New RBBB and subtle NSTEMI

This 49 year old male presented with chest pain.

Initial ECG: sinus with QRS of 128 ms and RBBB, though not obvious.  There is T-wave inversion in lead III and a very large T-wave in aVL (very large only compared to the small size of the QRS, and it is proportional ST elevation and T-wave size that is important, not absolute size!)  One would predict high lateral MI from this ECG.

ECG from one year ago (baseline), with QRS of 105 ms.  This confirms that the RBBB and the ST-T findings in III and aVL are new.

His chest pain resolved, then recurred, and the following ECG was recorded 70 minutes after presentation:

ECG at t=70 minutes, showing dynamic T-waves (new T-wave inversion in II and deepening T inversion in III and aVF, and increasing ST depression in III, as well as increasing hyperacute T in aVL

His chest pain resolved again, he was started on heparin, and was admitted pain free.  Initial troponin I's were 0.25 and 0.46 ng/ml.

At midnight the patient was still pain free and another ECG was recorded:

ECG at t = 8 hours, minimally changed

At cath the next day, the culprit was a 99% proximal RCA with good flow.  There was a posterolateral (RPL-1) branch off of this RCA with a 90% stenosis.

I have changed the outcome of this case because there is uncertainty as to whether, angiographically, there was ischemia to the inferior (RCA) or the lateral wall (RPL-1). My assessment from the ECG is that it was high lateral, with reciprocal inferior ST findings.  But the angiographer thinks that it was the inferior wall that was most ischemic. 

New LBBB and Massive ST elevation: Do not automatically jump to activate the cath lab!

This 50 year old male presented with some atypical chest pain and a blood pressure of 220/150.

There is Left Bundle Branch Block with up to 6 mm of discordant ST elevation in V2 and V3.  Limb leads have neither concordance nor discordance, and that is because  the QRS is neutral: neither definitely positive nor negative.  There  are some biphasic T-waves in II and aVF, suggesting ischemia.  The discordant ST elevation in precordial leads, though large, is proportional to a very high voltage S-wave (50 mm, or 5 mV).  The ratio of the ST elevation as measured at the J-point = 6 divided by 50 = 0.12.  The mean in my studies of LBBB without occlusion (either no MI or NSTEMI) was 0.10 +/- 0.1 (95% CI), so this is very close to a normal ratio.

Here is the previous ECG:

This is a previous ECG from months ago, showing that the presentation ECG is indeed New LBBB.  Here there is profound LVH with secondary ST/T abnormalities.

This did not alarm me.  In ED patients with symptoms of ischemia and New LBBB, only about 2-4% have acute coronary occlusion (need for immediate reperfusion therapy).  Many more have MI as diagnosed by biomarkers.   This is typical evolution of severe LVH to LBBB in a patient with severe HTN.  There may well be MI as diagnosed by biomarkers, but it is not due to acute coronary occlusion, rather most likely to demand ischemia from severe hypertension (afterload, "type II" MI).

Troponin I had a rise and fall, but never went above the 99% reference value for the VITROS assay (in ng/ml): 0.017, 0.018, 0.029, 0.020.  So this also represents a case that had some tiny amount of myocardial necrosis but is by current definition not an MI. 

Syncope, Chest pain: subtle, dynamic ST elevation and hyperacute Ts with preceding ST depression

This 63 yo male with no cardiac history had 30 seconds of syncope.  When he awoke, he complained of progressively worsening substernal chest pain associated with nausea and diaphoresis.  He had 2 prehospital ECGs and 4 hospital ECGs before he was taken to cath.  Here is the succession:

Prehospital ECG with sinus bradycardia.   There is ST elevation and tall T-waves that looks like early repolarization. The ST segment and T-wave in lead III should raise suspicions for LAD ischemia.

First ED ECG 0349.  There is an apparent junctional rhythm.  The ST elevation is gone.  The T-wave in lead V2 is no longer tall.  Lead III still looks suspicious.  LAD high grade ACS is certain with these changes.  This was not appreciated.  A pulmonary embolism workup was done.

Second ED ECG 0432.  There is new ST depression in leads I, III, and V3-V6.  V3, with a large T-wave and ST depression, is "A New Sign of LAD occlusion" de Winter et al. N Engl J Med 2008;359(19):2071.  Still the cath lab was not activated.

See this post for more of these T-waves: http://hqmeded-ecg.blogspot.com/2009/02/hyperacute-t-waves.html

3rd ECG 0439.  Hyperacute Ts and ST depression mostly resolved.  The patient was admitted to cardiology.

4th ECG 0605.  Recurrence in V3 of hyperacute T with ST depression

At this point, the patient was taken for cath. He was found to have 100% LAD occlusion just after the D1 takeoff, but also had a severe 90% RCA co-culprit ruptured plaque.The LAD was getting some flow through right to left collaterals, which explains the subtlety of the ECG.  Maximum troponin I was 36 ng/ml.

After cath and PCI.  The R-waves are gone.  There are only QS-waves in V2 and V3.  There is some persistent ST elevation.  There is T-wave inversion in aVL.

Next day ECG: T-waves are beginning to invert in V2 and V3

Although the peak troponin is not extremely high, the ECG would suggest that much of the anterior wall infarcted in spite of minimal ST elevation.  In the de Winter's study, they report that the ST depression followed by a large T-wave was persistent and did not develop into ST elevation.  Whether this is true with all such patients is in doubt, as it requires ECGs to be done frequently.

Nevertheless, de Winter's T-waves should trigger the cath lab.

And so should the Transient ST elevation seen on the prehospital ECG.

Chest pain, resolved: don't forget to look at the previous and the prehospital ECG

This is a 58 year old woman with a history of inferior MI.  She has had a week of intermittent substernal chest heaviness associated with SOB.  Because it came again and lasted for one hour, she called 911.  The medics recorded a 12-lead, then gave her  aspirin and nitro, and her pain resolved completely.  It seems the physicians caring for her did not see this ECG, so I am not showing it first.  On arrival in the ED around midnight, she was pain free and had this ECG recorded:

First ED ECG.  Sinus rhythm with a couple of PACs.  Heart rate is close to 100, so one must entertain hemodynamic etiologies of chest pain, such as pulmonary embolism.  There are Q-waves with  minimal ST elevation in inferior leads and reciprocal ST depression in aVL, not significantly changed from baseline (ECG below).  There is also minimal ST elevation in V1 and V2 with the beginnings of T-wave inversion suggestive of anterior NSTEMI ("Wellens' syndrome").

 The first ECG is substantially different from the previous ECG 3 years prior:

Previous ECG from 3 years prior shows old inferior MI and baseline precordial ST elevation of early repolarization.  There is upward concavity and normally upright T-waves.

Prehospital ECG during chest pain, before nitro and aspirin.

  There is ST elevation and a large upright T-wave in V1, different from the baseline T-wave.  The LAD may well have been occluded during this recording. 

ECG 2.5 hours after presentation, no therapy other than aspirin:

 The terminal T-wave invesions are still present and perhaps more noticeable.  

At this point, the troponin returned at 0.14 ng/ml (limit of detection: 0.012; 99% reference value: 0.034, so this is a "positive").  

Here is a third ED ECG at 6 hours:

The terminal T-wave inversions in V2-V4 are more obvious.  This is typical of Wellens' pattern A.

The K was also 2.9 mEq/L, but this does not account for the ECG findings.  The patient had a negative PE workup and was admitted to the hospital.  She had a rise and fall of troponin, with a peak at 0.358 ng/ml.  She went for an angiogram the next AM; it showed mid-LAD culprit lesion with 95% stenosis and was stented.

This is after LAD stenting:

After stenting, there was another rise and fall of troponin. Now the Pattern A Wellens' waves are very well developed.

T-wave inversion in LAD ACS:

Wellens' syndrome is chest pain that is relieved with terminal T-wave inversion on the initial, pain-free, ECG.  There is preservation of R-waves, and there is evolution to deeper T-wave inversion (Wellens' Pattern B).  It is due to brief LAD occlusion with reperfusion.  This last evolution (Pattern B) did not occur in this case.

See here for a series of classic Wellens' evolution over 26 hours.

Here is a case in which the Wellens' waves appear and disappear. They do not evolve. And this is because there is no actual infarction (no troponin elevation).

Two cases of the same electrolyte disturbance(s). Diagnosis?

This patient presented after dialysis with weakness and reproducible chest pain.

Sinus rhythm with a normal QRS.  The QT is prolonged and this is due to a long ST segment.  There are prominent U-waves, best seen in II, V2, and V3.

This patient presented in shock with GI bleeding, cirrhosis, and a lactate of 33.

There is widespread scooped ST depression, a very long QT, a long ST segment, and prominent U-waves which are easily mistaken for T-waves (as if the T-wave were biphasic down then up).  The terminal portion of what appears to be a down up T-wave is really a U-wave, best seen in V4 and aVF.

These are both cases of simultaneous hypokalemia (U-waves and ST depression) and hypocalcemia.  In the first case, the K was 3.1 and Ca was 3.8 ionized.  In the second case, the K was 2.9 and Ca 6.3 nonionized.  Hypokalemia gives a prolonged QT, scooped ST depression, prominent U-waves, and often a generally wavy appearance to the ECG.  Hypocalcemia gives a long ST segment resulting in a long QT.

In the second case, troponin I was negative.  ST depression was not due to NSTEMI.  ST depression with a normal QRS ("primary") is due to ischemia, hypokalemia, digoxin, and an abnormal baseline (unknown etiology).  Of course there is also "secondary" ST depression, secondary to an abnormal QRS such as LVH, BBB, Brugada, WPW, etc.

Weakness, prolonged PR interval, wide complex, ventricular tachycardia

This 58 year old patient with a PMH of CAD  only (MI, 2 stents) presented awake with weakness and non-palpable pulses and no obtainable blood pressure.  By ED ultrasound, he had good cardiac contractility.  He was volume depleted [by ED ultrasound of Inferior Vena Cava].  He had spider angiomas and abdominal free fluid [by FAST exam].  He was ashen, with shallow breathing, no pallor.  I intubated him.  His prehospital ECG showed "left bundle branch block" (computer reading) with prolonged PR interval.  It was identical to the following initial ECG.  Based on this prehospital ECG, I gave 3 amps of calcium gluconate (as well as several liters of IV fluids for the volume depletion).

There is sinus rhythm with prolonged PR inteval.  There is a wide QRS with a wide R-wave in lateral leads and a negative complex in V1-V3, consistent with LBBB.  But the QRS duration is 180 ms, which is very long and suggests hyperkalemia.  In addition, there is peaking of the T-waves that is not characteristic of LBBB.

The K returned at 7.4 and Cr at greater than 20.  About this time, he started having incessant ventricular tachycardia over 30 minutes, during which time I gave him a total of 15 amps of Ca gluconate, 5 amps of bicarb, 2 amps of D50, 10 U of insulin, 0.25 mg of terbutaline. Sometimes the V tach would spontaneously resolve; 4x it required synchronized cardioversion.  He had 1 minute of asystole requiring chest compressions.  During VT, his pulses were still not palpable, and ED cardiac ultrasound showed asynchronous beating, so it was difficult to assure adequate cardiac output.  ED ultrasound of the carotid artery confirmed good cerebral blood flow.

A dialysis catheter was placed, and I did a radial arterial line cutdown because of a tiny radial artery. The patient stabilized, went to dialysis, and when his K was 4.7, this was his ECG:

The QRS is now 108 ms.  There is ST depression with biphasic (down-up) T-waves in II, III, aVF and slight ST elevation with T-wave (up-down) inversion in aVL.  This is suggestive of high lateral NSTEMI, but probably all due to demand ischemia.

His peak troponin I was 3.2 ng/ml, consistent with demand ischemia (Type II MI). 


1) Wide complex should always make you think of hyperKalemia.
2) The treatment for VT in hyperK is calcium.  No antiarrhythmic will work.
3) No amount of calcium is too much if the patient is unstable.

Anterior hyperacute T-waves: look at this upside down mirror image

One reader who trained in France learned that a good way to see the ST elevation better is to look at a mirror image of the ECG (upside down).  I have done this in order to see that the ST depression in V2 of posterior STEMI is ST elevation when viewed upside down (as it would be recorded from a posterior aspect).  I have never seen it done to highlight inferior reciprocal ST depression and to highlight anterior hyperacute T-waves.

This is a case I posted last week: http://hqmeded-ecg.blogspot.com/2011/01/hyperacute-t-waves-missed-by-computer.html

Hyperacute T-waves in V2-V4, see full description at previous blog post

 

Upside Down Mirror Image.  Notice now that what was reciprocal ST depression in II, III, aVF is now ST elevation.  Also notice that the hyperacute T-waves, when pointing down, look to have ST depression.

Excellent case of RBBB with STEMI on EMS 12-lead blog, here's the link

http://ems12lead.com/2011/02/09/an-unusual-case-of-right-bundle-branch-block-discussion/

Inferior hyperacute T-waves. The clue is T-wave inversion in aVL. Serial ECGs evolve to ST Elevation.

This is a 66 year old male with severe substernal chest pain.  He was intermittently bradycardic down to the 30's with a blood pressure in the 80's systolic.

This is the first ECG:

There is sinus rhythm with first degree AV Block.  The QRS is slightly long (113 ms) but there is no bundle branch block.  The T-waves in inferior leads have high voltage proportional to the QRS, very suspicious for inferior MI.  aVL has T-wave inversion, which raises suspicion even higher

4 minutes later, a Right Sided ECG:

RIGHT SIDE ECG, t = 4 minutes -- (the limb leads are standard, only the precordial leads are shifted to the right side) -- there is still sinus rhythm with 1st deg AVB.  The T-waves in the limb leads have less voltage than in the previous ECG, suggesting evolution (artery opening!), which supports the diagnosis of ACS.  The R side leads do not have any significant ST elevation.

T = 18 minutes:

t = 18 minutes.   There is sinus bradycardia with a very prolonged PR interval and some nodal escape beats.  Sinus beats that happen AFTER the nodal beat can be seen in the upstroke of the T-wave in the 2nd, 4th, 5th, 7th, and 9th complexes at the bottom in lead II.  MORE IMPORTANTLY, there is now clear ST elevation in inferior leads (artery now closing!), with reciprocal ST depression in aVL and also in V2-V4, diagnostic of simultaneous posterior STEMI. Inferoposterior STEMI.

The patient was taken for immediate angiography and PCI of a 95% thrombotic occlusion of the RCA.

Here is another case in which aVL was critical to the diagnosis of inferior STEMI:
http://hqmeded-ecg.blogspot.com/2010/07/inferolateral-st-elevation-might-be.html