ECG Blog #341 — WHY are the T Waves Peaked?

The ECG in Figure-1 — was obtained from a 60-ish year old man who was admitted following a syncopal episode in the bathroom. He complained of a short episode of abdominal pain a few weeks earlier — but had not had chest pain. He was hemodynamically stable at the time the ECG in Figure-1 was recorded.

• How would YOU interpret this patient’s initial ECG?
• Are ECG findings likely to be the result of hyperkalemia?

Figure-1: The initial ECG in the ED — obtained from a 60-ish year old man with a syncopal episode and abdominal pain. No chest pain.

MY Thoughts on ECG #1:

As always — I favor a systematic approach to 12-lead ECG interpretation (See ECG Blog #205).

• There is significant artifact — especially in the limb leads.
• The rhythm is sinus at ~65-70/minute. All intervals (PR, QRS, QTc) appear to be normal. There is marked LAD (Left Axis Deviation) — with at most, no more than a tiny initial positive deflection in the inferior leads.
• 
  
• PEARL #1: Although difficult to be certain because of the marked baseline artifact — it appears that QRS complexes in the inferior leads are fragmented (ie, notched). The combination of predominant negativity of the QRS + fragmentation — suggests that in addition to LAHB (Left Anterior HemiBlock) — there has also been infarction at some point in time.

Continuing with systematic assessment:

• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q waves: As already stated — while difficult (because of artifact) to determine if the initial QRS deflection in inferior leads is positive or negative (ie, Q wave or r wave) — this is an academic distinction, since predominant negativity with fragmentation in all inferior leads at the least qualifies as a “Q-wave-equivalent” pattern.
• 
  
• R Wave Progression: There is early transition (with R>S already by lead V2).
• 
  
• PEARL #2: Did YOU notice the rSr’ pattern in lead V1? (and the R-s-r’ pattern in lead V2?). While possible that this represents incomplete RBBB conduction — the finding of a similar terminal r’ deflection in lead aVR and the negative P wave deflection in lead V1 suggests that the V1 and V2 electrode leads in ECG #1 may have been placed too high on the chest (See ECG Blog #274 for clues how to quickly recognize V1,V2 misplacement). This is relevant to today’s case — because of how prominent T wave changes are in the anterior leads!

Continuing with S-T Changes:

• The most remarkable finding in ECG #1 — relates to the presence of tall, peaked and pointed T waves in the anterior chest leads. While their symmetric appearance, narrow base and extreme point at the peak of the T wave in leads V3 and V4 could clearly be consistent with hyperkalemia (and I would definitely want to check the serum K+ level) — lack of this extreme morphology in most other leads suggests something other than hyperkalemia as the cause.
• 
  
• The other remarkable lead area with prominent ST-T wave changes is in the inferior leads — where leads II,III,aVF all show ST segment coving (albeit no ST elevation) with moderately deep, symmetric T wave inversion.

ECG #1: Putting It All Together:

The patient in today’s case did not have chest pain. Instead — he was admitted to the hospital for a syncopal episode that occurred while he was in the bathroom. The patient also reported having an episode of abdominal pain several weeks earlier. Although less typical — these symptoms could represent an alternative presentation of recent or acute coronary disease.

• I did want to rule out hyperkalemia — but I thought the lack of more generalized T wave peaking to be against this electrolyte disorder as full explanation for the ST-T wave changes in this tracing.
• 
  
• Chest lead T wave peaking (with giant T waves >10 mm tall in leads V3,V4) could represent a form of deWinter-like T waves from LAD (Left Anterior Descending) coronary artery occlusion — BUT — the J-point ST depression of deWinter-like T waves is missing — leads with peaked T waves are not “fatter”-at-their peak and wider-at-their-base, as is typical with deWinter T waves — and, rather than ST elevation in the inferior leads, there is symmetric T wave inversion (See ECG Blog #183 — regarding the concept of deWinter-like T waves).
• 
  
• Alternatively, instead of hyperacute anterior T waves — T wave peaking in the chest lead distribution shown could reflect posterior wall reperfusion. This would be consistent with the symmetric T wave inversion in leads II,III,aVF of ECG #1, that might represent inferior wall reperfusion changes (See ECG Blog #266 — regarding distinction between deWinter T waves vs Posterior MI).
• 
  
• BOTTOM Line: I initially was not certain of the cause of the ST-T wave changes in ECG #1. That said, although today's patient did not present with new chest pain — he did present with other symptoms that could reflect recent or acute coronary disease. Regardless of my uncertainty about the potential presence and location of a "culprit" artery — the ST-T wave changes in ECG #1 looked acute!

The CASE Continues:

The patient remained hemodynamically stable. Serum K+ was normal ( = 4.5 mEq/L). Two troponins showed similar slightly elevated values. A 2nd ECG was obtained 30 minutes after the initial tracing (Figure-2).

• What (if any) ECG changes do you see in ECG #2?

Figure-2: Comparison of the initial ECG in today's case — with the repeat ECG obtained 30 minutes later. What (if any) ECG changes do you see?

The Repeat ECG:

There are some subtle changes in ECG #2, compared to the initial tracing. Appreciation of these changes is best accomplished by lead-to-lead comparison of both ECGs placed next to each other (as I have done in Figure-2). Note the following:

• QRS morphology and the frontal plane axis is similar in both ECGs shown in Figure-2. However, QRS morphology is different in the chest leads! Note that the terminal r' that was present in leads V1 and V2 of ECG #1 — is no longer present in ECG #2. In addition — there is no longer a negative P wave in lead V1. As a result — I suspect that the too-high lead V1,V2 placement of ECG #1 has been corrected in ECG #2. This is relevant — because the location of maximal T wave peaking has shifted more anteriorly in ECG #2.
• 
  
• BOTTOM Line: I found it difficult to determine IF there was (or was not) any significant change in ST-T wave morphology between the 2 tracings in Figure-2. That said — while the predominantly negative and fragmented QRS complexes in the inferior leads may have represented prior infarction — the tall, peaked chest lead T waves "looked" acute — with need to assume that they are acute until proven otherwise!

A Prior ECG was Found!

It turns out that a previous "baseline" ECG from 2016 was found. For clarity — I put this previous tracing together with ECG #2 in Figure-3.

• HOW does this baseline tracing help for understanding the probable time sequence of events in today's case?

Figure-3: Comparison of ECG #2 — with a prior ECG (ECG #3) from today's patient, obtained in 2016. How does this baseline tracing help in understanding the time sequence of events in today's case?

What the Prior ECG Tells Us:

A number of significant ECG changes have occurred in the 6 years since the prior (2016) ECG was obtained. These include the following:

• Although fragmentation and predominant negativity of the QRS in leads III and aVF was present in 2016 — a definite R wave was present in lead II of the baseline tracing. T waves in all 3 inferior leads were upright in 2016, with at most minimal J-point depression. This suggests that while a 1st inferior infarction may be "old" (those fragmented, predominantly negative QRS complexes in leads III and aVF of ECG #3) — loss of the R wave in lead II, with associated symmetric T wave inversion in all 3 inferior leads of ECG #2 are new findings since 2016!
• 
  
• Early transition with a prominent (nearly 15 mm tall) R wave already in lead V2 was present in the 2016 tracing. Whether this tall R wave in lead V2 of the 2016 tracing was serving as a marker of prior posterior infarction was uncertain from review of this baseline tracing.
• Note how deep the S wave in lead V2 of ECG #3 is (ie, >20 mm, with overlap into the lead V3 R wave). As a result — the tall anterior T waves (between 5-10 mm in height) that are seen in the 2016 tracing are not disproportionate. KEY Point: Seeing this 2016 baseline tracing helps explain why the T waves in ECG #2 are so very tall (and now so pointed). There has been superimposition of an acute T wave change on top of what previously was already quite tall anterior T waves.

Putting Together the Story from Figures-1, -2 and -3:

• There is no history of chest pain in today's case. Therefore — we are missing a very important "clue" to the timing of the acute event (assuming that retrospective questioning of today's patient does not yield recall of any additional symptoms in recent days-to-weeks).
• Against an acutely evolving event — is the lack of significant change in ST-T wave morphology between ECGs #1 and #2 — and the finding of 2 troponin values showing similar values that are only slightly elevated above normal.
• Presumably — a recent event occurred, given how tall and pointed the chest lead T waves are in ECG #2 (especially in comparison to their non-acute appearance in the 2016 baseline tracing).
• 
  
• Conclusion: From the information known — I think the most logical explanation for the above described ECG findings — is that ECGs #1 and #2 represent recent infero-postero MI (that probably occurred days-to-1-to-2 weeks ago) — with inferior T wave inversion and anterior tall, peaked T waves representing spontaneous reperfusion changes.

Cardiac Cath was Performed:

Angiography performed a number of days later — revealed extensive multi-vessel coronary disease (Figure-4).

• The main trunk of the LAD was patent. There was a ~70% stenosis of the 1st Diagonal Branch of the LAD.
• A critical 90% stenosis was present in the LCx (Left Circumflex). This was felt to be the "culprit" artery responsible for the patient's recent event.
• An 80% stenosis was present in the distal RCA (Right Coronary Artery).
• Two ~80% stenoses were present in the PDA (Posterior Descending Artery).

Figure-4: Cath images showing 90% narrowing of the LCx (the presumed "culprit" artery for the patient's recent event) — with additional high-grade lesions in the RCA and PDA.

Lessons To Be Learned:

• Multi-vessel disease can often explain unusual ECG findings (I was not initially sure of the culprit lesion from my review of the initial ECG in today's case).
• Not all patients with acute (or recent) MI have chest pain (See ECG Blog #228 — which includes an Audio Pearl on this subject). Among non-chest-pain symptoms that have been associated with "Silent" MI are syncope and abdominal pain (both of which were associated with today's case).
• The deWinter-like T waves of acute LAD occlusion vs tall anterior T waves from posterior wall reperfusion — can sometimes be very difficult to distinguish from one another. 
• Regardless of the cause and precise sequence events in today's case — ST-T wave changes in the initial ECG were obviously acute, with need for prompt investigation.
• The history is often KEY to explaining complex cases like this one (the brief recent episode of abdominal pain could represent the "silent MI" non-chest-pain equivalent symptom that explains all facets of today's case).

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
• 
  
• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit" artery. NOTE: The Audio Pearl reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI. 
• 
  
• ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.
• ECG Blog #80 — Reviews determination of the "culprit" artery and application of the Mirror Test for recognition of acute Posterior MI. 
•  
• ECG Blog #248 — Reviews a case that illustrates Causes of a Tall R Wave in Lead V1 (with the Audio Pearl in this post devoted to this subject).
•  
• 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).
•  
• ECG Blog #262 — Reviews a case of recent acute Infero-Postero MI with group beating from Wenckebach conduction and Low Voltage (with a list of the causes of Low Voltage).
• 
  
• 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 — Reviews another case of deWinter T Waves.
• 
  
• ECG Blog #318 — Provides another variation of de-Winter-like T waves — and — Reviews (and illustrates) the concept of T-QRS-D (Terminal-QRS-Distortion).
• ECG Blog #215 — Reviews a case with T-QRS-D.
• 
  
• ECG Blog #340 — Reviews yet another variation of deWinter-like T waves (with downsloping ST segments and ischemic-induced J-waves).
• 
  
• 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?"). 
• 
  
• The November 22, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the BOTTOM of the page for My Comment regarding ischemia-induced Osborn Waves).
• 
  
• ECG Blog #274 — Reviews the concept of R Wave Progression (and how to quickly recognize lead V1,V2 misplacement).

ECG Blog #340 — An Evolution to Make Note Of

The ECG shown in Figure-1 was recorded in a primary care clinic — from a patient who presented with new-onset chest pain.

• How would YOU interpret the ECG shown in Figure-1?
• Is this hyperkalemia? — or is there a “culprit” artery?

Figure-1: The initial ECG in today’s case — recorded in a primary care clinic from a patient who presented with new-onset chest pain.

MY Thoughts on ECG #1:

Although I would clearly verify with a blood draw that serum K+ is normal — I strongly doubt that the tracing shown in Figure-1 represents hyperkalemia because:

• This patient presented to an out-patient clinic with a history of new-onset chest pain. This is an unlikely presentation for acute hyperkalemia.
• Although T waves are tall and peaked (pointed) with a narrow base in a number of chest leads — there is dramatic J-point ST depression in each of these leads (which is not an expected finding of hyperkalemia).
• The ECG appearance in the 6 limb leads does not look at all like hyperkalemia.

Instead — the history and ECG picture in Figure-1 is highly suggestive of ACS (Acute Coronary Syndrome) — most likely with acute OMI (Occlusion-based Myocardial Infarction). I see the following:

• The rhythm is sinus at ~70/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: Each of the 3 inferior leads (II,III,aVF) show fairly large Q waves (especially in leads III and aVF) — when compared to R wave amplitude in those same leads. These Q waves are suggestive of inferior infarction at some point in time (See below). In contrast — the very small and narrow q waves that are seen in lateral chest leads V5 and V6 are most likely “normal septal q waves”.
• R Wave Progression: There is early transition in ECG #1 — with abrupt development (already by lead V2) of an R wave that is at least as tall as the S wave is deep. Thereafter — R wave amplitude continues to appropriately increase, with peak R wave amplitude attained in leads V4,V5.

Regarding ST-T Wave Changes:

The most remarkable ECG abnormalities in ECG #1 relate to ST-T wave changes.

• As noted — T waves are tall and peaked, with a narrow base in at least 4 (if not 5) of the chest leads (ie, in leads V2-thru-V5 — if not also in lead V6).
• Each of the leads with tall, peaked T waves manifest dramatic J-point ST depression (of between 3-to-5 mm in leads V2-thru-V5).
• 
  
• NOTE: There is prominent J-point notching in leads V3,V4,V5 (and more subtly in lead V6) — with “eye-catching” downsloping of ST segments in those chest leads with ST depression.
• 
  
• In contrast — ST-T wave changes in the limb leads look much less acute. There is a hint of ST segment coving with T wave inversion in lead III — but without ST elevation. Other limb leads show nonspecific ST segment flattening, with some ST depression in leads I and aVL — but not nearly to the same extent as is seen in the chest leads.

Putting It All Together:

As emphasized — Given the history of new-onset chest pain — and — the ECG picture in Figure-1 — We need to assume acute OMI until proven otherwise! Beyond this obvious conclusion — I found a number of interesting features associated with this tracing:

• I did not know what the “culprit” artery was from this initial tracing in Figure-1. The large inferior lead Q waves — with abrupt early transition in the chest leads — strongly suggests infero-postero infarction has occurred at some point in time. But IF myocardial injury in these 2 anatomic areas is all "new" — then the difference in acuity suggested by limb lead vs chest lead ST-T wave findings conveys a discrepancy in timing (since limb lead findings look much less acute compared to far more dramatic ST-T wave findings in the chest leads). 
• Other Possibilities: The infero-postero MI could be old — and the ST-T wave findings in the chest leads could represent an early stage in an acute ongoing form of deWinter T Waves (See ECG Blog #183). Alternatively — ECG #1 could reflect some other pattern of multi-vessel disease.
• 
  
• BOTTOM Line: Regardless of what the "culprit" vessel(s) turned out to be — Acute intervention was needed! Ideally — prompt cath would be done to define the anatomy and guide treatment. Alternatively — acute thrombolysis could be initiated.

CASE Follow-Up:

The patient was treated with Streptokinase. For illustrative purposes in Figure-2 — I've consolidated the evolution of QRST changes by focusing on the Chest Leads over the course of 6 serial ECG tracings.

• NOTE: Limb lead tracings over the course of these 6 serial ECGs failed to show any evolution of ST-T wave changes in the inferior leads. The inferior MI was old.

Figure-2: Chest lead tracings from the next 6 serial ECGs obtained on today's patient. Limb lead tracings failed to show evolution of ST-T wave changes in the inferior leads.

Evolution of the Chest Leads over 6 Serial ECGs:

For clarity — Figure-2 compares serial ECG changes in the Chest Leads over the course of 6 tracings. The timing of these 6 tracings is as follows:

• Panel A: T = 0 (ie, These are the Chest Leads taken from the initial ECG in today's case — the complete 12-lead of which is shown in Figure-1).
• Panel B: T = 1 hour (Chest leads from initial ECG that was recorded when the patient arrived in the ED).
• Panel C: T = 2 hours (from the ECG obtained just prior to STK).
• Panel D: T = 2 hours, 45 minutes (Obtained just after STK completed).
• Panel E: T ~ 4 hours (Obtained ~ 1 hour after STK).
• Panel F: T ~ 12 hours (Patient with minimal chest pain).

MY Thoughts on Figure-2:

Unfortunately — I could not obtain chest pain severity scores correlated to each of the tracings shown in Figure-2. Nevertheless — I thought the evolution of QRST changes in the chest leads of these 6 serial tracings to be remarkable and insightful for another variation of deWinter-like T Waves (See ECG Blog #183 and Blog #318 for more on deWinter-like T Waves).

Panel A (T = 0):

• Chest leads in the initial ECG from today's case highlight how dramatic both the J-point ST depression and T wave peaking can be during the very early stages of deWinter T Waves. 
• Rather than a uniquely upsloping ST segment that leads into the very tall deWinter T waves — the ST segment with this entity may initially be downsloping, as it is here.
• Note how prominent the J-point notching is at the onset of the marked ST depression in leads V3,V4,V5 (and to a lesser extent in lead V6). I believe these exaggerated J-point waves are ischemic-induced Osborn waves — that become smaller as this case evolves, eventually disappearing by Panel C (See My Comment at the bottom of the page in the November 22, 2019 post in Dr. Smith's ECG Blog).

Panel B (T = 1 hour):

• Just 1 hour later — this tracing is remarkable for the loss of anterior lead R wave amplitude! J-wave prominence and the amount of ST depression are greatly reduced. Although the absolute height of the tall T waves is not much different than it was in Panel A — considering the greatly reduced R wave amplitudes — these chest lead T waves are fatter-at-their-peak — wider-at-their-base — and now ever so much more disproportionate (hypervoluminous) to the QRS in their respective leads. These are the hyperacute T waves of an evolving deWinter pattern from acute LAD (Left Anterior Descending) occlusion in progress.

Panel C (T = 2 hours):

• Another hour later (just before Streptokinase was started) — there is subtle evidence of further evolution in that: i) Ischemic J-point notching is no longer seen; and, ii) Downsloping ST depression has been replaced by a steeper, rapidly-rising ascending ST segment that peaks into tall T waves. These are typical deWinter T waves.

Panel D (T = 2 hours, 45 minutes):

• This ECG picture immediately after completion of Streptokinase is not encouraging. There is further overall reduction in chest lead R wave amplitude. ST depression is now minimal — but T waves are massive with respect to the R waves in leads V2, V3, V4. Unfortunately — I do not have information correlating the presence and severity of chest pain before, during and immediately after Streptokinase infusion — but it appears that the result of thrombolysis is at best suboptimal.

Panel E (T ~ 4 hours):

• About 1 hour after completion of Streptokinase infusion — definite ST elevation is now apparent in lead V3. That this ST elevation is diffuse and increasing — is evident in the 12-lead ECG shown in Figure-3, that was obtained 30 minutes later (ie, about 90 minutes after completion of Streptokinase).

Panel F (T ~ 12 hours):

• Final evidence of failed thrombolysis is seen in the last set of chest leads — obtained the next day. QS complexes are now seen in leads V1-thru-V4 (in marked contrast to the tall R waves with early transition that were present in Panel A). ST-T waves have returned to baseline — but at no time were "reperfusion T waves" seen. The patient has lost significant myocardium.

The ECG in Figure-3:

I've labeled the 12-lead ECG in Figure-3 as ECG #E2, since this 12-lead tracing was recorded ~30 minutes after the 6 chest leads shown in Panel E of Figure-2 ( = about 90 minutes after completion of Streptokinase).

• Although we lack a continuous long lead rhythm strip — it appears that a bigeminal rhythm is present in Figure-3. 
• Every-other-beat is wide — manifests RBBB/LAHB morphology — and is not preceded by a premature P wave. Therefore — I suspect the rhythm is ventricular bigeminy, with beats #2 and #4 in both limb leads and chest leads being fascicular PVCs arising from the left posterior hemifascicle.
• 
  
• Clinical implications of fascicular PVCs are the same as the implications for PVCs arising from ventricular myocardium. Given the clinical context of today's case (ie, extensive LAD occlusion with suboptimal, if not "failed" thrombolysis) — frequent ventricular ectopy suggests ongoing ischemia.
• 
  
• Note in ECG #E2 (obtained ~90 minutes after completion of Streptokinase) — that there are anterior Q waves + persistent ST elevation in leads V2-thru-V5 (with marked ST elevation in leads V3,V4).
• 
  
• As a didactic point — Note that excessive ST elevation is also present in the fascicular PVCs. PEARL: On occasion — acute MI may be diagnosed by the presence of abnormal ST elevation in PVCs (but not be present in any of the standard 12 leads). As a result — it's good to routinely assess ventricular ectopy for the presence of abnormal ST elevation, especially when standard leads do not yield a definitive diagnosis.
• 
  
• BOTTOM Line: Today's case illustrates another variation of deWinter-like T waves — showing ST-T wave evolution over the course of 6 sequential chest lead tracings — with the unfortunate end result of suboptimal (if not completely failed) thrombolysis, with ultimate dramatic loss of R wave amplitude in the final set of chest leads (Panel F in Figure-2).

Figure-3: The 12-lead ECG obtained ~90 minutes after completion of Streptokinase infusion (ie, about 30 minutes after the chest leads shown in Panel E of Figure-2). Ventricular Bigeminy is present in the form of left posterior fascicular PVCs ( = beats #2 and 4 in the limb leads — and beats #2 and 4 in the chest leads). ST-T wave changes are minimal in the limb leads. In contrast — there is marked ST elevation in leads V3 and V4 of the chest leads in both sinus-conducted beats and in the PVCs! (with a lesser amount of ST elevation in neighboring leads).

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Acknowledgment: My appreciation to Eelin Siow and Kianseng Ng (from Malaysia) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
• 
  
• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit" artery. NOTE: The Audio Pearl reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI.  
• 
  
• ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.
• ECG Blog #80 — Reviews determination of the "culprit" artery and application of the Mirror Test for recognition of acute Posterior MI.
•  
• ECG Blog #248 — Reviews a case that illustrates Causes of a Tall R Wave in Lead V1 (with the Audio Pearl in this post devoted to this subject).
•  
• 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).
•  
• ECG Blog #262 — Reviews a case of recent acute Infero-Postero MI with group beating from Wenckebach conduction and Low Voltage (with a list of the causes of Low Voltage).
• 
  
• 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 — Reviews another case of deWinter T Waves.
• 
  
• ECG Blog #318 — Provides another variation of de-Winter-like T waves — and — Reviews (and illustrates) the concept of T-QRS-D (Terminal-QRS-Distortion).
• ECG Blog #215 — Reviews a case with T-QRS-D.
• 
  
• 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?"). 
• 
  
• The November 22, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the BOTTOM of the page for My Comment regarding ischemia-induced Osborn Waves).

ECG Blog #339 — Is it SA Block?

 

The ECG in Figure-1 — was obtained from an older old man who presented to the ED (Emergency Department) with chest pain.

• Providers were concerned about SA block. Do you agree?
• What else do you see?

Figure-1: Initial ECG of a patient with chest pain. Is there SA block?

MY Approach to the ECG in Figure-1:

As always – I favor beginning interpretation with assessment of the long lead rhythm strip — using the Ps, Qs & 3R Approach to recall the 5 KEY Parameters (See ECG Blog 185). I find it easiest (and most productive) to delay assessing the 12-lead ECG until after I’ve had a chance to look at the rhythm.

• The rhythm in Figure-1 is not regular — but it does show a "bigeminal" pattern of group beating (ie, repetitive groups of 2 beats — seen here as a repetitive pattern of alternating "longer-than-shorter" R-R intervals).
• 
  
• The QRS is narrow (ie, not more than half a large box in duration in any lead = not more than 0.10 second). Therefore — the rhythm is supraventricular.
• P waves are present. It's easiest to focus on the 2 long lead rhythm strips — in which details of QRS complexes and P waves are perhaps easiest to see in the long lead V1.

The Importance of P Waves:

IF one focuses on the long lead V1 rhythm strip in Figure-1 — it appears that a P wave precedes each QRS complex on this tracing.

• The PR interval is normal (ie, between 0.12-0.21 second in lead II) — and appears to be of equal duration for all 10 beats on this tracing.
• The 1st beat in each pair (ie, beats #1,3,5,7 and 9) — appears to be sinus-conducted (ie, upright P wave with a constant and normal PR interval).

PEARL #1: As discussed in ECG Blog #232 and Blog #312 — recognition of a bigeminal supraventricular pattern when the 1st beat in each pair is conducted, should suggest the following differential diagnosis:

• Sinus rhythm with atrial or junctional bigeminy (ie, every-other-beat is a PAC or a PJC).
• Sinus rhythm with atrial trigeminy — in which every-third P wave is a PAC that is "blocked" (non-conducted).
• Some form of SA ( = Sino-Atrial) Block.
• Mobitz I, 2nd-Degree AV Block ( = AV Wenckebach) with 3:2 AV conduction.
• Mobitz II, 2nd-Degree AV Block (with non-conduction of every 3rd P wave).

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Beyond-the-Core: Technically, there are a few additional causes of a bigeminal rhythm that need not be considered in today's case, because the rhythm is either not strictly supraventricular — or — because the 1st beat in each group is not sinus-conducted. These additional causes include:

• Ventricular bigeminy (ie, every-other-beat is a PVC).
• Atrial fibrillation, atrial tachycardia or atrial flutter with Wenckebach conduction.
• "Escape-Capture" (the 1st beat in each group is a junctional or ventricular escape beat — followed by a conducted beat).

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PEARL #2: Since atrial activity provides the essential clue to the etiology of a bigeminal rhythm — the KEY Question — is whether the morphology of all P waves in today's tracing is the same?

• IF P wave morphology (and the PR interval) are both the same for each of the 10 beats on today's tracing — then all P waves are sinus-conducted.
• IF on the other hand — P wave morphology for each of the early beats (ie, beats #2,4,6,8 and 10) is different — then these early beats must be PACs (Premature Atrial Contractions), and the rhythm is atrial bigeminy.
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• KEY Point: An ectopic P wave arising from a site in the atria that lies close to the SA node — may look very similar to a sinus P wave in one or more leads. But non-sinus P waves will not look the same as sinus P waves in all 12 leads. For this reason — it is important to closely examine P wave morphology in as many of the 12-leads as possible.

Take Another LOOK at today's tracing (See Figure-2):

• HINT: Compare P wave morphology in Figure-2 for the 3 leads with colored arrows. Is morphology for the RED and YELLOW-arrow P waves exactly the same for each of the 3 simultaneously-recorded leads that I have labeled?

Figure-2: I've labeled selected atrial activity from Figure-1 (See text).

ANSWER:

There are subtle-but-real differences in P wave morphology between the RED and YELLOW-arrow P waves in Figure-2:

• In lead II — the RED-arrow P wave is clearly larger than the YELLOW-arrow P wave. In support that this finding is real (and not the result of artifact or the normal variation that may be seen from one P wave to the next) — is the fact that the first P wave in each of the 5 groupings in the long lead II rhythm strip is larger.
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• In lead III — the YELLOW-arrow P wave is barely seen, whereas a definite P wave can be seen under the RED arrow.
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• In lead V1 — the negative component of the RED-arrow P wave is larger. Once again, we see that the negative component of the 1st P wave in each of the 5 groupings in the long lead V1 is larger.
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• PEARL #3: In my experience — SA block is rare! In contrast — atrial bigeminy is a common rhythm disturbance. As a result, I start from the premise that before I will diagnose SA block as the cause of a bigeminal rhythm — I know that I'll probably be able to see subtle-but-real differences in P wave morphology between the 2 beats in each group IF I look in enough different leads. Only when there truly is no difference in P wave morphology in multiple leads do I contemplate SA block.

IMPRESSION: There are subtle-but-real differences in P wave morphology between the 2 P waves in each grouping in Figure-2. Therefore — we can rule out AV block (both Mobitz I and Mobitz II) — because P waves should be both regular and have the same morphology with either form of AV block.

• We ruled out SA block — because morphology of all P waves should be the same with this rare arrhythmia.
• We can rule out blocked PACs — because the T waves of the 2nd beat in each grouping (ie, the T waves of beats #2,4,6,8,10) look identical to the T waves of the 1st beat in each grouping (ie, there is no sign of a "hidden" blocked PAC).
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• Therefore — the rhythm in Figure-2 is atrial bigeminy!

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What About the Rest of the 12-Lead ECG?

Returning to the 12-lead ECG in Figure-2 — this is a very abnormal tracing from this older man who presented to the ED with chest pain!

• Take Another LOOK at the 12-lead tracing (Figure-3):

Figure-3: For ease of interpretation — I show only the 12-lead ECG from today's case. We've already established that the rhythm is atrial bigeminy (ie, sinus rhythm + every-other beat is a PAC). 
— QUESTION: What else do you see? —

MY Thoughts on the 12-Lead ECG:

As previously noted — the underlying rhythm in Figure-3 is atrial bigeminy. Additional findings include the following:

• There is low voltage in the limb leads (ie, No limb lead >5 mm). There is also surprisingly low voltage in lateral chest leads V5,V6 (which usually manifest significant R wave amplitude).
• Intervals (PR, QRS, QTc) are normal. That said, although the QRS complex does not measure out to be “wide” (ie, It is not more than 0.10 second in duration) — the QRS in the limb leads “looks wide”, because there is fragmentation (notching) of QRS complexes in all 6 limb leads.
• There is marked LAD (Left Axis Deviation) — as a result of the all-negative fragmented QS complexes in each of the inferior leads. Whether this is the result of LAHB (Left Anterior HemiBlock) — inferior infarction of uncertain age — and/or some combination of both is uncertain.
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: As noted — There are fragmented inferior lead QS complexes. A Q wave is also seen in lead V6. Although small in size — given how tiny the R wave amplitude in lead V6 is — this is a significant (ie, infarction-related) Q wave.
• R Wave Progression: Transition (where the R wave becomes taller than the S wave is deep) — occurs appropriately (here between leads V2-to-V4). That said — the tiny R wave amplitude in lateral chest leads V5,V6 is clearly abnormal.
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• ST-T Wave Changes: There is ST segment coving and elevation, with terminal T wave inversion in each of the inferior leads. Subtle reciprocal ST segment depression is seen in lead aVL. The nonspecific ST-T wave flattening in the other high-lateral lead ( = lead I) — is probably also a reflection of reciprocal changes.
• In the Chest Leads — there is "shelf-like" ST depression in leads V1-thru-V4 (maximal in leads V2,V3). There is subtle-but-real ST elevation in lead V6.

Putting It All Together:

Given the History of this patient (ie, an older man who presented to the ED for chest pain) — the ECG in Figure-3 is diagnostic of recent or acute infero-postero-lateral OMI (Occlusion-based Myocardial Infarction).

• The marked fragmentation (notching) seen in virtually all limb leads (and also to a lesser extent in lateral chest leads V5,V6) — suggests "scar" from either infarction and/or cardiomyopathy. This finding, in addition to the QS complexes in each of the inferior leads — suggests that there has been inferior infarction at some point in time. That said, without a prior ECG for comparison — we can not rule out the possibility that these findings may be recent (or even acute). To Emphasize: Significant Q waves have been known to develop in as little as 1-2 hours after the onset of symptoms.
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• The amount of ST elevation seen in the inferior leads is modest, albeit this is difficult to assess given how small QRS complexes are in these leads. Similarly, the amount of reciprocal ST depression in high-lateral lead aVL is also modest. Therefore, without the benefit of a prior ECG for comparison — we simply can not say from this single ECG alone whether inferior lead changes are new — old — or — reflect an additional "new" event superimposed on prior infarction.
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• On the other hand — the marked shelf-like ST depression in anterior chest leads constitutes a positive "Mirror" Test for acute posterior OMI (See LINKS to related Blogs below) — and, in this patient with new chest pain — has to be assumed acute until proven otherwise!
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• The loss of R wave amplitude in lateral chest leads — in association with a small-but-definite Q wave with coved ST elevation in lead V6 must also be assumed to reflect acute lateral infarction until proven otherwise.
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• As to identification of the probable "culprit artery" — the finding of potentially acute ST-T wave changes in infero-postero-lateral lead areas — with a comparable amount of ST elevation in lead II and lead III — suggests either acute occlusion of the LCx (Left Circumflex) coronary artery and/or multi-vessel disease.
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• Finally — the finding of greatly reduced QRS amplitude ( = low voltage) in multiple leads, in a patient with acute infarction — may indicate myocardial "stunning" with markedly reduced LV function (See ECG Blog #272 for more on the causes and clinical significance of low voltage on ECG).
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• P.S.: Of Note — Our assessment of the cardiac rhythm in today's case determined that the bigeminal rhythm was not the result of AV block. Chances are that if (as) this patient recovers and regains normal LV function — that his atrial bigeminy will also resolve.

CASE Follow-Up:

Unfortunately — I did not receive clinical follow-up on today's case. I also did not receive any additional ECGs on this patient. Serial ECG could have been enlightening as to refining the anatomic area(s) of acute infarction — as well as shedding light on when the recent infarction most probably occurred. 

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Acknowledgment: My appreciation to Kire Todorov (from Macedonia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation. 
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #312 — Reviews the ECG diagnosis of SA Block (as well as the Differential Diagnosis of a Bigeminal Rhythm).
• ECG Blog #232 — More on the ECG diagnosis of a bigeminal supraventricular rhythm.
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• ECG Blog #272 — Reviews the causes and clinical significance of Low Voltage (especially in association with recent/acute infarction).
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery (and discusses the concept of why "OMI" is a much better term than "STEMI", which has become outdated).
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• ECG Blog #317 — More on use of the Mirror Test (compared to use of posterior leads) for detection of acute Posterior MI.
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• ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).
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• 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). 
• ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
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• The September 21, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI.
• The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.