Thursday, January 28, 2010
There is ST depression, greater than 3 mm in some leads, in I-III, aVF, and V3-V6. aVR also has ST elevation.
Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main origin.
This patient was treated with nitroglycerine, ASA, and heparin. His pain diminished substantially but did not go away altogether. An ED ultrasound showed an anterior, apical, and septal wall motion abnormality. Repeat ECG showed most of the ST depression resolved (but not all).
There is no ST elevation, no evidence of occlusion that will cause imminent necrosis of a myocardial wall. But there is evidence of a very unstable atherosclerotic plaque that could completely thrombose at any moment. Also, his ongoing pain signified ongoing ischemia, which is an indication for immediate angiography and PCI. Therefore he was taken emergently (in the evening) to the cath lab. There was a severe ostial LAD thrombosis that was very close to the left main.
He went for emergent bypass that evening and had a good outcome.
ST elevation in aVR is often thought to represent left main occlusion. However, it really just signifies widespread and diffuse subendocardial ischemia which could be due to left main or 3-vessel disease, or severe proximal LAD disease. Left Main occlusion generally causes rapid death; most who survive left main ACS have some flow and thus often have widespread ST depression.
Think of aVR as (-)aVR. (-)aVR is 180 degrees opposite aVR and thus is between leads I and II. Thus, if I and II have ST depression, the (-) aVR must have ST depression, and (+) aVR must have ST elevation.
There is sinus rhythm with a PVC, and Right Bundle Branch Block (RBBB). Normally there is no ST elevation with RBBB. In fact, normally, there are inverted T waves (discordant to a positive QRS due to the large R' wave, of the rSR') and from 0-1 mm of ST depression. Any ST elevation in V2 or V3 is very suspicious for LAD occlusion in a patient with chest pain.
The cath lab was activated, but the interventionalist disagreed with the interpretation. A stat echocardiogram revealed anterior wall motion abnormality and the patient was taken for angiography which revealed a 95% ostial thrombotic LAD lesion. She went for immediate coronary bypass surgery.
A similar case was posted on January 12, 2010. You can search for all the RBBB in the search box, or any of a great number of search terms to find other ECGs
Thursday, January 21, 2010
There is sinus rhythm and a normal QRS. But repolarization is abnormal: there is scooped ST depression in I and aVL; there is a very prolonged QT interval (I measure a QT of 440 ms and QTc of 580 ms, though the computer got it very wrong at 440 ms); there are prominent U-waves (the bump between the T-wave and p-wave) in V2-V5.
The ECG is pathognomonic of hypokalemia. When the level returned, it was 2.3 mEq/L.
In a derivation study (which we have submitted only as an abstract so far) of ECGs of patients with hypokalemia vs. controls, in which interpreters were blinded to the K, we found very high sensitivity and specificity for a K less than vs. greater than 3.0 with any one of QTc of 450 ms or prominent U-waves or a subjective reading of hypokalemia.
Friday, January 15, 2010
There is very minimal ST elevation in aVL (less than 1 mm). Now look at V2 where there is less than 1 mm of ST elevation. This cannot be normal (early repol) because there is a Q-wave. Also, the QTc is 483 ms. This is very suspicious for an LAD occlusion or subtotal occlusion.
The cath lab was activated and there was an 80% occlusive thrombus in the proximal LAD with TIMI II flow. A post cath ECG (below) shows even more ST elevation, with loss of R-wave in V2, and a much deeper Q-wave.
This was a very large territory at risk. The post-PCI ejection fraction was 40%, where it was normal before. The convalescent EF was 53%.
Even with a very subtle ECG, without the "required" 1 mm of ST elevation, there may be a subtotal coronary occlusion with very much myocardium at risk of permanent infarction.
In my study of 355 consecutive proven LAD occlusions, of which 212 were excluded because they were electrocardiographically obvious, there were 143 remaining consecutive electrocardiographically subtle proven total LAD occlusions. Of these 143, 17 (12%) had a mean (V2-v4) ST elevation at the J point of less than 1 mm and 14 (10%) had a mean equal to 1 mm. Thus, 22% of these subtle LAD occlusions, or at least 9% of all LAD occlusions, had a mean STE less than or equal to 1 mm. 19 had no lead with more than 1 mm and 8 had less than or equal to 1 mm in only one lead.
Low R-wave amplitude was a better predictor of LAD occlusion than was ST elevation. QTc was very helpful as well. I have published several abstracts on this and am in the process of analyzing the data for a full manuscript.
In subtotal occlusions such as this one, the proportion with such subtle ST elevation is much higher.
Tuesday, January 12, 2010
There is Right Bundle Branch Block with large R-wave in V1 (the first R wave of the rsR' is not present) and wide S-wave in lateral leads I, aVL, V5 and V6. There is a slight amount of ST elevation (1 mm) in lead V3, and slightly more in V4-V6. The T-wave is upright in leads V2 and V3. Usually, but not always, RBBB has an inverted T-wave with up to 1 mm ST depression in leads V2 and V3, so these upright T's with slight ST elevation is highly suspicious for anterior STEMI. The ST elevation in lateral leads is diagnostic.
In this case, the diagnosis was particularly easy because there was a prior ECG available:
Here the normal baseline is easy to see for comparison. There was an rsR' before (now the first R may be lost because of anterior wall ischemia), there was T inversion (normal) and ST depression (normal) in V2 and V3. There was no ST elevation in lateral leads (there never should be in RBBB).
The cath result was complex, but suffice it to say that there was TIMI-2 flow in the LAD by the time of cath.
this is the first ECG at 1559:
There is very subtle and < 1 mm ST elevation in II, III, and aVF. The T-waves in these inferior leads are much larger than normal, with almost the same voltage as the QRS, and are "fat". These are hyperacute T waves. Just as importantly, there is minimal reciprocal ST depression in aVL, with T wave inversion. This is diagnostic for inferior STEMI, even though it doesn't meet the arbitrary criteria of 1 mm ST elevation in 2 consecutive leads. The cath lab was activated and a distal RCA thrombus with TIMI-0 flow was seen. For technical reasons, it could not be opened. An ECG was repeated, showing the development of the inferior MI without reperfusion:
There is abormal deep T wave inversion in anterior leads suggestive of Wellens' syndrome, although true Wellens' should have better R-wave preservation. This ECG is diagnostic of MI, but is not a STEMI. Though this has never been explained or studied in the literature, it is clear to me that Wellens' is the consequence of a spontaneously reperfused STEMI. The Wellens' ECG is identical to the ECG of patients who reperfuse MI with fibrinolysis or PCI. Wellens' is always in a pain-free patient and the angiogram always shows tight LAD lesion with either good flow or collateral flow.
35 minutes later his son reported that he had a "funny feeling" and "tightness in the throat;" at the same time the initial troponin returned positive at a low level. A repeat ECG was recorded:
Now the T-waves are upright (not normal, but "pseudo"normal). This is indicative of re-occlusion. Where Wellens' is spontaneous reperfusion, pseudonormalization is spontaneous re-occlusion of a Wellens' syndrome.
This patient had an LAD occlusion.
HyperKalemia with Cardiac Arrest. Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia
For more on hyperkalemia, click here (includes a great case of incessant ventricular tachycardia).
For more on early repolarization, see these cases:
For differentiation of early repol from LAD occlusion, click here.
Hyperkalemia resulting in cardiac arrest
Although there is little high quality data on differentiating these entities, some general insights are useful, and illustrated with the following cases:
The first ECG is one of a 27 y.o. patient who presented with ventricular fibrillation.
ECG #1, hyperkalemia
Because of the large T-waves, this ECG was interpreted as "hyperacute T-waves". However, these T waves are pathognomonic of hyperkalemia because they are peaked, "tented", come to point, have a very flat ST segment, and there is a long QRS (114 ms).
Conventional wisdom (with no hard data, to my knowledge) says that when hyperkalemia has a normal QRS that the QTc should be short. This idea conforms with the complex electrophysiology of hyperkalemia, but may not always be true in real life.
ECG #2, LAD occlusion
In this ECG#2 above, the T-waves are slightly more blunt at the peak, there is a normal QRS duration with a long QTc at 450 ms, the ST segment is straightened (less upward concavity, steeper ST segment) which results in an area under the curve (integral) that is larger than in either hyperkalemia or early repol (i.e., the T-wave is "fat")
Below (ECG #3) is a case of a patient who presented feeling moderately ill:
EKG #3, hyperkalemia, QTc 497 ms, QRS 102 ms (normal is less than 110ms)
|See V4 especially. The ST segment is horizontal until it abruptly rises to a very peaked T-wave. The T-wave is "tented" to a point.|
EKG #4, early repolarization, QTc 455 ms, QRS 82 ms
|Notice the ST segments here are not nearly as flat, and the rise to a peaked T-wave, especially in lead V4, not nearly as steep|
This patient, then did not get immediate treatment for hyperK. He actually had a v fib arrest while in his room, before his K returned from the lab. This was a presumed hyperkalemic arrest. He was immediately resuscitated, then his K returned at 7.0 mEq/L.
Some say you don't need to treat hyperK unless there is QRS widening. They claim that peaked T-waves are not enough. This is only one case, and anecdotal, but we found no other etiology of arrest in this patient. I always treat immediately if the ECG is affected by hyperK.
In addition, the QRS duration difference is important; the difference in QTc seems to defy conventional wisdom.
There is a definite difference, with EKG#3 pathognomonic for hyperkalemia.