Infarction is diagnosed by examining the QRS complexes, ST segments, and T waves. Combinations of abnormalities are usually required to make the diagnosis. Changes over time may also be required to firmly diagnose infarction.
The ECG signs of impending, evolving, and completed infarction follow a course from peaked T waves to elevated ST segments, to development of Q waves, to development of T wave inversion and resolution of ST segment elevation. The abnormalities you should look for are: significant Q waves, loss of precordial R height, ST elevation in contiguous leads, and T wave peaking or inversion. Any combination of these abnormalities can be present during the evolution of infarction.
Tall, peaked T waves in the area of ischemia may be the first sign of tissue injury. These tall T waves are identical to those seen in hyperkalemia, but are localized to the leads looking at the area of injury. These waves are probably due to potassium leaking through damaged membranes.
ST segment elevation is seen in early transmural infarction. ST elevation is reversible if blood flow through the occluded coronary artery is restored. The ST elevation is seen in the leads directed towards the area of injury. Transmural infarcts (where the entire thickness of the heart muscle is affected) are usually caused by coronary artery thrombosis.
ST segment depression may also be seen in infarction. It may be: 1) primary ST depression due to a large area of relative ischemia surrounding a small area that is infarcting, such as in subendocardial infarction, or 2) reciprocal changes, where ST depression is seen in leads opposite those that show ST elevation. For example, anterior infarction can cause ST depression in the inferior leads.
The last sign of infarction to occur is the Q wave. Q waves appear only with larger, transmural infarctions. Most often, the Q waves become a permanent reminder of the infarct. They allow diagnosis of a previous infarct years after the event.
Clinical diagnosis of infarction uses the ECG as a tool to assist in the diagnosis. The ECG does not make the diagnosis. The ECG of a patient with acute anterior infarction may appear exactly the same as that of a patient with an anterior ventricular aneurism.
The usual criteria for clinical diagnosis of infarction (sufficient to warrant use of thrombolytic drugs) are: 1) typical, significant ST segment elevation in two or more contiguous leads, and 2) typical chest pain of over 15 minutes duration, not responsive to nitroglycerin. [Chapter Menu]
ECG leads can be divided into zones. Changes diagnostic of infarction within a zone of leads indicate infarction in the geographic area of the heart forming that zone of ECG leads. The four identifiable areas for infarction are inferior, lateral, anterior, and posterior, or a combination of these areas. Infarcts may also be classified as transmural (involving the entire wall of the heart) or subendocardial (affecting only the most sensitive inner area of heart muscle).
Infarction of the anterior wall is caused by occlusion of the left anterior descending coronary artery. Signs of infarction will usually be seen in lead I and V2-V4, and often in V1.
Anterior infarction may be diagnosed if significant Qs (or QS complexes) are seen in lead I and any of V2-V6, or if a significant Q is seen in lead L when at least 3 mm of R wave is present.
Also highly suspicious are significant Qs in V2-V6. In the anterior leads, even a small Q should be considered significant when the Q is followed by an R wave and larger S wave. Non-pathologic Q waves are seen in V2-V3 only if the heart is rotated counterclockwise (these leads would then correspond to V5 and V6, where small Qs are normal).
Poor R wave progression can suggest the possibility of anterior MI, but is not diagnostic. Normally, R waves become larger as the ECG moves from V1 to V4. An actual decrease in R wave height from one anterior precordial lead (V2 through V4) to the next is highly specific for infarction. [Chapter Menu]
Lateral wall infarction can result from occlusion of the left circumflex coronary artery, or from a lateral branch of the left anterior descending artery. ECG changes are seen in leads I and L, V5-V6.
Anterolateral infarction involves portions of the anterior and the lateral walls of the heart. Lateral branches of the left anterior descending artery are at fault. ECG evidence of anterolateral infarction is seen in the more lateral anterior precordials, as well as the lateral leads. Leads I, L, and V4-V6 will be involved, with some degree of involvement of V3 and possibly V2. [Chapter Menu]
Occlusion of a dominant right coronary artery produces inferior infarction, with ECG evidence seen in leads II, III, and F. The inferior portion of the heart is supplied by the right coronary artery in most persons, but can also be serviced by the left circumflex artery, or by both.
When significant Q waves are seen in all three inferior leads, this is highly specific for MI. (These Qs must be either 0.4 msec, deeper than 5 mm, or the Q must be over 1/4 the size of the R wave.) If Qs are seen in only II or F, but are both wider than 0.4 msec (1 box) and larger than 1/4 the R size, this is moderately specific for inferior infarction.
If the inferior portion of the heart is served by the left cirumflex artery, inferior infarction may be accompanied by lateral infarction, called inferolateral infarction. ECG signs are seen in both inferior leads (II, III, F) and lateral leads (I, L, and V5-V6). [Chapter Menu]
Occlusion of the right coronary artery may also produce posterior infarction with or without inferior infarction. True posterior infarction is difficult to diagnose.
True posterior infarction may produce changes only in lead V1 and V2. The ECG changes of posterior infarction are reciprocal changes, that is, they are seen backwards on the front of the heart in lead V1. Qs become big Rs, ST elevation is seen as depression, T inversion is seen as an upright T. Lead V1 and V2 have large R waves, which are reflected Q waves from the back of the heart. The ST segment depression is reciprocal or reflected ST elevation from the back of the heart. T waves will become upright.
In true posterior infarction, no abnormality is seen in the limb leads. However, posterior infarction is usually accompanied by infarction of another area, such as the inferior wall. [Chapter Menu]
One final location for myocardial infarction is global subendocardial. This infarction occurs when a person with diffuse coronary disease has an episode of hypotension and/or extraordinary myocardial oxygen demand.
The global subendocardial infarction involves widespread areas of the endocardium, with evidence of infarction showing up in anterior, inferior, and lateral leads. Widespread subendocardial infarction may be difficult to differentiate from pericarditis on initial ECG. [Chapter Menu]
All material referenced through this menu is excerpted from copyrighted works by Bruce Argyle, MD. You are welcome to use selected portions, as long as appropriate credit is given. The credit for the text referenced through this menu is:
Copyright© Mad Scientist Software Inc. All rights reserved.