropyridine angina advanced aortic oedema giving
es, mg Ca channel pectoris stenosis, , paracetamol
pharmacologic nicard blocker. It inhibits cardiogenic shock tachyca to : the
: calcium + 40 Ca ion from rdia, correct
channel ml) entering the slow hypoten patient, the
blockers channels or sion, correct
select voltage- palpitati dose, the
sensitive areas of on, correct time,
vascular smooth nausea the correct
muscle and vomitin route.
myocardium g, dry 2. Advise
during mouth, patient to
depolarization, haemat take
producing a uria medication
relaxation of exactly as
coronary directed,
vasodilatation. It even if
also increases feeling well

43
myocardial 3. Instruct
oxygen delivery in patient on
patients with technique
vasospastic for
angina. monitoring
pulse

44
Nurse Care Plan
NO Assessment Diagnosis Planning Intervention Rationale Evaluation
1. SD : Ineffective - Monitored the vital - Monitored the vital - Measure the - Vital sign :
Patient said feel Tissue sign sign patient vital sign HR : 87x/minute
tightness in the chest to Perfusion - Assessed neurogical - Assessed the GSC - Measure level RR : 24x/minute
the right status - Assessed the neurogical T : 36,1 ºC
- Assessed the saturation status - GCS :
OD : saturation - Giving patient - Measure the E4 V5 M6 (15)
- SpO2 : 96 % - Maintained the oxygen nasal saturation - SpO2 : 98 %
- Patient had a oxgen oxygen canule 2 @Lpm - Increase oxgen - Still wearing nasal
nasal canule 2 @Lpm - Check the ABG - Collaborate to take levels in the canule for
- Patient had a cold - Collaborate give an the ABG blood inhalation
sweat IV fluid - Giving patient IV - Know the result - Collaborate wih the
- CRT < 2 minute fluid ABG physician to give IV
- Maintance fluid fluid PNSS 1000cc/
in body 8 hours
2. SD : Ineffective - Assessed breating - Maintained on : - Maximize - Position the patient
Patient said compaining Breathing pattern semi fowler position patient to semi fowler
hard to breathe and fast Pattern - Assessed breath - Assessed for use of ventilations - Noted additional
sounds accessory muscle - Work of breath

45
OD : - Assessed for - Monitored SPO2 breathing - SPO2 : 98 %
- Patient had a cough respiratory disstress - Auscultate breath increases - Vesiculer sound
- Patient had a fast - Monitored SPO2 sounds greatly as lung - Patient noted
breath - Maintained the - Assessed for compliance tacypnea
- Patient had a shallow position of the patient breating pattern decreases
breath - Helpful tool to
- RR : 24x/ minute detect
- Patient had additional alterations in
breath muscles oxygenation
initially but for
CO2 monitoring
or ABG’s would
require being
obtained
- To detect
decreased or
adventitious
breath sounds
- Unusual
breathing

46
 patterns may
imply an
underlying
disease
process or
dysfunction in
the deep
cerebral or
diencephalon
related with
brain injury or
metabolic
abnormaities.
3. SD : Acute Pain - Assessed pain - Monitored the vital - Measure the - Vital sign :
Patient said that she felt - Monitored vital sign sign vital sign BP : 130/80 mmHg
pain on her chest - Teached patient - Assessed pain to - Know the level HR : 87x/minute
Assessed pain : about relaxation dan patient (PQRST) of pain RR : 24x/minute
P : Movement distraction - Teached patient - Reduce the T : 36,1 ºC
Q : Stabbing - Collaborate for give a take a deep breath level of pain - Assessed pain
R : Right chest medicine and distract - Reducing pain P : Movement

47
 S : 3 (1 - 5) attention levels using Q : Stabbing
T : Staying - Collborate to give therapy S : 2 (1 – 5)
analgesic T : Staying
- Patient can do it
OD : about to reduce the
- Patient felt painful on level of pain
her chest - Collaborate wih the
- Patient seemed to be physician to give
looking for a Trametadol 35 mg
comfortable position IV Line
- Patient seemed to
grimace in pain
- Vital sign :
HR : 87x/minute
RR : 24x/minute
4. SD : Activity - Assessed weakness - Assessed the - Know the - Causes of
Patient said every Intolerance of patient causesof fatigue in patient ability weakness in patient
activity is always - Monitored vital sign patient level of ecah is pain in the chest
assisted by family and before and after - Teaced the patient activity - Patient activity is
nurse activities about simple - Train the still partially

48
 - Monitored the ECG activites: eat and muscles in the assisted: eating
OD : - Teach the patient drink alone patient and drinking
- Vital sign about simple - Monitored vital - Know the vital assisted family
BP : 130/80 mmHg activities sign patient sign difference - Vital sign
HR : 87x/minute - Monitored ECG before and after (Before)
RR : 24x/minute activity BP : 130/80 mmHg
T : 36,1 ºC - Measure the HR : 87x/minute
SPO2 : 98 % ECG before RR : 24x/minute
- The patient seemed to and T : 36,1 ºC
be assisted by families SPO2 : 98 %
and nurses
- The patient seemed to (After)
be lying on the bed BP : 130/80 mmHg
HR : 98x/minute
RR : 25x/minute
T : 36,1 ºC
SPO2 : 97 %

- ECG :
(Before)

49
 Sinus rhythm

(After)
Sinus rhythm

5. OD : Risk For - Monitored vital sign - Monitored vital sign - An unexpected - Vital Sign :
- Patient had a iv line Infection - Assessed sign and (Temperature) increase in T : 36,1 ºC
- Patient had iv catheter symtoms infection - Assessed about body - Assessed infection
- Monitored five sign and temperature is :
laboratorium result symtoms infection: a sign of no sign and
- Use antiseptic kalor, dolor, rubor, infection symtomps infection
techniques when tumor, and - Know the five - Leukocytes :
performing actions to fungsiolesa signs of 7.250/mm3
patient - Monitored infection - Still handwash
- Give patient leukocytes symptoms: before and after
education about sign - Handwash before heat, pain, medical prosudure
and symptoms about and after give the redness, - Patient know about
infection medical prosudure swelling, and sign and symptoms
- Give information changes in of infection

50
 about infection tissue funcion
- Increase in
luekocytes is an
infection (4.000
– 10.000/mm3)
- Prevent
transmission of
infection by
hand
- Provide
information to
patient about
sign and
symtoms of
infection

51
 References

David.2016. Acute Coronary Syndrom.https://emedicine.medscape.com

/article/1910735-overview accessed on January 13, 2018
Overbaugh.2009.Acute Coronary Syndrome. AJN May 2009 t Vol. 109, No. 5
Fabian, et all, 2016Epidemiology of coronary heart disease and acute coronary
Syndrome
Belleza,Mariane.2017. Cardiovascular System Anatomy and Physiology
https://nurseslabs.com/cardiovascular-system-anatomy-physiology/
accessed on January 14, 2018

52