Iloilo Doctors’ Hospital, Inc.

Department of Internal Medicine

MCC San Antonio, Danniel D. January 20, 2022

I. General Data

This is the case of L.G., 59 year old, M

II. Chief Complain

Chest Pain

III. History of Present Illness

Night prior to admission, while resting on his bed, patient felt a pain on his chest
characterized as “daw naipit”, retrosternal location, which lasted for about 5 minutes with a pain
scale of 5/10. The pain was non radiating. No other symptoms noted. Patient took losartan to
alleviate the pain. No consults done.
On the day of admission, patient felt the same chest pain, characterized as “daw naipit
and masakit na”, retrosternal in location, which lasted for 15 minutes with a pain scale of 8/10.
The pain radiated to the left arm of the patient with associated diaphoresis. Patient felt cold,
clammy, and felt like he was going to faint during the episode. No medications taken. Patient
then decided to have a consult.

IV. Past Medical History

The patient was a known hypertensive for 10 years. Medications given were losartan and
trimetazidine BID which the patient was not compliant. Patient also self medicated with
omeprazole OD, every morning, for 2 years. Patient undergone cholecystectomy 10 years ago.

V. Family History

History of hypertension on both paternal and maternal side. No other heredo-familial

diseases noted.

VI. Personal History

The patient worked as a kargador for 10 years and is not working as of the moment. The
patient is an alcoholic drinker who drinks 3 – 4 times a week. Patient is also a smoker with a pack
– year of 7.5. Patient’s usual diet is beef, dried fish, and rice.
 VII. Physical Examination

General Survey

Patient came in stretcher borne exhibiting levine sign.

Vital Signs Value Normal Value Remarks

Temperature 36.7 O C 36.6 – 37.5 O C Normal
Heart Rate 92 bpm 60 – 100 bpm Normal
Respiratory Rate 27 cpm 12 – 20 cpm Tachypneic
Blood Pressure 160/90 mmHg <120/<80 mmHg Hypertensive

Anthropometric Data

Height 5 foot 5 inches/165 cm

Weight 71 kg
26.0 kg/m2
BMI Patient is obese 1.
(Asian BMI classification)

CHEST & LUNGS

Inspection: No chest deformities noted. No usage of accessory muscles of respiration.
Palpation: Symmetrical chest expansion.
Percussion: All lung fields of both lungs are resonant.
Auscultation: Bibasal crackles noted.

CARDIOVASCULAR
Inspection: Adynamic precordium
Palpation: Jugular Venous Pressure is normal. Point of maximum impulse located at the 6th Intercostal
space on the anterior axillary line.
Auscultation: Regular rate and rhythm. No murmurs or extra heart sounds heard.

ABDOMEN
Inspection: Globular abdomen. No scars, ulcers, prominent veins, striae, or masses seen.
Auscultation: Normal bowel sounds heard. No aortic, renal, or iliac bruits heard.
Percussion: Tympanitic on all quadrants.
Palpation: No tenderness, guarding, or rigidity on all quadrants.

EXTREMITIES
Inspection: No active lesions noted. No clubbing of nails.
Palpation: Cool and Clammy extremities. Grade 2 non - pitting edema noted. 5/5 Manual Muscle Test on
all extremities.

SALIENT POINTS
Pertinent Positives Pertinent Negative
Shortness of Breath Normal JVP
Levine Sign No murmurs
PMI on 6th ICS Left ACL No abnormal heart sounds (S3 and S4)
Grade 2 non – pitting edema
Rales
Cool and Clammy Extremities
Admitting Impression

Congestive Heart Failure secondary to acute coronary syndrome

Differentials:
- Myocardial Infarction
- STEMI
- NSTEMI

Approach to arrive at the diagnosis:

The patient came in and presented with chest pain. Chest pain is among the most common reasons for
which patients present for medical attention at either an emergency room or an outpatient clinic. Etiologies of
chest pain could be cardiopulmonary or non-cardiopulmonary. On the day of admission, the patient’s chest pain
was accompanied by a radiating pain on his left arm and was diaphoretic. Patient had no history of myocardial
infarction but is a known hypertensive for 10 years and was given Losartan as maintenance but was not
compliant. Personal history shows that the patient is also a chronic smoker of 7.5 pack years and an occasional
alcoholic beverage drinker. Physical examination findings that were remarkable include the patient being obese
1 with a BMI of 26.0 kg/m2 under Asia Pacific Classification, increased respiratory rate due to pulmonary
congestion, bibasal crackles, displaced PMI at 6th ICS L Anterior axillary line that suggests cardiomegaly, and a
Grade 2 non – pitting edema which is a cardinal manifestation of heart failure. History and physical examination
narrowed the differential diagnosis to Myocardial Infarction and acute coronary syndrome. Myocardial
Infarction and Acute Coronary Syndrome cannot be ruled out in this patient until further diagnostics (e.g.
electrocardiogram and cardiac biomarkers) are done.
 Diagnostic Flow Sheet

1. 12 – Lead Electrocardiogram

Since the patient presented with chest pain, ECG is warranted. Electrocardiography is crucial in the
evaluation of nontraumatic chest discomfort. The ECG is pivotal for identifying patient with ongoing ischemia
as the principal reason for their presentation as well as secondary cardiac complications of other disorders.
Abnormalities of Ischemic heart disease in ECG are ST-segment and T waves changes, LVH and disturbances
of cardiac rhythm or intraventricular conduction.

Interpretation: Sinus rhythm, normal axis with ST segment depression at anteroapical wall and
myocardial ischemia.

2. Cardiac Biomarkers

Elevated cardiac biomarkers differentiates STEMI and NSTEMI from UA. Patients with NSTEMI and
STEMI have elevated biomarkers of necrosis, such as cardiac troponin (cTn) I or T, which are specific,
sensitive, and the preferred markers of myocardial necrosis.

Results Reference Values

Cardiac Troponin I 300 pg/L 24-30 pg/L
CK MB 25 ng/mL 3-5 ng/mL
Remarks Elevated Elevated
3. Chest X-ray

Chest x-ray is needed to determine cardiomegaly and any engorgement in pulmonary vessels.

Interpretation: This is the case of a 59/M who came in with chest pain, Chest x – ray taken at PA
view. Trachea in the midline, no bone fractures/deformities noted, CT ratio was not measured.
No blunting of both costophrenic and cardiophrenic angle. Hazy densities noted on both upper
and lower lung field and also on the periphery of the middle lung field. Increase pulmonary
vasculature marking noted. No gastric bubbled nted on the lower left diaphragm. To rule out
bilateral pneumonia.

4. Lipid Profile

Lipid profile is requested to assess patients with NSTEMI of possible atheromatous cause when
LDL is elevated and HDL is decreased for men. High levels of triglycerides is a more significant risk factor
for CVD in women, not in men.

Values Reference Values

Serum Cholesterol 3.70 mmol/L 0.0 – 5.2 mmol/L
Triglycerides 3.67 mmol/L 0.00 – 1.70 mmol/L
HDL 0.94 1.04 – 1.55 mmol/L
LDL 1.09 0.0 – 2.6 mmol/L
5. Fasting Blood Sugar

To check for presence of Diabetes Mellitus which shows an elevated value, as an additional risk
factor included in assessing risk of thrombolysis in myocardial infarction.

Value Reference Value

FBS 4.6 mmol/L <7 mmol/L

6. Creatinine

Creatinine is requested to assess the patient’s kidney function prior to treatment. The patient’s
creatinine level is normal. It is also important to monitor creatinine levels as patients with severe heart
failure, particularly those on large doses of diuretics for long periods, may have elevated BUN and
creatine levels indicative of renal insufficiency owing to chronic reductions of renal blood flow from
reduced cardiac output.

Value Reference Value

Creatinine 83 umol/L 46 – 92 umol/L

7. Uric Acid

High levels of uric acid is indicative of increased lactic acidosis and dehydration that might be due
to an acute kidney injury.

Value Reference Value

Uric Acid 239 umol/L 155 – 357 umol/L

8. Serum Electrolytes

Electrolytes are requested to check for any electrolyte imbalances. The patient’s serum sodium
signifies hyperkalemia. The serum potassium is normal which helps to control the electrical signals of the
myocardium which keeps the heart beating.

Electrolytes
Na 155 mmol/L 136 – 145 mmol/L
K 4.06 mmol/L 3.5 – 5.10 mmol/L
 Therapeutic Flow Sheet
Name, Dosage and Mechanism of Action
Route of Drug
Nitroglycerine Organic nitrate which
patch causes systemic
venodilation, decreasing the
preload
Cellular mechanism: nitrate
enters vascular smooth
muscle and converted to
nitric oxide (NO) leading to
inactivation of ccGMP and
vasodilation
Aspirin Aspirin is a salicylate that
exhibits analgesic, anti-
inflammatory, and
antipyretic activities.
It is a selective and
irreversible inhibitor of
cyclooxygenase-1 (COX-1)
enzyme resulting in direct
inhibition of the
biosynthesis of
prostaglandins and
thromboxanes from
arachidonic acid.
It also inhibits platelet
aggregation.
Clopidogrel Clopidogrel selectively and
irreversibly inhibits
adenosine diphosphate
(ADP) from binding to its
platelet P2Y12 receptor and
subsequent ADP-mediated
activation of glycoprotein
IIb/IIIa complex, thus
reducing platelet
aggregation.
Indication for the Special Considerations
Patient and Responsibilities
For relief of ischemic pregnancy
discomfort
To reduce coronary Patient with dyspepsia
events or lesion of the GI
mucosa, asthma or
allergic disorders,
anemia, dehydration,
menorrhagia,
uncontrolled
hypertension, G6PD
deficiency,
thyrotoxicosis.
Patients undergoing
surgical procedures.
Moderate hepatic and
renal impairment.
Pregnancy.
Given in addition to Patients with platelet
aspirin to reduce disorders, bleeding
cardiovascular death, disorders, or at
MI, or stroke. increased risk for
bleeding (e.g. recent
trauma or surgery);
lesions with a
propensity to bleed (e.g.
gastrointestinal,
intraocular), acute
lower gastrointestinal
bleeding, coronary
artery stents; previous
hypersensitivity or
hematologic reactions
to thienopyridine use
(e.g. ticlopidine,
prasugrel).

Heparin Heparin potentiates the
action of antithrombin III,
thereby inactivates
thrombin as well as
activated coagulation
factors IX, X, XI, XII and
plasmin, and inhibits the
conversion of fibrinogen to
fibrin.
It also stimulates release of
lipoprotein lipase which
hydrolyses triglycerides to
glycerol and free fatty acids.
Fondaparinux Fondaparinux, a synthetic
pentasaccharide, acts as a
selective inhibitor of
activated factor X. It works
by binding selectively to
antithrombin III and
potentiates the
neutralization of factor Xa.
This will interrupt the blood
coagulation cascade and
inhibit both thrombin
formation and thrombus
development.
Enoxaparin (L) Enoxaparin is a type of low
molecular weight heparin
CYP2C19 intermediate
and poor metabolisers.
Patients undergoing
CABG or other elective
surgical procedures.
Temporarily discontinue
5-7 days before elective
surgery if antiplatelet
effect is not desirable.
Renal and moderate
hepatic impairment.
Elderly.
Pregnancy and
lactation.
Reduce recurrent Patient w/ increased
cardiac events risk of bleeding
complications, HTN,
DM, pre-existing
metabolic acidosis.
Do not use in catheter
lock flushing.
Hepatic and renal
impairment.
Elderly.
Pregnancy and
lactation.
To prevent and The major side effect of
treat venous fondaparinux is
thromboembolism bleeding. There is no
antidote
for fondaparinux.
Protamine sulfate has
no effect on the
anticoagulant
activity of fondaparinux
because it fails to bind
to the drug.
Recombinant activated
factor VII reverses the
anticoagulant effects
of fondaparinux in
volunteers, but it is
unknown whether this
agent
controls fondaparinux-
induced bleeding.
Reduce ischemic Bleeding is the most
events common complication.
Non-ST elevation (LMWHs). It binds to and
myocardial potentiates antithrombin III, Contraindicated in
infarction a serine protease inhibitor, patients with severe
(NSTEMI): 1 mg/kg to form a complex that uncontrolled
SC q12hr; irreversibly inactivates hypertension, known
coadminister with factor Xa. Enoxaparin has hypersensitivity to the
antiplatelet less activity against factor drug
therapy; continue IIa (thrombin) compared to
for duration of unfractionated heparin.
hospitalization or
until percutaneous
coronary
intervention (PCI)
performed
Dabigatran Dabigatran is a competitive, Reduce the formation Dyspepsia occurs in up
selective, reversible direct of harmful blood clots to 10% of patients
inhibitor of free and fibrin- in the body. treated with dabigatran;
bound thrombin. It also this problem improves
prevents thrombin- with time and can be
mediated effects including minimized by
cleavage of fibrinogen to administering
fibrin monomers, activation the drug with food
of factors V, VIII, XI, and XIII,
and inhibition of thrombin-
induced platelet
aggregation.
Propanolol (L) Propranolol is a For chest pain and Hypotension,
80-320 mg/day PO nonselective beta- hypertension bradyarrhythmia, may
divided q6-12hr adrenoreceptor antagonist, aggravate pulmonary
also classified as a class II congestion,
antiarrhythmic. It exerts its bronchospasm, nausea
response by competitively and vomiting
blocking beta-1 and beta-2
adrenergic stimulation in
the heart, which is typically
induced by epinephrine and
norepinephrine.
Atorvastatin Atorvastatin is an inhibitor Obesity. Also to reduce May cause elevation of
of 3-hydroxy-3- the risk of myocardial chylomicrons and can
methylglutaryl-coenzyme A re-infarction and stroke influence the
(HMG-CoA) reductase. This development of
enzyme catalyzes the pancreatitis
conversion of HMG-CoA to
mevalonate, an early
endrate-limiting step in
cholesterol biosynthesis.
Enalapril Enalapril is a prodrug of To keep blood pressure Enalapril may cause
enalaprilat, which inhibits under control. dizziness. If affected, do
conversion of angiotensin I not drive or take part in
 to angiotensin II (a potent
vasoconstrictor) resulting in
reduced angiotensin II-
induced vasoconstriction,
Na retention and
aldosterone secretion.
Nifedipine (L) Nifedipine is a peripheral Chest pain due to
arterial vasodilator which ischemia
acts directly on vascular
smooth muscle. The binding
of nifedipine to voltage-
dependent and possibly
receptor-operated channels
in vascular smooth muscle
results in an inhibition of
calcium influx through
these channels.
Furosemide (L) A loop diuretic, works to
increase the excretion of
Na+ and water by the
kidneys by inhibiting their
reabsorption from the
proximal and distal tubules,
as well as the loop of Henle.
Relax the blood vessels any activity in which you
to lower blood need to be alert.
pressure.
If you are taking this
medicine for the very
first time, take the first
dose of Enalapril at
bedtime to minimize
dizziness.
Excessive alcohol
consumption should be
avoided.
Dosage reduction and
close monitoring of
blood pressure is
advised in patients with
hepatic impairment.
Although no specific
guidelines are available,
the half-life and AUC of
nifedipine is markedly
increased in cirrhotic
patients.
Nifedipine is a
dihydropyridine
calcium-channel blocker
and is contraindicated in
patients with known
serious dihydropyridine
hypersensitivity.
Pulmonary edema Watch out for
electrolyte imbalance
and fluid loss as this
drug may have several
side including, blood
volume reduction,
hypotension,
hypokalemia and
hemoconcentration.
Ventricular arrhythmia,
thrombosis or acute
renal failure may result
from overdose.
 Case Discussion

Chest discomfort may be caused by several etiologies. Typical clinical features of major causes of
chest discomfort include cardiopulmonary; cardiac, vascular, pulmonary, and non-cardiopulmonary;
gastrointestinal, neuromuscular, and psychological. The importance of proper history taking and physical
examination is vital in narrowing down the diagnosis. Diagnostic procedures are as important as history
taking ang physical examination as it is used to support the clinical finding and diagnosis.

Heart Failure is a complex clinical syndrome that results from structural or functional impairment
of ventricular filling or ejection of blood. Heart failure is highly considered in this patient since the
patient is a hypertensive for 10 years and is not compliant with his medication. The pertinent findings on
physical examination include a grade 2 non – pitting edema, PMI displacement, and being obese 1 under
Asia Pacific classifications. In the chest x-ray, cardiomegaly was noted, although cp ratio was not
calculated as we were not able to obtain the actual x-ray results and solely depended on cardiac
examination. Maintenance medications that include furosemide, telmisartan, and lacidipine are given
with hypertension and heart failure as well. Patient’s NYHA classification was not elicited, thus, we
cannot classify this patient.

Non – ST elevation acute coronary syndrome is most commonly caused by an imbalance between
oxygen supply and demand. It is usually due to a partially occluding thrombus forming on a disrupted
coronary plaque or on eroded coronary artery endothelium. In this patient, NSTEMI is highly considered
since the patient exhibited chest pain that lasted for about 15 minutes on the day of admission and the
onset was the night before the admission. The chest pain as described by the patient was substernal in
location and was radiating to his left arm. The patient also had diaphoresis which is a symptom that
increases the likelihood of acute myocardial infarction. Physical examination of the patient revealed
bibasilar rales and pale cool skin which are the usual findings of NSTE – ACS. ECG showed an ST segment
depression at the anteroapical wall ischemia. Cardiac biomarkers of the patient were elevated with
values of; Trop I at 300 pg/mL and CK MB of 25 ng/mL. Electrocardiogram showed a normal sinus
rhythm, normal axis with ST segment depression at the anteroapical wall. Treatment of NSTE – ACS
include anti – ischemic treatment of nitrates which should be first given sublingually or by buccal spray, if
there is ischemic discomfort, IV nitroglycerin (5-10 ug/min using nonabsorbing tubing) is recommended.
Beta blockers are the other mainstay of anti-ischemic treatment which should be started by the
intravenous route in patients with severe ischemia but should be avoided in the presence of acute or
severe heart failure. Antithrombotic therapy consisting of antiplatelet and anticoagulant drugs represent
the second major cornerstone of treatment; aspirin, a cyclooxygenase inhibitor, should be started with a
dose of at least 162 mg of a rapidly acting preparation but in this case since in our setting, we only use
lower doses of 80 – 100 mg/d. For the anticoagulants, unfractioned heparin, long the mainstay of
therapy.

Anticoagulants

Indications for the

Drug MOA Special Considerations
patient
Heparin potentiates
Unfractioned Heparin Long the mainstay of
the action of
(UFH) therapy
antithrombin III,
 thereby inactivates
thrombin as well as
activated coagulation
factors IX, X, XII and
plasmin, and inhibits
the conversion of
fibrinogen to fibrin.
It acts by enhancing
Shown to be superior
the inhibition rate of
to UFH in reducing
Enoxaparin activated clotting Accompanied by a slight
recurrent cardiac
(Low – molecular – factors including increase in bleeding
events, especially in
weight heparin (LMWH) thrombin and factor Xa compared to UFH
patients managed by a
through its action on
conservative strategy.
antithrombin III.
A synthetic 20-amino
acid analogue of the
naturally occurring
hirudin. It is a specific
and reversible direct
thrombin inhibitor that Similar to UFH and
works by binding to LMWH but cause less
Bivalirudin the catalytic and bleeding and is used
anionic exosite of just prior to and/or
circulating and clot – during PCI
bound thrombin. It is
used as an
anticoagulant in
percutaneous coronary
intervention.
Works by binding
selectively to
antithrombin III and
potentiates the
Requires supplemental
neutralisation of Equivalent in efficacy
UFH or bivalirudin
Factor Xa. This will to enoxaparin but has
Fondaparinux during PCI to prevent
interrupt the blood a lower risk of major
procedure-related
coagulation cascade bleeding.
thrombosis.
and inhibit both
thrombin formation
and thrombus
development.

Excessive bleeding is the most important adverse effect of all antithrombotic agents, including
both antiplatelet agents and coagulants. Therefore, attention must be directed to the doses of
antithrombotic agents, accounting for body weight, creatinine clearance, and a previous history of
excessive bleeding, as a means of reducing the risk of bleeding. Patients who have experienced a stroke
are at the higher risk of intracranial bleeding with potent antiplatelet agents and combinations of
antithrombotic drugs.