Acute Coronary Syndrome Case Study
Acute Coronary Syndrome Case Study
Submitted by:
Marilyn D. Palpal
Submitted to:
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.
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
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)
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
coronary artery
Decreased left ventricular Elevated CK-MB, myoglobin,
function Troponin T, Troponin I
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.
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.
Additionally, the release of aldosterone and antidiuretic hormone promotes sodium and
water reabsorption, increasing preload and ultimately the workload of the myocardium.
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.
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.
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
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
Accumulation of lactate
Inhibition of Glycolysis
Altered cell
Myocyte death/ Necrosis
membrane integrity
A. Pharmacology
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.
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.
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
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
Impression: Patient needs narcotics to control pain and the and the like of independent nursing
measures as positioning and regulation of environment.
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 .
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]
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]
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









