CASE STUDY

Background
Case studies are based upon the real cases that are quite commonly encountered in the
every day practice of medicine and pharmacy. How the cases are presented and what a
pharmacist has to play a role is the basic theme of these case studies.

Learning objectives
Following are the learning objectives of the case studies:

• To have the knowledge of the disease and particular condition under

consideration
• What routine tests should be carried out once the patient is brought to the
emergency of a hospital
• To identify the practical implication of CORE, PRIME and FARM in a
pharmaceutical care
• What initial drugs may be prescribed
• Rationale for the use of different drugs and treatments used
• How a pharmaceutical care is planned (PWDT)
• How the drug therapy is monitored
• How the outcome of the therapy may be evaluated

Hashmi Furqan UCP, PU

CASE STUDY 01
52 years old Mr. ABC is brought to the hospital emergency following the onset of chest
pain approximately two hours earlier while he was replacing some plumbing in a house.
He tried several doses of sublingual glyceryl trinitrate (GTN), but his pain had not
resolved. He became increasingly breathless and clammy with tight crushing pain across
his chest and left shoulder. His past medical history reveals him as a patient of angina.
Mr. ABC was noted to be as obese; his past drug history revealed on admission was
nifedipine and isosorbide mononitrate (doses unknown at the time of admission).

On examination: blood pressure 150 / 110 mmHg with heart rate 112 beats / minute

Discussion:
Whenever such patient is with the presenting complaints is brought to the emergency
patient having typical attack of angina, it is suspected that patient is suffering from
myocardial infarction.

There are several questions which need to be addressed in dealing such type of patient.
SATGE I
Questions
1. What routine tests should be carried out to confirm a diagnosis of acute
myocardial infarction (AMI)?

Mr. ABC was initially prescribed one dose of each of the following drugs:
• Morphine 2.5mg I.V
• Metoclopramide 10mg I.V
• Aspirin 300mg P.O
2. What actions of morphine are particularly useful in AMI?
3. Why is metoclopramide necessary? What alternative anti-emetics could be
considered?
4. Why should intramuscular injections generally be avoided in patient suffering
with AMI?
5. What is the rationale for aspirin administration during AMI?
6. What other therapies should be considered at this stage?

The first step that is usually taken for such type of patients is ECG.
ECG revealed ST elevation (2—3mm) in leads V2—V4 which shows an evidence of
ischemia in the lateral leads indicating that Mr. ABC has suffered an anterior MI.

Having done ECG has revealed a typical case of AMI. The ECG is followed by routine
laboratory tests. Blood sample is drawn and sent to laboratory.
Laboratory findings
• Qualitative troponin (negative) (trop-T test)

Hashmi Furqan UCP, PU

 • Creatine kinase (CK) result not yet available (see discussion portion)
• Sodium 138mmol/L (135—145mmol/L)
• Potassium 3.8mmol/L (3.5—5.0mmol/L)
• Creatinine 104mmol/L (45—120)
• Urea 6mmol/L (3.3—6.7mmol/L)
• Glucose 18mmol/L (3—7.8mmol/L)
• Hb 14.2g (14—18)
• RBC 6.4 x 1012 /L (4.6—6.5)
• WBC 6.1 x 109 /L (4—11)
• Platelets 167 x 109 (150—400)

STAGE II

DAY 1 FINDING

On basis of analysis of the ECG a decision should be taken to thrombolyse Mr. ABC.
• A bolus dose of streptokinase (1 h infusion) / tenecteplace 50mg / alteplase (bolus
+ 90 min infusion) was administered.
• I.V heparin
• Sliding scale insulin infusion (high blood sugar as found in the lab report)

7. What is the rationale for thrombolysis in the management of AMI?

8. When should thrombolysis be administered to gain maximal benefit?
9. What are the contra-indications to thrombolysis?
10. What pharmaceutical issues should be considered when choosing a thrombolytic?
11. What monitoring should be undertaken for patients prescribed and administered
thrombolytic therapy?
12. What alternative strategies could be employed when thrombolysis is contra-
indicated?
13. Is I.V heparin indicated for this patient?
14. What other therapies might be considered at this stage?

Since Mr. ABC was successfully thrombolysed it should be transferred to coronary care
unit for further and better care.
On the arrival to CCU Mr. ABC was still breathless although his chest pain was resolved.
A repeat ECG is recommended at this stage—showed resolution of ST segment
indicating a successful thrombolysis.
As the patient is still breathless at this stage, chest X-ray should be requested—the X-ray
showed pulmonary edema. At this stage blood gas estimation should be done (pulse-
oxymetry can also be used). As a result of pulmonary edema the oxygen saturation is
usually reduced. So on this basis an oxygen therapy should be initiated.
For pulmonary edema furosemide I.V (dose selected on the basis of severity of edema)
should be infused over a period of 20 minutes.

Hashmi Furqan UCP, PU

Blood pressure and heart rate are monitored periodically (usually the ECG monitors
showing all parameters are in place as long as patient is kept in CCU).

At this stage B.P = 105/65 mmHg and HR 103 beats/min

Mr. ABC prescribed with

• Morphine 2.5—5 mg I.V (as required)
• Metoclopramide 10mg I.V q 8hr (may be PO depending upon patient condition)
• GTN 400mcg S/L (when required)
• Humidified oxygen at 4L/min
• Human insulin 50U in 500ml to run over 24hr s (sliding scale)
• Aspirin 75mg PO daily

STAGE II

DAY 2 FINDINGS

Following IV furosemide (three doses) Mr. ABC settled with no further episodes of chest
pain and oxygen saturation also improved. A repeat X-ray showed a good response to
diuretic therapy with resolution of pulmonary edema.
On the ward round a cardiac echo was requested alongside repeat blood tests.

B.P = 94/63mmHg HR = 88 beats / min

Laboratory results

• Na 143 mmol/L (135—145)

• K 3.1 mmol/L (3.5—5.0)
• Glucose 4.8 mmol/L (3—7.8)
• Urea 5 mmol/L (3.3—6.7)
• Creatinine 110 micromol/L (45—120)
• Hb 13.2g/dL (14—18)
• RBC 5.2 x 1012 /L (4.5—6.5)
• WBC 6.0 x 109 /L (4—11)
• Platelets 172 x 109 /L (150—400)

Total cholesterol 5.6 mmol/L

Triglycerides 4.2 mmol/L

On the basis of the above report there are several questions of concern

15. Outline a pharmaceutical care plan for Mr. ABC.

16. Why is his potassium level a cause of concern? What other electrolytes should be
monitored closely?
17. Comment on drugs Mr. ABC was taking prior to admission.

Hashmi Furqan UCP, PU

DAY 2 (PM)

Mr. ABC continued to respond well to treatment and was beginning to mobilize (BP =
92/50mmHg and HR = 72 beats/min)

Echocardiography report: marked hypokinesia of anteroseptal region of left ventricle

Ejection fraction of 35—40%-- indicating compromised
ventricular function.
Mr. ABC was started Ramipril 1.25mg initially then 2.5mg twice daily plus Pravastatin*
20mg at night.

Further questions of concern that may arise:

18. What is the rationale for ACE-I post-MI?

19. Should beta-blocker therapy be considered?
20. What advice should be given for initiation of beta-blockers?
21. Comment on Mr. ABC’s cholesterol.
22. How should the cholesterol be addressed?
23. How should the blood sugar levels be controlled over longer term?

DAY 5

Mr. ABC has made a good progress over past three days although he complained about
the dry cough.

• BP = 95/56mmHg HR 58 beats/min
• Na 141 mmol/L
• K 4.2 mmol/L
• Glucose 5.1 mmol/L
• Urea 5.3 mmol/L
• Creatinine 121 micromol/L

On discharge he was stablished on following regimen

RX

• Aspirin 75mg PO daily

• Ramipril 2.5mg PO q 12hr
• Carvedilol 3.125mg PO q 12hr
• Pravastatin 40mg PO daily at night
• Human insulin 70/30 8U in morning 10U evening
• GTN S/L as required

Hashmi Furqan UCP, PU

 24. What lifestyle issues should be discussed?
25. What issues should be highlighted during discharge counseling for this patient?

*Why a statin has been added? Why pravastatin?

No Questions Answers Discussion

1 What routine tests A 12-lead ECG should be • 12-lead ECG is the key diagnostic tool.
should be carried out to performed & blood • Cardiac enzyme measurements are used
confirm a diagnosis of sample for measurement to determine the presence or absence of
AMI? of troponin and/or myocardial necrosis. CK and CK
creatine kinase (CK) isozymes are routinely used for the
levels diagnosis of AMI.
• Other markers include Myoglobin &
lactic dehydrogenase.
• Limitations—CK may be raised after
several hours of the onset of MI. CK-
MB is increased only after significant
damage have occurred (cannot detect
smaller areas of ischemic damage)
• Troponin levels are raised within 3—12
hrs after the onset of pain (even on
slight damage)
• Any increase in the level of these
biomarkers indicates some degree of
myocardial damage. But only ECG
changes can help diagnose AMI, also
called as STEMI.
• Repeat CK and Troponin may be used
to confirm the working diagnosis and
extent of damage in AMI.
2 What actions of Morphine has analgesic, • All of these effects are beneficial in
diamorphine are anxiolytic and AMI.
particularly useful in vasodialating effects • Analgesia is required to provide
AMI? immediate relief form chest pain
• Vasodilatation caused by this drug
improves the blood supply to
myocardium and contribute to anti-
ischemic effects
• The anxiolytic effects calm the patient
and help in the administration of further
therapy
3 Why is During the acute phase of • Cyclizine 50mg up to three times a day
metoclopramide MI majority of the would a suitable alternative; this agent
necessary? What patients suffer from may reduce the blood pressure quite
alternative anti-emetics significant nausea and significantly resulting in reduced
could be considered? vomiting. cardiac output.
Metoclopramide can
easily be administered I.V
for rapid onset of action

Hashmi Furqan UCP, PU

4 Why should Ck levels can be
intramuscular increased following IM
injections generally be injection, which may
avoided in patient confuse the diagnosis of
suffering with AMI? AMI. In addition IV
injection allows rapid and
predictable onset of
action.
5 What is the rationale In acute phase the
for aspirin administration of aspirin
administration during has been shown to reduce
AMI? mortality at 5 weeks by
approximately 23%
6 What other therapies At this stage the diagnosis
should be considered at in unclear. A number of
this stage? potential therapies should
therefore be under
consideration (STAGE-I)
7 What is the rationale Thrombolytic therapy has
for thrombolysis in the shown to reduce five-
management of AMI? week mortality in patients
suffering AMI by 18%
with benefits being
maintained for up to 10
years
8 When should Thrombolytic therapy
thrombolysis be should be administered as
administered to gain soon as possible after the
maximal benefit? onset of symptoms to gain
maximum benefit from
the treatment
Hashmi Furqan
• A number of non-cardiac problems
including cardiac resuscitation, IM
injection, diabetes mellitus, skeletal
muscle damage and alcoholism can
increase CK levels (limiting CK
usefulness in MI diagnosis)
• Troponin release is not entirely specific
to MI, it should be cautiously
interpreted in the presence of acute
renal failure.
• A study demonstrated that
administration of aspirin has reduced
mortality & morbidity associated with
AMI.
• A dose of 300mg should be
administered immediately regardless of
its prior use.
• Patient is advised to chew the tablet
before it is swallowed, which aids early
absorption
• Aspirin also shown to reduce the
occlusion and reinfarction
• Aspirin should be continued
indefinitely post-MI at a dose of 75—
150mg / day.
• Heparin, glycoprotein IIb/IIIa receptor
antagonists or thrombolysis with or
without I.V beta-blockers my be
indicated
• Patients with ongoing chest pain and
ventricular dysfunction may be
benefited from I.V GTN.
• Oxygen should be administered to
improve the supply to myocardium and
prevent further ischemic damage.
• Majority of MIs are caused by
obstruction of blood flow in coronary
arteries due to the formation of blood
clot.
• Thrombolytic therapy is targeted to
break the occluded thrombus via
fibrinolysis.
• Thrombolytic therapy limits the infarct
size, preserves left ventricular function
& reduces deaths.
• An early treatment has shown to reduce
the mortality and survival from AMI.
• Thrombolytic therapy has significant
benefits when administered within 12
hrs of onset of symptoms.
• Thrombolytic activity within 6 hrs has
more benefits than used within 12hrs
UCP, PU
9 What are contra- Absolute contra- • Absolute contra-indication—previous
indications to indication—therapy must hemorrhagic stroke, any
thrombolysis not be administered cerebrovascular event within the
Relative contra-indication previous year, active internal bleeding
—the benefits and risks of • Relative contra-indication—
therapy must be uncontrolled hypertension (systolic BP
considered for individual > 180mmHg), anticoagulant therapy or
patient requiring bleeding disorder, recent trauma or
treatment major surgery, pregnancy.
10 What pharmaceutical A number of issues • A number of thrombolytic agents are
issues should be should be considered like licensed and can be distinguished from
considered when comparative efficacy, one another on the basis of their
choosing a dose, method of pharmacokinetic and pharmacodynamic
thrombolytic? administration and profiles.
adverse effects • The significance of alteplase is that it is
free from any allergic potential
compared to streptokinase
• 65% of the total dose is given during
the first 30 minutes of 90 minute
infusion.
11 What monitoring Patients should be • Blood pressure monitoring
should be undertaken monitored closely (hypotension may occur), heart rate and
for patients prescribed throughout thrombolytic rhythm should be monitored
and administered therapy as they are at risk • ECG carried out after 90 minutes
thrombolytic therapy? of hemodynamic should show resolution of ST-segment
instability, reperfusion indicating a successful thrombolysis
arrhythmias or other
• Allergic may occur (streptokinase)
complications. Clinical
efficacy of the • Complications may be –hemorrhagic
thrombolysis should be stroke, haematuria, epistaxis,
assessed at 90 minutes haematemesis
with repeat ECG. • Full blood count should be done before
and after the therapy
• Patients are at risk for up to 4 days
following the administration of
thrombolytic therapy.
12 What alternative The most effective • In patients presenting late myocardial
strategies could be strategy for managing damage is likely to be irreversible
employed when AMI is primary • Standard therapies like heparin, GTN &
thrombolysis is contra- angioplasty, this has aspirin may be considered if there is
indicated? shown to be superior to ongoing pain with referral for early
thrombolytic therapy angioplasty.
• I.V beta-blockers may also be used to
reduce the occurrence of ischemia
related tachyarrythmias
13 Is I.V heparin indicated Yes, I.V heparin should • The adjunctive use of heparin is
in this patient be administered at the necessary to protect against reocclusion.
same time along with • Streptokinase should not be co-
other thrombolytic agents administered with heparin due to
& be continued for a greater risk of cerebral bleeding and
minimum period of 48hrs. requires transfusions.
The use of heparin during • I.V. dose should be weight adjusted and
thrombolysis is agent
initiated with a bolus dose
dependent.

Hashmi Furqan UCP, PU

 • Close monitoring of APTT is required.
14 What other therapies In view of this patient’s • An aggressive blood sugar control
might be considered at high glucose levels an approach is required
this stage? intensive insulin regimen • Sliding-scale insulin therapy is
should be initiated to recommended for first 24hrs with blood
ensure tight control of glucose levels raised above 11mmol/L
blood sugar in order to
improve survival
15 Outline pharmaceutical Pharmaceutical care plan • Ensure evidence-based strategies are
care plan is made to address the introduced in a timely manner
needs of the patient & to • Drugs initiated at an appropriate time &
handle any drug-related dose titrations are undertaken
problems that may arise • Monitor efficacy, drug interactions &
during the treatment
adverse effects. Notify relevant staff an
advise on alternatives if necessary
• Ensure nursing staff is administering
I.V therapy correctly
• Ensure secondary preventive therapies
are initiated
• Ensure adequate lifestyle advice is
given and the patient is being followed
up by appropriate specialist
• Ensure appropriate information on aims
of therapy, doses (post-discharge),
duration of treatment and monitoring
are provided
• Counsel the patient on discharge
including rationale for therapy,
appropriate monitoring, possible side
effects & how to deal with them and
how therapies should be continued in
future
16 Why potassium level a A reduction in serum K • Fall in serum K levels is secondary to
cause of concern? may predispose the excessive catecholamine release in
What other electrolytes patient to post-infarction response to pain and anxiety caused by
should be monitored arrhythmias. Serum Mg & AMI.
closely? Ca should also be • In addition repeated insulin
monitored & corrected to administration and diuretic therapy
further protect against reduces serum K levels.
arrhythmia. Serum Na,
creatinine & urea should • I.V or oral K-supplements can be used
be monitored throughout
diuretic therapy
17 Comment on drugs Mr. The drug therapy of Mr. • Nifedipine may increase early mortality
ABC was taking prior ABC on admission i.e. post-MI and is not associated with
to admission Nifedipine & isosorbide reduction in cardiac events. It should
mononitrate should be therefore be discontinued
reviewed • Isosorbide mononitrate is an effective
anti-anginal therapy, it has not shown to
improve outcomes in such patients,
more suitable alternatives with
secondary benfits may be considered

Hashmi Furqan UCP, PU

18 What is the rationale A number of reference
for ACEI post-MI? studies have demonstrated
How should ACEI the benefits of use of
therapy be initiated? ACEI post-MI
19 Should beta-blocker Beta-blockers have been
therapy be considered shown to reduce mortality
at this stage? and morbidity post-MI &
should therefore be
considered for Mr. ABC.
Consideration should be
made of his concurrent
heart failure and reduced
ventricular ejection
fraction, which may make
early use of beta-blockers
inappropriate and will
also influence the choice
of agent and dose regimen
chosen
20 What advice would Beta-blocker therapy
you give about the should be initiated
initiation of a beta- cautiously starting at low
blocker? dose with careful
monitoring of BP and HR
and symptoms of heart
failure. The patient’s
symptoms may be
aggravated during dose
adjustment; a diuretic
therapy may be required.
Occasionally a step-down
in beta-blocker dose may
be required.
Hashmi Furqan
• ACEI therapy should be initiated in all
patients post-MI.
• The greatest benefits from therapy are
seen in patients with reduced
ventricular ejection fraction, anterior
infracts or tachycardia (refer to the
echocardiography report)
• An early initiation of ACEI (within
24hrs) is recommended.
• ACEI should be initiated at low doses
to avoid the problem of first-dose
hypotension (Mr. ABC’s BP & HR
should be monitored closely)
• Early use of IV beta-blockers is
recommended in most of the case but in
case of Mr. ABC its early use is
inappropriate because of left ventricular
dysfunction (echo cardiography).
• Beta-blocker therapy may be initiated
after few days based upon the evidence
that this patient remains clinically
stable. Carvedilol may be used (see
reference link ).
• The concomitant use of ACEI and beta-
blockers post-MI is recommended.
ACEI therapy should be optimized
before the addition of beta blockers
• Sometimes the concomitant use of both
ACEI and beta-blockers may be limited
on the basis of consistent low BP.
• Mr. ABC as found in the echo report
has left ventricular dysfunction
therefore the references found show that
beta-blockers may be used with caution
in such patients starting with low dose
and that requires monitoring of BP, HR
and blood gases as well
• It is always advisable that beta-blockers
should be initiated after a few days
followed by the settling of clinical
symptoms of the patient.
UCP, PU
21 Comment on Mr. Mr. ABC has raised • Cholesterol levels should be measured
ABC’s cholesterol. cholesterol level which within 24hrs of onset of symptoms, as
indicates an increased risk after 24hrs cholesterol levels have been
of coronary heart disease. shown to fall and remain low for
Lipid-lowering therapy approximately three months.
should be initiated as • In the case of Mr. ABC the cholesterol
reducing serum cannot be measured in fasting state
cholesterol has been therefore total cholesterol levels can be
shown to reduce the risk considered reliable.
of death, reinfarction or
other cardiovascular
events.
22 How should Mr. This patient should be • The patient is encouraged to reduce his
ABC’s cholesterol given dietary advice in total intake of fat in particular saturated
levels be managed? combination with fats.
initiation of a statin. • Increase intake of vegetables and fiber.
• If he smokes, cessation of smoking is
encouraged.
• Statin cause greater reduction in LDL.
Reducing cholesterol has reduced the
risks of death, reinfarction and other
cardiovascular events.

23 How should Mr. A S/C insulin regimen • The preferred regimen for this patient is
ABC’s blood sugar should be initiated on the combination of a long acting (basal)
levels be controlled cessation of his sliding- insulin with short-acting soluble insulin
over the longer term? scale I.V. insulin at meal time to mimic physiologic
insulin patterns.
• Patient assessment, careful selection of
insulin dose and administration device
and patient education is key to a
successful therapy

Hashmi Furqan UCP, PU

REFERENCES

• D.K.Scott, J.Dwight, coronary heart diseases, chpt. 20, Clinical Pharmacy &
therapeutics 4th ED. Roger Walker
• Linda J Dodds, Drugs in Use, 3rd ED
• Russell J Greene, Norman D Harris, Pathology & therapeutics for Pharmacists,
Chpt 3, Cardiovascular System.
• BNF 52, September 2007.
• David S. Tatro, Drug Interaction Facts 2008, The Authority on Drug
Interactions
• Stockley’s Drug Interaction 6th ED.
• James E. Tisdale, Drug-induced Cardiovascular Diseases. Kevin M. Swinski,
Ischemia and Myocardial Infarction.
• Brett Cucchiara, MD; Steven Messé, MD Scott E. Kasner, MD, Danger of
Treatment Protocols in MI.
• http://www.rxlist.com/cgi/generic/carvedilol_ids.htm (indicated in left ventricular
dysfunction following MI)

Ramipril  Aspirin

Hashmi Furqan UCP, PU