Instrumental, Laboratory Investigations And Differential Diagnosis Of Acute Myocardial Infarction
The ECG Machine
Electrocardiogram (ECG) taken within a few hours of symptoms show diagnostic changes in over 80% of cases. More than 95% show positive ECG findings if recorded 12-24 hours after the onset of symptoms. The changes depend upon the nature of lesion (Ischemia or infarction), site of infarct, presence of arrhythmias and conduction defects. Ischemia without infarction produces depression of the ST segment. Presence of infarction is recognized by the elevation of ST segment. Presence of Q-waves and inversion of the T-waves. The site of infarct can be determined depending on the leads which show abnormalities.
ECG leads showing changes
Location of infarct
V1 to V4
V4 to V6, L1 and aVL
aVF, L2 and L3
ST depression in V1 and V4
Posterior wall. In this case, leads recorded from the back of the chest show Q waves.
The infracted myocardium releases large amounts of its enzymes into the circulation, so that transient rise of these enzymes occurs within hours of infarction. These remain elevated for periods ranging from days to weeks, and then fall.
Serum glutamic oxaloacetic Transaminase (SGOT aspartate transaminase) Normal level is 5-40 IU/liter
Serum values rise after 8-12 hours. Reach peak levels in 18-36 hours and fall by 3-4 days.
Serum lactic dehydrogenase (LDH), normal level is 20-220 IU/liter
Starts rising by 12-24 hours, highest values are obtained in 2-6 days and the level comes down by 2 weeks.
Creatine Kinase (CK). Normal level is 20-200 IU/liter. Among the three isoenzymes of CK, (MM, BB and MB), the rise in MB-CK is specific for cardiac infarction
Rises by 6-8 hours. Peak is reached in 24 hours and it returns to normal in 3-4 days.
Elevation of enzyme levels correlate with the extent of infarction. Recurrence of infarction leads to second and third peaks in serum enzyme levels. Even when the ECG changes are minimal or not diagnostic, the enzyme levels help to diagnose myocardial infarction. All the enzymes except MB, CK are found in other tissues as well. Therefore elevation of these enzymes may occur in pulmonary infarction, necrosis of skeletal muscles, hepatic necrosis, etc.
An X-ray Machine
Acute myocardial infarction does not produce any radiological changes per se, but if left ventricular failure occurs, pulmonary edema may be visible in chest radiographs. In uncomplicated cases, the patient should not be moved for routine chest X-ray. Whenever indicated, X-ray should be taken at the bedside using a portable machine.
Myocardial perfusion scintigraphy using 201thallium gives evidence of diminished arterial perfusion and necrosis. Diagnosis of myocaridial infarction should be confirmed if two of the following three criteria are present:
- Typical history with the clinical features;
- ECG evidence; and
- Enzyme changes.
Acute chest pain may occur in pleurisy, pneumonia, pericarditis, penumothorax, pre-herpetic neuralgia, dissecting aneurysm of the aorta or lesions on the chest wall. Pericarditis may closely resemble acute myocardial infarction in respect of the pain and its radiation. Fever, leukocytosis and pericardial rub occur early in pericarditis, whereas these develop only 24 hours after the onset of myocardial infarction. Dissecting aneurysm of the aorta is uncommon. It causes tearing pain, which is abrupt in onset and severe from the beginning. Pain may radiate to the back, epigastrium, flank and lower extremities. Ventricular dysfunction is less common to develop.
Sometimes, the pain of myocardial infarction may be felt mainly under the jaws, shoulder, or epigastrium and these may be mistaken for primary disease at these sites.
© 2014 Funom Theophilus Makama