Written by Pendell Meyers, with some edits by Smith
A man in his 40s with many comorbidities presented to the ED with chest pain, hypotension, dyspnea, and hypoxemia.
The bedside echo showed a large RV (Does this mean there is a pulmonary embolism as the etiology?)
Here is his triage ECG:
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| What do you think? Lots of info here. |
The rhythm is 2:1 atrial flutter. The flutter waves can conceal or mimic ischemic repolarization findings, but here I don't see any obvious findings of OMI or subendocardial ischemia.
The QRS is around 100 msec wide (narrow), but with very abnormal morphology including a large R-wave in V1, deep S-wave in I, R-wave in aVR. If this were RBBB, it would need to be incomplete, as the QRS duration is less than 120 ms.
However, V1 does NOT have an rSR' as one would see in either complete or incomplete RBBB. Rather, there is a qR. (Exception: One might see a qR in RBBB if there is an old septal MI). There are also large R-waves in V2 and V3, all indicating right ventricular hypertrophy.
The ST depression in V1-V3 might make you think of posterior OMI; however, these are all discordant to the abnormal R-wave. The repolarization abnormalities are all secondary (as a result of) the abnormal QRS (RVH). These are very typical repol abnormalities for RVH.
When you suspect pulmonary embolism due to large RV on POCUS, always look for right axis deviation and a large R-wave in V1 because the large RV may be entirely due to chronic RVH, not acute PE. PE does not manifest a large R-wave in V1 unless it is RBBB or iRBBB.
Chronic RVH is due to chronic pulmonary hypertension, and these patients are extremely difficult to manage when they are acutely ill.
There is also a suggestion of hyperkalemia with peaked T waves, but I was not able to get a potassium level in this case.
A prior ECG was available for comparison:
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| There is sinus rhythm here; the QRS is the same |
We can see that the QRS is essentially the same as prior. The RVH is not new. Notice the STD maximal in V3-4. This is NOT indicative of posterior OMI because it is secondary to this very abnormal QRS made by RVH.
OMI recognition cannot be learned well by reading text, but our best "sentence" or "criteria" for helping learners see posterior OMI is: In the context of acute symptoms suspicious for ACS, ST depression maximal in V1-V4 (without an abnormal QRS cause) is specific for posterior OMI until proven otherwise. This is one of the times when the abnormal QRS is causing the STD maximal in V1-V4, by the principle of appropriate discordance.
The electronic medical record revealed that this patient had known history including pulmonary hypertension, sickle cell disease with frequent transfusions, CHF, restrictive lung disease with chronic hypoxic respiratory failure on oxygen at home, CKD, OSA on nightly BIPAP, and chronic pulmonary embolism. Obviously he has multiple reasons to have pulmonary hypertension.
How about management?
1) It would help to cardiovert to sinus rhythm
------This would improve the atrial contribution to ventricular filling.
2) Norepinephine to support Blood Pressure.
------This is critical for supporting RV perfusion. The RV is normally a low pressure chamber, and perfusion happens in both systole and diastole (unlike the LV, which only perfuses in diastole when the pump is not squeezing). But in pulmonary hypertension, RV perfusion is greatly diminished, especially when there is hypotension. This leads to a "vicious circle" in acute on chronic RV failure.
CT pulmonary angiogram revealed only his known chronic PE burden, no acute PE.
He was critically ill with a complex course, and ultimately did not do well.
See these other cases of RVH:
An elderly woman with shortness of breath and an ECG that helps understand it
This was texted to me by a former resident. An 80-something woman who presented with chest pain and dyspnea.
What is going on in V2 and V3, with a troponin I rising to 1826 ng/L at 4 hours?
55 year old woman with chest pain and precordial T-wave Inversions
- For clarity in Figure-1 — I've reproduced and labeled the 2 ECGs in today's case.
- NOTE: The reason I find today's initial ECG so challenging — is that both for the rhythm, as well as for the rest of this 12-lead tracing — there is a differential diagnosis, and not a single definite answer. Rather than a single diagnosis for the rhythm and the 12-lead — optimal interpretation in my opinion entails awareness of the need for additional clinical information before we can settle on "the Answer".
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| Figure-1: I've labeled the 2 ECGs in today's case. |
- Although the QRS complex in ECG #1 looks a little wide — I measure QRS duration = 0.10 second (ie, half of a large box on ECG grid paper) — which is at the upper limit of normal for QRS duration.
- There is atrial activity in ECG #1 — in the form of a negative deflection that occurs near the mid-point of the R-R interval in lead II (BLUE arrows).
- There is 1 different-looking beat ( = beat #6 in the long lead II rhythm strip of ECG #1). Presumably beat #6 is a PVC (Premature Ventricular Contraction) — since it is wider and very different-looking than the other beats in this tracing. Presumably there is also some fusion of this PVC with the underlying supraventricular beats.
- As I've often reviewed in my comments on Dr. Smith's ECG Blog (See the May 1, 2023 post, among many others) — review of a few considerations will usually narrow down this differential diagnosis within seconds.
- The rhythm in ECG #1 is not Sinus Tachycardia — because there is no upright P wave in lead II. Instead, we see a negative deflection (highlighted by the BLUE arrows) — as well as a rounded upright deflection to the right of the blue arrows that looks to broad too be a sinus P wave.
- I doubt that the rhythm is a reentry SVT. As I review in my comment at the bottom of the page in the March 6, 2020 post of Dr. Smith's ECG Blog — the negative atrial activity highlighted by the BLUE arrows looks to be misplaced for either AVNRT (in which the RP' interval is very short, usually not passing beyond the S in the QRS) — or for AVRT (in which the RP' interval usually does not pass beyond the midpoint of the ST segment). While possible that this rhythm could reflect the "fast-slow" form of AVNRT (ie, as shown in my Figure-3 of the March 6, 2020 post) — this "fast-slow" form of AVNRT is very uncommon, and usually manifests a sharper and deeper negative deflection for the retrograde P wave.
- It's possible that the rhythm could be ATach. That said — strict 1:1 conduction with ATach is a relatively uncommon form of SVT in an unselected emergency setting (ie, there more often will be group beating with Wenckebach conduction and/or some pause in the SVT).
- This leaves us with AFlutter. In my experience — AFlutter with 2:1 AV conduction is by far the most commonly overlooked cause of an undiagnosed SVT rhythm — especially when sinus P waves are absent, and the ventricular rate of the rhythm is close to ~150/minute (ie, usual range ~130-160/minute).
- The EASIEST way to avoid overlooking the diagnosis of AFlutter is to: i) Remind yourself that AFlutter is by far the most commonly overlooked SVT rhythm — such that we need to always think of this diagnosis whenever we see any regular SVT rhythm at ~130-160/minute, in which sinus P waves are absent; ii) Remember that when you see atrial activity near the midpoint of the R-R interval in a fast rhythm (as highlighted by the BLUE arrows) — that there very often will be 2:1 atrial activity (with a 2nd P wave hidden within the QRS complex); and, iii) Use calipers! (ie, Set your calipers to precisely 1/2 the R-R interval — and then search all 12 leads to see IF there is any kind of deflection that you can walk out with this 2:1 ratio).
- Setting my calipers to precisely 1/2 the R-R interval — I was able to walk out 2:1 atrial activity for the rounded positive deflections in leads III and aVF (RED lines) — as well as for the rounded negative deflections in lead aVL (PURPLE lines).
- Although not quite in the usual "sawtooth" pattern of typical AFlutter — this 2:1 atrial conduction — which given the ventricular rate of ~140/minute — would yield an atrial rate of ~140 X 2 ~ 270-280/minute, virtually confirming the diagnosis of AFlutter even before treatment (ie, reentry SVTs and ATach generally don't go quite this fast).
- Final Point regarding the Rhythm: I always look for a "break" in an SVT rhythm — as the slight change in the cadence of the rhythm often provides a "tell-tale" clue to etiology. I believe the BLUE lines in the long lead II rhythm strip support the diagnosis of AFlutter — by showing what appears to be uninterrupted flutter waves before and after the PVC.
- For example — Doesn't it look like there is ST coving with some inferior lead ST elevation in ECG #1 during AFlutter? Although we do not have a follow-up ECG on today's patient — I suspect that once the rate slows and the rhythm converted to sinus, that this "pseudo-ST-elevation pattern" will resolve.
- This patient has IRBBB (Incomplete Right Bundle Branch Block) — as determined by the qR pattern in right-sided lead V1 with predominant positivity in this lead — in association with slightly widened terminal S waves in all lateral leads (ie, in leads I, aVL, V6).
- As I mentioned above — the QRS is of upper normal duration, but not widened (ie, ~0.10 second) — which is why this is "incomplete" (and not complete) RBBB.
- As I've discussed in detail in my comment at the bottom of the page of the February 12, 2023 post of Dr. Smith's ECG Blog — the ECG diagnosis of RVH (Right Ventricular Hypertrophy) is difficult to make. This is because no single ECG finding by itself is diagnostic — but instead, the ECG diagnosis of RVH is made by identifying a combination of ECG findings in a patient with a clinical history consistent with RVH.
- IRBBB itself is one of the ECG findings consistent (suggestive) of RVH.
- While difficult to sort out potential ST-T wave inversion in the inferior and anterior leads in ECG #1 given the rhythm of AFlutter at a rapid rate, and the absence of a follow-up tracing — I suspect the negative deflections seen in leads III, aVF and V3 may persist following conversion to sinus rhythm, therefore suggesting the possibility of RV "strain".
- Although difficult to sort out from IRBBB (which by definition produces a terminal S wave in lead V1) — there appears to be an S1Q3T3 pattern in ECG #1.
- PEARL: Although possible for a RBBB conduction disturbance (complete or incomplete RBBB) to lose the initial positive deflection (r wave) in lead V1 because of septal infarction — in the presence of other ECG findings suggestive of RVH — a qR pattern in lead V1 often serves as a marker for pulmonary hypertension (illustration of the pathophysiology for this ECG finding in Figure-2 of my comment from the February 12, 2023 post).
- At this point — I got to see a prior ECG on this patient ( = ECG #2 in Figure-1) — and learned about the patient's History (ie, Sickle Cell Disease with frequent emergency visits for blood transfusions, heart failure, renal insufficiency and pulmonary hypertension from restrictive lung disease with chronic hypoxemic respiratory failure and a history of prior pulmonary embolisms).
- Sinus rhythm is present in the prior ECG (RED arrow in lead II of ECG #2). Note how this upright P wave with normal PR interval in ECG #2 contrasts with the negative deflection in the mid-point of the R-R interval in ECG #1 (BLUE arrow). Remember that atrial activity near the mid-point of the R-R interval in a fast rhythm often signals the presence of 2:1 atrial activity!
- Note that the precisely regular 2:1 atrial activity seen in ECG #1 (ie, the RED and PURPLE lines seen in leads III,aVF and aVL) were not seen in the prior ECG — supporting our impression that these rounded deflections represented 2:1 flutter activity.
- IRBBB with a qR pattern in lead V1 (YELLOW arrows in both tracings) + ST-T wave inversion in leads V1-thru-V4 were present in the prior ECG — consistent with this patient's longstanding history of end-stage pulmonary disease with pulmonary hypertension. This confirmed that none of these ECG findings were new.
- The T waves in leads I and V3-thru-V6 were not nearly as pointed in the prior tracing compared to ECG #1 — in support of Dr. Meyers concern that this chronically ill patient with longstanding renal disease may be hyperkalemic.
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