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Acute Coronary Syndrome Case Study

The document summarizes a case study of a 63-year-old male patient who presented with acute coronary syndrome. He was initially diagnosed with GERD at another hospital but later diagnosed with a myocardial infarction. He was admitted with NSTEMI and later showed ST elevation, so was transferred for emergency PCI. Key aspects of the case included the patient's risk factors, pain management, and transfer to another facility for specialized care.

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100% found this document useful (2 votes)
2K views26 pages

Acute Coronary Syndrome Case Study

The document summarizes a case study of a 63-year-old male patient who presented with acute coronary syndrome. He was initially diagnosed with GERD at another hospital but later diagnosed with a myocardial infarction. He was admitted with NSTEMI and later showed ST elevation, so was transferred for emergency PCI. Key aspects of the case included the patient's risk factors, pain management, and transfer to another facility for specialized care.

Uploaded by

Mari Lyn
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
  • Introduction
  • Personal Data
  • History of Present Illness
  • Clinical Manifestation
  • Pathophysiology
  • Diagnostic and Laboratory Tests
  • Theory of Disease Causation
  • Schematic Diagram
  • Medical Management
  • Nursing Care Map
  • References

HOLY ANGEL UNIVERSITY

GRADUATE SCHOOL OF NURSING

Master of Science in Nursing

ACUTE CORONARY SYNDROME: A CASE


STUDY
GSNARHI1: ADULT RESPONSE TO HEALTH AND ILLNESS

Submitted by:

Marilyn D. Palpal

Submitted to:

Victor C. Quimen, Jr., RN, PhD

August 2019
ACUTE CORONARY SYNDROME

I. INTRODUCTION

The cardiovascular system consists of a closed circuit: the heart, responsible for pumping
blood and the blood vessels where the blood circulates (Tortora, 2014). It provides oxygen and
nutrition to tissues while removing waste. Any condition affecting the functions or structures of
the involved body parts are termed as Cardiovascular Disorder (CHD). One of which is Acute
Coronary Syndrome and was the case chosen for this presentation.

Acute coronary syndrome (ACS) is a group of clinical symptoms compatible with acute
myocardial ischemia at rest and is caused by either a complete or partial occlusion of a coronary
artery by a thrombus composed of platelets and fibrin (Spinler, 2007). Consequences depend on
degree and location of obstruction and range from unstable angina to non–ST-segment elevation
myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI), and
sudden cardiac death. ACS is usually a result of plaque disruption in coronary arteries. The
common risk factors are associated to the development of atherosclerosis which includes
smoking, hypertension, diabetes, hyperlipidemia, physical inactivity, family obesity, and poor
nutritional practices (Singh, 2019).

A study in 2018 by James [Link] revealed that cardiovascular diseases cause approximately
one-third of all deaths in the world, of which 7.5 million deaths are estimated to be due to
ischemic heart disease (IHD). Acute coronary syndromes (ACS) and sudden death cause most
IHD-related deaths, which represent 1.8 million deaths per year. Global data epidemiologists
forecast that at the rate of 1.40% per year, the hospitalized incident cases of ACS will increase
from 1.29 million cases in 2013 to 1.47 million cases in 2023. In the Philippines, acute coronary
syndrome (myocardial infarction and unstable angina) accounted for 16.5% and 13.2% of total
deaths in 2000, increasing to 17.6% and 12.8% of total deaths, respectively. Moreover,
Philippine Heart Association registry demographics of ACS showed cases of 67% commonly
noted in males based on a 2 year results (2011-2013).

The diagnosis of ACS is based on clinical presentation, ECG changes and serum cardiac
biomarker levels. The typical clinical presentation of ACS is retrosternal pressure or heaviness
(‘angina’) radiating to the left arm, neck, or jaw, which may be intermittent (usually lasting
several minutes) or persistent. These complaints may be accompanied by other symptoms such
as diaphoresis, nausea, abdominal pain, dyspnea, and syncope (Rapezzi [Link], 2018). Atypical
presentations including epigastric pain, recent-onset indigestion, stabbing chest pain, chest pain
with some pleuritic features, or increasing dyspnea however are not uncommon.

In addition, American Heart Association guidelines maintain that any patient with
complaints suspicious of ACS must undergo an ECG within 10 minutes of arrival as the first step
of evaluation to differentiate between STEMI and NSTEMI unstable angina. A JOURNAL
WRITTEN BY Daga et. Al (2011) discussed that an ST segment deviation and T waves that may
remain normal or inverted may indicate NSTEMI while presence of ST segment elevation of at
least 0.1 mV in two contiguous leads may signify STEMI. The rapid diagnosis, early risk
stratification and institution of life saving interventions for such cases is made possible through
the high diagnostic accuracy of cardiac biomarkers, specifically troponin T and I in patients with
recent-onset angina. Troponin levels usually increase after 3-4 hours and is the most sensitive
and specific marker of myocardial injury available. Although it is not a component in the
diagnosis of STEMI, it is helpful in the event that STEMI is not diagnosed and other forms of MI
are suspected.

Recent updates indicated initial treatment for all ACS includes aspirin and heparin bolus
and intravenous heparin infusion if there are no contraindications. Current meta-analysis also
recommended antiplatelet therapy with ticagrelor or clopidogrel (Wang [Link], 2018). Supportive
measures like pain control with nitroglycerin or morphine/ fentanyl and oxygen in case of
hypoxia are advised as required in addition of continuous cardiac monitoring for arrhythmia. The
American Heart Association (AHA) recommends an emergent catheterization and percutaneous
intervention (PCI) for NSTEMI/Unstable Angina if the patient continues to have pain.
On the other hand, reperfusion therapy is recommended to all eligible patients with
STEMI with symptom onset within the prior 12 hours. Early revascularization, the goal being 12
hours, is a primary treatment goal in patients with STEMI (Steg [Link], 2012). Delayed reperfusion
is associated with poorer myocardial salvage and outcomes. ACS always warrants admission and
emergent cardiology evaluation. Computerized tomography angiography might also be utilized
for further workup depending on availability and cardiologist preference. Cases not amenable to
PCI are taken for CABG (coronary artery bypass graft) or managed medically depending upon
comorbidities and patient choice (Singh [Link], 2019).
The fast paced global modernization has led to a pandemic of coronary artery disease and
its manifestation as ACS, with profound implications for personal and universal health concerns.
Due to the alarming demographic changes on cases of ACS provided by epidemiological studies
with emphasis on adherence to the recommended therapy and prevention geared toward
modifiable risk factors, the case was chosen to be presented. The case was also memorable on a
personal note with how it was managed and transferred to other facility from our care.

II. PERSONAL DATA

Patient X 63 year’s old, male, married was brought to our institution with chief complaint
of chest pain. A brief clinical history taken showed that few hours prior to consultation, the
patient suffered from chest pain, crushing in character with a rated pain of 10/10 radiating to the
back. Numbness on both hands was also present, thus was brought to a nearby hospital by the
relative. ECG was done revealing an arrhythmia. Consequently, troponin level showed a
negative result. The patient was treated as a case of GERD but later was diagnosed as
Myocardial Infarction. The relative opted for transfer to our institution.

Initial investigations revealed ECGs consistent with NSTEMI. The patient still
complained of chest pain rated as 5/10. He was then admitted with a case of Acute Coronary
Syndrome- Non ST elevation Myocardial Infarction at the Intensive Care Unit. Continuous
monitoring of arrhythmias was done and repeat laboratory work-ups were also taken. Troponin I
and CKMB result are elevated while serum potassium and sodium were significantly low. The
patient was started on an Isoket drip and received morphine for pain control. During the course
of hospitalization, the cardiac monitor showed ST elevation in leads V3 and V4 with unresolved
chest pain. The attending physician recommended percutaneous coronary intervention and was
consented by the relatives. He was transferred thereafter to Philippine Heart Center for
emergency coronary angiogram 9 hours after admission with a final diagnosis of ACS - STEMI.
III. HISTORY OF PRESENT ILLNESS

Chief Complaint: Chest pain

 External Perspective Risk Factors


1. Current stressful situation/ Significant others’ noticeable worried reactions
 A study of Pimple et. Al (2015) revealed that myocardial ischemia induced by
mental stress is associated with higher frequency of retrospectively reported angina
during the day. Stressors vary from different persons, as for the case of our patient
witnessing his relatives react worriedly to the present situation is considered one.
 Pain or tightness in angina is often triggered by a consistent high level of activity,
such as during stressful times or walking upstairs after an emotional discussion.
Coping with the pain and emotional trauma of a cardiac disease is difficult. Patient
may fear death and/or be anxious about immediate environment. Ongoing anxiety
(related to concerns about impact of heart attack on future lifestyle, matters left
unattended or unresolved, and effects of illness on family) may be present in varying
degrees.
2. Pain management
 Nitrates, such as nitroglycerin, works by increasing blood flow to the heart and also
decreases the work of the heart by dilating (expanding) the arteries.
 Morphine may also be used to control pain in AMI patients, but should be
administered cautiously at low doses (Haru [Link], 2006). Potent narcotic analgesic
may be used in acute onset because of its several beneficial effects, e.g., causes
peripheral vasodilation and reduces myocardial workload; has a sedative effect to
produce relaxation; interrupts the flow of vasoconstricting catecholamines and
thereby effectively relieves severe chest pain.
3. Secondary Care services
 Patients may choose have the right to choose their own secondary care services.
Regardless of the location, the patients’ hospital of choice must be honored. In this
case, the patients’ relative opted for more cost effective institution rather than the
neighboring exclusive hospital.
4. Presence of support system
 Anxiety releases catecholamine, which increase myocardial workload and can
escalate and/or prolong ischemic pain. Presence of support system such as relatives
or health care provider can reduce feelings of fear and helplessness.
 Internal Perspective
1. Anxiety Level
 Anxiety has been associated with the incidence, and in some cases progression, of
cardiovascular disease. In patients without existing cardiac disease, anxiety has
been linked to the subsequent development of CAD. When someone is anxious,
their body reacts in ways that can put an extra strain on their heart. The physical
symptoms of anxiety can be especially damaging among individuals with existing
cardiac disease.
2. Pain threshold
 Several studies have found pain is as unique as the individual. Pain is both a
sensory and an emotional experience that is felt differently by everybody. What's
more, there is a difference between how you are confronted with pain and how you
go on to tolerate it.
3. Pain quality and timing
 Chest pain caused by angina or a heart attack may be similar to or different from
chest pain caused by other conditions. Depending upon the cause, chest pain can
have varying qualities (sharp, dull, burning), can be located in one or several areas
(middle of the chest, upper or left chest, back, arms, jaw, neck, or the entire chest
area), pain may worsen with activity and improve with rest.
 Ischemic chest pain is usually not felt in any specific spot, but rather throughout the
chest. The patient may actually have difficulty describing the exact location of the
pain
4. Hypokalemia
 A decrease in serum potassium (K) level has been suggested to be a fairly common
observation in patients with acute coronary syndrome (ACS), which has been
shown to increase the risk of cardiac events, including lethal ventricular
arrhythmias. In addition, a decrease in K level generally induces vasoconstriction,
which leads to further ischemia, thereby producing a vicious cycle.
5. Age
 Patient age is helpful in evaluating chest pain. Chest pain in children and young
adults (< 30 yr) is less likely to result from myocardial ischemia, although
myocardial infarction can occur in people in their 20s. Musculoskeletal and
pulmonary disorders are more common causes in these age groups.
IV. CLINICAL MANIFESTATION

Experiential Perspective
Manifestations Rationales
Disturbed sleep pattern - The patient o Chest pain causes discomfort and may alter the
verbalizes being unable to go to individuals comfort.
sleep because of the pain.

Limited mobility - The patient o Angina usually becomes worse with exertion or
stated “I’m afraid to change position movement and is relieved by rest. If the patient notes that
because the pain might worsen”. less exertion is required to cause the pain when going out
in cold weather or after eating a large meal, then the pain
is likely to be caused by coronary disease (Hickam,
1990).
Acute Pain - The Patient reported o Cardiac pain may radiate. Pain is often referred to more
chest pain, heaviness, or pressure superficial sites served by the same spinal cord nerve
that radiate to the shoulders and level.
upper abdomen.

Behavioral Perspective
Manifestations Rationales
Narrowed focus o Reduced perfusion of the brain can produce observable changes in
sensorium.
Dysrhythmias o Ischemia during angina attack may cause transient ST segment
depression or elevation and T wave inversion. Serial tracings
verify ischemic changes, which may disappear when patient is
pain-free. They also provide a baseline against which to compare
later pattern changes.
Needs assistance in ADLs o People with coronary disease have a higher risk of functional
limitations than their same-age counterparts without disease.
(Briton [Link], 2012)
o Elderly CHD patients have greater limitations in their functional
which may depend on the severity of the disease.
Hypotension o Pain and decreased cardiac output may stimulate the
sympathetic nervous system to release excessive amounts of
norepinephrine, which increases platelet aggregation and
release of thromboxane A2. This potent vasoconstrictor causes
coronary artery spasm, which can precipitate, complicate,
and/or prolong an anginal attack. Unbearable pain may cause
vasovagal response, decreasing BP and heart rate.

PHYSIOLOGIC PERSPECTIVE

Angina pectoris often results from ischemic episodes that excite chemosensitive and
mechanoreceptive receptors in the heart. Ischemic episodes release a collage of chemicals,
including adenosine and bradykinin that excites the receptors of the sympathetic and vagal
afferent pathways. Sympathetic afferent fibers from the heart enter the upper thoracic spinal cord
and synapse on cells of origin of ascending pathways. Excitation of spinothalamic tract cells in
the upper thoracic and lower cervical segments, except C7 and C8 segments, contribute to the
anginal pain experienced in the chest and arm (Foreman, 1999).

Patients with chronic chest pain include those who have recurrent episodes of pain
occurring in a relatively stable pattern. Myocardial ischemia sometimes occurs in the absence of
fixed obstructions of the coronary arteries, resulting in recurrent chest pain. Obstructive disease
of the intramural small vessels can cause ischemia. Conversely, patient with acute chest pain
include those whose episodes are of recent onset or those who have had a recent increase in the
intensity or frequency of recurrent pain. The pain often occurs at rest and is not relieved by
nitroglycerin. It may be accompanied by diaphoresis, dyspnea, or nausea (Hickam, 1990).
PATHOPHYSIOLOGY (ACS)

Risk Factors Change in the condition of the


plaque in the coronary artery

Antiplatelets
Activation of Platelets
Altered
Elevated ST
coronary artery repolarization of segment
Formation of thrombus the myocardium Q wave

coronary artery
Ischemia of tissue in the
region supplied by the artery
Myocardial Dysrhythmias Antidysrythm
irritability ias
coronary artery
Coronary blood supply less
than demand coronary artery coronary artery
Nitrates/ Beta
blockers Anaerobic Lactic acid
Myocardial cell death
Glycolysis production
coronary artery Nitroglycerin

Angina

Decreased contractility Release of lysosomal enzyme

coronary artery
Decreased left ventricular Elevated CK-MB, myoglobin,
function Troponin T, Troponin I

coronary artery coronary artery


Increased preload

coronary artery
Decreased cardiac Inotropes
output

coronary artery
Stimulation of the
sympathetic nervous system

coronary artery
Increased oxygen needs

coronary artery
Vasoconstriction Nitrates

coronary artery
Increased Heart rate
BOOK BASED (American Journal of Nursing 2009)

Non modifiable factors that influence risk for coronary artery disease include age, sex,
family history, ethnicity, or race. Men have a higher risk than women. Men older than age 45,
women older than age 55, and anyone with a first-degree male or female relative who developed
coronary artery disease before age 55 or 65, respectively, are also at increased risk. Modifiable
risk factors include elevated levels of serum cholesterol, low-density lipoprotein cholesterol, and
triglycerides; lower levels of high-density lipoprotein cholesterol; and the presence of type 2
diabetes, cigarette smoking, obesity, a sedentary lifestyle, hypertension, and stress and ethnicity
or race.

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. 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. Lactic acid formation gives rise to pain sensation
(Chest pain).

At this point, infarction—cell death—will occur unless interventions are begun that limit
or reverse the ischemia and injury. Cardiac cells can withstand ischemic conditions for about 20
minutes before cellular death takes place, after only 30-60 seconds of hypoxia, ECG changes are
visible. Clinically, it is important to identify those individual with those transmural infarction
who are at high risk for serious complication and who should receive definitive intervention
without delay. Those individuals usually have marked the elevation in the ST-segment on ECG
and are categorized as having ST-elevation or STEMI. Those without ST segment elevation are
said to have non STEMI.

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.

Oxygen deprivation also is accompanied by electrolyte disturbances specifically loss of


potassium calcium and magnesium from cells. Myocardial cells deprived of necessary oxygen
and nutrients loss contractility, thereby diminishing the pumping ability of the heart. 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.

In an attempt to support vital functions, the sympathetic nervous system responds to


ischemic changes in the myocardium. Initially, both cardiac output and blood pressure decrease,
stimulating the release of the hormones epinephrine and norepinephrine, which in the body’s
attempt to compensate increase the heart rate, blood pressure, and afterload, ultimately
increasing myocardial demand for oxygen. As oxygen demand increases at the same time that its
supply to the heart muscle decreases, ischemic tissue can become necrotic. Low cardiac output
also leads to decreased renal perfusion, which in turn stimulates the release of renin and
angiotensin, resulting in further vasoconstriction.

Additionally, the release of aldosterone and antidiuretic hormone promotes sodium and
water reabsorption, increasing preload and ultimately the workload of the myocardium.

Clinically, it is important to identify those individual with those transmural infarction


who are at high risk for serious complication and who should receive definitive intervention
without delay. Those individuals usually have marked the elevation in the ST-segment on ECG
and are categorized as having ST-elevation or STEMI. Those without ST segment elevation are
said to have non STEMI.
V. DIAGNOSTIC AND LABORATORY TEST

Laboratory Date Indication Results Normal Analysis &


ordered/resu Values Interpretation
lt in
Complete There is an elevation of
Blood Count WBC because of the
WBC DO: 7-04-19 13.54 4-11 X inflammatory process in
DI: : 7-04-19 10*9/L response to myocardial
Routine injury. (Sadovsky, R.,
examination 2001)
DO: 7-04-19 for possible 4.7 4.7-6 Normal
DI: : 7-04-19 infection or X10*12/L
RBC DO: 7-04-19 trauma 13.5 13.5-18 Normal
DI: : 7-04-19 g/dL
Hemoglobin DO: 7-04-19 39.7% 42-52% Normal
DI: : 7-04-19
Hematocrit DO: 7-04-19 301 150-400 Normal
DI: : 7-04-19 x10*9/L
Platelet
Troponin I DO: 7-04-19 Evaluation of Negative There is elevation of
DI: : 7-04-19 Chest pain troponin T and CK- MB,
and to this elevation indicates
DO: 7-04-19 determine <0.63 <0.30 ng/ml damage to the myocardial
5:30pm cardiac cells. (James. 2018)
DI: : 7-04-19 etiology.
CKMB DO: 7-04-19 26.14 0-7ng/mL
DI: : 7-04-19
Sodium DO: 7-04-19 General 132.8 135-148 Hyponatremia commonly
DI: : 7-04-19 health of a mmol/L occurs in acute coronary
patient and as syndrome and has been
a baseline recognized as a worse
data prognostic indicator in
patients with ST-segment
elevation myocardial
infarction
Potassium DO: 7-04-19 Evaluation of 3.28 3.5-5.3 A decrease in serum
DI: : 7-04-19 Arrhythmia mmol/L potassium (K) level is
suggested to be a fairly
common observation in
patients with acute
coronary syndrome
(Heirlitz. 1988)
Nursing Responsibilities Rationale
Before
1. Check the doctor‘s order. To ensure correct procedure to be done.
2. Explain to the patient the procedure, its To increase patient‘s awareness, gain cooperation
purpose, process of specimen collection and allay anxiety of the patient, and to determine if
and the stinging sensation that may be felt. there is a need for reemphasizing the procedure.
Ensure if the patient understood the
procedure and its nature well. Clarify their
doubts and answer questions accordingly
During: Assist the patient during the collection of To provide support and attend the needs of the
blood by the phlebotomist. patient.
After
1. Upon the arrival of the result, refer it to the To determine abnormal results and make
physician and then attach it to the patient‘s appropriate interventions that will address the
chart abnormal results.
2. Document the procedure. Documentation serves for legal purposes.
1. Carry out doctor‘s new orders as to the To immediately address the abnormal results and
managements for abnormal results. prevent further complications.

DIAGNOSTIC PROCEDURE

ELECTROCARDIOGRAM (ECG)

This procedure is used to measure any damage to the heart, how fast the heart is beating
and whether it is beating normally, the effects of drugs or devices used to control the heart (such
as the pacemaker and the size and position of the heart chambers. A doctor orders the procedure
if patient has chest pain or palpitations, scheduled for surgery, has had heart problems in the past
or has strong history of heart disease in the family.

Purpose: This diagnostic test was performed because it was necessary taking into consideration
the diagnosis of the client was acute coronary syndrome. This test will simply record the
electrical activity of the heart. Thus, any disease affecting the heart will yield an abnormal result
of ECG.
 Date performed: July 7, 2019 2:20 pm (1st Hospital)
Interpretation: Sinus arrhythmia
 Date performed: July 7, 2019 7:00 pm
Interpretation: Atrial Fibrillation in Controlled Ventricular Response
 Date performed: July 7, 2019 10:56 pm
Interpretation: ST Elevation Myocardial Infarction

Analysis: The Atrial Fibrillation in Rapid Ventricular Response indicates abnormal electrical
impulses in the atria, as a result, they quiver. The AV node — the electrical connection between
the atria and the ventricles — is bombarded with impulses trying to get through to the ventricles
which leads to a fast and irregular heart rhythm. This is due to increase in blood pressure with
decreased in cardiac output since the heart is unable to function well resulting to damage the
heart‘s structure particularly the myocardium (Ellis, 2013).

The ST elevation indicates the zone of injury which causes the rapid repolarization of the
myocardial cells than normal cells.

Nursing Responsibilities Rationale


Before:
1. Check the doctor‘s order For verification
2. Inform patient that the procedure is To promote compliance and to prevent anxiety.
painless.
3. Inform patient to remove any metal To promote accuracy of result.
attached in his body
4. Check all medicines the patient is taking. Some drugs can interfere with the results.
(eg. Mucolytics: N-Acetylcysteine)
After:
Encourage patient to rest To prevent further demand of oxygen.

CHEST X-RAY

Chest X ray is a painless, noninvasive test that creates pictures of the structures inside the
chest, such as the heart, lungs, and blood vessels.

Purpose: Chest X-ray (Heart and Lungs) was done to our patient to obtain pulmonary and
cardiac findings and to determine any abnormalities that would help in doing appropriate
interventions.
 Date performed: July 7, 2019 4pm
Impression: Cardiomegaly

Analysis: The peripheral vasoconstriction increases the workload of the heart. Hence, ventricular
hypertrophy to pump harder and to oppose peripheral resistance.

Nursing Responsibilities Rationale


1. Fill out the x-ray request form. The x-ray request form will serve as a record for
the health care workers on what specific procedure
was done to the patient.
2. Explain the purpose and the type of procedure to To increase client‘s awareness regarding the
be done to the client and the watcher. procedure to be done to facilitate full cooperation.
3. Inform the client to remove all metal objects Metal objects and jewelries may obscure the X-ray
including jewelry that he is wearing images
4. Instruct the patient to remain still during the Even a little movement can blur the images.
procedure

VI. THEORY OF DISEASE CAUSATION (Web of Causation Theory)

Physical
Age Activity

Atherosclerosis
Cholesterol
Education Fat Intake

Hypertension ACS
Income Alcohol

Smoking

Family
History
The Web of Causation is a theory used to explain that disease and disability are caused by
many factors. Originally termed the "chain of causation" by MacMahon & Pugh (1970) as cited
in (Wills & McEwen, 2014, p. 335).

Acute Coronary Syndrome usually results from the build-up of fatty deposits (plaques) in and
on the walls of coronary arteries, the blood vessels delivering oxygen and nutrients to heart
muscles. As per the concept of the theory, several risk factors (modifiable and non-modifiable)
contributes to the development of the disease.

Non modifiable risk factors of ACS include age; as older individuals have degenerative
changes causing hardening of blood vessel walls, income, and education that have significant
effect on the attitude and behaviour of a person. Family history may include mutated or defected
gene responsible on the lipid metabolism.

Modifiable risk factors includes cigarette smoking – it has been suggested that the adverse
effects of cigarette smoking on the heart and blood vessels involve the effects of nicotine and
carbon monoxide. Sedentary lifestyle causes sluggish blood flow because of the non-utilization
of muscles and deposition of calories in term of fats. Increase intake of fats (animal fats) could
increase the LDL source of the body. LDL carries cholesterol to tissues which includes the heart
and coronary arteries.

Hypertension initiating stress on the body‘s blood vessels, causing them to clog or weaken
and hyperlipidaemia that is proven to be highly related to the premature development of
atherosclerosis are considered partially modifiable risk factors.
VII. SCHEMATIC DIAGRAM

PRECIPITATING FACTORS:
 Lifestyle Factors: Occasional
Drinker, Smoker, Diet: PREDISPOSING FACTORS:
chicharon, sisig, lechon Age: 63
 Medical Conditions: High Blood Family History: DM, HPN, CVA
Pressure

Endothelial lining of arteries are injured

Platelets, WBC & Fibrin converge at


 Permeability to lipoproteins the injured site

Lipoproteins accumulated in the


intima of arterial wall

Macrophages infiltrate the area to


ingest lipids and die Formation of fibrous cap over dead fatty core (plaque)

Narrowed blood vessel Plaque protrudes in lumen of Plaque ruptures & causes
obstructs/impedes blood flow the vessel thrombus formation

Occlusion of an artery
↓ Myocardial perfusion
↓ Blood flow to myocardium

(+) Chest Pain radiating


Unstable Angina Myocardial Ischemia
to the left arm 07/04/19

Partially Ischemic Cells Accumulation of waste products

Inadequate supply of O2 and nutrients

Anaerobic Metabolism ↓ ATP production

Accumulation of lactate

Inhibition of Glycolysis
Altered cell
Myocyte death/ Necrosis
membrane integrity

Myocardial Infarction Unrelieved Chest


07/04/19
Pain 07/04/19
↓ K: 3.28 mmol/L
 WBC: 13.54 x 109 /L
Trop I & CKMB:
Elevated ST Elevation MI Non-ST Elevation
(STEMI) MI (NSTEMI)
VIII. MEDICAL MANAGEMENT

A. Pharmacology

Medication Date Description Indication Patient’s Response


Ordered
Enoxaparin is a low Enoxaparin is a rational In general, because
molecular weight heparin alternative to UFH in response to
(LMWH) used primarily to patients presenting with enoxaparin at
prevent and treat blood either unstable usual doses is
clots, such as deep vein angina/non-ST-elevation consistent from
Enoxaparin 07-04- thrombosis (DVT) and myocardial infarction or patient to patient,
2019 pulmonary embolism (PE). ST-elevation myocardial the anticoagulant
Enoxaparin has infarction, with a response to
antithrombotic properties clinically modest enoxaparin does
and decreases fibrin clot increase in bleeding not need to be
formation by specifically complications monitored.
inhibiting the coagulation
factors Xa and IIa

Nursing Responsibilities Rationale


1. Observe 10 R‘s in drug administration. To avoid error.
2. Check if patient has signs and symptoms of This is done in order to avoid severe blood loss
bleeding. If any, refer it to physician. which can lead to shock.
4. Inform patient and watcher to refer to health care In order to apply measure that can halt possible
providers if bleeding gums, dark stool and gastric bleeding occurrence and further injury.
upset are present.

Medication Date Description Indication Patient’s


Ordered Response
Clopidogrel bisulfate is a It was given to the Anginal pain
P2Y12 inhibitors anti-platelet patient in conjunction decreased but
drug, that is, a drug that with aspirin to treat was not
Clopidogrel 07-04- inhibits the ability of platelets worsening chest pain resolved. A PT
2019 to clump together as part of a and keep blood vessels and aPtt was not
blood clot. It prevents blood open by blocking performed
clots by irreversibly binding to platelets from sticking because relatives
the P2Y12 receptor on together and opted to transfer
platelets, preventing adenosine preventing them from the patient.
diphosphate (ADP) from forming harmful clots.
activating platelets.

Nursing Responsibilities Rationale


1. Observe 10 R‘s in drug administration. To avoid error.
2. Check if patient has signs and symptoms of This is done in order to avoid severe blood loss
bleeding. If any, refer it to physician. which can lead to shock.
3. Advise watcher to keep patient assisted, or to To prevent fall of patient which can lead to trauma
always put the side rails of bed up in order and injury.
4. Inform patient and watcher to refer to health care In order to apply measure that can halt possible
providers if bleeding gums, dark stool and gastric bleeding occurrence and further injury.
upset are present.

Medication Date Description Indication Patient’s


Ordered Response
Aspirin is a Nonsteroidal Anti- Mainly as Anginal pain
inflammatory Drug. The antiplatelet decreased but was
mechanism of action of aspirin is therapy. Aspirin not resolved. A PT
as a Cyclooxygenase Inhibitor. therapy reduces and aPtt was not
Aspirin 07-04- The physiologic effect of aspirin the clumping performed because
2019 is by means of Decreased action of platelets relatives opted to
Prostaglandin Production. The — possibly transfer the patient
chemical classification of aspirin preventing a heart
is Nonsteroidal Anti- attack especially
inflammatory Compounds in patient suffering
from NSTEMI.

Nursing Responsibilities Rationale


1. Observe the 10 R‘s in drug administration To prevent error.
2. Advise watcher to keep patient assisted, or to In order to prevent fall of patient which can lead to
always put the side rails of bed up trauma and injury.
3. Inform patient and watcher to refer to health care In order to apply measure that can halt possible
providers if bleeding gums, dark stool and gastric bleeding occurrence and further injury
upset are present.

Medication Date Description Indication Patient’s


Ordered Response
Morphine is one of the Administered for A total of 6mg was
natural plant alkaloids management of chest administered. Pain
Morphine 07-04- found in opium and is the pain. scale reduced from
2019 prototype opiate, against 8/10 t0 3/10. Chest
which other derivatives are pain was
measured in terms of unresolved
analgesic effects and side however.
effects.

Nursing Responsibilities Rationale


1. Monitor blood pressure prior to administration. Hold if systolic BP < 100 mm Hg or 30 mm Hg
below baseline. It can cause further decline of
blood pressure.
2. Reassess pain after administration of morphine. Assess effectivity of the drug or need of higher
dosage.
3. Monitor vital signs May cause respiratory depression and hypotension
4. Ensure Safety In order to prevent fall of patient which can lead to
trauma and injury.
5. Advise patient to change positions slowly Minimize orthostatic hypotension
6. Be aware on total dosage given Physical dependence, resulting from prolonged use,
may create the risk of withdrawal symptoms if drug
is completely discontinued

Medication Date Description Indication Patient’s Response


Ordered
Potassium chloride extended- Repeat laboratory
release tablets USP, is a sugar- revealed low level of
Potassium 07-04- coated (not enteric-coated) tablet potassium. Few hours
Chloride tablet 2019 for oral administration, Hypokalemia after administration, the
containing 600 mg of potassium patient heart rhythm
chloride (equivalent to 8 mEq) in was converted from
a wax matrix. NSTEMI to STEMI

Medication Date Description Indication Patient’s


Ordered Response
Isosorbide dinitrate is in a For severe and unstable Chest pain nwas
group of drugs called angina pectoris. not resolved
Isoket Drip 07-04- nitrates. Isosorbide Isosorbide dinitrate although pain
2019 dinitrate dilates (widens) (ISDN) causes a scale decreased
blood vessels, making it relaxation of vascular from 8 to 3/10.
easier for blood to flow smooth muscle thereby
through them and easier for inducing vasodilatation.
the heart to pump.

Nursing Responsibilities Rationale


1. Check 10 R's. To prevent and/or minimize errors in drug administration.
2. Check patency and regulation To ensure that the drug will go into the circulation thus,
achieving the effectiveness of the drug.
3. Monitor patient‘s blood pressure To prevent severe hypotension
4. Keep patient in a calm environment To prevent stress and rise of blood pressure.
5. Document To avoid duplication in the administration of the drug and
serve as for legal purposes.

Medication Date Description Indication Patient’s


Ordered Response
Dopamine, a Treatment of During the 9 hours
sympathomimetic amine hypotension, low of hospitalization,
Dopamine 07-04- vasopressor, is the cardiac output, and poor target BP of
Drip 2019 naturally occurring perfusion of vital 120/80 was not
immediate precursor of organs. achieved.
norepinephrine.
Nursing Responsibilities Rationale
1. Check Doctor's order and make an IV label. To verify the procedure that has to be done.

2. Put the IV label of the IV fluid bottle. To identify the desired IV intended for the patient.
3. Do 7 Checks. Check the IV site, for patency, To ensure proper administration of the IV Fluid.
the filter, the clamps, the tubing‘s, the air vents,
the fluid level and check if there is back flow.
4. Titrate fluid as ordered. To ensure that the desired fluid is being
administered at the right time.
5. Watch out for signs and symptoms for To address the underlying signs and symptoms
complications/problems associated with IV
therapy such as swelling on the IV site, cold to
touch, etc.
6. Monitor client's response. To ensure effectiveness and address complications
present.

Medication Date Description Indication Patient’s


Ordered Response
PNSS is an isotonic fluid For proper fluid balance Was able to keep
Plain Normal 07-04- that contains a total tonicity and tissue hydration. patient hydrated.
Saline 2019 of 308 mOsm/L of Sodium
Solution and 154 mOsm/L of
Chlorine

Nursing Responsibilities Rationale


1. Check Doctor's order and make an IV label. To verify the procedure that has to be done.

2. Put the IV label of the IV fluid bottle. Do not use To identify the desired IV intended for the
marking pen on plastic IV containers. patient. To prevent possibility of absorption
of the marker's ink
7. Do 7 Checks. Check the IV site, for patency, the To ensure proper administration of the IV
filter, the clamps, the tubing‘s, the air vents, the fluid Fluid.
level and check if there is back flow.
8. Regulate fluid as ordered. To ensure that the desired fluid is being
administered at the right time.
9. Watch out for signs and symptoms for To address the underlying signs and
complications/problems associated with IV therapy symptoms
such as swelling on the IV site, cold to touch, etc.
10. Monitor client's response. To ensure effectiveness and address
complications present.

B. Dietary: NOTHING PER OREM EXCEPT MEDS

The patient was put to NPO except meds for the meantime. Generally, it is prescribed as
safety precaution. In addition, metabolism increases increase demand of ATP from muscle
contraction and increase work of ventilation causing increased work by the heart muscle.
C. Activity: COMPLETE BED REST WITHOUT BATHROOM PRIVILEGE

In cardiac patients, minimal activity is encouraged to reduce workload of the heart.


Complete bed rest was ordered to avoid additional stress that can cause further complications.
Prolonged complete bed rest in conjunction with conventional forms of therapy is being utilized
in patients with cardiac disease and cardiac dilatation in an effort to unload the heart (Burch
[Link]., 1999). It is thought that the minimization of cardiac work, a good diet, avoidance of
alcohol and the like have per mitted recovery and return of heart size to normal in approximately
half of the patients treated thus far.

IX. NURSING CARE MAP

Electrolyte Imbalance

 NPO
 IV fluids
 Potassium 3.38
 Sodium 132.8
 Potassium Chloride
tablet
Pain Decreased Cardiac
Output
 Facial grimacing
 Verbalized chest Reason for seeking  BP = 80/60 mmHg
pain aggravated by health care:  Arrhythmias
movement or deep Unresolved Chest Pain  Heart Rate 58
breathing  Isolated PVCs
 Rated as 7-8/10  Dopamine Drip
 Restlessness
 Morphine Activity Intolerance
 Isoket Drip  Chest pain aggravated by
movement
 Exertional angina
 Body malaise
 Fall protocol
 Acute pain
Problem no 1: Pain
Goal: Control Pain
Outcome: Patient’s pain remain above 3 on a 10 point scale

Nursing Intervention Patient Response


[Link] present health condition [Link] chest pain rated as 8/10
aggravated by movement or deep
breathing; facial grimacing noted
[Link] [Link] to comfort
[Link] environment [Link] noise, decreased lighting and
was able to calm down
[Link] analgesics as ordered [Link] and Isoket drip given and was
able to decrease pain scale to 3-4/10

Impression: Patient needs narcotics to control pain and the and the like of independent nursing
measures as positioning and regulation of environment.

Problem no 2: Decreased Cardiac Output


Goal: Blood pressure and heart within normal range
Outcome: Before transfer, patients’ blood pressure was 90/60mmHg; heart rate of 55bpm

Nursing Intervention Patient Response


[Link] present health condition [Link], irregular pulse rhythm,
body malaise, and agitation were noted
2. Positioned to reverse trendelenburg. 2. Patient was not able to maintain position
because of pain. Assumed position of
comfort.
3. Provided restful environment. 3. Minimized noise, decreased lighting and
was able to calm down
4. Titrated inotropic drugs as ordered. 4. Reached maximum dose allowed for
patient.
5. Monitored patient’s response and noted 5. Was not able to raise blood pressure on
for signs of worsening condition. acceptable range. Patient was bradycardic
before discharged.

Impression: Positioning and regulation of environment helps in decreasing cardiac load by


decreasing stress level. Inotropes are administered to support cardiac function.
Problem no 3: Electrolyte Imbalance
Goal: Heart pace to normal sinus rhythm.
Outcome: Patient condition progresses from NSTEMI to STEMI

Nursing Intervention Patient Response


1. Assessed present health condition 1. Abnormal heart rhythm, hypokalaemia,
decreased blood pressure, body weakness,
and normal renal function were noted.
2. Ensured safety 2. Side rails raised and was able to provide
safety and comfort.
[Link] KCL tablet as ordered 3. Presence of ST elevation noted and
unrelieved chest pain present. Serum
potassium was not re assessed as the need to
transfer to other facility for percutaneous
intervention was facilitated

Impression: Mineral supplement as potassium chloride tablet is needed to increase level of


serum potassium to normal range.

Problem no 4: Activity Intolerance


Goal: Measurable increase in patient‘s activity tolerance
Outcome: There was a measurable increase in client‘s activity tolerance as manifested by
reduced chest pain with a pain scale of 3/10

Nursing Intervention Patient Response


[Link] present health condition 1. Limited mobility because of pain, body
weakness, agitation were noted.
[Link] [Link] to comfort
3. Assisted to activities of daily living as 3. Able to move with assistance.
bathroom needs.
[Link] rest periods 4. Able to save energy and stay calm.
5. Ensured safety 5. Side rails raised and was able to provide
safety and comfort.
[Link] analgesics as ordered 6. Pain scale decreased to 3/10.

Impression: The occlusion of the coronary arteries caused decreased in blood and oxygen
supply to the myocardium. With decreased blood supply to the myocardium, the pumping ability
of the myocardium becomes inefficient and unable to meet the oxygen demands of the other
tissues of the body hence activity intolerance
REFERENCES

Britton, A., Brunner, E., Kivimaki, M., Shipley, M. (2012). Limitations to functioning and
independent living after the onset of coronary heart disease: what is the role of lifestyle
factors and obesity?, European Journal of Public Health, Volume 22, Issue 6, December
2012, Pages 831–835, [Link]

Burch, M.D.J., Walsh, V.J., Ferrans, MD. [Link]., (1999). Prolonged Bed Rest in the Treatment of
the Dilated Heart .AJA Journals 1999

Daga, L.C., Rosengart, T.K., & Mansoor, A.H. (2011). Approach to STEMI and NSTEMI. The
Journal of the Association of Physicians of India, 59 Suppl, 19-25 .

Foreman, R. D. (1999). MECHANISMS OF CARDIAC PAIN. Journal Article. Annual


Review of Physiology

Haro LH, Decker WW, Boie ET, Wright RS. (2006) Initial approach to the patient who has chest
pain. Cardiol Clin. 24:1-17

Hickam DH. (1990). Chest Pain or Discomfort. In: Walker HK, Hall WD, Hurst JW, editors.
Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston:
Butterworths. Chapter 9. Available from: [Link]

James SK, Atar D, Badano LP, BlömstromLundqvist C, Borger MA, et al.(2012). ESC
Guidelines for the management of acute myocardial infarction in patients presenting with ST
segment elevation. Task Force on the management of ST-segment elevation acute myocardial
infarction of the European Society of Cardiology (ESC), Steg PG, Eur Heart J. 2012
Oct;33(20):2569-619

James, S., & Bueno, H. (2018-12). Epidemiology of acute coronary syndromes. In ESC
CardioMed. Oxford, UK: Oxford University Press,. Retrieved 27 Jul. 2019, from
[Link]

Herlitz J, Hjalmarson A, Bengtson A Clin Cardiol. (1988). Occurrence of hypokalemia in


Suspected acute myocardial infarction and its relation to clinical history and clinical course.
11(10):678-82.

Kristen J. Overbaugh (2009). ACUTE CORONARY SYNDROME. American Journal of


Nursing May 2009. Vol. 109, No. 5

McEwen, M., & Wills, E. M. (2014). Theoretical basis for nursing.


Pimple, P., Shah, A. J., Rooks, C., Douglas Bremner, J., Nye, J., Ibeanu, I. Vaccarino, V. (2015).
Angina and mental stress-induced myocardial ischemia. Journal of psychosomatic
research, 78(5), 433–437. doi:10.1016/[Link].2015.02.007

Rapezzi, C., Biagini, E., Branzi, A. (2008). Guidelines for the diagnosis and treatment of non
ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and
Treatment of Non-S Segment Elevation Acute Coronary Syndromes of the European Society
of Cardiology, European Heart Journal, Volume 29, Issue 2, January 2008, Pages 277–278,
[Link]

Seun Ayoade, Mister. (2017). "The Differences Between the Germ Theory, the Terrain Theory
and the Germ Terrrain Duality Theory". JOJ Nursing & Health Care.
4.10.19080/JOJNHC.2017.04.555631.

Singh A, Grossman SA. Acute Coronary Syndrome. [Updated 2019 Apr 15]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from:
[Link]

Spinler, Sarah. (2007). Managing acute coronary syndrome: Evidence-based approaches.


American journal of health-system pharmacy : AJHP : official journal of the American
Society of Health-System Pharmacists. 64. S14-24. 10.2146/ajhp070109.

Tortora, G. and Tortora, G. (2014). Principles of anatomy & physiology, 14th edition. 14th ed.
John Wiley & Sons, [Link] 17.3, page 577.

Wang, D., Yang, X. H., Zhang, J. D., Li, R. B., Jia, M., & Cui, X. R. (2018). Compared efficacy
Of clopidogrel and ticagrelor in treating acute coronary syndrome: a meta-analysis. BMC
Cardiovascular disorders, 18(1), 217. doi:10.1186/s12872-018-0948-4

HOLY ANGEL UNIVERSITY 
GRADUATE SCHOOL OF NURSING 
 
 
 
Master of Science in Nursing 
 
 
ACUTE CORONARY SYNDROME:
ACUTE CORONARY SYNDROME 
I. 
INTRODUCTION 
The cardiovascular system consists of a closed circuit: the heart, responsib
several minutes) or persistent. These complaints may be accompanied by other symptoms such 
as diaphoresis, nausea, abd
PCI are taken for CABG (coronary artery bypass graft) or managed medically depending upon 
comorbidities and patient ch
III. 
HISTORY OF PRESENT ILLNESS 
Chief Complaint: Chest pain 
 External Perspective Risk Factors 
1. Current stressfu
4. Presence of support system 
 Anxiety releases catecholamine, which increase myocardial workload and can 
escalate a
arrhythmias. In addition, a decrease in K level generally induces vasoconstriction, 
which leads to further ischemia, t
pain-free. They also provide a baseline against which to compare 
later pattern changes. 
Needs assistance in ADLs 
o P
PATHOPHYSIOLOGY (ACS) 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Activation of Platelets 
coronary artery 
 
Format
BOOK BASED (American Journal of Nursing 2009) 
Non modifiable factors that influence risk for coronary artery disease i

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