A 60-something who has non-specific generalized malaise and is ill appearing.

July 30, 2019, 4:04 am

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An anonymous paramedic sent this.

A 60-something with past history only of colon cancer called 911 for non-specific generalized malaise.

The medics state that he was ill appearing.

They recorded an ECG:

What do you think?

This is extremely wide, and even if it is VT, it is so wide that there must be hyperkalemia or a severe Na channel blocking overdose. The patient was not on a sodium channel blocker.

The paramedic knew instantly what it was (he credits his regular reading of this blog!)

The patient was only a couple blocks from the hospital, so there was no time for treatment before arrival.

K was 8.9 mEq/L.

Etiology was a combination of NSAID and obstructive nephropathy, with a Cr > 20 (!). Estimated GFR of 2.0.

The potassium was brought down and the patient ultimately did well.

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OMI Confirmed by POCUS Echo in a 50 year man

August 2, 2019, 7:27 am

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Case submitted and written by Alex Bracey

A man in his 50s with no significant past medical history presented from a local beach with epigastric "burning" pain that had been intermittent for 4 days until this morning when it became constant at rest. He had associated nausea and diaphoresis, but overall looked well and had arrived by private vehicle to front triage. An ECG was performed there and brought to me for review:

What do you think?

STE in V2-4 that might just barely meet STEMI criteria
STE in aVL, and to a lesser extent lead I
Obvious reciprocal STD in II, III, aVF

Regardless of whether this ECG truly meets STEMI criteria, it is obviously diagnostic of OMI, most likely LAD occlusion. There is possible beginning of terminal T-wave inversion in V4 -5 possibly suggesting some reperfusion, but overall the ECG clearly shows active occlusion.

Since it was on the border of meeting STEMI criteria, a "heart alert" was activated. The heart alert pathway at my hospital summons a cardiology fellow and interventionalist to review the case and ECG without yet activating other cath lab staff, thereby allowing for rapid evaluation of the need for PCI without additional resource utilization.

The cardiology fellow presented to the bedside and reviewed the following additional ECG that had been obtained just before his arrival:

STE still present in V2-V4 and aVL, but to a lesser extent than the initial
Developing terminal T-wave inversion in V2-5, I, and aVL, implying reperfusion

He proceeded to review the ECGs and the case. He inquired as to the patient's recent alcohol intake, which had been increased compared to usual as he was on vacation. He had discomfort with deep palpation of the epigastrium.

At this point the fellow was concerned but not convinced that the presentation and findings truly represented OMI and wanted to wait for a troponin level before activating the cath lab.

The patient continued to have pain despite the reperfusion pattern, so we administered heparin 4000 U IV in addition to aspirin.

At our facility, we unfortunately do not yet have access to emergent high quality contrast enhanced echocardiography for our heart alert cases. So we immediately performed a bedside echo.

Despite imperfect quality, this shows severe hypokinesis of the anterior wall with reduced LV function.

I reviewed the images with the cardiology fellow who agreed that the constellation of symptoms and findings was concerning enough to activate the cath lab at this point. No troponin had yet resulted.

There was only a delay of perhaps 20 minutes between our diagnosis of OMI and the cardiologists' decision to take him for emergent cath.

Pre intervention: proximal to mid-LAD 100% occlusion (TIMI 0 flow).

Post intervention: stent placement with resultant TIMI 3 flow

The initial troponin T returned at 0.61 ng/mL.

5.5 hours later a repeat troponin T was 9.0 ng/mL, consistent with very large myocardial infarction.

At the 24 hour mark a formal echocardiogram was performed which revealed severe hypokinesis of the anterior wall, septum, and apex with an ejection fraction of 27%.

Teaching points:

You must learn to identify OMI so that you can advocate for your patients.

What is obvious to you may not be to your colleagues and consultants. Adjunctive tests such as point of care ultrasound to look for wall motion abnormalities may make the difference between an emergent or delayed cath lab activation (think of it as the FAST exam for ACS!). You should routinely perform these POC echos in order to practice identifying wall motion abnormalities. An easy exercise is to start by performing a POC echo on all STEMI activations where it is clear there is a wall motion abnormality; when there is STEMI, if you do not see a WMA, then you are missing it.

Although this ECG is completely diagnostic, there is utility in emergent echo looking for wall motion abnormalities in cases where the ECG is less diagnostic, or when the provider(s) do not recognize OMI on a diagnostic ECG. Only high quality contrast echo done by a trained echocardiographer and read by an expert can approach true rule-out of a wall motion abnormality. An echo of any lesser quality can of course be used, with the understanding that it is really only helpful if you find a wall motion abnormality, thereby increasing your suspicion of OMI and helping the decision to proceed with emergent cath.

Do not let POCUS convince you of absence of OMI if the ECG is diagnostic. An inadequate echo, or one read by a non-expert, can be false negative.

Don't forget to obtain serial ECGs. Even if progression to STEMI is not seen, dynamic changes (e.g., development of reperfusion pattern) can help to expedite appropriate treatment.

↧

What are all these little spikes?

August 4, 2019, 6:57 am

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An elderly woman fell and had an ECG recorded:

What are all these spikes?
They can't be anything but artifact, but from what??

These are typical spikes for nerve stimulators. In this case, the woman did not remember that she has a bladder stimulator for neurogenic bladder, but deep chart review found that this is the case.

ECG artifact of bladder stimulators has been reported in the Journal of Electrocardiology:

https://search.proquest.com/openview/aafa4a4cf87e7229eddc54d300209a9f/1?pq-origsite=gscholar&cbl=6950

↧

A young woman with altered mental status and hypotension

August 7, 2019, 6:12 am

≫ Next: How does acute left main occlusion present on the ECG?

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Written by Pendell Meyers

I texted this Prehospital ECG with no clinical information to Dr. Smith.

What do you think?

Dr. Smith texted back "Pulmonary Embolism" within seconds.

Here is the clinical information:

A woman in her 30s with no known past medical history presented by ambulance for altered mental status and syncope. She was delirious, ill-appearing, hypotensive, tachycardic, afebrile, satting 99% on 2L/min masal cannula.

Sinus tachycardia
Acute RV strain pattern evidenced by the morphology of the QRS and T-wave in V1-V3, including small-moderate R-wave followed by deep S-wave, then concave ST segment into whole T-wave inversion. The fact that lead V3 does not have a deep S-wave like the other examples you will find in the link below is simply due to it being the transition lead in this case, where the QRS progresses from mostly negative to mostly positive. There is TWI in lead III as well, completing the "inferior and anterior T-wave inversion" characteristic sometimes seen in acute right heart strain.

See this post for many side-by-side examples of this exact morphology

Based on this ECG we had high suspicion of PE.

We performed bedside echo which showed a large RV, with "D sign" of the RV impinging on the LV septum. The IVC was plethoric with minimal respiratory variation. We looked at the legs briefly and were unable to find an obvious DVT.

Here is the initial ED ECG:

This is much less convincing, as only V1-V2 still have the morphology described above. This could be due to lead placement, but it is not possible to say for sure.

Despite the fact that the initial ED ECG was not as convincing of acute right heart strain, the EMS ECG was nearly diagnostic and we proceeded with massive PE as our working diagnosis, despite the absence of any hypoxia.

She was hypotensive requiring 5-10 mcg/min of norepinephrine prior to CT scan.

She was quite altered, so we elected not to begin anticoagulation before obtaining head CT scan to exclude intracranial hemorrhage as a cause of her altered mental status (her mental status did not improve significantly despite her mean arterial pressure being raised to 65-70 mmg Hg with norepinephrine).

We rushed her to CT scan which revealed no intracranial hemorrhage and bilateral mainstem pulmonary emboli.

We diagnosed massive PE and gave alteplase. There are many different ways to give alteplase in this scenario, but we elected to give 10 mg over 2 minutes, followed by 10 mg over the next 10 minutes, followed by 80 mg over the next 2 hours (total dose 100 mg).

Over the next hour, her vitals normalized and pressors were discontinued. Her mental status returned to normal as her vitals normalized.

We discovered that her sister also had a massive PE last week! Her formal DVT ultrasound showed nonocclusive DVT throughout her left leg. She had a recent flight to Italy.

We started heparin drip several hours after alteplase was given.

Her formal echo hours later could only detect "mild RV strain" at that time.

She was admitted to the ICU.

Hypercoagulability workup has thus far been unrevealing.

Case 2

Here are 2 ECGs recorded from one patient with pulmonary embolism just this week. The patient had sudden chest pain and SOB:

Notice again the T-wave inversion in V1-V3 AND lead III.
The T-wave inversion is domed, which is different from Wellens'
This ECG is deceptive because there is no tachycardia, which is unusual in a patient who is not on beta blockers

Here is a followup ECG:

The patient had an initial troponin of 0.100 ng/mL, which could easily have been mistaken for acute coronary syndrome, but a D dimer was measured and was 2000. CTPA confirmed pulmonary emboli. The patient was NOT on a beta blocker.

Learning Points:

Learn the morphology of acute right heart strain vs. Wellens' T-wave inversions here:
See this post for many examples.

Use point of care ultrasound to confirm ECG findings of PE, OMI, etc.

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How does acute left main occlusion present on the ECG?

August 9, 2019, 7:06 am

≫ Next: The ECG was correct. The angiogram was not.

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Post by Smith and Meyers

Sam Ghali (https://twitter.com/EM_RESUS) just asked me (Smith):

"Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?"

Smith and Meyers answer:

First, LM occlusion is uncommon in the ED because most of these die before they can get a 12-lead recorded.

But if they do present:
The very common presentation of diffuse STD with reciprocal STE in aVR is NOT left main occlusion, though it might be due to subtotal LM ACS, but is much more often due to non-ACS conditions, especially demand ischemia. In these cases, STE in aVR is always reciprocal to the ST depression of subendocardial ischemia elsewhere (ST depression vector towards II and V5).

Total LM occlusion can present with STE or STD in aVR.

When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI.

The pattern seen may, or may not, be unique to left main occlusion. Some total LAD occlusion manifest on the ECG similarly to some left main occlusions. All are, however, clearly massive STEMI.

To reiterate the most important part relevant to your question: LM occlusion does not present with isolatedSTE in aVR. Depending on where the STE vector of the LM occlusion shows up on the ECG, there may be either STE, or STD, or neither in aVR, and lead aVR will not be the important part of the ECG interpretation in these cases.

Below are 6 anecdotal cases of true complete left main occlusion with no collateral circulation:
3 have STE in aVR
1 has no ST shift in aVR
2 have STD in aVR

The ECG can have a variety of presentations in LM Occlusion. Here I explain:

First, you don't know for certain what the state of the artery was at the time of the ECG.

It might have been (barely) open but closed at the time of angiography.

That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories:

1. The anterior direction (anterior) due to LAD (STE in V2-V4, possibly V5, V6)

2. The lateral direction (leftward) due to:

2a. D1 (STE I, aVL, V5, V6) and

2b. Circumflex (STE in I, aVL V4-V6)

3. The septum (rightward) from LAD (STE in aVR, V1, ST depression in V4-V6)
This ST depression may cancel out or reverse the STE in V1 and aVR!!

4. Posterior (due to circumflex occlusion) (ST depression in anterior leads)
This ST depression may cancel out the STE in anterior leads!

5. Superior due to ischemia of the base of the heart (STE in V1, aVL, aVR)
This may result in ST depression in inferior leads

Each ST vectors will have different contributions in different patients. They will add up in varying magnitudes resulting in a variety of ECG presentations.

At the bottom of the post, I have re-printed the section on aVR in my article on the ECG in ACS from the Canadian Journal of Cardiology:

Case 1.

Chris Mondie of the Newark Beth Israel Emergency Medicine Residency sent case 1 below of a 100% LM occlusion. His comments/questions are inserted below the ECG:

A 50-something woman presented with 3 days of intermittent chest pain that became worse on the day of presentation, with diaphoresis and radiation to the left arm, as well as abdominal pain.

This is her ECG:

An obvious STEMI, but which artery?
ST elevation in aVR

The cath lab was activated and a 100% left main occlusion was found.

Chris' comments/questions:

"Every "ST elevation in aVR" case I've ever seen has been triple vessel, insufficiency, or demand/global subendocardial ischemia secondary to some underlying sepsis/increased metabolic demand."

"My question is this: we are taught that aVR elevation with diffuse ST depression can be indicative of LMCA."

Smith: this teaching is incorrect; see this post: ST Elevation in Lead aVR, with diffuse ST depression, does not represent left main occlusion.

"In my case above there is indeed significant STE in aVR as well as V1, there is also STE in aVL and V2 which seems to violate the "diffuse STD" claim....   Why is it that we
don't see lateral STE in the classically taught "STE in aVR, and diffuse STD". If the lesion is so proximal, wouldn't we normally expect to see lateral STE instead of STD in the lateral leads?"

Smith response to case: "It is not surprising that this ECG was from a patient with acute LM occlusion." and I sent him the above ST vector explanation.

Case 2.

Here is another proven left main occlusion in a young woman who presented with sudden pulmonary edema, had this ECG recorded, then arrested and was resuscitated after 30 minutes of CPR:

This has sinus tachycardia with RBBB and LAFB, and STE in V2-V6 as well as I, aVL
This pattern could just as easily be seen in LAD occlusion.
She had a proven 100% Left Main occlusion
No ST shift in aVR

See this paper by Widimsky et al, which shows the high association of RBBB, especially with LAFB, with LAD occlusion. Furthermore, among 35 patients with acute left main coronary artery occlusion, 9 presented with RBBB (mostly with LAFB) on the admission ECG.

Widimsky P et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy?

Case 3.

Here is another total left main:

Total eclipse of the heart -- written by Pendell

ST Depression in aVR

And with lines to point out the end of the QRS:

ST Depression in aVR

Case 4.

Here is another 100% left main that was contributed by Rohin Francis of Medlife Crisis (https://twitter.com/MedCrisis)

"Shark fin" ECG in I, aVL, V4 and V5. Which artery? Hint: patient is in shock and was put on ECMO

ST depression in aVR

Here is the angiogram from Rohin's case:

Case 5.

Here is a 95% Left Main with TIMI-1 flow:

A Hybrid of de Winter's T-waves and Diffuse Subendocardial Ischemia: Left Main Ischemia

ST Elevation in aVR
But this is a bit different: there is some minimal flow, as you can see from the angiogram below. And thus it is a hybrid of de Winter's T-waves and Diffuse subendocardial ischemia.

Here is the angiogram:

Black arrows are very narrowed left main, red arrow is LAD with flow, and yellow arrow is circumflex with flow.

Case 6.

Beware crescendo angina in patient with known CAD

ST Elevation in aVR

Case 7.

Another left main occlusion, but this one shows subendocardial ischemia. Why?

This was a 100% acute LM occlusion.
This defies my principle that diffuse ST depression, with reciprocal STE in aVR, is NOT seen in total occlusion.
Why?
Below is the angiogram.
You'll see that there is collateral circulation from the RCA.

LM is indeed 100% occluded

But the RCA angiogram shows that there are RCA collaterals supplying subepicardial flow to other territories:

All the flow on the upper right is flowing from the RCA into the LAD territory

This is copied from my article in the Canadian Journal of Cardiology:

Lead AVR in Acute Coronary Syndromes (61)

Many experts consider the ECG pattern of STE in aVR, with diffuse ST depression elsewhere (referred to here as the “aVR STE pattern”), to be representative of left main (LM) OMI.(7) The 2013 ACC/AHA STEMI guidelines consider this a “STEMI equivalent,” where thrombolytic therapy is not contraindicated (Evidence level B, no specific class of recommendation).(16) However, these conclusions are based on studies where LM lesions were not true subtotal or complete occlusion (i.e. TIMI 0/1 flow).(61,62) The interventional community defines occlusive LM disease as >50% by FFR, or ≥75% stenosis,(63) but urgent or emergent intervention on lesions not meeting these thresholds is only imperative if it is a thrombotic lesion and the patient has refractory ischemic symptoms (i.e. not resolved by nitrates, antiplatelet, and antithrombotic therapies). (See 3 examples in appendix: Figure S7a, S7b and S7c) Although nearly half of patients with ≥1 mm STE in aVR due to ACS will require coronary artery bypass surgery for revascularization,(61) the infarct artery is often not the LM, but rather the LAD or severe 3-vessel disease. More importantly, such ECG findings are frequently due to non-occlusive etiologies (E.g. baseline LVH, demand ischemia secondary to respiratory failure, aortic stenosis, hemorrhagic shock). Knotts et al. found that only 23% of patients with the aVR STE pattern had any LM disease (fewer if defined as ≥ 50% stenosis). Only 28% of patients had ACS of any vessel, and, of those patients, the LM was the culprit in just 49% (14% of all cases).(56) It was a baseline finding in 62% of patients, usually due to LVH.

Thus, a number of expert reviews emphasize the low specificity of the aVR STE pattern, preferring to label it as circumferential subendocardial ischemia; in this syndrome, STE in aVR is reciprocal STE, reciprocal to an ST depression vector towards leads II and V5.(8,10,61) The aVR STE pattern is also not sensitive for LM OMI. On the other hand, anterior STEMI with combined new right bundle branch block and left anterior fascicular block is highly suggestive of LM OMI.(64 65) (See example 12-lead in appendix: Figure S8) It should be re-emphasized that true LM OMI (i.e. TIMI flow 0) is rare in the ED, as most either die before arrival or are recognized clinically due to cardiogenic shock. Thus, reported specificities of STE in aVR for LM OMI result in very low positive predictive values. Of those who do get to the ED, many present with clear STE.(65, 64, 61) The ACC/AHA states that thrombolytics are not contraindicated for diffuse STD “associated with” STE in aVR. Given the poor specificity of this pattern for LM OMI, we suggest that thrombolytics should only be considered for those with profound ST depression that is clearly due to ACS, is refractory to all other medical management, and only when PCI is completely unavailable.

Lead aVR in STEMI

Some patients whose ECGs already meet conventional STEMI criteria may also have STE in lead aVR. This finding does not alter the need to pursue emergent reperfusion, although it may suggest a poorer prognosis.(61,66) In a patient with otherwise diagnostic STE, additional STE in aVR does not represent LM OMI and is not helpful in diagnosing the infarct-related artery or the site of occlusion.(67) Less than 3% of anterior STEMI has LM OMI, and most are recognized clinically due to cardiogenic shock. (68, 69)

References

7. Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing electrocardiogram interpretation and clinical decision-making for acute STelevation myocardial infarction. American heart journal 2010;160:995-1003, .e1-8.

16. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology 2013;61:e78-140.

61. Smith SW. Updates on the Electrocardiogram in Acute Coronary Syndromes. Current Emergency and Hospital Medicine Reports 2013;1:43-52.

62. Jong GP, Ma T, Chou P, Shyu MY, Tseng WK, Chang TC. Reciprocal changes in 12-lead electrocardiography can predict left main coronary artery lesion in patients with acute myocardial infarction. International heart journal 2006;47:13-20.

63. Stone GW, Sabik JF, Serruys PW, et al. Everolimus-Eluting Stents or Bypass Surgery for Left Main Coronary Artery Disease. The New England journal of medicine 2016;375:2223-35.

64. Fiol M, Carrillo A, Rodriguez A, Pascual M, Bethencourt A, Bayes de Luna A. Electrocardiographic changes of ST-elevation myocardial infarction in patients with complete occlusion of the left main trunk without collateral circulation: differential diagnosis and clinical considerations. J Electrocardiol 2012;45:487-90.

65. Widimsky P, Rohac F, Stasek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? European heart journal 2012;33:86-95.

66. Kukla P, Bryniarski L, Dudek D, Krolikowski T, Kawecka Jaszcz K. Prognostic significance of ST segment changes in lead aVR in patients with acute inferior myocardial infarction with ST segment elevation. Kardiologia polska 2012;70:111-8.

67. Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. The American journal of cardiology 2011;107:495-500.

68. Zoghbi GJ, Misra VK, Brott BC, et al. ST Elevation Myocardial Infarction Due To LEFT Main Culprit Lesions: Percutaneous Coronary Intervention Outcomes. Journal of the American College of Cardiology 2010;55:A183.E1712.

69. Kurisu S, Inoue I, Kawagoe T, et al. Electrocardiographic features in patients with acute myocardial infarction associated with left main coronary artery occlusion. Heart (British Cardiac Society) 2004;90:1059-60.

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The ECG was correct. The angiogram was not.

August 13, 2019, 5:41 am

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This was sent by Cam Mosley and Michael Truax, LSU-Baton Rouge Residency.

74 yo male with previous MI years ago presented with chest pain and nausea.

An ECG was recorded:

Sinus rhythm with PVCs.
What else?

My interpretation (and theirs: they activated the cath lab):

It is clearly a subtle proximal LAD occlusion (OMI).

Why?
-- Subtle STE in I, aVL, V2
-- Hyperacute T-waves in aVL, V2, V3
-- Q-wave in V2, which is always abnormal
-- reciprocal ST depression in III, aVF. Thus, the STE in V2 cannot be normal.

Here is the outcome he sent:

Cath negative other than 40% LAD stenosis.
They looked at aorta too and it was ok.
Initial troponin = 0.02 ng/mL (ref up to 0.030).

Here is my response:

"What did subsequent ECGs show? Same? Or resolution? That is the key. LAD can be briefly occluded with negative trops and no thrombus seen (the thrombus lyses). But if this is the case, then the ECG will resolve. If the ECG is the same, then it is truly a false positive. If the ECG resolves, then it was indeed what it looks like: LAD occlusion, though brief (transient)."

So he sent the post cath ECG:

Indeed, the ECG confirms reperfusion, with resolution of ST in I, aVL and V2, terminal T-wave inversion in aVL, full inversion in V2, and resolution of hyperacute T-waves.

As you can see, the angiogram is not the final arbiter of acute coronary syndrome. Angiograms sometimes show no evidence of ACS. The thrombus lyses and may not leave behind any visible culprit lesion. Although unusual, it is not rare.

In this study, approximately 10% of Transient STEMI had no culprit found:

Early or late intervention in patients with transient ST‐segment elevation acute coronary syndrome: Subgroup analysis of the ELISA‐3 trial

One must use all available data, including the ECG, to determine what happened.

Final Diagnosis?

If the troponin remained under the 99% reference, then it would be unstable angina. If it rose above that level before falling, it would be acute myocardial injury due to ischemia, which is, by definition, acute MI. If that is a result of plaque rupture, then it is a type I MI. The clinical presentation would be one of either unstable angina or type I MI, even if no culprit was found on angiography.

See this post for another case of OMI with a negative angiogram, and here are more references:

Inferior hyperacute T-waves and ST elevation. Angiogram is normal. What happened?

Bibliography, with edited abstracts

Article 1

There were 821 cath lab activations and 86% were treated by mechanical revascularization. In 76 patients (8.5%), no coronary artery stenosis was documented. Observations documented angiographically included coronary spasms (6.6%) and muscle bridges (5.3%). During a mean follow-up of 11.2±6.4 months, one patient developed an acute myocardial infarction requiring coronary intervention. All other patients were free of any cardiac event.

Article 2, full text

Of 898 patients who had cath lab activations for primary PCI, normal coronary angiograms were obtained for 26 patients (2.6%). Among these, the diagnosis at discharge was a small myocardial infarction in seven patients (0.7%), acute (peri)myocarditis in five patients, dilated cardiomyopathy in four patients, hypertension with left ventricular hypertrophy in three patients, pulmonary embolism in two patients and misinterpretation of the electrocardiogram (ie, no cardiac disease) in five patients. Seven patients with small infarctions underwent angiography within 30 min to 90 min of complete relief of the signs of acute ischemia, and thus, angiograms during pain were not taken. None of the 898 patients catheterized during ongoing symptoms of ischemia had a normal coronary angiogram. Spontaneous coronary spasm as the only cause (without underlying coronary atherosclerosis) for the evolving infarction was not seen. Thus, the causes of the seven small infarcts in patients with normal angiograms remain uncertain.

Article 3

Characteristics of 690 consecutive patients with presumed STEMI referred for primary PCI. 87 (13%) had angiographically normal coronary arteries and were compared with patients with angiographically shown culprit lesions (control group; n = 594). Nine patients with significant coronary disease, but no identifiable culprit lesion, were excluded. Electrocardiograms (ECGs) from both groups were reviewed by 2 cardiologists blinded to angiographic findings. On expert review of ECGs, 55% of patients in the normal coronaries group had ST-elevation criteria for STEMI (vs 93% in the control group, but the ECG was considered consistent with a diagnosis of STEMI by both observers in only 33% (vs 92% in the control group) Left branch bundle block independently correlated with normal coronary arteries on multivariate analysis (odds ratio for STEMI 0.016). The discharge diagnosis in the normal coronaries group was predominantly pericarditis (n = 72; 83%), but these were not adjudicated by the authors. Other diagnoses were myocarditis in 3 patients (3%), Takotsubo cardiomyopathy in 2 patients (2%), presumed coronary spasm secondary to intravenous drug abuse in 2 patients (2%), cryptogenic AMI in 1 patient (1%), dilated cardiomyopathy in 1 patient (1%), massive pulmonary embolus in 1 patient (1%), cholelithiasis in 1 patient (1%), and pneumonia in 1 patient (1%).

The most likely alternative diagnosis suggested by both observers for the non-AMI ECGs in the normal coronaries group was normal variant ST changes (25% observer 1 and 26% observer 2) and early repolarization abnormality (25% observer 1 and 14% observer 2).

Article 4

The medical records of 941 patients undergoing coronary arteriography for presumed ACS within 48 h of onset were critically reviewed. In 70 patients (7.4%, 35 males) no CAD was documented. Alternative substrates of acute myocardial ischemia included coronary artery anomalies (7 patients, 10%), coronary spasm (10 patients, 14.3%), spontaneous coronary dissection (2 patients, 2.8%), paradoxical embolism through a patent foramen ovale (4 patients, 5.7%), embolism from left atrium or calcified aortic valve (4 patients, 5.7%), imbalance between oxygen demand and supply (20 patients, 28.5%), mitral valve prolapse (11 patients, 15.7%). No alternative substrates were found in 12 patients (17.1%). Absence of CAD is an uncommon finding in patients undergoing coronary artery angiography for ACS.

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5 Cardiologists said this is not a STEMI. But was it an OMI?

August 15, 2019, 12:49 pm

≫ Next: Acute Chest pain in a 50-something, and a "Normal" ECG

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Written by Pendell Meyers

A male in his early 50s presented with waxing and waning chest pain starting at rest. He had multiple cardiovascular risk factors and the EM physician strongly suspected ACS.

Here is his initial ECG:

What do you think?

Sinus rhythm
-STE in V1-V5, possibly a tiny amount in V6, and small amount in I and aVL, and II
-Reciprocal STD (although perhaps isoelectric at J point, immediate STD after the J point) with very ischemic appearance in lead III (down-up T-wave is strongtly suggestive)
-Large T-waves in V2-V4, which may be either a normal variant or hyperacute
-Very tiny Q wave in lead V2, as well as V6, I, and aVL, which is not seen in normal variant
-STEMI criteria are not formally met; although V2 has sufficient STE (greater than 2.0 mm), neither of it's neighbors have enough STE to meet criteria (V1 is close at 0.5 mm of the "required" 1.0 mm)

This is all highly diagnostic of acute anterior MI, with the most likely etiology being OMI of the proximal-mid LAD.

The formulas would be formally contraindicated because of the Q-wave in V2, but if we use them anyway the results are (using QTc 397 ms):

4 Variable formula: 20.32
3 Variable formula: 24.08

Both formulas predict LAD occlusion.

The physician called the on-call cardiologist immediately to discuss this ECG, but the cardiologist reportedly said not to activate the cath lab because he/she was not convinced by the ECG. Over the next few hours, four other general cardiologists "signed off on the initial ECG without recognizing STEMI."

The first troponin I returned elevated at 0.11 ng/mL.

Serial ECGs were obtained, including this one several hours later:

Slightly more STE and longer QT than prior.

Although I do not see much difference between the ECGs, for some reason (perhaps ongoing pain or rising troponins) the case was reevaluated at this time and the decision was made to perform cath.

They found 100% acute mid-LAD Occlusion MI, stented with excellent angiographic result.

Peak troponin I was greater than 75 ng/mL (the assay does not measure higher than this apparently).

Learning Points:

STEMI criteria misses 25-40% of OMI, like this case for example.

Due to our paradigm which lags far behind the current achievable skill level, cases like this will continue to be missed or delayed until we solve the problem by replacing the paradigm.

This is another case demonstrating OMI with all ST segments concave.

Pay attention to even the tiniest Q-waves in the right context and assume they are new until proven otherwise. New Q-waves during MI are NOT wide ("greater than 40 ms") until later.

Any Q-wave in V2 in the presence of an otherwise normal QRS complex is abnormal.

Repeat ECGs are almost always helpful.

Use of the formulas would have improved recognition of this OMI.

Ongoing ischemia (by symptoms, ECG, or troponin) despite maximal medical management is an indication for emergent cath lab activation.

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Comment by KEN GRAUER, MD (8/15/2019):

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

Once again, the wrong question was asked in this case. That's because it should not matter IF the initial ECG in this case ( = ECG #1 in Figure-1) represents an acute STEMI or an acute OMI — since initial management should be the SAME:

Considering that this patient had multiple cardiac risk factors + a good story for ongoing new ischemic-sounding chest pain and, the ECG abnormalities seen in ECG #1 — prompt cath to define the anatomy, with goal of acute reperfusion if acute OMI is confirmed is the treatment of choice.
Unless a prior ECG on this patient can be found that shows identical findings as we see in ECG #1 — there is NO way to rule out acute OMI. As a result — it’s hard to justify not doing acute cath ...

Figure-1: The 2 ECGs in this case (See text).

MY THOUGHTS on ECG #1: Dr. Meyers has skillfully detailed the abnormal ECG findings. To facilitate visualization — I’ve put both tracings together and labeled the following key points:

There is loss of the initial r wave in lead V1 — with development of a small-but-real Q wave in lead V2 of ECG #1. Overall QRS morphology in lead V2 is strange, with this qRS complex being “sandwiched in” between an rS complex in lead V1, and an rS complex in lead V3 — so there may be some lead misplacement of lead V2. That said — the small q in V2 is almost certainly a real finding, and clearly abnormal.
There is more than 2 mm of ST elevation in lead V2 of ECG #1 (Compare the RED horizontal baseline with the RED arrow in this lead). The very wide T wave base, with T wave peak clearly exceeding R wave amplitude in this lead clearly defines the T waves in V2 as being hyperacute.
Disproportionate T wave amplitude (compared to R wave height) in leads V3 and V4 define those T waves as also being hyperacute.
Note that there is more ST elevation in lead V4 of ECG #1, than there is in lead V3 (Compare the RED horizontal baseline with the RED arrow in these leads). There shouldn’t be more ST elevation in V4 than in V3.
Finally (as per Dr. Meyers) — the ST-T wave in lead III is clearly abnormal (curved RED line) — with the scooped ST segment ending in a biphasic (negative-then-positive) T wave.

BOTTOM LINE: Without an identical-looking prior tracing — there is NO way to rule out the possibility (if not probability) of acute ST-T wave findings in at least leads V2-thru-V4 + Q in V2 + reciprocal change in lead III, in this patient with new chest pain. A millimeter definition of acute STEMI should not be needed to justify the need for prompt cardiac catheterization.

NOTE: With proximal LAD OMI — one typically sees: i) significant ST elevation beginning in leads V1,V2; ii) reciprocal ST depression in each of the 3 inferior leads (II,III,aVF); and, iii) significant ST elevation in lead aVL. Because we only partially see these features in ECG #1 — I would interpret this tracing exactly as Dr. Meyers did = probable “proximal-mid acute LAD occlusion”.

MY THOUGHTS on ECG #2: Several hours later — ECG #2 was obtained. As per Dr. Meyers — for the most part, there has been little change between the 2 tracings. That said:

I think there is now more ST elevation in lead V2 of ECG #2 than there was in ECG #1 (Compare the BLUE horizontal baseline with the BLUE arrow in this lead).
Note that there is once again more ST elevation in lead V4 than in lead V3 of ECG #2. This is not a normal finding.

BOTTOM LINE: Given the clinical history — ECG #2 should not have been needed for making the decision to take this patient to the cath lab ...

Our THANKS to Dr. Meyers for this insightful case!

↧

Acute Chest pain in a 50-something, and a "Normal" ECG

August 17, 2019, 11:13 am

≫ Next: Elderly with Paced Rhythm, Possible Ischemic symptoms, and an Equivocal Smith Modified Sgarbossa ECG

≪ Previous: 5 Cardiologists said this is not a STEMI. But was it an OMI?

Chris Mondie of the Newark Beth Israel Emergency Medicine Residency sent this case

A 50-something man presented with acute chest pain.

Here is his ECG:

As you can see, the computer called it completely normal
What do you think?

The computer did not even mention the ST elevation. It could at least say: "ST Elevation, consistent with normal variant," or "consistent with ischemia or normal variant," or "consistent with early repolarization." But it simply says "normal."

An interpretation of "normal" could, of course, deceive many providers.

Analysis

This could be normal variant ST Elevation in V2 and V3. There is 1.5 mm STE in at the J-point in lead V2 (relative to QRS onset, otherwise known as PQ junction). There is 1.0 mm in V3.

So this is a normal amount of STE in V2 and V3, defined by Universal Definition of MI as up to 2.0 mm in men over age 40. So there is definitely no STEMI, and the STE is normal. So the computer is correct in calling it normal.

But after reading this blog, you all know that most OMI do NOT meet STEMI criteria. Some patient's baseline ECG has zero STE. Some patient's baseline has normal variant STE. You don't know which kind of patient this is.

Some normal STE is actually due to OMI. Some normal STE is not due to ischemia at all.

It is your responsibility to determine if STE is ischemic or not.

How do we do so?

Use the formula.

QTc = 385
STE60V3 is at least 4.0 mm, maybe more
RAV4 = 6
QRSV2 = 18

Formula value = 19.94 (very high, indicating LAD occlusion).

Any value greater than 18.2 is likely to be LAD occlusion.

For graphs of sensitivity, specificity, and accuracy at various cutoffs, see this post:

More precise interpretation of the results of the 4-variable formula.

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

Chris Mondie's note:

"My read: Acute proximal LAD occlusion. Hyperacute T waves which tower above the preceding R waves, poor precordial R wave progression. Large T in V1. Smith subtle LAD equation indicative of acute LAD occlusion.

"Bedside echo revealed anteroseptal wall motion abnormality at which point I activated a code STEMI.

"Cardiology agreed to take the pt to the lab but thought it would likely be negative.

"100% proximal LAD successfully stented.

Defibrillated out of v fib in the cath lab.

Initial TnI was negative.

"I thank you for constantly updating your blog and allowing free open access education on EKG interpretation. I recognized this as a STEMI immediately and I was only able to do so solely because of your blog."

↧

Elderly with Paced Rhythm, Possible Ischemic symptoms, and an Equivocal Smith Modified Sgarbossa ECG

August 20, 2019, 7:03 am

≫ Next: Editorial by Meyers and Smith, full text: Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)

≪ Previous: Acute Chest pain in a 50-something, and a "Normal" ECG

An 80 year old presented with a couple days of SOB, weakness, and diaphoresis. There was no chest pain.

Here was her initial ECG:

What do you think?

-There is a paced rhythm.
-There is some concordant ST Elevation (STE) in V5 and V6.
-There is ST depression in V2.
-There is minimal concordant ST depression in V3 (remember there should be, if anything, appropriately discordant ST Elevation).

The treating physician did not think that there was sufficient concordant STE in V5 and V6. He saw the ST depression in V2, but did not see it as concordant or excessively discordant because the R-wave and S-wave were equal.

However, when the QRS is isoelectric in LBBB or paced rhythm, there should be zero ST shift!
Non-ischemic (baseline, normal) ST shift in Paced Rhythm and LBBB is due to Appropriate Discordance. If there is no dominance of the R-wave or S-wave, there cannot be appropriate discordance. Any ST shift in these cases is abnormal (ischemic).

So this is clearly ischemic ST depression.

In addition: While it is true that the concordant ST Elevation in V5 and V6 is not quite 1 mm, any concordant STE is highly suspicious. Moreover, this is in the context of a very low voltage R-wave, so a small amount of concordant STE is much more significant.

This ECG is diagnostic of Occlusion MI (OMI).

The provider did not immediately activate the cath lab.

There were a couple subsequent ECGs before angiogram which show some evolution (worsening)

Increased ST depression in V2

Clinical Course

An initial troponin T returned at 2.1 ng/mL. This is very high for an initial troponin, and nearly diagnostic of OMI by itself, but of Subacute OMI, consistent with this patient's long duration of symptoms.

She did then later go to the cath lab (uncertain how much later) where she went was intubated, and put on a balloon pump.

Circumflex was the culprit, as expected.

The RCA and LAD were also diseased (3-vessel disease).

They decided to do bypass surgery; but would do PCI if surgery considered too high risk.

She then developed cardiogenic shock and returned to the cath lab for PCI of the circumflex.

The doctor wrote:

She had a rocky course with pain and was eventually transitioned to hospice

"I am trying to learn from this case. Looking at it objectively—was a really criteria to activate the lab or was this an NSTEMI. I cannot make up my mind about V5 V6 but I don’t think there are any criteria in the other leads.

"From the catheter report and presentation I also don’t think she has OMI unless I am wrong….."

He is to be greatly commended for sharing this and trying to learn from it.

Comment:

This is a late presentation MI and it is unlikely that earlier treatment would have made a large difference.

Learning Point:

In LBBB and Paced rhythm, if the S-wave and R-wave are of equal amplitude, there should be zero ST shift, since there is no "appropriate discordance." Thus, any ST shift is likely to be ischemia.

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Comment by KEN GRAUER, MD (8/21/2019):

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Excellent example by Dr. Smith of a pacemaker tracing that is diagnostic of recent infarction in a patient with new chest pain. My comments are brief, and offer a slightly different perspective on the superb discussion by Dr. Smith.

For clarity — I’ve put the first 2 tracings in this case together, and have labeled some KEY findings (Figure-1).

Figure-1: The first 2 ECGs done in this case (See text).

MY THOUGHTS on ECG #1: Assessment of pacemaker tracings for acute ST-T wave changes is challenging. I find this even more difficult than ST-T wave assessment with complete LBBB — because of tremendous variability in what a normally paced tracing will look like. Often, it will be difficult (if not impossible) to detect acute MI when all beats are paced. That said, sometimes the SHAPE of the ST-T wave in one or more leads will clearly look abnormal. My preference focuses on identifying such clearly abnormal ST-T wave morphology.

There is an underlying sinus rhythm in ECG #1. Following a PR interval of ~0.20 second — all QRS complexes are paced. For the most part — QRS morphology resembles a LBBB pattern.
There are 3 leads in ECG #1 that manifest ST-T waves that are clearly not normal:
Leads V5 and V6 show coved (convex down) ST segments that appear to be elevated by at least 1 mm (coved RED lines in these leads — with the horizontal RED lines indicating the PR segment baseline). These are primary ST-T wave changes — because the shape and direction of these elevated ST segments is opposite expected ST-T wave morphology in a lateral lead with LBBB-like morphology (ie, the ST-T wave in leads I and aVL show the expected ST-T wave shape in a lateral lead).
Lead V2 also manifests a primary ST-T wave change — because the SHAPE of the depressed ST segment in this lead is clearly abnormal (curved RED line in V2).
Given the definite ST-T wave abnormality of leads V2, V5 and V6 in ECG #1 — we can suspect that the curved and slightly depressed ST segments in neighboring leads V1 and V3 — as well as the ST coving (albeit without any ST elevation) that we see in lead V4 are also abnormal. That said, in isolation (ie, without the definite ST-T wave abnormalities in leads V2, V5 and V6) — I wouldn’t be able to call a recent MI from the subtle abnormalities seen in leads V1, V3 and V4.
I see no acute changes in the limb leads of ECG #1.

It should be noted that this elderly woman presented with a several-day history of dyspnea, weakness and diaphoresis — but no chest pain. As a result — I would have NO idea from the appearance of ECG #1 as to WHEN an event may have occurred ...

Clearly, the above described chest lead ECG changes could be very recent, if not still actively ongoing. On the other hand — an MI could have occurred at the onset of symptoms, or even a few days before that. The patient did not have chest pain — and shortness of breath from MI-induced heart failure sometimes takes a number of days to develop.
Timely cardiac catheterization would help clarify the situation — although from the information given and the appearance of ECG #1 — cardiac cath might not need to be immediate. “Ya gotta be there … “.

MY THOUGHTS on ECG #2: Some time after ECG #1 — and 2nd tracing was done (ECG #2). Details of this case, including when ECG #2 was obtained, and how this 2nd ECG was interpreted are lacking.

The point to emphasize, is that IF decision to perform cardiac catheterization was not made after seeing ECG #1 — it definitely should have been made after ECG #2 was done. The shape and amount of ST depression in lead V2 has dramatically worsened. There is probably also slightly more ST depression in leads V1 and V3 of ECG #2 — but, it is the appearance of lead V2 in ECG #2 that tells us acute OMI is in progress until we prove otherwise.

BOTTOM LINE: Assessment of acute ST-T wave changes is often quite difficult in pacemaker tracings. This case is insightful in illustrating how leads V2, V5 and V6 in ECG #1 should have prompted more rapid recognition of potential acute change.

In my experience — SHAPE of ST-T wave changes is often more important than the amount of ST deviation.

Our THANKS to the clinician who presented this soul-searching case!

↧

Editorial by Meyers and Smith, full text: Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)

August 23, 2019, 8:17 am

≫ Next: An ECG sent to me with concern for hyperacute T-waves

≪ Previous: Elderly with Paced Rhythm, Possible Ischemic symptoms, and an Equivocal Smith Modified Sgarbossa ECG

Read this full text article on the OMI paradigm, from International Journal of Cardiology:

https://authors.elsevier.com/a/1Zbyec5r~MxXk

↧

An ECG sent to me with concern for hyperacute T-waves

August 26, 2019, 3:56 pm

≫ Next: What is the differential of this very unusual ECG?

≪ Previous: Editorial by Meyers and Smith, full text: Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)

Written by Pendell Meyers

A woman in her 70s with diabetes, hypertension, and hyperlipidemia suddenly developed nausea, diaphoresis, and brief syncope while eating at a restaurant. She did not report any chest pain or pressure.

She was brought to the Emergency Department and this ECG was recorded while she was still feeling nauseous but denied chest pain, shortness of breath, or other symptoms:

What do you think? No baseline was available for comparison.

Sinus rhythm
Grossly normal QRS complex
Less than 1mm STE in II, III, and aVF, as well as V4-6, all with extremely upward concavity
aVL has the smallest possible amount of STD in aVL with a shallow negative T-wave
The T-waves in the inferior leads seem to have potentially large amplitude compared to their QRS complexes
STEMI criteria are not met

Although inferior OMI commonly presents with submillimeter STE in the inferior leads with very subtle reciprocal STD and/or T-wave inversion, the morphology of this ECG is not convincing to me. The T-waves have significant amplitude but they are not "fat" enough to be hyperacute. The morphology of STE is not diagnostic of being due to acute transmural ischemia. It is difficult to describe exactly why, but is something that simply comes with time, after following up hundreds of cases to see the ECG progression and patient/angiographic outcomes.

This ECG was texted to me with no clinical information, with the sender being concerned for possible hyperacute T-waves and STE in the inferior leads.

I replied: "I see why you would be worried about hyperacute T-waves, but they just don't look fat enough to be hyperacute. There is definite STE inferior and lateral but it just doesn't look like true positive STE to me. I wouldn't activate the lab for this EKG alone, but if the patient is clinically compatible with ACS you could call a heart alert. I would do echo for WMA, q15 min EKGs - if it's real it will be dynamic and become clear soon. Let me know what happens." If I had known there was no definite chest pain or pressure this would have been slightly more confident.

I later found out that the cath lab was activated soon after arrival.

The patient went emergently to the cath lab, where all coronary arteries were found to be normal.

Note: Normal coronary arteries at the time of cath of course does not rule out the possibility of OMI. There can be OMI at the time of the ECG followed by spontaneous (or medication induced) lysis, such that the artery is open at the time of cath. This can be so brief that even troponins do not significantly rise. Of course that is very rare. But it demonstrates the point that the angiogram alone cannot be used to adjudicate the presence or absence of OMI. The ECG progression, clinical picture, and biomarkers are also involved in the full diagnosis of OMI. The ECG progression in particular is important: True positive OMI findings on ECG must always resolve or evolve. Conversely, an ECG that remains static throughout the entire clinical course means that the ECG findings were not due to OMI (even if OMI was truly present!).

Serial troponins were negative.

Echo showed no wall motion abnormality.

Most importantly, several repeat ECGs were basically unchanged:

This is the ECG the next day. This one likely does meet STEMI criteria in II, III, and aVF. But it is the same morphology as the first ECG. Absolute STE is irrelevant - the fact that the prior ECG did not meet criteria and this one does, is meaningless in my opinion.

Learning Points:

This was an example of a false positive cath lab activation due to ECG findings that were thought to represent OMI.

Learning how to differentiate hyperacute T-waves from normal variants like this is difficult and requires comparing cases like this with our database of true positive hyperacute T-waves. True hyperacute T-waves are tall, fat, wide, symmetric, and by these properties have large area under the curve compared to the size and morphology of the QRS complex.

Take this example: first I'll show you a close up of leads II, III, aVF, and aVL from a true positive inferior hyperacute case. Below you'll see the same leads from this case.

These are fat, symmetric, true positive hyperacute T-waves in III and aVF, with their reciprocal counterpart in aVL. This patient had RCA OMI. From:

A female in her 60s who was lucky to get expert ECG interpretation

This case. False positive, proven by no evolution and no evidence of OMI, negative trops, and normal angiogram.

Use these cases to see more true positive inferior hyperacute T-waves:

You have two hours to save this patient's life

A female in her 60s who was lucky to get expert ECG interpretation

A male in his 50s with chest pain. What is your interpretation?

A male in his 60s with chest pain

A Male in his 60s with Chest pain. What is the ECG Diagnosis?

Inferior hyperacute T-waves and ST elevation. Angiogram is normal. What happened?

The development of an inferior-posterior STEMI, from prehospital to hospital

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

Inferior Hyperacute T-waves

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Comment by KEN GRAUER, MD (8/26/2019):

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

I find this an important case for helping to clarify the semantics surrounding use of the term “hyperacute” when referring to T wave appearance. I fully AGREE with Dr. Meyers astute ECG assessment and management plan for the initial ECG in this case ( = ECG #1 in Figure-1).

That said — I offer a different perspective on the semantics that I favor to describe the ECG findings in this case.

Figure-1: The 2 ECGs shown in this case (See text).

MY THOUGHTS on ECG #1: The most remarkable findings in ECG #1 are seen in the inferior leads. That said, systematic assessment of this tracing reveals a number of additional findings of interest:

There is baseline artifact in several leads. In ECG #1 — this is most marked in leads II, III and aVF. Since electrical derivation of these 3 leads is shared by involvement of the left leg electrode — this is the probable source of this artifact. I’ll emphasize that despite the artifact — this tracing is clearly interpretable. The reason I note the artifact, is that on occasions when artifact does impair interpretation, it may be helpful to recognize from which extremity the artifact arises (Details on this subject are beautifully described in this article by Rowlands and Moore.)
Beyond-the-Core: In contrast, the limb lead artifact in ECG #2 is maximal in leads I, II and aVR, with electrical derivation of these 3 leads shared by involvement of the right arm electrode — which is the probable source of artifact in ECG #2.

Additional findings of interest in ECG #1 include the following:

There are multiple small and narrow Q waves. These are seen in leads I, II, aVL, aVF; and V3-thru-V6. There appears to be a small-but-present initial r wave in lead III. The clinical significance of these Q waves is uncertain — but their presence should be noted because this finding might be relevant if there was ongoing infarction.
There is early transition — because the R wave becomes predominant (ie, taller than the S wave is deep) as early as lead V2. This finding could also be relevant — because posterior infarction is among potential causes of early transition.
Finally — I was struck by how similar the appearance is for QRS complexes and ST-T waves in leads V3-thru-V6 of ECG #1. This made me wonder if there might not be a potential technical mishap in this recording.

I AGREE completely with Dr. Meyers that:

There is <1 mm ST elevation in the inferior and lateral chest leads.
There is ST segment flattening with no more than minimal T wave inversion in lead aVL. Lead aVL does not have the appearance of a true “reciprocal change”.
The T waves in the inferior leads of ECG #1 are each taller-than-expected considering the appearance of the QRS complex in each of these leads.
Criteria for a STEMI are definitely not met in ECG #1.
The T waves in each of the inferior leads in ECG #1 are not as “fat” as the T waves in the true positive example of inferior hyperacute T waves that Dr. Meyers shows above.
Although this 70yo woman with cardiac risk factors did have acute symptoms (ie, nausea, diaphoresis and syncope) — she did not report any chest discomfort! On the whole — her history is not convincing for acute OMI (although we need to remember that not all acute MIs are associated with chest pain).
I would not activate the cath lab on the basis of ECG #1 alone.

Where My Perspective Differs: While the history for this patient is not at all convincing for acute OMI — and, reciprocal changes are lacking — and, chest leads fail to show acute changes — we still have the unescapable finding of T waves that are taller-than-they-should-be in each of the 3 inferior leads. That said:

ECG #1 is not diagnostic of acute OMI.
I would not have activated the cath lab on the basis of ECG #1 alone.
BUT — this patient did present to the ED with new non-chest pain symptoms (including syncope) that could reflect an acute cardiac event.
AND — in my opinion, in the absence of a prior ECG for comparison — we can not rule out the possibility that these might be hyperacute T wave changes in the inferior leads of ECG #1.

Why this is all Symantics: Regardless of how one classifies the T waves in the 3 inferior leads of ECG #1 — optimal management will be similar:

A definitive diagnosis can not be made from ECG #1 alone.
Continued close observation of this patient + frequent serial ECGs + stat Echo in the ED (looking for wall motion abnormality) + serial troponins — will almost certainly yield the correct diagnosis in very short order.

MY THOUGHTS on ECG #2: There is essentially NO change in the appearance of ECG #2 compared to ECG #1. We are told that several other ECGs done after the initial tracing all looked the same.

I find it of interest that both early transition and a similar appearance of the QRS complex and ST-T waves in lateral chest leads persist in ECG #2 done the next day. This makes a technical mishap much less likely — and makes me wonder if an unusual body habitus might account for these findings ...

BOTTOM LINE: Dr. Meyers and I are essentially saying the same thing. Considering this patient presented to the ED with new symptoms (including syncope — albeit without chest pain) — ECG #1 is not a normal tracing.

Regardless of whether or not you classify the inferior T waves in ECG #1 as possibly hyperacute or not — additional testing, including repeat serial ECGs, troponin + stat Echo are all needed to arrive at a more certain diagnosis.
“Ya gotta be there” to make the decision of whether or not to activate the cath lab on the basis of the history and ECG #1. While fully acknowledging that “hindsight is 100% in the retrospectoscope” — for learning purposes, I’ll put forth the thought that repeat ECG, stat Echo and initial troponin could probably have been enough to dissuade the decision to activate the cath lab in this case.

Our THANKS to Dr. Meyers for presenting this case!

↧

What is the differential of this very unusual ECG?

September 2, 2019, 12:18 pm

≫ Next: Do you recognize this ECG yet?

≪ Previous: An ECG sent to me with concern for hyperacute T-waves

Take a look at this ECG first without clinical context:

What do you think?

There is sinus bradycardia with very unusual shortened QT interval (approximately 400 ms), for a QTc (Bazett) 358 ms. The T-waves have high amplitude and narrow bases, reminiscent of hyperkalemia, maybe also with hypercalcemia. The T-waves are not bulky or fat, and are therefore not hyperacute regardless of their amplitude.

Short QTc is rare, but has been described as less than 360 ms for males and less than 370 ms for females. Furthermore, less than 330 ms (males) or less than 340 ms (females) can be termed "very short QTc" and, in the absence of reversible causes, is considered by some to be diagnostic of Short QT Syndrome (SQTS) in an appropriate setting.

Now for the clinical context:

This was a young man with a gunshot wound to the head, who arrived comatose and critically ill. CT scan showed severe brain injury and cerebral edema.

As we have shown on this blog, intracranial hemorrhage can cause various ECG findings, sometimes imitating ischemia, often with bizarre long QT syndromes reminiscent of takotsubo / stress cardiomyopathy. However this is the first time I have seen dramatically shortened QT in this setting. There was no prior for comparison, but this finding would be extremely unlikely to be present on baseline, in the absence of congenital short QT syndrome.

The potassium and calcium levels were within normal limits.

Learning Points:
This ECG in another clinical context should make you consider hyperkalemia and/or hypercalcemia, but would not be consistent with hyperacute T-waves.

ICH / Brain injury can manifest in many bizarre ways on the ECG, usually with long QT with bizarre morphology, but many other findings may be possible. These ECG findings typically correlate with worse outcomes, however most practitioners would say that ECG findings rarely, if ever, add prognostic information beyond standard clinical evaluation in this setting.

Reference:

Viskin S. The QT interval: too long, too short or just right. Heart Rhythm 2009 May;6(5):711-5.

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Comment by KEN GRAUER, MD (9/2/2019):

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Great case by Dr. Meyers about an important ECG entity that is not commonly seen. As I suspect many of those reading this column did — I initially put hyperkalemia at the top of my differential diagnosis list.

That said — these T waves would be among the tallest and “skinniest” I’ve ever seen, if the etiology of this T wave appearance turned out to be hyperkalemia ...

Dr. Meyers highlights that an equally impressive finding as T wave appearance in this tracing is the shortened QTc interval. And, there’s another finding ...

For clarity — I’ve numbered the beats in the long lead V1 rhythm in Figure-1.

QUESTION #1: What is the rhythm in Figure-1?

Figure-1: The ECG shown in this case. What is the rhythm?

ANSWER: The QRS complex is narrow. Although easy to overlook if not carefully measured — the R-R interval in the long lead V1 rhythm strip is not regular. Figure-2 shows the variation in R-R intervals (BLUE numbers indicating R-R interval duration in milliseconds).

Upright P waves with a fixed PR interval precede beats #3,4,5 and 6 (RED arrows in the long lead V1 rhythm strip). Presumably, these are sinus P waves — albeit the P wave is extremely small in amplitude, and the PR interval looks to be relatively short.
We only see 1 QRS complex for lead II. This is beat #1 — which is not preceded by any P wave at all.
I believe the small-amplitude negative “dip” preceding beat #2 in the long lead V1 is artifact. I don’t believe any P wave precedes beat #2.
Beat #7 is cut off — and, the RED question mark, followed by a drop in the PR interval indicates there is artifact. I don’t believe any conclusion can be made about atrial activity for beat #7.
BOTTOM LINE: The longest R-R interval in the long lead V1 is between beats #1 and 2 (Figure-2) — and neither of these 2 beats is preceded by any P wave. Therefore, beats #1 and 2 are junctional escape beats. The underlying rhythm in Figure-1 is marked sinus bradycardia with sinus arrhythmia — and when the sinus rate slows enough, junctional escape beats arise.

Figure-2: I’ve numbered and labeled key parts of Figure-1 (See text).

QUESTION #2: How short is the QTc?

ANSWER: The QTc is determined by taking the longest QT interval that you can confidently measure on the 12-lead ECG — and then correcting this QT interval for heart rate.

With heart rates over 60/minute (if using the Bazett formula) — the QTc will be more than the QT interval that you measure.
With slower heart rates (under 60/minute, if using the Bazett formula) — the QTc will be less than the QT interval that you measure.

Looking at the 12-lead tracing in Figure-2 — I thought the longest QT interval that I could clearly measure was in either lead V2 or V3. I measured 360 ms (thin vertical BLUE lines in V3 showing from where I measured). The R-R intervals both preceding and including this longest measured QT interval correspond to a heart rate of ~43/minute.

MD CALC is a handy link that provides near instant correction of the measured QT according to heart rate — allowing you to calculate the QTc by any of the 4 most commonly used corrective formulas ( = Bazett — Fridericia — Framingham — Hodges).

A measured QT interval of 360 ms = 9 small boxes on ECG grid paper. Plugging in this number into MD CALC for a heart rate of 43/minute yields the following results for the QTc:

Bazett formula QTc = 305 ms.
Fridericia formula QTc = 322 ms.
Framingham formula QTc = 299 ms.
Hodges formula QTc = 330 ms.

Conclusions:

None of the formulas are perfect. Each has its advocates. There is some variation in QTc value determinations — but it’s clear in Figure-2 that the QTc is very short.
Because the heart rate is so slow — the QTc turns out to be significantly less than the longest measured QT interval (which was 360 ms).

QUESTION #3: What is the “Short QT Syndrome” ?

ANSWER: A nice review of Short QT Syndrome (SQTS) appears in Arrhythm Electrophysiol Rev (2014 — by Rudic et al) — CLICK HERE.

As emphasized in this article — SQTS is an inherited cardiac channelopathy determined by the presence of symptoms (syncope, cardiac arrest), positive family history, and the ECG finding of an abnormally short QTc interval.
SQTS is a relatively new diagnosis that has only been recognized as a distinct clinical entity since 2000. The disorder is rare — but its importance is as a potential cause of atrial and ventricular arrhythmias, including cardiac arrest. Treatment is by ICD (implantable cardioverter defibrillator).
Males with a QTc ≤330 ms — and females with a QTc ≤340 ms are defined as having SQTS, even if they are asymptomatic.
Males with a QTc ≤360 ms — and females with a QTc ≤370 ms are said to have a “short” QTc. Such patients may have SQTS if, in addition to the "short" QTc there is a history of cardiac arrest, unexplained syncope or atrial fibrillation at an early age.

QUESTION #4: What are the ECG features of “Short QT Syndrome” ?

ANSWER: A series of gene mutations have been described in association with SQTS (See link to the Rudic article above). By definition — these gene mutations are all associated with a short QTc interval, as defined above in answer to Question #3.

Sometimes, the only ECG abnormality is an overly short QTc interval.
BUT — some patients with SQTS manifest specific ECG patterns. One of these patterns consists of T waves that are tall, peaked, symmetrical and narrow-based with a morphology that is completely consistent with the T waves in Figure-2 (especially the T waves in leads V2, V3 and V4).
U waves are often prominent with SQTS (This is best seen in lead V2 of Figure-2).
Sometimes the ST segment is absent (ie, the QRS complex may seem to immediately follow the T wave). This was not the case in Figure-2 — as a short ST segment is present here.

BOTTOM LINE: This tragic case of a young man critically ill with a gunshot wound to the head provides us with the fascinating ECG shown in Figure-1.

The principal findings of exceedingly tall, peaked and pointed T waves with narrow base + an exceedingly short QTc were not explained by either hyperkalemia or hypercalcemia — as both electrolytes were within the normal range.
CNS catastrophes (as in the case of this comatose patient) — typically present with marked QTc prolongation — and morphologically, with broad T waves that fan out to a broad base. If anything — bradycardia should further prolong the QT. Other than this bradycardia, one would not expect the ECG findings seen here with coma from CNS trauma.
I learned from this case that the T wave morphology seen in Figure-1 is perfectly consistent with one of the ECG patterns of SQTS, in this patient with a markedly shortened QTc.
As per Dr. Meyers (and in the absence of a prior ECG for comparison) — we can strongly suspect that the ECG of this patient incidentally revealed a previously undetected congenital SQTS.
P.S. — It is easy to overlook a short QTc. Don't forget to look for this in patients with syncope, cardiac arrest and/or unexplained arrhythmias.

↧

Do you recognize this ECG yet?

September 8, 2019, 3:47 pm

≫ Next: Chest pain, pelvic and abdominal pain, hypotension, and severe ischemia on the ECG

≪ Previous: What is the differential of this very unusual ECG?

Case contributed by Dr. David Gordon

See if you can recognize this ECG without the clinical context:

Sinus tachycardia
Wide QRS
Terminal R-wave in aVR, V1, and V2 with STE and coved downsloping ST segments
Slightly peaked T-waves, most evident in V5-6

Together, these features make this ECG consistent only with hyperkalemia or another toxic/metabolic abnormality such as Na channel blockade. Sometimes a patient with profound metabolic acidosis may have this pattern as well, generally in the context of profound metabolic intoxication, usually critically ill, with down time, peri-arrest, post-ROSC, etc. V1-V2 morphology would be consistent with Brudaga pattern, but this should generally be more isolated to V1-V3 and would not generally have findings in all leads as we see here.

The differential of the ECG is short, and the most common, most rapidly deadly, and most treatable etiology is hyperkalemia.

Now for some context:

The patient was a male in his 30s with type 1 diabetes presenting with chest pain and RUQ abdominal pain. His fingerstick read "Hi" and he stated he couldn't remember if he took his insulin the night before. Vitals were within normal limits with tachycardia.

The team recognized the ECG as possibly due to hyperkalemia, especially in the clinical context. Labs were not yet back.

They gave 2 gm calcium gluconate, then recorded this ECG:

The QRS is more narrow, however the peaked T-waves and Brugada morphology in V1-V2 persist.

The team administered another 2 gm calcium gluconate.

The initial K returned at 7.3 mEq/L.

After 4 gm calcium gluconate was adminstered, this repeat ECG was obtained:

Resolution of the peaked T-waves, as well as the STE and Brugada pattern in V1-V2.

Three serial troponins were negative. Hyperkalemia and DKA were effectively treated, and the patient did well.

Learning Points:

Hyperkalemia can mimic almost anything on the ECG, including Occlusion MI, Brugada, etc. However, this pattern of STE in V1-V2 is an especially common and notable variant which we have reported many times on this blog:

You MUST recognize this pattern, even if it is not common

Right Bundle Branch Block with ST Elevation in V1?

ST elevation in aVL with reciprocal ST depression in the inferior leads

"Steve, what do you think of this ECG in this Cardiac Arrest Patient?"

A Tragic Case, related to the last post

Calcium in hyperkalemia should be titrated to ECG normalization, and no there is no upper limit when the patient is critically ill or when the ECG shows severe effects of hyperkalemia.

See this article for more information on hyperkalemia

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

Comment by KEN GRAUER, MD (9/9/2019):

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

Our THANKS to Dr. David Gordon — for his contribution of this case! The title of this blog post = “Do You Recognize this ECG Yet?”, is indeed an appropriate one — since recognition of the pattern shown here is clinically essential for emergency providers.

That said — I’ll offer a different perspective on how one might describe the ECG findings in this case, along with differential diagnostic possibilities that this type of ECG pattern should prompt.
For clarity — I’ve lightened the 3 tracings in this case, and show them together in Figure-1.

Figure-1: The 3 sequential ECGs shown in this case (See text).

MY THOUGHTS: Dr. Ed Burns of Life-In-The-Fast-Lane has an excellent review on the ECG features of Sodium-Channel Blockade (CLICK HERE). These ECG features include:

Sinus tachycardia.
QRS prolongation to ≥0.10 second. (I would add that it is especially the terminal portion of the QRS complex that is prolonged with sodium channel blockade.)
RAD (Right Axis Deviation).
Addition of a significant terminal R wave component to the QRS complex in lead aVR (that is usually ≥3 mm in amplitude).

NOTE: The initial ECG in this case ( = ECG #1) illustrates each of these features of Sodium-Channel Blockade:

Sinus tachycardia (seen in ECG #1 at a rate of ~130/minute).
The QRS complex is clearly prolonged. Most of this QRS widening is a result of widening of the last part of the QRS complex.
The frontal plane axis is rightward — as demonstrated by predominant negative component to the QRS complex in lead I.
There is a tall, terminal R wave component in lead aVR.

THEREFORE: As per Drs. Gordon and Meyers — ECG #1 is completely consistent with any toxicity producing Sodium-Channel Blockade (ie, tricyclic antidepressant overdose; proarrhythmia from antiarrhythmics such as flecainide or procainamide — or other agents, as listed by Dr. Burns at the above LITFL link).

Beyond-the-Core: Returning for a moment to ECG #1 — I was not at all certain in my initial assessment of this tracing that there were P waves deforming the terminal portion of the T wave in the inferior leads (BLUE arrows in ECG #1). These deflections were not distinct, and they were not seen everywhere (PURPLE arrow) — so, given QRS widening in ECG #1 without indisputable sign of atrial activity — VT was among my diagnostic considerations for ECG #1.

That said — other features strongly supported the empiric treatment approach taken — and, without much slowing of the rate at all, clear evidence of sinus P waves emerged in the next 2 tracings ( = ECGs #2 and #3) following treatment with Calcium Gluconate (as shown by RED arrows in ECGs #2 and 3).

As per the title of this blog post by Drs. Gordon and Meyers ("Do You Recognize this ECG Yet?" ) — we need to consider (and, depending on the History — we need to assume!) HyperKalemia as the cause of the findings in ECG #1 until we prove otherwise because:

The QRS complex is wide — and this widened QRS does not manifest a typical bundle branch block morphology.
Atrial activity was not clearly seen in ECG #1.
There is T wave peaking in some of the leads!

PEARL #1: By the time hyperkalemia has significantly widened QRS complexes — there will not always be diffuse, “Eiffel-tower-like” T wave peaking. Instead, you might only see slightly-more-pointed-than-expected T wave peaks in no more than a handful of leads (as suggested by the pointed T wave peaks in leads I, V4, V5 and V6 of ECG #1).

PEARL #2: As per Drs. Gordon and Meyers — Sometimes with severe hyperkalemia, more than 1 dose of Calcium Gluconate may need to be given!

QUESTION: How do you know when you need to repeat Calcium Gluconate?

ANSWER: You don’t always know! That said:

If the cause is severe hyperkalemia — the patient may die without more Calcium. So if you suspect this diagnosis — then repeat the Calcium.
The HISTORY often provides an essential clue. (The patient in this case presented with DKA, without any hint in the history of drug overdose or toxicity — and severe acidosis may result in marked increase in extracellular K+.)
And — after giving the 1st dose of Calcium Gluconate in this case — the next ECG done shortly thereafter ( = ECG #2) clearly shows improvement, in the form of: i) Less RAD (the S wave in lead I of ECG #2 is not as negative as it was in ECG #1); and, ii) The QRS is less wide (most noticeable in seeing that the S waves in leads I, V4, V5 and V6 of ECG #2 are not as wide as they were in ECG #1).

MY PERSPECTIVE: There is a Brugada-1 ECG pattern in ECG #1, which if anything — is even more pronounced in leads V1 and V2 of ECG #2.

In my opinion — the ECG appearance of ECG #1 is not hyperkalemia that “looks like a Brugada pattern” — but rather a manifestation of Brugada Phenocopy — in which a Brugada-1 ECG pattern is seen as a result of some other factor. I discuss this distinction in detail in My Comment to the January 30, 2019 Dr. Smith post — and, beginning at 9:17 in my ECG Video on Brugada Syndrome.
If you want more on Brugada — Check out Josep Brugada’s 2018 State-of-the-Art Review on Brugada Syndrome.

NOTE: I fully acknowledge that you might call it “semantics” as to whether ECG manifestations that we see in ECG #1 reflect hyperkalemia vs Brugada Phenocopy caused by hyperkalemia — because in either case, these ECG manifestations resolve once hyperkalemia is treated (Note resolution of QRS widening, RAD, T wave peaking, and Brugada-1 ECG changes in ECG #3!). That said — I feel it important that:

Clinicians appreciate that there is an entity known as Brugada Phenocopy — in which a Brugada-1 ECG pattern identical to that seen in true Brugada Syndrome may be seen as a result of some other cause.
That among the LIST of potential “other causes” of a Brugada-1 ECG pattern are certain DRUGS (calcium channel blockers; ß-blockers; antianginals; psychotropics; ETOH; cocaine; others …) — acute febrile illness — variations in autonomic tone — hypothermia — electrolyte imbalance (hyperkalemia; hypokalemia) — ischemia/infarction — bradycardia — post-cardioversion/defibrillation. There may be others ...
That the entities I just listed should be considered in your differential diagnosis whenever you see a Brugada-1 ECG pattern.
The GOOD NEWS — is that if instead of true Brugada “Syndrome”, the reason for the Brugada-1 ECG pattern in your patient turns out to be Brugada Phenocopy precipitated by one or more of the above causes — and, that IF you find and “fix” the precipitating cause (as was done in this case of hyperkalemia due to DKA) — then longterm prognosis of the patient may not be adversely affected (and an ICD may not be needed, as it would be if true Brugada Syndrome was present)!

↧

Chest pain, pelvic and abdominal pain, hypotension, and severe ischemia on the ECG

September 12, 2019, 4:31 am

≫ Next: Unusual: Troponin Trajectory to Help Determine Ongoing/Recurrent Infarction vs. Completed Infarction.

≪ Previous: Do you recognize this ECG yet?

An elderly male was lethargic at the nursing home and complained of some pelvic pain, but then also chest pain and abdominal pain. He was hypotensive. His medications include beta blockers.

BP on arrival was 66/31, pulse 80, saturations 90% room air. The patient was lethargic and shocky.

An ECG was recorded:

There is severe diffuse ST depression of subendocardial ischemia, with the obligatory reciprocal ST Elevation in aVR.
One might also think there are hyperacute T-waves in inferior leads, with reciprocal STD and T inversion in aVL.

A bedside echo showed good LV function, no pericardial effusion, and normal right ventricle. There were no B lines and the inferior vena cava looked somewhat flat.

Is this Acute Coronary Syndrome? What do you think?

The cath lab had been activated by the time I walked into the critical care area and saw this.

However, I was skeptical that this was ACS. Not all severe ischemia is due to ACS. Shock/Hypotension can be the cause of ischemia or the result of ischemia.

How do we differentiate?

If ACS is the cause, then shock/hypotension is cardiogenic shock. Cardiogenic shock has 3 etiologies:
1. pump failure
2. dysrhythmia (too fast or too slow)
3. valve dysfunction

The rhythm is sinus. The bedside echo showed good pump function. There was no evidence of valve dysfunction on our bedside echo.

Because of the above considerations, I thought ACS was very unlikely. I suspected some other catastrophe as an etiology of hypotension which then caused a decrease in coronary flow and consequent ischemia.

The patient responded to fluids, but also developed pulmonary edema. Although ACS with valve dysfunction must be considered, this was not the etiology. (Among the investigations was an aortic CT which was negative.)

Without going into detail, sepsis was discovered as the etiology of hypotension, which in turn resulted in ischemia. Beta blockers prevented any compensating tachycardia.

In spite of adequate BP, his ECG did not improve by the next AM, but peak troponin I was only 0.200 ng/mL, confirming that acute ACS was not the initiating factor.

Learning Points:

1. When the ECG shows ischemia, it does NOT show the initiating event of the ischemia.
2. If there is good LV function and no dysrhythmia, and no valve dysfunction, then shock is not cardiogenic, and ACS cannot be blamed as the instigating factor.
3. Thus, you need to look elsewhere for the many etiologies of shock. Do not fixate on ACS just because there is severe ischemia.
4. ST Elevation in aVR does NOT mean left main occlusion. Usually it does not even represent ACS.(1)

(1) Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.

How does acute left main occlusion present on the ECG?

↧

Unusual: Troponin Trajectory to Help Determine Ongoing/Recurrent Infarction vs. Completed Infarction.

September 17, 2019, 5:02 pm

≫ Next: Teach your learners: when the QRS is wide, the J-point will hide, so trace it down and copy it over!

≪ Previous: Chest pain, pelvic and abdominal pain, hypotension, and severe ischemia on the ECG

A 40-something male with no PMH of any kind presented to urgent care on a weekend (cath team is at home) with cough starting 2 weeks prior and SOB one week prior.

He underwent a chest x-ray:

As this was consistent with "pulmonary edema vs. viral infection," and he was transferred to the ED

The faculty physician did an immediate cardiac and lung ultrasound:

Many B lines (probable pulmonary edema)

Parasternal short axis cardiac ultrasound:

The anterior wall is closest to the transducer and shows an obvious wall motion abnormality

Further history:

The patient denied chest pain but stated that he had had about 3 episodes of chest pressure, lasting 5 minutes each, in the past week.

The physician was alarmed by these findings and ordered an ECG:

This is diagnostic of Anterior MI, but:

Is this an "old" MI, a completed transmural anterior MI, or is there ongoing myocyte necrosis?

The QS-waves suggest that there is no myocardium left.

The T-waves are taller than one would expect in a completed MI, but the highest T/QRS ratio of V1-V4 is still only about 0.33, close to diagnosing acute STEMI, but not quite (see discussion of ratio below).
A ratio less than 0.36 is still consistent with a subacute STEMI.

Is it old, or is it subacute and ongoing? We usually determine this from ongoing chest pain, but this patient NEVER had chest pain.

The ECG in a true "old anterior MI with persistent ST Elevation," usually associated with an aneurysm, looks like this proven LV aneurysm:

Notice that there is anterior ST Elevation and QS-waves. This could easily be mistaken for a STEMI. The difference is that STEMI has a taller T-wave, at least when it is less than 6 hours after occlusion.

I derived and validated a formula to differentiate anterior LV aneurysm from acute anterior STEMI.

This formula depends on the fact that an acute MI has a tall T-wave and that the T-wave is proportional to the QRS. If any lead from V1-V4 has a T/QRS ratio greater than 0.36, then acute STEMI is most likely, unless the duration of symptoms is greater than 6 hours (as the infarct progresses, the T-wave gets smaller).

So in this case, it is difficult to ascertain symptom duration because the patient never had any pain. However, he has been SOB for a week, so it is likely that the infarct started 1-2 weeks ago.

However, was it:
1) a completed infarct that is now complicated by pulmonary edema? or
2) a small infarct with a lot of viable, but ischemic and stunned (wall motion abnormality) myocardium, or
3) did he have a small infarct and now a recurrent occlusion with impending transmural infarction?

The distinction is critical, as if there is new, recurrent occlusion, then he needs the artery opened NOW in order to save that myocardium. If the myocardium is all dead, then there is no great urgency.

The QS-waves suggest that it is completed, but QS-waves are not definitive.

Usually you can tell by the presence or absence of chest pain whether there is ongoing ischemia or not. But this patient never had and does not have chest pain. His SOB is due to pulmonary edema, which will be there whether there is active ischemia or not, as his ejection fraction is poor either way.

So how can we get some indication of the trajectory?

We decided to check the troponin trajectory. This is not usually an accurate way to assess the current state of the artery, and if the troponin is rising, you will not know whether there is ongoing infarction (rising troponin can be from ongoing necrosis or from release of troponin from already infarcted myocardium).

However, if the troponin is falling, then it is likely that there is no more ongoing infarction.

This is NOT the way to approach a case of acute symptoms, as in these cases, the troponin lags far behind the ECG, and waiting for the initial troponin, or especially for a 2nd troponin, takes too long and will result in unnecessary infarction. For example, the initial troponin is negative in approximately 50% of STEMI cases. While the 2nd is almost always positive, by that time all the damage is done.

The first troponin I returned at 2.53 ng/mL.

Here is the one hour ECG:

Not much changed

The second trop I returned at 2.417 ng/mL. So we decided that angiogram could wait for the next day.

He was treated with IV Nitroglycerin and furosemide.

There might even be some advantage to waiting, other than doing it in work hours:

Occlusions that have organized over days may be difficult to open, difficult to pass the wire.

Some think that heparin therapy for 12-24 hours before angiogram helps in softening the thrombus and thus helps to open the artery (This was conveyed to me by one of our cardiologists. I had never heard it and cannot find any literature on it. If anyone knows, please forward!)

Here is the 5.5 hour EKG:

T-waves are not as tall.
Does this mean that the artery is opening? Possibly, but it is more likely due to improving hemodynamics with nitro and furosemide.

Here is the ECG the next AM:

T-wave are smaller still.
This really looks like an LV aneurysm, though it is really too early to tell whether an aneurysm will form or not.

Troponin profile

Angiogram:

There was indeed a 100% LAD occlusion, and it was very difficult to pass the wire. The interventionalist estimate from the characteristics of the lesion was of a 2 week old thrombus.

↧

Teach your learners: when the QRS is wide, the J-point will hide, so trace it down and copy it over!

September 20, 2019, 7:45 am

≫ Next: A 40-something healthy male with transient chest squeezing

≪ Previous: Unusual: Troponin Trajectory to Help Determine Ongoing/Recurrent Infarction vs. Completed Infarction.

Case submitted by Alexis Cates, written by Pendell Meyers

A middle aged man with history of HTN, DM, and VSD repair at age 6, presented to the ED with chest pain and diaphoresis while exercising.

Here is his initial ECG:

What do you think?

Hopefully this is too easy for most readers, but it it shows a massive, obvious inferoposterior OMI, in the setting of sinus tachycardia with RBBB and LPFB. It may be too easy for you, but there is a very valuable teaching point for you as you spread ECG knowledge to your group, your residents, your learners.

Over the past 3 years I have shown this ECG and many similar ones to many residents and medical students, and it has become apparent to me that there is a very powerful pitfall in beginner ECG interpretation that happens when an abnormal and/or bizarre QRS complex attempts to hide the J-point from the learner. Their mental framework is to find the ST segment and then measure the ST deviation. This framework is obviously very inaccurate for its purpose of identifying Occlusion MI, but at least it provides an approach for the beginner. This is easily doable for the learner in regular QRS complex conduction, but then they encounter an abnormal QRS conduction and things get much more difficult because the classic STEMI paradigm teaching basically only applies to normal QRS complexes. In my medical school curriculum, there was essentially no teaching or understanding of what to do in the STEMI paradigm if the QRS is abnormal, or when the J-point isn't readily obvious, with the one exception of LBBB.

Here are the key take home points in my lecture to first year residents, which of course I first learned here on this blog:

1) "When the QRS is wide, the J-point will hide."

2) "When you aren't sure where the J-point is, your next move is to find it in any lead where you're more sure about it, then trace it down and copy it over."

"Trace it down and copy it over" means you find the J-point in any lead where you are more certain about it, then you trace it down to the rhythm strip to find the J-point on the rhythm strip, and now you can use that point on each QRS complex in the rhythm strip to find the J-point in all 12 leads.

Here is the result in this case:

Massive STE in leads III and aVF, with reciprocal STD in aVL. V2-V5 with clear STD, maximal in V2-4, indicating posterior OMI in addition to inferior. RBBB + LPFB would be concerning by itself for possible LAD occlusion even without clear STE, however would also be a consistent with many of the congenital heart disease surgeries, one of which this patient had at age 6. The morphology of the STE is somewhat unusual (downsloping), with reciprocal upsloping STD, but we have seen this morphology most often in the setting of RBBB + LAFB/LPFB (see this in several of our links at the end).

Another teaching point: New or possibly new RBBB, or RBBB + LAFB/LPFB, in a sick looking ACS patient is a very bad sign which correlates with LAD occlusion. The LAD supplies the bundles, and thus acute LAD OMI may present with new bundle blocks. In my experience the most likely blocks, in order of occurence, are first RBBB, second LAFB, last LPFB. I would be much more worried about a patient with new RBBB + LAFB than a patient with new LBBB (without any of the modified Sgarbossa criteria).

The 2017 ESC Guidelines partially address these issues by stating that left and right BBB are considered equal for recommending urgent angiography in the setting of persistent ischemic symptoms, however one could argue that we have already had the recommendation for years that ANY patient with ongoing ischemia (regardless of QRS, regardless of ischemic findings on ECG) should be considered for emergent angiography.

Back to the case:

The team taking care of this patient was not fooled and immediately understood that this patient likely had Occlusion MI. They activated the cath lab.

The cath report showed:
- severe triple vessel disease
- culprit: 100% ostial, large circumflex with TIMI 0 flow, with successful PCI with restoration of TIMI 2-3 flow
- 100% occlusion of the prox RCA (TIMI 0), believed to be chronic due to L to R collaterals
- 80% mid LAD, also with 99% stenosis after a large, believed to be intramyocardial vessel, probably "second LAD"

Initial troponin I: 9.91 ng/mL

Troponin I 6 hrs after cath: 968.3 ng/mL (enormous MI)

Learning Points:

When the QRS is wide, the J-point will hide

When you can't find the J-point, you first find it in any lead, then trace it down and copy it over.

Use this case and the following ones to train yourself and teach your learners:

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

68 minutes with chest compressions, full recovery. Plus recommendations from a 5-member panel on cardiac arrest.

Giant R-waves. What are they?

"Shark Fin": A Deadly ECG Sign that you Must Know!

↧

A 40-something healthy male with transient chest squeezing

September 22, 2019, 6:02 am

≫ Next: A 50-something woman with chest pain, BP 230/120, and LBBB with 7 mm ST Elevation

≪ Previous: Teach your learners: when the QRS is wide, the J-point will hide, so trace it down and copy it over!

A 40-something man with Hx of treated HTN had chest "squeezing," with SOB and diaphoresis, 10 hours prior to presentation. It lasted 5 minutes then resolved. There was an exertional component. Then, 1 hour before arrival, it recurred, again lasting 5 minutes. His 3rd and last episode was worse, had radiation to both arms, and was 10/10.

911 was called and this prehospital ECG was recorded at time zero:

Limb leads:

Note the artifact that is simultaneously recorded in all limb leads. This was mistaken by the treating physicians for ST depression initially.

Precordial leads:

What do you think?

This is diagnostic of LAD OMI. There is STE that does not meet STEMI criteria in V1-V6. There are normal size T-waves in V1-V3, but these T-waves are enormous relative to the QRS amplitude. These are hyperacute T-waves. Moreover, any time there is ST Elevation of any amount, it must be explained: is it normal STE? Or ischemic?

One sign that eliminates the possibility of normal STE is "Terminal QRS distortion." That is the absence of both an S-wave and a J-wave in EITHER V2 or V3. Here there is no S-wave in V3 and also no J-wave. This is diagnostic of ischemic STE and of LAD OMI.

See these previous posts on Terminal QRS distortion:

Paper published: Terminal QRS distortion not found in any ECG of Early Repolarization

Best Explanation of Terminal QRS Distortion in Diagnosis of Electrocardiographically Subtle LAD Occlusion

An intoxicated, agitated, 20-something with chest pain

Incredible case of evolution of terminal QRS distortion, then resolution after thrombolytics

4 Cases Discussing Terminal QRS Distortion in Diagnosis of Anterior MI

Case continued:

The patient received a sublingual NTG and his pain resolved (is this a result of NTG? Or coincidental? -- unknown).

This pain free ECG was recorded:

All STE is resolved.
The S-wave in V3 is restored!
The artery has reperfused
If you didn't believe it before, then this dynamic ECG proves it.

He had multiple subsequent prehospital ECGs, all identical to the last one and all pain free.

He received an aspirin.

On arrival, this was recorded:

Normal

Cardiology was consulted and they did not want to take the patient to the cath lab emergently.

Heparin was given.

A POCUS cardiac showed no WMA.

First troponin was 0.042 ng/mL (elevated above 99th %-ile URL of 0.030 ng/mL).

1.5 hours later, this ECG was recorded:

Still normal

Several more were recorded, with no change.

This was recorded at 8 hours:

There is the beginning of terminal T-wave inversion in V2.
This is Wellens' syndrome, but, in Wellens', you don't always get an ECG recorded during pain as we do here. This shows that a patient with Wellens' had OMI at the time of their pain and that the T-wave inversion of Wellens' is due to spontaneous reperfusion of an OMI.

This was recorded the next AM:

Evolution of Wellens', with more widespread and deeper T-wave inversion.

See this:

Classic Evolution of Wellens' T-waves over 26 hours

And a bit of further evolution here.

Troponin profile

The patient underwent angiography and had a 90% thrombotic proximal LAD lesion that was stented.

Here is his formal echo report:

Normal left ventricular size, mildly increased concentric left ventricular wall thickness and normal systolic function.

The estimated left ventricular ejection fraction is 61 %.

There is no left ventricular wall motion abnormality (WMA) identified.

This patient's ischemia was so brief that it did not cause any myocardial stunning. It is common to have a persistent WMA after resolution of ischemia (thus, the ECG is a better indicator of instantaneous ischemia than echo), but we see here that a normal echo does not rule out transient STEMI/OMI.

↧

A 50-something woman with chest pain, BP 230/120, and LBBB with 7 mm ST Elevation

September 25, 2019, 1:11 pm

≫ Next: Chest pain with NonDiagnostic ECG but Diagnostic CT Scan

≪ Previous: A 40-something healthy male with transient chest squeezing

A 50-something woman with history of CHF of unknown etiology, and of HTN, presented for evaluation of chest pressure.

Her BP was 223/125, Sp02 98% on RA. HR 106, RR 18.

Here was her ED ECG:

There is sinus rhythm with Left Bundle Branch Block (LBBB)
There is a large amount of ST Elevation in V2 and V3 (more than 5 mm)
Thus, this meets the unweighted Sgarbossa Criteria of 5 mm of discordant ST Elevation
But it does NOT meet the Smith Modified Sgarbossa Criteria, which depend on the ST/S ratio.

This ratio is critical because LBBB with very large depolarization voltage (QRS) also has very large repolarization voltage (ST/T).

Here the highest ratio is 6-7/60, which is 10-11%, which is normal

There is no concordant STE or concordant STD in V1-V3

The patient was given NTG with improvement of pain.

This was recorded 3.5 hours later.

There is no evolution

A bedside echo showed good function, concentric LVH, and no wall motion abnormality could be seen.

Her first troponin was elevated at 0.217 ng/mL, but this does not absolutely differentiate between acute and chronic myocardial injury.

Patients with heart failure and cardiomyopathy frequently have elevated troponins from chronic injury, but not usually this high.

Acute MI is a subcategory of acute injury (Injury caused by ischemia).

Type I MI is acute MI caused by plaque rupture, whereas Type II MI is caused by supply/demand mismatch or endothelial dysfunction and a few other entities.

By far most likely this will be acute MI, but it is very uncertain whether it is Type I or Type II. Severe hypertension with LVH causes increased demand (pumping against high pressure) and decreased supply (massive LVH constricting blood flow in arteries that perforate into the myocardium).

Here is the troponin profile:

Earliest on top

Now we can see a rise and fall of Troponin. A rise and/or fall is necessary to diagnose acute myocardial injury (vs. chronic myocardial injury, which has relatively stable troponins

A Nitro Drip was started, as was heparin (in case this might be a type I MI).

Cardiology did not think it was type I.

They did a Sestamibi stress test:

1. Normal perfusion study with a high degree of certainty.
2. There was no evidence of relative ischemia during regadenason-induced
hyperemia.
3. Left ventricular size was normal with pharmacologic stress while the
ejection fraction was 56%.
4. There were no regional wall motion abnormalities.
6. The patient did not experience anginal symptoms.
7. Stress EKG was uninterpretable for ischemia due to baseline left
bundle-branch block.
8. No prior studies available for comparison.

The echocardiogram showed:

Normal left ventricular size, moderate to severe concentric left ventricular hypertrophy and normal systolic function.

The estimated left ventricular ejection fraction is 61 %.

There is no left ventricular wall motion abnormality identified.

2 days later:

No change, proving that this is the baseline ECG.

Learning Points:

1. This is a baseline ECG with LBBB and huge but proportional discordant ST Elevation.
2. Myocardial infarction may be present without plaque rupture. This is called type II (or type 2) MI and may be due to severe hypertension or other causes of poor supply (anemia, hypotension, thick ventricle) or excessive demand (tachycardia, hypertension).

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Chest pain with NonDiagnostic ECG but Diagnostic CT Scan

September 27, 2019, 9:43 am

≫ Next: A man in his 70s with chest pain during a bike ride

≪ Previous: A 50-something woman with chest pain, BP 230/120, and LBBB with 7 mm ST Elevation

An elderly woman presented with chest pain that radiated to the back for several hours.

Here is here initial ECG:

There is only a nonspecific flat T-wave in aVL. It is essentially normal.

The first troponin returned at 0.099 ng/mL (elevated, consistent with Non-Occlusion MI)

Providers were concerned with aortic dissection, so they order a chest aorta CT.

This showed no dissection but did show the following:

Notice the area of the lateral wall (lower right) that has no contrast enhancement
(It is dark, where areas of enhancement are light-colored).
This transmural ischemia, but not necessarily completed infarction (yet).

A slice at a slightly different level:

Again, an area with absence of contrast enhancement (dark-, not light-colored).

These were read by our fantastic chief of radiology, Gopal Punjabi, who has his own blog on Spectral CT: https://www.ctspectral.com/

With continued symptoms, an elevated troponin, and no other explanation, this is acute MI with ongoing ischemia until proven otherwise.

The CT scan confirms no other explanation and also confirms that this is acute Transmural ischemia diagnostic of OMI (Occlusion MI).

If the patient were no longer symptomatic, one could conclude that the infarct is completed, and emergent angiogram +/- PCI would not be necessary.

The cardiologists did not want to go to the cath lab.

She had subsequent ECGs:

First at 1.5 hours:

This possibly shows some inferior STD, but probably it is baseline wander.

This one at 5.5 hours:

No significant change

She was admitted on a Nitro drip.

Her troponins went like this:
0.099 ng/mL
1.250
3.712
6.073
8.092
12.170
15.680
21.051
23.159 (this is not a small MI)

Next day echo:

The estimated left ventricular ejection fraction is 60%.

Regional wall motion abnormality-inferolateral

Angiogram:

Culprit for NSTEMI is thrombotic occlusion of small-medium caliber OM1. It was stented.

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A man in his 70s with chest pain during a bike ride

September 30, 2019, 12:40 pm

≫ Next: Look at this ST Depression

≪ Previous: Chest pain with NonDiagnostic ECG but Diagnostic CT Scan

Case written and submitted by Ryan Barnicle MD, with edits by Pendell Meyers

While vacationing on one of the islands off the northeast coast, a healthy 70ish year old male presented to the island health center for an evaluation of chest pain. The chest pain started about one hour prior to arrival while bike riding. It was a constant ache on the left side of his chest that forced him to stop cycling and call for an ambulance. It was radiating to his bilateral upper arms. It was associated with nausea but he denied dyspnea, dizziness, and headache.

He explained that he had the same chest pain the day prior as well, on and off. That episode started while climbing a long set of stairs from the beach to the parking lot. His pain radiated to his shoulders throughout the evening and the night but it did not prompt him to seek medical attention.

The patient stated he had a long history of well-controlled hypertension for which he was compliant with his ACE-inhibitor. He was also treated for erectile dysfunction but had not taken any medications recently. He had no prior MI and recalls a “negative” stress test in the recent years.

His vital signs on arrival were HR 77, BP 148/95, RR 16, SpO2 95%. He was in obvious discomfort.

Below was his first ECG, obtained within minutes of arrival.

What do you think?

Meyers comment: Ryan texted me this ECG with no information and my response was "Tough one. I'm worried about inferior posterior OMI but not convinced yet. Would get serial ECGs to help. Is there active pain at the time of this? Tell me more."

I later sent this same ECG without any context to Dr. Smith who replied: "Super subtle inferior OMI, and posterior. Great case."

First, you will likely notice the small amount of ST depression in V2-V6, seemingly maximal in V3-V4. It is even more subtle in I and aVL. The morphology in V2 is also concerning and it appears that the ST segment is being pushed down, as in ST depression. In lead III there is the tiniest possible amount of STE which is difficult to measure due to the very low-voltage. These findings are concerning for inferior wall ischemia with possible posterior wall involvement.

Repeat ECG minutes later (one shown below) showed no significant change.

No significant changes, ongoing pain.

Fortunately, we were able to obtain a copy of his only known prior ECG from his cardiologist (from another state) via facsimile remarkably fast. It was from four years prior.

All the noted abnormalities are proven new in comparison. At baseline, the patient has some expected, normal STE in lead V2, further demonstrating that the STD morphology in the presentation ECG above is "true" and diagnostic.

You will note that it is essentially an unremarkable electrocardiogram except for some PACS. This raised our concerns that the findings on his initial one were real. At the same time, his point-of-care labs came back and were most notable for a cardiac Troponin-I of 8.7 ng/mL.

The case was discussed with the cardiology fellow at the nearest tertiary care center and arrangements were made to fly the patient via HEMS. He was expected to arrive at the tertiary care center within 60 minutes of the call. He was loaded with aspirin, ticagrelor, and heparin. No arrhythmias occurred en route.

The patient’s ECG on arrival at the emergency department is shown below. Note the slightly more obvious ST elevation in III with more distinct ischemic morphology.

His initial cTnI at the receiving hospital was 27 ng/mL, and no further troponins were measured thereafter. He was taken emergently to the cardiac catheterization lab and found to have multi-vessel coronary artery disease with a near-occlusive culprit lesion in the RCA, possibly reperfused. Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent.

In the available view, the RCA appears fully occluded.

To our knowledge, the patient did well. Unfortunately there is no echocardiogram accessible because the patient checked himself out of the hospital in order to get back to his home state before it could be completed. No further follow up information is available.

Learning Points:

Everything is proportional. A very small QRS complex can only mount a very small amount of STE. This patient had a full RCA occlusion with the smallest visible STE.

Baseline and serial ECGs make you much more likely to identify OMI.

Using the STEMI paradigm would have resulted in significant delays for this patient, which correspond with the doubled mortality and morbidity of NSTEMI Occlusions seen in over 50,000 subjects in NSTEMI trials.

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MY Comment, by KEN GRAUER, MD (9/30/2019):

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Our THANKS to Dr. Ryan Barnicle for sharing this case — with excellent commentary on the key features by Dr. Meyers. ECG findings in this case are subtle — and worthy of repetition. To this, I’ll add a few additional points — with focus on the 1st and 3rd ECGs shown above in this case.

For clarity — I’ve put these 2 tracings together in Figure-1.

Figure-1: The initial ED ECG ( = ECG #1) — with comparison to the patient’s baseline ECG done 4 years earlier ( = ECG #3).

MY THOUGHTS: It is precisely because ECG findings are subtle — that we need to pay special attention to the details in this case:

The History states that this patient presented to medical attention for “evaluation of chest pain”— and that these symptoms had begun ~1 hour prior to being seen. BUT — the history also states that he had the same chest pain the day before. Duration of symptoms for at least 24 hours may account for the finding of ECG changes that did not look overly acute.

When confronted with subtle ECG changes that almost make me question IF they are real — I like to: i) Look for 1 or 2 leads that I KNOW are abnormal; and then, ii) See HOW MANY leads I can find that also show subtle abnormalities. In a patient with worrisome chest pain — the more leads that manifest abnormal findings, even if subtle — the more likely these findings are real.

The ECG finding that I KNOW is real in ECG #1 is the mirror-image appearance of ST-T waves in leads III and aVL. We have often referred to this almost magical mirror-image relationship for ST-T waves in leads III and aVL — which when present, means acute inferior OMI until you prove otherwise (See My Comment on the 8/9/2018 SSmith Blog Post). While ST elevation is minimal (barely perceptible) in lead III of ECG #1 — a mirror-image reflection of the coved (“frowny”-configuration) ST segment in lead III is seen in lead aVL. When you invert the scooped ST segment in lead aVL (as I have done in the magnification placed just above lead III in ECG #1) — Doesn’t this coved ST segment shape now look virtually the same as the ST coving that we see in lead III?
In support that the ST coving in lead III of ECG #1 is real — Don’t we see this same coved shape in lead aVF?
The other high-lateral lead ( = lead I) — also shows slight-but-real ST segment flattening and depression (0.5 mm).
Dr. Meyers highlighted the slight-but-real J-point ST depression in leads V2-thru-V6. Even before the prior ECG ( = ECG #3) was found — the point to emphasize is that the J-point in these chest leads looks like it is slightly depressed below the PR segment baseline, even though the amount of this depression is minimal.
Putting This All Together — In this patient with worrisome chest pain, we have in ECG #1 mirror-image ST-T wave changes in leads III and aVL + subtle-but-real ST-T wave abnormalities in no less than 9 of the 12 leads (ie, leads I, III, aVL, aVF and V2-thru-V6). Add in the fact that symptoms began at least 24 hours ago — and these subtle-but-real ECG findings suggest a recent event until we can prove otherwise.
Availability of this patient’s baseline ECG (done 4 years earlier) — added support that findings in ECG #1 are new. As per Dr. Meyers — the scooped ST segment in lead V2 of ECG #3 was clearly higher than in ECG #1 — and, the J-point in leads V3-thru-V6 of ECG #3 was not depressed. The magical reciprocal relationship for ST-T waves in leads III and aVL was also not seen in the baseline ECG.
Beyond-the-Core: Did you notice that the R wave becomes predominant in lead V3 of ECG #1 — whereas transition did not occur until later in the patient’s baseline tracing. Early transition (with a predominant R wave by lead V3) could be another sign of posterior infarction in this patient.

QUESTION: What Was the Rhythm in ECG #3?

HINT: If you said either sinus or sinus with PACs — Take another look!

ANSWER: Doesn’t P wave size and morphology, as well as the PR interval and the R-R interval change with almost every beat in the long lead II rhythm strip? P waves preceding beats #1, 3, and 4 are notched — the P wave preceding beat #6 is tiny — P waves preceding beats #8 and 9 are peaked — and P wave amplitude is not constant for the other rounded, upright P waves. I never see 2 P waves in a row with the same morphology. Given minimal artifact on this tracing — I believe this variation in P wave morphology is real!

BOTTOM LINE: This is not a sinus rhythm. It is also not a wandering pacemaker — because change in atrial pacing site is gradual with that disorder. Instead, given the change in P wave morphology and PR interval from one-beat-to-the-next — this would suggest MAT (Multifocal Atrial Tachycardia) — except that the rate is clearly not tachycardic!
Some cardiac rhythms do not read the textbook! Having observed this phenomenon over many years — I’ve noticed that rather than black-or-white classifications for rhythms such as wandering pacemaker; sinus with many PACs; and MAT — that there is a spectrum for these rhythm disorders. (CLICK HERE — for my detailed discussion of this subject).
Clinically — the rhythm we see in the long lead II of ECG #3 behaves similar to MAT, even though there is no tachycardia. A majority of patients with MAT have longstanding pulmonary disease. Rather than antiarrhythmic medication — optimizing pulmonary function is the best treatment approach. Beyond-the-Core: There are a number of findings on ECG #3 consistent with pulmonary disease (ie, an incomplete RBBB pattern; relatively low voltage in the limb leads; numerous S waves [ie, in leads I,II,III and in all chest leads]). The rhythm we see in the long lead II is not a common one. Therefore — I’d like to know if this patient had pulmonary problems, a smoking history, or some other significant systemic disorder at the time ECG #3 was obtained ...
PEARL: Over the 3+ decades that I've been teaching ECG interpretation — the most common error I've observed even experienced interpreters to make — is to overlook a non-sinus rhythm. The temptation is great to assume sinus rhythm, and jump to the "interesting" findings on the tracing. Guaranteed, it will take no more than 3 seconds for your "educated eye" to begin the interpretation of each and every ECG you are given with a QUICK SCAN of the long lead II rhythm strip under the 12-lead — in order to assess IF each QRS complex is preceded by an upright P wave with a constant PR interval. IF it isn't — then a simple sinus rhythm is not present ...

Our THANKS to Drs. Barnicle and Meyers for presenting this case!

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