A young man with back spasms

Written by Pendell Meyers

First see this ECG without clinical context:

What do you see? Do you agree with the computer's read of "nonspecific ST abnormality?"

The ECG is diagnostic of hypokalemia. There is diffuse minimal STD, with prolonged QT interval and characteristic "up-down" T-wave morphology in the precordial leads which is being caused by U-waves. V2 has an especially pronounced U-wave, but there is also a slightly wandering baseline. This morphology is very unlikely to be due to ischemia, and to an experienced electrocardiographer is nearly pathognomonic of hypokalemia +/- other concomitant factors such as hypomagnesemia, medication-induced long QT, etc.




Now here is the clinical scenario:

A young male in his 20s presented with back pain which he described as "back spasms" and weakness worsening all week and which became severe yesterday after lifting some boxes. Only upon review of his chart, I became aware that he had a history of CKD and eating disorder resulting in extreme electrolyte disturbances.

So I ordered this ECG:

We diagnosed hypokalemia based on the ECG and history. The computer read the QT and QTc intervals as 449ms and 488ms, respectively.

Do you agree?

No!

Here is the QT interval measured out:

It is actually almost impossible to measure the QT interval because of the U-wave.
So let's measure the QU interval.
QT interval = 560 ms. Using Bazett's formula, with HR=71 bpm, then QTc = 609 ms. Using Fridericia's formula, 592 ms.

We gave him magnesium 2 gm IV before labs returned. We waited to give potassium as he had history of CKD and appeared to be clinically dehydrated, had not urinated at all the day of presentation, raising concern for acute kidney injury which may limit the rate we can replete potassium. Despite that concern, this ECG is diagnostic of hypokalemia.

Labs showed:

Na                 133 mmol/L
K                   2.6 mmol/L
Cl                  61 mmol/L
Bicarbonate  60 mmol/L
BUN             75 mg/dL
Creatinine     7.75 mg/dL (baseline 2.5)
Anion Gap   18 mmol/L
Calcium       10.6 mg/dL
Phos             3.0 mg/dL
Mg               2.3 mg/dL

ABG (hours later during admission) showed:
pH               7.49
pCO2          66 mm Hg
HCO3         49 mEq/L
BE              25.5 mEq/L

This shows a chronic metabolic alkalosis with respiratory compensation. These disorders are clearly not acute because the bicarb has had time to elevate and the pH is close to normal despite significant abnormalities.

In the setting of metabolic alkalosis, the expected compensatory CO2 can be calculated as follows:

0.9(HCO3) + 16 +/- 2 = expected CO2

0.9(49) + 16 +/- 2 = 60.1 +/- 2

Therefore the CO2 is nearly in the expected range based on the primary metabolic disturbance.

The primary mechanism in this case appears to be chronic vomiting resulting in large losses of HCl. While you could choose to think about this process as loss of H+ (therefore net gain of HCO3-), others argue that H+ and HCO3- are simply the dependent variables of acid-base processes, with the actual independent variables being strong ions, CO2, and weak acids. In this view, it would be the loss of Cl and free water that best explains the severe metabolic alkalosis. Hypochloremia causes metabolic alkalosis.

Loss of Cl and free water (with SID=0) in this case results in a Strong Ion Difference (SID) = Na - Cl = 133 - 61 = 72. In this case, the SID is much much greater than the normal SID of 38 (resulting from normal values of Na = 140 and Cl = 102). An elevated SID is an independent variable causing alkalosis because there is a relative excess of positive strong ions compared to the normal milieu (relatively more Na+ than Cl-). As biologic physical processes are beholden to the principle of maintaining electrical neutrality, the body fills the relative void of negative ions with the single negative ion to which it has unlimited supply (dependent variable): HCO3-. This is how a high SID causes metabolic alkalosis in the teaching of the Stewart acid-based model.

See Dr. Smith's Acid Base Lecture and EMCrit's Acid-Base Series for more acid-base practice.




These results were similar to prior admissions. We decided to use normal saline as our rehydration fluid based on these results. Mirtazapine was also identified as a medication which could contribute to his long QTc.

He did not have any documented arrhythmias. Troponin was ordered by the inpatient team, negative x 3.

After several days of potassium repletion and supportive care, here is his ECG:

Normalized

Learning Points:

Don't trust the computer to measure QTc.

Hypokalemia (+/- hypomagnesemia) can be reliably diagnosed based on morphologic features on the ECG.

This ECG, recorded in triage, was shown to me immediately, with no other info.....

This ECG, recorded in triage, was shown to me immediately, with no other info.....

What do you think?
Computer read is: "Moderate ST depression"

I said:
"Inferior OMI (Occlusion Myocardial Infarction - see the Manifesto).  Activate the cath lab."
Dr. Laura Schrag also saw this immediately and that is why she showed it to me.

Then I asked: "Chest pain?  Is it a good story?"

Answer: The patient was a 60-ish woman with 3 risk factors who had had stuttering chest pain for a week, now constant.

What makes this diagnostic of OMI when there is less than 0.5 mm of ST Elevation?
--ST elevation is large relative to QRS size (the QRS above is very small)
--"Bulky" T-waves
--Absence of upward concavity of ST segments (which is what makes the T-wave bulky)
--Reciprocal ST depression in aVL
--Down-up T-wave in V2 (indicative of posterior MI)

A note on specificity of these findings:

I post here a lot of subtle OMI ECGs that people show me or send me.  I do not show enough subtly NEGATIVE cases.  The vast majority of cases that are texted to me or showed to me in real time, that physicians are worried about, I tell them: "This is not worrisome.  Do NOT activate the cath lab."  I always add: "The ECG can be normal in the setting of OMI, so I cannot say that there is no OMI; I can only say that it does not show on the ECG. If you are worried, then get serial ECGs, echo, etc."

But in this case, it definitely shows, and the findings are VERY specific.  In this case, the interventionalist (a great guy and friend of mine) wrote in his note "Nonspecific ST changes."  Many or most physicians would call these "Nonspecific ST-T abnormalities."  But these are most definitely NOT "Non-diagnostic" findings.  These are not "Non-specific." 

She was taken to the cath lab and had a 95% hazy RCA lesion that was stented.

Here is the post PCI ECG:

All STE is gone.  T-waves have normalized, or inverted in lead III.

Here are a bunch of ECGs with inferior ST Elevation that is NORMAL (normal variant STE):

I repeat:
You can see from the below ECGs that normal ST elevation may be very elevated, whereas the case above has hardly any ST elevation.   It is features OTHER THAN ST ELEVATION which mark the above as acute MI, and the below as NOT acute MI.
Here are the features of OMI vs. normal STE:
--ST elevation is large relative to QRS size (the QRS above is very small)
--"Bulky" T-waves
--Absence of upward concavity of ST segments (which is what makes the T-wave bulky)
--Reciprocal ST depression in aVL
--Down-up T-wave in V2 (indicative of posterior MI)

Widespread ST Elevation. Activate the Cath Lab?

Cases 2 and 3.

Inferior ST Elevation: what is the Diagnosis?

Case 2

Case 3.

This was a false positive cath lab activation.
It is clearly not an OMI.

Cases 4. and 5., at the bottom of this post:

Chest Pain in a Male in his 20's; Inferior ST elevation: Inferior lead "early repol" diagnosed. Is it?

Case 4. 

Case 5.

Case 6. 

Increasing ST elevation. STEMI vs. dynamic early repolarization vs. pericarditis.

Case 7.

Even with STE in V5 & V6, inferior STE without reciprocal STD in aVL is unlikely to be STEMI

Case 8.  At the bottom of this post.

Even with STE in V5 & V6, inferior STE without reciprocal STD in aVL is unlikely to be STEMI

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Comment by KEN GRAUER, MD (10/14/2018):

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Important blog post by Dr. Smith — which provides instant support of his October 9, 2018 post, in which we highlighted the importance of the Triage ECG interpreted by a capable clinician skilled in ECG interpretation (despite several published papers to the contrary).

• I focus my comments here on some additional fine points confirming why the initial ECG in this case (recorded in triage) — is definitive for OMI (Figure-1):

Figure-1: Comparison between the initial triage ECG in this case (TOP) — with the post-PCI ECG (BOTTOM) after reperfusion of a high-grade RCA stenosis  (See text).

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ECG #1 = the initial Triage ECG (TOP) — I repeat below (and illustrate in Figure-1) points made by Dr. Smith above, as well as some additional points:

• QRST amplitude in the inferior leads is often quite modest. As a result, OMIs may not declare themselves by as much ST elevation as is written into some “guidelines”. Instead, ST-T wave SHAPE takes on prime importance — as well as integration into our “Gestalt analysis” of the relative amount of ST-T wave deviation in cases when there is no more than modest QRS amplitude.
• There is debate among clinicians as to whether the PR or TP segment baseline should be used to assess the amount of ST segment deviation (Figure-2). BOTH are potentially correct — depending on the case at hand. There may be significant artifact or baseline wander that blurs definition of what constitutes the “baseline” in any given tracing. I prefer the PR segment baseline in those tracings in which this landmark is distinct — keeping in mind that the PR segment typically shortens (and is not always straight) as heart rate increases. Other clinicians prefer the TP baseline. SUGGESTION: Be open to using either the PR or TP segment as your “baseline” — and sometimes (when there is lots of artifact/baseline wander) using your “Gestalt average” of the two when neither is clear. (CLICK HERE — for the source of Figure-2).

Figure-2: Use of either the PR or TP segment to determine the “baseline” (See text).

Continuing with our discussion of the subtle ECG changes in Figure-1:

• There is significant baseline artifact in Figure-1. That said, I believe we still can confidently determine the baseline. I’ve drawn in RED horizontal lines that correspond to the PR segment baseline. Based on these — there is ST elevation in each of the 3 inferior leads. The relative amount of this ST elevation is ~50% of the height of the tiny r waves in leads III and aVF, which most definitely is clinically significant!
• NOTE: Even if you selected the TP baseline instead of the PR baseline — there still is ST elevation with straight takeoff of the ST segment, and hyperacute-appearing T waves in each of the 3 inferior leads in ECG #1 of Figure-1.
• Although subtle — there is some ST depression in lead aVL (ie, the ST segment in this lead clearly dips below the horizontal BLUE PR segment baseline). In addition, there is terminal positivity of the T wave in lead aVL (BLUE arrow) — which correlates well with acute OMI.
• Dr. Smith emphasized the “down-up” T wave in lead V2 as strongly suggesting associated acute posterior infarction. This finding is subtle, but real! For clarity — I’ve drawn in a PINK arrow over the initial negative portion of this T wave — and a PURPLE arrow over the terminal positivity. (NOTE: This is the same phenomenon I just described with the BLUE arrow in lead aVL).
• The ST-T waves in leads V3-thru-V5 are also clearly abnormal! Note straightening of the short ST segment (especially in V3,V4) prior to abrupt rise to a taller-than-expected symmetric T wave (especially in V3,V4). I interpret these findings as further support of associated ongoing acute posterior infarction.
• Finally — I believe there is subtle-but-real ST elevation in lead V1 — or at-the-least ST segment coving in this lead that is not typically seen (RED arrow within the RED circle in V1). In the setting of an ECG suggesting acute RCA occlusion — this suggests probable acute RV involvement (thought right-sided leads would be needed to confirm this).
• NOTE: This makes for a total of 9/12 leads on the triage ECG ( = ECG #1) that show subtle-but-real acute ST-T wave findings. This is the BEST way to confirm OMI — namely that acute findings (even if subtle) are found in so many leads!

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ECG #2 = the post-PCI ECG (BOTTOM) — Confirmation of each of the findings I cite above is forthcoming from comparison of ECG #1 with the 2nd ECG in this case, obtained after reperfusion.

• FIRST — Note that there has been a change in frontal plane axis in ECG #2. This is important to appreciate, because we need to take into account the different QRS appearance when assessing ST-T wave changes (ie, there is now LAHB). That said, I believe lead-by-lead comparison in both limb and chest leads between ECG #1 and #2 does provide valid indication of what has changed.

These are the differences I note between ECG #1 and #2:

• ST elevation in the inferior leads has resolved.
• ST depression has resolved in aVL.
• ST coving with slight elevation is no longer present in V1.
• The biphasic T wave in V2 is gone (the T is purely positive now).
• Leads V3-thru-V5 now look normal. Note that the ST segment prior to onset of the T wave in V3 and V4 now shows normal gradual upsloping (instead of ST segment straightening) — and the T waves in these leads are smaller and less symmetric than they were in ECG #1.

LEARNING POINT: The BEST way to hone your ECG interpretation skills is to regularly compare pre- and post-reperfusion tracings — to see what has changed! This confirms that subtle initial abnormalities were real — and makes you better the next time at recognizing subtle-but-important ECG findings from the start.

• Our THANKS to Dr. Smith for this highly instructive case! 

Another Inadequate Paper Published on Triage ECGs, whose Conclusions Need Scrutiny.

This paper was just published:

Noll S. et al.  The utility of the triage electrocardiogram for the detection of ST-segment elevation myocardial infarction.  Am J Emerg Med 36(10):1771-1774.  October 2018.

https://www.sciencedirect.com/science/article/pii/S0735675718300974

In this paper, in a department in which they state they have only 50 STEMI per year, they looked at only 8 days worth of triage ECGs for a total of 538.  They did not find one STEMI on their triage ECGs (no surprise! They only get 1 per week!).  They did have 16 NonSTEMIs, but do not describe the ECG of these 16, nor even investigate the consequences of the ECG in these 16.  "While in the ED, one patient progressed to have ECG changes consistent with STEMI although the initial triage ECG did not meet STEMI definition guidelines."  It would be instructive to see that ECG: perhaps it showed an OMI, but not STEMI, just like the one below which was recorded just a couple days ago in triage.  They did not look to see how many of the NonSTEMI had an occluded artery at angiogram.  As far as I can tell, they did not view the ECGs!  They only looked at ED diagnosis, not at any angiogram or even at discharge diagnosis.  They do a "cost analysis" based on charges of $125 per ECG and state that it would cost $54,000 to detect 1 STEMI based on 50 STEMI per year.  

Conclusion: "Given the extremely low yield and high associated charges, current guidelines for triage ECG for identifying a possible STEMI should be reviewed."

Fair enough.  I will briefly review the guidelines here and now: 

One should never use charges to calculate cost.  Charges and cost have no relation to each other in hospital billing.  In our ED, a health care assistant (HCA) records all ECGs, in triage and elsewhere.  It takes at most 10 minutes (this is an exaggeration).  At total compensation of $50,000 per year, working 1800 hours, an HCA could record over 10,000 ECGs if that is all they did.  That is $5.00 per ECG in cost.  Let's double it to be certain, to $10.00.  Then it takes a staff physician all of 10 seconds to read it (at most!).  Is that $125.00 of cost?  No, again, charges and cost have no relation to each other in hospital billing.  One must add in the cost of paper, and the system, and the ECG machine, all of which are negligible per ECG.  

Let's say, then, that the true cost of an ECG is $20.00 (this is an exaggeration -- it would cost even less).  We at HCMC have 30 walk-in STEMIs per year; the rest come by ambulance.  We also detect at least 5 OMI patients who do not meet STEMI criteria. We record ECGs in triage on every patient with chest pain, and some other indications, and this amounts to 8000 ECGs in triage each year, costing at most $200,000 (8000 x $20.00).   That is 35 OMI detected out of 8000 triage ECGs; that is 1 OMI for every 229 ECGs, and 1 OMI for every 10.4 days.  Thus, it costs us at most $5700 to detect one OMI.  Given the dire consequences of missing a STEMI or OMI, including cardiac arrest (see cases below), $5700 is extremely cheap.  

Saving just one person from death or heart failure by early diagnosis of STEMI is worth far more than $5700, or even than $54,000, or even than $200,000.  Moreover, the costs of litigation of just one missed STEMI or delayed diagnosis, with subsequent severe heart failure or death, can run into the millions.  

By recording triage ECGs, we make the early diagnosis of OMI in not just 1 patient, but 35 patients, per year.  

That the triage ECG must be shown to the physician is demonstrated again by the following ECG, recorded just this week.

A patient with chest pain:

See the computer analysis.
Is it normal, as the computer says?
Notice there is only trace ST Elevation in several leads (a normal amount!).

For those of you who read this blog regularly:

You will know that these are clearly hyperacute T-waves, diagnostic of proximal LAD occlusion.

This was immediately recognized by the physician and the cath lab was immediately activated. 

V2 is actually a de Winter's T-wave.  

Cath lab needs activating.

Imagine if this patient had no triage ECG and had to wait 2 hours for placement into the ED.

Imagine if the computer read of "normal ECG" prevented it from being seen by the MD.

For those of you who are new to this blog, see these cases:

10 Cases of Anterior Hyperacute T-waves in V2-V3

10 Cases of Anterior/Lateral Hyperacute T-waves in V4-V6

10 Cases of Inferior Hyperacute T-waves

Missed hyperacute T-waves followed by death

Hyperacute T-waves that never manifested STE despite serial ECGs with total anterior wall infarction

30 year old with hyperacute T-waves diagnosed prehospital

Missed hyperacute T-waves followed by cardiac arrest during discharge

Hyperacute T-waves called "normal" by computer

Another prehospital hyperacute T-wave case




Computer "Normal" ECGs in Triage:

A case of arrest:

Chest pain relieved by Maalox and viscous lidocaine

Another case of arrest:

Chest pain and a "normal" ECG

Another case of arrest:

Subtle Dynamic T-waves, Followed by LAD Occlusion and Arrest

A 50-something woman with chest pain and 2 "normal" ECGs at triage

A middle-aged woman with chest pain and a "normal" ECG in triage

Chest Pain Diagnosed as Gastroesophageal Reflux

An Elderly Male with "Indigestion"

Should Emergency Physicians be interrupted by ECGs that are read as "Normal" by the computer?

It is easy to be led astray by the computer....

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Comment by KEN GRAUER, MD (10/9/2018):

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I agree with Dr. Smith — This is a faulty study for many reasons. In addition to the highly problematic issue of “cost analysis” (What is a fair and reasonable “true cost” — and what is the “value” of stemi detection in patients with chest pain?) — the methodology used indicates this was a retrospective chart review of “all patients seen in an ED over an 8-day period of who had a triage ECG performed”.

• The intervention that should have been assessed (in my opinion) — is the potential benefit (if any) of doing a triage ECG (ie, of doing an ECG within 10 minutes of arrival when the presenting complaint is for symptoms of concern for possible stemi).

QUESTION: Isn’t there “potential benefit” — IF by doing an ECG on a patient who presents to the ED, a capable clinician decides that the patient needs to be formally assessed sooner than simply “waiting his/her turn” in a busy ED?

• To do such a study — data must be prospectively obtained. You simply have NO idea as to how much may have been missed by retrospective analysis.
• As per Dr. Smith — we have NO idea how many OMIs may have been missed that didn’t quite satisfy “stemi” criteria (like the triage ECG that Dr. Smith posts above).
• In addition to looking for STEMIs and OMIs — there are other potential ECG findings that may merit expediting formal evaluation by a clinician in the ED.
• Since the intervention being studied involves ECG interpretation — more than a single physician should interpret each tracing, with allowance for how to resolve discrepancies in interpretation.

BOTTOM LINE: I believe the wrong question was asked in this study. In addition, the wrong methodology was used. I don’t think any valid conclusions can be drawn from the results.

• COMMENT: I find it hard to imagine how there cannot be benefit from ensuring that a triage ECG is promptly performed (ie, within 10 minutes of arrival) for patients who present to an ED with symptoms concerning for possible acute STEMI.
• A study is not needed to determine potential benefit of parachutes for those who jump out of airplanes. Do we need to study if a triage ECG on patients who present to an ED with acute symptoms is a reasonable concept?
• P.S.: Our very next case ( = on October 14, 2018) — shows the value of having a capable ED physician promptly review the Triage ECG!

Hyperacute T-waves and Concordant ST Elevation seen in PVCs only

This comes from Steffen Grautoff, who is an Emergency Physician and Cardiologist who works on the Emergency Vehicles in the Northwest of Germany.

Steffen writes this case:

"A few weeks ago I was able to recognize a STEMI because of what I had seen on your blog."

"I have enclosed the ECG from a 50-something year old male who complained of chest pain. I was on scene at his working place (in Germany physicians are on the Emergency vehicles). Surprisingly enough he had undertaken a tour on the bike just two days ago without any complaints." 

"He had no further risk factors for atherosclerosis besides hypertension. However, I was a little unsure on scene whether it was a problem of his coronaries." 

"But when I took a look at the 12 lead-ECG I got a big smile on my face, because I remembered the ECG from your blog."

These are recorded at 50 mm/sec:

What do you think?

Here I have compressed them so they look as if they are recorded at 25 mm/sec.  I also put them side by side:

What do you think?

Steffen wrote:

"I remembered the ECG from your blog titled: "STEMI Seen Best in PVC, Diagnosed by Medic, Ignored by Physician" from 2013. The ECG looked similar (although at paper speed 50 mm/s) and – no surprise - an LAD occlusion was found in cath."

What is Steffen referring to?

Look in leads V2 and V3.  The PVC has a RBBB configuration (qR or rSR') because it originates in the left ventricle.  The ST segment in RBBB should be in the opposite direction to the terminal R'-wave.  That is, the ST segment should be somewhat depressed.  But it is elevated, concordant to the R'-wave.  This is a very specific sign of OMI (Acute Anterior MI due to LAD occlusion).

Notice also that the PVCs in V4-V6 have hyperacute T-waves that are much more pronounced than the only moderately hyperacute T-waves of the normal beats.  In fact, of the normal beats, only V4 shows a clearly hyperacute T-wave.

There are also Hyperacute T-waves in the PVCs in the limb leads.


Here is that case Steffen was referring to:

STEMI Seen Best in PVC, Diagnosed by Medic, Ignored by Physician

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Comment by KEN GRAUER, MD (10/8/2018):

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Our thanks to Dr. Steffen Grautoff for submitting this case that highlights a PEARL for facilitating recognition of acute STEMI by the morphology of PVCs! His case provides a perfect example of how sometimes acute coronary occlusion may only be recognized by PVC morphology!

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Figure-1: Compressed version of the ECG in this case (See text).

For clarity — I’ve labeled the compressed 12-lead tracing of this 50-ish year old man with new chest pain (Figure-1).

• The rhythm is ventricular bigeminy. As per Dr. Smith — assessment of the normal (sinus-conducted) beats on this tracing is not definitive for acute OMI (Occlusion-related Myocardial Infarction). There is slight ST elevation in leads V1 and V2; suggestion of a hyperacute T wave in lead V4 (and possibly V3); and subtle reciprocal change in the inferior leads — but not enough to confirm the diagnosis.
• As was astutely picked up by Dr. Grautoff — there is enough ECG evidence to confirm acute OMI based on PVC morphology!
• The most remarkable abnormality in PVC morphology is seen in lead V2. To clarify the points emphasized by Dr. Smith above — I’ve drawn a vertical RED line parallel to solid grid lines that indicates the end of the QRS complex of the PVC in leads V1 and V2. The dotted RED lines follow this demarcation point downward, so as to clarify the end of the QRS complex for the PVC in leads V3-thru-V6, as well indicating the end of the QRS complex for the PVC in the limb leads. The short horizontal YELLOW lines indicate the ST segment baseline.
• There is no ST segment elevation for the PVC in lead V1 — which is what one normally expects in PVCs when there is no ongoing OMI. However, it should be obvious that the PVCs in leads V2 and V3 manifest significant J-point elevation that just-shouldn’t-be-there. In addition, there is terminal T wave inversion for the PVC in lead V2 (RED arrow). If one steps back a little bit from this ECG to study the appearance of the ST-T wave for the PVC in lead V2 — Doesn’t this look like the ST-T wave appearance of an acute STEMI? (Look within the BLUE rectangle).
• ST-T wave morphology for PVCs in many other leads manifest exaggerated T wave amplitude — which in the context of the diagnostic PVC morphology changes in leads V2 and V3 is consistent with hyperacute T waves in these PVCs. And, in the context of clear abnormal J-point ST elevation for the PVCs in leads V2 and V3 — the dotted RED lines in leads V3-thru-V6 suggest there is also abnormal ST elevation for the PVCs in these leads. The overall picture strongly suggests acute LAD occlusion!

BOTTOM LINE: The great majority of acute OMI tracings identified by ECG will be diagnosed on the basis of ST-T wave morphology changes in sinus-conducted beats. But over the last decade-plus, since I started paying attention to ST-T wave morphologic changes in ventricular beats — I have seen a surprising number of cases in which acute OMI was evident from morphologic change in the PVCs. And on occasion (as is the case here) — acute OMI may only be evident from assessment of ST-T wave morphology of PVCs.

• PEARL: If you can identify one or two leads in which there is NO doubt that ST-T wave morphology of the PVCs is abnormal (as is the case here in leads V2 and V3) — it then becomes much easier to appreciate abnormal ST-T wave morphology for PVCs in other leads.