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).

 

 

 

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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).

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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 3 KEY leads ( = leads I, V1 and V6) — which show a 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 #21, which 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; and, ii) 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.

 

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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 #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?

 

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).

 

 

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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).

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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 V1, V2 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; and, iii) 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; ii) Loss 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); and, iv) 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).

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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-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.

ECG Blog #217 — 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?

 

 

 

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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).

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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. (NOTE: For 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.

 

 

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

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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”.