LORMA COLLEGES

COLLEGE OF PHYSICAL AND

RESPORATOY THERAPY
Carlatan, City of San Fernando, La Union

CASE STUDY:
MULTIFACTORIAL SECONDARY
TO ACUTE CORONARY
SYNDROME NSTEMI
(Non-ST- Elevation Myocardial
Infarction)

SUBMITTED TO:
ARELLANO, ALESSANDRO JR.

SUBMITTED BY:
TELIAKEN, HENRIC NICOLE P.
 I. ADMITTING HISTORY AND PHYSICAL EXAMINATION
A. DEMOGRAPHIC DATA

NAME: F.E. GENDER: FEMALE

ADDRESS: Parian, San Fernando City, La Union CITIZENSHIP: FILIPINO

AGE: 60 years old DATE OF CONSULTATION: 06-14-19

BIRTHDATE: November 23, 1960 BIRTHPLACE: San Fernando, La Union

MARITAL STATUS: Married RELIGION: Roman Catholic

OCCUPATION: N/A

B. CHIEF COMPLAINT
Difficulty of breathing

C. BRIEF HPI
2 weeks prior to admission, she was admitted and diagnosed of ACS NSTEMI S/V
with onset of difficulty breathing. Patient was then rushed at V/O hospital.
Procedures and medications given were unrecalled.

1 hour prior to admission, she was transferred at ITRMC, patient was then referred
to PT Rehab for more evaluation and PT management.

D. PAST MEDICAL HISTORY

(+) Diabetes Mellitus
(+) HPN 2017
(+) Pneumonia (CAP).
(+) Stroke 2017
(-) Cancer
 (-) Arthritis

E. FAMILY HISTORY
FATHER MOTHER
DM (-) (-)
HPN (-) (-)
Cancer (-) (-)

F. SOCIAL HISTORY

Patient has secondary lifestyle

(-) cigarette smoker

(-) alcoholic drinker

G. REVIEW OF SYSTEMS

HEENT:

Lid margins moist and light pink, lashes short, evenly spaced and curled outward. Bulbar
conjunctiva is clear with tiny vessels visible, palpebral conjunctiva is light pink with no
discharge, white sclera. Lips and surrounding tissue relatively symmetrical. No lesions,
swelling and drooping. Neck is symmetric with head centered and without bulging masses.

CHEST AND LUNGS

The color of his chest is similar to his complexion. Chest symmetry is equal, thorax is
straight, the RR of the patient is 26 breathe/min. Dyspneic with nasal flaring,

CARDIOVASCULAR:

The PR of the patient is 82bpm and a BP of 130/80 mmHg.

ABDOMEN

Flat abdomen; no tenderness, lesions and masses.

VITAL SIGNS

BP = 150/80 mmHg PR = 82 bpm SpO2 = 98% Temp = 37℃ RR = 26 breathe/min

I. DIAGNOSTICS AND PROCEDURES

A. HEMATOLOGY (06-21-19)

LABORATORY NORMAL VALUE RESULT

HEMOGLOBIN M = 14-18g/dL 92
F = 12-16g/dL
HEMATOCRIT M = 0.40-0.54 0.28
F = 0.37-0.47
RED BLOOD CELLS 4.0-5.4 3.0
WHITE BLOOD CELLS 4.0-10.0 23.7
DIFFERENTIAL COUNT

EOSINOPHILS 0.00-0.05 0.03

BASOPHILS 0.00-0.30
LYMPHOCYTES 0.20-0.40 0.18
MONOCYTES 0.00-0.07 0.04
BAND -
SEGMENTERS - 0.75
PLATELETS 150-450 442

B. ARTERIAL BLOOD GAS

EXAMINATION RESULT
pH 7.524
PaCO2 27.5
HCO3 22.9
PaO2 156.4
SaO2 99.6

INTERPRETATION: Uncompensated respiratory alkalosis with over corrected oxygenation via TT @ 40%
FiO2.

DISEASE DISCUSSION

INTRODUCTION
Coronary artery disease is an umbrella term used to cover any group of clinical symptoms
compatible with acute myocardial ischemia. Acute myocardial ischemia is a chest pain due to insufficient
blood supply to the heart muscle that results from coronary artery disease, also called coronary heart
disease. Multiple factors can be identified as contributing to the declined in CAD. These factors include
more effective medical treatment and an increase awareness and emphasis on reducing the major
modifiable cardiovascular risk factor (e.g. high blood pressure, smoking, high cholesterol, obesity, and
diabetes.
In Acute Coronary Syndrome, it is believed that the atherosclerotic plaque in the coronary artery
ruptures, resulting in platelet aggregation (“clumping”), thrombus (“clot”) formation, and vasoconstriction.
The amount of disruption of the atherosclerotic plaque determines the degree of obstruction of the coronary
artery and the specific disease process (unstable angina or myocardial infarction). Between 10% and 30%
of the client with unstable angina progress to having an MI (myocardial infarction) in 1 year and 29% die of
MI in 5 years.
Acute coronary syndrome (ACS) is a condition of unstable cardiac ischemia. ACS includes
unstable angina and acute myocardial ischemia with or without significant injury of the myocardial tissue.

Acute coronary syndrome is used to describe three types of coronary artery disease:

 Unstable angina

 Non-ST-segment elevation myocardial infarction or heart attack (NSTEMI)

 ST-segment elevation myocardial infarction or heart attack (STEMI)

If the supply of oxygen to the cells becomes too low, the cells of the heart muscles can die. The lack
of blood supply to any tissue is called ischemia. The death of the cells results in damage to muscle tissue,
and this is a heart attack or myocardial infarction. In some cases, the cells do not die, but damage due to
an inadequate supply of oxygen results in heart muscles that do not work correctly or efficiently. The
problem may be temporary or permanent. Unstable angina is the term used to describe the condition when
acute coronary syndrome does not lead to cell death. The location of the blockage, the length of time that
the blood flow is blocked, and the amount of damage that occurs determines the type of acute coronary
syndrome. Doctors classify the coronary syndromes based on:
  The presence of certain substances in the blood released by the damaged heart

 Symptoms

 Electrocardiography (ECG) results

ETIOLOGY AND EPIDEMIOLOGY

The etiology of NSTEMI varies as there are several potential causes. The median age at the time
of presentation for ACS in the United States is 68 years. Males outnumber females by a 3:2 ratio. The
incidence of ACS in the United States is over 780,000, and of those, approximately 70% will have NSTEMI.

CLINICAL MAIFESTATIONS

 Chest pain or discomfort

 Pain or discomfort in one or both arms, the back, jaw, neck, or stomach

 Shortness of breath

 Dizziness or feeling lightheaded

 Indigestion

 Nausea or vomiting

 Sweating

RISK FACTORS

 Older age - men of 45 years or older, women aged 55 years or older

 High blood pressure or cholesterol

 Smoking

 Lack of physical activity

 Unhealthy diet, obesity, or overweight

 Diabetes

 Family history
PATHOPHYSIOLOGY

PREDESPOSING FACTORS: PRECEPITATING FACTORS:

 AGE (75 YRS OLD)  DIET (CHOLESTEROL RICH

 GENDER (MALE) FOODS)
 STRESSFUL LIFESTYLE

PLAQUE FORMATION

ATHEROSCLEROTIC PLAQUE RUPTURES OR ERODES

THROMBIN IS GENERATED AND FIBRIN IS DEPOSITED

PLATELET AGGREGATION

CLOTS ARE BEING FORMED

THICKENING AND NARROWING OF ARTERIAL VESSELS

OBSTRUCTION IN BLOOD FLOW

CELLS BECOME ISCHEMIC

 PATHOPHISIOLOGY CONT’

MYOCARDIAL CELL CONTRACT LESS EFFECTIVELY LACTIC ACID IS

SECRETED DECREASE O2
SUPPLY TO
MYOCARDIUM
DECREASE CARDIAC OUTPUT STIMULATE PAIN
RECEPTOR

DECREASE O2 SUPPLY TO THE DIFFERENT PARTS OF CHEST PAIN

THE BODY

DIFFICULTY PALLOR
OF
BREATHING

BODY WEAKNESS

MANAGEMENT

Primary Prevention

The ACC/AHA guidelines continue to emphasize the importance of primary prevention of ACS by
decreasing coronary artery disease risk factors, including hypertension, hypercholesterolemia, diabetes
mellitus, and smoking.1 Family history of coronary artery disease is also a risk factor.

Initial Management

At the individual level, patients should be advised to chew a nonenteric coated aspirin (162 to 325 mg) at
first recognition of ACS symptoms, unless they have a history of severe aspirin sensitivity.4 At the
community level, local areas should create and maintain emergency medical service systems that support
STEMI care. Initial care should include a full assessment of clinical symptoms and coronary artery disease
risk factors, as well as 12-lead electrocardiography. Electrocardiographic findings that may reflect
myocardial ischemia include changes in the PR segment, QRS complex, and the ST segment.1 Part of the
initial assessment also involves obtaining cardiac biomarkers that include troponin (I or T). Primary
percutaneous coronary intervention (PCI) is the recommended reperfusion method; therefore, all efforts
should be made to transfer a patient with suspected STEMI to a PCI-capable hospital. If none is available
within a 30-minute travel time, medical management should occur in the nearest emergency department.
The goal of medical management is to administer fibrinolytic therapy within 30 minutes of first medical
contact.

Medical Management

The medications used to manage ACS.4,5 Dual antiplatelet therapy is highly recommended in the
treatment of STEMI to support primary PCI and fibrinolytic treatment strategies. With either strategy, aspirin
therapy (162 to 325 mg per day) should be started as soon as possible and continued indefinitely. For
patients undergoing primary PCI for STEMI, a P2Y12 receptor antagonist, such as clopidogrel (Plavix; 600
mg), should be administered as early as possible or at the time of PCI, and a maintenance dosage of 75
mg per day should be continued for one year in patients who receive a stent. Patients undergoing
fibrinolysis for STEMI should receive a loading dose of clopidogrel (300 mg in persons younger than 75
years, or 75 mg in persons 75 years and older) before treatment. Clopidogrel, 75 mg per day, should be
continued in patients receiving fibrinolytic treatment for at least 14 days and up to one year. Glycoprotein
IIb/IIIa inhibitors (such as tirofiban [Aggrastat], eptifibatide [Integrilin], and abciximab [Reopro]) have shown
benefit when used during PCI in persons with STEMI and as an adjunct to PCI in persons with NSTE-ACS;
however, triple antiplatelet therapy has been associated with an increased risk of bleeding.

RESPIRATORY CARE TREATMENT PROTOCOLS

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease work of breathing, and decrease myocardial work.

Mechanical Ventilation Protocol

Because ACS has decreased oxygen supply and due to severe difficulty in breathing.
Subjective Objective Assessment Plan

Chief Complaint: GS:

“nahihirapan huminga at Unconscious in a fowlers
nawalan ng pakiramdam position on mechanical
yung kaliwang kamay” ventilator.
as stated by the watcher
LOC:
Unconscious
GCS 3

V/S:
Diagnosis: HR:82
Multifactorial secondary RR:26 Tachypnic Monitor vital signs for
to acute coronary BP:150/80 Hypertensive any changes
syndrome nstemi T°:37
(non-st- elevation
myocardial infarction)
Cough: None
 weak Purulent Suctioning
 Productive
 Greenish

MV Parameters
Mode: SIMV
Vt/PIP: 360 Monitor mv settings and
FiO2: 40 look for any changes
BUR: 15

ABG:
pH: 7.524 Uncompensated
PCO2: 27.5 Decrease RR, decrease
respiratory alkalosis with
PaO2: 156.4 VT
HCO3: 22.9 overcorrected
SpO2: 99.6 oxygenation via TT @
FiO2: 100%
40% FiO2.

CXR:
N/A
REFERNCE:

https://www.ncbi.nlm.nih.gov/books/NBK513228/
https://www.scribd.com/doc/129680755/Acute-Coronary-Syndrome
https://emedicine.medscape.com/article/1910735-overview
https://www.aafp.org/afp/2017/0215/p232.html