MYOCARDIAL INFARCTION
PRESENTED BY SAEED AKRAM, FINAL YEAR MIT, SZMC, RYK
INTRODUCTION
DEFINITIONS :
Acute ischemic necrosis of an area of myocardium is known as
myocardial infarction.
OR
Myocardial necrosis occurring as a result of critical imbalance
between coronary blood supply and myocardial demand is called
myocardial infarction.
In majority of patients Ml develops in left ventricle; right ventricular
infarction frequently accompanies left ventricular inferior wall Ml.
2
CLINICAL FEATURES
Chest pain
The pain is reterosternal similar to angina in location and radiation
(left shoulder, arm, jaw) but it occurs at rest or with less activity and
is more severe and lasts longer (> than 30 min). It is not relieved by
nitroglycerine.
pain may also begin in epigastrium and simulates abdominal
disorders. (nausea / vomiting).
They describe their pain with clenched fist held against the sternum.
(FIST SIGN)
In some patients especially elderly, Ml manifests clinically not by
chest pain but rather by symptoms of dyspnea, chest tightness or
marked weakness or syncope. 3
CLINICAL FEATURES
There is profuse cold sweating which may drench the bed
clothes.
Pale color on examination
Tachycardia: Due to anxiety, low cardiac output or arrhythmias.
Bradycardia: If there is inferior wall infarction.
Hypertensive (>160/90 mmHg)
Majority of patients with MI develop fever within 24-48 hours
that resolves by fourth or fifth day.
Raised JVP, 3rd Heart Sound (S3), Quiet 1st Heart Sound
4
INVESTIGATION
According to the WHO criteria myocardial infarction can be
diagnosed, if two of the following three factors are present:
1. A history of ischemic type chest pain.
2. ECG changes of myocardial infarction.
3. Initially a rise and then fall of cardiac enzymes.
PRESENTATION TITLE 5
INVESTIGATION
1. ECG
ST segment elevation, T Wave inversion
2. Cardiac Enzymes
(A) Troponin T and troponin I:
These enzymes are highly specific to cardiac injury and can detect
small infarctions that are below the detection limit for CK-MB.
Troponin T and I rise early (within 2-4 hours ) and remains
elevated (troponin I, 7-10 days and troponin T, 10-14 days).
PRESENTATION TITLE 6
INVESTIGATION
(B) Creatine Kinase (CK)
It rises within 4-8 hours, peaks at 24 hours and generally returns to
normal by 2-3 days. Creatine kinase has three isoenzymes
CK - MB - Present in heart
CK - MM - Present in skeletal muscles
CK - BB - Present in brain
(C) Serum Myoglobin
Myoglobin released from injured myocardium comes into circulation
quite early and is very sensitive for detection of infarction (1-4
hours), however it is not very specific because minor skeletal muscle
trauma also releases myoglobin. 7
INVESTIGATION
3. Chest X-Ray
It may demonstrate pulmonary edema.
Heart size is usually normal.
4. Echocardiography
5. Radionuclide Scan
OTHER SERUM MARKERS
CBC
ESR
LDH
AST 8
MANAGEMENT
All patients with suspected myocardial infarction should be confined to strict
bed rest and admitted in hospital preferably in CCU.
GENERAL MEASURES:
1. Activity: Complete bed rest for the first 12 hours, then sitting upright or in a
chair within 24 hours, if no hypotension patient is allowed to ambulate in his
room or shower himself on third day. By day 4-5 after MI progressively
increased ambulation to a goal of 600 feet at least 3 times daily.
2. Diet: Nothing by mouth or clear liquids by mouth for the first 4-12 hours
because there is risk of vomiting and aspiration.
3. Bowel: A bedside commode facility should be available. Give laxative if
there is constipation.
4. Sedation for anxiety such as alprazolam.
5. Oxygen supplementation, if oxygen saturation is low. 9
MANAGEMENT
MEDICAL TREATMENT
1. Control of cardiac pain is typically accomplished with combination of
nitrates, morphine, oxygen and beta-blocker.
2. Morphine relieves pain and anxiety. If morphine causes hypotension
or bradycardia give atropine and for respiratory depression naloxone
as an antidote.
3. Aspirin
4. Nitrates
5. Beta-blockers (Metoprolol)
6. Thrombolytic therapy
7. Streptokinase injection
8. Anti-coagulants (Heparin)
10
9. Primary percutaneous coronary intervention (Primary PCI)
PRESENTED BY SAEED AKRAM, MIT, SZMC, RYK