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

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!

Chest pain with NonDiagnostic ECG but Diagnostic CT Scan

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/    https://twitter.com/CtSpectral

Here is the image using Spectral CT:

It is much more obvious with this technique!

See more images of this case at Gopal's Spectral CT Blog:

It's all about confidence

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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MY Comment by KEN GRAUER, MD (9/27/2019):

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As suggested by the title of this Blog post — confirmation of the diagnosis in this case was made not by ECG — but instead by chest aorta CT! That said — there are some Observations that should be made about the first 2 ECGs in this case.

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

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

OBSERVATION #1 — This case describes a high-prevalence situation — because the patient is an elderly woman with new-onset chest pain of several hours’ duration. Once dissecting aneurysm was ruled out by chest aorta CT — the possibility of acute ischemic heart disease becomes paramount.

• Given this History — our scrutiny for detecting ECG abnormalities is heightened. The onus falls on us to prove questionable ECG findings are not acute — rather than the other way around.

OBSERVATION #2 — While not diagnostic — the initial ECG in the ED ( = ECG #1) is not normal (Figure-1). Descriptive Analysis of ECG #1 reveals that the rhythm is sinus @ 80-85/minute — all intervals are normal — small septal q waves are seen in leads V4-6 — and transition (where the R wave becomes taller than the S wave is deep) occurs normally between leads V2-to-V3. Findings to note on ECG #1 include the following:

• There is some baseline artifact. Given that artifactual baseline undulations are largest in leads II, III and aVF — the left leg is most likely the source of this artifact. This artifact was no longer seen in the next 2 tracings. NOTE — While the amount of artifact in ECG #1 is small (ie, not enough to prevent accurate interpretation of this tracing) — knowing how to quickly determine which extremity is the cause of the artifact (due to tremor, a faulty lead connection/inadequate skin contact, etc) is helpful, because this may expedite correction, which may be important when artifact does impede interpretation. (BONUS — The 3 page article by Rowlands and Moore that I’ve posted in Figures-2, 3 and 4 below is the BEST description I’ve seen of how to quickly determine which extremity is the source of the Artifact).
• Returning to ECG #1 — There is probably some type of misplacement of lead V2 (perhaps due to body habitus of this elderly woman — perhaps due to placement of the V2 electrode too high on the chest). It just doesn’t make good physiologic sense for there to be an rSr’ only in lead V2, and not in V1. That said, given nearly identical QRS morphology in all leads for the 3 tracings shown in this case — this technical point does not affect assessment or management in this case.
• The T waves in leads V2 and V3 in ECG #1 look disproportionately tall and peaked compared to R wave amplitude in these respective leads. One reason this abnormal T wave morphology stood out to me — is that the ST segments prior to onset of T wave ascent are relatively flat. Whether this T wave appearance in leads V2 and V3 of ECG #1 is a benign longstanding finding — or — whether it might represent either hyperacute T waves and/or reperfusion changes in this elderly woman with new chest pain of several hours’ duration is (in my opinion) not known from assessment of this single ECG.
• There clearly is voltage for LVH in ECG #1 (ie, R wave amplitude in lead V5 ~25mm — CLICK HERE for Review of Criteria for ECG Diagnosis of LVH). The next bullet tells why recognition of voltage for LVH is relevant in this case.
• What does this patient’s baseline ECG show? Was there LVH with an ST-T wave repolarization abnormality (ie, with LV “strain” ?) on the baseline ECG? IF so — then perhaps the ST segment flattening in V5,V6 with relatively small T wave amplitude in lead V6 represents the combination of baseline LV “strain” (ie, ST-T wave depression) + hyperacute T waves that result in an “intermediate pattern” that might not look acute in the lateral chest leads of ECG #1.

BOTTOM LINE: In my opinion, at the point that we saw ECG #1 in this case about this elderly woman with new chest pain of several hours’ duration — it would be impossible to rule out acute changes on the basis of this single initial ECG.

• Finding a prior ECG on this patient could be invaluable! Otherwise — more information will be needed (ie, serial ECGs, troponin, Echo, etc.) before we'll be able to tell if the findings I describe above might be acute ...

OBSERVATION #3 — Compared to ECG #1 — the 2nd ECG (obtained 1.5 hours later) in this case ( = ECG #2) — does show a change that should be noted and which may be relevant (Figure-1).

• Isn’t T wave amplitude in both leads V2 and V3 of ECG #2 proportionately taller than it was in ECG #1, compared to R wave amplitude in these respective leads? That is — the T wave in lead V2 of ECG #2 measures 5 mm tall, whereas it was only 3 mm tall in ECG #1. In lead V3 — the T wave in ECG #2 is clearly taller than the R wave in this lead — whereas in ECG #1 — the T wave in lead V3 was clearly not as tall as the R wave in this lead. BOTTOM LINE: From comparison of ECG #1 with ECG #2 — I do not know how to rule out the possibility that T waves in leads V2 and V3 have become more hyperacute in ECG #2.

CONCLUSION of this Case: The 3rd ECG (done at 5.5 hours) did not show significant change compared to ECG #2 — so at this point, it had become apparent that this patient’s serial ECGs were not acutely evolving. And, as noted in detail by Dr. Smith — serial troponins had become markedly positive — the chest aorta CT showed regional contrast enhancement abnormality — and, Echo the next day confirmed regional wall abnormality. Therefore — the ECG findings I point out above were not needed in this case for diagnosis. That said, in the interest of optimizing ECG interpretation ability:

• Please take another look at the tracings in Figure-1 if you did not initially note the findings I described above. While it turned out in this case that serial ECGs did not evolve — this could not have been known from assessment of only those first 2 ECGs!
• Keep in mind that finding a prior ECG on your patient can sometimes prove invaluable! I wish a prior ECG on this patient was available! IF a prior ECG had been available — it is possible that recognition of an acute cardiac event could have been accomplished much earlier (ie, as early as the moment ECG #1 was recorded)!
• As should be apparent from the unique clinical correlations routinely provided on Dr. Smith’s ECG Blog — the BEST way to continue honing your ECG interpretation skills — is to GO BACK and review tracings in each case after the definitive diagnosis is revealed. In this particular case, the most important teaching point to me — is to appreciate that we can not be certain the ECG findings I describe above for ECG #1 are not acute on the basis of this single initial ECG. It was not until time had passed and the 3rd ECG recorded at 5.5 hours was obtained, that lack of serial ECG evolution became evident ...

Our THANKS to Dr. Smith for this illustrative case!

BONUS — The 3 Figures below reproduce the article by Rowlands and Moore for determining the source of artifact when a single limb lead is responsible. 

• Knowing which extremity is at fault is helpful for expediting correction (ie, from a faulty lead connection/inadequate skin contact, etc.).

Figure-2: Page 475 from Rowlands — Determining the extremity responsible for Artifact (See text).

Figure-3: Page 476 from Rowlands — Determining the extremity responsible for Artifact (See text).

Figure-4: Page 477 from Rowlands — Determining the extremity responsible for Artifact (See text).

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

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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Comment by KEN GRAUER, MD (9/25/2019):

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Providers sometimes overlook the concept of proportionality when assessing the amount of ST segment elevation. As emphasized by Dr. Smith above — the Smith-Modified-Sgarbossa Criteria for assessing ST elevation in the presence of LBBB tells us that despite 7mm of ST elevation in the initial ECG of this case — this is not abnormal given dramatic depth of anterior S waves.

I focus My Comment on 3 additional Take-Home Points regarding the initial ECG in this case.

• For clarity — I’ve put this initial ECG from the ED ( = ECG #1) — together with the 3rd ECG, done 2 days later ( = ECG #3) in Figure-1.

Figure-1: The initial ED ECG in this case, and ECG #3 done 2 days later (See text).

POINT #1 — Don’t forget about half-standardization.

• Although obvious that anterior S waves in ECG #1 are HUGE — it is exceedingly difficult to accurately measure S wave amplitude. This is because of marked overlap of QRS complexes in leads V1, V2, V3, and in that portion of the long lead II rhythm strip that lies directly below these 3 anterior leads. Immediately repeating the recording of this ECG at half-standardization could simplify measurement — allowing instant clarification of the relative amount of J-point ST elevation with respect to S wave depth, as is needed for application of Smith-Modified Sgarbossa Criteria.

POINT #2 — Despite the presence of complete LBBB — we can call LVH on these ECG tracings! Echocardiography is clearly superior to ECG for assessment of ventricular wall thickening and chamber enlargement. That said, a major focus of this ECG Blog — is to optimize clinical ECG interpretation. Because complete LBBB changes the sequence of ventricular depolarization — the usual voltage criteria for ECG determination of LVH are altered in the presence of this conduction defect. However — there are other ECG criteria that have high correlation for LVH when there is LBBB.

• IF S waves in one or more of the anterior leads (ie, leads V1, V2 V3) are very deep (ie, >25-30mm) in a patient with LBBB — this greatly increases the likelihood of LVH. All 3 of the anterior leads in ECG #1 easily surpass this threshold!
• The QRS complex in ECG #1 is extremely wide (I measure ≥0.16 second in some leads). Although I’m not aware of data directly correlating QRS width on ECG to degree of LVH — excessive QRS widening as seen here in this patient with such dramatic anterior S wave amplitude clearly suggests more significant underlying structural abnormality.
• Finally — is the matter of statistics. Unlike complete RBBB — complete LBBB virtually never occurs in the absence of underlying heart disease — and, most patients with complete LBBB will also have LVH. Considering this patient’s age, her history of HF (Heart Failure) and longstanding hypertension — and her presenting BP = 223/125 — it would seem almost certain that this patient must have LVH even before you saw her ECG. Now when we add in the excessive anterior S wave depth described above — all doubt should be removed.

POINT #3 — There is RAA (Right Atrial Abnormality) — and — the size of these enlarged P waves decreases as this patient’s clinical condition improves!

• Atrial abnormality is diagnosed independent of QRS amplitude. The finding of tall, peaked and pointed P waves in the “pulmonary leads” (ie, inferior leads) that look “uncomfortable to sit on” and, which achieve a P wave amplitude of ≥2.5 mm satisfy criteria for RAA. The 4 mm P wave amplitude that we see in lead II of ECG #1 is huge!
• NOTE: For those wanting a user-friendly review on ECG Diagnosis of Right & Left Atrial Abnormality — CLICK HERE.
• Finally — It has been my observation over the years that P wave amplitude sometimes varies from one day-to-the-next due to fluctuations in intravascular volume and/or intracardiac pressures. I found it especially interesting in this case to see progressive decrease in P wave size in lead II as this patient’s clinical condition improved (See P wave size in lead II of ECG #3).

Our THANKS again to Dr. Smith for this interesting case!