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!


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

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.

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

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-2: Summary of KEY findings in the ECG diagnosis of acute PE.



    Figure-3: 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.

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

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).
=================================

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).


     



    Friday, June 7, 2024

    ECG #433 — Which Lead Convinced Me?


    The ECG in Figure-1 was obtained from a previously healthy older man — who presented to the ED (Emergency Department) with new but atypical CP (Chest Pain) for several hours.


    QUESTIONS:
    • Given this history — How would YOU interpret this ECG?
    • Which lead is the most concerning?

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


    MY Initial Thoughts on Today’s ECG:
    The older age of today’s patient — and the fact that he presents to the ED for new CP immediately places this patient in a higher-prevalence risk category (albeit there is some reduction in risk — given the “atypical” nature of his CP). Clearly, more information (ie, assessment of his initial ECG) will be needed for optimal decision-making.
    • The initial ECG that is shown in Figure-1 is not normal! That said — the abnormal findings are subtle.

    Looking Systematically (as per ECG Blog #205):
    • The rhythm is sinus. All intervals (PR, QRS, QTc) are normal. The axis is vertical — but still within normal limits (ie, the QRS is slightly more positive than negative in lead I — so the frontal plane axis is +75-80 degrees). There is no chamber enlargement.

    Regarding Q-R-S-T Changes:
    • Small and narrow Q waves are seen in the inferior and lateral chest leads (ie, in leads II,III,aVF; and in V5,V6).
    • R Wave Progression — is normal, with transition (where the R wave becomes taller than the S wave is deep) taking place normally (seen here in ECG #1 — to be between leads V3-to-V4).

    Regarding ST-T Wave Changes:
    • PEARL #1: The one lead that immediately "caught my eye" in today's tracing — is lead I (within the RED rectangle in Figure-2). There simply is no way that the ST-T wave in lead I is normal because: i) The ST segment is straightened in lead I (as per the horizontal RED line that I drew over the ST segment in this lead); and, ii) The J-point of this straightened ST segment is depressed (and considering the tiny size of the QRS in lead I — this ST depression is significant!).

    • There is subtle-but-real J-point ST elevation in lead III and lead aVF (BLUE arrows in these leads). I was not initially certain of what (if anything) to make of this slight J-point ST elevation in these inferior leads, given the gentle upsloping (ie, "smiley"-configuration) shape and the lack of any J-point ST elevation in the 3rd inferior lead ( = lead II).
    • I considered that the symmetric T wave inversion in lead aVL might represent a reciprocal change (BLUE question mark in this lead) — BUT — PEARL #2: The T wave may normally be inverted in lead aVL when the frontal plane axis is vertical, as it is in Figure-2.

    • PEARL #3: I considered that the small q waves seen in leads II,III,aVF might represent the injury marker of inferior infarction — but in addition to normal septal q waves being commonly seen in one or more lateral leads (as they are here in leads V5,V6)normal septal q waves may also normally be seen in the inferior leads when the frontal plane axis is vertical, as it is in Figure-2.

    • BOTTOM Line: Were it not for the ST-T wave appearance in lead I — I would not have been at all certain that the above described changes in leads II,III,aVF and aVL were acute, and not simply a manifestation of a repolarization variant in a patient with a vertical frontal plane axis. BUT — Given that I knew that the ST-T wave appearance in lead I was definitely abnormal — My "working diagnosis" was acute inferior OMI until proven otherwise.

    PEARL #4: Because of the common blood supply to the inferior and posterior walls of the LV (Left Ventricle) — I always look for subtle signs of acute posterior OMI when I am looking for a way to support my suspicion of acute inferior OMI. Normally — leads V2 and V3 manifest slight-but-real, gently upsloping ST elevation. The fact that if anything — the J-point in lead V3 of ECG #1 is slightly depressed (BLUE arrow in this lead) — strongly suggests that there is an acute posterior OMI in Figure-2.
    • NOTE: The more leads that manifest ST-T wave abnormalities — the greater the support that there is an ongoing acute process. My "eye" was next captured by the ST-T wave appearance in leads V4,V5,V6 (within the BLUE rectangle in Figure-2). As per the BLUE lines I've drawn over the ST segments in these leads — there is flattening and slight J-point depression.

    • Putting This All Together: Given the history that the older man in today's case presented with new symptoms — and, has ST depression in lead V3 suggestive of posterior OMI — which lends further support to the limb lead changes suggesting inferior OMI — plus also manifesting ST flattening with ST depression in lateral chest leads (V4,V5,V6) — my "working diagnosis" expanded to an acute infero-postero OMI (plus my suspicion that this older patient may well have multivessel disease).

    Figure-2: I've labeled the initial ECG in today's case. 


    ==============================
    QUESTION:
    • Is there misplacement of any electrode leads?
    • IF so — WHY is this relevant?



    ANSWER:
    The only 3 leads that I've not yet mentioned in today's tracing are leads aVR, V1 and V2. 
    • Lead aVR in Figure-2 — shows slight ST elevation. I thought this finding consistent with the finding of ST depression in lateral leads I; V4,V5,V6 — and possibly indicative of multivessel disease (ie, Diffuse Subendocardial Ischemia — as discussed in ECG Blog #400).

    • I strongly suspect that the electrode leads for V1 and V2 may be placed too high on the chest. As discussed in ECG Blog #274 — the clues that suggest there is too-high placement of leads V1,V2 include: i) The negative P wave in leads V1 and V2 of Figure-2; ii) The subtle r' that we see in lead V2; and, iii) How similar the QRST complex in leads V1 and V2 look to the QRST in lead aVR! It is especially this last clue that makes me so suspicious of V1,V2 misplacement — because the symmetric T wave inversion we see in lead V2 looks totally "out-of-place", compared to the ST-T wave appearance in neighboring lead V3 (the BLUE question mark over the T wave in lead V2).

    PEARL #5:
     The clinical importance of recognizing lead V1,V2 misplacement — is that this potentially negates the diagnostic value of assessing leads V1,V2 in this patient for whom we are trying to diagnose acute posterior OMI.
    • ST depression with posterior OMI tends to be maximal in leads V2, V3 and/or V4 (with ST depression often beginning in lead V1). Losing the diagnostic utility of leads V1 and V2 in Figure-2 — therefore hinders our ability to recognize posterior OMI in today's patient. 

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

    The CASE Continues:
    The clues to acute infero-postero OMI that I discussed above were not recognized.
    • Even when several initial high-sensitivity troponin values came back with definite (albeit modest) elevation — the possibility of acute OMI was not recognized.
    • The initial ECG was not repeated for several hours ...
    • Troponin values continued to rise — and frank ST elevation was finally seen on repeat ECGs.


    Additional LESSONS To Be Learned:
    ECG findings in Figure-1 are subtle — but they are definitely present. At the least — these ECG changes should have raised concern for a potential acute event.
    • When in doubt about an acute event — Repeat the ECG! In acutely evolving coronary occlusion — "dynamic" ST-T wave changes may occur in as short of a time period as several minutes. As a result — I favor repeating ECGs every ~10-20 minutes until you are comfortable that acute OMI is or is not occurring.
    • In a patient with new symptoms and subtle ECG changes — the finding of even modest troponin elevation tells us to accept this as evidence of acute OMI until we prove otherwise. Prompt cath is indicated.
    • Correlate each serial ECG with notation of the presence and relative severity of symptoms. Improvement of symptoms that correlates with improvement in ECG findings does not mean "all is well". Instead, it most probably indicates "dynamic" ST-T wave changes in a patient with an evolving OMI. Prompt cath and PCI are likely to be needed.
    • Even without ECG changes — persistent ischemic-sounding chest pain is indication for prompt cath.
    • Finally — the EASIEST way to ensure that you will be able to tell a complete "story" as to the presence and relative severity of symptoms at the time that each ECG was recorded — is if written notation is made on each ECG as it is done on a scale from 0-to-10 of the patient's chest pain at that time.


    ==================================
    Acknowledgment: My appreciation to Giuseppe Trainito (from Butera, Italy) 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" = 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 (and also Diffuse Subendocardial Ischemia).

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

      • ECG Blog #274 — How to tell if leads V1,V2 are misplaced.