Thursday, April 29, 2021

ECG Blog #219 (ECG MP-36) — Is this an Irregular VT?

The 12-lead ECG shown in Figure-1 was obtained from an 87-year-old man who presented to the ED (Emergency Department). Unfortunately — no other information is available on this patient.

  • How would you interpret this tracing?
  • How certain are YOU of your diagnosis?


Figure-1: 12-lead ECG obtained from an 87-year-old man (See text).





NOTE #1: Some readers may prefer at this point to listen to the 7:45 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-36).


Today’s ECG Media PEARL #36 (7:45 minutes Audio) — Reviews distinction between Ventricular Tachycardia vs AFib when the Wide Tachycardia is Not Regular.



MY Approach to this Tracing:

As always — I favor use of a Systematic Approach for assessment of every 12-lead ECG I encounter (This Systematic Approach reviewed in ECG Blog 205). The first part of this 12-lead Systematic Approach entails assessment of the Rhythm.

  • Unfortunately — there is no long lead rhythm strip associated with the 12-lead ECG shown in Figure-1. That said — there are more than enough beats on this 12-lead tracing to adequately assess the cardiac rhythm. I favor the Ps, Qs & 3R Approach (Reviewed in ECG Blog 185).
  • P waves are absent.
  • The QRS is wide.
  • Regularity: Although parts of this rhythm look regular — when measured, the R-R interval is constantly changing. The rhythm is irregularly irregular.
  • Rate: The rate is rapid. It looks like the average R-R interval is about 2 large boxes — which corresponds to a rate of ~150/minute (A total of 26 beats are seen on this tracing — which is 10 seconds long — which means the actual rate = 26 X 6 = 156/minute).
  • Related: Since P waves are absent — there is no "relation" between P waves and the QRS.
  • Therefore — The rhythm is AFib with a rapid ventricular response.


PEARLS/Comments regarding this Tracing:

  • Although at times — VT (Ventricular Tachycardia) may manifest an element of irregularity, it should not be as irregularly irregular as the rhythm in Figure-1. This is AFib.
  • Coarse undulations in the baseline (best seen in lead II) represent "fib waves". 
  • Further support that the rhythm in Figure-1 is supraventricular is forthcoming from QRS morphology, which is consistent with RBBB (Right Bundle Branch Block). As reviewed in ECG Blog #204 — ECG diagnosis of the bundle branch blocks is made from assessment of QRS morphology in the KEY leads ( = leads I, V1 and V6) — which show RBBB-equivalent pattern in lead V1 (predominantly upright qR complex in V1 and, wide terminal S waves in leads I and V6.
  • NOTE: Finding a prior ECG on this patient could be very helpful — especially IF you see identical QRS morphology on a prior tracing during sinus rhythm (which would establish beyond doubt that the etiology is supraventricular — and that the rhythm is rapid AFib).
  • QRS morphology in Figure-1 is consistent with a Bifascicular Block = RBBB/LPHB (Reviewed in the video ECG Media Pearl #21which is found in ECG Blog #203). In association with RBBB — a deep and very steep (straight) S wave downslope in lead I suggests LPHB (Left Posterior HemiBlock). LPHB is not common. When seen — it is almost always associated with RBBB, and usually implies significant underlying heart disease.
  • QRS morphology in lead V1 lacks the characteristic triphasic (rsR') appearance of RBBB. The finding of an initial Q wave in lead V1 (which is clearly seen in 6 of the 7 QRS complexes in this lead) — suggests there has been prior septal infarction
  • Although difficult to tell because of baseline undulations — there appears to be a Q wave in lead III — and possibly in lead aVF (at least in some of the complexes in this lead). This is of uncertain clinical significance.
  • There is no sign of chamber enlargement (although assessment of LVH and RVH is always challenging when there is BBB).
  • There are nonspecific ST-T wave changes — but these do not appear to be acute.



NOTE: The reason I departed from  the sequential systematic approach outlined in ECG Blog #205 — is that the QRS complex is wide!

  • The 1st things to do on recognizing QRS widening are: i) Ensure that the patient is hemodynamically stable; andii) Make sure that the rhythm is not VT. As noted above — the absence of P waves and complete irregularity of the rhythm told us this is AFib.
  • Once established that the rhythm is supraventricular — the next step is to determine the type of conduction defect. The reason this should be done before assessing axis, chamber enlargement and QRST changes — is that criteria for these parameters will be different when there is bundle branch block.


In Summary: The ECG in Figure-1 shows AFib with a rapid ventricular response. There is bifascicular block (RBBB/LPHB) — with a Q wave in lead V1 that suggests prior septal infarction. Nonspecific ST-T wave changes are present — but these do not appear to be acute.

  • Finding a prior ECG on this patient would be helpful in determining which (if any) of the above changes might be new.
  • Clinical correlation is needed to determine optimal managment. Unfortunately — no additional clinical information was available on this patient.



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 #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach
  • 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 ECG Media Pearl #21 in this blog post. 
  • ECG Blog #211 — WHY does Aberrant Conduction occur?


Monday, April 26, 2021

ECG Blog #218 (ECG MP-35) — What is a Hyperacute T Wave?

The ECG in Figure-1 was obtained from a man in his 40s — who presented with new-onset chest pain that began 1 hour earlier.

  • HOW would you interpret this tracing?
  • Should you immediately activate the cath lab?
  • OR — Could the anterior T waves represent a repolarization variant?



Figure-1: Initial ECG obtained from a man in his 40s — who presented with new-onset chest pain (See text).




NOTE #1: Some readers may prefer at this point to listen to the 5:20 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-35).


Today’s ECG Media PEARL #35a (4:50 minutes Audio) — WHEN is a T Wave Hyperacute? (ie, How to distinguish from the T wave of repolarization variants?).



MY Approach to this Tracing:

As always — I favor a Systematic Approach for every ECG I encounter (This Systematic Approach reviewed in ECG Blog 205). My descriptive analysis of the ECG shown in Figure-1 is as follows:

  • The rhythm is fairly regular at ~55-60/minute. Upright P waves with a constant PR interval are seen in lead II — so the rhythm is sinus bradycardia. Intervals (PR, QRS, QTc) and the axis (which is about +45 degrees) are normal. There is no chamber enlargement.


Regarding Q-R-S-T Changes:

  • There may be the tiniest of Q waves in the inferior and lateral chest leads.
  • R wave progression is normal — with “transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V2-to-V3. If anything — there is already a prominent R wave (of ~11 mm) by lead V3 — suggesting preservation of anterior forces.


Assessment of ST-T waves:

  • Especially in this patient, who presents to the ED with new-onset chest pain that began just 1 hour earlier — there are a number of abnormal findings on this ECG that I have labeled in Figure-2.

Figure-2: I’ve labeled KEY findings from the ECG in Figure-1 (See text).




Assessment of ST-T waves:

  • The most remarkable finding in Figure-2 is the disproportionately tall T waves in leads V2 and V3. As discussed in the above Audio PEARL ( = ECG MP-35) — T waves are considered hyperacute when they are taller-at-their-peak and/or wider-at-their-base than expected (considering relative R wave and/or S wave amplitude in the particular lead you are looking at). Therefore — the 10 mm tall T wave in lead V2 especially (given the tiny r wave in this lead) — as well as the disproportionately tall T wave in lead V3 — are both clearly beyond the expected height for T waves in these leads. 
  • Note also how wide the T wave base is in both leads V2 and V3 (compared to a more normal width for the base of the T wave in leads V5 and V6).
  • The RED dotted lines show 2-to-2.5 mm of ST elevation in leads V2 and V3. Whereas some ST elevation may normally be seen in these leads — the amount seen here seems excessive considering the worrisome history and the hyperacute T wave appearance (given relatively modest QRS amplitude in these leads).
  • In the context of what we have just described regarding the ST-T wave appearance in leads V2 and V3 — the ST-T wave in lead V4 also appears to be abnormal (ie, showing ST elevation and a wider-than-expected T wave base).
  • Normally — you do not see ST elevation in lead V1, and certainly not the coved ST segment shape (“frowny”-configuration) with subtle-but-real ST elevation as seen here in lead V1 of Figure-2.

PEARL #1: I find the concept of patterns of neighboring leads” extremely helpful when assessing for potential acute ST-T wave changes. There should be no doubt that the ST-T waves in leads V2 and V3 are abnormal in this patient with new-onset chest pain

  • The ST-T wave changes I describe in neighboring leads V1 and V4 are less pronounced — but in the context of obvious marked abnormality for leads V2 and V3 — it is virtually certain that the ST-T waves in these neighboring leads represent an extension of the changes we see in lead V2 and V3.

PEARL #2: The last clear abnormality in ST-T wave appearance in the anterior leads of Figure-2 — is the terminal T wave inversion that we see in leads V1V2 and V3 (BLUE arrows)

  • This terminal T wave inversion in Figure-2 resembles the shape of the terminal T wave inversion seen with Wellens’ Syndrome (fully discussed in ECG Blog #209). In a patient with new-onset chest pain, this terminal T wave inversion that follows after disproportionately tall and hyperacute anterior T waves is definitely not a normal finding. Whether it represents some component of spontaneous coronary reperfusion is uncertain from viewing this single ECG — but what is certain — is that these ST-T waves in leads V1-thru-V3 do not represent a simple repolarization variant.


MY Impression of Figure-2 at this Point:

  • In this patient with new-onset chest pain — we see a combination of abnormal ST-T wave findings in the anterior chest leads. These include: i) Hyperacute T waves in leads V2, V3, V4; ii) Abnormal ST elevation in leads V1-thru-V4; andiii) Terminal T wave inversion in leads V1-thru-V3.
  • These ST-T wave findings alone clearly justify immediate cath lab activation — with a presumptive diagnosis of acute proximal LAD (Left Anterior Descending) Occlusion until proven otherwise. Onset of abnormal ST elevation as early as in lead V1 (in association with terminal T wave inversion in this lead) — is the reason for suspecting a proximal LAD occlusion.

PEARL #3: The more leads you see that show abnormal ST-T wave changes — the greater the likelihood that an acute cardiac event is ongoing.

  • After identifying the definite ST-T wave abnormalities (that we see in leads V1-thru-V4) — I always take another much closer look at the remaining leads. Although there is no ST depression in the inferior leads in Figure-2 — the ST segments in leads III and aVF are clearly straighter than normal (short, horizontal BLUE lines in these leads). 
  • Although admittedly subtle (!) — Can’t YOU see a difference between these straightened ST segments, compared to the more normal, gentle upsloping of the ST segment in lead I?
  • Lead aVL is a KEY lead to focus on in association with anterior infarction. Although there is no ST elevation in this lead — I thought the ST segment takeoff looked a bit straighter-than-expected (horizontal BLUE line in lead aVL).
  • NOTE: These changes in leads III, aVL and aVF are exceedingly subtle! The only reason I mention them — is that in the context of this patient with new-onset chest pain and clearly abnormal ST-T waves in leads V1-thru-V4 — identifying other subtle abnormal findings adds support that an acute cardiac process is ongoing.


FOLLOW-UP on Today’s Case:

  • Unfortunately, I do not have follow-up ECGs on today’s case. IF I did — I would have satisfied my personal curiosity by looking for: i) Evolution of the anterior hyperacute T waves into more profound ST elevation; iiLoss of anterior R wave forces (which would be expected if reperfusion was delayed); iii) Deepening of the shallow, terminal T wave inversion (if chest pain resolved and reperfusion was successful); andiv) Looking to see IF those very subtle ST-T wave changes I noted in leads III, aVL and aVF evolved over time.
  • What Happened: On seeing the initial ECG in today’s case — the cath lab was immediately activated. As shown in Figure-3 — there was 100% occlusion of the proximal LAD — with achievement of excellent reperfusion following successful PCI.

Figure-3: Cath films on this patient before and after PCI. LEFT: WHITE arrows in the before-PCI picture highlight complete absence of the LAD, due to 100% occlusion of this vessel at the ostium. RIGHT: RED arrows show successful reperfusion of the LAD following PCI (See text).


Acknowledgment: My appreciation to 林柏志 (from Taiwan) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205). 
  • ECG Blog #183 — Reviews recognition of deWinter-like T waves vs repolarization variants. 
  • ECG Blog #193 — 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.
  • ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data. 
  • ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome.

Friday, April 23, 2021

ECG Blog #217 (ECG MP-34) — Is this VT on this Holter?

The 2-lead rhythm strip shown in Figure-1 was obtained from the Holter monitor of a middle-aged adult.

  • Does this tracing show a 4-beat run of VT or aberrant conduction?
  • How certain are YOU of your diagnosis?


Figure-1: A simultaneously-recorded 2-lead rhythm strip, obtained during Holter monitoring. Does this tracing show a 4-beat run of VT or aberrant conduction?





NOTE #1: Some readers may prefer at this point to listen to the 6:00 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-34).


Today's ECG Media PEARL #34 (6:00 minutes Audio) — Are YOU really seeing AV Dissociation in that WCT Rhythm? (ie, Is the rhythm VT?).




MY Thoughts regarding the Rhythm in Figure-1:

The underlying rhythm in this 2-lead Holter tracing is sinus — as indicated by normal-appearing upright P waves with a fixed PR interval preceding each of the narrow beats (RED arrows in Figure-2).

  • After the first 2 sinus beats — the rhythm is interrupted by a 4-beat run showing a very different QRS morphology (ie, beats #3-thru-6).
  • Sinus rhythm resumes with beat #7 for the last 3 beats in the tracing.


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

What is the Cause of the 4-Beat Run?

I am 100% certain that the 4 different-looking beats that are seen in Figure-2 constitute a short run of NSVT ( = Non-Sustained Ventricular Tachycardia). My reasons for saying this are the following:

  • Statistically ( = according to the literature) — When the underlying rhythm is sinus, sudden occurrence of a wide run of different-looking beats (as we see in Figure-2) will turn out to be VT at least 80% (if not 90%) of the time. Therefore — Always assume VT until proven otherwise (ie, Our “mindset” should be that we need to prove aberrant conduction — rather than the other way around).
  • There is no reason for aberrant conduction to occur in Figure-2. Aberrant conduction of supraventricular beats is most often seen when the run of wide beats occurs early in the cycle (ie, when the coupling interval is short) — because this increases the chance that the run will begin during the RRP (Relative Refractory Period). But in Figure-2 — the first wide beat ( = beat #3) occurs late in the cycle, at a time when it is very unlikely that the conduction system will still be refractory. Thus, there is no “reason” for aberrant conduction(NOTEFor more on WHY certain supraventricular beats conduct with aberration — Please see ECG Blog #211).
  • QRS morphology for the different-looking beats shows marked QRS widening and a totally different appearance. Supraventricular beats that conduct with aberration often manifest a similar initial direction and slope of the QRS complex — because supraventricular beats often initially conduct down the normal AV nodal pathway until they encounter that part of the conduction system that is refractory. But, as opposed to the rapid R wave upslope that we see for sinus beats in both lead A and lead B of Figure-2 — beats #3-thru-6 show a marked difference in the very initial part of the QRS complex.
  • I am uncertain which specific leads rhythms A and B in Figure-2 correspond to. The most common leads monitored are a standard lead II — and either a right- or left-sided lead (corresponding to lead V1 or MCL-1  or — lead V5 or V6 or MCL-6). Knowing the specific lead(s) used in monitoring helps — because aberrant conduction is much more likely when QRS morphology is consistent with some type of conduction defect (ie, RBBB, LBBB, LAHB, LPHB, or some combination thereof). 
  • I suspect rhythm A corresponds to a lead II recording — in which case the excessively wide initial R wave and terminal S wave fragmentation are not characteristic of LAHB conduction. And, regardless of the lead that rhythm B corresponds to — QRS morphology would not be typical for any known form of conduction defect. Thus, QRS morphology in Figure-2 is atypical for any of the common forms of conduction defects — and, this is another factor against aberrant conduction. (NOTE: This atypical QRS morphology by itself does not rule out the possibility of aberrant conduction — but it does make aberrant conduction less likely).
  • Most Convincingly: There is AV Dissociation in Figure-2! This is subtle — but it is present (PINK arrows). Calipers are needed to find this! — but the notching that is highlighted by PINK arrows in rhythm A — corresponds perfectly to subtle notching that is also seen in rhythm B (as shown by the vertical BLUE timelines) — and — these PINK arrows occur with a P-P interval that is perfectly consistent with the slight underlying sinus arrhythmia. Demonstration that sinus P waves continue on-time throughout the rhythm strip in both leads A and B confirms that there are independent atrial and ventricular rhythms. This constitutes AV dissociation (ie, P waves that transiently are not related to neighboring QRS complexes) — and identification of AV dissociation proves that beats #3-thru-6 constitute a 4-beat run of NSVT.

P.S. — Some Definitions:

  • There are many different names for early-occurring ventricular beats. I favor the term PVC (Premature Ventricular Contraction).
  • 2 PVCs in a row are called a ventricular Couplet.
  • 3 PVCs in a row are called a ventricular Salvo or a “Triplet”. 
  • The definition of “VT” (Ventricular Tachycardia) — is 3 or more PVCs in a row. 


KEY Point: Rather than simply noting the presence of “VT” — it is important to describe the rhythm by a number of KEY parameters. These include: 

  • Duration of the VT run (ie, How many beats or for what period of time does the VT last?)
  • Rate of the VT? 
  • Regularity of the wide rhythm? (ie, Not all VT is regular — as seen for the 4-beat run in today’s case).
  • QRS Morphology? (ie, Do all VT beats look the same — or is there changing morphology?).
  • What happened just before? — and immediately after the VT episode? (ie, Was the patient in sinus rhythm or AFib before VT began? Was there a “post-ectopic” pause after the run terminated?)
  • Are there recurrent episodes of the VT rhythm? 
  • Has there been antiarrhythmic treatment?
  • Importantly: What is the patient's hemodynamic status during the VT episode? (ie, Is the patient symptomatic? Hemodynamically stable or unstable?)


Some Final Terms:

  • NSVT (Non-Sustained VT) —  The occurrence of 3 or more PVCs in a row up until the point when VT becomes “sustained”.
  • Sustained VT — Definitions for what constitutes “sustained” VT vary, depending on duration of the VT episode and/or the number of beats in the run. Most authorities reserve designation as “sustained” VT for runs lasting at least 30 seconds and/or VT that causes hemodynamic instability. 
  • Editorial Comment: My Simplified Definition  IF the run of VT is long enough to give YOU palpitations, then it is probably “sustained” VT.

  • “Slow” vs “Fast” VT — This gets into the definition of whether the VT rhythm is more likely to be associated with hemodynamic consequences or not. In general — AIVR ( = Accelerated IdioVentricular Rhythm or slow” VT) will often be surprisingly well tolerated — whereas fast VT (usually associated with a ventricular rate of at least 130/minute) is much more likely to be associated with hemodynamic consequences. 
  • NOTE: For more on AIVR and “slow” vs “fast” VT — Please check out ECG Blog #108.



In SUMMARY regarding Today’s Case:

  • The rhythm in Figure-1 shows an underlying sinus arrhythmia that is interrupted by a 4-beat run of an irregular NSVT at ~110-130/minute.




Acknowledgment: My appreciation to Zineddine Chleghoum (from Alger, Algeria) for the case and this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #211 — WHY does Aberrant Conduction occur? 
  • ECG Blog #133 — Illustrates use of Fusion beats and AV Dissociation in the diagnosis of VT.
  • ECG Blog #128 — Reviews the concept of Fusion Beats.
  • ECG Blog #129 — Late-cycle (End-diastolic) AIVR and Fusion beats in diagnosis of ventricular beats. 
  • ECG Blog #134 — A very subtle example of AV Dissociation to prove VT.
  • ECG Blog #108 — About AIVR — and review of why retrograde P waves with 1:1 VA conduction do not constitute AV “dissociation”.