Monday, August 1, 2022

KEEP-SAVE these LINKS for SSmith POSTS-flat ST- LA-RA Reversal- Brugada etc. (8-1.1-2022)


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Comment by KEN GRAUER, MD (7/28/2020):
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July 28, 2020 SSmith

https://hqmeded-ecg.blogspot.com/2020/07/a-woman-with-new-dyspnea-is-extreme.html



MY THOUGHTS on ECG #1: As always — I favor a systematic approach to ECG interpretation. Without a systematic approach — it might be all-too-easy to overlook that something is “off” here ...
  • Regardless of whichever systematic approach you favor for 12-lead ECG interpretation — the 1st Step should always be to interpret the rhythm. Once you’ve ensured that your patient is hemodynamically stable — the, “Watch Your Ps, Qs and 3Rs” memory aid reminds me of the 5 KEY parameters to assess (CLICK HERE — if interested in more on this Ps, Qs, 3R approach).
  • Although there is no long lead rhythm strip in ECG #1 — the rhythm is regular at a rate of ~80/minute. The QRS complex is narrow.
  • P waves are present — and, these P waves are clearly related to neighboring QRS complexes, because the PR interval is constant. This tells us that P waves are conducting to produce the QRS complex that follows them.
  • Did you recognize that the P wave in lead II is negative?

PEARL #1: If you see P waves that are conducting, but these P waves are negative in lead II — then you do not have a sinus rhythm. The only 2 exceptions to this are: i) If there is dextrocardia; and/or, ii) If there is some type of lead reversal.
  • PEARL #2: We can easily rule out dextrocardia for ECG #1 — because R wave progression is perfectly normal in the chest leads (there should be reverse R wave progression if the patient had dextrocardia).
  • This leaves us with distinguishing between a low atrial or junctional rhythm (which could be the cause of negative P waves in lead II) — vs some type of lead reversal.

Recognition of Lead Reversal:
Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — we like to periodically publish clinical examples of lead misplacement. To review a number of these — GO TO:

PEARL #3 — I’ve summarized in Figure-2 those tips that have helped me most over the years to rapidly recognize tracings in which lead reversal is likely (Taken from My Comment in the February 11, 2020 post in Dr. Smith’s ECG Blog).
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    MY Comment by KEN GRAUER, MD (9/5/2020):
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    September 5, 2020 — SSmith post
    https://hqmeded-ecg.blogspot.com/2020/09/a-patient-with-chest-pain-and-st.html


    As per Dr. Smith — today’s case features a series of pathognomonic ECGs of potential life-saving significance if recognized promptly.
    • Dr. Smith reviews key diagnostic features from the 5 serial tracings that are shown and discussed above. I limit my comments to several additional points regarding the 1st and 3rd ECG that were shown — which for clarity, I have put together in Figure-1.

      Figure-1: The 1st and 3rd tracings shown above in today’s case (See text).



    We’ve presented numerous cases of Hyperkalemia on Dr. Smith’s ECG Blog. Today’s case is informative because of the serial nature of findings as they evolve from an initial serum K+ = 9.3 mEq/L — until treatment returns the serum K+ level toward a normal range.
    • I illustrate the “textbook” sequence of ECG findings in hyperkalemia in My Comment at the bottom of the January 26, 2020 post of Dr. Smith’s ECG Blog. Many of these findings are seen in the ECGs from today’s case.

    My THOUGHTS on ECG #1: As per Dr. Smith — the initial prehospital tracing on the 56-year old man in today’s case ( = ECG #1) — is pathognomonic for hyperkalemia.
    • The QRS complex is markedly widened.
    • There is marked bradycardia (rate in the 40s).
    • P waves appear to be present in some places (RED arrows in lead V1) — but P wave amplitude is markedly reduced.
    • Conduction defects are present. Judging from the P waves we see for the 2 QRS complexes in lead V1 (RED arrows) — the PR interval appears to be constant, and markedly prolonged (1st-degree AV block).
    • The presence of P waves elsewhere is less certain. That is — I’m less certain that the question marks in leads I and II represent atrial activity. With progressive hyperkalemia — P wave amplitude decreases until ultimately P waves disappear. Interestingly, the sinus node is often still able to transmit the electrical impulse to the ventricles, even though no P wave may be seen on ECG. This is known as a sinoventricular rhythm — which if not intermittently present in ECG #1 — is seen later on in this case.
    • T wave morphology in ECG #1 is telling. As I illustrate in the January 26, 2020 post — these T waves resemble the Eiffel Tower (ie, not only are T waves in multiple leads of ECG #1 tall, peaked and pointed — but these T waves are symmetric with an equal angle of rise and fall — with a very narrow T wave base). KEY Point: These T waves in leads II, III, aVF; and V3-thru-V6 of ECG #1 are too thin, too symmetric, and have too narrow of a base to be either a repolarization variant of deWinter T waves.
    • Finally — a Brugada-1 ECG pattern is seen in leads V1 and V2 of ECG #1. This is almost certainly a Brugada Phenocopy. As per Dr. Smith — it is common to see Brugada Phenocopy in association with severe hyperkalemia.

    Regarding BRUGADA Syndrome vs Phenocopy: We’ve presented many cases of Brugada ECG patterns on Dr. Smith’s ECG Blog. For an excellent State-of-the-Art Review on Brugada Syndrome — Please SEE this article by Brugada et al in JACC — Vol. 72; Issue 9; 2018.
    • A Brugada Type-1 ECG pattern is diagnosed by the finding of ST elevation of ≥2 mm in one or more of the right precordial leads (ie, V1, V2, V3) — followed by an r’ wave and a coved or straight ST segment — in which the ST segment crosses the isoelectric line and ends in a negative T wave (See Panel A in Figure-2).
    • A Brugada-1 pattern may either be observed spontaneously (with leads V1 and/or V2 positioned normally — or positioned 1 or 2 interspaces higher than usual) — or — a Brugada-1 pattern may be observed on provocative drug testing after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide.
    • NOTE #1: In the past, the diagnosis of Brugada Syndrome required not only the presence of a Brugada-1 ECG pattern — but also a history of sudden death, sustained VT, non-vasovagal syncope or a positive family history of sudden death at an early age. This definition was changed following an expert consensus panel in 2013 — so that at the present time, all that is needed to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern, without need for additional criteria.
    • Panel B in Figure-2 illustrates the Brugada Type-2 or “Saddle-back” ECG pattern. This pattern may be suggestive — but is not diagnostic of Brugada Syndrome (See Figure-2).
    • NOTE #2: A number of conditions other than Brugada Syndrome may temporarily produce a Brugada-1 ECG pattern. These include (among others) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia/infarction/cardiac arrest — and hyperkalemia. Patients with such conditions that may transiently mimic the ECG findings of a Brugada-1 pattern are said to have Brugada Phenocopy. The importance of being aware of this phenomenon of Brugada Phenocopy — is that correction of the underlying condition (ie, hyperkalemia in today’s case) may result in resolution of the Brugada-1 ECG pattern, with a much better prognosis compared to patients with true Brugada Syndrome. Note in the last (5th) ECG shown above in today’s case — that there is no longer any hint of a Brugada-1 or Brugada-2 pattern.


    Figure-2: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol. 72; Issue 9; 2018) — (A) Brugada-1 ECG pattern, showing coved ST-segment elevation ≥2 mm in ≥1 right precordial lead, followed by a negative T-wave. (B) Brugada-2 ECG pattern (the “Saddle-back” pattern) — showing concave-up ST-segment elevation ≥0.5 mm (generally ≥2 mm) in ≥1 right precordial lead, followed by a positive T-wave. (C) Additional criteria for diagnosis of a Brugada-2 ECG pattern (TOP: the ß-angle; BOTTOM: A Brugada-2 pattern is present if 5 mm down from the maximum r’ rise point — the base of the triangle formed is ≥4).



    Returning to Figure-1: I’ll complete my comments with a look at ECG #3 — which was obtained 28 minutes after today’s patient arrived in the ED (following treatment with calcium; glucose + insulin; and albuterol nebulization).
    • Although still wide — the QRS complex in ECG #3 is not as wide as it was in ECG #1.
    • The rate is a little faster (ie, ~60/minute) — but I no longer see any sign of P waves. Presumably — this is now a sinoventricular rhythm.
    • T waves are still tall, peaked and pointed — although not quite as tall as they were in ECG #1.
    • NOTE #3: We are beginning to see ST depression in ECG #3 — especially in the inferior and lateral precordial leads. This is clearly more marked than it was in ECG #1. It’s important to appreciate that the ECG effect of severe hyperkalemia may mask other underlying ST-T wave abnormalities. Only on repeat ECG, after serum K+ returns to normal will we be able to accurately assess for the presence or absence of acute ST-T wave changes.
    • NOTE #4: I found it interesting that certain leads in ECG #3 (especially leads aVL, V2) — look much narrower than they really are. This highlights the importance of using all 12 leads to assess for QRS duration. I’ve added 2 sets of vertical lines in ECG #3 — in which the vertical BLUE line marks the onset of the QRS complex (as seen in the long lead II rhythm strip) — and the vertical PURPLE line marks the end of the QRS. The reason the QRS complex in certain leads looks deceptively narrow — is that part of the QRS in those leads lies on the baseline.
    • NOTE #5: As per Dr. Smith — a Brugada-1 ECG pattern persists in leads V1 and V2 in ECG #3. In addition — we now also see a Brugada-2 (saddleback) ECG pattern in lead V3! That said — the fact that the last (5th) ECG done in this case shows no trace of any Brugada-type pattern essentially confirms we were seeing Brugada Phenocopy associated with severe hyperkalemia on the earlier tracings.





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    Comment by KEN GRAUER, MD (10/27/2018):
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    October 27, 2018
    https://hqmeded-ecg.blogspot.com/2018/10/our-residents-are-getting-really-good.html

    Superb case by Dr. Smith with prompt recognition and treatment of acute coronary syndrome resulting in rapid cardiac cath before any actual infarction occurred. The patient was lucky in that the 80% RCA “culprit lesion” spontaneously reperfused. The lesion was stented in the hope of preventing a future event.
    • I focus my comments on the ECG definition of a “normal” ST segment (Figure-1) — and on some additional fine points regarding ECG interpretation of the first 2 tracings shown in this case (Figure-2):
    Figure-1: Compare the ST segment in Panel A with Panel B. What is the difference? Is this likely to be clinically significant?  (See text).
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    Recognizing Subtle ST Segment Changes — Consensus among expert electrocardiographers is lacking regarding the definition of a normal ST segment. Much of this relates to semantics — since minor ST-T wave abnormalities in a non-acute setting generally provide no more than a nonspecific suggestion to potential etiologies. That said — I feel it important to hone in on recognizing even minimal abnormalities because: i) it is good to let others reading our interpretation be aware that we saw the abnormality in question, even if we may not have thought it clinically important for the case at hand; and, ii) in an acute setting — even subtle ST-T wave abnormalities may be very important!
    • The ST-T wave in Panel A of Figure-1 is normal. Note the smooth contour at the point of transition between the end of the S wave and the beginning of the ST segment. Note an equally smooth contour at the end of the ST segment and the point where the ascending limb of the T wave begins. There is a slight normal upward concavity at this transition between the end of the ST segment, and the beginning of the T wave.
    • In contrast — Note the sharp angle in Panel B at the point where the straight (flat) ST segment ends and the ascending limb of the T wave begins (RED arrow). While admittedly “splitting hairs” — the ST-T wave in Panel B is not normal. Instead — there is nonspecific ST segment straightening (ie, with loss of that smooth transition between the end of the ST segment and the beginning of the T wave ascending limb).
    • I’ll emphasize that in a non-acute setting, “nonspecific ST segment straightening” — is a descriptive finding. It is nonspecific. It may mean nothing — especially if only seen in a single lead. Or, it may suggest some other problem (ie, electrolyte disorder) — or, it may be a nonspecific indicator of underlying coronary disease.
    • On the other hand, in an acute setting (ie, in a patient with new-onset chest pain) — even subtle ECG abnormalities, especially if present in multiple leads — may be extremely important. For this reason — recognition of subtle ST-T wave changes is an essential skill for emergency providers to master.
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    Now look at Figure-2 — in which we compare the initial ED tracing (ECG #1) obtained during chest pain — with ECG #2 obtained 17 minutes later, at a time when chest pain had greatly decreased. To facilitate discussion of the ECG abnormalities noted by Dr. Smith above — I’ve added magnified inserts (within the RED rectangles) for the first 2 complexes in leads II and aVF of ECG #1. Similar changes in the ST-T wave are seen in lead III.
    • In addition to slight-but-real J-point ST elevation — note straightening of the ST segment takeoff. The normal upward-concavity appearance of the ST segment (that we saw in Panel A of Figure-1) has been lost in each of the inferior leads of ECG #1.
    • In contrast — a more normal upward-concavity appearance for the ST segment in the inferior leads has returned in ECG #2 (as shown within the YELLOW rectangle inserts for leads II and aVF). To be clear — the ST-T waves in the inferior leads for ECG #2 are by no means normal (!) — but there clearly is less ST segment straightening — and we now clearly can see some upward concavity to the ST segment in the inferior leads.
    Figure-2: Comparison between the initial ECG obtained in the ED (TOP = ECG #1) — with ECG #2 (BOTTOM) obtained 17 minutes later at a time when chest pain had markedly decreased (See text).
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    Additional fine points regarding the 2 serial ECGs in Figure-2:
    • Could this patient have had prior inferior infarction? After all — there are inferior Q waves that are actually quite large considering the small size of the QRS complexes in the inferior leads. We are told that the patient had “no history of prior infarction” — and, cardiac cath did not suggest any wall motion abnormality — but given presumed significant baseline RCA narrowing, with an episode of spontaneous resolution of acute occlusion — perhaps one or more similar episodes occurred in the past?
    • This is relevant — because (as emphasized earlier by Dr. Smith) — it is highly unusual with acute RCA occlusion (with inferior ST elevation) not to see reciprocal changes in lead aVL. Keep in mind that lead aVL in ECG #1 is not “normal” (ie, the ST segment is uncharacteristically flat) — but there is no ST depression. Could the reason for this be that the lead aVL “baseline” was abnormal from a prior event?
    • There is a change in lead aVL in ECG #2 — in that there is now ever-so-subtle-but-real T wave inversion. This probably is another reflection of this patient’s spontaneous reperfusion.
    • In ECG #1 — there is early transition by lead V2, with R = S in lead V1. This is not a normal appearance in lead V1, which typically shows predominant negativity. Could these findings (ie, R=S in V1 & early transition by lead V2) have similar implications as the inferior Q waves, namely reflect prior posterior infarction?
    • Finally, note in ECG #2 that the tiny QRS complex in lead V1 now manifests an rsr’ — which in conjunction with the narrow terminal s waves in leads I and V6 suggests incomplete RBBB. That said — I suspect the reason for this change in QRS appearance in lead V1 is more likely due to lead misplacement (too high) of V1 and V2 — because the P in V1 of ECG #2 is now all negative (it was biphasic in ECG #1); there is now a negative component to the P in V2 (the P wave was all positive in V2 of ECG #1) — and leads V3-thru-V6 are virtually identical in both tracings (suggesting a technical problem may be the cause of the change in V1 and V2).



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