Two cases texted to me for concern of inferior hyperacute T waves and a flipped T in aVL - do either, neither, or both need emergent reperfusion?

Written by Pendell Meyers


I received two texts recently, in both cases the practitioners were worried about possible inferior hyperacute T-waves with an inverted T-wave in aVL. I was not given any clinical history.

What would you tell the team in these two cases?

Case 1

Case 2

My responses:

Case 1: "Not hyperacute. The T-wave in aVL is likely that way at baseline, send baseline if available. What's the story?"

Case 2: "Agree with concern for inferior posterior. This is almost completely diagnostic barring an identical baseline. What's the story?"



Did you agree with my assessments? Why do I say that Case 1 is not hyperacute and Case 2 is? Was I even correct?



Case 1:
The T-waves are tall in absolute millimeter terms, but they are not "fat" enough (the area under the ST-T is not enough compared to the QRS complex). The QRS complex is narrow and negative in aVL, which means it is possible or even likely than the baseline T-wave is also negative in that lead. So when I see the negative T-wave in this case it does not necessarily alarm me because it is not fat, and it may simply be the baseline T-wave in this lead for this patient. A repeat would be helpful to confirm this suspicion, however it was not available.

After I gave my opinion, the team told me that the patient was a middle aged male in the ED for seizure activity with a history of seizure disorder and had not been taking his medications. He had no chest pain or shortness of breath. Troponin was negative. He did not have ACS.


Case 2:
Atrial fibrillation with slow response. This patient also has a narrow, normal QRS complex. In this case, the axis is such that the QRS is positive in aVL. Leads III and aVF have a suspiciously straight ST segment morphology, with a large amount of area under the ST-T segments compared to the small, normal QRS complexes. Because the QRS is normal and upright in aVL, the negative large volume T-wave in that lead is highly diagnostic for reciprocal change. This is supported by STD in lead I which is not appropriate for its normal QRS complex. There is also STE in leads III and aVF, though whether it formally reaches 1mm in both leads is questionable and cannot be agreed upon by a majority of people to whom I have shown this ECG. I also had suspicion for posterior involvement because of the morphology in lead V2 which has an "awkwardly" straight, isoelectric ST segment from the J-point to the abrupt start of the T-wave, which to me is suggestive of relative ST depression and straightening although there is no absolute STD.

Comparison with a baseline would be your next step for Case 2, and here it is:

Baseline on file, showing normal relationship between the area under the ST-T curve compared to the QRS. This is proof that the findings on presentation ECG are new and diagnostic in comparison. Notice that the T-wave is negative in aVL at baseline, but the ratio of area under the T-wave is greatly increased and exaggerated between the two ECGs. 

A repeat ECG was performed shortly thereafter:

Similar findings, possibly slightly more obvious hyperacute T-waves in the inferior leads.

These hyperacute T-waves were diagnosed immediately by the ED team, and cardiology was called for emergent cath. However, this may not meet formal STEMI criteria because there may not be a full millimeter of STE in lead aVF depending on the exact baseline. It is very close if not diagnostic. The cardiologists believed that it did not meet our ACC/AHA criteria, and so emergent cath was cancelled.

First troponin T was undetectable. Second trop was 0.01 ng/mL. Third was 0.02 ng/mL. The fourth troponin shot up to 0.61ng/mL, then no further trops were measured.

He went for delayed cath ~28 hrs later, where they found 100% mid-distal LCX occlusion (TIMI 0). PCI was performed with good angiographic result.

Here is his post-intervention ECG:

Post-intervention, showing terminal T-wave inversions in the inferior leads indicative of reperfusion. 

Because troponin measurements were stopped around 9 hours after presentation, we do not know the peak troponin level. There was an inferoposterior WMA on echocardiogram, with 45% EF at that time (no old echo available).


Learning Points:

Hyperacute T-waves are recognizable with experience, and appear to the experienced electrocardiographer as fat, symmetric, large-volume T-waves judged against the size and morphology of the preceding QRS complex.

A patient with Occlusion MI should theoretically receive greater mortality benefit from reperfusion at the hyperacute T-wave stage of OMI than the ST elevation stage. Because our current paradigm does not provide recommendations or education regarding hyperacute T-waves, you must learn this on your own initiative if you are interested in providing this benefit for your patients.

As you begin to orient yourself to normal vs. hyperacute T-waves in actual practice, you must understandably go through a calibration period where you see many normal variants which appear alarming to you before you have enough experience to tell them apart from true positive hyperacute T-waves. Like any other process in medicine that cannot simply be achieved by reading a table written by the ACC/AHA, this takes time and effort. You and the learners you teach will predictably go through a period of decreased specificity (many false positives) before achieving expertise, and this temporary period should not dissuade you from further study!

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Comment by KEN GRAUER, MD (11/12/2018):

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I LOVE this post by Dr. Pendell Meyers regarding comparison between 2 ECGs texted to him out of concern for potential hyperacute inferior T waves with reciprocal change in lead aVL. I made my impressions about these 2 tracings before knowing the history for each patient — and before reading Dr. Meyers interpretation. Although I independently reached the same conclusions as Dr. Meyers — my path to this conclusion offers a different perspective.

• For ease of comparison — I’ve reproduced both initial tracings in Figure-1.

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Case #1:

• I was initially very concerned in Case #1 about the appearance of the T waves in the inferior leads. Despite the fact that the T wave peak is not overly “fat” — T wave amplitude in each of the inferior leads is clearly taller-than-it-should-be given the height of the QRS in these leads. In support of possible acute change, the deep T wave inversion in lead aVL is indeed a “mirror image” of the taller-than-expected inferior T waves. Adding to my initial concern was the biphasic T wave in lead V2 ...

That said — the reason I suspected the picture we see in Case #1 was probably not acute was a combination of the following factors:

• The ST-T waves in leads V3, V4, V5, and V6 look virtually identical to the ST-T waves in leads II, III and aVF. This makes no less than 7 out of 12 leads with a near-identical picture — and, that is highly uncharacteristic of acute MI. That’s because acute MI usually localizes to one or two lead group areas. In contrast — repolarization variants and ECG abnormalities due to metabolic factors are far more likely to be generalized.
• There really isn’t ST elevation in the ECG for Case #1.
• The fairly deep, symmetric T wave inversion in lead aVL is not necessarily abnormal. The T wave axis often follows fairly close behind the QRS axis — so T wave inversion per se in lead aVL may normally be seen when the QRS complex is predominantly negative (as it is in Case #1). And, if it turns out that the multiple prominent T waves in Case #1 are not due to acute ischemia — then the depth of the T wave inversion in lead aVL is not out of proportion to what might be expected for a repolarization variant given an all negative QRS in lead aVL.
• The fairly deep, T wave inversion in lead V1 is also not necessarily abnormal — especially given how tall T waves are in 7/12 leads.
• Despite its worrisome appearance — the biphasic T wave in lead V2 may simply be a “transition T wave” between the deep T inversion in V1 and the surprisingly tall T wave in lead V3.
• NOTE — Although duration of the QT interval looks long (ie, I measure the QT to be at least 480msec) — significant bradycardia with a heart rate below 50/minute makes it difficult to know what (if anything) this longish QT interval might mean.
• BOTTOM LINE for Case #1 — I was not certain that the initial ECG in Case #1 was not acute — BUT — the generalized nature of nearly identical-looking T waves in 7 out of 12 leads, along with a clearly potentially benign rationale for the findings in leads aVL, V1 and V2 — made me suspect that the findings in ECG #1 were probably not acute. As per Dr. Meyers — I wanted to know the history. As soon as I learned that this patient had a history of seizures, and did not have any acute chest pain — I became much more confident that this was not an acute tracing.

Figure-1: Comparison between the initial ECGs recorded for Case #1 and Case #2 (See text).

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Case #2:

• The rhythm for the initial ECG in Case #2 is slow AFib. There is some baseline artifact that distorts ST-T waves, and accounts for slight difference in the shape of some of these ST-T waves for successive beats in the same lead. That said — IF this ECG was obtained from a patient with new acute symptoms — it is virtually diagnostic of acute OMI ( = Occlusion-based Myocardial Infarction).
• Dr. Meyers has astutely highlighted the problem with the current paradigm for assessing acute tracings. Whether or not 1 mm of ST elevation is attained in ≥2 neighboring leads should be irrelevant to deciding what constitutes optimal care for the patient in Case #2. There simply is NO WAY that the ST segment straightening + slight-but-real J-point ST elevation + T wave “fattening” at its peak in leads III and aVF is normal.
• In the context of these changes in leads III and aVF — the fatter-than-expected T wave peak in lead II is also consistent with acute change.
• As per Dr. Meyers — leads aVL, V2 and V3 should serve to confirm a diagnosis of OMI if this patient was having new chest pain until one can prove otherwise on acute cath. Given the modest height of the R wave in lead aVL — a textbook picture of mirror-image reciprocal change is seen for the ST-T wave in aVL (including slight-but-real J-point depression that is the mirror-image opposite of the slight J-point ST elevation in leads III and aVF). The shape of the T waves in leads V2 and V3, coming after relative straightening of the preceding ST segment sticks out like a “sore thumb” — and strongly suggests acute posterior wall changes (as are usually seen in association with acute inferior OMI).

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FINAL THOUGHT — Take a last look at the 2 tracings in Figure-1. Isn’t it striking in Case #1 how similar the ST-T waves are in 7 out of the 12 leads?

• When upright T waves are more-prominent-than-expected in multiple leads without localization as a result of a non-ischemic cause — you’ll often see prominent non-ischemic deep T wave inversion in several of the remaining leads (as we do here) — and, sometimes you’ll even see a non-ischemic “transition” biphasic T wave (as we do here in lead V2 of Case #1).
• In contrast — Note localization of hyperacute ST-T waves to the inferior leads in Case #2 — with localization of reciprocal changes as expected with inferior OMI to leads I and aVL — with ST-T wave abnormalies suggestive of associated posterior OMI localized (as expected) to leads V2,V3. That’s WHY I suspected the ECG for Case #1 was probably not acute — but that the ECG for Case #2 was virtually diagnostic of acute OMI despite the initial cardiology decision to cancel immediate cath.

Extreme Bradycardia: a Case-Based Lesson in Pacing

I tell the residents: "The pacemaker is just common sense: if there is no beat, it provides one; if there is one, it keeps itself from pacing."

This is similar to Ken Grauer's comment at the bottom: 
"What would I do if I were a pacemaker?"

DDD pacer = Dual paced, Dual sensed, Dual response (triggered and inhibited)
Dual means that this occurs in both the atrium and the ventricle.

As you can see from the chart below, a VVI pacer is ventricle only and cannot be triggered by an atrial beat.  It can only be inhibited by an intrinsic ventricular beat.

So a DDD pacer can pace the atrium (if needed), then wait a defined period (e.g., 200 ms, like a PR interval) and pace the ventricle (if needed).  Either or both functions can be inhibited if the atrium or ventricle (or both) fires before the interval passes.

One of the reasons I'm presenting this case is that several residents misunderstood the concept of "failure to sense," believing it to be a cause of absence of pacing.  This made me realize that pacemaker function is not as well understood as I thought.

However, failure to sense is NOT a reason for absence of pacing.  Failure to sense results in inappropriate pacing: when the pacer is not sensing intrinsic activity that is present (failure to sense), it fails to have its pacing appropriately inhibited.  (If a heart beat comes soon enough, the pacer should sense it and inhibit pacing so that there is no pacing when it's not needed.)

In fact, when a pacemaker fails to generate an impulse (fails to pace), one reason may be oversensing, not undersensing.  

This is why we use a magnet when there is failure to pace!  To stop oversensing and thus stop inhibtion of pacing.  The magnet turns off the sensing function and the pacer becomes "asynchronous," meaning it will fire at a regular rate regardless of the intrinsic activity of the heart.  We place the magnet because a failure to pace may be due to oversensing (not undersensing) with inappropriate inhibition of pacing.

Case

A patient called 911 for weakness.

She had recently had a DDD pacemaker placed.

Her prehospital ECG showed failure to pace by the internal pacer.  External pacing was attempted but not tolerated and, because the patient was only mildly hypoperfused, she was transported to the ED without further intervention.

Exam revealed a fresh surgical scar at the area of pacemaker placement with significant swelling due to hematoma at the site of insertion.

Here is the first ED ECG:

What are you seeing?
Try to figure it out before reading the explanation below.

So what is happening here?  Failure to capture.  There may also be failure to sense, but it is not having any effect.

I'll explain with the arrows:

Black arrows show P-waves marching out regularly at a rate greater than 100.  They are not conducting at all (complete AV block) and thus are not affecting the ventricles at all.  The fact that the sinus node is tachycardic tells us that the sinus node is probably "trying" (teleologically speaking) to compensate for inadequate cardiac output. 

Green arrows show ventricular pacer spikes.  

These spikes come at a fixed interval (200 ms) after every P-wave.  

Therefore, the atrial pacing lead must be sensing the sinus activity and P-wave.  The ventricular pacer is programmed to fire at a fixed time period after the P-wave in order to synchronize atrial and ventricular activity.   If the ventricle had depolarized on its own (had there been no AV block), AND the ventricular sensing function also sensed the depolarization, then there would be no ventricular pacing spike.  

Why are there no atrial pacing spikes in this DDD pacer which has that capacity?  Because they are not needed and are thus inhibited: the sinus node is doing its job; it is firing and resulting in atrial depolarization (P-wave).  The atrial lead would pace if, after a programmed period of time, it did not sense an atrial beat (usually 1 second, corresponding to a rate of 60). For instance, if there were inappropriate sinus bradycardia at less than 60 bpm, the atrial pacer would take over if it is programmed to wait 1 second before firing.  (The atrial pacer would also fire if it failed to sense the atrial activity.)

However, the pacer is clearly not capturing the ventricle (not resulting in depolarization of myocardium, so no QRS).  There are 2 pacer spikes which are missing (between 3rd and 4th arrows and between 6th and 7th).  They may be there and hard to see (hidden); alternatively, they are not there at all.  
If the spikes did not happen at all, that would be a result of the pacer sensing the QRS, resulting in inhibition of pacing [even if it cannot pace (cannot capture)].  This would be unusual, as when the pacer lead is able to sense it is also usually able to pace.
If the spikes are there and just hidden, then the pacer is also not sensing: the escape QRS should inhibit pacing if that beat is sensed.  This latter one is the more likely explanation: that is to say that hidden pacing spikes due to absence of sensing is more likely than sensing + inhibition of pacing.)

Red arrows show escape beats at regular intervals, which in lead II (across the bottom) appear narrow, but if you look up at the leads above, especially at V1 above the 3rd escape beat, you see that it is RBBB morphology and therefore is an escape from the left ventricle (an escape from the junction or bundle of His, along with RBBB, would have the same morphology but at a faster rate).
A couple of these complexes are distorted by coincidental P-waves
The T-wave of the third escape beat is larger than the others because of a coincidentally superimposed P-wave.

The Dark Blue Arrow points to a pacing spike that occurs directly at the onset of a QRS, but that QRS looks exactly like those of the escape beat.  Therefore, it is just a coincidence that it happened at the same time as the onset of the QRS.  It is not capturing and not resulting in a QRS. 

The Light Blue Arrows point to pacing spikes that are followed immediately by wide beats (see brown arrows) that are typical of paced beats and different from the escape beats.  These are beats in which the pacer captured.
The T-waves of both of these beats have, coincidentally, a superimposed P-wave

Clinical course:

The potassium was normal, there was no ischemia or drug toxicity.

She went for emergent pacemaker revision.  It turned out that the hematoma at the "pocket" of the pacemaker had displaced the pacemaker, pulling the ventricular lead out of position.  This was fixed.

Etiologies of Failure to Capture

This was a failure to pace due to Failure to Capture (not due to oversensing, as there were pacer spikes), the differential diagnosis of which is:

--Hyperkalemia
--Ischemia
--Drug toxicity
--Poor electrode contact (as in this case)
--Fibrosis around electrode tip

Failure to Pace also includes these etiologies, none of which will produce a pacing spike on the surface ECG:

--Oversensing
--Broken leads (assess by Chest X-ray)
--Leads detached from generator
--Generator malfunction, including battery depletion and programming error

Emergency Management:

1. Treat hyperkalemia or drug toxicity
2. Treat ischemia (Cath lab)
3. Magnet application if no pacer spikes.
4. External pacing
5. Transvenous pacing
6. Chronotropic support with Isoproterenol, Epinephrine, or Dopamine to increase ventricular escape rate.

____________
John Larkin, of the ECG of the week (http://jhcedecg.blogspot.com/), has this simple thought process:

Hi Steve,
Great case as always, I just thought I'd share my very simple interpretation of some of the issues seen with PPMs. 
Sensing is about how many spikes are there and how many should there be.
Capture is about what is the effect of the spike.
Regarding under vs over sensing I use a very simple aide memoire of:
Over-sensing = Under pacing (less pacing spike than you'd anticipate, due to excessive inhibition)
Under-sensing = Over pacing (more spike that you'd anticipate, reduced / lack of inhibition from native cardiac activity).
John L

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Comment by KEN GRAUER, MD (11/9/2018):

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Interpretation of pacemaker tracings used to be straightforward and surprisingly simple when all the provider had to worry about were VVI pacemakers. These devices paced the ventricles — sensed the ventricles — and were inhibited by a QRS complex. Systems are far more complex these days, with dual chamber pacemakers and numerous pacing schemes, including less intuitive rate-responsive functions. As a result, determining whether a pacemaker is appropriately functioning or not has become exceedingly challenging — especially when parameters that the pacer has been set to are not known. Two thoughts have always helped me when confronted with a problematic pacemaker tracing:

• FIRST — Trying to imagine,“What would I do if I was the pacemaker” — with my sole function in life being to respond at a certain heart rate if no spontaneous impulse “from above” is forthcoming — and/or — inhibit myself if a response from above does arrive within an appropriate time period; and,
• NEXT — Remembering that most of the time, these amazing devices (pacemakers) are appropriately performing what they have been programmed to do — so our task as ECG interpreters is often best served by assuming the pacemaker is probably correct, and trying to figure out WHY the pacer is acting as it is.

The above said — this case clearly is one in which the pacemaker is not functioning correctly. As is superbly illustrated and explained by Dr. Smith — the pacemaker IS sensing spontaneous atrial activity — and IS appropriately putting out pacer spikes — but for the most part, is not capturing the ventricles. There is no way this pacemaker could be functioning appropriately with an effective ventricular rate in the 20s!

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10th Anniversary of Dr. Smith's ECG Blog: First Post was November 7, 2008

This was the first post 10 years ago today:

ST depression: is it ischemia? No, hypokalemia.

A bit of history:

K. Wang formerly sent out a paper ECG through interoffice mail called "The EKG of the Week."  When he left Hennepin to go to the University of Minnesota, I decided to start sending out the "EKG of the Week" by email to any residents and faculty in our department who wanted it.  Scott Joing, the founder of our department educational site www.hqmeded.com suggested that it would be easier just to blog it and send out the link to the blog. 

It sounded like a good idea.  He set it up and called it "Dr. Smith's ECG Blog."  I am not much of a techie myself, so would not have thought of it. 

Soon after, I noticed that there were viewers from outside Hennepin, there were comments, and the numbers went up.  This was a complete surprise, and totally unplanned.  

By December 2010, Scott Weingart gave the blog high marks on EmCrit, and viewership exploded, so that by May 2011, there were about 30,000 pageviews per day.

Viewership really exploded with the use of Facebook.  Now whenever I post, I promote on FB and get at least 20,000 views there, and up to 85,000, and most of the traffic to the blog comes from FB.  I also promote on Twitter, but get far less traffic from there.

There are now 945 published posts.  I have 249 drafts in various stages of writing, many (if not most) abandoned because I just can't get them into a form which has a distinct message.

There are over 13,000,000 pageviews on the blog now.  There were 40,000,000 views on Google image search when they stopped counting 2 years ago.  There are 55,000 Facebook followers and 14,000 on Twitter.  I never expected any of this!

Why did the blog catch on? What made it different from the multitude of other ECG sites or textbooks?

I believe there are several factors:

1. It is free FOAMed.

2. It is always in clinical context: how does this ECG help to manage this patient?

3. I have developed unique ways of diagnosing ischemia and acute coronary occlusion which were, and still are, not well known, and I can illustrate these here on the blog.

4. Every ECG finding has many different manifestations, and this wide variety can be displayed online.  Every de Winter's T-wave looks different.  Every subtle occlusion looks different.  These many morphologies could only be displayed online, never in a book, as there is not enough space in a book.  

5. Similarly, ECGs are dynamic; they evolve.  Books show only one, or sometimes 2 sequential ECGs.  I can post a half dozen or more to show this evolution.

Now Pendell Meyers and Ken Grauer are adding a lot of insight to the blog.

We are going to keep it going!  Thanks for reading!!

Steve Smith

A young man with back spasms

Written by Pendell Meyers with edits by Steve Smith

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 highly suspicious for hypokalemia. There is diffuse minimal STD, with prolonged QT interval and characteristic "down-up" 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!

Because of the prominent U-wave merging with the end of the T-wave, it is almost impossible to measure the QT interval, so let's measure the QU interval:

It is difficult, or even impossible, to determine the end of the T-wave because of a prominent U-wave. You can see here that there is a huge U-wave visible in V2. If we draw the line down to lead II across the bottom, you can see that what appeared to be the end of the T-wave in lead II is really the end of the U-wave. 

Because the T-wave is not discernible, we cannot calculate a QT or QTc interval. We could calculate a QU and QUc interval (QU = 560 ms; using Bazett's formula with HR=71 bpm, then QUc = 609 ms), however this is not really necessary or particularly helpful.

The important lesson here is that a large U-wave, especially as it is often due to critical hypokalemia, may be just as dangerous or more as a long QT without prominent U-waves. Here are some key points of logic and evidence that should leave you with the assumption (until proven otherwise) that prominent U-waves and long QUc should portend risk of arrhythmias:

1) The more cells repolarizing later, then the larger the U-wave, the more it fuses with the T-wave, the greater the amplitude of the T-U wave, and the higher the risk of arrhythmia. This assertion is indirectly supported by data from Kirchof et al, who compared ECG findings of 35 patients with LQTS (15 congenital, 20 acquired) with 40 patients with PVCs and normal QTc (1). Kirchof et al found that blinded analyzers often could not differentiate between the T- and U-waves in the recordings of patients who had imminent TdP, and that the amplitude of the largest T-U wave immediately preceding TdP was more than 3 times larger in LQTS patients with TdP compared with the LQTS patients without TdP. In fact, they found that "a marked increase in T–U-wave amplitude (3-fold higher amplitude compared with ECGs without TdP, 80% increase compared with the largest repolarizing wave in the entire ECG recording) was specific for imminent TdP."

From Kirchof et al: Graph A: The T–U-wave amplitude before TdP in LQTS patients, before PVC in patients with other heart disease (control subjects), and before PVCs that did not initiate TdP in LQTS patients. You can clearly see that those with TdP had higher TU amplitude than those without.

2) Early afterdepolarizations (EADs) are widely considered to trigger Torsade de Pointes (TdP). It has also been shown that low extracellular potassium augments EADs. (2) Low extracellular potassium is frequently associated with prominent U-waves, as we have shown countless times on this blog.

3) Kirchof et al (1) also found that the U-wave in long QTc syndrome closely correlated with EADs at the cellular level, and also that most episodes of TdP occur from EADs occurring on giant T-U waves and many occur on U-waves when there is a normal QT interval.



Back to the case:

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.



References:

1) Kirchhof P, Franz MR, Bardai A, Wilde AM. Giant T-U waves precede torsades de pointes in long QT syndrome: a systematic electrocardiographic analysis in patients with acquired and congenital QT prolongation. J Am Coll Cardiol. 2009;54(2):143-149.

2) Rautaharju PM, Surawicz B, Gettes LS, et al; American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; American College of Cardiology Foundation; Heart Rhythm Society; Endorsed by the International Society for Computerized Electrocardiology. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and U waves, and the QT interval: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society.J Am Coll Cardiol. 2009; 53(11):982-991.

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Comment by KEN GRAUER, MD (11/7/2018):

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Insightful post by Drs. Meyers & Smith — regarding recognition that this ECG is highly suggestive of hypokalemia. I’d add the following thoughts to their excellent discussion.

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• The initial ECG (ECG #1) is most dramatically abnormal in lead V2 (See TOP tracing in Figure-1). However, at first glance of this tracing — I was not at all certain about what I was seeing for the ST-T(-U) wave in this V2 lead — because: i) There is marked artifact in this lead (ie, the ST-T-U wave baseline changes from beat-to-beat and shows multiple extra undulations for each of the 3 beats in this lead); and, ii) Other than lead V2 — it is not easy to say if the upright deflection near the middle of the R-R interval in ECG #1 represents a T wave, U wave, or some “fused” combination of the two.

Figure-1: Comparison between the 2 ECGs recorded in this case (See text). 

KEY POINT — It could be all-too-easy to overlook the long QT (QU) interval in ECG #1. To avoid such oversight: i) You might repeat the initial ECG — to clarify what we are truly seeing in lead V2; and, ii) Be sure you religiously incorporate a Systematic Approach in the ECG interpretation of each and every tracing you encounter! Doing so is the only realistic way to ensure that you do not omit potentially important ECG findings in your interpretation. 

• I favor including assessment of the QT as one of the 3 ECG “Intervals” to look for (ie, the PR, QRS duration & QTc) — and, being sure to look at Intervals early in my interpretation. That’s because IF the QRS complex is wide, it is important to determine WHY the QRS is wide before proceeding further with your interpretation. (For the Systematic Approach that I favor — CLICK HERE).
• Assessment of the QT interval should be performed using measurements that you are certain of (ie, in which you can clearly see the beginning and end of the QT interval) — and, taken from that lead in which the QT interval looks to be longest! For example, we would not select lead I or V1 in ECG #1 to assess the QTc — because the QT interval does not look abnormal in these leads. The end of the T wave in lead I is also indistinct. 
• Even if we exclude lead V2 from our assessment — the QTc in ECG #1 looks prolonged in leads such as lead II, in which the QT clearly exceeds half the R-R interval (CLICK HERE and scroll down to Figure-9 for the “eyeball” approach to rapid assessment of the QTc).
• As per Dr. Meyers — it probably does not matter clinically on this initial ECG if we are measuring the QT or QU interval — since prolongation of either interval portends similar clinical consequences. Practically Speaking — the specific numerical value of this interval matters less than considering potential Causes of a Long QT (or QU) Interval. I favor consideration of this easy-to-remember LIST: i) Certain Drugs (and/or combinations of drugs); ii) “Lytes” (low K+/Mg++/Ca++); and/or, iii) CNS Catastrophes (ie, stroke, seizure, coma, head trauma, CNS bleed). NOTE — Several other conditions (ie, BBB, MI/ischemia) may also cause QT prolongation. However, the presence of these other conditions will usually be obvious from inspection of the ECG. PEARL — Whenever you see a prolonged QTc in the absence of ischemia, infarction or QRS widening — Think Drugs/Lytes/CNS as the possible cause(s). Then correlate clinically. (For more regarding use of this Long QTc List— Click HERE and HERE).

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FINAL THOUGHT — The BEST way to hone your skills for recognizing subtle abnormalities such as the QTc prolongation in ECG #1 — is to do Lead-to-Lead Comparison of the initial ECG (TOP tracing in Figure-1 — obtained when serum K+ = 2.6 mmol/L) — with ECG #2, which was obtained after electrolyte repletion.

• In my experience — the ECG is less sensitive and specific with milder degrees of hypokalemia. But in this case (as per Dr. Meyers) — given the clinical history of renal disease + an eating disorder with prior history of electrolyte abnormalities — a diagnosis of presumed hypokalemia should be immediately thought of on seeing ECG #1 until proven otherwise.