Saturday, February 16, 2019

How much time are you willing to wait for OMI to become STEMI (if it ever does)?

Written by Pendell Meyers, few edits by Smith

A man in his 60s with history of stroke and hypertension but no known heart disease presented with chest pain that started on the morning of presentation at around 8am.

Here is his triage ECG when he presented at 1657:
What do you think?

There is sinus rhythm with normal QRS complex and ST depression in V2-V5, maximal in V3-V4. There is no ST depression in V6, II, III, or aVF, and no significant ST elevation in aVR, all confirming that the ST vector is not consistent with diffuse subendocardial ischemia, but rather a focal ST vector pointed at the posterior wall. It is posterior OMI until proven otherwise.

This ECG is quite obvious for long-time readers, and you may think this far too easy to be presented on this blog.

But in actual practice, similar patients are routinely missed and under-treated, as you will see as this case progresses. "Posterior STEMI" may not even technically exist according to the current (2013) ACC/AHA STEMI guidelines, as it is not described as a "STEMI equivalent" and the only relevant statement in the guidelines is: "In addition, ST depression in 2 precordial leads (V1-V4) may indicate transmural posterior injury."  JACC 61(4):e78-140; page e83.

Furthermore, the term "STEMI equivalent" has no reliable or definable meaning except between two practitioners who both agree on the list of entities that they believe are STEMI equivalents and can agree on how to identify it.

It is true that other documents occasionally describe "abnormal ST segment elevation" in the posterior leads (commonly accepted criteria is 0.5 mm in just one lead V7-9), but as far as I can tell all of these documents specifically avoid calling this condition STEMI and specifically avoid using any terminology similar to "STEMI equivalent."  The once exception I have found is the NCDR guidelines, which actually do give a definition: "ST elevation in the posterior chest leads (V7 through V9), or ST depression that is maximal in V1-V3, without ST segment elevation in other leads, demonstrating posterobasal myocardial infarction, is considered a STEMI equivalent and qualifies the patient for reperfusion therapy." I find this definition problematic because the maximal STD in posterior OMI frequently extends out to V4 rather than V3.

So it is very unclear to me whether or not "posterior STEMI" is actually a recognized entity under our current guidelines. It is my opinion that this lack of clarity is part of the reason why patients with posterior OMI are frequently underecognized and undertreated. Regardless of its formality, the more important problem is that it is certainly not recognized in widespread current practice.

Back to the case:

As is unfortunately common practice, a repeat ECG was only performed after the initial troponin T returned elevated at 0.19 ng/mL 1.5 hours after arrival.

Persistent posterior injury. The ST depression which was present in V5-V6 is now gone, which may be either resolution or relative ST elevation of the lateral wall (which would be common with posterior involvement), either way it is dynamic and further proves the existence of ACS.

This was interpreted as "no significant change." Cardiology was called, but elected not to take the patient to the cath lab for some reason, but instead simply admitted him.

The second troponin returned at 0.25 ng/mL. There is no mention of whether the patient had ongoing symptoms. The records show that heparin drip had been ordered in addition to aspirin which had already been given.

The third troponin returned at 22:05 at 0.92ng/mL. A repeat ECG is recorded at 2333, along with a posterior ECG minutes later:

Leads labelled V4-V6 are actually V7-V9 on the posterior thorax. Obvious inferoposterior STEMI.

At this time, just before midnight, the cath lab was activated. The acute finding is reported as a 100% thrombotic lesion of the proximal left circumflex (TIMI 0 flow). In the views below, I would have guessed that this vessel was a ramus intermedius as it seems to be the middle vessel of a trifurcation of the left main, but I will simply defer to the true angiographers. See the occlusion here:

Here is the ECG after intervention showing resolution:

The peak troponin T was 2.35 ng/mL (fairly large MI). The patient had no further complications. Unfortunately an echo was not available.

I hope you are surprised at this case, but I fear that most readers recognize this as the sad reality that exists across many institutions as of 2019. I attribute this mostly to the inadequate current paradigm of myocardial infarction which inspires failure for all such cases that are not obvious according to the STEMI criteria. If this case were an acute occlusion of ANY other important artery (say for example, the superior mesenteric artery, or the middle cerebral artery), 7 hours from arrival to diagnosis despite ongoing evidence of occlusion would be seen as an important and unacceptable delay to diagnosis. Yet in our STEMI vs. NSTEMI paradigm this is simply not understood as an emergent arterial occlusion syndrome. "Time is muscle," but somehow only for occlusions that cause STEMIs, not for occlusions that are more subtle.

Hopefully fixing the paradigm by reframing this disease as an acute arterial occlusion will help people understand this problem. This patient had an Occlusion MI (OMI) and needed emergent reperfusion therapy. It is common sense that such patients have a higher probability of survival and of myocardial preservation if such an OMI is reperfused early, and there is no study that contradicts this notion.

Cases like this will be carefully quantified and studied in our ongoing retrospective study designed to quantify the difference in accuracy between advanced ECG interpretation and the current STEMI criteria. Specifically, cases such as this one will detail the difference in time between diagnosis of Occlusion MI by expert ECG interpreter vs. the current STEMI criteria. This case, for example, would be nearly 7 hours of ischemic time between arrival and cath lab activation.

How much time are you willing to wait for OMI to become "STEMI" (if it ever does)?

Comment by KEN GRAUER, MD (2/16/2019):
The importance of early recognition of an acute OMI (instead of waiting until it becomes a “stemi” ) can not be overstated! The consequences of failing to appreciate this critical concept is made painfully evident in this case by Dr. Meyers — in which it took over 6 hours until this man with new chest pain was finally taken to the cath lab. Superb review (above) by Dr. Meyers about the details of this case. I focus My Comments on 3 of the ECGs that were shown in this case (Figure-1).
Figure-1: The 1st, 3rd and 4th ECGs shown in this case (See text). 
The crux of this case — is the failure to appreciate that acute posterior OMI was clearly evident in the initial ED ECG ( = ECG #1). The abnormal findings in ECG #1 are localized (ie, ST depression in leads V2-thru-V5) — and, in the setting of new chest pain — ECG #1 should be interpreted as acute posterior OMI until proven otherwise. Had the treating clinicians recognized these concepts — they would have: iobtained a 2nd ECG long before 18:33 (~ 1 1/2 hours after ECG #1 was done); and, iithey would have advocated for activating the cath lab.
  • SUGGESTION: Consider use of the Mirror Test”. I’ve been teaching this concept for over 36 years (since including it in my first ECG publication that I wrote in 1983). The mirror test is a simple visual aid: It helps the clinician recognize acute posterior infarction. The mirror test is based on the concept that none of the standard 12 leads directly view the posterior wall of the LV — BUT — the anterior leads provide a mirror image of electrical activity in the posterior wall. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the mirror-image” of leads V1, V2 and V3. It should be readily apparent that the mirror-image view of leads V2 and V3 in ECG #1 (just to the right of ECG #1 in Figure-1— shows a QRST complex that is almost shouting out, “I’m having an acute posterior OMI (ie, large Q waves; coved ST elevation and symmetric T wave inversion in this mirror-image). With a little bit of practice — use of the Mirror Test should facilitate near-instant recognition of subtle changes such as the slightly-taller-than-expected anterior R waves in leads V2 and V3 of ECG #1 (which “become” Q waves in the mirror image view) — and the “shelf-like” shape (ie, nearly straight) ST depression in leads V2,V3 of ECG #1 (which “becomes” ST elevation in the mirror-image view).
ECG #2 (which is not shown in Figure-1— was done ~1 1/2 hours after ECG #1. It showed slightly less ST depression than was seen in ECG #1 — but no sign of ST elevation (ie, no “stemi” ).
Review of ECGs #3 and #4 is especially interesting. ECG #3 was done 6+ hours after ECG #1. It shows downward slanting and slightly greater ST depression in a number of chest leads compared to ECG #1 — but still NO ST elevation in the inferior leads, and NO reciprocal ST depression in lead aVL.
  • ECG #4 was done just a few minutes after ECG #3 for the purpose of directly assessing posterior leads V7, V8 and V9. These posterior leads show obvious ST elevation. But DID YOU SEE that this 4th ECG (done just minutes after ECG #3) now shows: iST elevation in leads III and aVF that was not present in ECG #3; iireciprocal ST depression in lead aVL that was not present earlier; andiiisignificantly more ST-T depression in leads V1, V2, V3 compared to what was seen JUST MINUTES EARLIER in these same leads in ECG #3. This means we are just now in ECG #4 catching acute evolutionary changes, that are evolving in front of us over these very few minutes between the time when ECGs #3 and 4 were done.
  • KEY POINT Although many providers advocate for doing posterior leads when looking for acute posterior involvement — realize that the magnitude of ST elevation that you are likely to see in posterior leads with acute posterior infarction is usually modest. The reason the amount of ST elevation in leads V7, V8 and V9 in ECG #4 is as large as it is — is because this ECG #4 was obtained during the very moments that acute evolution was developing (ie, Note there is now inferior lead ST elevation in ECG #4 — and note how profound is the downsloping ST depression in leads V2 and V3).
  • Finally — Note how obvious acute posterior infarction is in the Mirror Test of leads V1, V2, V3 in ECG #4 (insert to the right of ECG #4 in Figure-1). While use of posterior leads (V7,V8,V9) clearly showed ST elevation in ECG #4 — Are posterior leads really needed to make the diagnosis of a STEMI in this case? I am not saying that you should never do posterior leads — but rather, that with a little bit of practice — it’s possible to make the diagnosis of acute posterior OMI much more quickly by just using the standard 12 lead ECG. COMMENT  I don’t think I’ve seen a case in which posterior leads told me something that I did not immediately know from use of the standard 12-lead ECG (with Mirror Test of the anterior leads).
Our THANKS to Drs. Meyers and Smith for presenting this highly insightful case.
  • For another example of the Mirror Test CLICK HERE.

Tuesday, February 12, 2019

ST Depression and T-wave inversion in V2 and V3.

A middle aged male dialysis patient was found disorganized and paranoid.  He had no chest pain or dyspnea.

An ECG was recorded.  The clinician was worried about his ECG and showed it to me:
What do you think?

When I saw this ECG, I immediately recognized right ventricular hypertrophy as the cause of the ST depression and T-wave inversion in leads V2 and V3.   In other words, I was certain that this was a chronic finding on the ECG.  The worried clinician stated there are no old ECGs to compare with, and no records.  I remained certain that this was RVH as the findings are classic: Large R-wave in V1, large S-wave in lead I, and typical right precordial ST-T that mimic posterior STEMI.

If the QRS were normal, and the patient had chest pain, I would have said this was posterior MI, or possibly hypokalemia (see this post: Are These Wellens' Waves??).

Later, however, we found written records from an outside hospital:

EKG read:
Normal sinus rhythm
Right ventricular hypertrophy with repolarization abnormality
Nonspecific T wave abnormality
Prolonged QT
Abnormal ECG
No significant change since 05-17-18

Previous echo
Final Impressions:
1. Normal LV size, moderately increased wall thickness, normal global systolic function with an estimated EF of 60 - 65%.
2. Right ventricular cavity size is severely enlarged, global systolic RV function is severely reduced.
3. Severely enlarged right atrium.
4. Mildly enlarged left atrium.
5. Severe tricuspid regurgitation.
6. Severely increased estimated pulmonary pressures by tricuspid regurgitation velocity and right atrial pressure (96 mmHg plus RAP).
7. The inferior vena cava is dilated, respiratory size variation less than 50%, consistent with elevated right atrial pressure.

Learning Point:

Whenever there is abnormal repolarization (abnormal ST-T), look for abnormal depolarization (abnormal QRS).  This might include RVH, LVH, LBBB, RBBB, IVCD, WPW, paced rhythm and more.  If present, assess whether the ST-T abnormalities fit with the abnormal QRS.

2. Learn this pattern, as it is classic for RVH.  Here are some more cases of RVH, and/or large R-wave in V1, with ST-T abnormalities:

Young Woman with history of repaired Tetralogy of Fallot presents with chest pain

ST Depression and T-wave Inversions after ROSC from Resp and Cardiac Arrest after Head Trauma

A 50-something male with Dyspnea

Comment by KEN GRAUER, MD (2/12/2019):
Excellent case presented by Dr. Smith from the perspective of ECG teaching. For clarity — I’ve labeled the ECG in Figure-1.
Figure-1: ECG in this case — obtained from a middle-aged dialysis patient. No chest pain or dyspnea. (See text regarding labeling).
The interesting teaching points that impressed me about this case include the following:
  • How the History is of such critical importance! As per Dr. Smith — the fact that this middle-aged man had neither chest pain nor dyspnea dramatically reduced the likelihood of an acute cardiac or pulmonary event even before looking at the ECG. I would have interpreted this tracing very differently had the patient presented to an ED with severe new-onset chest pain or new dyspnea.
  • It is helpful that records from an outside hospital contained written interpretation of a prior ECG on this patient. This suggested that at least some of the findings present in ECG #1 (in Figure-1) were present previously. CAUTION: While clearly much better than nothing — in my experience, written report of ECG findings (even from a cardiologist) is NO substitute for finding an actual prior ECG in the old chart. Too-numerous-times-to-count I have found important ECG findings either undercalled or overcalled in a prior written report. The tracing in this case (in Figure-1) is complex. In my opinion, the only way to know if all findings are old is by lead-to-lead comparison with a prior ECG.
  • Availability of a previous Echo report can be an invaluable teaching tool — as well as proving to be tremendously helpful clinically in this case. Access to the previous Echo report in this case makes up for not having an actual copy of the prior ECG — because the previous Echo confirms high likelihood that ECG findings in this case are probably not new.
  • Regarding use as a teaching tool — the previous Echo showed severe RAE, severe RVH and markedly increased right-sided pressures — as well as mild LAE and moderate LV wall thickening. How well does the ECG in Figure-1 predict each of these findings? (See below).
The ECG in Figure-1 shows sinus rhythm at ~85/minute. Additional ECG findings (as well as non-findings) that I see include the following:
  • No sign of either LAE or RAE. Although the sinus P wave in lead II is a good size (RED arrow) — it is neither notched (as is common with LAE), nor tall enough or pointed enough in any of the inferior leads to qualify for RAE. The negative component to the P wave in lead V1 is neither deep enough nor wide enough to qualify for LAE. The positive component to the P wave in leads V1 and V2 is neither tall nor peaked, as may be seen with RAE.
  • No sign of LVH. The Echo showed moderately increased LV wall thickness. While sensitivity of the ECG is limited for picking up this type of LVH — I always find it insightful to correlate ECG findings with the far more accurate anatomic assessment possible in Echo evaluation.
  • Incomplete RBBB is presentI measure QRS width at between 0.09-0.10 second — which is within the normal range. A multiphasic (rsR’s’) complex is present in lead V1 (within the BLUE oval in V1) — in association with narrow terminal S waves in both leads I and V6 (within BLUE ovals in these leads). This qualifies as incomplete RBBB. It is common with either complete or incomplete RBBB to also see an rsR’ complex in right-sided lead III (as we do here). It is not common to see a 4-phase QRS complex (rsR’s’) in lead V1 due to simple complete or incomplete RBBB. That said, I still feel description of QRS morphology here best qualifies as incomplete RBBB. NOTE: Some anterior ST-T wave depression may be seen with incomplete RBBB. However, the amount of anterior ST-T wave depression seen here is clearly more than one should expect from simple incomplete RBBB.
  • ECG findings in favor of RVH in Figure-1 include — the relatively tall R’ wave in lead V1 — presence of numerous S waves on this tracing (ie, in leads I, II, aVL; and V2-through-V6) — the presence of incomplete RBBB — and, ST-T wave depression in leads V1-V3 consistent with RV “strain”. Clearly, the QRS complex is not wide enough to qualify as complete RBBB. Most of the time with incomplete RBBB — the R’ deflection in lead V1 is not nearly as tall as it is in Figure-1, unless there is also “something else” (ie, RVH).
  • ECG findings atypical for the dramatic degree of RAARVH and increased right-sided pressures indicated by Echo include: iLack of ECG findings suggestive of RAA; andiiLack of any hint of RV “strain” in the inferior leads. The 2 lead areas to look at when assessing for RV “strain”, are the inferior leads (II,III,aVF— and the anterior leads (V1,V2,V3). While true that RV “strain” will not always be seen in both of these lead areas — the fact that there is no sign at all of inferior ST-T wave depression (within the PURPLE rectanglesand, the somewhat less usual pattern of ST-T wave depression in the anterior leads (within RED rectangles, showing maximal ST-T wave depression in lead V2, despite only modest R wave amplitude in this lead) — to me suggested that the anterior ST-T wave depression might reflect acute cardiac or pulmonary disease. I’ll emphasize that the negative history for chest pain and dyspnea + dramatic abnormalities on the previous Echo strongly support supposition that the ECG findings in Figure-1 are not acute. My point is simply that I would not be at all certain of the chronicity of these findings had I just seen this ECG without benefit of the history and prior Echo report.
Our THANKS to Dr. Smith for presenting this highly insightful case.

  • For “My Take” on the ECG diagnosis of RVH  CLICK HERE.
  • For “My Take” on the ECG diagnosis of LAE & RAE  CLICK HERE.

Saturday, February 9, 2019

Right sided heart failure and tachycardia.

A middle-aged male presented with tachycardia, dyspnea, and 4+ bilateral leg edema.
What is the rhythm?

There had been an ice storm, and it was the busiest day in the history of our emergency department because of falls.  I reduced 12 fractures that evening and was in constant motion.   I looked at this and saw the negative component of the P-wave in V1, and immediately diagnosed sinus tachycardia.

I did a bedside echo:
There was good LV function
You can see a very large RV (closest to probe) and RA (on far right).
Lungs were clear to auscultation and there were no B-lines.

Volume overload was confirmed with this:
This shows the distended inferior vena cava (IVC), further supporting high right sided pressures and right heart failure.

So he clinically had right heart failure, subacute in onset.  If I had simply looked carefully through his chart, I would have found that this was not all new, but rather an exacerbation of a chronic problem.

Not having done that, pulmonary embolism was on the differential and we obtained a CT pulmonary angiogram:
This shows a massive right atrium and dilated right ventricle

Another slice of the CT showing the same thing:
A massively dilated right atrium

Later, I looked back at the first ECG; Here it is again:
It was suddenly clear to me from lead II across the bottom that this was atrial flutter.

Why is there a negative component to the atrial wave in V1?

Normally, one of the rapid ways to differentiate sinus from flutter is too look for a biphasic up-down atrial wave (sinus) vs. an upright atrial wave (flutter).

It turns out that there was a previous ECG to compare to:
This is clearly sinus, but with a mostly upright P-wave.
It is biphasic as usual, but the "up" component is (which is the right atrial component) is far larger than the subsequent negative deflection (representing the left atrium)

The answer has to do with the massive right atrial hypertrophy.  Normally, the P-wave in V1 is biphasic.  The initial upright part is the right atrium and the latter part, inverted, is the left atrium.  In this case, the right atrium is massively enlarged and results in almost all of the P-wave being upright.

Further complicating the problem, when the patient goes into atrial flutter, as with this presentation, the flutter wave has a large negative component due to the right atrial enlargement.

Thus, the atrial morphology is reversed in this patient, deceiving the physician (this physician) into believing it was sinus when it was really flutter.

And atrial flutter was the precipitating etiology of the patient's worsening right heart failure.

He required furosemide and ablation of the atrial flutter.

Formal Echo:

The estimated left ventricular ejection fraction is 50-55 %.
There is no left ventricular wall motion abnormality identified.
Mitral valve insufficiency mild.
The estimated pulmonary artery systolic pressure is 20 mmHg + RA pressure.
Right ventricular enlargement .
Paradoxical septal motion severe.
Decreased right ventricular systolic performance.
Tricuspid valve insufficiency severe.
Right atrial enlargement.
Based on the appearance of the IVC, the RA pressure is elevated.


RV function is probably worse than on the study of 2016. This is reflected
by more pronounced paradoxical septal motion, a lower PA pressure and
probably more TR.

Learning Point:

Atrial Flutter may have a mostly negative atrial wave on the ECG, mimicking sinus tachycardia, when there is marked right atrial enlargement.

Comment by KEN GRAUER, MD (2/9/2019):
Illustrative case by Dr. Smith — regarding acute arrhythmia interpretation. It’s so helpful to have clinical and echocardiographic correlation, with availability of a prior tracing for comparison. I focus my comments on the 2 ECGs shown in this case (Figure-1).
Figure-1: The initial ECG (= ECG #1at the time the patient presented to the ED, with comparison to a prior ECG (= ECG #2on this patient (See text).
ECG #1 (= the initial ECG in the ED)The approach to arrhythmia interpretation that I favor — is to: iFirst assess the patient hemodynamic status; and, iito use a Systematic Approach to Arrhythmia Interpretation.
  • The patient in this case presented in acute right-sided heart failure. That said, from what I surmise — immediate cardioversion was not needed — which meant there was at least “a moment” to better assess clinical parameters, including the cardiac rhythm.
  • I favor the following memory aid for recalling the 5 KEY parameters for arrhythmia interpretation: “Watch your Ps & Qand the 3 Rs”. Thus, we look for the presence of waves (or for sign of atrial activity if clear sinus rhythm is not present— QRS width — and the Rs (Rate and Regularity of the rhythm — and IF atrial activity is present, whether atrial activity is Related to neighboring QRS complexes).
  • PEARL #1: The reason I favor a systematic approach to rhythm interpretation (ie, NOT jumping to a single diagnosis — but first assessing each of the 5 KEY parameters cited above) — is that otherwise you risk premature fixation on a single rhythm diagnosis without considering other possibilities.
  • The 5 KEY Parameters: Although at first glance, it looks like sinus P waves may be present in ECG #1 — the PR interval in sinus mechanism rhythms usually shortens when heart rate increases — and, it looks like the PR interval for the upright deflection in lead II, as well as for the negative deflection in lead V1 is relatively longer-than-expected for a sinus mechanism rhythm in view of how fast the heart rate is. In addition, several leads (ie, all inferior leads, aVR, V5,V6) suggest that there may be 2:1 atrial-to-ventricular conduction. I was therefore not-at-all certain in my initial impression of ECG #1 that the rhythm was sinus.
  • It is difficult to accurately assess QRS duration for the rhythm in ECG #1. This is because of baseline artifact — and, as we’ll see in a minute — because of the underlying rhythm. So although I thought the QRS appeared to be at least of borderline duration (ie, ~0.11 second) — QRS morphology to me suggested a supraventricular rhythm.
  • The rhythm in ECG #1 is regular. I estimate the ventricular rate to be ~135/minute.
  • I’ll defer the 5th parameter (ie, Is atrial activity related to the QRS?) for a moment.
ASSESSMENT — What we have described in ECG #1, is that there is a Regular SVT at ~135/minute, without clear sign of sinus P waves. Recognition of a regular SVT with uncertain atrial activity should prompt the following Differential Diagnosis — iSinus Tachycardia (perhaps the deflections we see are sinus P waves after all …?); iia Reentry SVT (ie, AVNRT, AVRT); iiiAtrial Tachycardia; and, ivAtrial Flutter. Although other entities are possible (ie, SA nodal reentry tachycardia) — these 4 entities make up the overwhelming majority of regular SVTs that the emergency provider will see.
  • PEARL #2: By far (!!!) — the most commonly overlooked diagnosis in all of arrhythmias is atrial flutter. This is because flutter waves may be atypical in morphology, and because flutter waves may be hidden within the QRS complex and/or ST-T wave. In adults, the rate of flutter circulating within the atria in patients who have not yet been treated with an antiarrhythmic agent (that may slow the rate) is ~300/minute (usual range ~250-350/minute). By far, the most common conduction ratio in untreated AFlutter = 2:1. As a result, the ventricular rate in untreated AFlutter is almost always ~150/minute (within a range of ~135-165/minute). Therefore, the BEST way not-to-overlook the diagnosis of AFlutter is to always suspect it whenever you see a regular SVT with uncertain atrial activity at a rate of ~150/minute (ie, at a rate between ~135-165/minute). This is precisely the situation we have in ECG #1.
  • PEARL #3: Using CALIPERS facilitates diagnosis. The way I “look” for AFlutter — is to search all 12 leads for sign of atrial activity. We know lead II is the best lead for assessing sinus rhythm. The next best lead for assessing sinus rhythm is lead V1. When searching for possible 2:1 flutter activity — the best leads in my experience are leads II, IIIaVF; aVR; and V1. I generally look at these 5 leads first. After that — I then look at each of the remaining 7 leads for possible atrial activity. Set your calipers to precisely ONE HALF the R-R interval. Then see if there is any lead in which you can precisely walk out 2 deflections for each QRS complex.
  • In ECG #1  Lead aVF shows 2:1 deflections best (RED arrows). These deflections march out precisely with my calipers. There is a constant PR interval in front of each QRS complex. Since there are 2 deflections for each QRS — this means that the atrial rate = 135 X 2 = 270/minute. It would be rare indeed for ATach to go this fast (and neither sinus rhythm now reentry SVTs go this fast) — therefore the rhythm in ECG #1 is almost certainly AFlutter. And, if you step back a little bit from this tracing — there does appear to be a sawtooth pattern in each of the inferior leads.
  • In support that the RED arrows in ECG #1 truly indicate atrial activity — I’ve drawn in some vertical RED LINES that show similar 2:1 deflections in simultaneously-obtained lead aVR and lead II. Other leads that seem to show the same 2:1 activity include leads III, and possibly V5 and V6.
  • IF needed — one could confirm diagnosis of AFlutter with either a vagal maneuver or a “chemical” vagal maneuver (ie, use of Adenosine) — but using calipers has virtually already confirmed your diagnosis!
  • As per Dr. Smith — abrupt onset of the tachyarrhythmia, with resultant reduction in hemodynamically effective atrial contraction appears to be the reason for exacerbation of this patient’s condition. Management should focus on conversion to sinus rhythm.
  • P.S.: The vertical PURPLE lines in ECG #1 show that the prominent negative deflection before each QRS complex in lead V1 is not a sinus P wave. Instead it appears to be part of the flutter wave.
ECG #2 ( = the prior ECG on this patient)There are a number of interesting findings on this patient's baseline ECG:
  • Clear indication of sinus rhythm (ie, an upright P wave with fixed and normal PR interval in lead II ).
  • QRS widening in a pattern consistent with RBBB. Vertical BLUE lines in lead V1 of ECG #2 show QRS duration to be ~0.11-0.12 second, which is long enough to satisfy criteria for RBBB. Note the rSR’ pattern in lead V1 + wide terminal S waves in lateral leads I and V6 (within the BLUE circles) — which solidifies the diagnosis of RBBB.
  • There is RAE in ECG #2! Most often RAA is diagnosed by the finding of tall, peaked and pointed P waves in the inferior leads. On occasion however, you will only see a prominent pointed P wave in leads V1 or V2 — which given the clinical history here, is diagnostic of RAE in this case.
  • Note T wave inversion in leads V1 and V2 in ECG #2 (BLUE arrows). This could reflect RV “strain” — or — it could simple reflect commonly seen secondary ST-T wave changes in association with RBBB — or — it could represent both a reflection of RBBB + RV “strain”.
  • Now go back to ECG #1, and take another look at the QRS complex in lead V1. I suspect there was also RBBB in ECG #1, albeit much more difficult to see in ECG #1 due to the baseline artifact and flutter activity.
  • The Echo in this patient showed significant RAE and RVH. Note how difficult it is to diagnose RVH from the 2 ECGs in this case. This is common — as the ECG diagnosis of RVH is typically difficult, and often not apparent until late in the process. Signs consistent with RVH that we do see include relatively low voltage, lots of S waves, RBBB, T inversion on ECG #2 in leads V1 and V2 — and RAE. Keep in mind that there is only one condition in medicine that produces right atrial enlargement without also producing RVH ( = tricuspid stenosis) — so clear ECG diagnosis of RAE (as was done in ECG #2 by the prominent, peaked P waves in leads V1,V2) is an indirect clue that RVH is likely to be present (supported by the above noted ECG findings) — albeit definitive diagnosis of RVH required Echo.
  • Regarding "My Take" on a Systematic Approach to ECG Interpretation — CLICK HERE. For the part regarding systematic Rhythm Interpretation — Scroll down to Figure 4 on this web page, for the “First 2 Parameters = Rate & Rhythm).
  • For “My Take” on the ECG diagnosis of RVH  CLICK HERE.
  • For “My Take” on the ECG diagnosis of LAE & RAE  CLICK HERE.

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