CASE STUDY

By:
SHIUNY SOLIH
IUTHISAM HASSAN LATHYF
NAASHITHA NAASIR
SUBAATHAA ABDHULLAH



INTRODUCTION
This case study is based on 82 year old patient Hussain Ahmed who resides at Jasthukafaage/ B.
eydhafushi with a family of 3 girls and 1 boy. He was an active fisherman and retired 15 years
back as his children didnt want him to work since he was getting old. Therefore in order to earn
for his family his son came to male. When we inquired about his diet, his son explains that his
father preferred eating spicy food and mostly had garudhiyya and rice and avoided vegetables
with less fluid intake. Moreover he also was a smoker, but he quit smoking 20 years back.
Furthermore his walking had decreased 3 years ago.
According to his son one week back his father started having breathing difficulty, chest pain
followed by fever and cough for which local medication was given. However the fever
deteriorated and his father became disoriented and restless. Thus they took him to the atoll
hospital from where they were referred to IGMH.
He also explained that there was no past medical history of his father and also his family has no
history of cardiovascular diseases.
Myocardial infarction
Heart attack or myocardial infarction is a medical emergency in which some of the hearts blood
supply is suddenly and severely reduced or cut off causing the heart muscle myocardium) to die
because it is deprived of its oxygen supply
PATHOPHYSIOLOGY
In an MI, an area of the myocardium is permanently destroyed. MI is usually caused by reduced
blood flow in a coronary artery due to rapture of an atherosclerotic plague and subsequent
occlusion of an artery by a thrombus. In unstable angina the plague ruptures, but the artery is not
completely occluded. Because unstable angina and acute MI are considered to be the same
process but different points along a continuum, the term acute coronary syndrome (ACS) may be
used in lieu of these diagnoses. Other causes of MI include vasospasm ( sudden constriction or
narrowing) of a coronary artery or decreased oxygen supply ( acute blood loss, anemia or low
blood pressure), and increased demand for oxygen (e.g.; from a rapid heart rate, thyrotoxicosis or
ingestion of cocaine). In each case a profound imbalance exist between myocardial oxygen
supply and the demand.
Coronary occlusion, heart attack, MI are terms used synonymously, but the preferred term is MI.
the area of infarction develops over minutes to hours. As the cells are deprived of oxygen
ischemia develops, cellular injury occurs, and the lack of oxygen result in infarction, or the death
of cells. The expression time is muscle reflects the urgency of appropriate treatment to
improve patients outcomes. (Smeltzer s. C., Bare, L.Hinkle, & Cheever, 2008)
INCIDENCE
Potential for intervention
There are 32.4 million myocardial infarctions and strokes worldwide every year. Patients with
previous myocardial infarction (MI) and stroke are the highest risk group for further coronary
and cerebral events. Survivors of MI are at increased risk of recurrent infarctions and have an
annual death rate of 5% - six times that in people of the same age who do not have coronary
heart disease. Similarly, patients who have suffered a stroke remain at an increased risk of a
further stroke (about 7% per annum).
There is considerable scientific evidence that specific interventions will reduce the risk of further
vascular events in patients with MI and stroke. If these interventions are appropriately
implemented, nearly one third of the fatal and non-fatal MI and strokes could be prevented.
http://www.who.int/cardiovascular_diseases/priorities/secondary_prevention/country/en/index1.
html





CLASSIFICATIONS OF MI
Types of heart attack
Heart attacks can be classified by a measurement known as the ST segment. The ST segment is
an electrical measurement recorded by an ECG. It corresponds to the level of damage inflicted
on the heart.
The higher the ST segment, the greater the damage is likely.
Acute coronary syndrome
A heart attack is a form of acute coronary syndrome (ACS); where there is a significant blockage
in the coronary arteries.
There are three main types of ACS:
ST segment elevation myocardial infarction (STEMI)
non-ST segment elevation myocardial infarction (NSTEMI)
unstable angina
The three types are described in more detail below.
ST segment elevation myocardial infarction (STEMI)
A STEMI is the most serious type of heart attack where there is a long interruption to the blood
supply. This is caused by a total blockage of the coronary artery, which can cause extensive
damage to a large area of the heart.
A STEMI is what most people think of when they hear the term heart attack.
Non-ST segment elevation myocardial infarction (NSTEMI)
An NSTEMI can be less serious than a STEMI. This is because the supply of blood to the heart
is only partially blocked, rather than completely blocked.
As a result, a smaller section of the heart is damaged. However, NSTEMI is still regarded as a
serious medical emergency.


Unstable angina
Unstable angina is the least serious type of ACS although, like NSTEMI, it is still regarded as a
medical emergency.
In unstable angina, the blood supply to the heart is still seriously restricted, but there is no
permanent damage so the heart muscle is preserved.
http://www.nhs.uk/Conditions/Heart-attack/Pages/Diagnosis.aspx
CLINICAL MENIFESTATION
The first symptom of acute myocardial infarction is usually, severe chest pain. The pain is
similar to angina pectoris but is more severe and persistent and is not relieved by nitrate. It may
be described by heavy crushing such as a truck sitting on my chest. Radiation to the neck, jaw,
back, shoulder or left arm is common. Some individuals, especially who are elder or diabetic,
experience no pain, thereby having a silent infarction. Infarctions often stimulate a sensation of
unrelenting indigestion. Nausea and vomiting may occur because of reflex stimulation of
vomiting centers by pain fibers. Vasovagal reflexes from the area of infarcted myocardium also
may affect the gastrointestinal tract. Catecholamine release results in sympathetic stimulation,
producing diaphoresis and peripheral vasoconstriction that causes the skin to become cool and
clammy. Fever may develop in the first 24 hours and persist for 1 week because of inflammatory
activity within the myocardium.
A variety of cardiovascular changes may be found on physical examination. With an acute
myocardial infarction, blood pressure may initially decease. Abnormal extra heart sounds (s
3,
s
4
)
reflect ventricular dysfunction. Inflammation causes pericardial friction rub, along with a variety
of cardiac murmurs. (L.McCance & Huether, 1994)





RISK FACTORS OF MI
NON MODIFIABE RISK FACTORS
Personal elements that cannot be altered or controlled are
Age
Gender (men are at high risk when compared to women)
Family history
Ethnic background

MODIFIABLE RISK FACTORS
Elevated serum cholesterol level
Smoking
Hypertension
Impaired glucose tolerance (e.g. diabetes)
Obesity
Physical inactivity
Stress
(Ignatavicius & Workman, 2002)






RISK FACTORS OF PATIENTS
NON MODIFIABLE RISK FACTORS
Age
Gender
MODIFIABLE RISK FACTORS
Smoking
Physical inactivity

CAUSES OF MI
Atherosclerosis
Arterial spasm
Hypotension
Aortic stenosis
Hypoxia
CAUSE OF MI IN PATIENT
Patient is a smoker, who doesnt eat a healthy diet (oily and spicy food can lead to
atherosclerosis). His age can also lead to atherosclerosis, since the elasticity of the arteries will
be less, leading to plague formation



DIAGNOSTIC TEST FOR MI
The diagnosis of MI is made on the basis of ECG, serial enzyme alterations, radio-nucleotide
imaging, and physical examination (L.McCance & Huether, 1994)
Electrocardiography
An electrocardiogram (ECG) is an important test in suspected heart attacks. An ECG should be
carried out within 10 minutes of being admitted to hospital.
An ECG measures the electrical activity of your heart. Every time your heart beats, it produces
tiny electrical signals. An ECG machine records these signals onto paper, allowing your doctor
to see how well your heart is functioning.
An ECG is painless and takes about five minutes to perform. During the test, electrodes (flat
metal discs) are attached to your arms, legs and chest. Wires from the electrodes are connected to
the ECG machine, which records the electrical impulses.
There are two reasons why an ECG is so important:
it helps confirm the diagnosis of a heart attack
it helps determine what type of heart attack you have had, which will help
determine the most effective treatment for you
http://www.nhs.uk/Conditions/Heart-attack/Pages/Diagnosis.aspx
Serial 12 lead ECG may reveal characteristic changes, such as serial ST-segment depression in
non-Q-wave MI (subendocardial MI that affects the inner most myocardial layers) and ST-
segment elevation In Q-wave MI (transmural MI with damage extending through all myocardial
layers). The q waves are considered abnormal when they appear greater than or equal to 0.04
second wide and their height is greater than 25% of the R wave height in that lead. An ECG can
also identify the location of MI, arrhythmias, hypertrophy, and pericarditis. (Pagana & Pagana,
1998)



Blood tests
Damage to your heart from a heart attack causes certain proteins to slowly leak into your blood.
Enzymes are special proteins that help regulate chemical reactions that take place in your body.
If you have had a suspected heart attack, a sample of your blood will be taken so it can be tested
for these heart proteins (known as cardiac markers). Your protein levels will be measured
through a series of blood samples taken over the course of a few days.
This will allow damage to your heart to be assessed, and also help determine how well you are
responding to treatment.
http://www.nhs.uk/Conditions/Heart-attack/Pages/Diagnosis.aspx

CPK level can rise within 6 hours after damage. If damage is not persistent, the level peaks at 18
hours after injury and returns to normal in 2 to 3 days. Serial cardiac enzymes and proteins may
show a characteristic rise and fall of cardiac enzymes, specifically CK-MB, and the protein
troponin T and I, and myoglobin to confirm the diagnosis of MI. (Pagana & Pagana, 1998)

AST
This test is used in the evaluation of patients with suspected coronary occlusive heart disease or
suspected hepatocellular disease. The enzyme is found in a very high concentration within highly
metabolic tissues such as heart muscle.
When disease or injury affects the cells of these tissues, the cell, lyses. The AST is released,
picked up by the blood and the serum level rises. The amount of AST elevated is directly related
to the number of cells affected by the disease or injury. Furthermore the elevation depends on the
length of time that the blood is drawn after injury. Serum AST level becomes elevated 8 hours
after the cell injury, peaks at 24 36 hours, and returns to normal in 3 to 7 days. If the cellular
injury is chronic then level will be persistently elevated. (Pagana & Pagana, 1998)

Leukocyte level
Laboratory testing may reveal elevated white blood cell count and erythrocyte sedimentation rate
due to inflammation, increased glucose levels following the release of catecholamines, and
changes in electrocytes- all of which provide information about the patients potential for
developing arrhythmias and can identify the cause of an arrhythmia that accompanies chest
discomfort.
(Kowalak, 2003)

Chest X-ray
A chest X-ray can be useful if diagnosis of a heart attack is uncertain and there are other possible
causes of your symptoms, such as a pocket of air trapped between the layers of your lungs
(pneumothorax).
A chest X-ray can also be used to check whether complications have arisen from the heart attack,
such as a build-up of fluid inside your lungs (pulmonary edema).

Echocardiogram
An echocardiogram is a type of ultrasound scan that uses sound waves to build up a picture of
the inside of your heart.
This can be useful to identify exactly which areas of the heart have been damaged and how this
damage has affected your hearts function.

Coronary angiography
Coronary angiography can help determine whether a blockage or narrowing has occurred in the
coronary arteries and, if so, to locate the exact location of the blockage or narrowing.
The test involves inserting a thin tube, known as a catheter, into one of the blood vessels in your
groin or arm. The catheter is guided into your coronary arteries using X-rays.
A special fluid, known as a contrast agent, is pumped through the catheter. This fluid shows up
on X-rays. Studying how it flows around and through your heart can help locate the site of any
blockage or narrowing.
A coronary angiogram is often performed just before surgery because the results can help guide
the efforts of the surgeon. See treating a heart attack for more information
http://www.nhs.uk/Conditions/Heart-attack/Pages/Diagnosis.aspx

DIAGNOSTIC TESTS DONE IN PATIENT
Urine analysis 25/02/2014 5:06PM
Microscopy
Test Result Reference range Remarks
Pus cells 08 0-5 /hpf High
Red cells 10 0-2 /hpf High
Epithelial cells 01 0-15 /hpf Normal
Casts Not found
crystals Not found

Hematology 25/02/2014 3:06PM
Coagulogram Result Reference range Remarks
Prothrombin time (test) 15.8 sec 10-13 High
Prothrombin time (control) 12.5 sec
INR 1.3
APTT control 24.4 sec
APTT test 36.3 sec 25-35 High
Thrombine time 15.3 sec 17-25 Low


Clinical chemistry 25/02/2014 3:06PM
Test Result Reference range Remarks
Random blood sugar 118 60-139 mg/dl Normal
Blood urea 31.0 19-43 mg/dl Normal
Serum creatinine 1.1 0.8-1.5 mg/dl Normal
CK 367 55-170 u/L High
CK-MB 28 0-24 u/L High
Troponin-T Positive
Serum sodium 120 137-145 mmol/L Low
Serum potassium 4.8 3.5-5.1 mmol/L Normal
Serum calcium 7.9 8.4-10.2 mg/dl Normal
LIVER PROFILE
Total bilirubin 1.9 0.2-1.3 mg/dl High
Direct bilirubin 0.0 0-0.3 mg/dl Normal
Total proteins 6.7 6.3-8 g/dl Normal
Serum albumins 3.1 3.5-5.0 g/dl Low
Serum globulin 3.6 2.3-3.5 g/dl High
Albumin/Globulin
ratio
0.9
Serum alkaline
phosphate
69 38-126 u/L Low
AST 75 17-59 u/L High
ALT 66 21-72 u/L Normal
CRP(Quantitative) 20 0-10mg/L


Hematology 25/02/2014 3:06PM
Test Result Reference range Remarks
Haemoglobin 11.2 12-18 g/dl Normal
PCV 31.3 35-48% Low
Total leucocyte 10.47 4-11 *10^3 /uL Normal
Differential leucocyte count
Neutrophils 88.6 40-72% High
Lymphocytes 5.9 20-40% Low
Monocytes 5.3 2-10% Normal
Eosinophils 0.0 1-6% Low
Basophils 0.2 0-1% Normal
Platelet count 206 15-400 *10^3 /uL Normal
E.S.R 77 1-10 mm/1Hr High










MEDICATIONS
CEFTRIAXONE
Generic name: ceftriaxone sodium
Availability: 250mg, 500mg, 1g, 2g injection.
Indication: infections caused by susceptible organisms in lower respiratory tract, skin and skin
structures, urinary tract, bones and joints; also intra-abdominal infections, pelvic inflammatory
disease, uncomplicated gonorrhea, meningitis and surgical prophylaxis.
Indication related to the patient
To treat infection
Route and dosage
Moderate to severe infections
Adult: IV/IM 1-2g q12-24h x 4-14days. (max: 4g/day)
Child: IV/IM 50-75mg/kg/day in 2 divided doses x 4-14days (max: 2g/ day)
Bacterial Otitis media
Child: IM 50mg/kg(max:1g)
Meningitis
Adult: IV/IM 2g q12h
Child: IV/IM 100mg/kg/day in 2 divided doses (max:4g/day)
Surgical prophylaxis
Adult: IV/IM 1g 30-120 min before surgery
Uncomplicated gonorrhea
Adult: IM 250 mg as single doses
Child: IM 12 mg as single dose
Route and Dose of patient
1gram intravenously BD
ADVERSE EFFECTS
(1%) Body as a whole: pruritus, fever, chills, pain, induration at IM injection site; phlebitis (IV
site). GI: Diarrhea, abdominal cramps, pseudomembranous colitis, biliary sludge. Urogenital:
genital pruritus; moniliasis.
SIDE EFFECTS RELATED TO THE PATIENT
Patient doesnt show any side effect yet

PANTAZ
Generic name: pantoprazole sodium
Indication: short-term treatment of erosive esophagitis associated with gastro esophageal reflux
disease (GERD) hypersecretory disease.
Unlabeled uses: peptic ulcer disease.
Indication related to the patient
To relieve side effects of other medication such as gastritis
Route and dosage
4mg, intravenously, BD
Eroive esophagitis
Adult: PO 40 mg daily 8-16 wks.
IV 40mg daily x7-10 days.
Hyper-secretory disease
Adult: PO 40mg b.i.d. (doses up to 240mg/day have been used).
IV 80mg b.i.d. ; adjust based on acid output.
Route and Dose of patient
40 mg, IV BD
Renal impairment/Hepatic Impairment dosage adjustment
Adjustment not needed
Hemodialysis Dosage adjustment: drug not removed
Adverse effects
(1%)GI: diarrhea, flatulence, abdominal pain.
CNS: headache, insomnia
Skin: Rash.
SIDE EFFECTS RELATED TO THE PATIENT
Patient doesnt show any signs of side effects from this medication yet







T.ECOSPRIN
Generic name: Aspirin
Availability: 81mg chewable tablets;325mg,500mg tablets; 81mg, 165mg, 325mg, 500mg,
650mg, 975mg enteric coated tablets; 650mg, 800mg sustained released tablets; 120mg, 200mg,
300mg, 600mg suppositories.
Indication: to relieve pain of low to moderate intensity. Also for various inflammatory
conditions, such as acute rheumatic fever, systemic lupus, rheumatoid arthritis, osteoarthritis,
bursitis and calcific tendonitis and to reduce fever in selected febrile conditions. Used to reduce
recurrence of TIA due to fibrin platelet emboli and risk of stroke in men, and to prevent
recurrence of MI; as prophylaxis against MI in men with unstable angina.
Unlabeled uses: As prophylactic against thromboembolism; to prevent cataract and progression
of diabetic retinopathy; and to control symptoms related to gluten sensitivity.
Indications of patient
To prevent recurrence of MI; as prophylaxis against MI in men with unstable angina.
Route and dosage
Mild and moderate pain, fever
Adult: PO/PR 350-650 mg q4h (max: 4g/day)
Child: PO/PR 10-15mg/kg in 4-6hr (max: 3.6g/day)
Arthritic conditions
Adult: PO 3.6-5.4g/day in 4-6 divided doses.
Child: PO 80-100mg/kg/day in 4-6 divided doses (max:130mg/kg/day)
Thromboembolic disorders
Adult: PO 81-325mg daily
TIA prophylaxis
Adult: PO 650mg b.i.d.
MI prophylaxis
Adult: PO 80-325 mg/day
Route and dose of patient
75mg, PO, OD
ADVERSE EFFECTS
(1%) Body as a whole: hypersensitivity (urticarial, bronchospasm, anaphylactic shock
(laryngeal edema).
CNS: Dizziness, confusion, drowsiness.
Special senses: tinnitus, hearing loss.
GI: nausea, vomiting, diarrhea, anorexia, heartburn, stomach pains, ulceration, occult bleeding,
GI bleeding.
Hematologic: thrombocytopenia, hemolytic anemia, prolonged bleeding time,.
Skin: petechiae, easy bruising, rash.
Urogenital: impaired renal function.
Other: prolonged pregnancy and labor with increased bleeding.





T.ATORIN
Generic name: atorvastatin calcium
Availability: 10mg, 20mg, 40mg tablets.
Indication: adjunct to diet for the reduction of LDL cholesterol and triglycerides in patients with
primary hypercholesterolemia and mixed dyslipidemia, prevention of cardiovascular disease in
patients with multiple risk factors.
Indication of patient: Prevention of cardiovascular disease in patients with multiple factors.
Route and dosage
Hypercholestolemia/ prevention of cardiovascular disease
Adult: PO start with 10-40mg daily, may increase up to 80mg/day.
Child/adolescent (10-17y): PO start with 10mg daily, ma increase up to 20 mg/day.
10mg, HS, PO
Adverse effects
(1%)body as a whole: back pain, asthenia, hypersensitivity reaction, myalgia, rhabdomyolysis.
CNS: headache.
GI: abdominal pain. Constipation, diarrhea, dyspepsia, flatulence, increased liver function tests.
Respiratory: sinusitis, pharyngitis
Skin: rash.




T.AZITHROMYCIN
Generic name: Azithromycin
Availability: 500mg, 600mg tablets, 100mg/5m, 200mg/5ml, 1g/packet oral suspension; 500mg
injection; 1% ophthalmic; Zmax: extended release: 176mg/5ml oral suspension.
Indication: pneumonia, lower respiratory infection, pharyngitis/tonsillitis, gonorrhea,
nongonococcal arthritis, skin and skin structure infections due to susceptible organisms, otitis
media, mycobacterium avium-intracellulare complex infections, acute bacterial sinusitis.
Zmax: acute bacterial sinusitis and community acquired pneumonia.
AzaSite: bacterial conjunctivitis
Unlabeled use: bronchitis, helicobacter pylori gastritis.
Indication in patient: Infection
Route and dosage:
500mg , PO OD
Bacterial infections
PO 500mg on da 1, then 250mg q24h for 4 more days
IV 500mg daily for at least 2days, administer 1mg/ml over 3h or 2mg/ml over 1h
Child (6m or older): PO 10mg/kg on day 1, then 5mg/kg for 4 more days (max: 250mg/day)
Acute bacterial sinusitis
Adult: PO 500mg once daily 3 days. Zmax: single one time dose of 2g.
Child (6m or older): PO 10mg/kg once daily x 3days


Otitis media
Child(older than 6 mo): PO30mg/kg as a single dose or 10 mg/kg once daily (not to exceed
500mg/day) for 3 days or 10mg/kg as a single dose on day 1 followed by 5mg/kg/day on days
2-5
Gonorrhea
Adult: PO 2g as a single dose
Chancroid
Adult: PO 1g as a single dose
Child: PO 20mg/kg as single dose(max: 1 g)
Bacterial conjunctivitis
Adult: ophthalmic 1 drop b.i.d x 2 days than daily x 5 days
Renal impairment dosage
CrCl less than 10mL/min: use with caution

Adverse reaction
(1%)CNS: headache, dizziness.
GI: Nausea, vomiting, diarrhea, abdominal pain; hepatotoxicity, mild elevations in liver function
tests.





INJ.LASIX
Generic name: furosemide
Availability: 20mg, 40mg, 80mg tablets; 10mg/ml, 40mg/5ml oral solutions; 10mg/ml injection
Indication: treatment of edema related with CHF, cirrhosis of liver, and kidney disease,
including nephrotic syndrome. May be used for management of hypertension, alone or in
combination with other antihypertensive agents, and for treatment of hypercalcemia. Has been
used concomitantly with mannitol for treatment of severe cerebral edema, particularly in
meningitis.
Indication in patient : Treatment for hypertention and hypercalcemia
Route and dosage
20 mg Iv,OD
Edema
Adult: PO 20-80mg in 1 or more divided doses up to 600mg/day if needed IV/IM 20-40mg in 1
or more divided doses up to 600mg/day.
Child :PO 2mg/kg, may be increased by 1-2mg/kg q6-8h (max: 6mg/kg/dose)
Neonate: PO 1-4mgg/kg q12-24h IV/IM 1mg/kg q12-24h
Hypertension
Adult: PO 10-40 mg b.i.d. (max: 480mg/day)
ADVERSE EFFECTS
(1%)CV: postural hypertension, dizziness with excessive diuresis, acute hypotensive episodes,
circulatory collapse.
Metabolic: hypovolemia, dehydration, hponatremia, hypokalemia, hypochloremia, metabolic
alkalosis, hypomagnesemia, hypocalcemia (tetany), hperglcemia, glycosuria, elevated BUN,
hyperuricemia.
GI: nausea, vomiting, oral and gastric burning, anorexia, diarrhea, constipation, abdominal
cramping, acute pancreatitis, jaundice.
Urogenital: allergic interstitial nephritis, irreversible renal failure, urinary frequency.
Hematologic: anemia, leukopenia, thrombocytopenic purpura; aplastic anemia, agranulocytosis
(rare).
Special senses: Tinnitus, vertigo, feeling of fullness in ears, hearing loss(rarely permanent),
blurred vision.
Skin: pruritus, urticarial, exfoliative dermatitis, purpura, photosensitivity, porphyria cutanea
tarda, necrotizing angitis (vasculitis)
Bod as a whole: increased perspiration, paresthesias; activation of SLE, muscle spasms,
weakness, thrombophlebitis, pain at IM injection site.









Nursing care given to the patient
On admission, patients vital signs, ECG taken and also severity, location, type, and
duration of pain was assessed and recorded.
Rational for: -
Vital signs: - respiration may be increased as a result of pain and associated
anxiety. Release of stress-induced catecholamine increases heart rate and blood
pressure.
ECG: - serial ECG and stat ECG record changes that can give evidence of further
cardiac damage and location of myocardial ischemia.
Severity, location, type, and duration of pain: - assisting the client in quantifying
pain may differentiate pre-existing and current pain pattern as well as identify
complication.
Oxygen administered as prescribed by the doctor.
Rational: - Increase myocardial supply of oxygen
Medication administered as prescribed by doctor.
Rational: - Morphine is an opiate analgesic and alters the clients perception of pain and
reduces preload time vasoconstriction. Nitrates relax the smooth muscle of coronary
blood vessels, decreasing ischemia and hence decreasing the pain.
Patient was on cardiac monitor for continuous monitoring.
Rational: -Monitoring ST is important because elevation of ST segment indicates
myocardial tissue injury; ST segment depression indicates decreased myocardial
perfusion.
Patient was on catheter, urine output monitored every 8 hourly and total 24hrs.
Rational: - Urine output less than 0.5ml/kg/hr may reduced renal perfusion and
glomerular filtration as a result of reduced cardiac output.
Bed rest provided as much as possible.
Rational: - Stress activates sympathetic nervous system and increase myocardial oxygen
needed.
Bed bath and care of pressure point (back care) given daily
Rational: - Increases circulation and prevent skin damage (bed sore). (Black & Hawks,
2005)

Things that need to be improve
Urine output should be monitored every 2 hourly instead of 8 hourly
Rational: - Urine output less than 0.5ml/kg/hr may reduce renal perfusion and
glomerular filtration as a result of reduced cardiac output.
Change position every 2 hours.
Rational: - Increase circulation and reduce the time that weight deprives at any one area
of blood flow.
Provide mouth care every 8 hourly (during every shift).
Rational: - Oxygen therapy may dry mouth and frequent mouth care would be
refreshing.
Since patient is on bed rest, pain medication he is at a risk for constipation so ensure that
he is getting a more bulk diet and also laxatives are administered.
Rational: - straining during defecation increase myocardial work load.
Provide comfortable, quite environment for the client and family.
Rational: - A comfortable environment enhances coping mechanism and reduces
myocardial workload and oxygen consumption. (Black & Hawks, 2005)







Discharge plan
Discharge plan begins on the day of admission. During patients stay at hospital the
relatives are explained about the care given and how it can be done at home. Possible side effects
of medications are explained to the patients relatives. They could notify the nurse if such side
effects are seen in patient. If patient feels unrelieved pain, decreased activity tolerance, sudden
onset of SOB, weight gain, would seek immediate medical essential so patient should be shown
to a doctor.
Diet
Eat five servings of fruits and vegetables each day
Fruits and vegetables contain substances that help to prevent heart attacks and strokes. They
protect blood vessels and heart and brain tissue.
You should eat at least five servings of fresh fruit and vegetables every day (400-500 grams
daily)
One average size banana, apple, orange, or mango would be a serving of fruit. Two table spoons
of cooked vegetables or one big tomato would be a serving of vegetable.
Avoid salt and salty foods
Many preserved foods like pickles and salt fish, contain a lot of salt. In addition, fast food, like
French fries, often has a lot added salt. Prepared foods, such as frozen dinners, can also be very
salty.
Try not to add salt in your food. A good guideline is to use less than 1 teaspoon (5 grams) of salt
each day.
Eat more fiber
Fiber protects against heart attack and strokes. Sources of fibre include beans, lentils, peas, oats,
fruits and vegetables.
Eat at least two servings of oily fish a week
Fish oils contain good fats called omega 3 fatty acids, such as EPA (eicosapentanoic acid) and
HAD (docosahexaenoic acid). They protect people from heart attacks and strokes by preventing
blood clots. One serving of fish is about the size of a peak of playing cards. Fish oil supplements
are also good.
Limit fatty foods
All fats are high in energy and will make you gain weight unless you burn them off by staying
active. Some fats are more likely to increase your risk of heart attack and stroke;
Saturated fats and trans-fats lead to bad cholesterol in your blood, and increase you risk
of heart of heart diseases. Try to restrict use of these fats.
Unsaturated fats are risky, but they still make you gain weight. You should eat them in
moderation
Cooking tips for reducing fat
Use only a very little cooking oil.
Instead of frying foods, bake, boil, grill, steam, roast, poach, or microwave them.
Trim the fat and skin off meal before cooking.
Eat chicken instead of red meat like beef, pork, and mutton. (Avoiding Heart Attackd and
strokes: Dont be a victim - protect yourself, 2005)








Health education
To extend and improve the quality of life, a patient who has had an MI must learn to adjust
his/her life style to promote heart-healthy living. With this in mind the nurse and patient develop
a programmed to help the patient achieve desired out comes.
Changing life style during convalescence and healing
Adaptations to an MI are a process and usually require some modifications of the lifestyle. Some
specific modifications include:
Avoiding any activity that produces chest pain, extreme dyspnea, or undue fatigue.
Avoiding extremes of heat and cold
Lose weight, if indicated.
Stopping smoking and use of tobacco, avoiding second-hand smoke.
Using personal strengths to support lifestyle changes.
Developing heart-healthy eating patterns and avoiding large meals and hurrying while
eating
Modifying meals to align with the therapeutic life style changes (TLC) or dietary
approaches to stopping hypertension (DASH) diet.
Adhering to medical regimen, especially in taking medications.
Following recommendations that ensure blood pressure and blood glucose are in control.
Pursuing activities that relieve and reduces stress.
Adopting activity program
Additionally, the patient needs to undertake an orderly program of increasing activity and the
exercise for long term rehabilitations as follows:
Engaging in regimen of physical conditioning with a gradual increase in activity
intensity.
Walking daily, increasing distance and time as prescribes
Monitoring pulse rate during physical activity until the maximum level of activity
is attained.
Avoiding activities that ensure the muscle; isometric exercise, weight-lifting, any
activity that requires sudden burst of energy.
Avoiding physical exercise immediately
Alternately activity with respiration periods( some fatigue is normal and expected
during convalescence)
Participating in daily program of exercise that develops into program of regular
exercise for a lifetime. (Black & Hawks, 2005)














REFLECTION
During this case study we were able to gain a lot of knowledge about MI and what nursing care
should be given to a MI patient. We also learned about the diagnostic tests which could be done
to diagnose MI. Moreover we gained some knowledge of why the tests are done and how they
interpret the result. We also included health education and what kind of a diet MI patient should
take, which provided us with more knowledge about health education.
It could have been more effective if we got the opportunity to stay and care for the patient during
the patients stay at hospital. Thus we could gain more knowledge about patient condition and
observe him in order to get more information about his condition.










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