Monday, September 28, 2020

"It isn't a STEMI," so cath lab refusal (again). Were they right?

Sent by Anonymous, written by Pendell Meyers

An elderly female called EMS for acute epigastric pain. EMS arrived and recorded this ECG on the way to the hospital:

This case was sent to me with only the details above, and my response was: 

"It's posterolateral (and probably also inferior) OMI until proven otherwise. I'd also give a little calcium because it's slow, wide, and a couple leads have almost pointy Ts. But I don't really think it's hyperK. This one is OMI. Either LCX or RCA, or perhaps an Obtuse Marginal that supplies those regions."

Interpretation: There is an absence of sinus activity, including an absence of retrograde P waves. The rhythm is probably a junctional escape at a rate of approximately 45, with RBBB and likely also LAFB (given the leftward axis despite RBBB). Alternatively, it could be a posterior fascicular escape. There is STD in V2-V5 that is maximal in V2 and V3. This STD is excessively discordant in V2, and concordant in V3. The inferior leads show Q waves with STE in lead III, and there is some slight reciprocal STD in I and aVL. Interestingly, many of the T waves have a slightly peaked appearance. Along with bradycardia and conduction block, this would be alarming for potential hyperkalemia, which of course can also cause OMI mimics. We have shown several cases on this blog that appear to have both OMI and severe hyperkalemia.

Additionally, both 1) no spontaneous sinus activity (sinus arrest or extreme sinus brady) and 2) no retrograde activity, which implies AV block as well

Cardiology was summoned immediately to bedside but they thought that this ECG "isn't a STEMI" and refused to take the patient to the lab. 

The initial troponin T returned highly elevated at 4.04 ng/mL. The potassium was 4.1 mEq/L. Cardiology was recalled to bedside to reevaluate.

Smith comment: When Pendell texted this to me, I thought it was both hyperkalemia and inferior posterior OMI.  V4 and V5 especially have the appearance of hyperK.  This just goes to show that there are always false positives and false negatives.

Another ECG was recorded:

These are almost certainly posterior leads, though they were not labelled as such (V4-V6 are really V7-V9 on the posterior thorax). 
How do we know? We can tell this because of the very low QRS amplitude and the Q-waves.  The slight ST elevation is diagnostic of posterior STEMI, which in posterior leads only requires 0.5 mm in just one lead to meet "criteria."

There are possible atrial waves but it is not definitive with this low quality ECG. If the possible atrial waves are real, it could be sinus bradycardia with 2:1 AV block. Otherwise, this would be complete heart block with junctional escape. The rate is approximately 30 bpm. Apparently the patient was mentating and had a normal blood pressure with this, and did not require pacing at that moment.

We do not recommend posterior leads in this situation because they are unnecessary (the initial ECG is diagnostic of posterior MI) but they might be falsely negative and dissuade you from your diagnosis. 

Why are posterior leads falsely negative?  2 reasons: 
1) they are often recorded at a later time, after the artery has reperfused.  It is easy to recognize this if you are aware: V1-V3 will still be recorded and visible, and the STD in these leads will be gone.
2) the voltage of posterior leads may be very small because the signal needs to traverse the lungs.


The patient was taken to cath where a 100% (TIMI 0) LCX occlusion was found and stented. No further troponins were ordered.

The patient survived so far.

Learning Points:

RBBB should have a small, proportional amount of appropriately discordant STD and T wave inversion in leads with large R' wave (usually just V1 and V2). At some point, STD in these leads becomes out of proportion. This case is an excellent example of excessively discordant STD in RBBB, maximal in V2-V4, which signifies posterior OMI in RBBB.

Make sure to keep hyperkalemia on the differential for any sick patient with bradycardia, wide QRS, AV blocks, and bizarre morphology. It would have been an excellent choice to give this patient IV calcium on arrival to see if the ECG responded, while also treating for OMI simultaneously.


MY Comment by KEN GRAUER, MD (9/28/2020):


Superb interpretation of the presenting ECG in this case by Dr. Meyers!

  • As per Dr. Meyers — the combination of QRS widening + bradycardia + lack of sinus P waves should immediately suggest the possibility of Hyperkalemia — especially since T waves in no less than 8/12 leads (ie, in leads I,II,aVL,aVF; and in V3-thru-V6) in the initial ECG look more-peaked-than-they-normally-should-be. For this reason — Dr. Meyers appropriately suggests that empiric Calcium would be a reasonable option in this circumstance, even before knowing the serum K+ level.
  • NOTE — I would bet that No One who regularly follows Dr. Smith’s ECG Blog has trouble recognizing hyperkalemia when all of the typical findings are present. That said, many of our patients simply “don’t read the textbook” — and recognition of hyperkalemia becomes much more challenging when T wave peaking isn’t obvious (ie, when T waves aren’t so pointed with such a narrow base — or, when other abnormalities such as RBBB are present). For this reason — I thought it worthwhile to review some less appreciated ways in which hyperkalemia may present.

Regarding HyperKalemia & Brady Rhythms: We have previously discussed on numerous occasions in Dr. Smith’s ECG Blog, the multiple ECG manifestations of various degrees of HyperKalemia. Among these:

  • Review of sequential ECG changes of Hyperkalemia — in My Comment at the bottom of the January 26, 2020 post.
  • And, relevant to the bradycardia and lack of P waves in today’s tracing — My review of the mechanism for the various ECG changes (My Comment in the July 3, 2020 post) — which I restate here: The characteristic T wave peaking of hyperkalemia is seen early in the process — due to an acceleration by elevated K+ levels of terminal repolarization. With more severe K+ elevation — there is depression of conduction between adjacent cardiac cells, eventually with depression of SA and AV nodal conduction. This may result in a series of conduction defects, including PR and QRS interval prolongation — frontal plane axis shift — fascicular and/or bundle branch block (including interventricular conduction defects— and/or AV block with escape beats and rhythms. Ultimately, QRS widening may lead to a sine-wave appearance (fusion of the widened QRS with the ST-T wave — such that distinction between the two is no longer possible). If this severe hyperkalemia remains untreated — VT, VFib or asystole are likely to result as the terminal event.
  • As serum K+ increases — P wave amplitude decreases. Ultimately, P waves may disappear. This is because atrial myocytes are exquisitely sensitive to the extracellular effects of hyperkalemia (much more so than the SA node, AV node, the His, and ventricles). As a result — despite lack of atrial contraction (ie, loss of P waves on ECG) — there may still be transmission of the electrical signal from the SA node over the conduction system and to the ventricles. Thus, rather than a junctional rhythm or fascicular escape rhythm — a bradycardic rhythm without visible P waves in severe hyperkalemia may be a Sino-Ventricular Rhythm (in which despite lack of P waves on ECG — the rhythm IS still initiated in the SA node, with electrical transmission through to the ventricles). But because P waves disappear and the QRS is often wide with a hyperkalemic sino-ventricular rhythm — it is EASY to mistake this rhythm as either AIVR (Accelerated IdioVentricular Rhythm) or VT.
  • BOTTOM Line: The bradycardia, altered P wave activity and the different forms of widened QRS morphologies may make for multiple potential ECG manifestations when there is severe hyperkalemia. The only way to prevent overlooking the diagnosis in some of these patients — is to always consider the possibility of HyperKalemia whenever presented with a tracing such as the one that was seen in today’s case.

— BUT — Serum K+ in this case turned out to be normalTherefore — the ST-T wave appearance in today’s case is not the result of hyperkalemia.

QUESTION: If I were to show you the ECG that appears in Figure-1 — Would you have any doubt that this is an acute STEMI?

  • HINT: The answer is “No”.

Figure-1: How would YOU interpret this tracing?

MY Thoughts on ECG #1: In the context of the obvious acute STEMI-like ST elevation in leads V1, V2 and V3 of Figure-1 — supportive ECG findings that we see in other leads should become unmistakably obvious:

  • There is definite ST elevation in lead III — with reciprocal ST depression in high lateral leads I and aVL. These high lateral leads also manifest suspicious-looking terminal T wave positivity of surprisingly high amplitude.
  • The T wave in lead II is obviously hyperacute (much more “voluminous” than-it-should-be, given modest depth of the S wave in this lead).
  • In this context — the T wave in lead aVF is probably also hyperacute (given small depth of the S in this lead).
  • All 3 of the lateral chest leads (leads V4,5,6) manifest clearly hyperacute T waves given modest QRS amplitude of the complexes in each of these leads. In addition, ST segments leading up to these hyperacute T waves are abnormal (depressed in V4; straightened in V5; and straightened with a rising takeoff in V6).

COMMENT: Despite the above described obvious abnormalities in 11/12 leads (actually in all 12 leads if you count the ST elevation in aVR) — in this elderly patient with new-onset potential chest pain “equivalent”symptoms — this case presents yet one more instance of the cardiology team stating, “Not a STEMI — therefore NO indication for acute cath.” I have to admit that I just do not understand this refusal ... (We’ve published many similar examples of this type of oversight — the most recent of which in our September 21, 2020 post).

CONFESSION: The 12-lead tracing I show above in Figure-1 was altered by me. I simply inverted the 3 leads within the RED rectangle (to project the mirror-image of leads V1, V2 and V3).

  • I show the actual initial ECG in today's case in Figure-2 — to which I’ve added the inverted (mirror-image) view of leads V1, V2 and V3 to the right of ECG #1.
  • As I’ve described in many prior posts on Dr. Smith's ECG Blog (See especially My Comment from Sept. 21, 2020) — the Mirror Test is no more than a simple visual aid that inverts anterior leads, thereby facilitating recognition of the shape of an acute posterior MI. It is based on the principle that the mirror-image of anterior leads provides insight into the appearance of ongoing electrical activity in the posterior wall. With a little practice — you’ll find posterior leads are rarely (if ever) needed — because use of the Mirror-Test allows instant recognition of virtually all cases when there is acute posterior MI.
  • NOTE: Regardless of whether you call the ST-T wave appearance in the anterior leads of ECG #1 (in Figure-2) a “STEMI-equivalent” (since technically there isn’t ST “elevation” ) or simply an OMI — this pattern in a patient with new symptoms reliably identifies acute Occlusion-based MI.
  • Final POINTS: The shape of the ST-T waves in leads V2 and V3 of ECG #1 in Figure-2 is clearly abnormal! Note how much J-point ST depression there is for the ST segment in lead V2. This is not seen with simple RBBB. The 2 mm of J-point ST depression with shelf-like straightening of the ST segment in lead V3 is also not a “normal accompaniment” of simple RBBB. Some ST-T wave depression is expected with uncomplicated RBBB — but generally this should be maximal in lead V1 (and not increasing as we move laterally toward leads V2, V3, as we see in Figure-2).

Figure-2: The initial ECG in this case, with the mirror-image of leads V1, V2 and V3 placed to right of ECG #1 (See text).

Saturday, September 26, 2020

40 Something Man with Palpitations and Grouped Beating: Is it Wenckebach?

From Dr. Smith: A 40 something male complained of palpitations.  See the ECG below and how Ken Grauer dissects this grouped beating.


MY Comment by KEN GRAUER, MD (9/26/2020):


The 12-lead ECG and accompanying long lead II rhythm shown in Figure-1 was obtained from a 40-something year old man who was found to have a fairly slow and irregular heart rate. He was hemodynamically stable at the time this tracing was done. Imagine this is the only history available.

  • What is the rhythm? Is this Wenckebach?
  • Clinically — WHY might it matter?

Figure-1: 12-lead ECG and rhythm strip from a 40-something year old man with an irregular heart rate (See text).

MY Thoughts on ECG #1: This is a challenging tracing. My purpose in discussing this case is to highlight distinction between AV block vs mimics of AV block. Treatment indications for being able to quickly make this distinction are obvious = A pacemaker may be needed for more severe, symptomatic forms of AV block — whereas a pacemaker will usually not be needed for most AV block “mimics”.

As always — I favor beginning with the cardiac rhythm (in the long lead rhythm strip) before assessing the rest of the 12-lead ECG. By the 5 Parameter Ps, Qs & 3R Approach — I noted the following:

  • P waves are present. However, it is not immediately apparent how consistent atrial activity is (More on this below).
  • The QRS complex is narrow in all 12 leads. Therefore, this is a supraventricular rhythm.
  • The Rhythm is not regular. That said — there appears to be group beating (ie, 4 groups of 3 beats each, with a similar pattern of spacing throughout the long lead II rhythm strip).
  • Since the ventricular rhythm is not regular — the Rate is changing! The longest R-R intervals are approximately 7 large boxes in duration (corresponding to a rate in the low 40s). The shortest R-R intervals are about 3 large boxes in duration (corresponding to a rate of ~100/minute).
  • We can estimate the overall heart rate by the fact that the entire rhythm strip is 50 large boxes in duration (ie, ~10 seconds) — during which time 11 beats occur. Therefore — 11 beats X 6 = 66/minute as the average overall rate.
  • The 5th Parameter is the 3rd R — which stands for Related (ie, Are P waves related to neighboring QRS complexes?). We can tell at a glance that at least some of the P waves are related to neighboring QRS complexes — because the PR interval preceding each of the QRS complexes that terminate each of the short pauses is equal (ie, a normal PR interval ~0.15 second precedes the QRS complex of beats #4, 7 and 10).
  • NOTE: For those interested in more on “My Take” on the Ps, Qs & 3R Approach for Systematic Rhythm interpretation — CLICK HERE.

PEARL #1: I have emphasized on a number of occasions in Dr. Smith’s ECG Blog, that whenever group beating is seen — one should immediately consider the possibility of some type of Wenckebach conduction. Clearly — Not all group beating will turn out to be the result of Wenckebach conduction (ie, atrial bigeminy or trigeminy, among other rhythms — may manifest “group beating” that is not the result of Wenckebach). That said — Keeping in mind this concept of group beating has allowed me to recognize literally hundreds of Wenckebach cases in record time!

  • The most common form of Wenckebach conduction is 2nd-degree AV block, Mobitz Type I (also known as AV Wenckebach) — and this is the type of Wenckebach conduction that I will consider here. KEY Point: For there to be 2nd-degree AV block of the Mobitz I type — the atrial rhythm (ie, P-P interval) should be regular (or at least almost regular, if there is underlying sinus arrhythmia).
  • The utility of this PEARL — is that simple use of calipers allows you within seconds to establish that regardless of what you interpret as P waves in the long lead II rhythm strip in Figure-1  the atrial rhythm is not regular. Therefore, despite group beating — 2nd-degree AV block of the Mobitz I type is not present in ECG #1!
  • NOTE: For those interested in my video on ECG recognition of the AV Blocks — CLICK HERE. (If you click on SHOW MORE under the video on the YouTube page — you’ll see a detailed linked Contents to key topics in the video).

PEARL #2: The following truism has served as my arrhythmia “mantra” over the past 4 decades — “The commonest cause of a pause is a blocked PAC” (taught to me by the incomparable Henry J. L. Marriott).

  • Statistically — Blocked PACs are a far more common cause of pauses than any form of AV block. By repeating this truism to myself whenever I see a short pause (such as for the 3 short pauses in ECG #1) — I avoid overdiagnosis of AV block, and, I tremendously increase my ability to quickly spot even the most subtle of blocked PACs.

Figure-2: I’ve labeled key points from Figure-1 (See text).

PEARL #3: In my experience, the 2 simple steps of labeling P waves and numbering the beats in a complex arrhythmia have proved invaluable for facilitating recognition of the mechanism of the arrhythmia — and, for being able to communicate your thoughts to colleagues (ie, It’s impossible to do this with any time efficiency unless you number the beats). I illustrate my approach in Figure-2.

  • I start with what I know. As mentioned earlier — the QRS complex that terminates each of the 3 pauses in ECG #1 is preceded by a sinus P wave with a constant (and normal) PR interval. RED arrows highlight these 3 sinus beats (ie, beats #4, 7 and 10).
  • Similar events regarding additional atrial activity seem to be occurring within each of the groups. In Figure-2 — I focus on the group that consists of beats #4, 5 and 6 — and have labeled the atrial activity that I believe is occurring.
  • The P wave labeled “a” is the sinus P wave of beat #4 that begins the cycle.
  • The next P wave in this group of 3 beats appears to be added on to the end of the T wave of beat #4 (labeled “b”). The fact that “b” occurs at the very end of the T wave of beat #4 allows us to see what a “normal T wave” looks like ( = the 1st BLUE T in the long lead II — that is contained within the BLUE rectangle).
  • Compare the shape of the T waves of beats #5 and 6 (labeled with a PURPLE T’ ) — with the shape of the “normal” T wave that follows beat #4. Aren’t these T waves of beats #5 and #6 more peaked than the normal T wave? This extra peaking is the result of premature P waves “c” and “e” that are hidden within these T waves.
  • One more P wave occurs in this 3-beat group (labeled “d”  which precedes beat #6 with a longer PR interval than the PR interval for sinus beat #4).
  • The P waves that are hidden within the T waves of beats #5 and #6 (labeled “c” and “e”) are both blocked. That neither of these P waves are conducted makes sense — because these P waves occur very early in the cycle, presumably during the absolute refractory period.

BOTTOM Line: The above findings make for a repetitive sequence, in which a short pause is terminated by a sinus-conducted beat — which is then followed by 4 successive P waves (PINK arrows highlighting b, c, d and e) — and then the cycle repeats (ie, similar events occurring within the next group consisting of beats #7, 8, 9 — and one more time with the last 3-beat group = beats #10, 11, 12).

  • It is admittedly difficult to distinguish between a single sinus beat followed by repetitive PACs vs being followed by short runs of ATach (Atrial Tachycardia). I favor the former because: i) The P-P intervals between a, b, c and d are not all the same (ie, the P-P interval between c-to-d is noticeably shorter than the other P-P intervals); andii) P wave morphology seems to vary during these successive P waves — whereas I’d expect a similar P wave morphology if these were runs of ATach (Note different shapes for P waves in several leads highlighted by the small YELLOW vs BLUE arrows).

The Rest of the 12-Lead ECG: The remainder of the 12-lead tracing for ECG #1 is fairly unremarkable.

  • There is a leftward axis — though not negative enough to qualify for LAHB (since the QRS in lead II is isoelectric and not predominantly negative). The QTc is not prolonged. There is no chamber enlargement. Blocked PACs (within many of the T waves) account for much of the extra T wave peaking. ST-T wave changes do not appear to be acute.

Putting It Together: The underlying rhythm is sinus. The primary rhythm disturbance appears to be repetitive sequences of successive PACs. These terminate with a blocked PAC that results in a brief pause (of <1.4 second) — and then the cycle resumes.

  • The rhythm disturbance is not AV Wenckebach. No pacemaker is needed.
  • Management will depend on symptoms — frequency of PAC episodes over time, and whether longer runs of PACs are sustained (whether this develops into runs of ATach) — and, the presence or absence of underlying heart disease or other predisposing factors. Unfortunately — additional follow-up was unavailable on this case.
  • P.S. Re-entry SVT rhythms (such as AVNRT) often begin with multiple PACs. Whether to begin a trial of empiric therapy (ie, with a ß-blocker or other agent) — or to assess with a longer period of monitoring would be a decision for the treating clinician.

ADDENDUM (9/26 pm): Dr. Smith wrote me just as today’s post was published, asking me, “Could I add a laddergram?”. The reason I did not do this initially — is that there are several potential explanations for the atrial activity we see, and I did not feel there was enough monitoring to delineate an exact answer.

  • As is often the case with complex arrhythmias (especially when the amount of monitoring recordings is limited) — there may be more than a single plausible theory for the mechanism of an arrhythmia. I illustrate 3 possibilities in the Laddergram that I’ve just derived (Figure-3). I still do not think we can know for certain what is going on — but it may be instructive to contemplate possibilities:
  • For the 1st Grouping ( = beats #4,5,6) — The initial beat in this grouping is sinus-conducted (beat #4). There follows 4 successive PACs. I used different colors to suggest origin from different sites in the atria — but one or more of these PACs could be coming from the same site. Reasons why the PR intervals preceding beats #5 and #6 are longer than the PR interval for sinus-conducted beat #4 could be: i) These PACs originate from an atrial site further away from the AV node; or, ii) There could be some partial retrograde conduction (dotted butt ends traveling backward) that delays forward conduction. The last PAC (labeled “e” — and the GREEN circle in the laddergram) presumably occurs during the absolute refractory period, and is therefore blocked (non-conducted).
  • For the 2nd Grouping ( = beats #7,8,9) — The laddergram depiction is similar to my proposed mechanism for the 1st Grouping — with the exception that beat #9 might be sinus-conducted (albeit with a prolonged PR interval due to delay caused by partial retrograde conduction from the previous PAC that is shown in YELLOW).
  • For the 3rd Grouping ( = beats #10,11,12) — There could simply be atrial tachycardia (ie, all P waves after sinus-conducted beat #10 arise from the same atrial focus — shown in GREEN). NOTE #1: Given the frequent prolonged PR intervals we see in this tracing — it seems likely that if ATach ever became established and sustained — that this ATach would manifest Wenckebach conduction. NOTE #2: ATach is not always a perfectly regular arrhythmia — as could be the case in this last Grouping.

P.S.: I’ll emphasize that regardless of whatever the precise mechanism for this arrhythmia turned out to be — my initial approach to management would be the same.

Figure-3: I’ve added a laddergram to Figure-2, showing 3 possible theories for the mechanism of atrial activity in this arrhythmia (See text).


  • NOTE: My sincere THANKS to Feroz Haroon (from Srinagar, India) for sharing this tracing with us!


ADDENDUM #2 — by David Richley (9/28/2020): Dave has followed up on his 9/26 comment with his own laddergram (Figure-4). Although we still do not know for certain what the correct answer is — I think it instructive to show how sometimes a number of possibilities exist.

  • I’ll once again emphasize that even though we are not certain of the mechanism of this interesting rhythm — my initial approach to management would still be the same.

David Richley said the Following: I think this could simply be sinus rhythm with an atrial bigeminy, in which the atrial premature beats (APBs) are alternately conducted and non-conducted, as illustrated in this laddergram (Figure-4). According to my theory, beats #1, 3, 4, 6, 7, 9, 10 and 12 are sinus beats; beats #2, 5, 8 and 11 are conducted APBs — and immediately following beats #3, 6 and 9 is a non-conducted APB.

  • The reason every other APB does not conduct is because it has a slightly shorter coupling interval than the conducted APBs, something that is most clearly seen in lead V1.
  • The sinus beat at the end of each group of 3 beats has a longer PR interval than the one at the start of the group — because the AV node, having had less time to recover, is still partially refractory and conducts more slowly.
  • The big weakness with my explanation is that the 2nd beat in each group has a taller T wave than the first. This is easily explained by Ken’s theories because he proposes that there is a premature P wave on top of this T wave, whereas I don’t think there is. My best explanation for the tall T wave of the 2nd beat, is that this QRS has a taller R wave and greater overall positivity than the 1st beat, particularly in some of the chest leads — and that a taller T wave might therefore be expected.
  • The big weakness of Ken’s theories – in my opinion – is that there is absolutely no evidence of a P wave on the T wave of the 2nd beat in each group in V1. Ken thinks that there is a P wave here, and I think there isn’t — and this is the main difference between us in how we see the ECG and therefore interpret it.

Figure-4: David Richley’s laddergram (See Addendum #2).

Thursday, September 24, 2020

Repost: Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

I came across this post from 2015 while answering a question on Twitter, and decided to repost it:

Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3
An elderly male had a syncopal episode.  911 was called.  When medics arrived, the patient was alert and following commands.  In the presence of the medics, he lost consciousness and became apneic and underwent 30 seconds of chest compressions, after which he started moaning and was again able to communicate and follow commands.   No shock was ever delivered.

A 12-lead was recorded:
Without a rhythm strip, this rhythm is difficult.  In any case, there is bradycardia.  There is either RBBB (see rSR' in V1) or there is a left sided escape rhythm that gives RBBB morphology.
There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia.  There is no ST elevation.

The patient was moaning upon arrival to the ED, looked ashen, and had agonal respirations.  He was unresponsive to painful stimuli.

He was in profound shock.

He was intubated.

A bedside cardiac ultrasound was recorded:
If this video does not work, you can view it here:

Here is a still image of the echo:
The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber.
What do you think?

There is no pericardial fluid to account for shock.  The RV is huge.  This essentially rules out hypovolemia as the etiology (no GI bleed, no ruptured AAA, etc.).  It makes pulmonary embolism (PE) very likely.  It also makes large right ventricular infarct possible, but much less likely than PE.  The small LV implies very low LV filling pressures, which implies low pulmonary venous pressure.  RV pressure appears to be high (large RV), so there is obstruction between the RV and LV (PE).

Alternatively, the RV is so ischemic as to be unable to generate high pressures (RVMI).  This is much less likely than PE.

Along with supportive cares, this first ED ECG was recorded:
What do you think?
Annotated with arrows:
The arrows show what I believe are P-waves.  So this is third degree AV block.  There is a wide QRS, so there is infra-HIS escape.  It is RBBB morphology (left bundle escape).
There is obvious ischemic ST elevation in V1-V3, maximal in V1.
There are slightly large T-waves inferior, with ST depression in aVL

What is going on?

First, what kind of arrest was this?  It was a PEA or bradyasystolic arrest, not a shockable rhythm.  There is 3rd degree heart block.  Although most cardiac arrest from MI is due to ventricular fibrillation, some is due to high grade AV block, and so this could indeed be due to large acute STEMI.

Second: what does the ultrasound tell us about the condition? Is this an anterior (LV) MI?  No!          --The large RV and small LV on ultrasound make this a right ventricular process.  A standard anterior MI would have a large LV with poor function, not a small LV.  This LV is not filling.

Third: what does the ECG tell us about the left ventricle?  The STE is anterior, but is it anterior LV or anterior RV????   LV anterior STEMI does not give maximal ST elevation in V1.  So this ECG is typical of right ventricular (RV) STEMI.

Fourth:   RV STEMI is almost always accompanied by profound inferior STEMI.  Though there is some evidence of this in inferior leads, it is not convincing.

          Therefore, the ultrasound looks like PE, and the location of the ST elevation tells us that it is an RV STEMI (which manifests in "anterior" leads, as they overlie the anterior RV).  But it does not tell us whether this RV STEMI is due to type 1 MI (plaque rupture with thrombus) or due to type 2 MI (severe hypotension and increased RV pressure prevents RV perfusion)

Fifth: the ultrasound in RV MI can look identical to that of PE: there can be both McConnell's sign and "D" sign, as well as enlarged RV with poor function.

Sixth:  Severe shock (e.g., due to PE) may result in STEMI (and, if anterior, it can be from anterior LV or anterior RV ischemia, or both) from low coronary pressure and flow, simply due to the shock.  Here we have evidence of massive RV dysfunction.

Seventh: When the severe shock that is the etiology of STEMI is due to PE, the ST elevation likely reflects the RV, as there is both: 1) very low coronary flow in the RV marginal branch (due to BOTH low blood pressure AND due to high RV pressure), and high oxygen demand (increased volume increases wall stress and increased oxygen demand) leads to very low supply and high demand leads to subepicardial ischemia and ST Elevation.

Eighth: STEMI even if from low flow, not ACS, can cause ischemia of the conduction system and result in complete AV block, even infra-HIS AV block.

Ninth: Type II MI can be exacerbated by fixed coronary stenoses.  It may be that there is a stenosis of the proximal RCA, but it need not be thrombotic for this situation to cause extreme ischemia.  There need not be any stensosis at all.

All of this favors PE with resulting RV STEMI, but initiated by PE.

1.  If this had been a shockable rhythm, STEMI would be most likely.  But it is bradyasystolic, so pulmonary embolism must be high on the differential.
2.  The echo shows that, if this is MI, it is most likely an RV MI.  It is not an (LV) anterior MI.
3.  The ECG also shows RV MI, not LV anterior MI
4.  So is this an isolated RV MI with shock?  Possible, but huge pulmonary embolism is more likely.

In a patient with such a differential diagnosis, and in profound shock, near death, the treatment is IV thrombolytics.  A 1/2 dose (50mg) of full dose (100 mg) bolus may be given when the patient is in extremis as this patient is.

Such isolated RV STEMI is rare, but pulmonary embolism is not.  Thus, this is most likely pulmonary embolism, not STEMI.  However, thrombolytics will treat both.  

Lytics are very effective early in the course of STEMI.  

Moreover, their use of lytics does not precluded subsequent angiography and PCI if this turns out to be RV STEMI.

Clinical course

The clinicians thought this was LV STEMI due to the "anterior" ST elevation.  The cath lab was activated.  In the cath lab, the coronaries were clean.  Pulmonary embolism was suspected a right side cath with pulmonary angiogram confirmed it.

Here is the left pulmonary artery
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There is extensive clot in the main pulmonary artery

Here is the right pulmonary artery
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Less thrombus here

Catheter-Based thrombectomy was undertaken.

Here is the post thrombectomy angiogram:
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There is now good flow in both trunks.

Unfortunately, the patient was too ill to survive.


MY Comment by KEN GRAUER, MD (9/25/2020):


Brilliant explanation by Dr. Smith on this tremendously challenging case! I limit my comments to some advanced points regarding interpretation of the 2 ECGs shown in this case.

  • For clarity — I’ve reproduced these 2 tracings in Figure-1.
  • NOTE: Management of this case is not affected by the advanced points I make. My purpose is solely academic to highlight some additional observations in the hope of enhancing ECG interpretation.

Please Take ANOTHER LOOK at the 2 ECGs in this case.

  • Is there evidence of atrial activity?
  • Are there any sinus-conducted beats in either tracing?
  • Does ECG #1 portend what happens in ECG #2?

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

I will again emphasize the brilliant problem-solving discussion of this case by Dr. Smith. As deduced by him (and confirmed by cath + pulmonary angiogram) — the primary event appears to have been a massive pulmonary embolism. The resultant severe shock led to RV MI with ischemic-induced conduction defects that proved too great for this elderly man to overcome.

The Rhythm in ECG #1: As per Dr. Smith — interpretation of the cardiac rhythm is ECG #1 is all but impossible in the absence of a simultaneously-recorded long lead rhythm strip. I fully acknowledge that I am in no way certain of the rhythm. Nevertheless, a number of observations can be made:

  • There is atrial activity! The 4 RED arrows in lead I of Figure-2 identify similar-looking low amplitude, notched deflections at an almost-regular rate. I believe these are real — and identify atrial activity. These may not be P waves arising from the SA node, because the deflections we see in lead II are smaller than those highlighted by RED arrows in lead I.
  • YELLOW arrows highlight what looks to be atrial activity in other leads — but amplitude is low and morphology inconsistent.
  • The QRS complex is wide in ECG #1 — with morphology consistent with a RBBB pattern (rSR’ complex in lead V1 + wide terminal S waves in lateral leads I and V6). The overall ventricular rhythm is fairly regular at 60-65/minute.
  • At the least — there appears to be high-grade 2nd-degree AV Block — as many of the deflections thought to be P waves are not conducted, and the PR interval preceding QRS complexes seems to be constantly changing.
  • Two of the clues that I commonly look for when trying to distinguish between high-grade vs complete AV block are: i) Do any QRS complexes occur unexpectedly early? (which often indicates that such early beats are conducted); andii) Does QRS morphology change, with this change not being due to a premature beat? (ie,Such a change often signals that some beats are being conducted). None of the beats in ECG #1 occur unexpectedly early in ECG #1. The QRS complex of 2 of the beats in ECG #1 do look different (ie, beats #1 and 3) — but I’m hard pressed to know what (if anything) this means. Lead aVF makes one think beats #4 and 5 are conducted — but potential atrial deflections in other leads are not consistent with this.
  • BOTTOM Line: I do not know what the rhythm in ECG #1 is. And, we lack a long lead rhythm strip. I think there is clearly some atrial activity — which is probably not conducting. I suspect at the least there is high-grade AV block with a fairly regular left bundle branch escape rhythm.

About ST-T Wave Changes in ECG #1: It is clearly more difficult to assess ST-T wave morphology for changes of ischemia when the QRS complex is wide. That said — since the escape focus in ECG #1 appears to be in the bundle branch system, we can often see ischemic ST-T wave changes.

  • As I noted above — QRS morphology in ECG #1 is typical for RBBB (rSR’ complex in lead V1 + wide terminal S waves in lateral leads I and V6). What is not typical for simple RBBB — is the shape of the ST segment in each of the chest leads.
  • With simple RBBB — one should not see ST segment coving — as highlighted by the curved RED lines in leads V1-thru-V5 of ECG #1.
  • T wave inversion with simple RBBB is deepest in lead V1 — not in leads V2-thru-V4, as shown in ECG #1.
  • Marked J-point depression (as is seen in leads V4, V5 and V6 in ECG #1) is not part of simple RBBB.
  • The angled shape of the ST segment depression in lead V6 is clearly abnormal (RED lines in V6).
  • Finally — with simple RBBB, the ST segment should be slightly depressed below the baseline in lead V1. The inverted T wave that we see in lead V1 of ECG #1 is an expected finding of RBBB — but the coved ST segment in lead V1 lies clearly higher than it should! Shortly thereafter, ECG #2 was obtained — and we now see the coved anterior ST segments from ECG #1 have evolved into marked ST elevation in leads V1-thru-V3.

Figure-2: I’ve labeled the 2 ECGs in this case — and added a laddergram for the 2nd tracing (See text).

The Rhythm in ECG #2: As per Dr. Smith — the long lead II rhythm strip in ECG #2 now shows consistent, regular deflections that clearly look like sinus P waves at ~48/minute (PURPLE arrows).

  • There once again are regular, wide QRS complexes for the first 8 beats that manifest a very typical RBBB pattern.
  • None of the P waves (PURPLE arrows) appear to be conducting during these first 8 beats in ECG #2.
  • The R-R interval for ventricular beats is just under 6 large boxes in duration — which corresponds to a ventricular rate of ~52/minute. Given the typical RBBB pattern of these ventricular beats — the escape focus again seems to be in the left bundle branch.

Did YOU notice at the very end of the long lead II rhythm strip in ECG #2 that the QRS complex for the last beat ( = beat #9) looks different? IF you measure with calipers — beat #9 occurs ever-so-slightly EARLIER than the 8 different-looking QRS complexes that precede it.

  • The reason beat #9 looks different and occurs slightly earlier compared to the R-R interval for the 8 beats that precede it — is that beat #9 is conducted! Note that the PR interval preceding beat #9 is different (shorter) than the PR interval preceding each of the 8 beats before it that were not conducted.
  • Therefore — there is AV dissociation by “default” (ie, due to sinus bradycardia) — but the rhythm in ECG #2 is not complete AV block, because when a P wave does occur at the “right time”, it can conduct. How severe the AV conduction disturbance is can not be determined solely from the rhythm we see in ECG #2. Alas, the cause of this patient’s demise was not a result of his conduction disturbance.

Our THANKS again to Dr. Smith for his superb problem-solving analysis. Bradyasystolic arrest from massive pulmonary embolism portends an ominous prognosis. Unfortunately, nothing could save this patient.

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