1. Introduction to ECG Recognition of Myocardial Infarction
When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with subendocardial or transmural ischemia, followed by necrosis, and eventual fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time. Rupture of an atherosclerotic plaque followed by acute coronary thrombosis is the usual mechanism of acute MI. The ECG changes reflecting this sequence usually follow a well-known pattern depending on the location and size of the MI. MI's resulting from total coronary occlusion result in more homogeneous tissue damage and are usually reflected by a Q-wave MI pattern on the ECG. MI's resulting from subtotal occlusion result in more heterogeneous damage, which may be evidenced by a non Q-wave MIpattern on the ECG. Two-thirds of MI's presenting to emergency rooms evolve to non-Q wave MI's, most having ST segment depression or T wave inversion.
Most MI's are located in the left ventricle. In the setting of a proximal right coronary artery occlusion, however, up to 50% may also have a component of right ventricular infarction as well. Right-sided chest leads are necessary to recognize RV MI.
In general, the more leads of the 12-lead ECG with MI changes (Q waves and ST elevation), the larger the infarct size and the worse the prognosis. Additional leads on the back, V7-9 (horizontal to V6), may be used to improve the recognition of true posterior MI.
The left anterior descending coronary artery (LAD) and it's branches usually supply the anterior and anterolateral walls of the left ventricle and the anterior two-thirds of the septum. The left circumflex coronary artery (LCX) and its branches usually supply the posterolateral wall of the left ventricle. The right coronary artery (RCA) supplies the right ventricle, the inferior (diaphragmatic) and true posterior walls of the left ventricle, and the posterior third of the septum. The RCA also gives off the AV nodal coronary artery in 85-90% of individuals; in the remaining 10-15%, this artery is a branch of the LCX.
Usual ECG evolution of a Q-wave MI; not all of the following patterns may be seen; the time from onset of MI to the final pattern is quite variable and related to the size of MI, the rapidity of reperfusion (if any), and the location of the MI.
A. Normal ECG prior to MI
B. Hyperacute T wave changes - increased T wave amplitude and width; may also see ST elevation
C. Marked ST elevation with hyperacute T wave changes (transmural injury)
Often a difficult ECG diagnosis because in LBBB the right ventricle is activated first and left ventricular infarct Q waves may not appear at the beginning of the QRS complex (unless the septum is involved).
Suggested ECG features, not all of which are specific for MI include:
Q waves of any size in two or more of leads I, aVL, V5, or V6 (See below: one of the most reliable signs and probably indicates septal infarction, because the septum is activated early from the right ventricular side in LBBB)
Reversal of the usual R wave progression in precordial leads (see above )
Notching of the downstroke of the S wave in precordial leads to the right of the transition zone (i.e., before QRS changes from a predominate S wave complex to a predominate R wave complex); this may be a Q-wave equivalent.
Notching of the upstroke of the S wave in precordial leads to the right of the transition zone (another Q-wave equivalent).
rSR' complex in leads I, V5 or V6 (the S is a Q-wave equivalent occurring in the middle of the QRS complex)
RS complex in V5-6 rather than the usual monophasic R waves seen in uncomplicated LBBB; (the S is a Q-wave equivalent).
"Primary" ST-T wave changes (i.e., ST-T changes in the same direction as the QRS complex rather than the usual "secondary" ST-T changes seen in uncomplicated LBBB); these changes may reflect an acute, evolving MI.
5. Non-Q Wave MI
Recognized by evolving ST-T changes over time without the formation of pathologic Q waves (in a patient with typical chest pain symptoms and/or elevation in myocardial-specific enzymes)
Although it is tempting to localize the non-Q MI by the particular leads showing ST-T changes, this is probably only valid for the ST segment elevation pattern
Evolving ST-T changes may include any of the following patterns:
Convex downward ST segment depression only (common)
Convex upwards or straight ST segment elevation only (uncommon)
These are ECG conditions that mimic myocardial infarction either by simulating pathologic Q or QS waves or mimicking the typical ST-T changes of acute MI.
WPW preexcitation (negative delta wave may mimic pathologic Q waves)
IHSS (septal hypertrophy may make normal septal Q waves "fatter" thereby mimicking pathologic Q waves)
LVH (may have QS pattern or poor R wave progression in leads V1-3)
RVH (tall R waves in V1 or V2 may mimic true posterior MI)
Complete or incomplete LBBB (QS waves or poor R wave progression in leads V1-3)
Pneumothorax (loss of right precordial R waves)
Pulmonary emphysema and cor pulmonale (loss of R waves V1-3 and/or inferior Q waves with right axis deviation)
Left anterior fascicular block (may see small q-waves in anterior chest leads)
Acute pericarditis (the ST segment elevation may mimic acute transmural injury)
Central nervous system disease (may mimic non-Q wave MI by causing diffuse ST-T wave changes)
7. Miscellaneous Abnormalities of the QRS Complex:
The differential diagnosis of these QRS abnormalities depend on other ECG findings as well as clinical patient information
Poor R Wave Progression - defined as loss of, or no R waves in leads V1-3 (R £2mm):
Normal variant (if the rest of the ECG is normal)
LVH (look for voltage criteria and ST-T changes of LV "strain")
Complete or incomplete LBBB (increased QRS duration)
Left anterior fascicular block (should see LAD in frontal plane)
When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with subendocardial or transmural ischemia, followed by necrosis, and eventual fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time. Rupture of an atherosclerotic plaque followed by acute coronary thrombosis is the usual mechanism of acute MI. The ECG changes reflecting this sequence usually follow a well-known pattern depending on the location and size of the MI. MI's resulting from total coronary occlusion result in more homogeneous tissue damage and are usually reflected by a Q-wave MI pattern on the ECG. MI's resulting from subtotal occlusion result in more heterogeneous damage, which may be evidenced by a non Q-wave MI pattern on the ECG. Two-thirds of MI's presenting to emergency rooms evolve to non-Q wave MI's, most having ST segment depression or T wave inversion.
A. Normal ECG prior to MI
(Pathologic Q waves are usually defined as duration >0.04 s or >25% of R-wave amplitude)
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