Showing posts with label ST Elevation. Show all posts
Showing posts with label ST Elevation. Show all posts

Sunday, November 20, 2011

ECG-Myocardial Infarction

Source: ABC of ECG (BMJ)


Hyperacute T waves
The earliest signs of acute myocardial infarction are subtle
and include increased T wave amplitude over the affected area.
T waves become more prominent, symmetrical, and pointed
(“hyperacute”). Hyperacute T waves are most evident in the
anterior chest leads and are more readily visible when an old
electrocardiogram is available for comparison. These changes
in T waves are usually present for only five to 30 minutes after
the onset of the infarction and are followed by ST segment
changes.


ST segment changes
In practice, ST segment elevation is often the earliest recognised
sign of acute myocardial infarction and is usually evident within
hours of the onset of symptoms. Initially the ST segment may
straighten, with loss of the ST­T wave angle . Then the T wave
becomes broad and the ST segment elevates, losing its normal
concavity. As further elevation occurs, the ST segment tends to
become convex upwards. The degree of ST segment elevation
varies between subtle changes of < 1 mm to gross elevation of > 10 mm.



Pathological Q waves
As the acute myocardial infarction evolves, changes to the QRS
complex include loss of R wave height and the development of
pathological Q waves.
Both of these changes develop as a result of the loss of
viable myocardium beneath the recording electrode, and the
Q waves are the only firm electrocardiographic evidence of
myocardial necrosis. Q waves may develop within one to two
hours of the onset of symptoms of acute myocardial infarction,
though often they take 12 hours and occasionally up to 24
hours to appear. The presence of pathological Q waves,
however, does not necessarily indicate a completed infarct. If
ST segment elevation and Q waves are evident on the
electrocardiogram and the chest pain is of recent onset, the
patient may still benefit from thrombolysis or direct
intervention.
When there is extensive myocardial infarction, Q waves act
as a permanent marker of necrosis. With more localised
infarction the scar tissue may contract during the healing
process, reducing the size of the electrically inert area and
causing the disappearance of the Q waves.



Resolution of changes in ST segment
and T waves
As the infarct evolves, the ST segment elevation diminishes and
the T waves begin to invert. The ST segment elevation
associated with an inferior myocardial infarction may take up to
two weeks to resolve. ST segment elevation associated with
anterior myocardial infarction may persist for even longer, and
if a left ventricular aneurysm develops it may persist indefinitely.
T wave inversion may also persist for many months and
occasionally remains as a permanent sign of infarction.



Reciprocal ST segment depression

ST segment depression in leads remote from the site of an
acute infarct is known as reciprocal change and is a highly
sensitive indicator of acute myocardial infarction. Reciprocal
changes are seen in up to 70% of inferior and 30% of anterior
infarctions.
Typically, the depressed ST segments tend to be horizontal
or downsloping. The presence of reciprocal change is
particularly useful when there is doubt about the clinical
significance of ST segment elevation.

Reciprocal change strongly indicates acute infarction, with a
sensitivity and positive predictive value of over 90%, though its
absence does not rule out the diagnosis.
The pathogenesis of reciprocal change is uncertain.
Reciprocal changes are most frequently seen when the infarct is
large, and they may reflect an extension of the infarct or occur
as a result of coexisting remote ischaemia. Alternatively, it may
be a benign electrical phenomenon. The positive potentials that
are recorded by electrodes facing the area of acute injury are
projected as negative deflections in leads opposite the injured
area, thus producing a “mirror image” change. Extensive
reciprocal ST segment depression in remote regions often
indicates widespread arterial disease and consequently carries
a worse prognosis.



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Thursday, November 17, 2011

ST Elevation


Knowledge

The ST level is measured relative to the PR interval. While the U-P level theoretically would be preferred it cannot be used because it disappears with tachycardia. When there is a short PR interval, it can be particularly difficult for computer algorithms to find the isoelectric reference level. The direction of the ST vector and the relative position of the electrode measuring the vector determine whether the ST amplitude is positive (elevation) or negative (depression). For instance at rest, since the main ST vector projects along the long axis of the heart toward the apex, AVR will register a negative ST amplitude and V5 will register a positive ST amplitude (early repolarization). With tachycardia or ischemia the direction changes, as does the ST amplitude. As for any vector shift that is perpendicular to an electrode, no amplitude will be registered. Pathological processes that cause ST elevation shift the entire vector from it's long axis of the heart orientation and move it through the area of inflammation (pericarditis) or transmural ischemia (infarction or spasm). Thus, pathological ST depression does not localize but reflects a global subendocardial process while pathological elevation occurs directly over the involved area.
It is important to determine if the ST elevation was documented on previous ECGs and if the ST level is currently changing or is stable.
  • Acute or dynamic ST elevation can be due to severe transmural ischemia secondary to thrombus, spasm or a tight fixed coronary artery lesion or a combination of these situations. It can be the first ECG manifestation of an evolving myocardial infarction and it represents the ECG criteria for thrombolytic therapy. However, if the pain does not persist, it more likely is due to variant or unstable angina. The elevation localizes the ischemic lesion to the coronary artery supplying the area of myocardium reflected by the ECG leads. It represents transmural ischemia and is very arrythmogenic.
  • Chronic or persistent ST elevation could be due to an aneurysm when it occurs over Q waves or to chronic pericarditis (i.e., with uremia), but it most commonly occurs with a normal ECG pattern and is known as early repolarization. It may actually be due to late depolarization and is a very normal finding even to 3-4 mm in amplitude. Normally early repolarization lessens with increases in heart rate while ischemic ST elevation increases.

Recommendations

If the ST elevation has been present on prior ECGs:
If the ST elevation has been present on prior ECGs, the ECG does not exhibit diagnostic Q waves (no Q wave is wider than 35 millisec or 25% larger than the following R wave), and the elevation lessens with increases in heart rate then the benign finding of early repolarization is probable. The ECG with this finding usually will be obtained in a healthy, asymptomatic individual but it can also be obtained in a patient presenting with non-cardiac chest pain or with complaints due to another pathological process which makes the diagnosis more complicated. In this later circumstance, the early repolarization does not rule out a cardiac process but makes other diagnoses more likely.
If the ST elevation has been present on prior ECGs and occurs over diagnostic Q waves (Q wave wider than 35 millisec and 25% larger than the following R wave), a LV aneurysm or large wall motion abnormality is likely. In the case of an anterior location (i.e., V1-4), an abnormal precordial movement may be noted on examination. An echocardiogram would be the best way to evaluate LV function to see if an ACE inhibitor or other vasodilator was necessary to improve survival and lessen admissions for CHF.
When the ST elevation is a new finding:
The patient must be carefully questioned regarding ischemic symptoms including angina pectoris, chest pain, and shortness of breath, chest squeezing or pressure.
q      If the symptoms are consistent with myocardial ischemia, an aspirin and nitrates should be given immediately. If due to coronary spasm, the symptoms and elevation should resolve. If they do not, then thrombolysis should be given unless there are contraindications (bleeding disorder, recent stroke, operation or bleeding, etc). Enzymes should be drawn but treatment need not be delayed for their analysis. The ECG often also exhibits increased R and T wave amplitudes and the elevation usually is in the area of the coronary artery with spasm or thrombus.
q      If the patient's pain is pleuritic and positional, then consider pericarditis. A history of a URI or pneumonia, prior pericarditis, auto-immune disease and arthritis support the diagnosis of pericarditis. Physical exam may reveal a multi-component rub. ECG findings that also support pericarditis are PR depression, low amplitude T waves and ST elevation in multiple areas. If diagnosed, laboratory studies are indicated including renal function for uremia and patients should be closely followed for cardiac tamponade (distant heart sounds, narrow pulse pressure, pulsus paradoxus, hypotension). Echocardiography and cardiology consultation is usually indicated.
q      If the patient is asymptomatic, then the most likely diagnosis is Early Repolarization. To confirm this, the ECG can be repeated to see if the pattern is stable. "Silent Ischemia" , ischemia occurring without symptoms, is a rare possibility that usually need not be considered.

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