Wednesday, January 22, 2020

This middle-aged patient presented with SOB, weakness, and mild pulmonary edema.

This middle-aged patient presented with SOB, weakness, and mild pulmonary edema.

She previously had Atrial fibrillation with LBBB.

Here is her ED ECG:
Does this reveal the etiology of her symptoms?

This shows atrial fibrillation.  There is a regular, slow response.  The fact that the response is regular proves that the atrial fibrillation is NOT conducting.  When atrial fib conducts, the ventricular rate must always be irregular.

This is atrial fibrillation with complete (3rd degree) AV block.

The QRS morphology is RBBB with a vertical axis.  This suggests an LV escape rhythm, possibly from the left anterior fascicle.

She previously had known LBBB, so she is lucky that her left sided escape can make it out of the LV through the left sided conducting system to the right side.  She could have developed an escape that is not able to use the conducting system at all; such an escape would be very wide and bizarre, with uncertain efficacy.  She could even have developed asystole.

There are 3 etiologies I always think of with bradycardia and AV block:
1. Medications -- she had been on metoprolol for 4 years at the same dose, so this is unlikely to be the etiology
2. Hyperkalemia.  Her K was normal
3. Ischemia.  There was no evidence of ischemia.

Thus, this is a sick AV node.

She had a permanent pacemaker implanted.

After pacer AND conversion to sinus rhythm:
Computer diagnosis:
What is missing from this interpretation?


Many computer algorithms do not make any attempt at atrial rhythm diagnosis when the ventricle is paced.  This is puzzling to me, because it is very important!

It is common for physicians to ignore the atrium in this situation and forget the stroke risk.

See this terrible case:

Computer often fails to diagnose atrial fibrillation in ventricular paced rhythm, and that can be catastrophic

MY Comment by KEN GRAUER, MD (1/22/2020):
Our THANKS to Dr. Smith for presenting this extremely interesting case. In the interest of academic discussion — I’ll present another perspective on selected aspects this case.
  • Pertinent information for clinical decision-making is not mentioned among the details we are provided with ... For illustrative purposes — I will “walk through” mthought process on examining the 2 ECGs in this case (Figure-1).

Figure-1: The initial ECG recorded in the ED (See text).

Clinical Points Regarding ECG #1:
We are told that the patient is a middle-aged woman — and that she previously had been in AFib with LBBB.
  • PEARL  Realizing that complete information is not always available (and it may not have been available in this case) — I always look through the old chart for the actual ECG at the time the patient was said to be in AFib with LBBB. I learned the importance of doing so through unfortunate personal experience, in which regardless of the capabilities of the provider who wrote out the ECG interpretation — many times I would catch findings not mentioned (or erroneously interpreted) in the written description. KEY  It’s always BEST for YOU to see the actual ECG before accepting a written interpretation by someone else as valid.
  • This is relevant in this case. IF this patient was previously in LBBB — and now manifests RBBB — then we have alternating BBB, which is an extremely high-risk situation for abrupt development of ventricular standstill. Permanent pacing would then be clearly needed.
  • In ECG #1 — We see a combination of baseline artifact presumed “fib waves”. Atrial activity could easily be lost within all the baseline undulations that we see. Therefore — knowing this patient was truly in AFib before would help me to be more comfortable that we are truly dealing with regularization of AFib” in ECG #1 — and not just a simple junctional escape rhythm without AFib (or even something else ...).
  • As per Dr. Smith — the rhythm in ECG #1 is regular, with the exception of 1 PVC ( = beat #5). Keep in mind that the phenomenon of regularization of AFib” (to this degree of regularity) is not common! By far (!!!) — the most common cause of this phenomenon is Digoxin Toxicity — such that it is worth searching through all of the pills that enter this patient’s mouth (We’ve all seen patients who forget some of the meds they are taking, that may not have accompanied them to the hospital). While I agree that AFib + complete AV block is the most likely rhythm diagnosis — I'd like to see additional monitoring strips to be sure ...

Assuming we are dealing with AFib + regularization of the ventricular response due to complete AV block — I do not think the site of the escape rhythm is in the ventricles ( = my opinion). I say this because: i) QRS morphology is precisely consistent with typical complete RBBB (ie, triphasic rSR’ with taller right rabbit ear and S wave that descends below the baseline in lead V1 + wide terminal S waves in lateral leads I and V6, with triphasic opposite qRS morphology in lead V6). In contrast, fasicular escape tends to manifest less typical “pure” RBBB morphology — and — fascicular escape should manifest resemblance to bifascicular block (either RBBB/LAHB or RBBB/LPHB), which is not present in this case; andii) The rate of the escape pacemaker is exactly 50/minute — which is most consistent with a junctional escape focus.
  • This is relevant — because junctional escape with RBBB (instead of postulating a ventricular site of escape— would confirm alternating BBB, which is strong indication for permanent pacing.
  • It is also relevant — because assessment of ST-T wave morphology is clearly more valid when dealing with a supraventricular QRS morphology (See below).

The question then arises as to whether this patient has SSS ( = Sick Sinus Syndrome) — and — whether sufficient investigation has been completed to confirm this diagnosis.
  • SSS is by far the most common cause of permanent pacing in the U.S. The syndrome is characterized by a long “prodrome” period (often 10-20 years) — during which a series of suggestive rhythm disorders evolve. These include sinus bradycardia & arrhythmia — sinus pauses/sinus arrest — associated “sick AV node” disease — SA block/AV block of varying degrees — slow AFib — slow AV nodal escape rhythms — and often periods of “tachyarrhythmias” (ie, “tachy-brady” syndrome), including fast AFib, ATach, reentry SVT — ultimately, with delayed SA node recovery time (leading to long pauses) after tachyarrhythmias terminate.
  • While the diagnosis of SSS may become readily apparent early on in many patients — clear indication for pacing usually does not become established until there is profound, symptomatic bradycardia — usually requiring pauses of at least ≥3.0 seconds in duration.
  • Although SSS can be seen at any age — it is by far (!!!) most commonly seen in an older population (patients at least 60, and often much older)NOTE  The patient in this case was only “middle-aged” — so SSS would not yet be expected in most patients in this age range ... — which makes one ask IF something else (ie, underlying coronary disease) was going on?
  • Finally — SSS is a diagnosis oexclusion. In addition to ruling out rate-slowing medication — serum electrolyte disorders — and/or ischemia/infarction as potential causes of bradyarrhythmias — one should also rule out hypothyroidism + sleep apnea.
Ischemic Heart Disease can be recent or longstanding. We are not told how “ischemia” has been ruled out in this case ...
  • Has this patient been cathed? Given the heart failure and markedly abnormal ECGs — I would expect cardiac cath at some point to have been performed.
  • In my opinion — there are ischemic changes on ECG #1. These are not acute changes — but I see definite ECG findings not expected in simple RBBB.
  • With typical RBBB — the ST-T wave should be oppositely directed to the last QRS deflection in leads I, V1 and V6. While the T wave in V1 is inverted as expected with RBBB — the ST segment in both V1 and V2 is not at all depressed (RED arrows). This is not what should be expected with simple RBBB ...
  • Typically, the most J-point ST depression with RBBB is seen early (ie, in leads V1, V2). Instead, we see more J-point ST depression in lead V3 (highlighted by the dark BLUE arrows) than we do in leads V1 and V2.
  • J-point ST depression continues in leads V4, V5 and V6 (light BLUE arrows).
  • The ST segment in lead I is uncharacteristically straight (straight RED lines in this lead).
Conclusion  The above are all subtle-but-real abnormal ST-T wave findings that should not be seen with simple RBBB. They clearly do not suggest acute coronary occlusion — but they are consistent with ischemia. I’d want to know more information (ie, prior tracings, more history, serial troponins, follow-up ECGs, cardiac cath results) — before confirming the need for pacing, and before ruling out potentially treatable ischemic heart disease as a cause.

Clinical Points Regarding ECG #2:
We are then shown ECG #2, in which conversion to sinus rhythm has occurred — and a permanent pacemaker has been implanted (Figure-2).

Figure-2: The 2nd ECG in this case, that was obtained some time after conversion to sinus rhythm, and after insertion of a permanent pacemaker (See text).

The following are thoughts to consider regarding the limited information we have been given in this case.
  • WHEN in the process was ECG #2 obtained? A day after ECG #1? or many days later? Clinically — What has happened in the interim?
  • HOW was this patient converted to sinus rhythm? NOTE  Given apparent long-standing AFib in this patient with severe conduction system disease — restoration of sinus rhythm is far from an easy task (ie, the longer a patient has been in AFib — the more difficult it becomes to cardiovert the patient, and then maintain sinus rhythm) = all the more reason to search for additional monitoring strips before the pacer was inserted, to verify that the initial regular rhythm (that was laden with artifact) in ECG #1 was indeed AFib ...

Regarding ECG #2:
I’m not bothered by lack of computer algorithms commenting on the underlying rhythm in pacer tracings. In my experience — the aspect of interpretation that computer algorithms do most poorly in, is interpretation of complex arrhythmias. I hold little hope that computer algorithms will provide useful information given the subtleties of complex pacer tracings.
  • NOTE  Despite conversion to sinus rhythm in ECG #2, there remain significant baseline undulations. This is relevant — because I raised the valid question in ECG #1 as to how much of the undulations we saw at that time were the result of “fib waves” (from presumed AFib with regularization of the ventricular responsevs baseline artifact. Looking at ECG #2 suggests that a large part of the undulations we saw in ECG #1 probably were artifact and not “fib waves”.
  • I believe we see an underlying sinus rhythm in ECG #2 (with spontaneous P waves) — which is followed ~0.24 second later by ventricular pacing spikes. I’ve added dark BLUE arrows at selected places where we clearly see ventricular pacing spikes. But note that we do not see these everywhere, and that the clarity of these pacing spikes sometimes varies for consecutive beats in certain leads. Nevertheless — I believe all QRS complexes (except the PVC = beat #11) are ventricular paced.
  • It is of interest that the QRS of paced beats in the long lead II rhythm strip looks narrow. A look at simultaneously-recorded other leads however, confirms that these paced ventricular complexes are indeed wide.
  • Following the PVC (beat #11) — there is a short pause. The RED arrow suggests that this pause was long enough to initiate atrial pacing of the P wave before beat #12.
  • Although I do not see any ventricular pacing spike in front of beat #12 — the fact that this QRS looks identical to all other paced beats in the long lead II tells us that beat #12 is also ventricular paced.
Conclusion — It appears that there is a DDD pacemaker that is functioning appropriately (ie, both sensing and pacing both atria and ventricles). Details could be confirmed, depending on pacer specifications (ie, rates, intervals) that were set, which we are not privvy to. 

P.S.  There is NO way any computer algorithm would be able to sort out this degree of complexity that we see in ECG #2, in which there is so much confusion generated by the baseline artifact.

Sunday, January 19, 2020

A woman in her 70s with bradycardia and hypotension

Submitted by Anonymous, written by Pendell Meyers

A woman in her 70s with HTN and DM had been experiencing lower chest / upper epigastric pain off and on for approximately one week until it acutely worsened, with diaphoresis and extreme fatigue. Her family called EMS and EMS recorded hypotension and this ECG:

What do you think?

This is an obvious inferoposterior OMI. There is STE in III and aVF which does not meet STEMI criteria due to insufficient STE in lead aVF. There is reciprocal STD in I and aVL. There is STD in V1-V5, maximal in V2-3, which is diagnostic of the posterior component. The quality is not perfect, but I believe this is sinus rhythm at about 100 bpm with prolonged PR interval.

It is impossible to determine from this ECG if there is also a right ventricular MI, but there is a suggestion of RVMI: the STD in V2 is very deep and yet minimal in V1. STD in V2 from posterior MI can "pull down" the STE in V1 and negate it.

On arrival in the ED, she was profoundly hypotensive, nearly obtunded, and bradycardic.  Resuscitation was initiated and this ECG was obtained:

Likely AFib (irregularly irregular) with bradycardia. ST changes persist, however this ECG shows some signs of reperfusion including terminal T-wave inversion in the inferior leads with tall posterior reperfusion T-waves in V2-4. 

Of course, the electrical and mechanical aspects of reperfusion are not always perfectly coincidental - just because there appears to be transient electrical reperfusion pattern does not mean that the inferior and posterior walls (or the SA and/or AV nodes) are functioning.

The cath lab was activated. The interventionalists insisted that the ECGs did not meet STEMI criteria and cancelled the activation, stating that they would consider urgent cath after further stabilization.

Atropine produced no response. The patient was placed on pressors and transcutaneous pads (which failed to capture). She was intubated and a transvenous pacemaker was inserted with good capture. She received PR aspirin.

Bedside echo showed obvious inferior wall motion abnormality and good TVP placement, no effusion.

At about 30 minutes after presentation, the patient had acceptable vital signs with the TVP and low dose epinephrine drip. Another ECG was obtained during pacing:
Mostly paced rhythm with PVCs (#3, #6, #9, #12). The PVCs have obvious STE in III and aVF and V6, with STD in I, aVL, V2-3. The paced beats show a clear OMI pattern as well, by the modified Sgarbossa criteria: lead III for example has 3.5 mm STE with 9.5 mm QRS = 37%, well over 20-25% as we have described. Proportionally excessive discordant STE is present in II, III, aVF, and V6. V5 has a barely concordant appearance, probably not a full millimeter.

The ED team again pointed out the evidence of inferoposterior OMI, this time by the modified Sgarbossa criteria. The cardiologists were not familiar with this and insisted that the ECG in paced rhythm could not be used to "look for a STEMI". After some discussion, cardiology insisted that they would need a native rhythm ECG to evaluate for STEMI criteria.

So they paused the TVP and obtained this ECG:

First beat is paced, then the rest are native. There appear to be very small possible P waves which may be conducting with huge PR interval and heart block, but this is irrelevant clinically. The QRS is narrow and shows a clear inferoposterior OMI pattern like all the ECGs before.

The ED team believed that this ECG met STEMI criteria, however the cardiologists felt that there the inferior leads had significant J-waves at the J-point, followed by STE that does not meet STEMI criteria.

At this point it was approximately 90 minutes after patient arrival.

Cardiology requested a head CT before cath for unknown reasons, which was negative. First troponin T was positive at 0.06 ng/mL.

Cardiology then requested 2U PRBC transfusion for Hgb 7.5 prior to cath, which was started.

During this time, the patients blood pressure continued to decline, requiring 4 pressors to sustain hemodynamics.

The patient expired approximately 2.5 hours after arrival, before cath was performed.

Learning Points:

We must not let STEMI criteria prevent identification and/or treatment of Occlusion MI. We must hold ourselves and our consultants to a higher standard to protect our patients.

Use the modified Sgarbossa criteria to detect OMI in the setting of ventricular paced rhythm.

Consider thrombolytics for OMI when PCI is not an option.

MY Comment by KEN GRAUER, MD (1/19/2020):
There is a LOT to talk about regarding the series of tracings in this unfortunate case. I’ll limit my comments toward reinforcing concepts brought forth by Dr. Meyers — with additional focus on rhythm interpretation.
  • I must respectfully disagree with Dr. Meyers regarding his comment that rhythm interpretation of ECG #4 is “irrelevant clinically”. On the contrary (as I’ll emphasize below) — more accurate rhythm interpretation would have provided one more way that the cardiology team could have (should have) been convinced that this patient was evolving an acute OMI in front of their eyes.
  • For clarity — I'll reproduce the 4 ECGs in this case.
  • PEARL  As I’ve said many times before, use of Calipers is EASY, and it instantly makes you “smarter”. I had NO idea whether the atrial rhythm in ECGs #3 and #4 were regular — until I measured P-P intervals with calipers. This did not delay my interpretation — on the contrary, using calipers allowed me to accurately assess the underlying atrial rhythm much faster than trying to guess what might or might not be regular.

NOTE: Some of my comments below regarding rhythm interpretation are quite sophisticated ( = advanced). It is fine if you don’t follow them all — since it is the overall concepts that are important to enhancing and appreciating clinical interpretation of the essentials in this case.

Figure-1: ECG #1 — recorded by EMS on the scene (See text).

Clinical Points Regarding ECG #1:
  • I do not understand why the cardiology team was “stuck” on requiring “STEMI criteria” in this case. This 70-something year-old woman had symptoms for ~1 week prior to admission. While the additional history of “acute worsening” of symptoms might indicate the time of acute occlusion — given that she had symptoms for days prior to calling EMS — the cardiology team should clearly have considered the possibility that the initial event occurred before the day of admission to the hospital!
  • The patient was hypotensive in association with the initial ECG ( = ECG #1)Regardless of whether “STEMI criteria” are (or are not) strictly met — a recent acute event in a dramatically symptomatic patient (this woman was profoundly hypotensive, with reduced mentation) is in-and-of-itself clear indication for prompt diagnostic/therapeutic cardiac catheterization.
  • As per Dr. Meyers — ECG #1 shows an obvious inferoposterior OMI. There should be NO doubt that despite only 1mm of ST elevation in leads III and aVF — these are acute changes, given hyperacute ST-T waves in both leads III and aVF mirror-image opposite ST-T wave reciprocal depression in lead aVL (further supported by 1 mm of flat shelf-life ST depression in lead I).
  • Among the reasons why it may be that no more than 1 mm of ST elevation is seen in leads III and aVF are: iThat the QRS is tiny in these leads (as it often is with inferior MI) — so percentage-wise, the amount of J-point ST elevation is actually >25% R wave amplitude in leads III and aVF; andii) This patient’s symptoms have been ongoing for ~1 week — so some of the ST elevation may have receded by this point in the process.
  • As per Dr. Meyers — there is very deep ST depression in anterior leads, that approach 3 mm deep in lead V2. Many experts view this shape of ST depression in one or more anterior leads as the “reciprocal” of what is ongoing in the LV posterior wall — which should (for practical purposes) translate to more-than-enough acute ST deviation to qualify for “STEMI criteria”.
  • Dr. Meyers’ point regarding the possibility of associated acute RV involvement (because of no more than minimal ST depression in lead V1, in the face of marked ST depression in V2) — is extremely relevant in this patient with profound hypotension — since need for volume replacement is a prominent part of resuscitation. Right-sided chest leads would have provided a more definite answer regarding associated acute RV involvement.
  • While not part of “written STEMI criteria” — the unexpected 2 mm of J-point ST elevation for the PVC in lead aVF of ECG #1 provides additional evidence of recent (and/or ongoing) acute OMI.
  • Unfortunately — the quality of ECG #1 + baseline artifact prevent accurate rhythm interpretation. That said, I agree with Dr. Meyers that this most likely represents a sinus rhythm at ~95/minute + 1st-degree AV block — though we’d need a better quality rhythm strip to know for certain what the rhythm is. That said — Remember that we suspect 1st-degree AV block (this becomes relevant with rhythm assessment of subsequent tracings!).

Figure-2: ECG #2 — recorded on arrival in the ED (See text).

Clinical Points Regarding ECG #2: I found the rhythm in ECG #2 especially interesting:
  • I agree with Dr. Meyers that there is likely to be some underlying AFib in ECG #2 — because the R-R intervals preceding beats #3, 4 and 7 are all different — and we do not see clear sign of P waves in any of the 12 leads on this tracing.
  • That said — note that QRS morphology changes in the long Lead V1 rhythm strip. Using Calipers allows you to instantly measure R-R intervals — and it is not by chance that the R-R interval preceding each of the 3 beats with incomplete RBBB morphology is identical ( = 8.3 large boxes in duration).
  • This confirms that these 3 beats ( = beats # 2, 5 and 6) are escape beats. Since the QRS complex is no more than slightly prolonged for these 3 beats, with a very similar initial deflection that manifests incomplete RBBB/LPHB morphology (LPHB morphology is seen for beat #2 in simultaneously-recorded leads I,II,III) — the site of this escape focus is in the conduction system, most likely arising from the left anterior hemifascicle.
  • In addition to marked bradycardia — could there be high-grade AV block? Intermittent conduction defects (such as the incomplete RBBB/LPHB seen here) — are most commonly associated with acceleration of the heart rate — yet they are seen here with increased bradycardia — which leads me to suspect a progression of AV block in this patient with ongoing and evolving inferior MI. Acute inferior MI is notorious for its association with stepwise progression from 1st-degree — to 2nd-degree AV block, Mobitz I — to 3rd-degree AV block — and perhaps we are seeing this?

Figure-3: ECG #3 — recorded after ~30 minutes in the ED, after placement of a transvenous pacemaker (See text).

Clinical Points Regarding ECG #3:
  • As per Dr. Meyers — ECG #3 shows a paced rhythm with ventricular trigeminy (every 3rd beat is a PVC).
  • Using Calipers allows you to establish an underlying regular atrial rhythm! I’ve highlighted with RED arrows in ECG #3 those low-amplitude P waves that I am nevertheless certain about. Following through this P-P measurement with my calipers, allows detection of the likely remaining P waves (PINK arrows).
  • I suspect the mechanism of this rhythm is not sinus — because we really don’t see atrial activity in lead II (therefore, an ectopic atrial rhythm is likely).
  • While hard to diagnose coexistent underlying AV block given regular ventricular pacing in ECG #3 — the fact that the PR interval constantly changes, but without any evidence of conduction suggests there is some underlying AV block (probably high-grade 2nd-degree).

Figure-4: ECG #4 — recorded by the cardiology team after pausing pacing after beat #3 (See text).

Clinical Points Regarding ECG #4:
  • IF you were skeptical about my statement that there is an underlying regular atrial rhythm in ECG #3 — then review of ECG #4 should resolve any skepticism. There can be NO doubt that regular (albeit non-sinus) atrial activity is evident in ECG #4 (RED arrows).
  • There can also be NO doubt that 2nd-degree AV block, Mobitz Type I (ie, AV Wenckebach) is present in ECG #4. There is group beating — with the R-R interval between beats #6-7 and #8-9 being identical — and then with the preceding R-R intervals (between beats #5-6 and between #7-8) also being identical. The PR intervals preceding beats #4, 6 and 8 are all identical ( = 0.54 second) — with identical PR intervals for the 2nd beat in each of these groups ( = 0.58 second). There is NO way this is by chance!
  • NOTE: Two pacing spikes are seen in ECG #4 — and this resets some of the PR interval relationships. Beat #1 is paced (Note the very wide and different-looking QRS complex). We also see a pacing spike just in front of beat #3 — but since the QRS complex of beat #3 looks identical to that of all other beats on this tracing — I postulated that beat #3 was conducted with a PR interval = 0.36 second.

BOTTOM Line: While some details about the rhythm in ECG #4 are less than certain — there can be NO doubt that 2nd-degree Ablock, Mobitz Type I is present in ECG #4 — in this 70-something woman with ~1 week of symptoms (with recent exacerbation) + clear evidence of ongoing acute infero-posterior (probably also RV) OMI.
  • Recognition of the rhythm disturbances in this case is relevant (in my opinion), since what appears to be 1st-degree AV block — then high-grade 2nd-degree AV block — then clear evidence of Mobitz I — is so characteristic of AV conduction disturbances seen with evolving inferior OMI, as to supply further confirmation that there has been a recent acute cardiac event that is still ongoing.
  • CONFESSION: I do not understand why the cardiology team involved in this case refused to cath this profoundly symptomatic patient.
  • I hope feedback is provided to the involved cardiology team ...

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