Wednesday, July 10, 2024

ECG Blog #438 — A Paramedic Diagnosis ...


The ECG in Figure-1 was obtained from a previously healthy middle-aged woman — who was awakened by new-onset CP (Chest Pain) that began ~3 hours before this ECG was obtained. She was stable hemodynamically — but still with CP at the time ECG #1 was recorded.
  • The patient reports 3 shorter episodes of CP the day before.


QUESTIONS:
  • Given this history — How would YOU interpret this ECG?
  • Should the cath lab be activated?

Figure-1: The initial ECG in today's case (See text).


MY Thoughts on Today’s ECG:
In view of the above history — the initial ECG in today's case is clearly of concern. The rhythm is sinus at 70-75/minute — with normal intervals (PR,QRS, QTc) — normal axis — and no chamber enlargement.
  • My "eye" was immediately attracted to leads V2 and V3 (within the RED rectangle in Figure-2). There is early transition in these chest leads (with surprisingly tall R waves in leads V1,V2 — and the R becoming taller than the S wave is deep by lead V3).
  • The ST segment in leads V2 and V3 is inappropriately straightened (as often emphasized in this ECG Blog — there should normally be slight, gently upsloping ST elevation in these leads).
  • Continuing wth neighboring leads V4, V5 and V6 — the T waves in these leads look hyperacute (BLUE arrows) — in that their ST segment takeoff is straightened, with these T waves being larger-than-expected in size with a widened base.
  • PEARL #1: By itself — the appearance of the T wave in lead V4 does not necessarily look abnormal. However, in the context of the clearly abnormal ST-T wave findings in leads V2,V3 — and the more acute-looking appearance of the T waves in leads V5 and V6 — I interpreted the T wave in lead V4 as representing the beginning of this hyperacute change.

MY Impression of ECG #1:
 Given the history of new-onset CP in this middle-aged woman — this initial prehospital ECG in Figure-2 suggests posterior OMI beginning and/or ongoing over the past day that this patient has had symptoms.
  • Given her new episode of CP that awakened her from sleep just 3 hours earlier (and which is still ongoing)the cath lab should be activated! 

  • PEARL #2: Admittedly — the ECG findings in this initial ECG are subtle. But abnormalities are present in each of the chest leads in this patient with new CP. In this clinical context — this ECG is diagnostic of acute posterior OMI. 
  • It should be appreciated that the reason for the lack of clear ST depression in leads V2,V3 — and the lack of ST elevation in leads V4,V5,V6 — may be the ongoing clinical course in this patient, that includes multiple CP episodes over the past day (ie, There could be spontaneous opening and reclosing of the "culprit" vessel over this period of time). It may be that the ECG in Figure-2 represents some pseudo-normalization of what might have be more prominent ST-T wave changes on an earlier ECG.

  • PEARL #3: In addition to posterior involvement — the hyperacute T waves in the lateral chest leads suggest there is acute postero-lateral OMI, which in the absence of obvious inferior lead changes — points to the LCx (Left Circumflex) as the most likely "culprit" artery.

  • PEARL #4: The unexpectedly tall R waves in leads V1,V2 lend support to concern that there may be completed posterior infarction (See ECG Blog #354) — as the mirror-image reflection of deepening Q waves is increasing amplitude of the R wave in anterior leads. Unexpectedly tall anterior R waves is especially likely to signal completed posterior infarction IF this finding is new compared to prior ECGs.

Figure-2: I've labeled KEY findings in the initial ECG.

===========================

The CASE Continues:
Serial ECGs were obtained by the prehospital team. Figure-3 offers a comparison between one of these repeat ECGs — and the original prehospital ECG (with ~30 minutes separating the time between the recording of these 2 tracings).
  • WHAT do you learn from the repeat ECG in Figure-3?

Figure-3: Comparison of the initial ECG — with the repeat ECG done in the field ~30 minutes after the initial ECG.


===========================

What We Learn from the Repeat ECG:
IF there was any doubt after seeing ECG #1 about the need for prompt cath lab activation — that doubt should be removed by the "dynamic" ST-T wave changes that are evident in virtually all leads in the repeat ECG.
  • PEARL #5: The BEST way to compare one serial ECG with another — is to put both tracings side-by-side — and to then go lead-by-lead, always comparing one lead area to the corresponding lead area in the 2nd ECG.
  • Instead — it is all-to-common for clinicians to ignore this important procedural point. Instead, the tendency is to try to "gain time" by looking at 1 tracing in its entirety — and then the 2nd tracing in its entirety without taking the time to directly compare each lead area with the corresponding lead area in the 2nd tracing. The reality is that unless you compare the 2 tracings by going lead-by-lead — it is all-too-easy to overlook subtle but important findings.
  • Along the way — it is also important to ensure that our lead-by-lead comparison is "comparing apples with apples, and not with oranges". By this I mean — that we want to ensure that any changes in ST-T wave morphology are not the result of a significant frontal plane axis shift or due to a change in chest lead electrode placement.

Applying this Comparison Technique
in Figure-4:
Although there is a slight frontal plane axis shift (from about +40 degrees in ECG #1 — to +60 degrees in ECG #2) — this small change is unlikely to alter our assessment of comparative limb lead ST-T wave appearance. Chest lead QRS morphology appearance is essentially the same in both tracings. Therefore — any ST-T wave changes that we note between these 2 ECGs are likely to be "real".
  • In the Limb leads of ECG #2 — there now is subtle-but-real ST elevation in each of the inferior leads (as seen by respect to the dotted RED line baseline in each of these leads)
  • ST-T waves in these inferior leads have a more acute appearance than they did in ECG #1 (ie, there is more straightening of the elevated ST segment takeoff) — and we may be seeing the beginning of small inferior lead Q waves.
  • The BLUE arrow in lead aVL — highlights ST segment straightening that was not present in ECG #1. I interpreted this as a reciprocal change to the new inferior lead ST elevation.
In Chest Leads:
  • BLUE arrows in leads V2 and V3 — highlight an increase in ST depression.
  • In leads V5 and V6 — there should be no doubt that there is a more acute appearance with straightening of the ST segment takeoff and increased ST elevation (with respect to the dotted RED lines in these leads).

MY Impression of ECG #2: In this patient with ongoing CP — the repeat ECG in Figure-4 confirms "dynamic" ST-T wave changes. 
  • Prompt cath is indicated! — in this symptomatic patient with acute ongoing infero-postero-lateral OMI.

Figure-4: I've labeled findings in the repeat ECG.


CASE Follow-Up:
  • Serial troponin values were markedly elevated.
  • Cardiac cath revealed normal left main and LAD branches — and, a small but non-obstructed RCA. The main trunk of the LCx (Left Circumflex) showed a 50% lesion in the middle of this vessel — with severe narrowing proximally in the 1st Obtuse Marginal branch of the LCx, which was felt to be the "culprit" artery. Angioplasty was successfully performed.




==================================
Acknowledgment: My appreciation to Konstantin Тихонов (from Moscow, Russia) for the case and this tracing.
==================================


Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = an acute coronary Occlusion MI).
=================================
  • CLICK HERE  for my new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
  • CLICK HERE  for my new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).
=================================
    • Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
    • Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators— See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 

    • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
    • ECG Blog #230 — Reviews how to compare serial ECGs.
    • ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
    • ECG Blog #268 — Shows an example of reperfusion T waves.
    • ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.

    • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).







    Thursday, July 4, 2024

    ECG Blog #437 — A 2-Part Answer ...


    I was sent the ECG in Figure-1 — but without the benefit of any history. 

    QUESTIONS:
    • How would YOU interpret this tracing?
    •   WHY do I say there is, "A 2-Part Answer?"

    Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). 


    MY Thoughts on Today's CASE: 
    As important as providing a brief, relevant history is for optimal clinical ECG interpretation — Cases like the one today often prove even more educational, because we are not given any history (and therefore need to deduce the most likely clinical setting to explain the ECG in front of us).
    • As per the title I selected — there is a 2-Part Answer to today's post, which entails: i) Determining the cardiac rhythm; and, ii) In light of this rhythm — interpreting how this 12-lead tracing is highly suggestive of the cause of this rhythm!


    Take Another LOOK at the ECG in Figure-1.
    • WHAT is the rhythm?
    • HOW does knowing what this rhythm is — help in determining the cause of this rhythm?
    ===============================


    ANSWER:
    Let's presume that the patient in today's case is hemodynamically stable. I favor starting with the long lead II rhythm strip — by use of the Ps, Qs, 3R Approach (See ECG Blog #185 for more on the Ps, Qs, 3Rs).
    • The ventricular rhythm in Figure-1 looks Regular — with the exception of slight irregularity seen at the end of the tracing (most notably for the R-R interval between beats #13-to-14, which is clearly longer than all other R-R intervals).
    • The overall ventricular Rate is ~100/minute, as the R-R interval for all but the last 2 beats is ~3 large boxes in duration (and 300 ÷ 3 = 100/minute).
    • The QRS complex is narrow in all 12 leads. Therefore — the rhythm is supraventricular.
    • P waves are present!

    PEARL #1: The simple steps of numbering beats and labeling those P waves that we definitely see — greatly facilitates our recognition of what is going on.
    • Starting with beat #2 in Figure-2 — RED arrows highlight each of the P waves that we definitely see. 


    QUESTION:
    • Do YOU Think that the atrial rhythm in Figure-2 remains regular throughout the entire rhythm strip?

    •   HINT: Do you see any indication that an additional on-time P wave may be occurring between beat #12 and beat #14?

    Figure-2: I have added RED arrows for P waves I definitely see.


    ANSWER:
    • PEARL #2: When the underlying atrial rhythm is regular (with possible exception of 1 or 2 P waves that are not clearly seen) — the chances are excellent that those 1 or 2 "missing" P waves may be present (and may be occurring on-time) — but are simply hidden within a QRS complex or ST-T wave. 
    • Using calipers facilitates the search for any potentially "missing" P waves that might be in hiding — because you know where to look

    Consider the following in Figure-3:
    • IF the underlying atrial rhythm in Figure-3 was to be regular — Wouldn't we expect to see another "on-time" P wave at the point marked by the YELLOW arrow?
    • Doesn't knowing where to look in Figure-3 — help us to identify that there is an extra deflection (just under the YELLOW arrow — at the very end of the QRS complex of beat #13?).

    Figure-3: I've added a YELLOW arrow at the point where I'd expect to find another on-time P wave.


    We now have the elements needed to solve today's arrhythmia:
    • Colored arrows in Figure-4 highlight that there is an underlying regular atrial rhythm.
    • The QRS complex is narrow.
    • The slight pause in the rhythm (that occurs between beats #13-to-14) — ends with a sinus-conducted P wave (ie, the PINK-arrow P wave in Figure-4). This PINK P wave produces sinus-conducted beat #14, which manifests a minimally prolonged PR interval.
    • The next P wave is on-time — and is conducted with 1st-degree AV block (ie, the PURPLE-arrow P wave in front of beat #15 which manifests a PR interval = 0.31 second).
    • Working backward — no QRS follows the YELLOW arrow P wave in Figure-4. This suggests that the RED arrow P wave that precedes beat #13 is being conducted, albeit with a very long 1st-degree AV block (ie, PR interval >0.52 second).
    • This suggests that each of the previous RED arrow P waves in Figure-4 are also conducting with very long PR intervals to produce the next QRS complex in front of them.

    • Conclusion: The rhythm in today's case is 2nd-degree AV block, Mobitz Type I ( = AV Wenckebach).

    PEARL #3: The reason it is so challenging to recognize Mobitz I in today's tracing — is that there is a very long cycle until a beat is dropped.
    • With long Wenckebach cycles — the increment in PR interval from one beat to the next may be minimal and hard to appreciate by visual comparison. In such cases — the easiest way to verify that the PR interval is increasing, is to LOOK at the PR interval just before the pause (ie, the PR interval before beat #13 in Figure-4) and compare it to the PR interval that starts the next cycle (ie, the PR interval from the PINK arrow P wave in Figure-4 — until beat #14).
    • That today's rhythm is Mobitz I, 2nd-degree AV block — is confirmed by the presence of other "Footprints" of Wenckebach, which are: i) Regular atrial rhythm; ii) The pause containing the dropped beat is less than twice the shortest R-R interval; and, iii) Progressive increase in the PR interval, which is easy to see in Figure-4 in the next Wenckebach cycle (ie, The PR interval formed by the PURPLE arrow P wave is clearly longer than that formed by the PINK arrow P wave). For more on the "Footprints" of Wenckebach — See ECG Blog #164.

    Figure-4: The diagnosis of Mobitz I becomes apparent from the colored arrows at the end of this tracing (See text).


    How Does Knowing the Rhythm Help to Interpret the 12-Lead?
    As I often emphasize — 2nd-degree AV block, Mobitz Type I is most commonly seen in association with acute inferior and/or posterior OMI.
    • Knowing that today's rhythm is Mobitz I therefore prompts me to look especially closely for any suggestion of acute inferior and/or posterior OMI.

    In Figure-5 — I've labled the 2 leads in today's 12-lead tracing that immediately "caught my eye". 
    • Lead V3 (within the RED rectangle) — is the most remarkable lead. Normally, there should be a slight amount of gentle upsloping ST elevation in leads V2 and V3. In view of this — there is no way the ST segment straightening seen without any hint of ST elevation in lead V3 can be a "normal" finding.
    • Lead V2 (within the BLUE rectangle) — also manifests an inappropriately straightened ST segment, thereby supporting our impression that the ST-T wave in neighboring lead V3 is not normal.
    • ST-T wave changes in other leads show nonspecific ST-T wave flattening, and are non-diagnostic.

    • To Emphasize: The ST-T wave changes highlighted above are subtle. That said — Given 2nd-degree AV block, Mobitz Type I for the rhythm — the ECG appearance of the 2 leads in Figure-5 (within the colored rectangles) — have to be interpreted as suggestive of acute posterior OMI until proven otherwise!

    Figure-5: I've highlighted the 2 leads that "caught my eye".


    Today's LADDERGRAM:
    For clarity — I've drawn a laddergram in Figure-6.
    • Several of the essentials for Wenckebach periodicity are present in Figure-6. These include: i) Regular atrial rhythm; — ii) The pause that contains the dropped beat is less than twice the shortest R-R interval; — and, iii) Progressive PR interval lengthening is seen in the last 2 beats on the tracing.

    • NOTE: Isn't it virtually impossible to discern any change in the PR interval for the first 12 beats in this tracing?
    • That said, the YELLOW P wave in Figure-6 is not conducted — and — the PR interval just before the pause in this rhythm is clearly longer than the PR interval at the end of the pause. This makes it obvious that today's rhythm is Mobitz I, 2nd-degree AV block.

    Figure-6: Laddergram for today's rhythm.



    ==================================
    Acknowledgment: My appreciation for the anonymous submission of this case to me.
    ==================================


    Related ECG Blog Posts to Today’s Case:

    • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

    • ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).
    ================================= 
    • CLICK HERE  for my new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
    • CLICK HERE  for my new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).
    =================================
      • Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
      • Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators— See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 

      • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
      • ECG Blog #230 — Reviews how to compare serial ECGs.
      • ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
      • ECG Blog #268 — Shows an example of reperfusion T waves.
      • ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.

      • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).

      • ECG Blog #351 — for review of the ECG diagnosis of acute posterior OMI (with links to additional examples of posterior OMI in the references at the end of this post).











      Friday, June 28, 2024

      ECG Blog #436 — Bigeminy or Alternans?


      The ECG in Figure-1 — was obtained from an older man with known coronary disease. He was on a number of medications — including antiplatelet agents, a statin drug and Digoxin.
      • The patient presented to the ED (Emergency Department) for an episode of syncope. He developed cardiac arrest shortly after the ECG in Figure-1 was recorded.

      QUESTIONS:
      • How would YOU interpret the ECG in Figure-1?
      •   What is the most likely cause of this arrhythmia?

      Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). 


      MY Thoughts on the ECG in Figure-1:
      A repetitive bigeminal pattern is seen in Figure-1 — in which QRS morphology alternates with each beat. 
      • There are 2 different QRS morphologies — both of which clearly manifest a wide QRS complex when this rhythm is viewed in certain leads. Thus, although one of these QRS morphologies looks narrow in lead V3 — a glance at leads III, aVR, aVL, V1 and V2 confirms that the QRS is wide!
      • NOTE: Although QRS morphology from one-beat-to-the-next looks similar in certain leads (ie, in leads aVR, V4,V5,V6) — there can be no doubt about the presence of 2 distinct QRS morphologies when one looks at leads I, III, aVL, aVF — and leads V1,V2,V3.

      • The overall rate of the rhythm in Figure-1 is fast (at least 150/minute).
      • There are no P waves.

      • And, the patient is older (ie, prone to reduced renal function) — and he is taking Digoxin.

      IMPRESSION: Given the presence of a wide tachycardia — with 2 distinct QRS morphologies, and no sign of P waves — a presumed diagnosis of BiDirectional Ventricular Tachycardia has to be made.
      • As discussed in ECG Blog #231 — Bidirectional VT is a special form of VT, in which there is beat-to-beat alternation of the QRS axis. This unique and very uncommon form of VT is distinguished from PMVT (PolyMorphic VT) and from pleomorphic VT — because a consistent pattern (ie, alternating long-short cycles) is usually seen throughout the VT episode. As implied in its name, there are 2 QRS morphologies in bidirectional VT — and they alternate every-other-beat (CLICK HERE — for this case report Review by Femenia et al on Bidirectional VT in a patient with CPVT = Catecholaminergic Polymorphic VT).

      • KEY Point: There are a limited number of causes of Bidirectional VT — with the 2 most common causes being Digoxin toxicity and CPVT. Given that today's patient was taking Digoxin — Digoxin Toxicity was immediately suspected as the most likely cause. 
      • Since Digoxin is primarily renally excreted — older age, that is commonly associated with reduced renal function, would predispose to developing Digoxin toxicity.

      As reviewed by Almarzuqi et al (Vasc Health Risk Mgmt 18:397-406, 2022)  Potential Causes of Bidirectional VT include:

      • Digitalis toxicity.
      • CPVT (Catecholaminergic PolyMorphic VT).
      • Acute myocardial ischemia.
      • Familial hypokalemic periodic paralysis.
      • Cardiac Sarcoidosis.
      • Primary Cardiac Tumors and/or Cardiac Metastasis.
      • Andersen-Tawil Syndrome ( = Long QT Syndrome, Type 7).
      • Acute Myocarditis.
      • Certain drug overdoses (Aconitine poisoning, severe caffeine poisoning).

      To Emphasize: Bidirectional VT is rare. That said, it does occur — and awareness of the entities associated with this diagnosis may be important in evaluation and treatment.


      ==============================

      CASE Conclusion:
      As noted above — today's patient developed cardiac arrest shortly after arrival in the ED. Despite prolonged resuscitation with multiple defibrillation attempts — the patient could not be saved.



      ==================================

      Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and these tracings.

      ==================================

       

      =======================

      Related ECG Blog Posts to Today’s Case: 

      • ECG Blog #36 — Reviews irregular wide tachycardias (with distinction between Torsades de Pointes vs Polymorphic VT discussed in Figure-3 in this post). 
      • See My Comment in the June 1, 2020 post in Dr. Smith's ECG Blog — for review of Pleomorphic VT.
      • ECG Blog #231 — for review on the types of VT (including monomorphic — polymorphic — pleomorphic — and bidirectional VT).

      • Bidirectional VT: Challenges and Solutions (Almarzuqi et al — Vasc Health Risk Mgmt 18:3997-406, 2022)

      • Pleomorphic VT and Sudden Cardiac Death — Editorial by Liu and Josephson on potential mechanisms to explain the ECG appearance of Pleomorphic VT. 
      • Case Report on BiDirectional VT — by Femenia et al on this patient with BiDirectional VT from CPVT (Catecholaminergic Polymorphic VT).
      • ECG Blog #197 — Reviews the concept of Idiopathic VT (including recognition and treatment of Fascicular VT and RVOT VT).
      • Multifocal vs Polymorphic VT — September 23, 2011 post from Dr. S. Venkatesan's insightful and user-friendly Cardiology Blog (from which I adapted his figures to derive my Figure-3).










      Saturday, June 22, 2024

      ECG Blog #435 — Did Cath Show Acute Ischemia?


      The ECG in Figure-1 — was obtained from a middle-aged woman with positional tachycardia and diaphoresis with change of position from suprine to sitting. Although CP (Chest Pain) was not a prominent symptom — ACS (Acute Coronary Syndrome) was suspected from the chest lead T wave inversion seen on this ECG.


      QUESTIONS:
      • How would YOU interpret the ECG in Figure-1?
      •   Do you agree with the diagnosis of ACS?
      •     WHY — or Why Not?

      Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). 


      My THOUGHTS on the ECG in Figure-1:
      The rhythm is sinus tachycardia at ~105/minute (ie, The R-R interval is regular — and just under 3 large boxes in duration). The PR interval is normal. The QRS complex is narrow — but the QTc appears to be prolonged (although this is more difficult to assess given the tachycardia). No chamber enlargement. A small, narrow (and normal) septal q wave is seen in leads I and aVL.

      Additional relevant ECG findings include:
      • There is an rSr' pattern in leads III and aVF — but not in right-sided lead V1. Although an rSr' pattern in either lead III or aVF is more of a descriptive finding — the potential relevance of this pattern in today's case is that this terminal right-sided activity (that writes the r' in these vertical/right-sided leads) sometimes serves as a proxy for an IRBBB (Incomplete Right Bundle Branch Block) pattern.
      • There is poor R wave progression — with transition (where the R wave becomes taller than the S wave is deep) being delayed until between leads V5-to-V6.
      • S waves persist in the chest leads through to lead V6.

      Regarding ST-T wave findings:
      • The most remarkable ECG finding in Figure-1 — is the fairly deep and symmetric T wave inversion, that begins in lead V1 — and continues through until lead V5
      • Nonspecific ST-T wave flattening is seen in most of the remaining leads.
       
      IMPRESSION:
      While the History in today’s case was not especially suggestive of ACS (ie, There was no mention of CP) — this history was also not suggestive of any other specific diagnosis. That said — the ECG in Figure-1 should prompt the following considerations:
      • The symmetric chest lead T wave inversion in ECG #1 could be a sign of coronary disease, potentially with acute ischemia. And as per ECG Blog #350 —  this could represent Wellens' Syndrome IF this chest lead T wave inversion was new and occurred in a patient who initially had a normal ECG, and then had an episode of transient CP that had resolved at the time this ECG with chest lead T wave inversion was recorded.
      • PEARL #1: Before attributing the chest lead T wave inversion seen in ECG #1 to Wellens' Syndrome — it is essential to inquire IF the patient had a prior episode of CP that has now resolved at the time the T wave inversion is seen.

      • Alternatively — the symmetric chest lead T wave inversion in ECG #1 could be a sign of Takotsubo Cardiomyopathy — especially given hemodynamic instability reported in the history — and, what appears to be QTc prolongation (See ECG Blog #277).

      • As another alternative consideration — Diffuse ST-T wave abnormalities (including T wave inversion) as are seen in ECG #1 could be the result of a non-cardiac condition — including marked metabolic and/or electrolyte disturbance, CNS catastrophe (ie, stroke, intracerebral or subarachnoid bleed, trauma, tumor), severe anemia, "sick" patient, etc.

      MY Hunch:
       Before going further — We need to consider the possibility of acute PE (Pulmonary Embolism)!
      • PEARL #2: Acute PE remains one of the most commonly overlooked diagnoses. As per links that I provide below — IF the diagnosis of acute PE is not thought of, this entity will be missed! (See ECG Blog #313 — as well as My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog).

      • As emphasized in previous ECG Blog posts — Figure-2 lists the series of ECG findings most commonly associated with acute PE. Of these — acute RV "strain" is the most suggestive ECG sign. Statistically, in an adult population with new symptoms — the finding of symmetric, anterior lead T wave inversion (as seen in Figure-1) is much more likely to reflect RV "strain" than acute coronary disease.

      • Additional, potentially supportive ECG signs of acute PE in Figure-1 include: i) Sinus tachycardia; ii) Poor R wave progression, with persistence of S waves through to lead V6; and, iii) The rSr' morphology (ie, IRBBB proxy) seen in leads III and aVF.

      • To EMPHASIZE: While the ECG picture in today's tracing is clearly not definitive for the diagnosis of acute PE — seeing anterior T wave inversion in association with sinus tachycardia in this patient with signs of hemodynamic instability (ie, positional tachycardia with diaphoresis on change of position from supine to sitting) — should at least prompt consideration of this diagnosis.

      Figure-2: ECG Findings associated with acute PE.



      CASE Conclusion:
      As noted in my presentation above — the ECG in Figure-1 was initially interpreted as suggestive of ACS. Cardiac cath was planned — until the patient had an episode of syncope with severe hypotension.
      • Stat Pulmonary CT angiography was ordered — and confirmed acute PE.

      ==========================================

      P.S. = PEARL #3: An Often Forgotten Clinical NOTE ...
      Initial assessment of the patient for possible acute PE begins by counting the respiratory rate. During my decades of working with residents when hospital Attending — by far, the most commonly overlooked vital sign was respiratory rate.
      • KEY Point: The respiratory rate that is written on the chart does not count! I cannot tell you how many times such "written" documentation was off, due to the tendency to inscribe a normal number instead of counting for 30 seconds because "the patient looked like they were breathing normally".
      • Patients may "look" like they are breathing normally — when in fact they are tachypneic if you simply take the time to watch them and count the number of rapid, shallow respirations. All it takes is a few seconds of concentration for you to determine how fast the patient is breathing. And, IF the patient's respiratory rate is increased — and their initial ECG looks like the initial ECG in today's case — You have made the diagnosis of acute PE until proven otherwise!


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      Acknowledgment: My appreciation to Mahtab Parvizpour (from Khorramabad, Iran) for the case and these tracings.

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      Related ECG Blog Posts to Today’s Case: 

      • ECG Blog #313 — Reviews in detail a case that illustrates the ECG diagnosis of acute PE.
      • ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
      • ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
      • My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).

      • ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
      • ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”

      • ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome (What it is — and what it is not! ). 

      • ECG Blog #277 — Reviews findings in Takotsubo Cardiomyopathy.

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      ADDENDUM (6/21/2024): 
      • I've excerpted below in Figure-3 and Figure-4 — several pages from my ECG-2014-ePub — that summarize the ECG findings of acute PE (Pulmonary Embolus) — as well as an Audio Pearl relevant to today's topic.

          
        Figure-3: Summary of KEY findings in the ECG diagnosis of acute PE.



        Figure-4: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE. 


        ECG Media PEARL #49 (7:40 minutes Audio) — Reviews the ECG finding of Anterior T Wave Inversion (with emphasis on not overlooking acute PE as the cause!).

       









      Friday, June 14, 2024

      ECG Blog #434 — WHY Did this Patient Arrest?


      The ECG in Figure-1 — was obtained from a middle-aged man who presented to the ED (Emergency Department) in cardiac arrest. ROSC (Return Of Spontaneous Circulation) was obtained — and ECG #1 was recorded.
      • In view of this history — How would YOU interpret the ECG in Figure-1? Should you activate the cath lab?

      Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio)

      MY Initial Thoughts:
      Although there are different approaches regarding decision-making as to which patients with ROSC following OHCA (Out-of-Hospital Cardiac Arrest) should undergo prompt cardiac catheterization — what does appear to be clear, is that the post-ROSC ECG helps to identify patients at highest risk who may benefit from coronary reperfusion (Gentile et al — JAHA 12:3027923, 2023 — and — Baldi et al — JAMA Netw Open 4(1): e2032875, 2021).
      • Prompt cath is therefore advised if the post-ROSC shows an acute STEMI.
      • The decision of whether to cath patients with a less definitive post-ROSC ECG is less clear. Waiting a few extra minutes to repeat the ECG in such patients may help reduce false positive results when there are equivocal findings on the initial post-ROSC tracing.

      The Post-ROSC ECG in Today’s CASE:
      The initial ECG following ROSC in today’s case is clearly abnormal. I’ve highlighted KEY findings in Figure-2.
      • Although there is significant baseline artifact in the limb leads of ECG #1 — the underlying rhythm is sinus — as conveyed by the presence of upright P waves with a constant and normal PR interval in lead II (BLUE arrows in lead II of Figure-2). The rhythm is regular — at a rate just over 100/minute = sinus tachycardia (ie, the R-R interval is just under 3 large boxes in duration).

      • PEARL #1: In general — lead II is the best lead for assessment of P waves to determine if sinus rhythm is present. Sinus rhythm is defined by the presence of upright conducting P waves in this lead. 
      • The above said, when for whatever reason sinus P waves are not well seen in lead II — the 2nd-best lead when looking to determine if sinus rhythm is present, is lead V1. Recognition of a negative P wave deflection with fixed PR interval before the next QRS (similar to that highlighted by BLUE arrows in lead V1 of Figure-1) — confirms that the rhythm in today's ECG is sinus.

      PEARL #2:
       We can tell at a glance in Figure-1 — that the "culprit" causing the artifact in today's ECG is the RA (Right Arm) extremity. The cause of the abnormal baseline deflections seen in Figure-2 is most likely muscle tremor artifact (See Bouthillet T — ACLS Med Training, Dec, 2015). A quick LOOK at the patient would confirm this — but unfortunately, there is no information about the patient's appearance.
      • NOTE: Abnormal baseline deflections in Figure-2 are maximal in leads I,II and aVRAs discussed in ECG Blog #255 — the extremity primarily responsible for a certain type of artifact — can be quickly recognized by the finding of greatest artifact amplitude in 2 of the 3 standard limb leads (ie, in leads I and II for Figure-2) — and, minimally or not seen at all in the 3rd standard limb lead (ie, artifact is minimal in lead III). By Einthoven's Triangle — this localizes the "culprit" extremity to the RA electrode.

      • SHORTCUT (To find the "culprit" extremity within seconds! ): When 2 of the standard limb leads clearly show greater artifact amplitude than the 3rd standard limb lead — then whichever augmented lead shows maximal amplitude indicates the "culprit" extremity (which is lead aVR in Figure-2 = which means that the RA is the "culprit" extremity).
      • Clinically — Rapid determination of the "culprit" extremity may facilitate quick correction (ie, If you could quickly know to look if the RA electrode had become loose — this may be easy to rectify).

      Figure-2: I've labeled the initial ECG.

      Continuing with assessment of ECG #1 in Figure-2:
      • The rhythm is sinus tachycardia at ~110/minute. The QRS complex is obviously wide. QRS morphology is consistent with RBBB (ie, all positive QRS in right-sided lead V1 — with wide terminal S wave in left-sided leads I and V6).
      • The all negative QRS complexes in each of the inferior leads indicate marked LAD (Left Axis Deviation). That said, rather than LAHB (Left Anterior HemiBlock) — the all-negative QRS in leads II,III,aVF is really a “QS” wave — which therefore suggests inferior MI at some point in time (possibly with or without associated LAHB).

      • The most worrisome part of this tracing is in the chest leads. RED arrows in leads V2,V3,V4 mark the J-point, which defines the end of the QRS complex in these leads. Everything to the right of these arrows entails the ST segment. As can be seen when compared to the dotted RED lines that mark the baseline in these leads — there is marked ST segment elevation, which is most dramatic in leads V3 and V4. This is followed by especially “bulky” (hyperacute) T waves in leads V5,V6, that are clearly taller, “fatter”-at their peak and wider-at-their base than expected given amplitude of the QRS complex in these leads.
      • Adding support to the occurrence of proximal LAD OMI — is the ST elevation that is clearly seen in lead aVL. Although harder to appreciate because of the variable baseline — there is also a hyperacute T wave in lead I.

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      PEARL #3: Today’s ECG provides an excellent example of T-QRS-D (Terminal QRS Distortion)When present — T-QRS-D may provide invaluable assistance for distinguishing between a repolarization variant vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI = Occlusion-based Myocardial Infarction)

      I illustrate the ECG finding of T-QRS-D below in Figure-3, which I've excerpted from My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog. To review:
      • T-QRS-D — is defined as the absence of both a J-wave and an S-wave in either lead V2 or lead V3 (and/or probably also in lead V4). Although simple to define — this finding may be subtle! It takes a while to become comfortable and confident in its recognition.

      A picture is worth 1,000 words. I’ve taken thlead V3 examples in Figure-3 from previous cases posted on Dr. Smith’s ECG Blog:
      • TOP in Figure-3 — Despite marked ST elevation in lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
      • BOTTOM in Figure-3 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).

      Figure-3: Comparison between ST elevation in lead V3 due to a repolarization variant (TOP — from 4/27/2019) — vs acute OMI (BOTTOM — from 9/20/2015), which manifests T-QRS-D (See text).


      To Emphasize: The phenomenon of T-QRS-D is not needed in today's case to recognize the acute STEMI. Once the J-point is recognized in the chest leads (RED arrows in leads V2,V3,V4 of Figure-2) — the marked ST elevation becomes obvious.
      • In my experience — T-QRS-D is not a common finding among patients with acute coronary occlusion. That said, the importance of being aware of this phenomenon — is that on occasion other signs of acute OMI may not be obvious, such that seeing T-QRS-D may be a KEY finding in support of acute infarction (See ECG Blog #318).
      • Today's case is also noteworthy in that T-QRS-D is seen in association with RBBB — which has only been described on rare occasions (See the March 28, 2021 post in Dr. Smith's ECG Blog).
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      CASE Conclusion:
      As noted above — the middle-aged man in today's case presented to the ED in cardiac arrest. Retrospective questioning of the driver who brought this patient to the hospital revealed that he was having chest pain as the reason for presenting to the ED. He became unconscious on arrival.
      • A series of VFib episodes followed — each time with successful defibrillation. ROSC (Return Of Spontaneous Circulation).
      • Cardiac cath was not performed — because the interventionist did not recognize the ECG signs of acute MI.


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      Acknowledgment: My appreciation to Nirdosh Ashok Kumar (from Karachi, Pakistan) for the case and this tracing.

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      Related ECG Blog Posts to Today’s Case:

      • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

      • ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" should be replaced by "OMI" = Occlusion-based MI).
      =================================
      • CLICK HERE  for my new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
      • CLICK HERE  for my new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).
      =================================
        • Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
        • Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators— See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 

        • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
        • ECG Blog #230 — Reviews how to compare serial ECGs
        • ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
        • ECG Blog #268 — Shows an example of reperfusion T waves.
        • ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.

        • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).

        • ECG Blog #282 — reviews a user-friendly approach to the ECG diagnosis of the Bundle Branch Blocks (RBBB, LBBB and IVCD).

        • ECG Blog #203 — reviews ECG diagnosis of Axis, Hemiblocks and Bifascicular Blocks.

        • ECG Blog #318 — reviews the concept of T-QRS-D (Terminal-QRS-Distortion).