ECG Blog #425 — Are there P Waves?

I was sent the ECG in Figure-1 — told only that the patient was 70 years old, and had a history of an ASD (Atrial Septal Defect). 

• Serum K+ was normal.
• The patient was hemodynamically stable with ECG #1.

QUESTIONS:

• How would YOU interpret the rhythm in Figure-1?
• Are there P waves?

Figure-1: The initial ECG in today's case.

MY Initial Thoughts on Today's CASE:

Knowing that today's patient has a history of an ASD (Atrial Septal Defect) — is relevant to the interpretation of today's interesting tracing!

• There are many variations of ASDs — with severity of this entity and the age at which the patient presents dependent on multiple factors. Surprisingly, patients with an ASD may present for medical attention at any age. 
• Many patients go years without significant symptoms. That said — most patients eventually do become symptomatic (Webb and Gatzoulis: Circulation 114: 1645-1653, 2006).
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• PEARL #1: Given a potentially longterm course for the patient with an ASD — it's important to appreciate that a lack of symptoms does not necessarily exclude the possibility of hemodynamically significant heart disease.
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• PEARL #2: The ECG may provide clues to the underlying severity of the ASD in a given patient — especially in the adult patient who is not overtly symptomatic. Thus, the finding of any of the following may all portend more significant underlying disease: i) Rhythm disturbances (ie, AV block; AFib/AFlutter; other atrial arrhythmias); ii) Signs of RVH and/or pulmonary hypertension (RAA, right axis, tall R and/or qR pattern in lead V1; ST-T wave changes of RV "strain"; incomplete or complete RBBB); and/or iii) LVH.
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• Given complexity of the multiple facets of ASD management during the course of a patient's lifetime — lifelong adult CHD (Congenital Heart Disease) care is recommended, as potential timing of surgical repair in adulthood is a very challenging determination to make (Cotts — Eur Heart J 43:2260-2671, 2022 — and — Lopes and Mesquite — Arq Bras Cardiol 103(6):446-448, 2014).
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• NOTE: For more on ECG recognition of RVH and/or pulmonary hypertension (re the qR pattern in lead V1) — See ECG Blog #234 and Blog #248.

Regarding the Initial ECG in Figure-1:

Realizing some technical faults with ECG #1 (slight folding and angulation of the ECG — therefore some distortion of measurements) — there appears to be a regular WCT (Wide-Complex Tachycardia) at ~135/minute, but without clear sign of sinus P waves.

• I've labeled the initial ECG in Figure-2 — to highlight the areas of uncertainty that I had in assessing this tracing. Specifically — I was not at all certain whether the BLUE arrows and question marks represented P waves with a long PR interval — or — T waves from the preceding QRS with a long QTc — or — the combination of T waves that are "fusing" with underlying atrial activity?
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• KEY Point: Given obvious QRS widening in ECG #1 — distinction between P waves vs T waves vs a combination of both is an essential determination for whether today's rhythm is likely to be supraventricular or VT (Ventricular Tachycardia).
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• PEARL #3: Knowing that today's patient has an ASD led me to suspect some form of SVT (SupraVentricular Tachycardia) instead of VT, because of how common RBBB conduction defects are in the patient with a significant ASD. And although QRS morphology in Figure-2 is somewhat unusual — the findings of QRS widening with a QR pattern in lead V1, with wide terminal S waves in lateral leads I and V6 — especially given marked fragmentation (notching) in multiple leads — could certainly be consistent with adult CHD in which the patient had a longstanding, hemodynamically significant ASD with significant underlying structural abnormality. 

Figure-2: Do the BLUE arrows and question marks represent P waves? — T waves? — and/or a fusion of T waves with underlying atrial activity?

PEARL #4: If the BLUE arrows and question marks in Figure-2 are the result of sinus P waves (that are perhaps fusing with preceding T waves) — then the PR interval would be prolonged.

• That said, as the rate of a sinus rhythm increases — the PR interval tends to shorten, probably the result of reduced basal vagal tone. Because of this, it is uncommon to see sinus tachycardia with a prolonged PR interval.
• While there are some patient who have baseline PR interval prolongation, who continue to manifest a certain amount of PR interval prolongation with sinus tachycardia — most tachycardias that seem to show a "sinus P wave" near the mid-point of the R-R interval turn out to have 2:1 AV conduction (from either ATach or AFlutter).
• As discussed in ECG Blog #227 — this principle is known as the Bix Rule, named after the Viennese cardiologist who first cautioned against "accepting" the diagnosis of "sinus tach with 1st-degree" before meticulous search for an "extra" P wave hidden within the QRS complex.
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• KEY Point: If I was able to identify 2:1 atrial activity — this would virtually confirm my suspicion that today's rhythm was some form of SVT (and not VT) — since coincidental occurrence of 2:1 atrial activity with perfectly timed simultaneous VT is extraordinarily rare.

Searching for Extra P Waves:

I illustrate in Figure-3 — how to assess the possibily of 2:1 atrial activity in today's tracing. 

• IF today's tracing was the result of an SVT with 2:1 AV conduction (from either ATach or AFlutter) — then we would expect to see evidence of an additional atrial deflection (P wave or flutter wave) at that point precisely midway between successive atrial deflections (ie, between successive RED lines in Figure-3).
• Whereas it is impossible to tell if an extra atrial deflection might be lying under the PURPLE lines in leads aVF and V3 (since the PURPLE line occurs in the middle of the QRS in these leads) — I would have expected to see some form of upright deflection under the PURPLE arrow in leads I and V2 if there was 2:1 atrial activity.
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• BOTTOM Line: While important to consider the possibility of an SVT rhythm with 2:1 AV conduction in Figure-3 — I see no evidence to support this theory.

Figure-3: How to assess for possible 2:1 atrial activity.

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Putting It All Together:

At this point in my assessment of today's rhythm — I fully acknowledge that I did not know for certain the etiology of this arrhythmia.

• I had established that today's rhythm was a regular WCT at ~135/minute — but with uncertain (if any) atrial activity. The differential diagnosis is between some form of SVT vs VT (especially since we were told that serum K+ was normal).
• Given the history of an ASD — I thought an SVT would be more likely than VT, because QRS morphology in today's rhythm looked potentially consistent with adult CHD in a patient with longstanding, underlying structural disease (ie, given the widened QR pattern in lead V1 — with wide terminal S waves in lateral leads + marked fragmentation of several QRS complexes).
• I was hoping to find evidence for 2:1 atrial activity — because if present, this would virtually confirm that today's rhythm was supraventricular. Unfortunately — my search for 2:1 atrial activity (as shown in Figure-3) was unsuccessful.
• This could have been an optimal time to try a Lewis Lead — which sometimes reveals atrial activity not evident with standard lead placement (See ECG Blog #223).
• Finding a prior tracing on today's patient could also prove insightful — especially if at a slower heart rate with sinus rhythm, the same QRS morphology is seen as appears in Figure-3. Unfortunately — no prior tracing was available at this time.
• The "good news" — is that today's patient was hemodynamically stable, which meant there was at least a moment of time to try to attain greater certainty as to the etiology of the rhythm.
• Learning more about the patient's history could be insightful.

The CASE Continues:

• The patient's medical record was found. Recent Echo showed a large Ostium Secundum ASD defect — with left-to-right shunting and huge dilatation of right-sided chambers.
• It turns out the patient had been symptomatic — with progressively increasing exertional dyspnea over the past few months.

The initial ECG was repeated — and is shown in Figure-4.

QUESTIONS:

• How would you interpret the repeat ECG shown in Figure-4?
• 
  
• Does ECG #2 clarify what the initial rhythm was?

Figure-4: ECG #2 is a repeat ECG, done later that day. 

MY Thoughts on the Repeat ECG in Figure-4:

For clarity with measurements in ECG #2 — I've drawn in 5 large boxes on the ECG grid (seen in between leads I and II in Figure-4). Note when comparing this repeat tracing with the initial ECG in today's case — that because many more beats are captured in ECG #2, that the relative size of a large box on ECG grid paper is different between these 2 tracings.

• Group beating in the form of a bigeminal rhythm (alternating shorter-then-longer R-R intervals) is present in ECG #2. This bigeminal rhythm is most easily appreciated in leads V5, V6. 
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• Sinus rhythm has been restored! (RED arrows in Figure-5 showing clearly defined P waves in this repeat ECG in multiple leads — with return to sinus rhythm defined by the presence of upright P waves with fixed PR interval in lead II).
• Every-other-beat in Figure-5 is a PAC (highlighted by YELLOW arrows that show a slight-but-real different P wave morphology for these PACs, that are clearly narrower than the RED-arrow P waves of sinus beats).

Figure-5: I've labeled the repeat ECG — which shows a bigeminal rhythm in which every-other-beat is a PAC (YELLOW arrows).

CASE Conclusion:

Comparison of the 2 ECGs in today's case allows a definitive diagnosis of the rhythm in the initial ECG to be made retrospectively. Consider Figure-6:

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• Please NOTE in Figure-6: When comparing leads aVF and V6 from ECG #2 — with ECG #1 — that the relative size of a large box on ECG grid paper in my illustration is different between ECG #1 and ECG #2.

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• It is because the overall heart rate has slowed in ECG #2 — that we are able to see sinus P waves emerge from where they were hiding within the preceding T waves. Sinus P waves (RED arrows) are now clearly seen for even-numbered beats in leads aVF and V6 of this repeat tracing.
• We are able to see the pointed P waves of the PACs in lead aVF of ECG #2 (YELLOW arrows).
• However, in lead V6 — we are not able to clearly distinguish the P waves of PACs, because these YELLOW-arrow PACs in lead V6 "fuse" with the preceding T wave.
• Now imagine in your "mind's eye" if the rate of the atrial bigeminy rhythm in lead aVF of ECG #2 was a little bit faster. Wouldn't fusion of the RED-arrow sinus P waves in lead aVF with the T waves preceding them be expected to produce a similar picture of fused P wave and T wave, as is seen in lead aVF of ECG #1?
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• BOTTOM Line: Retrospectively — the return of sinus rhythm with atrial bigeminy in ECG #2 strongly suggests that the rhythm in ECG #1 was sinus tachycardia at ~135/minute, in which tall, pointed inferior lead P waves from this patient's longstanding ASD fused with the T waves that preceded them to produce the unusual QRS appearance in ECG #1.
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• PEARL #5: The KEY to proving that the mechanism of a tachycardia is sinus — is frequent ECG monitoring that once the cause of sinus tachycardia is treated, will result in enough slowing of the tachycardia rate to allow sinus P waves to emerge from where they were hiding in the preceding T waves. This is precisely what we see in Figure-6.

Figure-6: Comparison between today's initial ECG — and leads aVF and V6 in the repeat tracing. Slight slowing of the heart rate with return to a sinus mechanism allows sinus P waves to emerge from where they were hiding in the preceding T waves.

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ADDENDUM (4/14/2024):

Based on some questions that have arisen regarding the PR intervals in ECG #1 and ECG #2 — I've added Figure-7, that I hope will clarify my discussion.

• I fully acknowledge that the difference in size of the ECG grid in the 2 tracings that I show here is potentially confusing. Rather than digitizing both tracings (which risks introducing error inherent with digitization of fine measurements from ECGs that are not completely flat and completely straight) — I thought it better to show the original ECGs.
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• I've added PINK lines in Figure-7 to show that by my measurements — the PR interval in the initial ECG (TOP = lead II rhythm strip) measures just under 1 large box (corresponding to a PR interval = 0.18 second).
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• By my measurements — this is the same PR interval ( = 0.18 second) that I measure for the sinus beats (RED arrow P waves) in lead aVF of ECG #2.
• The PR interval for the PACs (YELLOW arrow P waves) in ECG #2 appear to have a slightly longer PR interval — but PR interval duration of PACs may vary depending on from where in the atria the PACs arise, as well as conduction velocity through the atria, which may be altered by early occurrence of these supraventricular impulses.
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• BOTTOM Line: I wish I had additional tracings. I wish I had tracings that were scanned completely flat and straight. And I wish I had record of ECG monitoring just before — and during — and just after the rhythm changes from the regular tachycardia in ECG #1 — to the bigeminal rhythm in ECG #2. Unfortunately — I lack this information. 
• That said — I thought my discussion in today's case to be a valid explanation based on the 2 tracings that I have (in which I believe that the PR interval is virtually the same for sinus-conducted beats in ECGs #1 and #2). But I fully acknowledge that other explanations may be possible.

As always — Comments from my readers are welcome! — :) 

Figure-7: In the hope of clarifying PR interval duration in ECG #1 and ECG #2 — I've written out the measurements I've made (See text).

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Acknowledgment: My appreciation to Ella Hmayer (from Tunisia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• ECG Blog #220 — and ECG Blog #361 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a regular WCT rhythm.
• ECG Blog #263 and Blog #283 — More WCT Rhythms ...
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• ECG Blog #227 — Reviews the "Bix Rule" (Looking for 2:1 atrial activity when you see a long PR interval with a tachycardia).
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• For more on ASD in Adults — Webb and Gatzoulis: Circulation 114: 1645-1653, 2006.
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
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• ECG Blog #323 — Review of Fascicular VT. 
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #361 — A regular WCT in a middle-aged man.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Review of criteria for distinguishing VT vs aberrant conduction.
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• ECG Blog #422 — Reviews another case of adult Congenital Heard Disease.

ECG Blog #424 — Proportionality and the "Cut Off"

The ECG in Figure-1 was obtained from a middle-aged woman — who presented with low back pain, shortness of breath and marked hypertension — but no CP (Chest Pain).

QUESTIONS:

• In view of this history — How would YOU interpret this ECG?
• Are the large, peaked T waves (especially in lead V2) — likely to indicate hyperacute deWinter T waves?

Figure-1: The initial ECG in today's case.

PEARL #1: Did YOU notice that S wave amplitude is cut off in leads V2 and V3? (and possibly also in lead V1). 

• As a result — We have no idea how deep the S wave really is in these leads! This is especially true in lead V2, given slight-but-real separation between descending and ascending limbs of the S wave in this lead (See dotted RED lines highlighting abrupt S wave "cut-off" in Figure-2).
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• It is extremely likely that voltage criteria for LVH (as listed in the ADDENDUM below in Figure-3) would have been easily satisfied IF this ECG had been recorded at half-standardization, so as to enable us to capture full dimensions of the QRS complex in the anterior leads. Given the age of today's patient — and her markedly elevated BP on exam, the finding of LVH is not at all unexpected.
• KEY Point: In the United States, there is a limit to the amount of voltage that prehospital ECGs in most EMS (Emergency Medical) Systems are able to display. As a result — QRS amplitudes are automatically truncated once they exceed that limit (which typically is 10 mm for the deepest S wave and tallest R wave).
• Once aware of this automatic truncation of ECG amplitudes that is used in most EMS systems in the United States — it becomes EASY to spot (as shown below in Figure-2).

Figure-2: I've labeled with dotted RED lines the S wave "cut-off" in leads V2,V3. I've also added the mirror-image view of leads V2,V3 (within the RED inserts) — showing how likely it is that today's patient has LVH (See text). 

More Technical Misadventures in Today's CASE:

In addition to automatic truncation of anterior S waves — 2 additional "technical misadventures" are seen in today's tracing:

• There is significant baseline artifact. Although worse in leads aVR,aVL,aVF — fine undulations alter the baseline in virtually all leads in Figure-2. While we are still able to interpret ST-T wave morphology — this baseline artifact clearly renders our assessment less clear. 
• The lead V1 ectrode is most probably placed too high on the chest because: i) There is an rSr' complex in lead V1; ii) QRS morphology in lead V1 looks very similar to QRS morphology in lead aVR; and, iii) There is a significant negative component to the P wave in lead V1 (See ECG Blog #274 — for review on how to quickly recognize too-high electrode lead placement of leads V1,V2). Since the focus of our attention in today's case is on the anterior leads — alteration of ST-T wave appearance in lead V1 because of erroneous placement of the lead V1 electrode clearly affects our interpretaton.

PEARL #2: Sometimes with LVH — instead of seeing tall R waves with LV "Strain" in the lateral chest leads — we see the "mirror-image" opposite picture in right-sided leads V1,V2 (ie, LVH may be manifested by deep anterior S waves — with ST elevation in leads V1,V2 and/or V3). This is precisely what we see in today's case!

• LOOK at the RED inserts in Figure-2 — that show the mirror-image of leads V2 and V3. The dotted RED line highlights that the R wave of this inverted complex would almost certainly be a good bit taller — IF there wasn't "automatic truncation" of the S waves in leads V2,V3 on this EMS ECG.
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• DON'T the ST-T waves in these inverted RED inserts look identical to the ST-T wave appearance of LV "strain"? (ie, Panel C in Figure-4 below in today's ADDENDUM).
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• KEY Point: The concept of "proportionality" is essential to recognize! Today's patient with marked hypertension has LVH that is manifest on ECG by deep anterior S waves (in leads V1,V2,V3) — except that these S waves are "cut off" because of the automatic truncation inherent in this EMS ECG. As a result, the ST elevation (with especially tall, peaked T wave in lead V2) — is not indication of acute ischemia. Instead, it is the manifestation of LV "strain" that is best seen in this anterior lead. IF anterior S wave depth would not have been cut off — then the tall, peaked T wave in lead V2 of Figure-2 would probably be proportional to the deep S wave in this lead.
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• A picture is worth 1,000 words. For additional examples of this phenomenon whereby automatic truncation of an EMS ECG may mistakenly result in LVH serving to mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020 — March 31, 2019 — March 29, 2019 — and the December 27, 2018 post.

PEARL #3: Another reason why some clinicians may have been concerned about anterior (or anteroseptal) infarction from today's initial ECG — is the Poor R Wave Progression (ie, There is virtually no r wave in Figure-2 until lead V4!).

• While it may not be possible on this single ECG to absolutely rule out anterior (anteroseptal) infarction at some point in time — it's important to remember that marked LVH that is primarily manifest by deep anterior S waves (rather than by tall lateral R waves) — produces a vector in which the hypertrophied, posterior-lying left ventricle opposes normal anterior forces. Thus, it is at least in part because of the deep anterior S waves from LVH that R wave progression in Figure-2 is much less than expected.

PEARL #4: The remaining finding of note on today's ECG — relates to the ST segment coving with symmetric T wave inversion in leads V5,V6 of Figure-2.

• The KEY lies in the history. Today's patient is a middle-aged woman who presented with low back pain, shortness of breath and marked hypertension — but no chest pain.
• As suggested by Figure-4 below in the ADDENDUM — assessment of the ST-T waves in leads V2,V3 and V5,V6 — is consistent with ischemia and/or LV "strain". While perfectly appropriate to obtain serial ECGs and troponin values in this acutely ill patient — I suspect troponins will be negative, and serial ECGs will confirm that there is no acute OMI. 
• The PEARL is that LVH with "strain" may mimic ischemia — and this ECG finding of lateral lead ST coving with symmetric T wave inversion is often seen in patients who present with marked hypertension, especially in the absence of new chest pain as a presenting complaint.

FINAL Thoughts:

I unfortunately do not have clinical follow-up on today's case. That said — My final thoughts on the case include:

• The need to find out WHY this patient is short of breath.
• Wanting to see the initial hospital ECG — in which there should be no limitation of voltage on the ECG recording. I would expect this hospital ECG to show very deep anterior S waves, consistent with LVH.
• Ruling out an acute event (As noted above — I would expect serial ECGs and troponins to be negative for acute OMI).

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Acknowledgment: My appreciation for anonymous donation of today's case.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
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• ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
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• The November 4, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews 3 ECG Clues for rapid recognition of erroneous lead V1,V2 placement. 
• For cases similar to today, in which LVH may mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020 — March 31, 2019 — March 29, 2019 — and the December 27, 2018 post.
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• ECG Blog #266 — Reviews some considerations when distinguishing between deWinter T Waves vs Posterior MI.
• ECG Blog #183 — Reviews a case of deWinter T Waves (with the Audio Pearl in this post discussing some variants of the deWinter T wave pattern). 
• ECG Blog #53 — and ECG Blog #340 — Review more cases of deWinter T Waves.
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• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

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ADDENDUM (4/6/2024): I've added below in Figure-3 and Figure-4 additional material to facilitate ECG diagnosis of LVH and LV "strain".

 

Figure-3: The voltage and other criteria I favor for ECG diagnosis of LVH (Please see ECG Blog #73 for additional details).

Figure-4: Illustration and description of LV “strain” and a “strain equivalent” pattern (See text).

ECG Blog #423 — Flank Pain, Heartburn & an ECG

I was sent the ECG in Figure-1 with the information that this man in his 60s presented to the ED (Emergency Department) — for flank pain of several days duration (that he thought was from a kidney stone) and an intermittent "heartburn" sensation over the past few weeks.

QUESTIONS:

• Given the above history — How would YOU interpret this patient's initial ECG, that was obtained on arrival in the ED?
• 
  
• 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). 

Would YOU Activate the Cath Lab?

Many providers would look at the initial ECG shown in Figure-1 — and say, "This is not a STEMI — therefore there is no need to activate the cath lab at this time". 

• STEMI Criteria are not satisfied in ECG #1 — because in this man ≥40 years old, ≥2 mm of ST elevation is not attained in consecutive anterior leads V2 and V3.
• Unfortunately, following the outdated, millimeter-based STEMI Paradigm in today's case — would result in needless delay in reperfusion of acute coronary Occlusion, with potential loss of a significant amount of salvageable myocardium.
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• KEY Point: To interpret ECG #1 in the absence of awareness of the newer, superior OMI Paradigm is to risk missing at least 30% of all acute OMIs (acute MIs resulting from acute coronary Occlusion) — as discussed in detail in our ECG Video Blog series in Blog #406 — Blog #407 — and Blog #408.

MY Thoughts on Today's Initial ECG:

The initial ECG in today's case (as shown in Figure-1) — is not "normal".

• The rhythm is sinus at ~75/minute (with upright P waves and a constant PR interval in lead II). All intervals (PR, QRS, QTc) and the frontal plane axis are normal (ie, The isoelectric QRS complex in lead aVF, with maximal net R wave amplitude in lead I — suggests a frontal plane axis near 0 degrees). There is no chamber enlargement.

Regarding Q-R-S-T Wave Changes:

• Q waves: Tiny (normal) septal q waves are seen in lateral leads I, aVL and V6. It is hard to determine if a tiny initial positive deflection (r wave) is or is not seen in lead III — but neither of the other 2 inferior leads ( = leads II,aVF) manifest a Q wave.
• R wave progression: Normal-sized R waves are seen in anterior leads V1,V2 — with normal transition (Height of the R wave becomes greater than depth of the S wave between leads V2-to-V3, which is normal).

The ECG findings of potential concern relate to the ST-T Wave Changes — that I highlight in Figure-2.

• Did YOU See these areas that raised my concern?

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

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To Emphasize: The History in today's case is not typical for acute MI, in that this patient did not present with CP (Chest Pain). Instead — today's patient presented with a potential "CP-equivalent" symptom (ie, a "heartburn" sensation), albeit this sensation of "heartburn" was of uncertain duration.

• PEARL #1: As emphasized in ECG Blog #228 — Not all patients with acute MI have chest pain. Instead, the estimated incidence of "Silent" MI may be as high as between 20-40% of all MIs (depending on the definition used). As a result — lack of chest pain in today's case does not rule out the possibility of acute MI given the patient's age (in his 60s) — and given the description of "a heartburn sensation", as this symptom is commonly confused with cardiac CP.
• 
  
• PEARL #2: One of my favorite history questions to ask is, "What happened today (instead of yesterday, or the day before) — that led you to come to the ED?" To emphasize that we do not know the answer to this question from the brief history provided above at the beginning of this case.
• IF the reason this patient presented to the ED today is that his "heartburn" got significantly worse — this would be important imformation that would greatly increase the likelihood that even subtle ECG changes may be an important clue to an ongoing acute cardiac event.

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The ECG Changes of Concern in Today's Case:

I was concerned by the appearance of 6/12 leads in Figure-2:

• For me in Figure-2 — the most "eye-catching" ST-T wave abnormality is in lead V2 (within the RED rectangle).
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• PEARL #3: Normally, there should be a small amount of gradually-upsloping ST elevation in anterior leads V2,V3. Instead — the amount of J-point ST elevation in lead V2 is excessive (ie, as per the PURPLE arrow in this lead). In addition — the gently upsloping shape of the ST segment in lead V2 has been replaced by the abnormally straightened ST segment "takeoff" (straightening of the RED line in this lead).
• 
  
• PEARL #4: I favor looking for 1 or more leads that I know are abnormal. Once found — then more subtle findings in neighboring leads become much more likely to be supportive of an acutely evolving cardiac event. For example, in Figure-2 — the amount of J-point ST elevation in lead V3 is not excessive — but in the context of the definitely abnormal amount and shape of the elevated ST segment in lead V2 — the ST segment straightening that we also see in lead V3 is also abnormal!

PEARL #5: The more leads in a given tracing with abnormal ST-T wave changes — the greater the likelihood that an acute evolving cardiac event is ongoing. So while important to appreciate that not all anterior OMIs manifest reciprocal ST depression in the inferior leads — IF you do see inferior lead ST depression, this provides additional support that even subtle ST elevation in the anterior leads is likely to be acute.

• Each of the 3 inferior leads in Figure-2 manifest reciprocal ST segment depression (within the BLUE rectangles in leads II,III,aVF).
• By far — lead aVF manifests the most abnormal ST depression, given how small amplitude of the QRS complex is in this lead. There is therefore no doubt that the scooped, downsloping ST segment with terminal T wave positivity in lead aVF has to be assumed acute until proven otherwise!
• In the context of knowing that the ST-T wave in lead aVF is abnormal — the more subtle-but-real ST segment straightening with slight depression in leads II and III adds further support to our impression that there is reciprocal inferior lead ST depression.
• KEY Point: Any doubt that I may have had about whether ST-T waves in anterior leads V2 and V3 were truly abnormal — was eliminated the moment I saw the definitely abnormal ST-T wave in lead aVF!
• 
  
• PEARL #6: The isolated finding of T wave inversion in either lead III and/or lead aVF in association with a predominantly (or entirely) negative QRS — is not necessarily abnormal. BUT — the finding of ST segment straightening with some amount of ST depression in lead III, instead of just T wave inversion (as highlighted by the BLUE arrow in Figure-2) — is clearly not normal. And, ST flattening with some ST depression in lead III is even more definitely abnormal when it occurs in association with ST-T wave depression in the other 2 inferior leads! (as it does in today's case).
• 
  
• PEARL #7: My "Go-To" Lead when I find myself contemplating the possibility of an acute anterior OMI — is lead aVL. The presence of even subtle ST elevation (as highlighted by the BLUE arrow in Figure-2) solidifies our suspicion of an acute cardiac event in today's case.
• Note that there is fulfillment of the "magical" reciprocal (ie, mirror-image opposite) shape of the ST-T wave for the subtle ST depression in lead III — and the equally subtle ST elevation in lead aVL. This provides yet one more indication that despite the lack of new CP in today's case — the collective abnormal ST-T wave findings in the 6 leads highlighted in Figure-2 strongly suggest an acute evolving cardiac event!
• 
  
• PEARL #8: Among the actions to undertake at this point in today's case are the following: i) Go back and carefully question the patient — trying to get a better "feel" for the likelihood that his "sensation of heartburn" may or may not represent a "CP equivalent" symptom — with focus on how much this sensation increased today, and how severe it was at the time the initial ECG was done; and, ii) Assuming at least 10 minutes have passed since ECG #1 was recorded — Repeat the ECG.
• 
  
• To Emphasize — In the absence of acute symptoms, immediate activation of the cath lab may not yet be indicated on the sole basis of ECG #1. That said — IF an acute cardiac event is indeed ongoing — then serial ECGs (repeated as soon as between 10-30 minutes after the initial ECG) — in conjunction with clinical information (ie, initial troponin values, correlation with the presence and ongoing severity of symptoms with each serial ECG that is done) — are actions likely to quickly confirm the need for prompt cardiac catheterization.

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Today's CASE Continues:

A prior ECG on today's patient was found. For clarity in Figure-3 — I have put this previous ECG together with today's initial tracing:

QUESTION:

• What do we learn from this prior tracing?

Figure-3: Comparison between the 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). 

What We Learn from the Prior ECG:

While the ST-T wave changes in today's initial ECG are subtle and do not satisfy millimeter-based STEMI criteria — there can be no doubt from comparison with the prior tracing shown in Figure-3 — that ST-T wave findings highlighted in the initial ECG are new!

• Despite no significant change in chest lead QRS morphology — the ST segment straightening in leads V2 and V3 was not previously present! In addition — there previously was no ST elevation in lead V2 — and there was even a hint of ST depression in lead V3.
• In the limb leads — inferior lead ST depression was far less than in today's initial ECG — and there previously was no ST elevation in lead aVL.
• 
  
• BOTTOM Line: While questions remain from brevity of the history as to when the ECG findings noted in ECG #1 may have developed — there is no doubt that the above-noted ST-T wave findings in today's initial ECG are new since the prior tracing from ~1 year ago was done. As a result — an acute and/or recent LAD (Left Anterior Descending) OMI must be assumed until proven otherwise. 
• 
  
• Cardiac Cath was ultimately performed in today's case — almost 7 hours after arrival in the ED. It revealed multi-vessel disease, with "culprit" lesions in both the proximal LAD, as well as in the 1st Diagonal Branch of the LAD. Reperfusion with PCI was successful.
• Among the actions undertaken during the hours until cardiac cath was performed, were: i) Return of 3 abnormal troponin assays, with progressively increasing values; ii) Several repeat ECGs, including one in which the acute ECG findings highlighted in Figure-2 had greatly improved (albeit no notation was made regarding the presence and/or relative severity of the patient's symptoms at this time); and, iii) Coronary CT scan — showing subtotal occlusion of the proximal LAD.

Final COMMENT: Cardiac catheterization in today's case should not have been delayed for nearly 7 hours.

• Although assessment of today's case was understandably made more difficult by the lack of chest pain — the possibility that the patient's "heartburn" might be an acute "CP equivalent" was apparently not explored.
• Even without a history of "new CP-equivalent symptoms" — the abnormal findings in the initial ECG (as detailed in discussion of Figure-2) — place the onus on medical providers to assume acute OMI until proven otherwise. 
• 
  
• As soon as the prior ECG was found — it should have been obvious that the ST-T wave changes in the initial ECG were definitely acute. In this context — any troponin elevation is a mandate for prompt cath.
• 
  
• "Dynamic" ST-T wave changes (ie, the improvement of ECG findings on a serial tracing) — should have served as additional indication for prompt cath.
• 
  
• In the context of the above events — further delay to perform coronary CT scan serves no useful purpose. The above described ECG findings (especially in association with any even minimally elevated troponin value) — defines today's case as an acute OMI in need of prompt cath. This need for prompt cath would not be changed regardless of coronary CT scan results (ie, Spontaneous reperfusion is suggested in today's case by the "improvement" in abnormal ECG findings — which could have shown up as a "non-critical stenosis" = "negative" result on coronary CT scan). 
• As emphasized often in this ECG Blog — prompt cath with PCI is still indicated after spontaneous reperfusion because of the high risk in ensuing hours of spontaneous reocclusion (See ECG Blog #326 — Blog #337 — and Blog #320, among many others).

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Acknowledgment: My appreciation to Hans Helseth (from Minneapolis, Minnesota, USA) 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.
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• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (and review of why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• 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.
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• 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 #387 — Dynamic change in 2 minutes.
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• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).
• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
• 
  
• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• 
  
• The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.
• For review on when despite acute OMI — the initial hs-troponin may come back normal — See the March 24, 2023 post in Dr. Smith’s ECG Blog.

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ADDENDUM (3/31/2024): 

• I've added a series of Audio Pearls relevant to today's case. 

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ECG Media PEARL #1 (3:00 minutes Audio) — Reviews the concept of deWinter T waves (and the many variations on this "theme" ).

 

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ECG Media PEARL #35a (4:50 minutes Audio) — WHEN is a T Wave Hyperacute vs a Repolarization variant?

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ECG Media PEARL #39a (4:50 minutes Audio) — Reviews the concept of dynamic ST-T Wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated).

 

 

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ECG Media PEARL #46a (6:35 minutes Audio) — How to compare serial ECGs (ie, Are you comparing "Apples with Apples" — or — with Oranges?).

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ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.

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ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.