Acute Coronary Syndromes

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FACULTY OF MEDICINE AND HEALTH SCIENCES

UNIVERSITI SAINS ISLAM MALAYSIA (USIM)

ACUTE CORONARY SYNDROMES


1) Patient’s data
Mrs. X, 80-year-old malay lady.
Date of admission and clerking: 22th June 2009
Source of information: Patient’s daughter who lived with her.
a) Presenting complaint/illness
a known case of
- diabetes mellitus since 30 years ago
- hypertension since 30 years ago
- End stage renal failure since 3 years and chronic anemia since a year ago
- Ischemic heart disease since a year ago
presented with chest pain for 4 hours prior to admission.
b) History of presenting complaint/illness
She was apparently well before she developed the chest tightness,
which was sudden after going to toilet at 1am, in the morning. The retrosternal
pain was heavy and gripping in nature, radiating to jaws. The pain was
continuous and lasted for four hours and progressively resolving with one
sublingual tablet of glyceryl trinitrate, given by her daughter immediately after
the attack. The daughter also given her mother sweet, in fear of hypoglycemic
attack and later went to emergency department. The chest pain was scale as 2
out of 10, where 10 are equivalent to the pain of childbirth.
The chest pain was associated with shortness of breath, palpitation,
nausea and vomiting. There were no syncope, peripheral edema, orthopnea,
paroxosyml nocturnal dyspnoe, fever, loss of weight and loss of apetite. There
were no muscle and bones weakness and pain, and no spontaneous bleeding.
Shortness of breath was continuous, exacerbates on exertion and is relieved by
lying with two pillows. Palpitation was sudden, fast and irregular. The vomitus
was fluid, approximately 50 ml in volume and was delayed more than 3hours
after eating. No haematemasis.
She had a similar attack previously on February 2008, after having a
tiring peritoneal dialysis in hospital and was more severe than this one. ECHO
was done and claimed that there is enlargement of the cardiac.

c) Systemic review
Respiratory system

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No wheezing, cough, and night sweating.
Gastrointestinal system
There was no pain in abdominal region. No alteration in bowel habits. The
stool was blackish as hair in colour and being claimed due to the haematinic
agent that she ingested.
Genitourinary system
Urination was about 8 times per day. There was polyuria and urgency but no
hematuria, swollen ankle nor urinary incontinence.
Central Nervous system
No syncope, parasthesia, weakness of limbs, fits, and paralysis.
d) Past medical history
She was a known case of diabetes mellitus, and now it is well controlled.
Admitted to ward two times per month to undergo peritoneal dialysis,
depending on doctors’ impression. Having fluid restriction, consuming 500ml
of fluid for three days.
e) Past surgical history
Nil
f) Drug/medication history
Amlodipin, statin, haematinic agent, calcium carbonates, and diuretics.
No allergies to drugs and was not consuming traditional medicine
g) Transfusion history
Transfusion of blood, type AB on 18/2/09 due to underlying chronic anemia.
h) Family history
Husband and all children have hypertension and diabetes. The family
members love to drink bicarbonate drinks.
i) Social history
No history of smoking and drinking alcohol. She was previously working in
estate before retiring at the age 55 and becomes housewife. She lived at
ground floor of her house that have western toilet.

2) Physical Examination
a) General Examination

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Patient was laying at 45, look slightly pallor, weak, and conscious.
Nasal prong attached with flow rate at 3litres/minuts. She looked fairly
hydrated and is alopecia. The vital signs were:
- Blood pressure: 199/92 mmHg
- Pulse rate: 58 beats per minute (bradycardia), regular and small volume
- Respiratory rate: 16 breath per minute (normal)
- Temperture: 37 and 02 saturation: 100% on air
Hands was cold, no excessive sweating, no clubbing, no stigmata of
infective endocarditis, no peripheral cynosis, capillary refill was normal,
no muscle wasting and flapping tremor. There was no radio-radial and
radio-femoral delay.
Pallor was present; xanthelasma was present and no jaundice. No
central cynosis, hydration was fair and oral hygiene was good. There was
no high-arched palate. Mild pitting pedal oedema was present.
b) Systemic Examination
Cardiovascular system
The chest wall shape was normal. There was visible apex beat. No
extra pulsation observed, no surgical scars.
The apex beat was present at 5th intercostal space and slightly displaced
to left. Parasternal heaves was present. There were no thrills and palpable
P2. No other pulsation found.
Jugular Venous Pressure was normal, 2.8cm. Carotid pulse was
adequate in volume.
The first and second heart sounds were present and normal. There were
no murmur and added heart sound heard.
No palpable liver. No sacral oedema.
Respiratory system
Chest moved with inspiration. No usage of accessory muscles. There
was no spine abnormality.
No ribs tenderness. Chest expansion and tactile fremitus were equal on
both sides of the lung.
Lung percussion was resonance on both sides.

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Slight reduced in air entry in the right lung. Minimal and occasional
fine bibasal crepitation present.
Abdomen
Tenkoff catheter was attached to the abdomen. Abdomen is flattened,
not distended and umbilicus was centrally located and inverted. It moved
with inspiration. There were no scratch marks, obvious mass, dilated veins
or any obvious peristaltic activities.
The abdomen was soft. No rebound tenderness, rigidity and mass were
found. No organomegaly detected.
Abdomen was dull with no shifting dullness.
Bowel sound present and normal. No renal and liver bruits were heard.
Central Nervous System
Patient was well oriented with time, place and person. The speech,
cranial nerves, sensation, motor function and reflexes, cerebellar function
and gait were normal.
CASE SUMMARY
Mrs X, a 80-year-old Malay lady presented with chest pain for 4hours
prior to admission. It was associated with shortness of breath, palpitation,
nausea and vomiting. She was a known case of diabetes mellitus,
hypertension, end stage renal failure and ischemic heart disease. Physical
examination shows slight displacement of apex beat and present of
parasternal heaves.
3) Provisional Diagnosis
-Unstable angina/ acute coronary syndrome without ST elevation.
Having history of ischemic heart disease, diabetes and hypertension are risk
factors for developing acute coronary syndromes. The diagnosis is supported:
a) Sublingual nitrates relieved the pain.
b) There was no ST elevation in ECG.
c) The cardiac enzymes were not raised.
Investigations done 6hour after the attack were:
1) ECG results shows second-degree heart block with “Mobitz type 2”
phenomenon. Left ventricular hypertrophy, left anterior hemiblock, left axis
deviation, negative T wave (lateral) and S waves. No ST elevation.
- T waves inversion is highly suggestive of an Acute Coronary Syndromes.

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- However, the presence of conductive block may complicate a myocardial
infarction.

2) Cardiac enzymes:
LDH 328U/L (N: 240-461U/L)
CK 38U/L (N: 24-170U/L)
AST 23U/L (N: 0- 40U/L)
- There were no changes in the level of cardiac enzymes, which was not
suggestive of myocardial infarction.

4) Differential Diagnosis
a) Acute myocardial infarction (AMI)/ Acute coronary syndrome with ST
elevation.
-AMI can generally be differentiated with unstable angina by several
characteristics:
1) MI pain typically lasts from 20 minutes to several hours.
2) Not relieved by sublingual nitrates
3) Dyspnea is common and is caused by impaired myocardial contractility,
with resultant pulmonary congestion and edema.

-The diagnosis of AMI is based on the presence of 2 out of 3 criteria (WHO)


a) Clinical history of ischemic type chest discomfort
b) Evolutionary changes in serially obtained ECG changes.
c) A rise and fall in serum cardiac enzymes

b) Hypoglycemic attack secondary to underlying diabetes mellitus


Hypoglycaemia attack is having plasma glucose less than 3mmol/L.
Symptoms ranging from rapid onset of palpitation and sweating, as what
the patient had felt. The daughter even had given her mother sweets in fear
of some hypoglycemic attack occurring.
Yet, this was unlikely to occur since the daughter claimed that her
mother’s diabetes mellitus is controlled after she developed end stage renal
failure. Upon arrival, the random capillary blood sugar is 6.4mmol/L.
(Fasting Blood Glucose; N: 3.5-5mmol/L)

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c) Chronic anemia secondary to chronic renal failure (CRF).
CRF can cause anemia as the synthesized erythropoietin is reduced.
This is supported by the full blood count on the day of admission:
Hgb 9.4 g/dL (N: 12-16.0 g/dL)
MCV 91fL (N: 81-99fL)
MCHC 34.3g/dL (N: 33-37g/dL)
The patient was having normocytic normochromic anemia and it was
unlikely to cause sudden onset of the symptoms unless it was a severe
anemia (Hb< 7g/dL).
5) Discussion
The doctors did still not confirm the exact diagnosis. They diagnosed it
as acute coronary syndrome; yet the differentiation between unstable
angina and myocardial infarction is important, as the management will
differ. Further investigation to support and complement the diagnosis:
1) ECG, to rule out myocardial infarction (MI). It should be repeated when
the patient experienced chest pain, continuous ST-segment monitoring is
recommended.
2) CK-MB and troponins. The cardiac enzyme of CK is not specific, and
can be found in brain and skeletal muscle. Measuring blood levels of CK-
MB and troponins is more sensitive and specific in confirming the
diagnosis. Cardiac troponin and CK-MB are equally sensitive at early
stages of an MI, however, persistence of elevated troponins levels for
approximately 10 days allows the diagnosis of an acute MI long after CK-
MB has returned to normal.
3) Arterial Blood Gases, to determine acid base balance in the body.
Early management involved admitting the patient to CCU, gives high
flow oxygen, morphine as analgesics and sublingual nitrates in sequence.
Management for MI includes thrombolysis, B-blocker to reduce
palpitation and sympathetic response, and ACE inhibitors, as left
ventricular failure can complicate MI. Management for unstable angina
includes B-blocker, low molecular heparin as anticoagulant and nitrates as
vasodilators by inducing smooth muscle relaxation.

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