Saturday, April 30, 2011

Apparent ST depression in lead III. Is it MI?

A few days ago, I posted this ECG with "inferior" ST depression that was reciprocal to high lateral MI due to a 2nd diagonal occlusion.
Here is the post, with a previous baseline ECG:
Here is a repost of the ECG:
there is minimal but real ST depression at the J-point, in III and aVF.  Lead aVF has J-wave notching, typical of early repolarization, and should have, if anything, a bit of ST elevation (the ST segment on the baseline ECG was actually isoelectric).  The ST depression in III and aVF is reciprocal to real ST elevation of the J-point in lead aVL (and I).

The next day I saw this ECG:
One might say this has the same findings, but if you look closely, the J-point in lead III is isoelectric, as is lead aVF.

I immediately saw this as a normal ECG, but realized that some would see the downsloping in lead III and think that there is ST depression, same as the former ECG.  They are different and the difference is sublte but real.

The second is normal and I sent the patient home with noncardiac chest pain.

Thursday, April 28, 2011

Coved ST elevation with reciprocal ST depression: what is the diagnosis?

This 82 year old presents with atypical chest pain:

There is slow atrial fibrillation and a slightly wide QRS (109 ms), with high voltage in precordial leads (LVH).  There is ST elevation in II, III, and aVF, with reciprocal ST depression in I and aVL. 

There is one very important feature of the ECG I have not mentioned.  What is it?  What is the diagnosis?  See below.

The QT interval is extremely short (QTc = 323 ms).  That, along with the strange scooping of the ST depression and domed shape of the ST elevation, as well as the atrial fibrillation, should alert to possible Dig effect rather than STEMI.  Indeed, she turned out to be on Digoxin.

Diagnosis: Dig effect. There was no STEMI.  STEMI would have a longer QTc.

Tuesday, April 26, 2011

"Inferior" ST depression: What is the diagnosis?

This 58 year old man presented at noon with chest pain that began the previous evening and became constant less than one hour prior. 
Now there is still sinus rhythm but with 2 complexes that are PACs with aberrancy [not PVCs (thanks to VinceD for correcting me on that!)].  There is subtle ST depression in "inferior" leads II and aVF. This should always alert to ST elevation in the opposite, high lateral, leads especially aVL.  Looking at aVL, there is indeed subtle ST elevation and also in lead I.

Here is the previous ECG for comparison:
This baseline ECG is normal

Subendocardial ischemia may have ST segment depression, but it does not reliably localized to any wall.  "Inferior" ST depression is really reciprocal to high lateral ST elevation.

The chest pain resolved with nitroglycerine, the cath lab was activated, and a 99% LAD D2 (large second diagonal off the LAD) was found and stented.

Subsequently, there was no wall motion abnormality and the maximum troponin I was 1.0 ng/ml.

Here is a followup ECG 42 hours later:
ST segments have normalized.  There are now "reperfusion" T-waves (inverted) in I and aVL, verifying a high lateral MI

1) ST depression in III and aVF should be assumed to be reciprocal to high lateral ST elevation
2) This ST depression may be the most visually arresting part of the ECG

Sunday, April 24, 2011

ST segment depression: what is the etiology?

This 86 year old woman had syncope.  There is no chest pain or SOB.  She is uncertain of her past medical history.

There is atrial fibrillation and profound ST depression.  What else do you see? What else do you want to know?

Answer below:

Here is the same ECG with some arrows:

The QTc is 387 ms, very short for ischemia.  There are also prominent U-waves (arrows).

Any patient in atrial fibrillation might be on Digoxin.  Etiologies of ST depression with a normal QRS ("primary" ST depression, in contrast to "secondary" ST depression that is due to abnormal QRS such as in LVH, LBBB, RBBB, WPW, hyperkalemia, Brugada, RVH, or paced rhythm) include hypokalemia, digoxin, and ischemia, as well as baseline ST depression of unknown etiology.

Digoxin results in ST depression with a short QT and often with prominent U-waves such as in this case.  Hypokalemia results in a long QT with prominent U-waves.

Ischemia results in ST depression with a relatively long QT, and is likely to be accompanied by ischemic symptoms.  Syncope is not an ischemic symptom; it is a relatively rare sole manifestation of ischemia.

It is important to keep in mind that ST depression due to digoxin happens at therapeutic concentrations, and is not a sign of Dig toxicity.

Saturday, April 23, 2011

Why is this patient weak?

35 year old presents with diffuse weakness.

Answer is below:

There are very large U-waves best seen in precordial leads V2-V5.  U-waves that are this prominent are almost always the result of profound hypokalemia.  The patient had a potassium of 2.2 mEq/L, and has hypokalemic periodic paralysis.

For other cases of hypokalemia, go here:

Wednesday, April 20, 2011

Dyspnea, resp failure, DNR/DNI, what to do?

79 yo patient with no known previous history of MI and a history of severe dementia presented with acute dyspnea, pulmonary edema, BP 110/70 and tachycardic, requiring noninvasive ventilatory support.  CXR confirmed pulmonary edema.  Bedside echo showed severe anterior wall motion abnormality and very poor EF.  Here is the ECG:

Obvious Acute Anterior STEMI.  There are wide and deep Q-waves, with some R-wave preservation (QR-waves).  Is this previous MI with persistent ST elevation (LV aneurysm morphology)?  No!  The presence of an R-wave makes this very unlikely.  More important, the T/QRS ratio is very high.  We have shown that a high T/QRS ratio is very unlikely in LV aneurysm.  Only acute MI has such a ratio.  However, subacute MI (duration > 6 hours commonly has a low T/QRS ratio).  It is also possible that this is an acute STEMI superimposed on old MI.

A previous ECG was found from 3 years prior:

No evidence of anterior MI

After exhaustive inquiry, it was determined definitively that this patient would not want to be intubated under any circumstances.  He could not undergo PCI without intubation and paralysis.  We considered fibrinolytic therapy, heparin, GP IIbIIIa inhibitors, but decided to give aspirin alone.

Interestingly, the next AM he was much better, he was no longer SOB, his troponin peaked at only 2.7 ng/ml.  A formal echo showed severe anterior wall motion abnormality with dyskinesis and EF of 15%.  Dyskinesis usually implies LV aneurysm and is unusual in acute STEMI, so it is quite possible that he had a previous undiagnosed anterior MI since 2008, and that he now has a superimposed STEMI.  

He never had a subsequent ECG, but I can only surmise that he had spontaneous reperfusion (this occurs in up to 25% of STEMI).  If he indeed underwent reperfusion, and does not re-occlude, his ejection fraction will mostly recover.

When we are certain that our therapy saved the patient, cases like this should give us a bit of humility!

Saturday, April 16, 2011

Cath lab activated. What do you think? (#2)

This 45 year old male called 911 for increasing SOB and CP over 2 weeks.  His BP was 220/150.  The medics did a prehospital ECG, shown here.  They tried to activate the cath lab, but the message did not get through.

There are several worrisome findings: Upright T-wave in V1, large T-wave with ST elevation in V1-V4.  The medics activated the cath lab based on this.

What the medics did not see is that the S-waves are cut off.  You can see that they are very wide where they are cut off, and if you project them down they will be very deep S-waves.  On arrival, we cancelled the cath lab activation and started a high dose nitroglycerin drip, up to 200 mcg/min. 

We recorded this ED ECG:

This is similar to the above, but does not cut off the S-waves, which you can now see are very deep.
The patient had pulmonary edema due to severe hypertension, and he ruled out for myocardial infarction. 

One must read the ECG in this order: rate, rhythm, axis, interval, QRS (voltage, morphology), ST, T, U.  If you do that here, you will see that the QRS voltage is extremely high. When you see ST elevation, the first thing you must do is determine if it is secondary to an abnormal QRS.  In this case, it is secondary to high voltage, or LVH. 

His SOB resolved with high dose NTG, his maximal troponin I was 0.115 ng/ml (demand ischemia, type II MI).

Cath lab activated. What do you think?

This is a 47 year old African American man with substernal and right sided chest pain, worse with inspiration. EMS was called. Prehospital EKG showed ST elevation V2 and V3 with (reportedly, tracing unavailable) some ST depression in leads II and III. The pain improved with nitro. He has a h/o smoking and hypertension.   Here is his ED ECG:

There is sinus tachycardia.  There is ST elevation in V1-V4, but there is also very high S-wave voltage in these leads.  There is a high voltage R-wave in V5.  There are no reciprocal changes.
I was shown this ECG without the clinical info and it was clear to me that this is not STEMI because the large T-waves and ST elevation are proportional to the high voltage.  Additionally, tachycardia is not common in STEMI without cardiogenic shock.  AND tachycardia can exaggerate ST elevation and T-wave amplitude.

Further history: There was also a productive cough. CXR showed right sided infiltrate. In spite of all this, the cath lab was activated.  Coronaries were clean. 

Tachycardia was due to dehydration.  Chest pain due to pneumonia.  ST elevation due to LVH.

LVH is one of the most common pseudoinfarction patterns.  High S-wave voltage is followed by discordant ST segments; that is, by ST elevation in precordial leads, sometimes striking.

However, LAD occlusion in these cases is very uncommon.  In fact, I have only seen 2 cases of LAD occlusion in the presence of clear V1-V6 LVH.  I believe, but cannot prove, that this is not because these individuals do not get LAD occlusion, but because when they do, it attenuates the voltage and erases the LVH.  I am in the process of studying this.

For other cases of LVH mimicking STEMI, go here:

Thursday, April 14, 2011

Marked ST depression refractory to maximal medical therapy

This 62 year old man, heavy smoker, with no previous medical history, presented after 2.5 hours of substernal chest pressure.   He stated he had been having chest pressure with exertion for one month.

His prehospital ECG (I cannot find them) showed marked ST depression in V2-V6, with 1 mm ST elevation in aVR.  He received 3 sublingual NTG in the ambulance with improvement of pain, but no resolution.  He received a 325 mg aspirin.

On arrival, BP was 130/70.   A nitro drip, heparin bolus and drip, and eptifibatide bolus and drip were started.

This is his second 12-lead ECG.  I will shortly post his initial ECG which I have had a hard time locating.  Here there is less ST depression than in the prehospital ECGs and less STE in aVR.  But there is ongoing ischemia.

Sinus rhythm with slightly wide QRS, ST depression in V2-V6 (less than prehospital ECGs) and 1 mm ST elevation in aVR.
You can read more about STE in aVR.

If there is at least 1 mm of STE in aVR, 3-vessel disease or left main disease is likely, and CABG is the likely outcome.   Therefore, do not give clopidogrel which results in unacceptably high CABG bleeding risk for 5 days.

After titrating IV nitroglycerin to 180 mcg/min, the chest pain was gone and the BP was 100/60. However, there remained ST depression:
Sinus rhythm with slightly wide QRS, ST depression in V2-V6 (less than prehospital ECGs) and now minimal ST elevation in aVR.

Chest pain is not a sensitive indicator of ischemia; the ECG established ongoing ischemia in spite of resolution of chest pain.

Thus, the patient had ACS with ischemia refractory to maximal medical therapy.  It is important to note that aVR does not count as an ST elevation indication for thrombolytic therapy.  But refractory ischemia is an indication for emergent angiography with possible PCI.  I called the interventionalist and he agreed, however the patient refused to go.

He was admitted to the ICU.  His troponin peaked at 7.0.  He continued to have ST depression the next AM, at which time he agreed to cath, which showed 100% RCA (probably chronic), 99% LAD, and 95% Circumflex disease.  A balloon pump was placed, with subsequent resolution of ST depression.  He went for 3 vessel CABG, and immediately after coming off pump, his ejection fraction was greatly improved, the balloon pump was removed, and he is doing well.

Here is the postoperative ECG:

Monday, April 4, 2011

ST elevation in aVR, with widespread ST depression

This case and ECG was already posted here:

However, because of a new article, I want to post it again.

The patient presented with chest pain and had this ECG which is a very high risk situation.  There was a severe ostial LAD thrombosis that was very close to the left main.  He went for emergent bypass that evening and had a good outcome.

ST elevation in aVR is often thought to represent left main occlusion. However, it really just signifies widespread and diffuse subendocardial ischemia which could be due to left main or 3-vessel disease, or severe proximal LAD disease. Left Main occlusion generally causes rapid death; most who survive left main ACS have some flow and thus often have widespread ST depression.

There is an important recent article relevant to this:  

Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol;107(4):495-500.

They show that if there is not at least 1 mm STE in aVR, then ACS is highly unlikely to be due to severe 3-Vessel disease or Left Main.  Why is this important?  Because if such severe CAD is present, the patient is likely to need CABG.  If they need CABG, then the surgeon will usually be unhappy if the patient received clopidogrel.  

So, here is a potential strategy: if there is no STE in aVR, then you can safely give clopidogrel to this NSTEMI patient.  If there is at least 1 mm STE in aVR, then a GP IIbIIIa inhibitor should be given instead.

Saturday, April 2, 2011

Is it pulmonary embolism?

This is a 41 year old male with severe asthma who barely avoided intubation.  His troponin I returned at 0.130 ng/mL, and here is his ECG:

There is sinus tach with anterior T-wave inversion of the same morphology as the previous cases of PE which I have posted (see link below).  There is no TW inversion in lead III, so this is not pathognomonic.  Whether or not there is T-wave inversion, this ECG could be due to PE or any cause of right heart strain.

Here are some cases of pulmonary embolism.

This is to illustrate that these T-wave inversions are due to acute right heart strain, which is caused by many etiologies other than PE, including but not limited to acute severe asthma and acute pneumonia.  Hypoxia causes pulmonary vasoconstriction (pulmonary hypoxic vasoconstriction) which puts strain on the right heart.

Pulmonary embolism was ruled out.

Answer: pulmonary embolism. Now another, with ultrasound....

This 18 year old presented with syncope and tachycardia.

Similar to the last case (the "quiz"), there is sinus tachycardia with precordial T-wave inversion with TW inversion in lead III also.  The morphology of these T inversions is highly suggestive, but unlike the previous case, not diagnostic.  There is also, arguably, S1Q3T3 depending on whether one considers the S-wave to be "prominent."  There is no right axis deviation, but there is a S-wave.  (Does anyone know of a definition of "prominent" S-wave in S1Q3T3?)

Immediately, a bedside echo was done.  Here is the video:

This shows a huge and poorly functional RV.

Here is a still picture from the video:

The RV is on the left, the LV on the right (thick-walled).  The RV is very enlarged and looks like a "D".  Accordingly, this is called the "D" sign.

  This is diagnostic for pulmonary embolism, which was subsequently proven. Thrombolytic therapy might have been given, but at least partly because of head trauma from syncope, it was not.

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