Fatigue and Weakness and a computer interpretation of STEMI

This case was sent by David Carroll, a 2nd year EM resident, and his attending physician Brad Caloia.

A 60-something male presented to the ED with weakness and fatigue.  He was diagnosed with a viral syndrome and discharged.  

He returned later and had a lab and ECG workup.  He had no cardiac history.  There was no chest pain or shortness of breath.

Here is his ECG:

The computer interpretation:

Rate: 93 | PR 146 | QRSD 112 | QT/QTc(Bazett) 353/439

Normal sinus rhythm

Anterolateral infarct, acute / ***ACUTE MI***

 What do you think?

Dr. Carroll astutely realized something was amiss: what is it?

There is no ST Segment (i.e.,the ST segment is extremely short).  The T-wave follows immediately after the end of the QRS.  There is also a domed T-wave.  Both of these are typical of hypercalcemia, and Dr. Carroll recognized this.  However, usually the short ST results in a short QT also.  But in this case the QT is accurately measured by the computer.  The domed T-wave mimics STEMI. 

Being a careful clinician, while awaiting the result of blood tests, he recorded another ECG 33 minutes later:

This did not look much different

I think the QRS is slightly wider

The calcium returned at 20.0 mg/dL (twice normal).  He began therapy for hyperCa and obtained a chest X-ray:

Metastatic cancer

 6 hours later, the Ca was down to 14.5 and another ECG was recorded:

The ST segment is still short.  The T-waves are less domed.  But the QT is the same.

Here are 2 more examples of hypercalcemia, both with short QT and short ST segment:

This is from K.Wang's book (V1-V6 only):

How are these cases related?

Learning Points:

1. Hypercalcemia shortens the ST segment

2. The QT can be normal in the setting of a short ST segment if the remainder of the QT is long

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MY Comment by KEN GRAUER, MD (10/30/2020):

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I thought today’s case provided a wonderful example of an important ECG finding that often goes unrecognized. CREDIT to Dr. David Carroll — who quickly picked up on this finding!

• Although 3 serial ECGs are presented in above in this case — I did not think there was a significant difference between them. As a result — I focus my comments on the initial ECG, which I’ve reproduced in Figure-1.

Figure-1: The initial ECG in today’s case (See text).

MY Thoughts regarding ECG #1:

As we emphasize repeatedly — the History is critical (!) for optimal clinical ECG interpretation. The presenting complaint of the 60-something man whose ECG is shown in Figure-1 was weakness and fatigue — but not chest pain!

• Although I’ve drawn attention on a number of occasions to the entity of “silent MI”, in which acute OMI may occur in the absence of chest pain — the history in today’s case should preferentially heighten awareness of a possible non-cardiac cause for this patient’s weakness and fatigue.
• As to the ECG itself — the rhythm in ECG #1 is sinus at a rate of ~85/minute. All intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes in ECG #1:

• There are no Q waves (other than in lead aVR, which is not clinically significant).
• R wave progression is normal (with transition where the R wave becomes taller than the S wave is deep occurring normally, between leads V3-to-V4). S waves persist through to lead V6.
• There is ST segment coving in leads V2-thru-V6. There appears to be some ST elevation in each of these leads — though quantification of the amount of J-point ST elevation is difficult to do because of how smooth the ST coving is. There is non-specific ST-T wave flattening in each of the limb leads.

Putting It All Together: Regarding my Clinical IMPRESSION of the above noted ECG findings in ECG #1 — I would highlight the following:

• PEARL #1 — There is significant baseline artifact in the limb leads of ECG #1. As I’ve noted previously — the EASY way to quickly identify the “culprit” extremity causing the artifact is to see IF artifact is maximal in 2 of the limb leads, and in 1 of the augmented leads. According to Einthoven’s Triangle — since the artifact in ECG #1 is maximal in limb leads I and II — and in augmented lead aVR — the “culprit” extremity is most probably due to a problem (ie, tremor) in the RA ( = Right Arm).
• NOTE: For detailed description on HOW to identify the “culprit extremity” causing artifact — Please SEE My Comment at the bottom of the page in our September 27, 2019 post in Dr. Smith’s ECG Blog.

PEARL #2: As per Dr. Smith’s calculations above — the QTc interval is normal in ECG #1.

• I measure a QT interval of 350 msec in several of the chest leads, which given the heart rate of ~85/minute — I estimated a QT corrected-for-rate of ~420 msec ( = clearly within the normal range).
• That said, despite this normal QTc value — the QT interval “looks” short! As noted above by Dr. Smith — the reason the QTc looks short, is that there is virtually no ST segment in ECG #1.
• While ST coving in association with J-point ST elevation in a number of consecutive chest leads can clearly be the result of acute ischemia — We need to remember that the differential diagnosis of a short QTc (or a QTc that looks short) is limited = short QT syndromes and/or hypercalcemia.
• It also helps to remember that the QTc tends to be longer with acute ischemic heart disease. Lack of a longer QTc in ECG #1 supports a non-ischemic etiology.

Hypercalcemia to at least a moderate degree (ie, serum calcium level >12 mg/dL) is not a common diagnosis in an unselected ED population. Instead, the prevalence of this electrolyte disorder will be much higher in an oncology population (ie, more than 90% of patients with hypercalcemia have either primary hyperparathyroidism or malignancy).

• This is where the History in today’s case comes in — as this 60-something man presented with weakness and fatigue, but no chest pain (ie, Malignancy rises as a diagnostic consideration).
• PEARL #3: While the textbook description of ECG findings of hypercalcemia is often limited to “QT interval shortening” — QT shortening is not an easy ECG finding to recognize (even when you are looking for it!). In addition, what is not described in textbooks — is how high the serum Ca++ must go before such QT interval shortening occurs. Over my 3 decades as family medicine Attending (working in and out of the hospital) — I religiously scrutinized the ECGs of all patients I encountered in whom serum calcium levels were elevated. In my experience — NO change in ECG appearance was noted in the overwhelming majority of hypercalcemic patients until their serum Ca++ level was significantly elevated (ie, generally over 12 mg/dL). Therefore — Do not expect to pick up hypercalcemia on ECG unless serum Ca++ is increased by a lot.
• PEARL #4: More than simply QT interval “shortening” — the principal ECG finding of significant hypercalcemia is a short-Q-to-peak-of-T interval. By this I mean that the time it takes for the T wave to attain its peak is shortened with significant hypercalcemia. I know of no measurement to quantify this shortened time-until-T-wave-peak. Instead — it is a subjective judgment — that with experience (armed by an increased index of suspicion for the case-at-hand) YOU can learn to appreciate.
• Regarding ECG #1 — I found it extremely difficult to appreciate the time-until-T-wave-peak in this tracing because the coved ST segment is so smooth in most chest leads. I did draw in vertical BLUE lines in leads V4 and V5 of ECG #1 at the point in these leads where I thought definite “peaking” was seen. Subjectively — the time until attaining this T wave peak seemed short to me with respect to the vertical RED line that marks the end of the T wave in these leads.

CASE Continuation: As discussed above — the serum Ca++ level obtained at the time ECG #1 was recorded, was dramatically increased to 20.0 mg/dL. Diffuse metastatic cancer was obvious on chest X-ray.

• As I noted earlier — I did not see significant change in the 2 ECGs shown above that were obtained after ECG #1 (despite the fact that serum Ca++ had decreased significantly to 14.5 mg/dL by the time the 3rd ECG shown above was obtained).

PEARL #5: To better illustrate what I mean by a short-Q-to-peak-of-T interval — I’ve reproduced an ECG from My Comment at the bottom of the page in the July 1, 2020 post in Dr. Smith’s ECG Blog (Figure-2).

• Once again — the History in this July 1, 2020 case was insightful. My years in primary care taught me to be leery of older patients presenting with an unusual history of atypical pain in some specific part of their body. While clearly patients with “frozen shoulder” may experience exacerbations in the degree of their shoulder pain — I immediately became suspicious after hearing this history and seeing the ECG in Figure-2, that the patient had hypercalcemia secondary to malignancy. The remarkable ECG finding in this tracing is a short QTc interval.
• Vertical BLUE lines in leads V2 and V3 of this ECG from July 1, 2020 are placed over the peak of the T waves in these leads. Doesn’t the time until attaining this T wave peak “look” short? The serum Ca++ level corresponding to this ECG was 15 mg/dL — and the patient was found to have lung cancer with shoulder metastases accounting for the increase in his extremity pain.
• Now look at the Inserts in leads V2 and V3 in Figure-2. I’ve placed one QRST complex within each insert from the repeat ECG after correction of the elevated serum Ca++ level. Doesn’t the time until T wave peaking (marked by vertical GREEN lines within the inserts) now look longer (and more normal) after correction of the serum Ca++ level?
• BOTTOM Line ( = My Synthesis): I have not found much literature regarding clinical correlation between various serum Ca++ levels and time-until-T-wave peaking. Despite as high of a serum Ca++ level ( = 20 mg/dL) as you will probably ever see for the patient in today’s case — and despite a QT interval that “looks” short in ECG #1 — the QTc (corrected for rate) for the ECG in Figure-1 was not short. Significant reduction in the serum Ca++ level obtained 6 hours later did not produce appreciable change in ECG appearance. In contrast — the ECG in Figure-2 did show subtle-but-real ECG changes of hypercalcemia that did improve once serum Ca++ levels returned to normal. My "Take” — Each patient is different, and even with experience it is challenging to appreciate subtle ECG changes in many patients with hypercalcemia.
• Final PEARL: Awareness of the clinical history often provides invaluable assistance when interpreting tracings such as the ECGs shown in Figures 1 and 2.

Figure-2: This ECG is reproduced from My Comment in the July 1, 2020 post in Dr. Smith’s ECG Blog (See text).

P.S. — For another example of ST elevation from hypercalcemia — CLICK HERE —

ADDENDUM (11/2/2020):

Credit to Praneet Manekar — who picked up on an additional finding associated with hypercalcemia. I would be remiss not to add this to My Comment.  As I’ve indicated on a number of occasions — although Osborn waves are most commonly associated with hypothermia — they can on occasion be seen with other conditions (SEE My Comment at the bottom of the page in the November 22, 2019 post in Dr. Smith’s ECG Blog).

• The Osborn wave is described as a deflection with a dome or hump, that occurs at the point where the end of the QRS complex joins with the beginning of the ST segment. This is the J-Point (ie, it Joins the end of the QRS with the beginning of the ST segment) — so Osborn waves are exaggerated J-point waves.
• In addition to hypothermia — Osborn waves have been reported with brain inury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib, severe ischemia — and, as in the above case, hypercalcemia (RED arrows in the inferior leads of ECG #1 — as shown in Figure-3).
• I would have loved to see a follow-up ECG on this patient after serum Ca++ had returned to normal — in order to see if these inferior lead Osborn waves resolved. (Otero & Lenihan show resolution of hypercalcemia-induced Osborn waves after correction of serum Ca++ in this case report — Tex Heart Inst J 27:316, 2000 ).
• My THANKS again to Praneet Manekar.

Figure-3: I’ve added RED arrows to ECG #1 to highlight hypercalcemia-induced Osborn waves in the inferior leads (See text).

Is this Septal STEMI/OMI? Many examples of Septal STEMI/OMI

 This ECG was texted to me with the implied question "Is this a STEMI?":

What do you think?

I responded that it is unlikely to be a STEMI.  

Why?

1. There is a saddleback.  I have only seen 2 Saddlebacks with LAD occlusion.  Links to these two are below.

2. There is high voltage. It does not quite meet LVH criteria, but all I can say is that it has "the look"

3. The QS-wave in V2 is associated with a biphasic P-wave.  This P-wave indicates that the leads were placed too high.  When the V1, V2 leads are placed too high, a frequent result is a QS-wave in V2.

4. The QT is short.  You can eyeball it at 280 ms. The computer measured it at 284, with a QTc (Hodges correction is used by our computer) of 352 ms.  If the correction were Bazett, then it would be 393 ms, which is short for LAD occlusion (though by no means impossible).

5. Septal STEMI often has ST depression in V5, V6, reciprocal to V1.

Then I found out that the presentation is fever and headache in a 32 year old.

I suggested serial ECGs and troponins.

Serial ECGs were unchanged.  2 high sensitivity troponins were both = 4 ng/L (LoD less than 4).  This rules out acute MI, both OMI and Non-OMI.

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Learning Points:

As above, think about:

1. Saddleback

2. QT interval

3. Leads placed too high

4. High voltage

5. Looking for ST depression somewhere, especially in V5, V6

6. Then combine with clinical presentation and low pretest probability

2 Saddleback STEMIs

A Very Subtle LAD Occlusion....T-wave in V1??

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

See these examples of Septal STEMI:

A man in his 50s with "gas pain"

A woman in her 70s with chest pain

Chest Pain and RBBB. What do you think?

Chest pain in a patient with previous inferior STEMI. Scrutinize both the ECG and the history!

Septal STEMI with lateral ST depression, then has collateral reperfusion resulting in Wellens' waves

Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6

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MY Comment by KEN GRAUER, MD (10/28/2020):

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We are told that Dr. Smith was texted the ECG that I have reproduced in Figure-1. No clinical information was provided.

Please TAKE another LOOK at this ECG in Figure-1.

• What would YOU say IF this tracing was texted to you?

Figure-1: The ECG that was texted to Dr. Smith in today’s case. No clinical information was provided (See text).

MY Thoughts on ECG #1:

I’d begin by systematically interpreting this tracing. My Descriptive Analysis of ECG #1 (looking sequentially at Rate – Rhythm – Intervals – Axis – Chamber Enlargement & QRST Changes) is as follows:

• The QRS complex is narrow. The Rhythm is regular and rapid. This is sinus tachycardia at a Rate of ~115/minute.
• All Intervals are normal (ie, the PR interval is not more than 1 large box in duration — the QRS is not more than half a large box — and the QTc is not prolonged, albeit more difficult to assess at this rapid a rate).
• The frontal plane Axis is markedly leftward. Since the QRS complex in lead II is clearly more negative than positive — the axis is more negative than -30 degrees (probably about -45 degrees) — which satisfies criteria for LAHB (Left Anterior HemiBlock).

Regarding Chamber Enlargement:

• There is a deep, negative component to the P wave in lead V1. This suggests that there may be LAA (Left Atrial Abnormality).
• Although the P wave is fairly prominent in lead II — it is not quite pointed, and not quite 2.5 mm tall — so I would not call RAA (Right Atrial Abnormality). That said — there appears to be subtle-but-real P wave notching in a surprising number of leads (ie, in leads II, III, aVR, aVF; and V2-thru-V6).
• IF the patient is an adult who is at least 35 years of age — then several voltage criteria for LVH would be satisfied: i) R in lead aVL ≥12 mm; ii) Cornell Criteria would be met, since the sum of the R in aVL + the S in V3 is ≥20 mm (for a woman) and/or >28 mm (for a man); and, iii) Peguero Criteria would be met, since the deepest S in any chest lead + the S in V4 is >23 mm (for a woman) and/or >28 mm (for a man).
• NOTE: For those wanting more on my approach to assessing LAA/RAA — CLICK HERE. For review of ECG criteria for LVH that I favor (including a user-friendly Table of LVH Voltage Criteria) — Please scroll down to the bottom of the page for My Comment in the June 20, 2020 post in Dr. Smith’s ECG Blog.

Regarding Q-R-S-T Wave Changes:

• Small and narrow (probably septal) Q waves are seen in high lateral leads I and aVL. In addition — there is an unusual Qr pattern (with a very deep and wide initial Q wave) in both leads V1 and V2.
• After the initial Qr pattern in leads V1 and V2 — the R wave progresses as we move across the precordial leads, albeit with slightly delayed transition (with the R wave becoming taller than the S wave is deep between V4-to-V5). S waves do persist in the chest leads through to lead V6.
• Regarding ST-T wave changes — there are several abnormal findings. These include: i) No less than 2-3 mm of ST elevation in lead V2, albeit with a saddleback (upward concavity) appearance; ii) At least 2 mm of J-point ST elevation in lead V3, with some ST segment straightening and a lesser amount of ST elevation in lead V4 (albeit slight PR depression in leads V3 and V4 makes assessing the amount of ST elevation more difficult); iii) There is also slight ST elevation in lead V1; iv) Shallow T wave inversion in lead aVL, that is potentially consistent with LV “strain”; and, v) Nonspecific ST-T wave abnormalities in inferior leads (ie, ST straightening/coving in leads II and aVF) — with a peculiar notching of what appears to be the terminal T wave in lateral leads I, V5, V6.

Clinical IMPRESSION of ECG #1: There are a lot of descriptive ECG findings on this tracing! As a result — we absolutely need some History in order to clinically interpret the numerous ECG findings noted above.

• IF the Question being raised is whether the cath lab should be activated because of the ST elevation that is most marked in lead V2 (but also seen in leads V1, V3 and V4) — then I agree with Dr. Smith, who indicates above how rare it is for the saddleback form of ST elevation to be associated with acute LAD occlusion. That said — IF the history was of an older patient presenting with worrisome new-onset chest pain — I would be less confident ruling out acute OMI on the basis of this single ECG.
• Looking closer — Although the shape of the ST-T wave in lead V2 (and to a lesser extent in lead V1) resembles that of a Brugada Type-2 or “Saddleback” pattern — the ß-angle is not wide enough to qualify as a Type-2 Brugada pattern. (For more on the “saddleback” shape and the various Brugada ECG patterns — Please SEE My Comment at the bottom of the page in the September 5, 2020 post of Dr. Smith’s ECG Blog).
• Dr. Smith raised the question of possible lead misplacement of the V1 and V2 electrodes (being placed too high on the chest) as the reason for the unusual Qr pattern seen in these leads. While certainly possible — I’m used to seeing an rSr’ (instead of a Qr pattern with such wide Q waves) — in association with negative P waves and negative T waves (that resemble the QRST appearance of lead aVR) — when leads V1 and V2 are placed too high on the chest. That said — a combination of LVH and the above noted saddleback pattern + misplacement of leads V1 and V2 could certainly cause the picture seen here. (For more on the ECG findings when leads V1 and V2 are placed too high on the chest — Please SEE My Comment at the bottom of the page in the November 4, 2018 post of Dr. Smith’s ECG Blog).
• NOTE: It would be EASY to determine if leads V1 and V2 were placed too high on the chest. Simply repeat the ECG after verifying correct lead placement. This is clinically relevant — because if leads V1 and V2 are properly placed, then we would have to explain the LAA and the 2 wide Q waves in these leads.

A number of other findings were noted above in ECG #1, that might suggest underlying structural heart disease if the clinical setting was “right”. These include:

• P wave notching in multiple leads (which might reflect an intra-atrial conduction defect, such as is commonly seen in patients with underlying heart disease).
• LVH (in which case the shallow T wave inversion in lead aVL might reflect LV strain).
• LAHB.
• ST-T wave abnormalities in multiple leads that could be ischemic.

FOLLOW-UP to Today’s Case: As per Dr. Smith — it turns out that the patient in today’s case was a 32-year old who presented to the ED with headache and fever. Serial ECGs were obtained — and we are told these were unchanged compared to ECG #1. Two high-sensitivity troponins were negative.

• Awareness of this History is essential to clinical interpretation of the ECG in this case. The negative troponins and lack of change on serial ECGs essentially rules out OMI.
• Increased QRS amplitude is much less likely to reflect true LV chamber enlargement given the young adult age of this patient. The P wave notching is less likely to be significant — and, one wonders how much of an effect the sinus tachycardia may be having on ST-T wave morphology.
• P.S. — The fact that serial ECGs were “unchanged” makes me question IF the health care providers recognized the possibility of lead V1,V2 misplacement?

Fascinating case of dynamic shark fin morphology - what is going on?

 Case submitted by Magnus Nossen MD from Norway, written by Pendell Meyers

A man in his 50s with no pertinent medical history suffered a witnessed cardiac arrest. EMS found the patient in VFib and performed ACLS for 26 minutes then obtained ROSC. 12 minutes later, the patient went back into VFib arrest and underwent another 15 minutes of resuscitation followed by successful defibrillation and sustained ROSC. In total, he received approximately 40 minutes of CPR and 7 defibrillation attempts. 

Here is his first ECG recorded after stable ROSC:

Originally recorded in 50 mm/s (the standard in Norway), here converted to 25 mm/s. There is sinus rhythm with a relatively normal QRS complex followed by a hint of STD that is maximal in V4-V6, which appears to me to be an expected amount of supply-demand mismatch ischemia from his immediately post-ROSC state. I do not see clear evidence of OMI or reperfusion at this time.

The patient was transferred immediately for angiogram which revealed no significant CAD, and no intervention was performed. The patient received therapeutic hypothermia at 33 degrees C for 24 hours. Echo revealed morphologically normal left and right ventricles with normal ejection fraction and no wall motion abnormalities. Troponin T peaked at 330 ng/L, then trended down. After rewarming he was noted to be neurologically intact. An ICD was placed due to suspicion of a primary arrhythmia. MRI showed a small area of the lateral wall that could potentially represent infarct. 

Several weeks later the patient presented with epigastric pain and lightheadedness. ICD interrogation showed episodes of polymorphic VT. After cessation of VT, bizarre QRS morphology was noted and is shown below. Repeat echo showed no wall motion abnormalities. He was started on amiodarone and admitted for telemetry.

While on telemetry the patient remained asymptomatic, however recurrent episodes of ECG abnormalities were recorded. These episodes are characterized by rapidly dynamic ST segment and T wave abnormalities that rapidly change from normal to hyperacute T waves to shark fin morphology and back to normal. This progression occurs and resolves rapidly, within seconds on telemetry, with clear beat-to-beat changes. The telemetry alarm states "ventricular rhythm" but it is clearly massive ST segment elevation. All of these episodes occurred without any symptoms reported from the patient, even after pointed questioning during the telemetry events.

Here are the telemetry recordings (each line is a long rhythm strip, followed immediately by the line underneath it):

This event lasts two minutes and shows rapid evolution from normal to hyperacute T waves, to terminal QRS distortion, to STE, to a progressively altered terminal portion of the QRS with STE and QRS morphology worsening in tandem. By the halfway point of the two minutes, the rhythm strip shows complete shark fin morphology, which then resolves abruptly in the last rhythm strip over the course of seconds. This is literally the OMI progression caught in action, but with the twist of adding the shark fin morphology to the classic OMI progression.

This event similarly starts with a progression from normal to enlarging T waves with simultaneously increasing STE. In this event the QRS retains a more normal, narrow appearance until longer in the progression, allowing us to see obvious huge STE and terminal QRS distortion still with a narrow QRS. During the fourth line of the telemetry image, the shark fin appearance re-emerges. During the fifth line the rhythm changes likely to a brief run of polymorphic VT, then quickly back to sinus with rapid resolution of all findings. 

He had many 12-lead ECGs obtained during various episodes (keep in mind that these ECGs are recorded using 50 mm/s):

Dr. Nossen comments on his thought process at this point: "With this rapid ST-E development and regression there was in my mind only one plausible explanation. Coronary spasm causing massive current of injury with shark fin ECG. I suspect LAD or LM. I would not expect ST-E to vanish in four beats with dissolving thrombus (also we know that the coronaries were clean). Immediately restored blood flow as with cessation of spasm I speculated is the only explanation for the fast resolution. The patient was not experiencing any typical coronary chest pain at these short episodes of ST-E. My understanding of this is that the transmural ischemia is sudden, massive and triggering a very pro-arrhythmic state before ischemic symptoms appear. Thus presenting clinically with malignant arrhythmia without the classic ischemic symptoms."

The patient was referred for a provocative test for coronary spasm based on these findings. While awaiting testing the patient was re-admitted due to short episodes of chest pressure. Telemetry again showed the same shark fin appearance multiple times. He was started on treatment for suspected coronary spasm. One incident was complicated by multifocal PVCs and a short episode of polymorphic VT, which self-terminated with regression of STE. 

The patient was sent for provocative angiogram which revealed significant spasm of the LAD, shown in the video below.

Here is the LAD before provocative testing:

Here is the mid LAD spasm induced during the procedure:

Here is a still image of the LAD spasm:

The patient is now doing well on long acting nitrates and diltiazem. ICD interrogations have been unremarkable. The patient underwent another ambulatory 48 hour holter ECG which showed only sporadic PVCs with no evidence of shark fin morphology or STE. He has been asymptomatic and doing well since.

Learning Points:

The myocardium doesn't know the etiology of OMI (ACS, spasm, dissection, embolus, etc.), and all acute coronary occlusion causes may cause the same ECG findings and progression of OMI. This reminds us that the ECG is a surrogate for what we are actually trying to figure out, and it cannot be expected to differentiate the etiologies of OMI. That said, ACS is by far the most common and treatable cause.

Serial ECGs and continuous 12-lead telemetry can be very helpful for both diagnosis and for learning the ECG.

When OMI is extremely brief, there may not be any clear ischemic symptoms during the brief episodes, and there may be no large troponin increase measured, and the ECG may not exhibit the classic reperfusion sequence after the episodes as they would for an OMI that was more sustained and cause significant MI.

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MY Comment, by KEN GRAUER, MD (10/26/2020):

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Superb discussion by Dr. Meyers of this fascinating case captured in intricate detail by Dr. Magnus Nossen.

QUESTION: How many of YOU recognized the ECG format used for the 1st tracing shown above in this case? Please TAKE another LOOK (Figure-1):

• This was the 1st ECG recorded following ROSC after a long course of ACLS. We are told that this ECG was originally recorded at 50 mm/sec speed — but had been converted to 25 mm/sec. But — WHAT about the limb lead arrangement?

Figure-1: The initial ECG shown above in today’s case (See text).

POINT #1: The ECG shown in Figure-1 has been recorded using the Cabrera Format. Electrocardiography is an international tool. While a standard ECG format (with no more than minor variation) is used throughout the United States — variations in format are used in some other countries.

• A number of ECG parameters may vary in these other ECG formats. These most commonly include the speed of recording (ie, use of 50 mm/second — instead of the standard 25 mm/second speed used in the U.S.) — and — the sequence of the limb lead display (which is different in the Cabrera format — as shown in Figure-1).
• Because we become accustomed to whatever ECG format is used in the country in which we practice — other ECG formats may be unfamiliar to us. As a result — the limb lead layout for the ECG shown in Figure-1 may have seemed strange when you first saw the initial ECG in today’s case. This is because the 1st limb lead displayed in Figure-1 is lead aVL — and, an aVR display occurs between leads I and II.

The Cabrera Format:

Initial description of the sequential limb lead format shown in Figure-1 was made by Fumagalli in 1949. Despite this — credit for this format is attributed to Cabrera. The Cabrera system has been in routine use in Sweden since 1977. A number of other countries also use the Cabrera format (ie, witness today’s case, contributed by Dr. Nossen from Norway). There are 2 Modifications in the Cabrera Format compared to the standard format used in the United States and in many (most) other countries: i) A recording speed of 50 mm/second is used in the Cabrera format; and, ii) A different limb lead sequence is used.

• As I “confessed” in the September 26, 2018 post of Dr. Smith’s ECG Blog — my brain is “programmed” to interpreting 12-lead ECGs and rhythm strips at the 25 mm/second speed that is standard in the United States. After 4+ decades of interpreting tens of thousands of tracings — there is an instant (automatic) process of “pattern recognition” that I find takes place in my brain, even before I begin systematic interpretation of any given tracing. This process is invalidated by the unfamiliar appearance of different-sized complexes that are produced when a 50 mm/second recording speed is used.
• POINT #2: Other countries (such as Germany) often use a 50 mm/second recording speed. Usually it will be obvious on sight when a 50 mm/second speed has been used — but sometimes it won’t be. This is especially true when assessing narrow QRS rhythms for heart rate (ie, a narrow QRS rhythm may appear widened and excessively slow if you fail to recognize a 50 mm/second recording speed). Therefore — it’s important to be aware of the recording speed (and to clarify if the tracing you are interpreting is from a foreign country — especially if the recording speed isn’t marked at the bottom of the ECG).

The Altered Limb Lead Sequence in the Cabrera Format:

The insert in the lower right-hand portion of Figure-2 shows the rationale for the altered limb lead sequence in the Cabrera format.

• Rather than using lead aVR — the Cabrera format uses negative aVR ( = lead -aVR) — which is situated directly opposite (ie, 180 degrees away) from positive aVR. As shown in the insert of Figure-2 — lead -aVR is situated at +30 degrees (within the BLUE rectangle).
• In many ways — the Cabrera Format offers a much more logical display of limb lead sequencing. As opposed to the traditional U.S. format (in which limb leads are grouped into standard leads I,II,III — and augmented leads aVR,aVL,aVF) — there is gradually progressive (equally spaced) sequencing with the Cabrera format, beginning with the most superior lead viewpoint = lead aVL (at -30 degrees) — and moving gradually rightward (at 30 degree intervals) — until finally arriving at the most rightward placed lead = lead III (at +120 degrees).
• The Cabrera format enhances the clinical utility of aVR — by effectively adding lead –aVR as a transition lead between lateral and inferior frontal plane location. This allows greater specificity for determining the extent of high lateral and inferior lead ischemia or infarction. It also simplifies both axis and ST-T wave vector calculation in the frontal plane — since no more than a glance at the 6 sequential Cabrera leads is now needed for instant determination of which lead(s) manifests greatest net QRS and/or ST-T wave deflection. For example, in Figure-2 — Note gradual transition of the ST segment straightening with slight depression that actually begins with lead -aVR instead of with lead II, as would have been suggested by the U.S. standard lead format.
• Another potential advantage of the Cabrera format for limb lead sequencing — is that comparison with serial tracings in a given patient is easier. This is because the more gradually progressive Cabrera format for limb lead sequencing makes serial variation in Q wave presence, QRS amplitude, and ST-T wave displacements much more evident as to what represents probable “real change” — vs change in ECG waveforms that is more likely the result of some change in lead placement.
• BOTTOM Line: Despite the above potential advantages that may be derived from use of the more logical limb lead sequencing of the Cabrera format — it seems unlikely to replace the non-sequential traditional U.S. format, at least for the immediate future. Old established habits are difficult to break ... — even when a newer approach seems technically easy to implement and clinically advantageous.

Figure-2: The insert that I've added to Figure-1 (in the lower right portion of this Figure) — shows the rationale for limb lead sequencing used in the Cabrera format (See text).

How I Interpret ECGs recorded at 50 mm/second Speed:

Ever increasing use of the internet has changed medicine, not to mention our life. Literally, hundreds of thousands of providers frequent the numerous ECG forums available on the internet — which means that whenever we participate in internet ECG case discussions — we are interacting with medical provider colleagues from all over the world. Tracings using both 25 mm/second and 50 mm/second recording speeds — as well as Cabrera and other formats will be posted. So it’s important to be aware that we may encounter a variety of ECG formats.

• When I first received Dr. Nossen’s submission of today’s case — I noted that many of the multi-lead telemetry recordings and 12-lead tracings he sent were in Cabrera format with 50 mm/second recording speed (ECG #1 was one of the exceptions — which Dr. Nossen had already converted for us to 25 mm/second speed).

Because of the difficulty that I’m happy to acknowledge regarding the interpretation of arrhythmias and 12-lead ECGs recorded at 50 mm/second speed — I wanted to share a quick and easy way I’ve developed for “visually correcting” the wider appearance produced by a doubling of recording speed to 50 mm/second.

• I’ve labeled the 6th ECG shown above in today’s case as ECG #6. This multi-lead monitor recording uses Cabrera limb lead sequencing and a 50 mm/second recording speed (LEFT panel in Figure-3). Especially because of the shark-tooth ST distortion during the first half of the recording — I initially had trouble conceptualizing what I was seeing.
• PEARL: To compensate for the 50 mm/second recording speed — I uploaded this tracing to Power Point and: i) I reduced the width of this tracing by 50% (ie, from 10 inches to 5 inches); and, ii) I unchecked the “Keep Proportions” ( = “Lock aspect ratio” box) in the Format Pane under Size options in Power Point. Doing so narrows the width of the ECG by 50% without affecting the height. As can be seen in the RIGHT panel in Figure-3 — You’ll get twice as many little boxes (which must be considered when assessing rates and intervals) — but QRS complexes and ST-T waves now look "normal" to my eye.

Figure-3: I’ve reproduced the 6th tracing shown above in today’s case, first in Cabrera format recorded at 50 mm/second speed (LEFT panel) — and then in the RIGHT panel, after “compensating” for 50 mm/second speed by reducing width of the tracing by 50% without altering tracing height (See text for full explanation).

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NOTE: My sincere THANKS to Dr. Magnus Berger Nossen (Norway) for sharing the tracings and this case with us!

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