Acute Dyspnea in a Dialysis Patient. K is 6.3 mEq/L. Are ECG findings due to hyperkalemia, or even due to Type 2 MI?

I was reading ECGs on the system and saw all of these, from one patient.  I read them without clinical context and looked at the clinical context later.

A 70-something dialysis patient presented and coronary disease had missed dialysis and then presented with acute onset of shortness of breath.  He denied chest pain.

There was mild hypoxia prehospital, lowest saturation 90%, 

On arrival, BP was 140/84, pulse 122, O2sat 100% and the patient had increased work of breathing. 

Bedside POCUS showed very poor LV function and a few pulmonary B lines.

He was put on BiPAP.  A Chest X-ray did not show pulmonary edema.

This ECG was recorded:

It is difficult to appreciate P-waves, but I believe this is sinus tachycardia.

Here is my interpretation:

As you can see, the QRS duration is quite long at 200 ms, and I think this is a pretty accurate measurement.  

In order to measure, one needs to find the end of the QRS, which I have done here:

The onset of the QRS is obvious.  And here the lines show the offset.  So indeed the QRS is approximately 200 ms.

Comment:

What is the normal QRS duration in LBBB?

In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, a QRS duration less than 170 ms (n = 262), vs. greater than 170 ms (n = 38), was associated with a significantly better ejection fraction (36% vs. 24%).  Only 13% had a QRS duration greater than 170 ms, and only 1% had a duration greater than 190 ms.

So a QRS of 200 ms in LBBB is indeed likely to be abnormal and due to hyperkalemia.

Here is a similar case involving right bundle branch block.

Case Continued:

A previous ECG was available: 

There is a normal QRS duration here, so there was no previous LBBB

The very wide QRS is very similar to LBBB.  Because it is so much wider than standard LBBB, there is additional concern for hyperkalemia.  It is possible that the entire reason for the wide QRS is hyperK, but not likely.  The morphology is not at all typical of HyperK, especially the inferior T-waves.  

I sent that first ECG to the PM Cardio Queen of Hearts AI Model:

The Queen thinks this is OMI

The providers thought that this ECG manifested hyperkalemia.  They treated for hyperK.

The K returned at 6.3 mEq/L.

Time 18 minutes after therapy for hyperK

The ECG is not significantly different.  

The Queen thinks this repeat is still OMI

Time 33 min:

No significant change, in spite of treatment for hyperK

Still OMI

Time 56 minutes.  Now the potassium is down to 5.0 mEq/L.

Now there is even more proportionally excessive discordant ST Elevation in inferior leads, with excessive reciprocal STD in aVL/

This is an unequivocally diagnostic ECG of inferior OMI in the setting of LBBB

She still says OMI

Unfortunately, nothing was done about this.

Time 7 hours lead reversal

There is limb lead reversal (QRS in I and aVL are now inverted), but nevertheless one can see that the ischemia appears to have resolved.  

Next day, with K = 4.6 mEq/L

The QRS is still very wide.  The evidence of OMI is gone. 

Old echo:

The estimated left ventricular ejection fraction is 30-35%.

There is akinesis of distal anteroseptum and entire apex.

New echo:

EF of 30-35%.

Regional wall motion abnormality--mid to apical anterior, mid

Anteroseptal, apical septal, and apical inferior akinesis.

So there is a new inferior severe wall motion abnormality.

The troponin peaked at 16,000 ng/L

Angiogram

Showed "No culprit".  This was attributed to a "Type 2 MI", which is acute MI that is not due to ruptured plaque, but rather due to "supply demand oxygen mismatch".

However: Supply demand mismatch must have a clinical correlate: 

Increased demand: extremely high blood pressure or pulse, or myocardial wall stress

Decreased oxygen delivery due to: hypoxia, hypotension, severe anemia, hemoglobin transport pathology (CO, met Hgb, etc)

This is far more likely to be MINOCA (Myocardial Infarction with Non-Obstructive Coronary Artery).  

Most MINOCA is due to ruptured plaque with thrombus that lyses and does not leave behind a visible culprit.  It must be diagnosed with IVUS or Optical Coherence Tomography.

See these posts:

Dynamic OMI ECG. Negative trops and negative angiogram does not rule out coronary ischemia or ACS.

"The dye don't lie" ...except when it does. Angiogram Negative, or is it?

This was most likely acute thrombosis of a coronary artery resulting in OMI:

The ECG changes were attributed to hyperkalemia.  But none of them were typical of hyperkalemia and they did not get better with treatment for hyperkalemia.

He had acute onset of shortness of breath.  Not gradual, as one would expect from fluid overload in a dialysis patient.  It is correct that he did not have chest pain, but we must remember that fully 1/3 of full blown STEMI do not present with chest pain.  

The EKG shows inferior OMI.  There is a positive Smith Modified Sgarbossa criteria which is a Cath Lab indication by the American College of cardiology.  

By 8 hours, the EKG is all resolved. 

The echo showed inferior apical akinesis, which was NOT noted on the previous echo. 

They made a final diagnosis of type II myocardial infarction.  However, he was never hypoxic, his heart rate never went above 120, he was not hypertensive or hypotensive.  

The highest troponin measured was 16,000.  This is extremely elevated for a type 2 MI and totally consistent with STEMI.  Moreover, a tiny fraction of type II MI have ST Elevation equivalent on the EKG.  To have a new wall motion abnormality with akinesis is unusual.

The clinical presentation is most consistent with an anginal equivalent of dyspnea due to acute coronary syndrome/occlusion.  The EKG is diagnostic of OMI.

It is a judgment call retrospectively, but to assume there is no ACS at presentation is very risky, especially in a patient with previously diagnosed severe CAD and poor LV function.

Finally, the patient was lucky that his artery opened spontaneously and the EKG normalized, but it may have been hours before that happened, and a troponin of 16,000 indicates a lot of myocardial loss.

===================================

MY Comment, by KEN GRAUER, MD (1/21/2025):

===================================

I found today’s case by Dr. Smith to be fascinating. I focus my comments on the initial ECG — as it contains many subtle-but-important ECG findings.

• To review historical features of today’s case — The patient is a 70-something man with known coronary disease, who missed his last dialysis treatment — and who now presents with acute dyspnea, but no chest pain. 

The Rhythm in Today's Initial ECG:

The 1st challenge in today’s initial ECG — is to verify the rhythm. In Figure-1 — I’ve labeled ECG #1, which confirms Dr. Smith’s suspicion of sinus tachycardia as the rhythm.

• PEARL #1: When it is difficult on an ECG to determine the presence and nature of atrial activity — LOOK for a “break” in the rhythm! In Figure-1 — there is a short “break” in the rhythm between beats #7 and #8. Because the R-R interval is slightly longer during this short "break" than it is for the preceding 7 beats — we are able to clearly see a sinus P wave (RED arrow in front of beat #8).
• Support that this is a “real” P wave (and not just artifact) — is forthcoming from the fact that we see a similar P wave deflection in a 2nd “break” in the rhythm, that occurs between beats #18 and #19. The fact that the PR interval before beat #19 is the same as the PR interval before beat #8 supports the fact that the 2nd RED arrow in Figure-1 highlights another sinus P wave.
• Further support that these 2 RED arrows highlight sinus P waves — is forthcoming from the PINK arrow that highlights a 3rd sinus P wave. The reason we are able to see this partially hidden PINK P wave — is that the R-R interval before beat #9 is also longer than the R-R interval preceding the 15 other beats in this tracing.
• 
  
• PEARL #2: The KEY for then determining if there are even more P waves in this tracing — is to define what a “normal” T wave looks like (ie, a T wave not deformed by superposition of another P wave) — and then to compare the appearance of this "normal" T wave (labeled "T" for the T waves of beats #7 and #18) — with the T wave of all other beats in this tracing.
• Note that all other T waves in ECG #1 are clearly taller and more peaked than the 2 “normal” T waves (ie, YELLOW arrows over the 15 beats in which sinus P waves are superimposed on T waves of each preceding beat).
• 
  
• PEARL #3: One of my favorite "tip-offs" to the presence of sinus P waves that are partially hidden in the preceding T wave (which may occur when the heart rate is fast) — is to look in lead V1 for a small, negative "dip" right after the T wave that falls before the next QRS complex. The 2 vertical RED lines that line up with the 2 sinus P waves that are superimposed on the T waves of beats #13 and #14 (highlighted by YELLOW arrows) — show that the small negative "dip" in lead V1 occurs simultaneously with the sinus P waves before beats #14 and #15 in the long lead II rhythm strip.

BOTTOM Line: The rhythm in today's initial ECG — is sinus tachycardia, with some variation in rate.

Figure-1: I’ve labeled the initial ECG in today's case — proving that the rhythm is sinus tachycardia.

How Wide is the QRS in Figure-1?

At 1st glance — I had trouble determining How WIDE is the QRS in today's initial ECG. I believe my difficulty was because: i) The QRS in the limb leads is both tiny and fragmented, as well as distorted by marked artifact in these limb leads; and, ii) S waves in leads V1-thru-V5 are extremely steep — such that I had trouble distinguishing what might be a narrow QRS with "shark fin" ST depression vs true QRS widening.

• KEY Point: Determining IF the QRS is wide or narrow is essential for accurate assessment of potential ischemic ST-T wave changes. The technique for clarifying QRS duration and the end point of the QRS complex, is similar to that used when assessing for "Shark Fin" ST-T wave deviations (For review of this concept — Check out My Comment in the May 3, 2024 post in Dr. Smith's ECG Blog).
• LOOK for a lead in which you can clearly define the onset and offset of the QRS complex. In Figure-1 — I chose lead I, because there is virtually no artifact in this lead. The dark BLUE vertical line marks the end of the QRS complex — and shows us where the QRS ends for each beat in the long lead II rhythm strip.
• I then drew light BLUE vertical lines upward from this QRS endpoint in the long lead II rhythm strip for the QRS of beat #11 and beat #17. Doing so confirms that the QRS is indeed wide — and doing so tells us precisely where the ST segment begins in each of the chest leads.

What Kind of Conduction Defect is Present in Figure-1?

Knowing that the mechanism of the rhythm in Figure-1 is sinus with a markedly widened QRS complex (of at least 0.18 second) — the type of conduction defect most closely resembles LBBB (Left Bundle Branch Block), albeit with some atypical features.

• LBBB is suggested by the predominantly positive QRS complex in left-sided leads (ie, in leads I, aVL, V6) — and predominantly negative QRS complexes in leads V1-thru-V5, especially given the steep S wave downslope.
• The atypical features for LBBB are the marked fragmentation in the limb leads — and the pseudo-Q-wave that we see in the fragmented QRS in lead V6. These features are most likely the result of significant underlying coronary disease.
• NOTE: As per Dr. Smith — Apart from QRS widening, the ECG appearance of today's initial ECG is not typical for hyperkalemia, as T wave peaking is limited to the first 4 chest leads, and the base of these T waves is not nearly as narrow as it typically is with hyperkalemia.

===================================

Did Today's Patient have a STEMI?

As per Dr. Smith — the Troponin peak of 16,000 is much more suggestive of a STEMI than of a Type II MI.

• As per Dr. Smith — the absence of CP (Chest Pain) does not rule out a STEMI. As I emphasize in My Comment from the December 6, 2022 post — the Framingham studies long ago taught us that up to ~30% of all MIs may occur without a complaint of chest pain! Instead — many of these patient have some other non-CP "equivalent" symptom.
• The most common non-CP "equivalent" symptom — is new shortness of breath, which is precisely what today's patient had.

For clarity in Figure-2 — I've labeled today's initial ECG with those finding that "caught my eye" as being clearly abnormal in association with LBBB.

• My "eye" was immediately drawn to the ST-T waves in the 3 inferior leads (within the RED rectangles). Keeping in mind that the dark BLUE vertical line marks the end of the QRS complex — I thought the ST-T waves to be hyperacute in leads II, III, and aVF (RED arrows showing subtle-but-significant J-point ST elevation considering tiny size of the QRS — and clearly abnormal ST segment straightening).
• Support that these inferior lead changes are real — is forthcoming from the abnormally straightened and depressed ST segment in lead aVL (within the light BLUE rectangle).
• Similar abnormal ST segment straightening with slight depression is seen in lateral chest lead V6.
• 
  
• MY Impression: In view of today's clinical presentation — the marked difference in today's initial ECG compared to the previous ECG (shown above in Dr. Smith's discussion) — and the lack of any change in the hyperacute inferior lead ST-T wave appearance 18 minutes later after treating any potential hyper-K+ — I was in favor of a diagnosis of acute OMI until proven otherwise.

Figure-2: I've labeled the limb lead findings suggesting acute OMI.