Page 450 - Textbook of Pathology, 6th Edition

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Figure 16.20 Some common ECG changes in acute myocardial infarction.

CHANGES IN EARLY INFARCTS. By special techniques iv) Shock: Systolic blood pressure is below 80 mmHg;
like electron microscopy, chemical and histochemical studies, lethargy, cold clammy limbs, peripheral cyanosis, weak
changes can be demonstrated in early infarcts before pulse, tachycardia or bradycardia are often present.
detectable light microscopic alterations appear. v) Oliguria: Urine flow is usually less than 20 ml per hour.
1. Electron microscopic changes. Changes by EM vi) Low grade fever: Mild rise in temperature occurs within
examination are evident in less than half an hour on onset of 24 hours and lasts up to one week, accompanied by
infarction. These changes are as under: leucocytosis and elevated ESR.
i) Disappearance of perinuclear glycogen granules within vii) Acute pulmonary oedema: Some cases develop severe
5 minutes of ischaemia. pulmonary congestion due to left ventricular failure and
ii) Swelling of mitochondria in 20 to 30 minutes. develop suffocation, dyspnoea, orthopnoea and bubbling
iii) Disruption of sarcolemma. respiration.
iv) Nuclear alterations like peripheral clumping of nuclear 2. ECG changes. The ECG changes are one of the most
chromatin. important parameters. Most characteristic ECG change is ST
SECTION III
segment elevation in acute MI (termed as STEMI); other
2. Chemical and histochemical changes. Analysis of tissues changes inlcude T wave inversion and appearance of wide
from early infarcts by chemical and histochemical techniques deep Q waves (Fig. 16.20).
has shown a number of findings. These are as follows: 3. Serum cardiac markers. Certain proteins and enzymes
i) Glycogen depletion in myocardial fibres within 30 to 60 are released into the blood from necrotic heart muscle after
minutes of infarction. acute MI. Measurement of their levels in serum is helpful in
ii) Increase in lactic acid in the myocardial fibres. making a diagnosis and plan management. Rapid assay of
+
iii) Loss of K from the ischaemic fibres. some more specific cardiac proteins is available rendering
+
iv) Increase of Na in the ischaemic cells. the estimation of non-specific estimation of SGOT of historical
++
v) Influx of Ca into the cells causing irreversible cell injury. importance only in current practice. Important myocardial
Based on the above observations and on leakage of markers in use nowadays are as under (Fig. 16.21):
Systemic Pathology
enzymes from the ischaemic myocardium, alterations in the
concentrations of various enzymes are detected in the blood i) Creatine phosphokinase (CK) and CK-MB: CK has three
of these patients. forms—
CK-MM derived from skeletal muscle;
DIAGNOSIS. The diagnosis of acute MI is made on the CK-BB derived from brain and lungs; and
observations of 3 types of features—clinical features, ECG CK-MB, mainly from cardiac muscles and insignificant
changes, and serum enzyme determinations. amount from extracardiac tissue.
1. Clinical features. Typically, acute MI has a sudden onset. Thus total CK estimation lacks specificity while elevation
The following clinical features usually characterise a case of of CK-MB isoenzyme is considerably specific for myocardial
acute MI. damage. CK-MB has further 2 forms—CK-MB2 is the
i) Pain: Usually sudden, severe, crushing and prolonged, myocardial form while CK-MB1 is extracardiac form. A ratio
substernal or precordial in location, unrelieved by rest or of CK-MB2: CK-MB1 above 1.5 is highly sensitive for the
nitroglycerin, often radiating to one or both the arms, neck diagnosis of acute MI after 4-6 hours of onset of myocardial
and back. ischaemia. CK-MB disappears from blood by 48 hours.
ii) Indigestion: Pain is often accompanied by epigastric or ii) Lactic dehydrogenase (LDH). Total LDH estimation also
substernal discomfort interpreted as ‘heartburn’ with nausea lacks specificity since this enzyme is present in various tissues
and vomiting. besides myocardium such as in skeletal muscle, kidneys,
iii) Apprehension: The patient is often terrified, restless and liver, lungs and red blood cells. However, like CK, LDH too
apprehensive due to great fear of death. has two isoforms of which LDH-1 is myocardial-specific.