Dr. Smith's ECG Blog

Chest pain and hypotension in a patient who is 3 weeks post STEMI

2012-01-28T14:19:00.004-06:00

A middle aged patient who was 3 weeks s/p STEMI came from cardiac rehab where he developed some chest pain, dyspnea and weakness on the treadmill. In the ED he had some continued chest pain and hypotension. Here was his ECG:

There are inferior and lateral Q-waves with T-wave inversion in the corresponding leads. There is minimal ST elevation. There is no acute STEMI. This is diagnostic of recent, reperfused STEMI. The T-inversions are "reperfusion T-waves."

This looks like the typical ECG of someone who had a recent Q-wave MI. The small amount of ST elevation is persistent, not acute. Acute STEMI would have upright T-waves. With re-occlusion, the T-waves become upright (pseudonormalize, as in these cases). The patient might be having cardiac ischemia, but if he is, it is unstable angina or non-STEMI, or perhaps he has not YET pseudonormalized, so serial ECGs may be important.

Below are his presenting STEMI ECG and his post-PCI ECG from 3 weeks prior:

Because of the hypotension, chest pain, and T-wave inversions, the physicians were worried about MI, took the patient to the critical care room, and called the cardiologists. However, these T-wave inversions should be expected at one month after MI. This is normal for these patients.

They also did an ED bedside ultrasound, shown here:

This shows a large amount of pericardial fluid, with some echogenic structures that appear to be thrombi or fibrinous exudate. The RV free wall collapses, indicating tamponade. If you are uncertain where the pericardial fluid is, I have annotated still images with arrows at the bottom of the post.

The differential includes hemopericardium from myocardial rupture, or from coronary artery rupture from PCI, or Dressler's syndrome of post-MI pericardial effusion.

After pericardiocentesis was unsuccessful, he was taken to the OR for a pericardial window. 300-450 ml of serosanguinous fluid was drained. The patient was given a probable diagnosis of Dressler's syndrome.

Differential of peri-infarct pericardial fluid
The differential includes 1) pericarditis with effusion or 2) hemopericardium.
1) Pericarditis with effusion:
   a) If 3 weeks after MI, then Dressler's syndrome (Dressler's syndrome is also known as post-myocardial infarction syndrome, post-cardiac injury syndrome and postpericardiotomy syndrome), which is a late post-MI autoimmune pericarditis occurring about 3-4 weeks after the MI. Dressler's syndrome appears to be quite rare, according to Shahar and Lichstein.
   b) Nonspecific pericarditis
2) Hemopericardium would be due to myocardial rupture, which could be due to:
   a) Rupture of a coronary artery due to PCI or
   b) Free wall Myocardial rupture (see below, next paragraph).

Myocardial rupture is not uncommon. It is found on 1% to 3.5% of autopsies of patients who died of MI. It is associated with transmural MI; since most STEMI are aborted with reperfusion therapy, it is not as common as it once was. It is more common in women, and in patients who have a first MI and have a good EF, as it requires a pump force from the healthy myocardium to produce high pressure which ruptures the infarcted myocardium. The "rupture" is not an explosion, rather a small tract through the myocardium which leaks blood into the pericardium, and kills by tamponade.
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Myocardial rupture is usually preceded by postinfarction regional pericarditis (PIRP). PIRP is indicated on the ECG by 2 findings: 1) persistently positive (upright) T-waves at 48 hours, or 2) premature reversal of inverted T-waves to positive deflection by 48 to 72 hours after STEMI. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual. There should be QS-waves indicative of completed transmural MI.
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Patients who present with chest pain or cardiac arrest and have an ECG diagnostic of STEMI could have myocardial rupture. Obviously, administration of heparin and/or lytics is hazardous. These patients may survive. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. 5 of 6 presented with chest pain and an ECG indicating reperfusion therapy, but were detected by bedside ultrasound.
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Plummer D et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of EM 23(6):1333-1342; June 1994.
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For more information, see chapter 28 of Smith's "The ECG in Acute MI."

Below are still images of the ultrasounds. White arrows point to pericardial fluid.

Left ventricular Aneurysm Morphology Distorted by Right Bundle Branch Block, Mimicking Acute STEMI with RBBB

2012-01-25T08:41:00.001-06:00

This is a complex case that I have reprinted from my article in the EMRA publication, EM Resident, with their permission. I'm starting with some didactics. If you want skip to the case, page down, but it is difficult to understand without knowing the background information.

GENERAL BACKGROUND

Prior Myocardial Infarction/Left Ventricular Aneurysm

Approximately 60% of patients with a previous anterior transmural MI, and fewer inferior MI patients, may have persistent ST Elevation (STE),¹ mimicking acute STEMI. Of those with anterior persistent STE, approximately 80% have an anatomic left ventricular (LV) aneurysm (LVA), which can be seen on echocardiogram as “diastolic distortion” or myocardial wall thinning.^{2, 3} In the reperfusion era, transmural MI is uncommon, and so the incidence of persistent STE is less than it once was. In a 1987 series of patients with a prior MI presenting with chest pain and STE, only 50% proved to have an acute MI.⁴ Persistent STE may also be associated with systolic dyskinesis, akinesis, or a large area of myocardial necrosis, even in the absence of anatomic ventricular aneurysm.⁵

LVA of the anterior wall results in Qr-waves (deep Q followed by a small r-wave) or QS-waves (single deep negative wave) in V1-V4, followed by a moderate degree of STE. The QS-waves indicate complete loss of anterior electrical forces during depolarization. The T-wave may be upright (but not large or hyperacute as in acute STEMI) or inverted (but not deeply inverted, as in acute Non-STEMI). Inferior LVA has STE and QR-waves, not QS-waves, and is thus much more difficult to differentiate from acute inferior STEMI.

We found the best discriminator of LVA vs. acute MI is the T wave amplitude/QRS amplitude ratio, and derived and validated this ratio: if (sum of the T wave amplitude) ÷ (sum of QRS amplitude) in V1-V4 is greater than 0.22, it favors AMI with good sensitivity and specificity.⁶ If any one lead has a ratio greater than 0.36, it is acute STEMI with equal accuracy. False negatives had a long time between symptom onset and ECG, so that the T-wave was no longer tall. We also validated this rule, published as an abstract (7). Just as useful is evaluation of an index ECG (prior ECG), but these are not always available. Echocardiography may also be useful if it shows dyskinesis (diastolic dysfunction); unfortunately, persistent STE after old MI also occurs without anatomic aneurysm. STE with echocardiographic regional wall akinesis or hypokinesis is present in both acute STEMI and old transmural MI. In some cases, coronary angiography will be required to make the diagnosis. New STEMI in the same location as previous Q-wave MI may also have deep QS-waves, but also has tall T-waves and an increase degree of STE.

An example of classic LV aneurysm morphology (figure 1).

There is QS pattern in V1-V3 with anterior STE. The T-wave amplitude is not sufficient for acute MI. If you apply either ratio rule, it turns out to be LV aneurysm. This is a classic LV aneurysm morphology.

Normal Right Bundle Branch Block (figure 2)

This is normal RBBB, with rSR’, slight ST depression in V2 and V3, and no ST elevation anywhere.

A non-pathologic RBBB has an rSR’ in V1-V3 and no ST elevation anywhere on the ECG. In RBBB, an absence of an r-wave in lead V1 only may be normal, but if it extends to V2 and beyond it is always abnormal, and the differential includes not only RBBB with MI but also RBBB with left ventricular hypertrophy, and RBBB with cardiomyopathy. There is usually up to 1 mm of ST depression in V2 and V3, discordant (opposite direction of) the positive R’ wave (see figure 2). If there is a very large voltage R’ wave, as in right ventricular hypertrophy, this ST depression may be greater than 1mm in the absence of acute ischemia. To determine the presence or absence of STE in RBBB, one must first determine the end of the QRS, which is the beginning of the ST segment (the J-point).

Case presentation: Right bundle branch block (RBBB) transforms a QS- into a QR-pattern, obscuring diagnosis of left ventricular aneurysm, and suggesting acute STEMI and RBBB.

A 79 year old man presented with dyspnea. He stated that he had sustained a recent myocardial infarction and that it had been painless. His presenting ECG is shown here (figure 3):

There is sinus rhythm at almost 100 beats per minute. There is a large R-wave at the end of the QRS complex in V1, and wide S-waves in lateral leads I, aVL, V5 and V6, with a QRS duration greater than 120 ms, diagnostic of RBBB. There is absence of r-wave in V1-V4, resulting in a QR, rather than an rSR’ wave. If the r-wave is absent, then it is a Q-wave, which strongly suggests a Q-wave MI (whether due to acute or old MI). Figure 4 magnifies V1-V3 and shows how to find the end of the QRS, which is the J-point and beginning of the ST segment.

Here is a magnification of V1-V3 (figure 4):

Arrows show the end of the QRS and thus the beginning of the ST segment; this is the J-point. It is apparent, then, that the ST segment is elevated.

Case continued:

Thus there are anterior Q-waves and anterior STE. So it is an acute STEMI, right? I saw this patient in the late 1990’s (and have seen others since) and administered tPA for acute MI. Before the tPA had time to work, the rate slowed and the RBBB disappeared and showed the ECG in figure 1 above.

Old records were retrieved, and indeed the patient’s previous ECG was the same. In fact, he had presented one week earlier with the exact symptoms and exact same RBBB ECG and received tPA from one of my partners!

How is this possible? Normally, anterior LVA has no or little R-wave amplitude. However, this patient has rate-related RBBB. His right bundle has a long refractory period so that when his rate increases, his right bundle is refractory and does not conduct. In RBBB, there is automatically a large R’-wave even if there the anterior wall is dead, simply because of the sequence of depolarization. So the LVA morphology gets replaced and distorted.

How can you suspect this? On the ECG, it is nearly impossible, as far as I can tell. So you must use other clinical data. First, you have to know that this is possible. Second, you can use echocardiography to assess for aneurysm (diastolic dysfunction or bulging), but if you see only systolic dyskinesis, it could be either LVA or acute STEMI.

In contrast to LVA, patients with acute STEMI who have Q-waves have a larger T-wave. See figure 5 for an example of a patient with QS-waves but with hyperacute T-waves, such that the T/QRS ratio is high. It was an acute LAD occlusion.

Figure 5. There are QS-waves as one would see in LV aneurysm, but there are large T-waves, as is seen in acute STEMI. The T/QRS ratio is high. It was an acute LAD occlusion.

References

1. Mills RM, Young E, Gorlin R, Lesch M. Natural history of S-T segment elevation after acute myocardial infarction. Am J Cardiol 1975;35(5):609-14.

2. Visser CA, Kan G, David GK, Lie KI, Durrer D. Echocardiographic-cineangiographic correlation in detecting left ventricular aneurysm: A prospective study of 422 patients. Am J Cardiol 1982;50(2):337-41.

3. Visser CA, Kan G, Meltzer RS, Koolen JJ, Dunning AJ. Incidence, timing and prognostic value of left ventricular aneurysm formation after myocardial infarction: A prospective, serial echocardiographic study of 158 patients. Am J Cardiol 1986;57(10):729-32.

4. Miller DH, Kligfield P, Schreiber TL, Borer JS. Relationship of prior mycardial infarction to false-positive electrocardiographic diagnosis of acute injury in patients with chest pain. Arch Intern Med 1987;147:257-61.

5. Arvan S, Varat MA. Persistent ST-segment elevation and left ventricular wall abnormalities: a two-dimensional echocardiographic study. Am J Cardiol 1984;53(11):1542-6.

6. Smith SW. T/QRS amplitude ratio best distinguishes the ST elevation of anterior left ventricular aneurysm from anterior acute myocardial infarction. American Journal of Emergency Medicine 2005;23(3):279-87.

7. Beeman W. Shroff G. Smith SW. T/QRS Amplitude Ratio Is Significantly Higher In Acute Anterior ST Elevation Myocardial Infarction Than In Previous Myocardial Infarction With Persistent ST Elevation (left Ventricular Aneurysm Morphology): A Validation (abstract 371). Annals of EM Oct 2011 Suppl 58(4): S302.

Subtle Anterior Transient Injury Pattern, Not Appreciated, LAD occlusion spontaneously reperfused

2012-01-20T08:30:00.001-06:00

This 41 yo male was cleaning using a chemical and experienced sudden substernal chest burning radiating to both arms with SOB, relieved by sublingual NTG. He called 911 immediately. Here is the prehospital ECG at 1143:

There are precordial hyperacute T-waves. The QTc is only 392, but there is very poor R-wave progression and the ST elevation, though less than 1 mm at the J-point, is 3 mm at 60 ms after the J-point, which indicates a steep ST segment. The equation value (see side bar of blog, with excel spreadsheet) is 25.1. A value greater than 23.4 indicates that this ST elevation is not a normal variant early repol, but anterior STEMI. More importantly, there is ST depression in "inferior" leads and this is reciprocal to extremely subtle STE in aVL and a T-wave that is massive when compared to the QRS. (There is also some subtle STD in V5 and V6, which is another clue to STEMI). The QRS is so small in aVL that the ST elevation can barely register. The computer had nothing to offer. The medics were worried.

Here is aVL blown up so you can see the relative size of the T-wave and QRS:

Tiny T-wave in aVL is giant when compared to the QRS. This is a hyperacute T-wave

On arrival, the pain was resolved and this ECG was recorded at 1201:

Notice the R-wave amplitude has recovered. STE at the J-point is no different, but it is less at 60 ms after the J-point because the T-waves are not hyperacute any more. The QTc is 401. The T-waves are less hyperacute. Equation value is now 22.5. There remain some abnormalities in "inferior" leads.

So we have here a patient with a proximal LAD occlusion that has reperfused on its own (or due to NTG).

The findings of the first ECG, and their difference from the 2nd ECG, were not entirely appreciated, so the cath lab was not activated.

A while later, the first ECG was shown to me without any clinical data and, due to all the characteristics I have described, I was able immediately to say that it is an anterior STEMI. Then, upon looking at the ED ECG, I immediately knew it was reperfused. I knew there was a 90% unstable proximal stenosis with thrombus.

A reperfused anterior STEMI is a dangerous situation. I once had a patient who reperfused the LAD, so I deactivated the cath lab, then he re-occluded and I re-activated the cath lab. The delay caused his death.

This could happen in this case, so it is imperative to at least treat aggressively with antiplatelet and antithrombotic therapy. The cath lab was in use, so this therapy was started, and cardiology was consulted.

Cardiology did an echocardiogram. I was worried that they would find a normal echo. This occlusion was so brief that the anterior wall, though it would have had a motion abnormality during occlusion, could completely and rapidly recover after reperfusion. Thus, a normal echo would give a false sense of security: if normal, it would not rule out previous anterior injury pattern. The ECG does not lie, and in the right hands is better than an echo. This is an unequivocal ECG, especially with the serial findings.

Fortunately, the echo showed some subtle abnormality in the septum, but it was read by one of the world's experts in echocardiography and perhaps most would not have seen this abnormality and would have dismissed the ECG findings. Then the patient might be admitted and re-occlude (and die?).

The first troponin was normal (so that is of no help).

The two of us talked and arranged for a cath.

Before his cath, this ECG was recorded at 1321:

There is further resolution of the findings and it is now normal.

Cath showed a 95% proximal LAD stenosis with thrombus. A stent was placed.

Here is the ECG the next AM:

QTc is 378, there is no ST elevation whatsoever. T-waves are much smaller than they were. This probably represents the patient's baseline ECG, but we can't know for certain.

The peak troponin I was 0.9 ng/ml. It is interesting that the ECG did not evolve any T-wave inversion, as might be commonly seen with Wellens' syndrome. This goes to show that not all brief LAD occlusions result in Wellens' pattern of reperfusion T-waves.

This was called by the interventionalist and cardiologists a "Non STEMI." Had the ECG findings not been seen in the ED, no one would ever have known that STEMI was missed.

Serial ECGs confirm initial suspicion of anterior STEMI (LAD occlusion)

2012-01-15T06:37:00.001-06:00

A 52 yo man began having substernal chest discomfort and presented 2 hours later. His prehospital ECG, which I cannot find, reportedly had some ST depression in precordial leads. He had this ECG recorded at 0658:

There are hyperacute T-waves in V1-V4. There is minimal ST elevation, almost 1 mm in V2 and less than 0.5 mm in V3, but this is diagnostic of anterior STEMI even without ST elevation. Using the equation (which may not be applicable because there is not enough ST elevation to even qualify for early repol), and the computerized QTc of 424, the value is 25.995 (greater than 23.4 is LAD occlusion).

The clinicians who saw this patient do not, like me, spend their lives analyzing the minutiae of ECGs, so they were not certain of the diagnosis, but they did suspect it, so they did the entirely appropriate management of obtaining serial ECGs, and a repeat ECG was done at0713:


Still suspicious for hyperacute T's but no ST elevation or significant evolution. The T-wave in V2 is less prominent, suggesting some reperfusion. QTc is 436 and equation remains greater than 23.4

So another was recorded at 0720:

Now there is ST elevation in V2 and V3, diagnostic of LAD occlusion

Another at 0726:

Not much changed

Another at 0744:

Now it is unequivocal

At this point, the cath lab was activated.

This is the post cath ECG:

Cath showed a complete mid-LAD occlusion. Peak troponin I was 120, even with a short door to balloon time, and even though the initial ECG was not striking. The echo showed a large anteroapical wall motion abnormality.

I suspect the prehospital ECG had de Winter's ST depression and T-waves.

Extremely subtle inferior MI

2012-01-07T10:28:00.001-06:00

A 45 yo woman with several coronary risks but no history of coronary disease developed 10/10 "gnawing" retrosternal chest pressure at rest at 7:30 PM. She thought it was reflux, but antacids did not relieve it. She did not arrive in the ED after pain all night (not certain if it was constant or intermittent) until the next AM when this ECG was recorded:

There is sinus bradycardia with a PVC, and an artifact on the 8th complex. There is a significant Q-wave in lead III, with very subtle ST elevation in leads III and aVF, and, importantly, some reciprocal ST depression in aVL. There is also high voltage suggestive of LVH, but no repolarization abnormalities that are typical of LVH.

Let's look at the limb leads enlarged:

Here the ST elevation in leads III and aVL is more clear, with reciprocal ST depression in aVL are more apparent

This is very suspicious for inferior MI of unknown age. It could be old MI with persistent ST elevation, or it could be subacute MI with new Q-wave, but is unlikely to be very acute (with a Q-wave and without large T-waves). If it is a subacute MI, there should be a positive troponin.

The first troponin I returned at 0.74 ng/ml, diagnostic of MI. Is this STEMI or NonSTEMI? That is an arbitrary definition, based on millimeters of ST elevation. Every physician should know that biologicial systems do not follow millimeter rules, so many "NonSTEMIs" are due to coronary occlusion.

The important thing is whether the patient has ongoing ischemia after almost 12 hours of chest pain, and as long as the ST segments are elevated or depressed, or the patient has chest pain, one must assume there is ongoing ischemia and do something about it. She did receive antithrombotic and antiplatelet therapy, and nitroglycerine, but her pain did not subside until she received hydromorphone. Then it was not until a second troponin returned at 4.40 ng/ml 4 hours later, that she was taken to the cath lab.

Cath revealed a 100% occlusion of the mid- first obtuse marginal (OM-1). Troponin I peaked at 49 ng/ml. Echo showed an inferolateral wall motion abnormality and concentric hypertrophy.

Here is her post cath ECG for comparison:

ST segments are back to baseline

Here it is enlarged:

Learning points:

1. Any ST depression in aVL is abnormal. Tikkanen et al. studied inferior early repolarization (baseline ECG with ST elevation). By personal communication, they have told me that only 1 of their 71 cases had reciprocal ST depression in lead aVL, and that this patient also had WPW. We are going to combine our data for inferior STEMI (159 of 160 had some ST depression in aVL) and our data on pericarditis (none of 39 had any ST depression) with their data on early repol to show that any ST depression in aVL is highly sensitive and specific for inferior MI.

2. "NonSTEMIs" may be large and due to complete persistent coronary occlusion that needs emergent reperfusion. Millimeters do not measure occlusion. Large MI may be very subtle on the ECG. This was not a small MI, with peak troponin of 49. I do not know what the convalescent ejection fraction or wall motion abnormalities were, but they might be significant here. (The initial echo shows stunned myocardium that may recover with time.)

3. Inferior MI does not always mean Acute MI. This patients initial ECG could represent old MI with persistent ST elevation, subacute MI, or old MI with superimposed acute MI. When the patient has such typical pain, and especially when you have a positive troponin, assume it is acute or subacute.

4. Opiates will obscure the diagnosis of MI. Morphine has been associated with higher mortality in ACS and I believe this is because the relief of pain is confused by physicians as relief of ischemia.

5. If in doubt, get an immediate echocardiogram. In this case, it would have confirmed MI and allowed for earlier cath lab activation. It may not differentiate old MI from acute MI, and I think the Q-wave here is diagnostic of old MI, so in this case echo is not so helpful.

6. Positive troponins alone are not grounds for cath lab activation. There must also be ongoing ischemia as evidenced by the ECG or ongoing pain, as in this case.

The Same Theme: Large Lateral STEMI is Subtle on the ECG

2012-01-03T13:19:00.001-06:00

This is a 34 yo female with no history of CAD who had the onset of chest pain at 0900. It was constant, achy, substernal, 7/10, non-radiating, aggravated by smoking and movement and relieved with short deep breaths. She took analgesics without relief. She had had an episode one week prior. She smokes 2 packs per day and has a family history of early CAD. She has diet controlled DM. She presented at 1930 and had this ECG recorded:

There is just under 1 mm of ST elevation in I and aVL, with reciprocal ST depression in inferior leads, especially III. This should alert you to the high probability of lateral MI. This STE is more pronounced than in this case which was a false positive, posted a few days ago. Notice also that there is less than 1 mm of ST depression in V1-V3. This is highly suspicious for concomitant posterior MI, and should raise your index of suspicion very high because lateral MI is frequently accompanied by posterior MI when the circumflex artery is involved.

The clinicians did not appreciate these findings. They administered aspirin and arranged for a telemetry bed. The patient continued to have pain and 2 more ECGs were recorded at 2145 and 2225, without any evolution. At 2059, the first troponin I returned at 14.19 ng/ml, confirming AMI of considerable duration. Apparently, the clinicians must have believed at first that it was a NonSTEMI because they waited until 2245 to activate the cath lab.

At cath, there was a 100% occluded proximal circumflex which was opened and stented. The troponin peaked at 300! (very large MI). Echo the next day showed a posterolateral wall motion abnormality and an ejection fraction of 40%. Here is the post cath ECG:

ST segments have resolved, confirming good microvascular reperfusion.

One week later, this was recorded:

Now there are clearly inverted T-waves in I and aVL (lateral reperfusion T-waves). If there were posterior leads, the T-waves would be inverted, but since they are recorded in anterior leads, we see instead a phenomenon that I call "posterior reperfusion T-waves"--the T-wave which would appear inverted on posterior leads appears larger on anterior leads.

Learning point: Lateral MI may be very large but electrocardiographically subtle. Inferior ST depression is nearly always seen in lateral MI. Concomitant right precordial (V1-V3) ST depression makes the case for lateral MI, as the posterior wall is often supplied by the circumflex.

Subtle Lateral ST elevation. False positive. This diagnosis is hard.

2011-12-27T10:39:00.001-06:00

Case 1. A middle-aged woman presented with severe substernal crushing chest pain radiating to the left shoulder. This was her presenting ECG:

There is a Q-wave in aVL and Minimal ST elevation in I and aVL (less than 0.5 mm) in the context of a 10 mm QRS. There is minimal reciprocal ST depression in III. There are some features of left anterior fascicular block, but there is not enough left axis deviation to meet criteria for this. This could be high lateral MI with circumflex or diagonal occlusion.

Management options are to get an immediate echocardiogram, look for old EKGs (there were none), do serial ECGs, or just do an immediate angiogram. The interventionalist was consulted and he opted to go for immediate cath. It was negative.

Below are 3 typical cases (cases 2-4) of lateral ST elevation with inferior reciprocal ST depression that were actually circumflex or diagonal occlusions. In these cases, the findings are not as subtle as in case 1. But when you look at the last case (case 5), you'll see how subtle real occlusion can be.

It is important to remember that only about 50% of lateral MI due to coronary occlusion have significant ST elevation, and for this reason the lateral wall is often called "electrocardiographically silent." Often this is due to low QRS voltage in lateral leads, and because ST elevation is always proportional to the QRS, the ST eleavtion is low voltage. (See Schmitt et al. Chest 2001;120(5):1540-6, free full text)

Case 2.

Acute Circumflex occlusion (also old inferior MI with Q-waves, and early repol giving anterior STE)

Case 3.

Lateral STEMI with very low voltage QRS in aVL, therefore very low voltage STE in aVL, but best seen by marked ST depression in inferior leads. Diagonal occlusion. Remember ST depression in inferior leads is not inferior ischemia, but rather reciprocal to lateral STEMI

Case 4.

Circumflex occlusion with hyperacute T wave in aVL and reciprocal inferior ST depression. Notice the precordial ST depression of concomitant posterior STEMI.

Case 5a.

D2 occlusion, lateral MI

Case 5b.

After nitroglycerine, inferior ST depression and STE in aVL resolve. D2 is open by the time of angiography.

Here is one of the most popular posts of all time, also relevant to this: ST depression does not localize: 2 cases of "inferior" ST depression of high lateral STEMI.

Ventricular fibrillation on a 12-lead ECG

2011-12-19T10:24:00.004-06:00

A 54 year old male suddenly collapsed. He had not complained of symptoms prior to this. He received bystander CPR, then was defibrillated when the medics arrived. He arrived in the ED awake. The following ECG was recorded:

There is sinus tachycardia with diffuse ST depression (I, III, III, aVF, V2-V6), with obligatory ST elevation in aVR (ST depression maximal in leads II and V4 establishes the ST vector as upward and rightward; there must be ST elevation in aVR).

This is typical of NonSTEMI with ischemia from acute 3-vessel ischemia or left main stenosis. It establishes ongoing ischemia, though sometimes may be residual after cardiac arrest. So a repeat ECG should be done a short time later in order to establish whether there is, indeed, ongoing ischemia. Thrombolytics are never given for such an ECG, but angiogram and PCI are indicated if medical therapy alone does not control the ischemia.

Amiodarone 150 mg was given, along with aspirin, heparin, and eptifibatide. Because of tachycardia and thus a risk for cardiogenic shock, no beta blocker was given. BP was adequate and so nitroglycerine drip was started. Clopidogrel (or any thienopyridine) was not used because the ST elevation in aVR makes the probability of CABG high.

15 minutes later, the patient was awake enough to take a history. He stated that he had ongoing chest pressure, strongly suggesting ongoing ischemia. The leads were placed for a repeat 12-lead ECG, and we were talking to the patient when the ECG tech said, "Hey, guys, uh......" We looked up and this is what we saw:

12-lead ventricular fibrillation. Not seen very often!! Notice how similar ventricular fibrillation is to torsade. By the way, the computer read: sinus tachycardia with frequent multiform PVCs!!!!

The patient was awake but becoming obtunded when he was defibrillated successfully with one shock; he did not remember it.

Recurrent v fib in the setting of ischemia is diagnostic of ongoing and uncontrolled ischemia. The only way to control this is with PCI, if angiogram shows a lesion amenable to therapy.

A second 150 mg dose of amiodarone was given.

Angiogram showed 3-vessel disease and 3 lesions in the LAD which were stented. He did well.

Right Ventricular MI seen on ECG helps Angiographer to find Culprit Lesion

2011-12-17T08:43:00.000-06:00

This is a video I made a while back. I thought it was worth a re-post. For those who don't have time to watch a video, you'll have to read the ECG as shown on this still frame because I lost it and cannot post it.

See down below for explanation if you don't want to watch the video.

A 56 year old woman with chest pain and hypotension:

There is inferior STEMI. But there is also ST elevation in leads V1 and V2. When you see this, think right ventricular (RV) MI. The hypotension is further evidence for RV MI. There was no right sided ECG.

I heard about the case, and saw the ECG, shortly after the patient left for the cath lab. I called the interventionalist while the patient was on the table and he told me that the occlusion was not in the proximal RCA, but further down. I asked if he was sure about this, because the ECG would indicate a proximal RCA occlusion with RV MI. He took another look and realized that the culprit was indeed in the proximal RCA and that the thrombus had embolized distally. And so he put the stent in the proximal RCA.

Learning point: Even when you have an angiogram, the ECG findings make a difference.

This ECG is nearly pathognomonic. What is it?

2011-12-13T20:34:00.001-06:00

A 45 yo male with a known history of MI presents with a few hours of chest burning, resolved now. Here is his presenting ECG:

There is ST elevation in precordial leads. What is the diagnosis? See below. The first troponin I returned positive at 0.467 ng/ml.

This is classic Left Ventricular Aneurysm morphology, otherwise known as persistent ST elevation after old MI. There are QS-waves in V2-V4 (QS-wave is a single negative deflection without any R-wave), moderate ST elevation, T-waves are not tall and may be (as in this case) slightly negative.

"LV aneurysm" morphology is so-called because it is associated with an anatomic aneurysm about 80% of the time. It is quite common after a completed MI (formerly known as transmural MI), one in which the artery did not reperfuse, nor was the affected wall reperfused by collaterals, so the entire wall is infarcted, throught the full thinkness. Over time, the scar thins out and bulges outward in diastole (diastolic dyskinesis on echo). Before the reperfusion era, they were the most common reason for ST elevation STEMI mimic, but now they are much less common than before.

LV Aneurysm can be inferior, anterior, or posterior. I have never seen a lateral LVA, but I suppose they could exist. Inferior aneurysm looks very much like acute MI because it does not get QS-waves, but rather QR-waves, which can also be present in acute MI. I will post a case of inferior aneurysm soon, but here is one.

The chest pain with troponin elevation establishes this as a Non-STEMI. There is no need to activate the cath lab emergently. In his case, next day echo confirmed apical and anterior dyskinesis, and he underwent risk stratification with a nuclear stress test, which was normal, and he did not undergo cath. [This is perfectly appropriate conservative care for NSTEMI if the patient is discharged on maximal medical therapy (statins, beta blockers, aspirin, clopidogrel)].

Here is an old post from 2009 that describes LV aneurysm in detail, and describes an ECG rule I developed to help differentiate it from STEMI.

Here are all the cases I have posted on LV aneurysm.

Subtle Inferoposterolateral STEMI

2011-12-09T10:18:00.000-06:00

This ECG comes from Tom Bouthillet, who is devoted to good STEMI care, runs the EMS12lead ECG site, and who has also produced an outstanding iPhone/iPad/Android 12-lead ECG challenge App for learning to recognize subtle STEMI and to differentiate STEMIs and look alikes.

Case 1. This was a 70 year old woman who had chest pain while exercising the day before, then developed chest pain on the day of the ECG and called 911. Here was her prehospital ECG.

There is very subtle ST elevation in inferior leads, with hyperacute T-waves, with subtle reciprocal ST depression in I and aVL, and T-wave inversion in aVL. There is minimal ST depression in V2. T-waves in V5 and V6 are perhaps a bit hyperacute, too.

For contrast, let's look at limb leads and V4-V6 side by side with a normal ECG:

Here the contrast in T-wave size is obvious. Normal has a wide range, and not all normal inferior T-waves are this small. But the ones on the left are clearly too large.

Here the contrast in T-wave size is obvious. Normal has a wide range, and not all normal V4-V6 T-waves are this small. But the ones on the left appear too large.

The medics did not see this. The computer did not see this. The patient was brought to the ED and discharged after ED evaluation. Unfortunately, we do not have any ED data on this case. What did the ED ECG look like? Was there an old one for comparison? It is hard to imagine that this was a baseline ECG.

I suspect this was a missed STEMI. Most patients with missed STEMI at least get admitted to the hospital for a rule out.

Case 2. Here is a similar case in which all the data is available:

A 65 year old woman with no previous cardiac history presented with 2 hours of typical chest pain.

There are inferior hyperacute T-waves, some minimal ST depression in V2, and lateral hyperacute T-waves. There is 0.5 mm of ST depression in aVL. In my opinion, this is diagnostic of inferoposterolateral MI.

Here is the patient's previous ECG:

It is not entirely normal, but there are no large T-waves anywhere. This establishes that the presentation ECGs findings are new.

These findings were also not recognized. The patient was admitted to the CCU. Troponin I peaked at 63 ng/ml 14 hours later. Angiography showed an occluded dominant left circumflex. Echo showed an infero-postero-lateral wall motion abnormality and EF of 55%.

Learning points: Scrutinize the ECG for T-wave size and morphology, especially in reciprocal leads III and aVL.

Several Cases of ST Elevation from Early Repolarization

2011-12-04T09:40:00.002-06:00

As I have pointed out in other posts, I have developed an equation to help in the electrocardiographic differentiation of anterior early repolarization from anterior STEMI. If the equation [(1.196 x ST Elevation in mm at 60 ms after the J-point in V3) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in mm in V4)] has a value greater than 23.4, vs. less than 23.4, it is quite sensitive and specific for LAD occlusion.

Remember: when you are uncertain, look for old ECGs, do serial ECGs, then, if you still need to, you can get an immediate echocardiogram, and if you ultimately cannot be certain that it is not STEMI, then you may have to risk a false positive cath lab activation. That happens.

Case 1. One of my partners phoned me when I was out. He was worried about this ECG. He used his iPhone to photograph it, then sent it to me by text message:

Computerized QTc was 391 ms, STE at 60 ms after the J-point is 2 mm, R-wave is 11.5. I looked at it at said I do not think it is STEMI. If you apply the equation, the value is 21.7 (less than 23.4, so it is early repolarization).

I told him that it is very unlikely to represent STEMI.

Here is a previous ECG from one year ago:

The new one looks different from this one, especially in V3, but this can happen in early repol

This was recorded the next AM, after the patient had ruled out with serial troponins:

Here are all 3 side by side:

Case 2.
A Hennepin residency graduate called me to ask about an ECG. I happened to be in the ED so I asked her to fax it. She was worried about diffuse ST elevation and whether there was MI or pericarditis.

There is 4 mm of STE at 60 ms after the J-point (2.5 mm at the J-point) in V2, so it looks scary. There is 1 mm STE in 2 consecutive of inferior and lateral leads. So it meets "criteria" for fibrinolytic therapy in every coronary distribution. But the computerized QTc is 370 ms, the STE at 60 ms after the J-point in V3 is only 2mm, and the R-wave in V4 is 19 mm. Equation value is 21.08, so this is unlikely to be an anterior STEMI. Is it lateral or inferior STEMI? The pronounced J-waves make early repol in inferior or lateral walls much more likely than STEMI. The absence of reciprocal ST depression in aVL makess inferior MI extremely unlikely.

As for pericarditis: the ratio of ST elevation to T-wave in V6 is less than 25 percent, so pericarditis is unlikely. Furthermore, there is no significant PR segment depression.

Case 3. A 19 yo with stab wound to the chest. After viewing the ECG, there was concern for LAD laceration.

Again, there is scary ST elevation. In fact, the ST segments in V2 and V3 are straight, not concave. In my study, I excluded ECGs with non-concave (straight or convex) ST segments because they are so specific for STEMI. Nevertheless, if you apply the equation, the value is only 20.52. The patient ruled out. The heart was not affected by the stab wound.

Atrial Flutter Mimicking ST Depression

2011-11-29T08:30:00.000-06:00

A 65 year old presented with altered mental status and had an intracranial bleed:

One could be fooled into thinking this is sinus tachycardia (with a short PR interval) with diffuse ST depression. But close inspection reveals flutter waves. In particular, a totally upright p-wave in V1 is very unusual and should alert you to atrial flutter. The fluttering baseline accounts for the apparent ST depression, although I cannot rule out some amount of true ischemic ST depression.

Here is the ECG after cardioversion:

Now there is sinus. Interestingly, this one also has an upright p-wave in V1 - so the rule is not universal!

Osborn Waves and Hypothermia

2011-11-25T12:14:00.005-06:00

Case 1. Temperature 30 degrees Celsius (86 degrees F) due to environmental hypothermia.

There is very slow atrial flutter (rate = 167) with 4:1 AV conduction. There is a wide QRS with a very large notch (in this case, a hump), or J-wave, at the end. This is the classic Osborn wave of hypothermia.

Case 2. A young paraplegic presented confused. Among the early tests performed was this ECG which was showed to me:

Sinus rhythm. Long QTc [about 500ms; the computer read 180ms (!)]. There is ST elevation which alarmed the residents. I did not think it looked like injury. There are J-wave notches at the end of the QRS, particularly in V3, which are rather large for early repolarization, which should make one think they may be Osborn waves.

I asked about the temperature.

Here is the patient's previous ECG:

No ST elevation, and much smaller J-wave notching, seen best in V4.

A rectal temperature was 30.8 degrees Celsius.

Here is the ECG after rewarming:

J-wave notching persists but is much smaller.

Here they are side by side to better see the difference:

The J-waves are subtly larger in the hypothermic condition

The ECG in hypothermia

Rhythm: The most common rhythms in hypothermia are sinus bradycardia, junctional bradycardia, and atrial fibrillation. Shivering artifact is common. Atrial flutter is seen in case 1. At temperatures below 30 C, the patient is at risk for ventricular fibrillation. In this study of 29 humans cooled to 28-30 C for cardiac surgery, 19 developed atrial fibrillation and 2 ventricular fibrillation.

QRS: Osborn waves are thought to be pathognomonic of hypothermia, but can also be seen in normothermic patients. "J-waves" or "J-point notching" is very common in early repolarization. Very narrow Osborn waves were reported in severe hypercalcemia (level 16.3). Sometimes a short ST segment of hyperCa can be misinterpreted as an Osborn wave (see image below); that is not the case in the aforementioned case report. J-wave syndromes are proposed to give a unifying pathophysiology to Osborn waves of hypothermia and early repolarization, as well as Brugada syndrome.

Very large and wide J-waves, as in case 1, are almost exclusively due to hypothermia. The etiology is beyond the scope of this blog, but may be read here.

Hypothermia and pseudoinfarction patterns: MI or ischemia (either ST elevation or depression) may be mimicked either by 1) repolarization abnormalities (As in Case 2, with ST elevation) or by 2) confusing the J-wave with the ST segment, as in this case in JACC (full text) and this case in Archives of Internal Medicine (no full text). This latter case also has ST segment depression as a repolarization abnormality.

Short ST segment (with resulting short QT interval) of hypercalcemia mimicking Osborn waves

This image courtesy of Dr. K. Wang from his Atlas of Electrocardiography. The major difference between the Osborn wave and the example of hypercalcemia is that the Osborn wave is followed by an ST-T complex, while the wave directly following the QRS in hypercalcemia is the T-wave itself.

Tachycardia with Pericardial Effusion

2011-11-19T08:36:00.000-06:00

A 52 year old man with a history of atrial fibrillation and prosthetic mitral valve replacement just 11 weeks prior presented with a complaint of a rapid regular heart rate; he could hear rapid clicking of his valve. He was otherwise asymptomatic. His medications included amiodarone for rhythm control of his atrial fibrillation. This ECG was recorded:


The treating physicians diagnosed sinus tachycardia at a rate of 127. They were worried about ST elevation in II, III, and aVF, with reciprocal ST depression in I and aVL. With the Q-waves, they were not sure if this was old or new ST elevation.

They looked for a previous ECG and found this:

There was no ST elevation at baseline. They were now worried about acute MI.

They did a bedside echocardiogram and found a large pericardial effusion. BP was stable and normal at 110/83. They infused a liter of normal saline, and the heart rate remained 127. A repeat ECG was identical.

70 minutes after arrival, the first troponin I returned elevated at 0.160 ng/ml. Now they were even more worried about MI.

What is the diagnosis?

Slow Atrial Flutter with 2:1 conduction. Slow because of the beta blocking effects of amiodarone.

1. Note the flutter waves in V1: one positive wave that appears to be a p-wave and another that immediately follows the QRS. The one that looks like a p-wave is positive, whereas the p-wave on the previous ECG is negative!
2. Any time the heart rate remains the same, in spite of time or fluids, it is almost certainly not sinus.
3. There is no ST Elevation. All of the apparent ST elevation is due to the baseline formed by the atrial flutter waves!

INR returned at 3.9. The patient was given propofol and electrically cardioverted in the ED. Here is the subsequent ECG:

Final diagnosis: Atrial flutter with pericardial effusion due to myocarditis due to postoperative Dressler's syndrome. Troponin elevation from demand ischemia. ST elevation from flutter wave. The effusion disappeared with time; no surgery or drainage was necessary.

Anterior ST elevation: is it STEMI?

2011-11-16T12:32:00.002-06:00

I received a call from an outside hospital. A 31 year old healthy auto mechanic had a prolonged exposure to Carbon Monoxide in his garage and presented with blunted level of consciousness and chest pain. There were others who were also affected.

I requested a transfer so that he could undergo immediate hyperbaric oxygen therapy at our hospital. After the ambulance left the other hospital, the physician called to state that the patient was having an anterior STEMI with "tombstones."

The CO level returned at 14, so I knew that any STEMI would be due to simultaneous and incidental acute coronary thrombosis, NOT due to the CO toxicity. I asked him to immediately fax the ECG, which is shown here:

What is it?

There is an R'-wave in V1 with downsloping ST elevation and an inverted T-wave. There is ST elevation in lead V2. This is not STEMI. It is Brugada pattern

Brugada is frequently mistaken for STEMI, although it can also mask anterior STEMI. I was not worried about this ECG. When the patient arrived, his Brugada pattern had resolved:

There is minimal STE and poor R-wave progression, but the QTc is 384, so this is early repolarization. The Brugada pattern is gone.

We sent him to the chamber. He was admitted to the hospital and ruled out for MI. The patient's CO level was only 14, but he had had a prolonged exposure, had enough toxicity to cause objective neurologic deficits, and the blood level had been measured after prolonged oxygen therapy.

Brugada pattern ECG is not Brugada syndrome, which requires more than simply an ECG. It is important to note that the pattern and the risk for cardiac arrest may not always be present, but may be induced by fever or sodium channel blocking drugs. This makes me wonder if CO poisoning could induce or unmask Brugada pattern on the ECG.

Also, V2 makes this Brugada pattern atypical.

The patient should be referred to an electrophysiologist.

Hyperacute T-waves, with a Twist

2011-11-11T07:13:00.001-06:00

A 30 year old male complained of chest pain and then collapsed. He was resuscitated from ventricular fibrillation. He arrived at 0700.

These two ECGs were recorded at 17 minutes apart.

Which was first?

There are hyperacute T-waves in V1-V5, with some depressed ST takeoff in V3-V5. There are also hyperacute T's in II, III, and aVF

There is ST elevation (injury) in V2-V4and II, III, aVF

The bottom one was recorded first, at 0719, the top one was recorded second at 0736. The patient's artery had reperfused between the first and the second.

This illustrates nicely how hyperacute T-waves are present not only shortly after occlusion, but also shortly after spontaneous reperfusion, or, as I sometimes say: "both as the ST segments are on the way up, and on the way down."

As it turns out, the artery reoccluded, and at 0801, the angiogram showed a 100% occluded type III ["wraparound" (to the inferior wall)] mid (after the second diagnoal) left anterior descending artery. A large thrombus was aspirated and the LAD was stented.

The EF later that day was 25%, with both inferior and anterior wall motion abnormalities. However, as expected from the short duration of complete occlusion, the troponin I peaked at only 20 ng/ml. A second Echo was done 4 days later: the stunned myocardium had recovered, and the EF was 65%.

He underwent therapeutic hypothermia and in spite of some initial hypoxic encephalopathy, he completely recovered.

Click here to see the most popular post of all time, on hyperacute T-waves.

Atrial Repolarization Wave Mimicking ST Depression

2011-11-09T09:06:00.002-06:00

A 25 year old woman presented with a caffeine overdose and chest discomfort. This is her ECG:

There is sinus tachycardia (rate = 120) with what appears to be diffuse ST depression in leads II, III, aVF and V2-V6. However, if you look closely, the PR segment is downsloping. This is due to a pronounced negative atrial repolarization wave (atrial T-wave, or "Ta-Wave"). The wave is still negative at the J-point, and thus depresses the J-point.

The ST segment is most commonly measured at the J-point and relative to the PR segment, but when there is a Ta-wave, this method is inaccurate. K. Wang (my mentor) recommends measuring the ST segment relative to the end of the PR segment (this is also called the PQ junction, and the recommended location for measurement according to ACC/AHA) However, in my experience, when there is a Ta-wave, the PR interval is still downsloping at this point and this method of measurement will underestimate the effect of the Ta-wave. Also, in my experience, and contrary to research I outline below (and which contradiction I cannot explain), the greatest part of the Ta-wave is back to baseline by 60-80 ms after the J-point. In the case above, if you measure the ST deviation at 60-80 ms after the J-point and relative to the TP segment, you'll see that there is no ST depression.

Many textbooks recommend measuring the ST segment at 60-80 ms after the J-point and relative to the TP segment, presumably because it helps to avoid the issue of the Ta-wave. However, especially in tachycardia, the TP segment may never come back to baseline after the T-wave; furthermore, the T-wave has often begun by 80 ms after the J-point, as in this case.

Below is a schematization of the Ta-wave:

The atrial repolarization wave lowers the baseline, but its amplitude, if present at all, is not great (maximum 0.2 mV, or 2 mm at normal recording). It is not finished until up to 180 ms after the J-point (see references below).

How do you recognize the Ta-wave? First, you have to be aware of it and look for it. Then, you have to imagine a curve, like this drawing:

The Ta-wave inscribes a parabolic curve that can be imagined when viewing the ECG

Learning point: Beware diagnosing ST depression before considering the atrial repolarization wave as the etiology.

More Detail on the Ta-wave:

The Ta-wave is a mean of 320 ms after the end of the p-wave, with a duration of 2-3x that of the p-wave and a polarity always opposite of the p-wave. The PTa duration (onset of p-wave to end of Ta-wave) is a mean 440 ms, though it varies with heart rate just like the QT interval. Thus, if the PR interval is 160 ms, the Ta-wave ends about 280 ms later. If there is normal conduction of 100 ms, the Ta-wave may still be present at 180 ms after the end of the QRS! Even if the patient has Bundle Branch Block with a duration of 140 ms, then the Ta-wave may still be present 140 ms after the end of the QRS.

Here is a short explanation of the atrial repolarization wave.

Here are two detailed articles measuring the Ta wave: one by Holmquist et al. and another by Debbas et al.

Left Bundle Branch Block (LBBB) with Chest Pain, concordant and excessively discordant ST depression V2-V6

2011-11-04T01:28:00.000-05:00

A middle-aged male presented pain free after an episode of chest pain. Here is the initial ECG (sorry some is cut off -- it is an iPhone shot from a friend):

There is LBBB with appropriate discordance of all ST segments. Anterior ST elevation is appropriate, with highest ST/S ratio of 3.5/28 = 0.125 (mean normal = 0.11; normal up to 0.19). There are concordant T-waves in V5 and V6. This is a nonspecific sign of NonSTEMI.

5 minutes later, the patient had crushing chest pain, and this ECG was recorded (again, some of limb leads are cut off):

Now there is concordant ST depression in V2 and V3. This is a relative change of approximately 5 mm(!). There is excessively discordant ST depression in V4-V6. (V4 ratio is 2/6 = 0.33; V5 ratio = 2.5/6.5 = 0.38; V6 = 2/6.5 = 0.31). Thus, there is ischemic ST depression in V2-V6. In normal conduction, ST depression from V2-V6 is often due to subendocardial ischemia, whereas when limited to V1-V4, it is usually posterior STEMI. Either way, this is a patient with acute coronary syndrome with chest pain. If you cannot control the symptoms with medical therapy, then the patient must go to the cath lab.

I have written about excessively discordant ST elevation, but have not mentioned excessively discordant ST depression. In our study of LBBB with and without coronary occlusion, just one lead with excessively discordant ST depression or ST elevation, as defined as a ratio of ST depression (or elevation) to the preceding R-wave (or S-wave), greater than 0.25, was very specific for ischemia (in our study, for occlusion). More recent analysis of the data showed that 0.20 was probably a better cutoff.

The physician called the interventionalist, who did not agree there was ischemia on the ECG. The patient was started on nitroglycerine IV and the pain subsided, as did the ECG findings.

The patient was admitted pain free on nitro and no immediate cath was done. The troponin I peaked later at 0.18 ng/ml.

The next AM, the patient had another episode of pain that could not be resolved with maximal medical therapy. He went for emergent cath, which showed a proximal lad 95% stenosis with deep ulcer and a 90% mid lad stenosis. Both were stented.

Later, the troponin peaked at 5.6, and echo showed anteroseptal hypokinesis with EF <40%.

So this was LBBB with concordant and excessively discordant ST depression, representing ST depression in leads V2-V6, completely consistent with subendocardial ischemia due to profound LAD ischemia.

Wellens' syndrome, no culprit, what happened?

2011-10-29T19:19:00.002-05:00

A 55 yo male with h/o smoking complained of 4 days of intermittent chest pain lasting up to a few hours each day. He presented to the ED pain free and had the following ECG at 1332:

There is a suggestion of terminal T-wave inversion in V2, highly suggestive for early Wellens' syndrome. There is T-wave inversion in I and aVL diagnostic of ACS.

The first troponin returned with "minor increase" on a qualitative troponin I, so another quantitative troponin was sent and it was elevated at 0.325 ng/ml. The patient remained pain free. Another ECG was recorded at 1555:

The T-wave inversion is more pronounced in V2, an evolution diagnostic of Wellens' syndrome. TWI in aVL again is clearly ischemic.

See here for classic evolution of Wellens' waves.

The patient was admitted to the hospital late on a Friday, and put on antithrombotics and antiplatelet agents. His troponin I peaked at 1.05 ng/ml that day.

On day 2, he had an echo which was suggestive of anterior wall motion abnormality. He had no ECGs that day.

Sunday AM at 0800, he had another episode of severe chest pain, waxing and waning. He had the following ECG recorded, and it is unclear whether he was having the pain at the time of the ECG.

Now there are deeper and more symmetric Wellens' waves. Is this just evolution of the waves seen 2 days ago? Or did something new happen?

Troponin rose again that day (day 3). So the patient was taken to the cath lab. He had no culprit, but a 50-60% narrowing of the proximal LAD. Fractional Flow Reserve was performed across the lesion and it was 0.88 to 0.90 (negative, showing no blockage of flow). Intravascular ultrasound revealed that the lesion had a minimal luminal diameter of 2.3 mm but a large plaque burden. Nevertheless, it did not appear to the angiographer to be the cause of the symptoms.

The patient went back to the wards. He had an identical episode of pain the next morning (day 4). It turns out that the patient was on an ST segment monitor and it had not been checked on day 3 after the previous episode of pain. So the interventionalist went and had it printed out. Here it is, a 12-lead monitor strip:

Obvious anterolateral STEMI.

This illustrates what Wellens' syndrome is: it is always recorded when the patient is pain free, after an episode of chest pain. The artery is always open but there is an LAD lesion that is at high risk of re-occlusion (as in this case). Wellens' is the aftermath of occlusion that has reperfused. The inverted T-waves are "reperfusion T-waves."

In this case there was no clear LAD lesion. This was probably spasm, but could have been an unseen thrombotic event. They went back and stented the LAD and all symptoms have resolved.

Four anterior STEMIs: acute and reperfused vs. won't reperfuse, subacute and reperfused vs. not reperfused

2011-10-26T17:37:00.002-05:00

These 4 recent cases illustrate acute and subacute MI with reperfusion and absence of reperfusion (or failed reperfusion). QS-waves and depth of T-wave inversion are very helpful in determining the duration of injury (the "acuteness" of the ECG), the viability of the myocardium, and patency of the infarct-related artery. Persistence of ST elevation helps to determine state of the myocardium after reperfusion.

Definition: total loss of R-wave means there is a QS-wave (a single deep deflection). Preservation of R-wave may mean and initial Q-wave followed by an R-wave (this is called a QR-wave. Upper case vs. lower case Q (q) or R (r) is used to designate smaller or larger waves.

1. This 57 yo diabetic male presented with generalized fatigue, myalgias, and arthralgias, mild subjective fever and chills, and nausea. He also stated his arms and head feel "heavy" and he had a headache, dry heaves, and dizziness, and some "indigestion" in his chest "like acid". His pulse was 114. Exam was otherwise normal.

There are QS-waves in precordial leads with some preserved R-wave in V2 (Qr-wave). There is persistent ST elevation, but no T-wave inversion. T-waves are not tall (tall, hyperacute T-waves are markers of ischemic but viable myocardium). The fact that they are not present here suggests that the MI is complete. That they are not inverted tells us that the artery is still closed. But the presence of a bit of R-wave gives some hope that there might be some viable myocardium left. [STE in lateral leads, with inferior reciprocal ST depression, tells us it is a proximal LAD ]

Cath showed a 100% proximal LAD and other disease. It was opened. Initial troponin I was > 50 ng/ml; followups are not available. Echo on the day after admission showed EF of 30-35% and antero-apical wall akinesis with an LV thrombus [these frequently form in complete or near complete (no early reperfusion) anterior STEMI because of akinesis/stasis]

2 more days later, this was recorded:

ST elevation is still present. Persistent ST elevation 3 days after a nearly transmural MI portends possible LV aneurysm.

Echo at this time showed some improvement in EF to 40%, but persistent akinesis and thrombus.

2. This 42 yo diabetic male presented with cough and foot pain. He had been awakened by cough at 3 AM 2 days earlier. In spite of aggressive questioning, he denied chest pain, but he did tell one triage nurse that he had had some chest burning, and so he underwent an ECG:

There are deep Q-waves and QS-waves in precordial leads V2-V3, with a bit of R-wave left in V4. ST segments are greatly elevated and T-waves are deeply inverted. There is also T inversion in I and aVL (Proximal LAD) and a Q-wave in III.

Symptoms have been prolonged but intermittent, and there has been little chest pain, if any. So all duration of injury must be estimated from the ECG. Even when there is chest pain, the ECG is a more reliable indicator of injury duration than are symptoms. Here there are some QS-waves, telling us that there has probably been a significant amount of completed infarction, but there is also persistent R-wave in lead V4 suggesting some viable myocardium. The deep T-wave inversion also tells us that there is a significant amount of viable myocardium left and that the artery is most likely open. It is very unlikely to be LV aneurysm morphology when the ST elevation is so high and the T-Wave inversion is so deep.

Cath showed a 95% LAD with flow. Echo showed anterior wall motion abnormality. Peak troponin I was 52 ng/ml (significant myocardial loss, but not the whole anterior wall)

3. This 67 yo male with h/o HTN and GERD only presented with 60 minutes of diaphoresis and GERD symptoms. He had a prehospital ECG:

Obvious anterolateral acute STEMI

The patient received aspirin only and his pain immediately resolved:

Clear resolution of all ST elevation, with only some residual T-wave inversion in I and aVL. The LAD has reperfused early.

An open 90% LAD was stented. Peak troponin I was 0.3, so almost no myocardium was lost.

Here is the ECG the next AM:

There was so little infarction that there are lateral, but no anterior reperfusion T-waves (normally, there would be Wellens' type waves after LAD reperfusion). The T-waves are smaller than they were immediately after reperfusion, illustrating how hyperacute T-waves are present BOTH shortly after occlusion (when ST segments are on the way up) and shortly after reperfusion (when ST segments are on the way down).

4. A 51 year old male with h/o stent presented with 30 minutes of chest pain:

Obvious anterolateral very acute STEMI with hyperacute T-waves

He went for immediate PCI, with successful reperfusion of a 100% occluded proximal LAD, and a door to balloon time of 35 minutes. This was recorded 2.5 hours later, after PCI:

There is a significant QS-wave in V2, with some persistent ST elevation, suggesting incomplete small vessel reperfusion and significant infarction.

The patient continued to have ischemia after PCI, and in fact had an episode of polymorphic VT shortly after while in the ICU. This was recorded the next AM:

There are QS-waves in V2 and V3, with rather shallow T-wave inversion, both indicative of significant myocardial loss.

Peak troponin I was 84 ng/ml and there was a large anterior wall motion abnormality, in spite of very fast treatment and a symptom onset to balloon time of 65 minutes.

Sometimes, even with very fast reperfusion, there is significant myocardial loss because of downstream obstruction of small vessels. This can be seen on angiogram as an absence of "myocardial blush" and is measured the the TIMI myocardial perfusion grade (TMP grades 0-3, just like TIMI flow grades 0-3).

As it turns out, the best measure of reperfusion is TMP (not TIMI flow) and the best noninvasive measure of TMP is the ECG, as measured by resolution of ST elevation on the ECG ("ST resolution"), with 70% resolution associated with high TMP grade. The ECG, as it turns out, is the best predictor, better the TMP grade because TMP measures microvascular patency, and the ECG measures cellular viability (see this full text article and this abstract).

I will specifically discuss acuteness on the ECG in a future post.

Here is some older but very interesting literature on TIMI myocardial perfusion grade and ST resolution:

1. Claeys MJ, Bosmans J, Veenstra L, et al. Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome. Circulation 1999;99(15):1972-7.

2. Gibson CM, Cannon CP, Murphy SA, et al. Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs. Circulation 2000;101(2):125-30.

3. Shah A, Wagner GS, O'Connor CM, et al. Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the "gold standard" for myocardial reperfusion treatment. J Am Coll Cardiol 2000;35(3):666-72.

4. van't Hof AW, Liem A, de Boer MJ, et al. Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction. Zwolle Myocardial Infarction Study Group. Lancet 1997;350(9078):615-9.

5. van't Hof AW, Liem A, Suryapranata H, et al. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade. Zwolle Myocardial Infarction Study Group. Circulation 1998;97(23):2303-6.

Wide complex tachycardia in a 36 year old

2011-10-22T10:18:00.002-05:00

A 36 year old male presented with palpitations. He has had these many times for many years, episodes lasting 30-60 minutes, without syncope or pre-syncope. He has a bit of chest pressure, but is otherwise comfortable. He has no other medical history and is on no significant medications.


There is a wide complex tachycardia at a rate of 179 bpm. The QRS duration is 139 ms. The frontal axis is 180 degrees.

What action do you want to take? Answer below.

But first:
If this is ventricular tachycardia (VT), is it likely to be a dangerous type? No. With no history of any structural heart disease, no syncope or pre-syncope in spite of many prolonged episodes, and no other medical problems, this is unlikely to be a life-threatening dysrhythmia. This does not mean that it cannot be VT. Some VT is not life threatening, and most of these are called "idiopathic."   The most well known of these are: 1) posterior fascicular, verapamil sensitive, "idiopathic" VT or 2) right ventricular outflow tract (RVOT, adenosine sensitive) idiopathic VT. Both of these entities occur in a structurally mostly normal heart with fairly normal ejection fraction. In terms of danger, they act more like SVT. Two other more rare types are: idiopathic propranolol-sensitive (automatic) VT (IPVT), catecholaminergic polymorphic VT (CPVT). See this excellent full text online review.

There are ECG instructors who warn against using adenosine for wide complex tachycardia. They warn that, if it converts, it might be the adenosine-sensitive VT, and you might discharge to home a patient with a diagnosis of SVT when in reality it is VT. I do not subscribe to this for three reasons: first, these are comparatively rare; second, these are not dangerous and it is ok to send the patient home; third, because it is wide complex, you will have the patient follow up with a cardiologist.

Why would any physician give adenosine rather than just sedate and cardiovert? While most recently trained emergency physicians routinely give propofol for sedation, there are many other physicians who are not so comfortable with it. For them, cardioversion may not be so safe.

FYI: I posted this case of SVT with aberrancy last month and many readers thought it was RV outflow tract VT. The reason that RVOT VT was very unlikely is that RVOT starts in the outflow tract and propagates inferiorly; therefore, inferior leads are all positive. In this case, there was an initial Q-wave in inferior leads. I'm sorry I do not have a case (yet) of RVOT VT.

--Best answer: sedate and cardiovert
--Acceptable answer: give adenosine (but it would not work)
--You are brilliant and very sure of yourself: verapamil
               --If you have the diagnosis right (idiopathic VT), this will work.
               --If it is non-idiopathic VT, verapamil is dangerous.

Let's take a close look at this one using Sasaki's system to diagnose wide complex tachycardia:

Step 1: Initial R in aVR?
--This means is there a large single (upright) R-wave (not a small r-wave) in aVR, indicating that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.

--If yes, then rhythm is VT. If no, step 2. Not here.

Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)? See image below.

--If yes, then rhythm is VT. If no, step 3. Not here.

Step 3: Initial r or q ≥ 40 ms in any lead?
--If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)

--If yes, then it is VT. If no, then it is SVT. "No" here, therefore it is SVT

However, this is one of the exceptions. This is VT that looks like SVT. Why? Because this is VT that originates in conducting fibers of the ventricle; therefore, the initial impulse is conducted quickly through conducting fibers, just as in SVT. So the initial part of the QRS is narrow, and the entire QRS is less than 140 ms (normal VT is usually greater than 140 ms). Andrade FR et al. [J Cardiovasc Electrophysiol January 1996; 7(1):2-8] found in all their 11 cases of fascicular VT that the QRS duration was 105 to 140 ms, and the RS interval, which in normal VT is more than 100ms, was always less than 80 ms.

In this case, there is a fast depolarization at the initial part of the QRS, just as you would see in SVT with aberrancy. However, there is also an RBBB morphology and a rapid narrow depolarization towards leads II and aVL, and a subsequent wide depolarization towards inferior lead III, with aVF relatively isoelectric. The axis is directly to the right. This is typical of an idiopathic fascicular VT. The most common form of fascicular VT originates in the left apical inferior septum, corresponding to the posterior fascicle, and therefore has an RBBB morphology with a leftward axis, as in RBBB + left anterior fascicular block. Less commonly, it originates in the anterior fascicle and has a rightward axis. So this would appear to be due to the less common variety. Fascicular VT is apparently due to "false tendons" which are conducting and which can be seen on transesophageal echo. See this excellent full text article (Thakur RK et al. Anatomic substrate for idiopathic left ventricular tachycardia. Circulation 1996;93:497-501.)

Further historical information: this patient had been to EDs many times, and received adenosine several times without success. He had been electrically cardioverted successfully several times. On this occasion, he was cardioverted, with this subsequent ECG:

Notice T-wave inversions in II, III, aVF and V3-V6. It is typical for the baseline ECG of patients with idiopathic VT to have some shallow abnormal T-wave inversions like this in inferior and lateral leads.

The patient was diagnosed with verapamil sensitive idiopathic fascicular VT. He was put on verapamil SR 240 mg per day, and this only partly controlled his symptoms.

Therefore, he underwent an EP study. This did not show the typical abnormalities one finds in posterior fascicular type (near the septum), but rather possible "false tendons" on the lateral wall. These were ablated and the patient has had relief from the frequency and severity of palpitations, but not complete.

Here is his baseline ECG after ablation:

Normal ECG, T-wave inversions are gone.

What is the diagnosis? A nearly pathognomonic ECG.

2011-10-21T12:14:00.001-05:00

A 50 year old woman complained of shortness of breath, but on closer questioning she seems to be weak. An ECG was recorded immediately. What is the diagnosis?

Answer below.

Notice large U-waves (arrows). One is tempted to think that the long hump after the QRS (between the two vertical lines) is the T-wave. Whenever you see this, you should think about both long QT and U-wave. But if you look closely, you see there are 2 bumps, so the second one must be a U-wave.

The diagnosis of hypokalemia was made 1 hour prior to return of the lab value. K was 1.8.

This patient presented with hypotension, shock, acidosis, hgb of 8. He stated he had been vomiting all day.

There is scooped ST depression in V4-V6, possibly due to ischemia, but mostly it is highly suspicious for hypokalemia. The K was 2.6.

ST elevation (Saddleback), is it STEMI?

2011-10-12T10:58:00.004-05:00

This 56 year old male presented with atypical chest pain and left arm numbness off and on for one week, worse on the day of presentation:

There is saddleback type ST elevation in leads V2 and V3, and diffuse T-wave inversion. But there is also very high voltage especially in V4 (35mm, sorry it is cut off) and V5 (27 mm). The QTc was 426 ms.

Answer is below:

This ECG was shown to me by a colleague, and I immediately said: "You thought it was a STEMI, but it is not." He had, in fact, activated the cath lab, and the coronaries were clean and the patient ruled out.

Saddleback ST elevation, in my experience, is rarely due to STEMI. I will not say it is never due to STEMI because I know of no research on this topic. It is usually a form of early repolarization that also usually meets criteria for type II or III Brugada pattern (see this post). I will post more on this topic later. In this case, it may be related to the LVH or be simultaneous early repolarization and LVH. The diffuse (both inferior and precordial) T-wave inversion is somewhat atypical of LVH.

Echocardiography confirmed marked concentric LVH.

In this case, you might want to try applying the early repol/anterior STEMI equation rule posted on the sidebar. However, it is not validated in the presence of LVH). You would get a value of 16.11, which is very low and argues strongly against LAD occlusion.

Inferior ST Elevation: what is the Diagnosis?

2011-10-05T10:01:00.008-05:00

You can read this post here, or watch a video presentation of it:

I was handed this ECG, without any clinical information, while on my way to see another patient:

There is sinus rhythm. There is ST elevation diffusely: 2 mm in V2, 3.5 mm in V3, 2.5 mm in V4, 1.5 mm in V5, and 1 mm in V6, 1.5 mm in lead II, 1 mm in leads III and aVF. R-waves are well formed, and in fact there is high voltage. T-wave to ST ratio is greater than 4 in lead V6, making pericarditis unlikely (also there were no symptoms of pericarditis). The computerized QTc is 386 ms. There are marked J-waves in II and V4-V6, with slurring of the R downstroke in III and aVF. There is no reciprocal ST depression anywhere except aVR; in particular, there is none in aVL. Not only is there no ST depression in aVL, there is actually a bit of STE in lead I. These are all classic signs of early repolarization.

I immediately recognized this as early repolarization of inferior, lateral, and anterior leads, and went on my way. Some time later, I found out that the residents had initiated an aggressive workup because they were worried about the ECG.

It turns out that this was a 27 yo African American male who presented with pressure-like (non-pleuritic) chest pain and dyspnea. He appeared very anxious and was hyperventilating and he had just had an episode of what sounds like carpal spasm. Clinically, he was having a panic attack. His ECG did not worry me.

Is there LVH on the ECG? By voltage there does seem to be, but this was a young thin male and high voltage without LVH is common in this situation.

Most early repolarization is in precordial leads, where it is so common that it is considered normal to have baseline ST elevation on the ECG. I have put up many posts on this topic, and on differentiating ER from LAD occlusion. But there is also early repolarization in inferior or lateral leads, and when present, it is virtually always present in anterior leads as well.

Here is a case of a 45 year old with chest pain:

There is ST elevation in inferior leads only, with no reciprocal ST depression in aVL. There is a slight T-wave inversion in aVL.

Inferior MI was diagnosed by the emergency physician and the patient needed to be flown by helicopter to the cath lab. The arteries were clean. There was no MI. This was the patient's baseline ECG. It was a false positive.

How would you be able to know this from the ECG alone? If there are no changes in aVL, it is highly unlikely to be inferior STEMI. If there is simultaneous lateral MI, it is possible that aVL may be silent, but in this case V5 and V6 have very minimal ST elevation. Would you be certain that it is not STEMI? No, but you should suspect that it is a false positive. If you have immediate echocardiography available, you could prove that it is early repolarization by showing good contraction of the inferior wall. Serial ECGs may be useful. Or perhaps you need to just activate the cath lab and risk a false positive.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation. Elevations in inferior leads were less than 0.5mm in 18 of 20 cases. Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

Is there danger to early repolarization itself?

Haïssaguerre et al. performed a case control study of patients with idiopathic ventricular fibrillation, and found that many more of these patients than of controls had baseline inferior or lateral early repolarization. Tikkanen et al. performed a longitudinal community study, following people for a mean of 30 years. They found early repol pattern in inferior and/or lateral leads in 3.5% and 2.5% a , respectively, and in both locations in only 0.1%. These patients had a small but significant increased long-term risk of death from cardiac causes (Relative Risk = 1.28 for 1mm, 2.98 for 2 mm of inferior STE).

No one is certain what to do with this information, and it certainly does not impact emergency medicine, in which the problem remains: is it STEMI or not?

1. Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358(19):2016-23.
2. Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med 2009;361(26):2529-37.
3. Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61.

Fusion Beat During Supraventricular Tachycardia: No criterion is absolutely accurate in differentiating wide complex tachycardia

2011-10-03T07:07:00.000-05:00

Yesterday, I posted this case of wide complex tachycardia, and some steps to help in differentiating VT from SVT with aberrancy.

One step was this:
"Do a quick look for obvious fusion beats and AV dissociation. If found, then VT." It is generally thought that fusion beats are diagnostic of VT.

This prompted our excellent electrophysiologist, Dr. Rehan Karim, to make the point that no criterion or algorithm can make a certain diagnosis of wide complex tachycardia. And so he provided me with the interesting tracing below (sorry, no 12-lead because this just happened to occur in the EP lab while they were recording):

There is a wide complex tachycardia; rate was 171. It was proven at EP study to be SVT. You can see the RBBB morphology, with rSR' in V1 (green arrow) and a wide S-wave in lateral leads (see lead I, red arrow). There is a fusion beat (black arrow) which was proven in the EP lab to be due to a PVC occurring in the midst of the SVT!!

Learning point: whatever system or rule you are applying, it is not perfect. Dr. Karim also wanted to make the point that Brugada's algorithm had very good sensitivity and specificity in the derivation group, but attempts to validate it were not nearly as successful. This may be just as true for Sasaki's rule.

Nevertheless, while appreciating the limitations of all algorithms, I like Sasaki's rule because it depends on many of same principles as the other algorithms (principles which, though fallible, are pretty reliable), but is quite a bit simpler to apply.

Wide Complex Tachycardia: Ventricular Tachycardia or Supraventricular Tachycardia with Aberrancy?

2011-10-01T08:32:00.011-05:00

Before we start, here is another popular post on wide complex tachycardia.

What is the ECG rhythm diagnosis?

Wide complex regular tachycardia at a rate of 209, so it is not atrial fibrillation.

Which is it?
1) VT

2) SVT with aberrancy (usually AV nodal reentry tachycardia with aberrancy)

3) AV reciprocating tachycardia [antidromic, up through AV node and down through bypass tract, (AVRT)]4) What can you do if you don't know? (Does it matter?)

4) I should briefly mention idiopathic VT, which occurs in structurally normal (or nearly normal) hearts, and is therefore not as dangerous as standard VT; this includes adenosine-sensitive VT (RV outflow tract, with LBBB morphology, monomorphic R-wave in inferior leads) and verapamil-sensitive VT (posterior fascicle, RBBB morphology). I will discuss this in a future post.

Here is the clinical data:
26 yo male with chest pain and SOB and no history of structural heart disease. He was not hypotensive or in shock.

A young person with no cardiac history is likely to have SVT, not VT, but let's consider the ECG alone:

When assessing for the rhythm in wide complex regular tachycardia, these are the assessments I make, though no method is foolproof:

1) Look for hidden p-waves before each QRS. Don't miss sinus rhythm! Not here.

2) If there is a transition from narrow to wide, is the rate the same? Then it must be SVT. Not here.
3) QRS duration: VT should be at least 140 ms (except for fascicular VT), and the longer, the more likely it is to be VT. Here it is 155 ms, so it is plenty long for VT.

4) Is there RBBB or LBBB morphology? Then it is very likely to be SVT. This one has LBBB morphology.

5) Do a quick look for obvious fusion beats and AV dissociation. If found, then VT. None here.

6) Do a quick look for concordance (all QRS's in the same direction in precordial leads, not the same as concordance when evaluating ST segments in LBBB). No concordance here: this is easy to see comparing V4 to V6.

7) Finally, because it is easy to apply, I like a new rule better than Brugada's or Vereckei #1 or Vereckei #2 (aVR). It is Sasaki's rule (Sasaki K. Circulation 2009; 120:S671), and it had 86% sensitivity and 97% specificity among 107 cases of wide complex tachycardia. It has not been validated; this is important: remember that Brugada's rule was much better in the initial study than in subsequent validation studies.

Step 1: Initial R in aVR?

This means is there a large single (upright) R-wave (not a small r-wave) in aVR. This indicates that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.

--If yes, then rhythm is VT. If no, step 2. Not here.

Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)? See image below.

--If yes, then rhythm is VT. If no, step 3. Not here.

Step 3: Initial r or q ≥ 40 ms in any lead?

If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)

--If yes, then it is VT. If no, then it is SVT. "No" here, therefore it is SVT

Treat without a diagnosing
If you don't know what to do, you can always use electricity, but you can also give adenosine. As long as the rhythm is regular, not irregularly irregular (atrial fibrillation), adenosine is safe. It will usually (safely) convert SVT with aberrancy and AVRT (antidromic reciprocating tachycardia) without harming a patient in VT, and may convert a patient with fascicular VT.

Obviously, synchronized cardioversion should be undertaken if the patient is unstable.

If it is irregular with a wide QRS, it could be WPW, in which case an AV nodal blocker could be life threatening (see this post).

Diagnosis: SVT with aberrancy; it resolved with adenosine.

Added Oct 22, 2011: many readers thought this was RV outflow tract VT. The reason that RVOT VT is very unlikely is that RVOT starts in the outflow tract and propagates inferiorly; therefore, inferior leads are all positive. In this case, there is an initial Q-wave in inferior leads.

Here is the post-conversion ECG:

There is slight slurring at the beginning of each QRS, suggestive of delta waves, and the QRS is thus 109 ms (borderline wide). The PR interval is 138 ms, so WPW is very unlikely. There is also some ST depression which appears to be secondary to this slightly abnormal QRS, and lends some further credibility to some sort of pre-excitation.

There is no further follow-up at this point.

Is it STEMI or Non STEMI? What you call it has consequences.

2011-09-28T10:46:00.000-05:00

This 53 yo male with no cardiac history developed chest pain 12 hours prior to admission. It was coming and going, waxing and waning, all night. At 8 AM, it increased to 9/10 and he called 911 and had this prehospital ECG recorded at 0858:

There is sinus rhythm with ST elevation in V1-V3, Q-waves in III and aVF, and ST depression in I, aVL, V5 and V6. It is obviously ACS, and, to me, clearly a STEMI. The computerized QTc is 429 and another ECG recorded shortly thereafter looked similar, with a QTc of 450.

The equation value was about 30, which clearly reflects LAD STEMI. In fact, this one is so obvious (due to the ST depression) that I would not have included it in my study comparing LAD occlusion to early repolarization. The computer (which often misses MI) read it as Acute MI. The cath lab was activated prehospital.

The patient received nitroglycerin and his pain greatly diminished (possibly even resolved). He arrived in the ED and had this ECG at 0947:

The ST elevation is somewhat less. There is now ST elevation in lead III, with reciprocal ST depression in aVL (which was also present on the prehospital, showing how aVL is more sensitive for inferior STEMI than are inferior leads). The QTc is now only 388 ms, and the equation value has dropped to 25.4 (STEMI less obvious, but still above 23.4).

The initial troponin was 2.4 ng/ml. The patient went to the cath lab with a door to balloon time of 50 minutes, where he had a 4 cm long 95% narrowing of the LAD that was nitroglycerin responsive, and thought to be spasm. It was a type III (wraparound) LAD to the inferior wall, explaining the inferior ST elevation. There is no mention of thrombus. It was stented. There was also a chronically occluded circumflex and RCA which both filled via collaterals from the LAD (he was hanging on by the 5% of the LAD that was open).

Of course the ECG cannot tell you the cause of the ischemia (thrombus, spasm, or even demand ischemia), so the fact that this was spasm does not affect the ECG diagnosis, and there would be no way to know this without doing the cath.

Troponin I peaked at 82 ng/ml. Echo showed anterior and apical, and inferior, WMA and EF of 35%.

The ECG the after PCI had the same appearance, and the next day there was slightly less STE and evolving T-wave inversions, seen here:

Persistent ST elevation in V1 and V2, with T-wave inversion in V3 - V6.

A cardiologists called this a NonSTEMI because he saw the ST elevation as normal. Normal ST elevation, as I have shown in my study yet to be published, has an equation value that is less than 23.4 in almost all cases. But not all. Could this have been a false positive?

No. See below.

However, the troponin peaked at 82 (large MI consistent with STEMI), the convalescent echo showed a persistent anterior wall motion abnomality and a persistently poor EF of 44%.

So there was significant Myocardial wall loss, consistent with STEMI.

Finally, here is his ECG months later:

Most ST elevation is gone, equation value is now 22.1 (less than 23.4), and the R-wave in V4 has recovered some.

I think this pretty clearly shows that the ST elevation was not baseline ST elevation, but rather a result of the acute coronary syndrome and therefore it was indeed a STEMI.

On review, the cardiologist sees that this is a STEMI. Partly by just looking again and also because he had not seen the prehospital ECG.

Learning points:
1. ACS should be called STEMI if there is ST elevation that is a result of the ACS.
2. When there is ST elevation that is the result of ACS, there is occlusion or near occlusion of the artery.
3. The diagnosis of STEMI vs. NonSTEMI should not be based on the degree of ST elevation; rather, it should be based on whether there is ST elevation due to occlusion or near occlusion. 1 mm, or 2 mm, are arbitrary measurements that do not have a physiologic basis.
4. Many STEMIs are erroneously called NonSTEMIs.
5. If you call it a NonSTEMI, you may delay cath lab activation that should be immediate.
6. Had this patient not gone immediately to the cath lab, he would not have shown up in missed STEMI statistics. This is one reason why, in the literature, STEMI has such a low miss rate. If true STEMIs are called NonSTEMIs, then of course the STEMIs are not missed so often.
7. If the door to balloon time had been 300 minutes, this would not have been reflected in the hospital statistics. How many hospitals are accurately classifying their MI cases as STEMI? When the door to balloon time is being tabulated, how often are cases like this called NonSTEMI just to buff the statistics?

ST elevation of early repolarization may vary with the rate

2011-09-25T15:58:00.004-05:00

This 49 yo black male presented with sudden substernal non radiating pleuritic chest pain on the day prior to presentation. Here is the presenting ECG:

There is ST elevation in anterior leads that is classic for early repolarization: there is excellent R-wave progression, QT is not long, T-waves are assymmetric (slower upstroke than downstroke), and well-formed J-waves. The equation value [1.196 x (ST elevation at 60 ms after the J-point)] + [QTc x 0.059] - [R amplitude in V4) x 0.326)] is low [= (2.0 x 1.196) + (418 x 0.059) - (25 x 0.326)], which is equal to 18.9. A value less than 23.4 is unlikely to be MI. Interestingly, the presence of J-waves did not add value to the prediction rule equation.

Bedside ultrasound showed no wall motion abnormality. A troponin drawn the next AM was negative. A repeat EKG showed increased ST elevation:

Equation value is: (4.5 x 1.196) + (0.059 x 400) - (0.326 x 28) = 19.9 (early repol)

Repeat echo again showed no wall motion abnormality.

Why is the ST elevation greater in the second ECG? One must remember that the ST elevation of early repolarization diminishes with increased sympathetic tone, such as during exercise. When the heart rate is faster, as in the first ECG, the ST elevation is likely to be less pronounced than when the heart rate is slower.

Kambara found in his longitudinal study of patients with early repolarization that, in 26% the ST elevation disappeared on follow up ECG and in 74% the degree of ST elevation varied on followup ECGs.

I do not have proof in this case, but I'm pretty certain that the difference in ST elevation is due to the difference in heart rate.

Learning point: The ST elevation of early repol is not constant. In particular, it may be diminished with exercise, sympathetic tone, and heart rate, and may be increased when the heart rate is slower.

Thanks to Steve Dunlop for this case.

Here is a good review article on early repolarization:

Cardiac arrest, LBBB with STEMI on the ECG, but no Acute Coronary Syndrome!

2011-09-20T21:16:00.002-05:00

This 80 year old with a history of CABG had a cardiac arrest. He was resuscitated after fairly prolonged down time, but regained consciousness, though he was confused. He did not state he had chest pain, but, then again, he couldn't remember anything. Here is the prehospital ECG at 1935:

Sinus rhythm with left bundle branch block (LBBB). There is concordant ST elevation in all inferior leads. Remember that, in LBBB, lead II should have discordant ST depression, and the fact that it does not indicates relative ST elevation. In Sgarbossa's study, just 1 mm concordant STE in just 1 lead was 92% specific for MI and earned the ECG 5 points. There is reciprocal ST depression (excessively discordant) in I and aVL, consistent with RCA occlusion. There is proportionally excessively discordant ST elevation in V1, consistent with RV involvement. There is concordant ST depression in V2 and V3, greater than 1 mm. Just 1 mm concordant ST depression in just 1 lead of V1-V3 was 96% specific for MI and would earn the ECG 3 points. So this ECG gets 8 points PLUS has excessive discordance in V1 PLUS has the finding in many leads, not just one. 3 points gets you an MI by Sgarbossa. There are also marked Q-waves in lead III.

We did a bedside cardiac ultrasound. Here it is:

This is a parasternal short axis view (a transverse cut through the heart; you see the left ventricle). You can see that the part of the heart closest to the transducer (top) is the anterior wall and is moving and contracting well. The part farthest (bottom) is the posterior wall and is not contracting. This is a posterior wall motion abnormality. This is consistent with MI, though one cannot tell if it is new or old. The structure at the bottom that is moving is the mitral valve, with anterior and posterior leaflets.

This is as clear a STEMI as you can get. Now, it is true that shortly after a non-ACS cardiac arrest, there can be transient diffuse ST depression, but not ST elevation in a coronary distribution, and there should not be a wall motion abnormality.

This was the initial ED ECG at 1951:

All the same findings are there, but they have diminished, consistent with reperfusion

There was some delay in cath team arrival since it was the middle of the night, so this right sided ECG was recorded at 2010:

The ST segments have normalized in the limb leads and in V1R (V2) and V2R (V1). The Q-wave in lead III persists.

The angiogram showed a chronically occluded RCA and an occluded SVG to the RCA. There was faint filling of the distal branches of the RCA by collateralss from the left coronary system.

As it turned out, the patient had an old inferoposterior MI that was scarred; this scar initiated primary V Fib arrest, which in turn resulted in temporary hypoperfusion of the inferior wall because of its very tenuous blood supply and resulting ST elevation on the ECG.

So this is classic inferoposterior STEMI on the ECG but is NOT acute coronary syndrome!

This could not have been known without the angiogram. The ECG and ultrasound could not have been differentiated from acute plaque rupture with occlusion of the RCA.

Weakness due to Bradycardia due to Sick Sinus with Sinoatrial block, with Ashmann's phenomenon

2011-09-19T14:15:00.000-05:00

This post is from last December, and shows sinoatrial block. A reader was puzzled by why one p-wave conducted and another did not.

I had not thought about it at the time, but K. Wang noticed that the preceding R-R intervals were different, and this led to Ashmann's phenomenon.

Respiratory Failure, Heart Failure, and Narrow Complex Tachycardia

2011-09-15T21:09:00.003-05:00

A 60 yo female presented by ambulance in resp distress, requiring noninvasive ventilatory support. She had pulmonary edema and was near respiratory failure.

Here is the prehospital ECG (will not comment on the interpretation until the end of the post, so you can ponder it for yourself):

Computer read: "Sinus tachycardia" at a rate of 143, and "***Acute MI***". Obviously, there is no clear STEMI.

She was continued on respiratory support, treated for COPD and CHF with nebs, steroids, lasix and nitro. Here is her first ED ECG:

The computer reads "sinus tach".

An ED bedside echo was performed from the subcostal view:

Here is a legend for what you are seeing on the echocardiogram: LA = Left atrium, LV = left ventricle, RA = right atrium, RV = right ventricle, MV = mitral valve. The LA is greatly enlarged. The LV is very small. The mitral valve is very echogenic and highly suggests stenosis, which we confirmed with doppler.

Chart review confirmed h/o porcine mitral valve replacement with subsequent development of prosthetic mitral valve stenosis (that is to say, it recurred in the new valve). This conforms with our ED echo.

The heart rate continued at 143, and by this time there was much less artifact. This strip was printed out:

Now there is clear atrial flutter.

A bit of history could be obtained at this point, and she said she had had rather sudden SOB about 15 hours prior, and had had some pink and frothy sputum.

A better 12-lead was obtained:

Now, again, the atrial flutter is obvious, and there are no signs of ischemia

So, we have a patient who is in respiratory distress, due to mitral stenosis and complicated by atrial flutter, which diminishes LV filling that is already compromised by mitral stenosis. ACLS would say to do electrical cardioversion for a patient with atrial flutter and rapid ventricular response who is suffering respiratory failure, but patients with mitral stenosis are at very high risk of thromboembolism and stroke (old literature). Cardioversion would increase this risk. Therefore, we decided on slowing the ventricular rate with diltiazem. Here is the subsequent ECG:

There is now atrial flutter with 4:1 block.

With more time to fill, the LV was able to pump better. The patient improved gradually, and refused a valve replacement. She returned a few days later in distress and will now get a new valve.

Look again at the first ED ECG:

Knowing that it is atrial flutter, you can now see (if you didn't before) the atrial spikes in V1 (2:1) that might have been interpreted to be artifact.

Learning points:
1) When the heart rate does not change, but stays rapid and constant, it is probably not sinus tachycardia and then you should...
2) Look for atrial flutter waves
3) ACLS is guidelines only. Sometimes the patient does better with less aggressive care (and, of course, sometimes with more). One must always think it through.
4) Bedside echo can be very useful

Subacute MI masked by a wide complex

2011-09-12T11:26:00.000-05:00

This is a post I put up about a year ago and had forgotten about until I noticed that it was getting a little traffic recently (how does this happen?).

I find it very interesting and worth another look.

Click here to see these ECGs that represent a subacute MI masked by a wide complex.

Forgive me if you've seen it before and find it too repetitive to post again.

Chest pain, tachycardia, diffuse ST elevation. What is the diagnosis?

2011-09-09T11:57:00.004-05:00

First, I want you to see the ECG without a lot of clinical information: this 45 year old male presented with left chest pain:

More clinical information:
One week prior, he was stabbed in the left chest and a chest tube was placed. His pulse was 120 and blood pressure 90/50.

ECG analysis:
There is sinus tachycardia. There is ST elevation in inferior, lateral, and anterior leads. The ST elevation in II is greater than III. There is no reciprocal ST depression in aVL. The ST elevation in anterior leads is marked, and scary. There is perhaps excessive PR depression (see esp. leads II, V5). This ECG is classic for pericarditis, but could conceivably be due to antero-infero-lateral STEMI due to proximal (before D1 to the lateral wall) occlusion of a type III (wraparound, to inferior wall) LAD.

Findings favoring pericarditis over diffuse MI:
1) no ST depression in aVL. We studied 160 inferior STEMI; only 1 had absence of any ST depression in aVL. We also studied 39 consecutive cases of pericarditis who presented to the ED with chest pain and ST elevation meeting "reperfusion criteria." None had any ST depression anywhere (except aVR, in which all had it).
2) The computerized QTc is 371 ms. This makes anterior MI very unlikely. In my study of 355 consecutive LAD occlusions, only 2 had a QTc less than 372 ms.
3) High anterior R-wave amplitude. The mean R-wave amplitude in V2-V4 is at least 18 mm. In my study of 355 consecutive LAD occlusions, zero had a mean R-wave amplitude this high.
4) STE in lead II greater than lead III. This is not very accurate, and is found in inferior MI due to circumflex occlusion; i.e., inferolateral MI may have this.
5) The equation value (incorporating ST elevation, R-wave amplitude, and QTc) is 22.32 (less than 23.4 is unlikely to be LAD occlusion when early repol is the alternate diagnosis, but this has not been tested against pericarditis)

I was shown this ECG with no clinical info the next day, and due to the above considerations, after a glance at the ECG I said, "It's not an MI."

Verifying the diagnosis of pericarditis by ED bedside echo
If this is STEMI, it is a massive antero-infero-lateral STEMI and the patient would probably present in cardiogenic shock. A bedside echo should show very poor LV function, and the patient should probably have pulmonary edema (which he did not). A bedside echo was done: there was no pericardial effusion and, though the LV was not what the clinicians thought should be appropriately hyperdynamic, there was only "possibly decreased LV function."

Further evaluation revealed a fever of 101. Fluids were given and the heart rate decreased, but an ECG 30 minutes later was unchanged. The cath lab was activated. Ultimately, he was not taken to the cath lab and troponins had a very tiny rise consistent with a very small degree of myocarditis in addition to pericarditis. He grew out MSSA from his blood and had an infected hematoma in his chest. The next day, he developed a pericardial friction rub, confirming the diagnosis of myo-pericarditis. No more ECGs were recorded.

Here are more cases in which pericarditis was on the differential diagnosis.

Missed Acute MI, with coronary occlusion, evidence only by T-wave inversion in V2 and evolving ST depression in V3

2011-09-06T12:49:00.001-05:00

A 39 yo otherwise healthy man with no risk factors was walking at the mall when he developed chest pressure. He presented to the ED after 30 minutes, now also feeling weak. He was diaphoretic. Here was his initial ECG:

There is sinus rhythm. There is abnormal T-wave inversion in V2 (in morphology, consistent with "persistent juvenile pattern" because the R-wave is not greater than the S-wave, but this would be very unusual in a 39 yo male). There is minimal, nondiagnostic ST elevation in inferior leads without any reciprocal ST depression in aVL. There are thin and normal inferior Q-waves. Thus, there are some suspicious abnormalities, but no definite signs of ischemia.

Because of persistent symptoms, another ECG was recorded 30 minutes later:

There is only one new finding on this ECG which suggests ischemia. It is very subtle but real. Look at lead V3, where there is now some ST depression. The previous ECG has a small amount of appropriate ST elevation in V3. Any ST depression in a young male is abnormal, especially if changed from previous. This is especially worrisome when combined with the abnormal T-wave in V2.

Let's look at both V3's, magnified:

The later ECG (bottom panel) shows minimal ST depression in V3. The top shows minimal ST elevation (normal). The difference is significant and highly suggests posterior ischemia.

This abnormality in V3 was apparently not seen by the treating MD, who is a nationally recognized expert in STEMI care (showing how difficult these diagnoses can be).

The initial troponin was negative. The patient was admitted to telemetry. At 4 AM, his second troponin returned at 1.8 ng/mL. Another ECG was recorded:

T-waves in V2 and V3 are now upright and larger, evolving. Are these posterior reperfusion T-waves?

He went for cath at 6 AM and had on occluded OM-2 that was opened and stented. Troponin I peaked at 99 ng/mL (large MI)!

So this is a NonSTEMI, right? Technically, yes, because there is not 1 mm of STE in 2 consecutive leads. But the definition misses the point. It is a coronary occlusion with a substantial myocardial territory at risk, that showed only very subtle ST changes.

Should you activate the cath lab for this?

Not from the ECG alone. However, if you notice the ST depression, you then realize that this is ischemic chest pain, not esophageal spasm. Once you know that the chest pain is ischemic in origin, and you cannot control it medically, then you must go urgently to the cath lab.

The patient should be treated with NTG, Aspirin (and clopidogrel, if your institution allows), metoprolol, antithrombotics, and GP IIb IIIa inhibitors. If the pain persists, and the ST depression persists, then talk to your interventionalist immediately.

Here is the followup ECG:

The ST abnormalities have resolved. There are new inferior Q-waves diagnostic of inferior MI. The R-wave is increased in V2, consistent with MI (analog of a Q-wave). There is no apparent resolution of the minimal and non-diagnostic inferior ST elevation.

I don't have all the data on this case, and do not know if there is an inferior wall motion abnormality, or if this OM-2 supplied the inferior wall. It probably did, as evidenced by the Q-waves; but it is very interesting that during the acute phase, there were no diagnostic ST changes in inferior leads, and the minimal ST elevation that was present did not evolve.

Many MIs are electrocardiographically "silent," especially when in the circumflex territory. I do wonder whether, in the studies that show this phenomenon, if an ECG expert evaluated the ECG for the subtle signs of ischemia. I suspect that many or most that are thought to be "silent" are really just "subtle."

Here are more electrocardiographically subtle MI.

What is the rhythm? Answer at the bottom.

2011-09-01T13:25:00.000-05:00

An elderly woman presented with abdominal pain. Here is her ECG:

This is easily mistaken for atrial flutter because the waves have a fluttering, wavy, sawtooth appearance. However, 3 things make atrial flutter impossible, 2 are related:
1) the rate of the waves is > 400
2) the QRS does not appear at the same part of the atrial wave cycle each time (which it must do in flutter)
3) the ventricular rate is irregularly irregular. In atrial flutter, the ventricular rate can be regular if there is a constant ratio (2:1 block, 3:1 block etc). It can also be regularly irregular, in which every QRS comes at a multiple of the atrial wave rate (if atrial wave rate is 300, it happens every 200 ms, and every R-R interval must be a multiple of 200ms)

2) and 3) are related: since 2) is true, 3) must also be true.

The woman had atrial fibrillation. It was misdiagnosed as flutter, and this may have contributed to a delayed diagnosis of mesenteric embolism.

This is a quiz. The ECG is pathognomonic. Answer is at the bottom.

2011-08-30T15:34:00.000-05:00

Hyperkalemia, with near sinusoidal pattern. Note very wide QRS, bizarre deep T-waves in V1 and V2, peaked T-waves in V4 and V5, long PR interval this case.

Whenever you see a wide QRS, you must think of hyperkalemia.

The K was 8.7 mEq/L. It responded to therapy.

Reversible T-wave inversion -- it reverses, then evolves, then reverses when ischemia is gone. Normalization of T-waves, NOT pseudonormalization.

2011-08-27T10:33:00.001-05:00

A 62 yo male has had chest pain with exertion for 2 weeks. He began having chest pain at rest at 2AM, and presented at 7 AM.

Here is his initial ECG:

Sinus rhythm. There is a QS-wave in V2 (old MI?) and very subtle terminal T-wave inversion in V3, and ST depression in V4-V6, highly suspicous for LAD NonSTEMI. I believe the extra wave in V1-V3 is artifact.

This was recorded 2 hours later, after troponin I confirmed acute MI at 0.485 ng/mL:

There is a PVC, but now the terminal T-wave inversion is gone. Some ST depression in V5 and V6 remains.

An angiogram revealed 3-vessel disease and a 90% LAD stenosis, 99% RCA, and 70% ostial right Posterior Descending Artery. No intervention was done because of consideration of CABG.

This was recorded 9 AM the next day. A simultaneous echo had very subtle WMA in the LAD territory.

Now there is classic biphasic terminal T-wave inversion (strictly speaking, it is not Wellens' because Wellens' requires preservation of R-waves). There is also subtle new Terminal T-wave inversion in aVF ("inferior Wellens").

On day 2, PCI of the rPDA and RCA was done. The troponins continued to trend down.

This ECG was recorded the next AM (day 3):

There is evolution of anterior T-waves, with T-wave inversion in V4 more pronounced now. T-wave in aVF is now upright.

On day 3, he had the LAD stented. Troponins bumped to 3.0 mcg/L after the PCI. This was recorded the next AM:

Now, the anterior T-waves have completely normalized.

Such reversal is usually due to reocclusion (pseudonormalization) and associated with chest pain. Wellens in the setting of significant troponin elevation usually evolves to deep and symmetric T-waves, then normalizes over weeks to months. This is an unusual case of T-wave normalization without re-occlusion that occurred in 24 hours.

In unstable angina, with no myocardial cell death, T-waves are more likely to normalize when ischemia is resolved.

Contrast this normalization of T-waves to the pseudonormalization of the last post.

Pseudonormalization of T-waves

2011-08-23T14:14:00.001-05:00

In a few days I will post a twist on pseudonormalization, but wanted to first post this classic case.

This 49 year old male presented after an episode of chest pain.

There is sinus rhythm. There are T-wave inversions in II, III, aVF and V4-V6. This is consistent with inferior and lateral Wellens' type reperfusion T-waves. There is also a large upright T-wave in V2 (and, in retrospect) I see this as a posterior reperfusion T-wave.

The first ECG is consistent with a patient who had an occlusion of an artery supplying the inferior and lateral walls, but is now reperfused.

In the ED, his pain recurred and this ECG was immediately recorded, 20 minutes later:

Now the T-waves are upright (not normal, but pseudonormalized). This is an obvious STEMI, but nicely illustrates the phenomenon of pseudonormalization. Lead V5 by itself looks normal unless you compare it to lead V5 20 minutes prior.

Pseudonormalization is a phenomenon or reocclusion of an artery that has recently reperfused. The reperfusion resulted in inverted T-waves (reperfusion T-waves, Wellens' T-waves). The reocclusion results in the T-wave becoming upright again. If seen in isolation, one may be lulled into thinking they are truly normal (see V5).

See here for more cases of pseudonormalization.

This also illustrates the importance of serial ECGs.

Bizarre T-wave inversion of Stokes Adams attack (syncope and complete AV block), with alternating RBBB and LBBB

2011-08-19T12:30:00.002-05:00

This is a 68 yo male with a history of aortic stenosis, on carvedilol, fell from a ladder approx 20 ft onto concrete, landing face down with likely loss of consciousness. Upon EMS arrival, pt was still face down in a pool of blood, but was responsive, alert, and neuro intact. His BP was stable en route, but he was bradycardic in the 30's.

On exam, he had multiple orthopedic injuries, but no significant head, neck, spinal, chest, or abdominal injuries. The patient had had no premonitory chest pain or SOB. His BP was 121/59 and he was well perfused. This was his initial ECG:

There are regular p-waves at a rate of about 90, but they do not conduct. Thus, there is 3rd Degree AV block with a probable Purkinje escape at a rate of 36; the wide QRS and RBBB pattern (rSR' in V1, wide S-waves in lateral leads) tell us that the escape is from the left bundle, creating an RBBB-like ECG. [Alternatively, there could be a nodal escape with RBBB]. There are also very wide, bizarre, inverted T-waves. The QT is 680 ms, and QTc = 527 ms. There are no ST changes indicative of STEMI.

First troponin returned at 0.11 ng/ml (slightly elevated). With all his injuries, he spent 2 hours in the ED, and a subsequent ECG is shown here:

Now the escape has an RBBB in the first part of the ECG, and LBBB pattern in the latter part, and the rate is 41. The escape has alternated to the right bundle [or there is a nodal escape with LBBB].

This is a classic ECG. A drop attack with third degree AV block is called a "Stokes Adams" attack, and is often associated with bizarre wide inverted T-waves. A google scholar search comes up with several articles: Giant T-wave inversion associated with Stokes-Adams syncope (sycope due to complete AV block).

The escape rhythm is dependent on the automaticity of the tissue that escapes. AV nodal escape is the fastest, then HIS bundle, then Purkinje fibers, then ventricular tissue (which results in a slow "idioventricular" rhythm)

In this case, there is either an alternating escape, or a nodal escape with alternating RBBB and LBBB. If it is the former, then you know that your bundles have appropriate automaticity and can support the rhythm without a stimulus from above. If it is the latter, then you have the risk of developing block of both the left and right bundles simultaneously, in which case the only escape possible is idioventricular.

Obviously, this is a dangerous situation, and you must place transcutaneous pacing pads and ascertain that they will capture if you need them too. Alternatively, an internal pacing wire can be placed.

A simple test of capture is nicely done by pacing and observing the heart with bedside ultrasound to be certain of capture.

Case continued:

Fearing possible beta blocker toxicity, glucagon was given in increments up to a total dose of 5 mg, but this was not effective. Atropone 1 mg was given without effect (this will not work in this situation, ever). An internal pacing wire was placed in the ED, but not used because, in the interim, dopamine had been started and titrated to 10 mcg/kg/min with an increase in the heart rate to the 50's. Pacer pads were also placed.

Subsequent troponins rose to a maximum of 8.5, suggesting that ACS may have had a role here. However, third degree heart block can develop for other reasons than acute MI.

An echocardiogram revealed moderately severe aortic stenosis with a valve area of 1cm2, with a mean pressure gradient of 50mmHg. There were regional wall motion abnormalities (apex, distal septum and
inferior) but these are difficult to interpret in the setting of LBBB.

Angiography and Ventrilography revealed worse AS, with valve area of 0.74 cm2. There was no coronary artery disease.

A permanent pacer was placed on hospital day 3.

This is the final ECG:

Perfectly normal paced rhythm. Note that all precordial QRS are negative. This is because the pacing lead is placed in the apex of the right ventricle, so that depolarization always proceeds away from the apex of the heart (on the chest, the point of maximal impulse). Thus, it depolarizes away from all precordial leads.

After many orthopedic procedures, the patient had his aortic valve replaced, and went home.

Altered Mental Status, possible ingestion. What does the ECG show?

2011-08-15T08:09:00.002-05:00

A middle aged man was heard to be falling in his apartment. He was found very agitated, intermittently screaming (and on presentation was intermittently roaring like a lion). There was no apparent etiology. He required 10 mg of droperidol for sedation. He underwent an ECG as a routine part of the evaluation of possible ingestion:

What jumps out at you?

Answer: There is sinus rhythm with one PAC. The notable feature is a very long QT interval. The computer read this as QT = 492 ms, with QTc = 518 ms. But when the QT gets very long, computers become inaccurate and you must read it by hand.

Some recommend reading in lead II or V5/V6. Some say to measure the longest of the 12 QT intervals. I tend to measure the longest of the 12 QT intervals on the ECG. I have not measured them all, but at a glance, it looks like V2 and V3 have the longest, and these typically are the longest. I have blown them up below:

The end of the T-wave has a small hump (wide arrow) which is probably a U-wave and this can make the end of the T-wave appear to be even more delayed than it is. The narrow arrow more accurately follows the projection of the T-wave to the baseline (horziontal black line). Using this at the end of the QT interval, I get 540 ms, with QTc as 540/(square-root of R-R interval) = 540/0.91 = 593 ms

(By my eyeballing it, the QT in V5 is also 540 ms.)

593 ms is dangerously long and may result in torsade de pointes (polymorphic VT), and could be a result of the droperidol, or of metabolic and electrolyte abnormalities, or to many drugs or even be familial. In any case, it is unsafe to leave it like this, so we gave 2 grams of Magnesium. A blood gas revealed a pH of 7.75 (entirely a respiratory alkalosis, drawn before intubation and due to his agitation and hyperventilation), which will also cause long QT and torsade. K was 3.2, which will also contribute. By this time, we had him on the ventilator and so we intentionally slowed his ventilations to lower the pH.

Repeat pH was normal and Mg was delivered, and we recorded another ECG:

I calculate the QTc at 488 now, which is safe.

The magnesium level returned at 1.2 (low).

Etiology of long QT in this case: 1) hypo Mg 2) hypoK 3) alkalosis 4) droperidol? 5) other drug (we still do not have a diagnosis and the patient is still unable to tell us what meds he is taking)

1) QTc over 500 ms can be dangerous. When near 600, it is very dangerous.

2) Give Mg, correct to 2.0.

3) Correct high pH (I once had a patient who required mechanical hypoventilation and intravenous HCl to prevent torsade)

4) Correct low K to 4.5. Hypokalemia causes a large amount of QT dispersion (see #6)

5) Check Ca (normal in this case). HypoCa causes long QT by lengthening the ST segment without lengthening the duration of the T-wave. It is uncommon for hypocalemic long QT to result in torsade because it results in only a small amount of QT dispersion. It is "homogenously prolonged".
6) both QT interval and QT "dispersion" (a measure of the difference, in ms, between the longest QTc and shortest QTc of the 12-leads) are risk factors for torsade. A QT dispersion of greater than 60 ms is high risk.

Details on measurement of the QT interval can be found here: free full text article.

One should average 3-5 leads, usually take lead II, or the lead that shows the end of the T-wave best, or the leads with the longest QT (which are usually V2 or V3). Correction for the heart rate must be done, but tends to overestimate the QT interval at fast heart rates and underestimate at low rates, and so other correction methods have been developed. The U-wave should generally not be included, especially if large, but if small and not distinguishable from the T-wave, the course of action is unclear.

QT dispersion

--Yelamanchi VP, Molnar J, Ranade V, Somberg JC. Influence of electrolyte

abnormalities on Interlead variability of ventricular repolarization times in 12-

lead ECG. Am J Ther 2001;8:117–122.

--Eryol NK et al. Effects of Calcium Treatment on QT Interval and QT

Dispersion in Hypocalcemia. Am J Cardiol 91:750-752; March 15 2003.

Droperidol

Droperidol has a black box warning regarding the QT interval prolongation. Our department has studied this extensively and found it to be a greatly exaggerated danger.

Here are two abstracts:

QT Lengthening after Parenteral Droperidol Administration

Stephen W Smith, Marc Martel, Michelle Biros, Marsha Zimmerman and Peter Chase

Hennepin County Medical Center: Minneapolis, MN SAEM, St. Louis 2002
ABSTRACT
Objectives: Recently, the Food and Drug Administration (FDA)warned of a prolonged QT interval and torsade de pointes asa complication of droperidol (DROP). We sought to determinethe frequency of a significantly prolonged QT interval (LQT)in patients who received DROP, and to compare this with theQT interval of patients not receiving DROP. Methods: The EmSTATelectronic patient database was searched from January 1, 1997,through November 30, 2001, for all patients who received DROP.Those who had an electrocardiogram (ECG) ordered at least 30 minutesafter administration of DROP were identified. These ECGs werereviewed and the computerized corrected QT intervals (QTc)were recorded. A medication-induced QTc of less than 480 ms is generallyconsidered safe; we defined LQT by QTc greater than 480 ms. Medical recordsof patients with LQT were further reviewed for previous ECGs,contributing medical conditions, and adverse events. The QTc'sof 100 consecutive patients who did not receive DROP were reviewedas controls. Data were analyzed with descriptive statisticsand Fisher's exact test. Results: 15,374 patients received18,020 doses of DROP; 682 had an ECG recorded after DROP, 450were obtained at least 30 minutes after administration. LQTwas found in 17 patients, 1 had left bundle branch block (LBBB),1 had a paced rhythm, 1 had right bundle branch block (RBBB),resulting in a total of 14 with a normal QRS and LQT (3.1%).Four of these 14 had previously documented LQT not associatedwith DROP. None had an adverse event related to LQT. Of 100consecutive patients in the control group, 4 had LQT (4.0%)(p = 0.76) Conclusions: Our study does not support an effectof DROP on the frequency of LQT.

QT Prolongation and Cardiac Arrhythmias Associated with Droperidol Use in Critical Emergency Department Patients

Marc Martel, James Miner, Seth Lashkowitz, Mark Danahy, Joseph Clinton and Michelle Biros

Hennepin County Medical Center: Minneapolis, MN SAEM Boston 2003
ABSTRACT
Background: QT prolongation and torsade de pointes (TdP) havebeen reported as a complication of droperidol (Drop). Objectives:To determine the change in the corrected QT interval (QTc) andthe incidence of cardiac arrhythmias in critically ill patientswho received Drop. Methods: The medical records of all criticalcare ED patients from 1/1/1997 to 12/31/2001 were hand searchedfor those who received Drop and an ECG in the ED. Drop dose,ECG time, QTc intervals, and cardiac rhythm were reviewed. ECGswith atrial fib/flutter, right or left bundle branch block,or paced rhythms were excluded. Data was analyzed in 3 groups,patients with an ECG recorded only before Drop, only after Drop, andthose with ECGs both before and after Drop. Data was analyzedusing descriptive statistics and chi-squared. Results: 11,583charts were reviewed, 1172 patients received Drop, and 396 hadboth an ECG and Drop in the ED. 44 patients were excluded dueto abnormal rhythm, bundle branch block, or paced rhythm. 96patients had an ECG only before Drop (mean 33.3min prior), averagedose of 2.75mg, and mean QTc of 435.0ms (95% CI 428.1–441.9ms).186 patients had an ECG only after Drop (mean 25.9min after),average dose of 3.68mg, and mean QTc of 433.3ms (95% CI 427.8to 438.8ms). 114 patients had ECGs before and after Drop (meantime 28.2min before, 108.8min after), average dose of 2.21mg,and mean QTc of 435.7ms (95% CI 426.7–444.7ms) and 435.8ms(95% CI 427.5–444.1ms) before and after Drop, respectively.The mean ratio of the QTc before and after Drop is 1.005 (95%CI 0.985–1.025). 2 patients had ventricular arrhythmiasin the before Drop group, 3 in the after Drop group, and 4 inthe before and after Drop group (p = 0.5). 1 patient had anunrecorded event of TdP with a QTc of 466ms after conversion.Conclusions: We detected no statistical difference in the changeof the QTc interval or occurrence of ventricular arrhythmiasin critically ill patients who received Drop.

Atrial Fibrillation with RVR and Inferoposterior ST elevation (Injury Pattern)

2011-08-11T13:02:00.000-05:00

This is an old post from June 2009 that has not received much attention, but should. Take a look!

This 80 yo woman had been increasingly lethargic for 2 days, and presented hypotensive (SBP =70), pale, and tachycardic. She had not been complaining of chest pain. It was uncertain whether she had chronic atrial fibrillation or not. She was afebrile. Here is the initial ECG.

There is an irregularly irregularly rhythm (atrial fibrillation) with a very fast ventricular response. There is an injury pattern, with ST elevation in II, III, aVF, reciprocal ST depression in I and aVL, and ST depression of posterior injury in precordial leads.

We did not activate the cath lab. We suspected GI bleed and this was confirmed with blood on rectal exam. An ultrasound of the heart showed hyperdynamic function and the inferior vena cava (IVC) confirmed low central venous pressure (IVC was flat). Had this been a primary cardiac event, the CVP would be high and the IVC distended, and the patient might have also been in pulmonary edema.

She was given blood and fluids until the bedside ultrasound showed good central venous pressure (distended inferior vena cava), but she remained hypotensive and tachycardic, and the ST elevation did not resolve. Thus, we sedated her and electrically cardioverted at 200J (biphasic), but this was unsuccessful x 3. We then intubated her and started an infusion of amiodarone 300 mg IV, but with no improvement, and a subsequent cardioversion was again unsuccessful. We then loaded her with 500 mcg/kg of esmolol and started her on a 50 mcg/kg/min drip, after which a fifth cardioversion was successful, and resulted in the second ECG shown here:

The rhythm is sinus (with a couple PACs), rate normal, and all ST elevation and depression is now resolved.

The blood pressure came up immediately. Hemoglobin returned at 7 and WBC count at 29,000. The troponin peaked at 19, and there was a subsequent inferior wall motion abnormality. EGD showed duodenal ulcers and erosions which had stopped bleeding.

A stress sestamibi showed no inducible ischemia, so no cath was done. Whether there was thrombus in the infarct-related artery, or whether this was only demand ischemia (Type II MI) is uncertain.

Convert atrial fibrillation with a rapid response when the patient is unstable; any injury pattern on the ECG constitutes instability.

Though demand ischemia usually shows as ST depression (or nonspecific findings) on the ECG, it may occasionally present with injury (ST elevation).

Young man with syncope while riding a bike [Arrhythmogenic Right Ventricular Dysplasia (ARVD)]

2011-08-07T13:08:00.010-05:00

This 31 yo who is otherwise healthy had sudden syncope while riding a bike. He remembers looking down, then becoming dizzy, then waking up on the ground with his feet still attached to the pedals. He thought he was unconscious by himself for 45 minutes (!). Then he awoke and called 911. He had no prodromal vasovagal symptoms such as flushing, nausea, or diaphoresis.

He had a several year history of palpitations without syncope, but had one presyncopal epsisode one month prior. He had been seen by a local cardiologist 3 years prior and had what is described in records as a normal ECG and normal Echo, and had been encouraged to resume exercise.

Here is his presenting ECG in the ED:

Sinus rhythm with some artifact. QTc may be slightly prolonged; I eyeball it at about 470ms. This is not long enough to be dangerous.

His symptoms are very alarming. There are 2 features which are high risk: no prodrome other than dizziness, and onset with exertion. When a young person who is otherwise healthy presents with high risk syncope, a normal exam, and NSR, it is essential to obtain an ECG not only to look for ischemia, blocks such as LBBB and RBBB, but also for inherited disorders that cause dysrhythmia. There are 5 that I think of: WPW, HOCM, Brugada, long QT, and Arrhythmogenic Right Ventricular Dysplasia (ARVD), which is a disorder of fatty infiltration of the RV that causes sometimes lethal ventricular tachycardia originating from the RV. ARVD is quite rare, not often thought of, and very difficult to recognize on the ECG.

Alas, this young man's presenting ECG shows none of these.

Surprisingly, the first troponin returned at 3.44 ng/ml, the second at 7.48. Clinicians thought they were dealing with a dysrhythmia due to ACS/NSTEMI, and started heparin and aspirin. He was admitted to the hospital.

An echo revealed segmental hypokinesis of the apex of the right ventricle only. The contour at this portion of the RV free wall was also unusual, and raised suspicion for ARVD.

MRI of the heart was done; here is the final report:

There is focal dyskinesia involving the RV apex and the anterior wall. On the T2-weighted sequence, there is linear increased signal in the RV myocardium suggesting fatty infiltration. There is no definite delayed enhancement in this area. These findings are suspicious for arrhythmogenic right ventricular dysplasia.

Coronary cath was normal. Troponins trended down.

Here is another ECG from 3 days later:

Now there is abnormal T-wave inversion in III, aVF, and V2. So the patient only has minor criteria by ECG, and only on the followup ECG (see below).

Case Conclusion:

He had an EP study that induced VT at a rate of 252. Here is the induced VT:

VT at a rate of 252 bpm. Short QRS for VT (116 ms). Not a typical LBBB morphology, but induced VT in ARVD need not be of LBBB morphology.

A heart rate like this would stress the heart and lead to troponin release.

An implantable cardioverter defibrillator was placed.

ARVD, also known as arrhythmogenic RV cardiomyopathy, is estimated to have a prevalence of 1 in 5000 adults and is responsible for approximately 11% of sudden death in young adults and 22% in a study of athletes in northern Italy. The diagnosis is not easy (see below).

Gemayel C, Pelliccia A, Thompson PD. Arrhythmogenic right ventricular cardiomyopathy. J Am Coll Cardiol. 2001;38(7):1773. Full text: http://content.onlinejacc.org/cgi/reprint/38/7/1773.pdf

There is a 2010 publication by the Task Force in Diagnosis of ARVD: Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria.

Free full text: http://circ.ahajournals.org/content/121/13/1533.full.

There are 6 categories of criteria:

1) Imaging

2) Pathologic

3) ECG Repolarization

4) ECG Depolarization

5) Arrhythmias

6) Family History.

ECG and historical Highlights of this publication are (Suspect ARVD with):

1) High risk syncope with no other etiology; Family History

2) Depolarization abnormalities (Major criteria):

a) Epsilon Waves

b) Localized prolongation (greater than 110 ms) of the QRS complex in right precordial leads (V1-V3)

3) Repolarization abnormalities in patients of age at least 14 years (because younger patients often have juvenile T-waves)

a) Minor: Inverted T-waves in right precordial leads V1-V2

b) Major: Inverted T-waves in right precordial leads V1-V3 or beyond (major criteria)

4) Arrhythmias

a) Major criterion:

i) VT of LBBB morphology with superior axis (negative or indeterminate QRS in leads II, III, aVF and positive in lead aVL) (major criteria)

b) Minor criteria:

i) VT of LBBB morphology with inferior axis (positive QRS in leads II, III, aVF and negative in lead aVL) (minor criteria)

ii) More than 500 PVCs per hour

5) Finally, it is a progressive disease and patients without ECG abnormalities may develop them over time.

Here is an example of an epsilon wave (image C). And another example. Here are some great examples from the post on RV dysplasia (translated by Google translate!) on Pierre Taboulet's great French site: #1, #2, #3

Here's a great example on Wave Maven.

Here is an explanation od the importance of leads V1 and V2.

Here is another nice example. I've taken the liberty of blowing up part of the ECG at this link for better viewing. Look closely at V1-V2:

There are Epsilon waves (small waves at the end of the QRS) and also a slight prolongation of the QRS at the very end.

A Southeast Asian with Tachycardia and Hypotension after taking a dangerous herbal medication (Birectional Ventricular Tachycardia from Aconite Poisoning)

2011-08-04T16:06:00.008-05:00

I published this case in Annals of EM 6 years ago. I figure it's ok to put it here now after all these years, especially since one cannot even read an abstract of it. The reference is below, so as not to give away the diagnosis.

This 59 year old Hmong woman presented with palpitations, nausea, vomiting, weakness, and numbness. She had intended to take "Hmong Medicine number 9" but unwittingly took "Hmong medicine number 12." When she realized her mistake, she knew that she would die, and her family called 911. Her BP was 65/40. Lungs were clear and exam was otherwise unremarkable.

This was her initial 12-lead ECG:

The family showed EMS the herbal root from which the patient ate shavings:

What is the rhythm????

Answer: Bidirectional Ventricular Tachycardia. There are alternating ventricular beats; the frontal and transverse axes alternate because there is alternating right bundle and left bundle branch block morphologies. This is, of course, not because there is actually RBBB and LBBB, but because the origin of the ventricular beat alternates from right ventricle (LBBB) to left ventricle (RBBB).

We treated her with esmolol without any effect. No therapy helped her, but she did spontaneously convert to NSR 8 hours later. A Chinese PharmD and herbal specialist identified the root as aconitum Carmichaelii.

Bidirectional Tachycardia is rare, and usually associated with digitalis toxicity. It has been reported to be unresponsive to electrical cardioversion and lidocaine, but responsive to flecainide. Aconite (also known as monkshood, or wolfsbane) seems to trigger automaticity by direct activation of inward sodium channels during phase II of the cardiac action potential; thus, flecainide, which blocks these sodium channels appears to be effective in rats.

I had some great questions on this from Beth Bilden, toxicologist:

1. 1. In a patient with a wide comlex dysrhythmia accompanied by hypotension (both likely caused by the unidentified toxin), I would have been tempted to give sodium bicarb which probably would have made things worse. My answer: Although the QRS is wide, it is not wide because of delayed conduction; it is wide because of bundle branch blocks morphology which indicated a focus of dysrhythmia in the ventricle, not a delay in conduction. Therefore, bicarb would not be indicated and was not given. In fact, the best treatment for this (flecainide), when taken in overdose is reversed with sodium bicarb!

2. Esmolol was used for rate control, right? If so, was a calcium channel blocker considered rather than a beta blocker since a sodium channel blocking toxin/toxicant would decrease inotropy and a sodium channel blocking agent had not been excluded from the differential? My answer: Again, I don't think the ECG is consistent with a sodium channel blocking agent. I have to admit, I had no idea what the toxin was and thus what I should do, so I tried esmolol, knowing I could shut it off if it did not work. No one else knew what to do, so she was only observed overnight and (very luckily) survived. Obviously, if I saw a case of this now, I'd know the differential and have a much better idea how to treat it. As would all of you readers!

Here is another case of bidirectional tachycardia. And another.

Smith SW et al. Bidirectional Ventricular Tachycardia Resulting From Herbal Aconite Poisoning (Case Report). Annals of Emergency Medicine 2005; 45(1):100-101.

Left Bundle Branch Block and Left Anterior Descending Artery occlusion: Serial ECGs then T-wave inversion after reperfusion

2011-07-31T17:15:00.001-05:00

A 50 yo male presented with chest pain. This ECG was recorded at 0415.

There is sinus tachycardia. There is left bundle branch block (LBBB). All ST-T complexes are discordant. However, the ST-T in V1-V4 is excessively discordant: with 6 mm ST elevation, V3 meets criterion 3 of Sgarbossa's criteria (giving 2 points, not enough for a diagnosis of "MI"). By the Smith modification of Sgarbossa's criteria, the ratio of the ST elevation at the J-point (6 mm) to the S-wave (24 mm) is 0.25. Since this is greater than the cutoff of 0.20, it would be diagnostic not just of MI, but of LAD occlusion.

The occlusion was not appreciated by the treating physicians, and another ECG was recorded at 0457:

Now the R-wave in V3 is gone (QS-wave), the S-wave is "fragmented" (an indication of infarction analogous to Q-waves), and the ST elevation remains at 6mm, with an S-wave of only 12 mm, for a ratio of 0.50. The injury is worsening.

The notching in V3 is also known as "Cabrera's sign" (prominent notching of at least 40 msec in the ascending limb of the S-wave in any of leads V3-V5).

The patient was taken to the cath lab and a 100% LAD occlusion was opened.

Here is the ECG after reperfusion:

There is less tachycardia, as the stroke volume is now higher with improved myocardial function. The ST elevation has mostly resolved. There are now concordent T-waves diffusely, especially in the LAD territory.

Such T-wave inversion is a frequent sign of reperfusion even in LBBB, and when seen alone (without the preceding ECGs diagnostic of STEMI) is a common sign of NSTEMI. T-wave concordance can be normal, so it is not a very specific nor sensitive sign of ischemia. But it should raise your suspicion. In the context of this case and the preceding ECGs, it is diagnostic of reperfusion and is definitely the result of ACS.

Should we activate the cath lab if the STEMI is spontaneously reperfused?

2011-07-14T14:36:00.001-05:00

Will be on vacation until August. Last post until then!

I received a question yesterday: "If spontaneous reperfusion (or aspirin/nitro assisted reperfusion) occurs, why is it so important to rush for reperfusion therapy?" This is a very good question. To my knowledge, there is no randomized trial of immediate PCI vs. delayed PCI for transient STEMI. There is a study that randomized patients with NSTEMI to early vs. delayed PCI. It showed that patients at high risk, as measured by a GRACE score of 140 or greater (corresponding to an in-hospital mortality of 3%), had better outcomes if they underwent immediate angiogram and PCI.
[Mehta SR et al. NEJM May 21, 2009; 360(21):2165.]

I do let the following anecdote affect my practice:

This was a 52 year-old male I saw a few years back. He was playing cards with his friends when his left hand became numb. He had no CP or SOB, no arm or jaw or other pain. His friends thought he was having a stroke and called 911. The medics wisely recorded the following ECG prehospital.

He arrived in the ED still without any chest pain, and the medics showed me this ECG:

There is marked ST elevation in anterior precordial leads, and reciprocal ST depression in inferior leads. This is diagnostic of proximal LAD occlusion.

I activated the cath lab at 2129 in spite of the fact that the patient was asymptomatic.

We then recorded this ECG:

There is some ST depression in V2 and V3 and hyperacute T-waves.

Hyperacute T-waves can occur "on the way up" or "on the way down" as I like to say; this means they can be present shortly after occlusion before ST elevation, or shortly after reperfusion, after ST segments have resolved. I considered this to be diagnostic of reperfusion.

So I de-activated the cath lab at 2135.

Then the patient became hypotensive. We recorded this ECG:

Obvious anterior STEMI

I re-activated the cath lab at 2145. The total delay, then, was 16 minutes.

Shortly after the LAD angiogram, which showed 100% occlusion, the patient arrested and could not be resuscitated.

If I had let the cath lab be activated in spite of reperfusion, he would be alive.

This was a big mistake of mine.

Any STEMI is very high risk, even if reperfused. I don't believe you'll ever be criticized for activating the cath lab if you have just one ECG that is diagnostic of STEMI.

Wait until after the ECG to give Nitroglycerine

2011-07-10T09:15:00.002-05:00

Here is the ED ECG of a 58 yo male whose chest pain is resolved:

There is sinus rhythm with a PAC (which has aberrant conduction -- RBBB). There is nondiagostic ST depression in V3 and nondiagnostic ST-T abnormalities in precordial leads.

Without any ECG from earlier when the patient had chest pain, this is nondiagnostic. With a negative troponin, the patient would be admitted for observation.

Let's go back to the beginning:

A 58 yo male with a h/o CABG developed on and off chest pain which became constant while playing golf.

911 was called. Here is his initial prehospital ECG at 1129:

There is sinus rhythm and clear posterolateral STEMI, with ST elevation in I and aVL and reciprocal ST depression in III and aVF. There is ST depression in right precordial leads diagnostic of posterior STEMI.

The computer read ***Acute MI***. The cath lab was activated prehospital.

He received aspirin and Nitroglycerin, had relief of chest pain, and had this ECG recorded at 1136:

There is now minimal ST elevation in aVL with minimal reciprocal ST depression. Clearly the artery is reperfused.

Did NTG cause this reperfusion? That can't be known. But had this second ECG been the first one recorded, there would be no indication for immediate reperfusion.
He arrived in the ED and had this ECG recorded at 1153:

This is the ECG shown first, above, with the PAC with aberrant RBBB conduction and non-diagnostic ST-T findings.

Imagine if you did not have the prehospital ECGs. It would be tough to diagnose ACS, in spite of a very high risk situation.

He did develop chest pain again, and had this ECG recorded at 1206:

Sinus rhythm with 2 aberrantly conducted (RBBB) PACs. Now there is again ST elevation in aVL with reciprocal depression in lead III

The initial troponin was normal. He was taken for immediate angiography, where a 99% 2nd diagonal (2nd major lateral branch off the LAD) lesion was found and opened.

The next AM he had a completely normal echocardiogram with EF of 65%. Peak troponin was 0.85 ng/ml. Here is his ECG the next AM.

Notice the reperfusion T-waves in I and aVL.

Thus, the next day, the ECG was more sensitive than echo for MI. This is not unusual, but sometimes, due to a negative echo, cardiologists can be convinced (in spite of contrary evidence), that no MI occurred. I have heard expressions of high faith in the sensitivity of echo for ACS.

Learning points:
1. NTG may cause reperfusion
2. Record an ECG before NTG
3. Always look at prehospital ECGs
4. Even after STEMI (if reperfused, with small amount of myocardium infarcted), and even when the ECG is diagnostic of ACS (as it was the next day), the simultaneous echocardiogram may be normal.

Here is an interesting abstract regarding NTG after the EKG:

Mahoney BD, Hildebrandt DA, Allegra P. Normalization of Diagnostic For STEMI Prehospital ECG with Nitroglycerin Therapy. Prehospital Emergency Care 2008;15:105, Abstract 24.

Hypothesis. The decision to take a patient for emergent reperfusion therapy is largely determined by an ECG diagnostic for ST Elevation Myocardial Infarction (STEMI). Hildebrandt et al have proven that prehospital 12 Lead ECGs followed by an immediate call for reperfusion team mobilization reduce door to balloon times.We hypothesize that prehospital ECGs will normalize in some STEMI patients after nitroglycerin (NTG)therapy or due to spontaneous reperfusion. NTG therapy before an ECG, or the absence of a prehospital ECG capacity in some services may lead to missing the early diagnosis of STEMI thus delaying reperfusion therapy. Methods. A prospective analysis of consecutive adult patients presenting to an urban/suburban two paramedic ambulance service fromJuly 15, 2006, to August 15, 2007, who have diagnostic ECGs for STEMI. Paramedics managing a possible myocardial infarction patient were instructed to obtain rapidly an ECG prior to treatment with NTG. If the initial ECG was diagnostic for STEMI the paramedic called to mobilize the reperfusion team. A second ECG was done prior to arrival at the ED. The ECGs were later reviewed by emergency physicians and cardiologists who confirmed the presence of a diagnostic prehospital ECG and STEMI. Results. During the 13 month interval, 87 patients had an initial ECG that was diagnostic for STEMI. These patients received no NTG from the paramedics prior to obtaining the first ECG. An average of 16 minutes 42 seconds later, 3 patients had an ECG that was no longer diagnostic for STEMI and 3 had a partial normalization in their ECG that made diagnosis of STEMI more difficult. Conclusions. Prehospital ECGs diagnostic for STEMI can normalize or become nondiagnostic after NTG administration or due to spontaneous reperfusion or evolution. In the absence of a prehospital ECG, it is possible that 6 of 87 (7%) of STEMI patients in this study would have had reperfusion delayed due to a rapid change in their ECG. Limitations includenocontrol groupreceiving NTG prior to the first ECG.

Missed STEMI, spontaneously reperfused

2011-07-05T06:39:00.001-05:00

Click here for other very instructive cases of missed STEMI.

This is a 48 yo female with no risk factors for CAD had sudden onset of arm numbness radiating to bilateral arms, followed by substernal chest heaviness that radiated to both sides of chest. She had some associated SOB. In previous weeks she had been having SOB when climbing 2 flights of stairs. She called 911. Medics arrived and recorded the following ECG at 1756:

There is sinus rhythm and a wandering baseline. There is no ST elevation nor hyperacute T-waves, nor ST depression anywhere. The ST segments are upwardly concave. R-wave progression is normal. It is a normal ECG.

The medics gave her sublingual NTG with some decrease in symptoms. They gave her an aspirin.

She presented to the ED at 1832 is some distress; the nurse's note mentions "grunting, mottled."

This is the patient's first ED ECG, recorded at 1845:

There is now 1 mm of ST elevation in V2 and minimal STE in V3. The ST segments are straight. There is poor R-wave progression. The T-waves are larger. This description makes it sound like MI, but really, at a glance, it is not terribly remarkable on its own -- until you compare it with the previous.

The physicians caring for the patient were unaware of the prehospital ECG, and did not go look for it. The patient remained in some discomfort, but no serial ECGs were obtained. The first troponin was negative. At 2016 the patient had no more grunting respirations.

With the ECG read as normal, a negative troponin, and a low risk patient, the providers did not have a high suspicion for ACS, so admitted her to observation with no further antiplatelet or antithrombotic therapy. By the time of admission to observation, she had no more chest pain. No more ECGs had been done.

Troponins

First trop at 1932 "normal" (negative)
2335: 34.8 (this returned at 0100, prompting the following ECG at 0111, 6.5 hours after the last one)

There are now Wellens' T-waves in V1-V5 and poor R-wave progression.

What happened?

One needs to view the prehospital ECG and the ED ECG side by side:

ED ECG is on the right. Notice the T-waves are taller and fatter, the ST segments straight, and the R-waves have less voltage. This is almost certainly a developing anterior STEMI.

Had this side by side comparison been done, the index of suspicion would have been much higher. Perhaps a second, or third, ED ECG would have been recorded. It almost certainly would have revealed more ST elevation and had indication for immediate reperfusion.

That her pain eventually spontaneously subsided indicates probable spontaneous reperfusion.

Subsequent troponins
0250: 41.7
0455: 35.6

An echocardiogram the next day showed an EF 55% and a regional wall motion abnormality in the distal septum, anterior and apex.

An angiogram later that day showed the culprit lesion at a 60% LAD stenosis (the patient did indeed have spontaneous reperfusion, but not before losing a significant amount of myocardium).

Learning points
1. This is labelled a NonSTEMI, and shows one of the many ways in which a damaging coronary occlusion is called a NonSTEMI rather than a STEMI: the fewer ECGs you record, the less chance your STEMI is called a STEMI.
2. Always do serial ECGs in patients with ongoing unexplained substernal chest pain.
3. Always compare the ED ECG with the prehospital ECG
4. Beware of straight ST segments, and any ST elevation that is not accompanied by well-formed R-waves. Early repolarization always has well formed R-waves. This is the main reason why my early repol vs. MI equation works (although, in the study, I excluded any patients with straight ST segments).

Would you activate the cath lab prehospital?

2011-06-28T15:52:00.002-05:00

A 54 yo with history of hypertension awoke in the AM with substernal chest pain. It did not abate, so at 0930, he called 911.

Medics arrived and recorded this ECG:

There is sinus tachycardia at 105 bpm. Leads II, III, and aVF have very minimal r-waves and rather large T-waves, with straightening of the ST segments. Leads V4-V6 have greater than 1 mm of ST elevation at the J-point (abnormal), as well as large T-waves. V1-V3 are unremarkable except for low voltage in V1 and V2. There is upward concavity in all leads. There is only very subtle reciprocal ST depression in aVL, with T-wave inversion. This helps to make the diagnosis of inferior MI.

This is highly suggestive of acute inferolateral STEMI, though not classic. By any millimeter criteria, one would have to call it STEMI. I would call it STEMI but it is not obvious. [Also, tachycardia should always alert you to impending cardiogenic shock, or to possibly another diagnosis such as pulmonary embolism; however, this has none of the other classic findings of PE.]

Our prehospital protocol is:
--If a patient has chest pain and the computer algorithm reads ***Acute MI***, then they are to activate the cath lab from the field.
--If only one of these is present, they are not to do so.

The computer algorithm made no comment on any of it.

Fortunately, our medics sometimes go outside the rules. That is what they did here: activate the cath lab.

The patient arrived in the ED at 1022 and had this ECG recorded at 1028:

Now there is new ST elevation in V2 and V3, with Q-waves forming. Diagnostic of anterior STEMI. Inferior leads now have much more ST elevation. Again, all leads have upward concavity and there is only very subtle reciprocal ST depression in aVL.

The patient was taken to the cath lab at 1039. As he was being transferred to the cath table he had a v fib arrest. He was defibrillated. Angiogram showed a type III (wraparound) LAD, occluded distally (but also with an 80% diagonal stenosis), such that he was having an infero-antero-apical STEMI. The thrombosis was opened, thrombus suctioned, and the lesion stented, with a door to balloon time of 45 minutes (thanks to prehospital activation by the medics).

Medics are getting very good at reading the ECG; maybe it is time to let them overrule the computer? --This requires a formal study.

Anyone want to study this?

General methods:

Take one or more EMS service(s) in which medics are well trained in reading the 12-lead. Search for all patients who had a prehospital ECG. Find the cath outcome, or troponin outcome if no MI. Find the computer read on the ECG. Have 2-4 medics read the ECG blinded to the computer and the outcome. Compare.

Chest pain, SOB, and tachycardia. What is the rhythm? Is it MI?

2011-06-24T17:53:00.001-05:00

This was sent to me by a reader from India (Thank you, Rama Krishna!). The patient presented recently (age unknown). He had a history of DM, HTN, COPD, and previous anterior wall MI.

Here is his presenting ECG:

The answer, as analyzed by the rhythm master, K. Wang, is below:

It is ventricular tachycardia with 1:1 retrograde conduction to the atria and also with electrical alternans. The small drawn circles, which appear to be p-waves, are not actually the p-waves. Rather, the small negative deflection following these circles (narrow black arrows along the lead II rhythm strip at the bottom), are retrograde p-waves. They are negative because of the retrograde conduction. The alternate QRS has a negative p-wave that is buried in the negative T-wave (green arrow). These p-waves are upright in aVR (see the blue arrows, and red arrow for the alternate QRS) Also, the retrograde p-wave can be seen in V1 (purple arrow).

As for repolarization, there is ST elevation in V2-V4 (thick black arrow) diagnostic of MI. It looks like it is old MI, not acute (see discussions of LV aneurysm on other posts). Of course, these discussions apply to normal conduction, not normally to ventricular tachycardia. But in this case it is fair to say that the ST segments are a result of MI [almost certainly old MI (which also fits the patient's history), possibly acute] rather than being due to the abnormal QRS.

Without reciprocal ST depression or hyperacute T's, inferolateral MI and myo- or pericarditis are impossible to distinguish

2011-06-23T07:05:00.002-05:00

A 63 y.o. female with a past medical history of lupus and MS presents with chest pain and SOB she has never had before, starting approximately 1615. The pain gradually diminished since onset. It was described as pressure, with SOB, and no radiation. There is some reproducibility with palpation, but the pain is not positional or pleuritic. She has no h/o CAD, HTN, or DM. There is no pericardial friction rub. NTG by EMS improved pain. The pain resolved after 1 hour in ED. Here is her initial ECG at 1954 (3.5 hours after onset of CP):

There is sinus rhythm with minimal inferior ST elevation (and no reciprocal depression in aVL). There is moderate ST elevation in V3-V6, not quite 1 mm. V3 and V4 have almost 1 mm of STE. STE is greater in II than III. There are no hyperacute T-waves. There is no ST depression anywhere. (For comparison, her previous ECG had no ST elevation anywhere.)

Inferior MI virtually always has reciprocal ST depression of some amount, or at least T-wave inversion, in aVL.

See this case and this case for patients who were erroneously thought to have pericarditis, whose ECGs had subtle reciprocal ST depression in aVL.

When there is inferior and lateral STEMI or inferior and anteroapical STEMI, the reciprocal ST depression can be attenuated or completely abolished by the lateral ST elevation. Thus, the ECG can look identical to myo- or pericarditis.

The reading by the cardiologist was: "diffuse ST elevation, consider pericarditis." Subsequent ECGs are of little interest, only showing some resolution of ST elevation, but no T-wave inversions or other diagnostic findings.

Clinically, the patient has pain more typical of ischemia. Her initial troponin I was 8.56 ng/ml! Therefore, whatever the process is, it must have been going on longer than 3.5 hours. Subsequently, every 4 hours, the levels were 9.96, 8.96, 8.40, 7.48, 6.62, so there is some rise and fall, though not dramatic. A steady state is typical of myocarditis, whereas a rise and fall is more typical of MI.

The differential diagnosis, then, is myocarditis vs. inferolateral STEMI (most likely).

Echocardiogram showed wall motion abnormalities of the distal anterior wall, apex, and septum as well as the inferior wall. This could be seen in either MI or myocarditis, but greatly favors MI, as myocarditis infrequently has focal myocardial dysfunction.

Her angiogram showed a Type III LAD ("wraparound LAD, that supplies the inferior wall). It had moderate diffuse disease in the distal segment of the vessel. There was no definite culprit or thrombus, so no definite explanation of the findings.

Therefore, an MRI was done with gadolinium, to assess for myocarditis.

MRI report
1) Mild to moderately reduced LV function with large apical wall motion
abnormality. Calculated ejection fraction is 45%.
2) Small, discrete focus of transmural enhancement, consistent with
myocardial scarring, in the mid inferior wall of the left ventricle. This
pattern of enhancement is unlikely to be from myocarditis, and is more
suggestive of a small infarct.

Thus, the diagnosis is myocardial infarction of the distal wraparound LAD, with STE in II, aVF, V3-V6.

As I've had more and more experience, I've noticed that most of what is thought to be myo- or pericarditis on the ECG turns out to be MI. As we have better and better tools to make the ultimate diagnosis, we find that cases that should have been diagnosed as MI were diagnosed with pericarditis. That was not the case here, but it did happen here.

Prehospital ST Elevation and pain resolve with NTG. ECG and Echo normal in ED.

2011-06-21T14:46:00.003-05:00

The resolution of symptoms and the ECG in this case is similar to the last post, but the ST and T-wave morphology of the ECGs are quite different, and the outcome is remarkable.

65 yo male with h/o HTN, DM, and hyperlipidemia had onset of intermittent chest pressure and SOB at 2 AM. He has never had anything like this and has no h/o CAD. The pain is substernal and radiates to the left arm. It is not reproducible, pleuritic, or positional. It became much worse at approximately 1230 and he called 911. Medics recorded this ECG with pain 10/10:

The computer calls this normal. The medics were worried about the ST elevation. The ST elevation could be MI or early repol, though one should be skeptical of early repol in patients of more advanced age as it becomes much less common. Additionally, there is straightening of the ST segments. The early repol vs. MI "score," based on STE 60 ms after the J-point of 3.0 mm, QTc of 425 ms, and R-wave V4 of 17 mm, is 23.773 (greater then 23.4 is the best cutoff for MI).

He was given sublingual NTG, and his pain improved to 7/10 at 1303, to 3/10 at 1309, and to 1/10 at 1313 after a second NTG.

At each of these times, he had another ECG recorded by the medics, and the resulting decrease in ST elevation and T-wave amplitude is demonstrated here, with all of them side by side, including the 5th ECG recorded in the ED. (I have also posted the entire 1st ED ECG, recorded at 1334, below this figure).

Here is the full 12-lead from the ED at 1334:

T-waves and ST elevation are subtly but significantly less pronounced. ER vs. MI score is now 20.324 (STE V360 = 1.5 mm, QTc = 408, R-wave amplitude = 17)

A formal echo was done at 1349 which was entirely normal. There was no anterior wall motion abnormality. It was read by one of the most experienced echocardiographers anywhere. Then his first troponin I returned at 0.18 ng/ml (0.10 is positive).

He was treated for NSTEMI. Subsequent troponins every 4 hours were: 0.41, 0.90, 1.14, 1.18, 1.01, then 0.98. Next day had angiography, which showed a 90% LAD stensosis (culprit) as well as severe 3-vessel disease.

He went for CABG on day 5, and this ECG was recorded after the operation:

There is new anterior infarction that has happened some time within the last few days.

A troponin was measured at over 80 ng/ml, indicating that the infarct had occurred some time between admission and operation, probably before the operation.

1. Transient ST elevation is hazardous
2. Pay attention to ECG changes
3. After the ECG has normalized, the echo may normalize as well.

The last post: why is it not pericarditis? (hint: previous ECG has LV aneurysm morphology)

2011-06-19T08:53:00.000-05:00

Yesterday, I posted this interesting transient STEMI.

I was asked why it is not pericarditis. I have edited the post (see red text) to add the following:

Added to description of presenting ECG:
The old ECG has a Q-wave with persistent ST elevation in lead III, and some reciprocal ST depression (typical for aneurysm morphology). The new ECG has relative reciprocal ST depression in lead III, with ST elevation in aVL. This rules out pericarditis, which essentially never has reciprocal ST depression.

Added to description of old ECG:
Notice the ST elevation in lead III that follows a deep Q-wave. This is "Persistent ST elevation after previous MI" or "LV aneurysm morphology". LV aneurysm is very different for inferior vs. anterior MI.

And have added the following to the conclusions:

4. This is not pericarditis because:

a. Pain was typical for MI (substernal, not postional or sharp, resolved with NTG)

b. There is relative reciprocal ST depression in lead III.

Pericarditis does not have reciprocal depression.

c. ST elevation of pericarditis is maximal in leads II and V5, V6.

Here the ST elevation is maximal in V2-V4.

d. Pericarditis does not have hyperacute T-waves.

e. Tight proximal LAD stenosis explains STE in precordial leads and I and aVL.

Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 ng/ml)

2011-06-18T11:13:00.001-05:00

This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up.

3 hours prior to calling 911 he developed typical chest pain.

The medics recorded this prehospital ECG at 1535:

There is ST elevation and tall T-waves in precordial leads, with reasonably good R-wave progression. He is a 45 year old male, so this could be male pattern benign early repolarization (BER, or ER). But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6.

How can one decide whether this is ER or MI? First, if an old ECG is available, then compare. Only rarely does early repolarization change from date to date, though it is possible.

Second, I have developed a score that helps to differentiate the two. His BER score, based on ST elevation at 60 ms after the J-point in lead V3, QTc (400), and R-wave amplitude in V4 is 23.9 (> 23.4 is likely anterior STEMI).

(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc) - (0.326 x RA in V4 in mm)

Third, one can do an immediate cardiac ultrasound.

Medics gave him nitroglycerine sublingual and his pain resolved. He arrived in the ED and had this ECG recorded at 1544

It is essentially the same as the previous, and the score is again about 24 (MI more likely than early repol). Also, compare with the patient's previous ECG below; concentrate on reciprocal leads III and aVL. The old ECG has a Q-wave with persistent ST elevation in lead III, and some reciprocal ST depression (typical for aneurysm morphology). The new ECG has relative reciprocal ST depression in lead III, with ST elevation in aVL. This rules out pericarditis, which essentially never has reciprocal ST depression.

Here is a blow-up of V1-V3:

A previous ECG was found:

This has no ST elevation, and T-waves are not tall. Notice the ST elevation in lead III that follows a deep Q-wave. This is "Persistent ST elevation after previous MI" or "LV aneurysm morphology". LV aneurysm is very different for inferior vs. anterior MI.

Here is V1-V3 of the old ECG:

The patient remained pain free, and this ECG was recorded at 1606:

Here is V1-V3:

He remained pain free. A bedside ultrasound was done by an emergency physician and simultaneously read by a cardiologist. They could see no anterior wall motion abnormality. Diagnosis of ACS was in doubt.

His old angiogram was reviewed and it was known that his disease was not amenable to PCI. He needed CABG. He was therefore treated with eptifibatide, heparin, and aspirin, and referred for CABG, but not immediately.

The next AM, this ECG was recorded:

There is some residual ST segment elevation. The T-waves are far less tall.

Here is V1-V3:

8 days later. All ST elevation resolved.

Here are V1-V3 8 days later:

There is finally no ST elevaton whatsoever

It is often difficult to see changes unless they are directly side-by-side. Here are V1-V3 from start to finish. I did not include the prehospital because it is identical to the first ED ECG:

Self explanatory, no?

All troponins were undetectable (< 0.04 ng/ml).

The patient had a critical LAD stenosis. Flow had spontaneously been restored, perhaps aided by nitroglycerin. He underwent CABG.

Conclusions:
1. Anterior STEMI can look very much like early repolarization. There are means to distinguish the two.
2. Transient ST elevation is very hazardous. Even when the serial troponins are negative, the ECG is critical to the diagnosis of ACS.
3. When flow is restored, wall motion may completely recover so that echocardiogram does not detect the previous ischemia.

4. This is not pericarditis because:

a. Pain was typical for MI (substernal, not postional or sharp, resolved with NTG)

b. There is relative reciprocal ST depression in lead III.

Pericarditis does not have reciprocal depression.

c. ST elevation of pericarditis is maximal in leads II and V5, V6.

Here the ST elevation is maximal in V2-V4.

d. Pericarditis does not have hyperacute T-waves.

e. Tight proximal LAD stenosis explains STE in precordial leads and I and aVL.

The development of an inferior-posterior STEMI, from prehospital to hospital

2011-06-15T07:52:00.002-05:00

For other cases of inferior hyperacute T-wave click here and here.
For more on lead aVL, click here and here. Also use labels on the right sidebar.

Case
A 65 yo woman called 911 for pain in her upper back (between the shoulder blades) and in the left shoulder and left biceps, and some "mild chest pressure" elicited by the medics. Exam was normal. All but the back pain resolved with nitroglycerine

Medics recorded 6 prehospital ECGs. Below are 3 of them:

1430

There are hyperacute T-waves in II, III, and aVF. Note T-wave inversion in aVL, which is the earliest finding in acute inferior STEMI, as well as in V2, suggesting posterior wall involvement

1432

No significant change

1445

Now there is clear ST elevation in inferior leads. T-wave inversions in aVL and V2 have evolved to ST depression.

They arrived in the ED at 1503. BP was 116/70. CXR and cardiac and aortic ultrasound were done to look for any evidence of aortic dissection. All were normal except for a possible inferior wall motion abnormality.

In the ED, the following ECGs were recorded.

1512

ST segments have almost normalized. Hyperacute Ts are less prominent, as is T inversion. There is probably some spontaneous reperfusion of the infarct-related artery. The computer noticed only some "minimal" ST depression.

1532

Inferior ST elevation is more obvious, with 1 mm in II and III, but T-waves have normalized. ST depression in V2 is clearly abnormal. Computer did not read MI.

1542

Now the most obvious findings are ST depression in aVL and V2

Cardiology was consulted. Again, a cardiology fellow opined that this was not a STEMI, and went to talk with the interventionalist.

A posterior ECG was recorded:

Only aVL was of great concern. There is no posterior ST elevation.

The interventionalist was very concerned and activated the cath lab. The patient was taken to the cath lab. The proximal RCA was 100% occluded. It was stented. Door to balloon time was 62 minutes. Peak troponin I was 5.15 ng/ml.

Post PCI ECG

T-waves and ST segments are back to normal

Chest pain and LBBB. LBBB resolves and there is V1-V3 T-wave inversion.

2011-06-11T11:23:00.001-05:00

A 59 year old man with no cardiac history was at work when he developed very typical substernal chest pressure. He went to a clinic across the street and had this ECG recorded:

There is sinus tach with LBBB with appropriate discordance and no excessive discordance.

To learn about appropriate and excessive discordance, please see this post:
http://hqmeded-ecg.blogspot.com/2011/05/lbbb-is-there-stemi.html

911 was called, the medics arrived, and recorded this ECG:

Again, there is sinus tach and no concordant ST elevation, all ST segments are appropriately discordant. The S-waves are not very deep, but that is because they are cut off. If projected, they are indeed very deep.

The patient arrived in the ED and had this ECG:

No difference. Sinus tach with appropriate ST segments.

The following ECG was recorded later:

Now the heart rate is 72 and LBBB is gone. There is, however, T-wave inversion in leads V1-V3, suggestive of Wellens' syndrome.

Is this an anterior STEMI with LBBB? Did the occlusion reperfuse, resolving the LBBB and leaving the patient with reperfusion T-waves (Wellens' syndrome)?

He was taken to the cath lab. All coronaries were completely normal. All troponins were undetectable.

Explanation:
The patient had a worrisome history: 59 yo with significant substernal chest pressure, so his pretest probability of MI (and even of STEMI) is reasonably high. However, he had a left bundle brach block with normal appropriate discordance on 3 EKGs. Only 5-13% of patients with chest pain and LBBB have MI; many fewer have coronary occlusion. Additionally, appropriate discordance is common in NonSTEMI, but very unusual in coronary occlusion (STEMI).

Moreover, and importantly, there was sinus tach. Whenever you see tachycardia with bundle branch block, you should suspect that it is rate related BBB. Indeed, once the heart rate came down, the BBB resolved.

After resolution, there was T-wave inversion in V1-V3, highly suggestive of ischemia. There are features of the T-wave inversion, however, which argue against ischemia. First, as I have pointed out in posts on pulmonary embolism (see links), T-wave inversion of anterior infarction (Wellens' syndrome) almost always has an upright T-wave in lead III. Also, anterior ischemia is unlikely to spare lead V4 as in this case.
http://hqmeded-ecg.blogspot.com/2011/03/chest-pain-sob-anterior-t-wave.html
http://hqmeded-ecg.blogspot.com/2010/03/anterior-t-wave-inversion-due-to.html

Cardiac Memory
There is another more likely explanation of this T-wave inversion: "Cardiac Memory." Cardiac Memory (CM) has been described for a couple decades. It is most common after termination of pacing and other etiologies of abnormal depolarization such as Left Bundle Branch Block. After resolution of the abnormal depolarization, there may be transiently inverted T-waves that last for hours to days (these T-waves are the heart's "memory" of the previous abnormal conduction). This phenomenon is poorly understood, but involves "transient electrical remodeling."
http://www.heartrhythmjournal.com/article/S1547-5271%2807%2900801-6/abstract

Shvilkin et al. described the way to differentiate CM from ischemia:
http://circ.ahajournals.org/cgi/content/full/111/8/969
In short, the combination of:
(1) positive T_aVL (as in this case) and
(2) positive or isoelectric T-wave in lead I (as in this case) and
(3)maximal precordial T-wave inversion greater than the T-wave inversion in lead III (as here: maximal precordial T inversion is in lead V2, at 4.5 mm, and T-wave inversion in lead III is only 2.5 mm) was

92% sensitive and 100%specific for CM, discriminating it from ischemic precordialT-Wave Inversion.

Thus, the very well informed physician could differentiate these ECGs from those of an LBBB patient with MI:
1) no concordance
2) no excessive discordance
3) LBBB with tachycardia, probably rate related
4) subsequent T wave inversion that, according to Shvilkin et al., is diagnostic of cardiac memory. It is NOT Wellens' syndrome.