_________________________________________________________________________________________

PHASE 3 MEDICINE REFLECTIVE JOURNAL

Date
13/11/14
1113hrs
(Day 1/5)

Events
Presenting Complaint
Mr. R. is a 43 year old Indian gentleman who presented with sudden onset chest pain and a
shortness of breath while exercising. This was associated with cold sweats, dizziness, and a
generalized feeling of weakness. The chest pain was poorly localized over his entire chest,
did not radiate to other parts of his body, and was described to be tightening and crushing in
nature with a pain score of 5/10. These were no prodromal symptoms such as prior visual
and auditory disturbances, palpitations, or a decrease in effort tolerance. There were also no
abdominal pain or acid reflux/heart burn symptoms.
As he had forgotten the ambulance hotline, he had to wait until his mother returned home. Mr.
R. couldnt remember the duration spent waiting, but remembers that he spent it immobile on
the floor due to the intensity of the pain and other symptoms. There were no exacerbating or
relieving factors, and no loss of consciousness or urinary and fecal incontinence. All his
aforementioned symptoms lasted even until he reached NUH Emergency Department, where
he was subsequently rushed to the Cardiac Catheterization Lab where a balloon angioplasty
was carried out with stent insertion.

Past Medical History

Mr. R. has a significant history of acute coronary syndromes (ACS), with an inferior STEMI
(ST Elevation Myocardial Infarction) in 2007, and an episode of stable angina in 2008. He
also suffers from hyperlipidemia discovered in 2007, for which he is on simvastatin 20mg ON.
The 2007 STEMI presented atypically as 2 days of insomnia with no relevant constitutional
symptoms whatsoever such as chest pain, shortness of breath or diaphoresis. This STEMI
was only discovered on an electrocardiogram (ECG) taken at the local polyclinic. Mr. R. was
then admitted to NUH, stented, and placed on lifelong dual antiplatelet therapy of aspirin and
Plavix (clopidogrel).
The 2008 angina presented as a 4-day duration of left sided tightening chest pain that
happened about twice a day, each time lasting about 15 minutes. This was associated with
exertion, and relieved with rest. Again in this case, there were no constitutional ACS
symptoms. Mr. R. apparently defaulted on his 2007 STEMI medications, claiming that he felt
it was of no use as he was already drinking and smoking so much even after his first heart
attack. This was diagnosed as stable angina due to its association with exertion, unraised
cardiac enzymes and no new ST or T changes on ECG.
He also has hyperlipidemia diagnosed in 2007 for which he is prescribed statins for. He does
not have any other significant past medical history such as hypertension, diabetes,
cerebrovascular accidents (CVA), or any diseases associated with alcoholism such as liver
cirrhosis.
Although his father was diabetic and had liver problems due to chronic alcoholism, he had no
known cardiovascular or coronary diseases. He died from hospital acquired pneumonia. His
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41 year old brother is currently well and does not have any significant medical history.
His current medications are as follows:
1. Aspirin 100mg OM
2. Plavix 75mg OM
3. Glycerol Trinitrate (GTN) 0.5mg PRN
4. Simvastatin 20mg ON
5. Enalapril 2.5mg BD
As mentioned earlier, he has a history of non-compliance to medications, and in this case, he
has also admitted to defaulting for seven months. He has no known drug allergies. He also
claims to not be using any phosphodiesterase-5-inhibitors such as Viagra or Cialis
(sildenafil/tadalafil respectively) that would be a contraindication to prescribing nitrates for his
chest pain.

Social History
Mr. R. is currently working as a security guard on day shift. He has approximately 7 pack
years as he has been smoking 5-6 sticks of cigarettes a day since he was 17 years old. He
has also been drinking about 3 bottles of beer every day since 17. He lives with his parents,
wife, and a domestic helper. He has not travelled out of the country in the past 6 months, and
has no significant contact history.

Physical Examination
On examination, the patient looked alert, oriented to time, person, and place, and able to
speak in full sentences. He was however in pain and distress, and was pale in appearance
and clammy to touch.
His vitals upon presentation were as follows:
T: 36.0C (afebrile)
HR: 84 bpm
RR: 26/min
BP: 121/72
SpO2: 96% on 2L/min
With the patients current complaint, past medical history and presenting condition, my
working diagnosis was that of an acute coronary syndrome. The physical examination was
therefore no longer simply an examination of his cardiovascular system or respiratory system,
but one that was guided by ACLS principles (Advanced Cardiac Life Support), which will be
further elaborated later.
Examination of his cardiovascular system revealed a regular but fast pulse rate of 84 beats
per minute. Heart sounds S1 and S2 were heard without any accompanying murmurs. There
were several signs of systemic hypoperfusion such as the aforementioned tachycardia,
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dizziness, generalized feelings of weakness, and his cool, clammy and pale skin. Patient was
however not hypotensive, and his cognition was intact, with a GCS of 15 (Glasgow Coma
Scale).
There were no signs of heart failure such as a raised jugular venous pressure, pedal edema
or bibasal crepitations. There were also no signs of pulmonary hypertension such as a
palpable pulmonary component of the 2nd heart sound, and signs of atrial fibrillation such as
an irregularly irregular, faint and thready pulse. There were also no sequelae of infective
endocarditis such as Oslers nodes and Janeway lesions.
Examination of his respiratory and neurological system, as well as an abdominal examination,
were all cursory in nature.

Investigations
The NUH Emergency Department was trauma activated by the Singapore Civil Defense
Force (SCDF) at 1113 hours. Upon arrival at 1120 hours, he was triaged stat at the P1 resus
area with his ECG taken within 10 minutes as per NUH ACS Protocol. The ECG is as follows:

Figure 1: ECG taken acutely at the ED, 1128 hours

The ECG showed doming ST segment elevations in Leads II, III and aVF and reciprocal ST
inversions in Leads I and aVL, findings which are characteristic of an acute inferior
myocardial infarction. There were no ST inversions in V1-V4, which would have indicated
right ventricular involvement as well.
In lieu of his acute condition, and taking into account the famous idiom time is muscle, not
many tests and investigations were carried out when Mr. R. presented to the ED. However,
other than the ECG, several tests were crucial, namely blood serum Troponin I levels and an
AMI screen (Creatine Kinase and Creatine Kinase-MB isoenzyme). These were done to
differentiate between a stable angina and a full blown STEMI for diagnostic, treatment and
prognostic purposes.
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In order to ascertain etiology of his acute coronary ischemia, a PT/INR and aPTT clotting
panel (Prothrombin Time/International Normalized Ratio, and Activated Partial
Thromboplastin Time) was done to rule out coagulopathy in lieu of potential antiplatelet
therapy. A Full Blood Count and Renal Panel 2 was also done to rule out infections, anemia,
and electrolyte derangements as a cause of his chest pain, as well as to gauge hematocrit
and hemoglobin levels.

Acute Management
As this is a medical emergency with all the symptoms of an acute ischemia and the
provisional diagnosis of an ongoing inferior STEMI, acute management of the patient was
indicated. This was done through the principles of ACLS. Patient was noted to be alert,
responsive and able to cooperate when asked about his symptoms and medical history.
Regardless, his vitals were taken via the attachment of a cardiac monitor, blood pressure cuff,
and oxygen saturation monitor. Supplementary oxygen was also given via non-invasive
ventilation through nasal prongs at 2L/min as required to maintain oxygen saturation (SpO 2)
>90%. IV access was also established. The NUH ACS Algorithm utilized is as follows:

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Figure 2: NUH ACS Algorithm

As he was already given 300mg of aspirin and a dose of 0.4mg GTN sublingually for a total of
3 doses, none were given at the ED. IV GTN was not deemed necessary after assessing his
blood pressure and pain score. As Mr. R. is younger than 75 (43 years old), heavier than
60kg (78kg) and does not have any prior history of strokes, transient ischemic attacks, or
intracranial hemorrhages, we decided to prescribe prasugrel 60mg over clopidogrel 600mg.
This was also done after considering the absence of other contraindications such as
symptoms or signs of an aortic dissection or other significant closed-head or facial trauma
within the last 3 months.
Following the ACS algorithm above, Mr. R. was subsequently rushed to the Cardiac
Catheterization Lab adjacent to the NUH ED in preparation for a PCI (percutaneous coronary
intervention) after proper discussion with the patient, where the provisional diagnosis and
management plan was discussed. The risks involved with a PCI, such as bleeding, a
periprocedural MI, and other complications that would require surgery were also brought up
and explained.
Mr. R. reached the cath lab approximately 1 hour after admission (1215 hours), where a
selective coronary angiography was done via the right common femoral artery, revealing a
mid RCA (right coronary artery) stenosis. His left coronary arteries were normal. Decision was
made to proceed with the PCI of his mid RCA, which resulted in a complete regain of arterial
vessel diameter (100% blockage to 0% blockage). As Mr. R. suffered an episode of vomiting
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in the cath lab, non-bilious non-bloody, another oral dose of 300mg aspirin and 60mg
prasugrel was administered. There were no other complications of his presenting complaint,
of the angiography and contrast, or of the PCI such as arrhythmias, ventricular failure and
cardiogenic shock.
Status post PCI, patient was alert and not in respiratory distress, though he still complained of
chest pain, now 3/10 on the pain score. Vitals were normal (BP 107/78, HR 77, SpO 2 100%
on room air). Pulse was regular, S1 and S2 heart sounds heard without any murmurs, lungs
were clear. Examination of the right groin was normal with no hematoma seen at the access
site. Distal pulses were all 2+.
The team decided to do 2 more sets of ACS and ECG to assess progression of STEMI. Plan
was made for post-PCI dual antiplatelet therapy with aspirin 100mg OM and prasugrel 10mg
OM for a year as well as atorvastatin 40mg ON and carvedilol 3.125mg BD. Patient was
extensively and thoroughly encouraged by the team to be compliant with the medications.

Investigational Results
Lab
Inx

Results

Cardia
c
marker
s

PT/INR
and
aPTT

Full
Blood
Count

Discussion

Troponin I:
0.364()
(normal 0.0000.039)
CK: 130
(normal 30-350)
CK-MB: 3.2
(normal 1.0-6.0)
PT 12.8
INR 1.03
aPTT 24.1()
(normal 21.035.0)
RBC 6.02()
(normal 4.325.72)
WBC 8.90
Hb 19.2()
(normal 13.517.5)
Plt 257 Hct
53.5

Taken 12 minutes after presentation at the ED

(1132 hours).
Only Troponin I is high. This is possibly due to its
high sensitivity and characteristic responsiveness
in the acute setting. Myocardial infarction present.
In lieu of characteristic ECG, STEMI diagnosed
Activated Partial Thromboplastin Time low. This
may be the etiology of patients ischemia.
However, this by itself is considered to have little
clinical relevance, though some research indicates
that it might increase risk of thromboembolism.
High RBC count. May be a response to chronic
ischemia or smoking. To rule out polycythemia
rubra vera as an etiology of patients ischemia. To
recheck FBC again tomorrow for trending.
Hb high, also possibly in response to chronic
smoking/ischemia.

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Renal
Panel

POCT
(pointof-care
testing
)

Na 139 K 4.1
Creatinine 84
Urea 2.7
Glucose 8.1()
(normal 4.0-7.8)
Anion Gap
20()
(normal 10-18)

1236h
rs
6.5

2006h
rs
6.9

Electrolytes normal. Also done to ascertain if the

polycythemia has a renal etiology.
Random blood glucose high. Possibly pre-diabetic
or diabetic
Anion gap of 20. Probably benign, no significant
cardiovascular causes of high anion gap.
To investigate high random blood glucose taken in
renal panel and as a workup for metabolic
syndrome.
Coupled with a fasting glucose, fasting lipid panel
and HbA1c subsequently done in a non-acute
setting.

After considering the ECG, raised cardiac markers, mRCA blockage seen on coronary
angiogram, and the subsequent successful relief of blockage and pain through an emergency
PCI, the diagnosis is as follows:
Acute Inferior ST Elevation Myocardial Infarction
on a background of coronary heart disease and non-compliance to dual antiplatelet therapy

Mr. .R. was subsequently shifted to Coronary Care Unit (Ward 28), where the right groin
access site appeared to start oozing blood (1455 hours). The CCU MO was informed and
compression was done for 10 minutes. Pressure bandages were subsequently applied for 1
hour with releases at 15 minute intervals. Bandages were removed at 1650 hours. At the
CCU, a cardiac rehabilitation plan was also emplaced which is run by the CCU Cardiac
Rehab Nurse.
Reflectio
n
13/11/14
(Day 1/5)

Evaluation of Mr. R.s Condition

Mr. R. presented with a sudden onset, poorly generalized chest pain associated with
shortness of breath, cold sweats, dizziness and a generalized feeling of weakness. This
cluster of symptoms is highly indicative of an acute coronary syndrome like an AMI. In fact it
was so evident that the SCDF paramedics started empirically administering GTN and aspirin.
While I admit that it is within their protocol to do so for any patient with chest pain, I am sure
that they were able to diagnose this as well with all their experience dealing with acute
conditions. There is a thin line between overzealously ruling out other differential diagnoses
like an aortic dissection, and blindly going straight for a PCI and giving anticoagulation
therapy. This problem can be overcome by taking an ECG and measuring cardiac markers,
the former often taking less than a minute.
In reality, such patients with characteristic ST elevations on ECG will immediately be rushed
to the CCU after the necessary bloods and tests are done. However, for academic sake, I will
discuss the differential diagnoses of chest pain. As there are many, I will broadly classify them
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according to organ systems as follows:

Cardiovascular: Aortic Dissection, Ruptured Aortic Aneurysm, and other ischemic

heart syndromes like unstable angina and NSTEMI (Non-ST elevated myocardial
infarction)
Respiratory: Pulmonary Embolism, Spontaneous Pneumothorax
Gastrointestinal: Gastroesophageal Reflux Disease (GERD)
Musculoskeletal: Costochondritis, Trauma (rib fractures)

The medical history of a past angina and STEMI was strong evidence to support our working
diagnosis of a STEMI. There was no significant medical history that would allude to any of the
differential diagnoses. The pain wasnt tearing in nature, and did not radiate to the back as
might be expected in a dissection. Although patient does smoke, it is extremely rare to find an
aortic aneurysm in such a young patient, much less a ruptured one. Patient also presented
much too well clinically to have a ruptured aneurysm, with a BP of 121/72 and a HR of 84
bpm. Patient also did not present with cyanosis, hemoptysis, or petechiae over his chest or
face that might indicate a PE. Both sides of his chest also moved symmetrically in respiration,
with no ascertainable difference in air entry upon auscultation. No acid reflux symptoms were
elicited. As pain was generalized instead of focal, and that of a crushing instead of a stabbing
nature, constochondritis is also unlikely. No history of trauma was present in Mr. R.s case.
Other factors that might indicate a STEMI would also include his gender (males higher risk),
race (Indians higher risk), history of drinking and smoking, slight obesity (BMI 27.3), noncompliance to medications (antiplatelets and statins) and occupation (shift work, long hours,
bad diet).
When an ECG was done, ST elevations were noted in the inferior leads, i.e. II, III and aVF.
Although ST elevations can occur in many other pathologies as well, such as myocarditis and
pericarditis, the findings consistent with a STEMI are as follows:
New ST elevation at the J point in 2 contiguous leads (in this case, leads II and III)
0.1 mV (1 mm) in all leads other than V2-V3, where the following diagnostic
threshold applies: 0.2 mV (2 mm)
Reciprocal ST inversions in leads V1, V2 and aVL
This provisional diagnosis was further supported by elevations in Troponin I. However, even
with concomitantly positive ECG and cardiac marker findings another possible diagnosis
would be acute myocarditis, which can also present with ST segment elevations and high
Troponin I. In a series of 60 patients who presented with a possible AMI but eventually turned
out negative, 50% had features of acute myocarditis. 8
Although his serum Troponin I was significantly raised, his CK and CK-MB levels were within
normal ranges. This is possibly due to Troponin I typically being the most responsive as more
Troponin is found in the heart per gram of myocardium. Troponin is also known to have a
higher sensitivity and specificity for myocardial infarctions as compared with creatine kinase
MB (CK-MB), as 18% of people with MI eventually turn out to have elevated troponin but
normal CK-MB values.4

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Figure 3: Graph of Cardiac Marker Concentrations against Time (in days) 6

Management
Cardiac markers can also be utilized for prognostication. In a recent study, in-hospital
mortality was highest when both troponin and CK-MB were positive (7.7%), intermediate
in troponin-positive/CK-MB-negative patients (3.9%), and lowest in patients in whom both
markers were negative and those who were troponin-negative/CK-MB-positive (1.7% and
2.3%, respectively).2 Another method of prognostication would be the Framingham Risk
Score, which estimates the 10-year cardiovascular risk of an individual. In lieu of Mr. R.s age,
total cholesterol and HDL levels (mentioned later), systolic blood pressure, and smoking
habit, it is estimated that he has an 11.4% risk of a heart attack in the next 10 years.
Mr. R. was prescribed with dual antiplatelet therapy (aspirin 100mg and prasugrel 10mg) of a
1 year duration in order to reduce the likelihood of another acute coronary syndrome. This
would also help to endothelialize the stent within the vessel wall and prevent stent
thrombosis. Also, based on 2013 ACC/AHA guidelines, patients with clinical atherosclerotic
cardiovascular disease will benefit from statin therapy. Mr. R. was therefore also prescribed
with atorvastatin 40mg. In Mr. R.s case, there was no sign of left heart failure such as lung
crepitations, or orthopnea, and IV furosemide (Lasix) was therefore not indicated. I would
consider giving him some morphine sulfate for his persistent discomfort, though in view of the
high priority given to PCI, there was insufficient time for that. His discomfort was also
expected to decrease status post PCI.
As mentioned above, a cardiac rehabilitation plan was also emplaced which is run by the
CCU Cardiac Rehab Nurse. The plan constituents include the explaining of patients heart
condition, reinforcement of treatment modalities, recognition of signs and symptoms of a
heart attack, dietitian and physiotherapist referrals, smoking cessation, and compliance to
medications and given TCU dates. I feel that this is especially important as a key etiologic
factor in Mr. R.s case is his noncompliance to medications, as well as his unhealthy diet and
daily activity, even after a past episode of STEMI with successful stenting. Some degree of
effort would therefore be required in this case to encourage proper medication compliance as
well as diet and lifestyle modifications.

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Events

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14/11/14
0600hrs
(Day 2/5)

Mr. R. was reviewed last night by the on-call cardiovascular medicine (CVM) MO as he
complained of persistent chest pain. His vitals were noted to be normal. A physical
examination of his heart and respiratory system also returned normal. Another ACS screen
was taken, as well as an ECG at 1917 hours which showed a possibly evolved inferior
STEMI, with new Q waves detected in the inferior leads. Mr. R. was also reviewed by the
CCU team during their morning rounds.

Coronary
Care Unit
(CCU)

Subjective
Mr. R.s pain seems to have resolved by the CCU morning rounds, and appears both alert
and comfortable at rest. He is not on any supplementary oxygen and is not in any respiratory
distress.
Objective
T: Afebrile
BP: 110/67 mmHg
HR: 58 bpm
RR: 20 bpm
SpO2: 98% on room air
On examination:
CVS: Pulse is regular. S1 S2 present. No murmurs heard. No signs of hypoperfusion, heart
failure, or fluid overload
Lungs: Clear, no basal crepitations
Abdomen: Soft non tender. Bowel sounds present
Right groin: 2X2cm hematoma over access site. Slightly tender upon palpation. No bruit.
Lower limbs: Distal pulses intact. Capillary refill time <2 seconds. Calves supple.
Results:
STEMI workup
1. Acute Coronary Syndrome Panel
As of 14.11.14, the ACS panel has been taken 3 times, one at the acute ED setting, one in
the evening for his persistent chest pain, and one the next day for trending purposes. The
figures of the 3 cardiac markers used (Troponin I, CK and CK-MB) are depicted in Figure 4.
13.11.14
13.11.14
14.11.14
1132hrs
1917hrs
1227hrs
Troponin I
0.364
65.600
52.700
CK
7.42
2629.00
1638.00
CK-MB
3.2
131.0
78.6
Figure 4: Cardiac Markers, trending
2. ECG
ECGs were taken at the acute ED setting, immediately after PCI, in the evening for his
persistent chest pain, early next morning and at noon. This trending of ECGs showed a
gradual decrease in heart rate back to normal levels. The one taken early next morning
(14.11.14) even noted sinus bradycardia. The amplitude of the ST elevation characterizing his
STEMI also gradually decreased in the affected leads (II, III and aVF). No new ST elevations
or T wave inversions were noted. As mentioned earlier, Q waves were seen in the inferior
leads indicating prior myocardial infarction.
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Diabetes and metabolic syndrome workup
3. HbA1c: 5.8% (normal)
4. Fasting blood glucose: 6.2() Impaired fasting glucose
5. POCT: Results as follows. As noted, all the values are acceptably below 7.8
13.11.14
1236hr 2006hr
s
s
6.5
6.9

14.11.14
0356hr 1121hr
s
s
6.7
5.3

6. Lipid Panel: Cholesterol 6.48() TG 1.96 HDL 1.50 LDL 4.09

Hypercholesterolemia detected. Triglycerides, HDL and LDL levels desirable.
Polycythemia workup
7. Red Blood Cell (RBC) and Hb values in Full Blood Count (FBC): As noted, the RBC
values are elevated above the normal range of 4.30-5.70. The Hb values are also
elevated above the normal range of 13.5-17.5. Although both entities seem to be
improving, it is not prudent to trend if only 2 datapoints are present.

RBC
Hb

13.11.14
1132hrs
6.02()
19.2()

14.11.14
0405hrs
5.84()
18.8()

8. Erythropoietin: results still pending at time of writing.

Assessment
1. Inferior STEMI (Day 2) status post PCI
- Background of coronary heart disease
- Complicated by non-compliance to dual antiplatelet therapy
2. Prediabetic
Impaired Fasting Glucose 6.2%
3. Hypercholesterolemia
- Serum cholesterol 6.48
4. Polycythemia
- RBC count high
- B/g of chronic smoking
- TRO polycythemia rubra vera
Plan
1.
2.
3.
4.
5.
6.
7.
8.

2D Echocardiography
To monitor ACS and ECG
To monitor right groin PCI access site, and to KIV ultrasound if worsening
Atorvastatin 40mg ON discontinued. On same day, restarted at 5mg ON by another
doctor
Lisinopril 2.5mg OM started
Diazepam 5mg single dose for delirium tremens prophylaxis
Thiamine 100mg OM for Wernickes prophylaxis
Physiotherapist review post PCI education regarding topics such as the signs and
symptoms of ACS and Phase
the usage
of GTN. Similar to CCU cardiac rehabilitation plan
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Reflectio
n
14/11/14
(Day 2/5)

Events
Evaluation of Mr. R.s Condition
It is important to continue doing ACS screens and ECGs to regularly trend and monitor the
patients coronary ischemia as it might progress and evolve. A second episode might also
occur in the days after. Doing so will also help in prognostication, and in gauging the severity
of complications. As can be seen in Figure 4, all 3 cardiac markers seem to be dropping,
objectively indicating the remission of the STEMI. This can be positively correlated with the
clinical findings and improvement of symptoms.
Management
Interestingly, the dosage of statins (atorvastatin) kept being modified as different doctors saw
the same patient. On day 1, 40mg ON was prescribed. This was then completely removed on
day 2 with the argument that statins are contraindicated in myopathy and rhabdomyolysis, 5
which was evident through the diagnosis of a STEMI and the high cardiac markers. The 3 rd
doctor that saw Mr. R. represcribed, but at a lower dose of 5mg ON with a KIV increase to
20mg ON when the CK values started dropping. Subsequent cardiac markers monitoring
would only include CK values to both monitor for statin complications, and to ensure that the
downtrending continues. The doctors involved varied in experience (MO vs senior consultant
ultimately it is obvious who had final say). This reminded me of the artistic nature of
medicine, and that there may never be a definitive right answer. Although it is quite well
accepted that statins do help in the acute post-AMI setting, 7 there is also the possibility of
contraindications and complications. Every patient is different and unique and although
pathways like the aforementioned ACS Algorithm do attempt to standardize treatment
regardless of practitioner, some scenarios have yet to be sufficiently researched and planned
for.
It is also important to treat the patient as a whole, and to remember that we are general
practitioners first, especially in this climate of clinical specialization. This was reinforced
through the screening of other cardiovascular and metabolic factors through a DM screen,
FBC, and a lipid panel, after noting patients past medical history of hyperlipidemia and his
smoking history. All turned out positive, with an impaired fasting glucose level of 6.2, a
polycythemic reading of 6.02, and a high cholesterol of 6.48 indicating possible
hypercholesterolemia. It would also be ideal to correlate these laboratory findings with clinical
signs and symptoms, asking for further risk factors in terms of dietary habits, exercise habits,
relevant symptoms including polyuria and polydipsia, and relevant signs on physical
examination including palmar erythema and xanthelasma.
Metabolic syndrome is a disorder of energy utilization and storage that increases the risk of
cardiovascular diseases such as diabetes and coronary heart disease. This is noted to be
present in 37% of patients with premature coronary artery disease (occurrence at an age <45
years old).1 Metabolic syndrome however, is diagnosed with the presence of 3 out of 5 of the
following: central obesity, elevated fasting plasma glucose, elevated TG, elevated BP, or low
HDL. In Mr. R.s case, the only criteria positive is the fasting plasma glucose, though there is
a possibility that more might be met in the near future if medication compliance, activity
modifications and diet interventions are not emplaced, especially in view of his currently high
BMI of 27.3. This highlights the importance of allied health professionals such as the cardiac
care nurse, physiotherapist and dietitian, who were instrumental players in this particular
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case.
It is also interesting to note the usage of diazepam and thiamine for his alcoholism, reiterating
the importance of a thorough and accurate history. As his regular alcohol intake consisted of
3 bottles of beer (approximately 665ml per bottle, making up 10 units of alcohol) per day, it
would be understandable to err on the side of precaution. This is especially as it is imperative
that he stay in hospital for at least 3-4 days in lieu of his acute condition, and because there is
no ration of alcohol in Singapore hospitals as of yet. Thiamine and diazepam administration is
typical in incidences where alcoholism is suspected, thiamine more often than diazepam
because of the relative lack of side effects and complications. In this case, both seem to have
been effective with no neurological sequelae noted throughout inpatient stay.

Date

Events

15/11/14
0720hrs
(Day 3/5)

Subjective
No overnight events. Mr. R. alert and comfortable at rest. No chest pain or shortness of
breath. Groin PCI access site better.

Coronary
Care Unit
(CCU)

Objective
T: Afebrile
BP: 84/56 mmHg
HR: 74 bpm
RR: 18 bpm
SpO2: 98% on room air
On examination:
CVS: Pulse is regular. S1 S2 present. No murmurs heard. Low BP noted.
Lungs: Clear, no basal crepitations
Abdomen: Soft non tender. Bowel sounds present
Right groin: 2X2cm hematoma over access site. Non-tender upon palpation. No bruit
heard.
Lower limbs: Distal pulses intact. Calves supple.
Results:
1. Acute Coronary Syndrome Panel
13.11.14
13.11.14
14.11.14
1132hrs
1917hrs
1227hrs
Troponin I
0.364
65.600
52.700
CK
7.42
2629.00
1638.00
CK-MB
3.2
131.0
78.6
Figure 5: Cardiac Markers, trending

15.11.14
0905hrs
Not done
663.00
Not done

2. ECG
Similar to that of previous ECGs, there was no indication of a new infarct. ST interval
was still mildly elevated in the inferior leads.
Phase III Medicine Clinical Posting Reflective Journal l Page 14

_________________________________________________________________________________________

Date

Events

Assessment
1. Inferior STEMI (Day 2) status post PCI
- Background of coronary heart disease
- Complicated by non-compliance to dual antiplatelet therapy
2. Prediabetic
Impaired Fasting Glucose 6.2%
3. Hypercholesterolemia
- Serum cholesterol 6.48
4. Polycythemia
- RBC count high
- B/g of chronic smoking
- TRO polycythemia rubra vera
Plan
1. Transferred down to General Ward (Ward 63)
2. Telemetry ordered
3. Atorvastatin increased to 20mg ON from 5mg as CK was noted to drop from
1638 to 663
4. Lisinopril temporarily stopped in view of low BP
Reflection
15/11/14
(Day 4/5)

Management
In view of Mr. R.s improving condition, he was subsequently shifted to the cardiology
General Ward, where telemetry could be carried out. He however, developed
hypotension of 84/56 mmHg. Any drastic drop in BP could be a sign of reduced ejection
fraction that can result from an AMI. Another ACS panel and ECG subsequently done
which disproved his possibility. The CK was noted to continue downtrending (1638
663), while the ECG also returned without any new anomalies. This drop in blood
pressure was therefore attributed to the lisinopril which he was started on yesterday at
2.5mg OM.
In view of the aforementioned drop in CK, atorvastatin was also increased to 20mg ON
as per previous orders. This was due to perceptions that the complications of statin use
(rhabdomyolysis) were not present in this patient. Benefits of statins therefore
outweighed the potential risks.
The right groin access site was also noted to no longer be tender to palpation, though
the hematoma was still noted to be present. Both the CK-statin and the PCI-hematoma
issue are examples of complications and benefit-risk analyses that must be made in
medicine. Despite the iatrogenic nature of the hematoma, it is no debate that the PCI
was essential and literally life-saving in this case. It is therefore crucial to alleviate and
reduce the severity of these complications and risks with proper monitoring and clinical
knowledge.

Phase III Medicine Clinical Posting Reflective Journal l Page 15

_________________________________________________________________________________________

Date

Events

16/11/14
0824hrs
(Day 4/5)

Subjective
No overnight events. Mr. R. alert and comfortable at rest.

Ward 63
(Cardio)

Objective
T: Afebrile
BP: 106/65 mmHg
HR: 75
RR: 20
SpO2: 98% on room air
On examination:
CVS: Pulse is regular. S1 S2 present. No murmurs heard. BP back to baseline levels
Lungs: Clear, no basal crepitations
Abdomen: Soft non tender. Bowel sounds present
Right groin: 2X2cm hematoma over access site. Non-tender upon palpation. No bruit.
Lower limbs: Calves supple.
Results:
1. Telemetry: Came back normal with no abnormalities detected
Assessment
1. Inferior STEMI (Day 2) status post PCI
- Background of coronary heart disease
- Complicated by non-compliance to dual antiplatelet therapy
2. Prediabetic
Impaired Fasting Glucose 6.2%
3. Hypercholesterolemia
- Serum cholesterol 6.48
4. Polycythemia
- RBC count high
- B/g of chronic smoking
- TRO polycythemia rubra vera
Plan
1.
2.
3.
4.
5.
6.
7.

Reflection
16/11/14
(Day 4/5)

To do a final ECG and CK

Chase 2DE
Lisinopril restarted at 2.5mg OM
FBC
Hematology outpatient review TRO polycythemia rubra vera
Spirometry and Lung Function Test as workup for chronic smoking
Alcohol counselling

Evaluation of Mr. R.s Condition

I find it useful to always ask myself if a patient can be discharged on that particular day,
and if not, what was keeping him/her in the wards. For Mr. R., the regular monitoring of
his cardiac condition through cardiac marker screens and ECGs have been thankfully
free from any progressions or new episodes. His telemetry also returned unremarkable.
Phase III Medicine Clinical Posting Reflective Journal l Page 16

_________________________________________________________________________________________

Date

Events
A final ECG and CK was therefore planned for him today in order to obtain a possible
baseline prior to discharge. His 2DE which was planned for since 2 days ago was also
yet to be done. Attempts were therefore made to chase the 2DE appointment so that Mr.
R. could be sent home if no thrombus or other life-threatening pathologies were
detected.
With the coronary management and follow-up completed, effort was also spent to
workup his problem list, with another FBC, a referral to Hematology, spirometry and lung
function tests to gauge the extent of his smoking complications and to obtain a baseline,
and a referral for alcohol counselling. It would also be ideal to provide him with an option
to follow up with Psychiatry for disulfiram medications. These help to ensure alcohol
abstinence through the severely unpleasant effects felt if a patient takes even a small
amount of alcohol while on it.
Another example of benefit-risk analyses is also depicted here, with the principal team
restarting Mr. R. on lisinopril at the same dosage (2.5mg OM) despite him experiencing a
hypotensive response just a few days ago. This however appeared to be a once-off
episode, with no reports of hypotension since.

Date

Events

17/11/14
0810hrs
(Day 5/5)

Nil complaints, feels well. Patient discharged with the following vitals and findings on
physical examination:

Ward 63
(Cardio)

Objective
T: Afebrile
BP: 131/87 mmHg
HR: 85
RR: 20
SpO2: 96% on room air
On examination:
CVS: Pulse is regular. S1 S2 present. No murmurs heard. BP now noted to be high.
However, when compared to other BP values taken before and after, the mean systolic
pressure is around the 95-100 range.
Lungs: Clear
Abdomen: Soft non tender.
Lower limbs: Calves supple, no pedal edema.

Phase III Medicine Clinical Posting Reflective Journal l Page 17

_________________________________________________________________________________________

Date

Events
Results:
1. Acute Coronary Syndrome Panel

Troponin I
CK
CK-MB

13.11.14
13.11.14
14.11.14
15.11.14
1132hrs
1917hrs
1227hrs
0905hrs
0.364
65.600
52.700
Not done
7.42
2629.00
1638.00
663.00
3.2
131.0
78.6
Not done
Figure 5: Cardiac Markers, trending

17.11.14
0848hrs
Not done
188.00
Not done

2. ECG
Another ECG was done along with the ACS panel for trending and monitoring purposes.
Similar to that of previous ECGs, there was no indication of a new infarct. ST interval
was still mildly elevated in the inferior leads.
3. Red Blood Cell (RBC) and Hb values in Full Blood Count (FBC):

RBC
Hb

13.11.14
1132hrs
6.02()
19.2()

14.11.14
0405hrs
5.84()
18.8()

17.11.14
0848hrs
5.45
17.4

4. 2DE
Normal, without any complications of the STEMI noted, such as wall motion
abnormalities, valve lesions, and a poor ejection fraction.
5.
-

Spirometry/Lung Function Test

FEV1: 79%, FVC: 75% (both <80%, abnormal)
FEV1/FVC: 83% (possibly restrictive nature)
Total Lung Capacity: 61% (confirmed to be restrictive in nature)
Diffusion Capacity of the Lungs for Carbon Monoxide (DLCO): 74% (<80%,
intrapulmonary restrictive pathology)

D/C TCU Dr Mark Chan in 1/12 with the following outpatient medications:
1. Aspirin 100mg OM X 2/12
2. Prasugrel 10mg OM X 2/12 (Dual antiplatelet therapy)
3. GTN 0.5mg PRN
4. Atorvastatin 20mg ON X 2/12
5. Carvedilol 6.25mg BD X 2/12
6. Lisinopril 2.5mg OM X 2/12
7. Vitamin B OM X 2/12
8. Diazepam 5mg BD X 1/7, then ON X 1/7

Patient discharged on 17/11/2014, 1142hours.

Phase III Medicine Clinical Posting Reflective Journal l Page 18

_________________________________________________________________________________________

Date

Events

Reflection
17/11/14
(Day 5/5)

Creatine Kinase values showed an appreciable drop from 663 on Day 3 to 188 on Day 5.
The 2DE results also returned unremarkable. Although the RBC and Hb values have
also now returned to normal (5.45 and 17.4 respectively), the team went ahead with the
TCU with Hematology in view of a strong suspicion of secondary polycythemia
secondary to smoking or polycythemia rubra vera, although it could also very well be an
incidental benign finding or a transient polycythemia. The spirometry/lung function
test/DLCO done also returned with results indicative of an intrapulmonary restrictive lung
pathology that is reducing total lung function. This is possibly due to his long smoking
habit.
Ischemic heart disease is a common but unfortunate disease. Although it is estimated
that 15 people in Singapore die from cardiovascular diseases (heart attacks and strokes)
every day, the total percentage of deaths due to these has decreased from 31.6% in
2009 to 30.4% in 2011.9 This may be due to government efforts in raising awareness and
actively promoting healthy lifestyles through agencies like the Health Promotion Board
and the Singapore Heart Foundation. I hope that this trend will continue with more
Singaporeans becoming aware of cardiovascular risk factors and means of modifying
them, such as through medication compliance, healthy lifestyles and diets, and the
cessation of smoking and drinking habits.
I feel that the management of Mr. Rs case has been satisfactory. All of his presenting
issues have been addressed suitably and according to the current standards of care. A
multidisciplinary inter-professional approach has also been utilized in all aspects of
patient care and decision making.

References:
1. Fauci, A. (2012). Harrisons Principles of Internal Medicine Self-Assessment and Board Review 18th
Edition. McGraw-Hill Professional.
2. Goodman, S., Steg, P., Eagle, K., Fox, K., Lpez-Sendn, J., Montalescot, G., ... Gurfinkel, E. (2006).
The diagnostic and prognostic impact of the redefinition of acute myocardial infarction: Lessons from the
Global Registry of Acute Coronary Events (GRACE). American Heart Journal, 151(3), 654-660.
3. Korte, M., Clarke, M., & Lefkowitz, M. (2000). Short Activated Partial Thromboplastin Times Are Related
to Increased Thrombin Generation and an Increased Risk for Thromboembolism. American Journal of
Clinical Pathology, 113(1), 123-127.
4. Saenger, A., & Jaffe, A. (2008). Requiem For A Heavyweight: The Demise Of Creatine Kinase-MB.
Circulation, 118(21), 2200-2206. Retrieved November 20, 2014.
5. Savage, R., & Tatley, M. (2004). Myopathy with Statins: Check CK Levels and Interactions. Prescriber
Update,
25(1),
4-5.
Retrieved
November
19,
2014,
from
http://www.medsafe.govt.nz/profs/puarticles/Statinmyop.htm
6. Siemens Corporation. (2014, January 1). Cardiac Troponin. Retrieved November 17, 2014, from
http://usa.healthcare.siemens.com/clinical-specialities/cardiovascular/laboratoryexpert/education/content/troponin/
7. Teshima, Y., Yufu, K., Akioka, H., Iwao, T., Anan, F., Nakagawa, M., ... Saikawa, T. (2009). Early
atorvastatin therapy improves cardiac function in patients with acute myocardial infarction. Journal of
Cardiology, 53(1), 58-64.
8. Villata, G., Bollati, M., Gambino, A., Biondi-Zoccai, G., & Sheiban, I. (2007). Comment on the 'pilot'
GRACIA-2 randomized trial. European Heart Journal, 28(19), 2417-2418.

9.

Singapore Heart Foundation. (n.d.). Singapore Heart Foundation. Retrieved November 23, 2014, from
http://www.myheart.org.sg
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