ECG Blog #365 — A 30yo with Pericarditis ...

The ECG in Figure-1 was obtained from a previously healthy 30-ish year old man — who presented to medical attention for vasovagal syncope. Based on this initial ECG — the patient was transferred to a PCI-capable center: 

• Do YOU agree with the need for transfer?

Hospital evaluation for this patient was negative for an acute coronary syndrome (ie, CT coronary angiogram was normal — troponin was not elevated — and Echo was negative, with no sign of pericardial effusion). The patient was discharged with a diagnosis of acute pericarditis — and treated with a full course of colchicine and ibuprofen.

• Do YOU agree with the discharge diagnosis and treatment prescribed?

Figure-1: The initial ECG in today's case. Based on this ECG — the patient was transferred to a PCI-capable center. The ultimate discharge diagnosis was acute pericarditis. (To improve visualization — I've digitized the original ECG using PMcardio).

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Editorial NOTE: Today's case was sent to me by Dr. Magnus Nossen from Norway — where the Cabrera Format for ECG recording is used. Given how the internet has changed the world in recent years — virtually all clinicians will periodically encounter different recording formats such as this one. The insert in the lower right portion of Figure-1 highlights the difference in limb lead sequencing with the Cabrera Format:

• Instead of beginning the limb lead display with standard lead I — the Cabrera format begins with the highest lateral lead ( = lead aVL, corresponding to an electrical viewpoint perspective of -30 degrees).
• The right augmented lead is displayed with reversed polarity = lead -aVR (corresponding to an electrical viewpoint perspective of +30 degrees).
• As suggested by the Axis Insert in Figure-1 — the Cabrera Format offers a more logical display of limb lead sequencing, in that there is a gradual progression of equally spaced (at increments of 30 degrees) limb leads, beginning with lead aVL (at -30 degrees) — and continuing until the most rightward frontal plane lead = lead III (at +120 degrees).
• In contrast, the standard U.S. format is not sequential — it views the right augmented lead from the remote perspective of the right shoulder — and it uses unequal spacing between neighboring leads.
• NOTE: The chest leads are unchanged with the Cabrera format. 
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• See ECG Blog #215 — for more on the Cabrera format.

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MY Thoughts on the ECG in Figure-1:

It's important to remember that the ECG in Figure-1 was obtained from a previously healthy 30-ish year old man who presented with an episode of vasovagal syncope — but there is no mention of chest pain in the history!

• Even before looking at today's ECG — the above clinical scenario suggests a low-prevalence likelihood for an acute cardiac event.

I interpreted the ECG in Figure-1 as follows:

• The rhythm is sinus at ~65/minute. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is normal at +75 degrees. 
• There is no chamber enlargement. Although QRS amplitude in lateral chest leads V4 and V5 is generous (with overlap of the S in V3 with the R in V4) — in view of this patient's young age (ie, ~30 years old) — criteria for LVH are not satisfied. 

Regarding Q-R-S-T Changes:

• There are small, narrow Q waves in the inferior and lateral chest leads. These are consistent with normal septal q waves (ie, Normal septal q waves may be seen in the inferior leads when the frontal plane axis is fairly vertical — as it is in ECG #1).
• R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.

Regarding ST-T wave Changes: — ST elevation is present in multiple leads (ie, in leads I-thru-III; and V3-thru-V6). That said — a number of features strongly suggest that this ST segment elevation looks like a benign repolarization variant. These benign-looking features include: 

• ST elevation is gently and smoothly upsloping (ie, "smiley" configuration) in all leads in which it is present. 
• The ST elevation is present in 9/12 leads — such that there is no localization (as is usually present with acute infarction). In particular, in 7 of these leads (ie, in leads -aVR-thru-lead III — and in leads V4-6) — the shape of the ST elevation and peaked T waves is virtually identical (whereas that is rarely the case with acute infarction).
• To emphasize — the inverted T wave in lead aVL of ECG #1 "looks" benign — since the T wave vector often follows close behind the QRS vector (ie, the negative T wave in lead aVL "follows" the negative QRS in this lead) — AND — the size of this inverted T wave is small and not disproportionate to the size of the S wave in this lead. When the frontal plane axis is vertical (as it is in Figure-1) — it is common to see a predominantly negative QRS with shallow T wave inversion in lead aVL.
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• The typical J-point notching that is characteristic of early repolarization is prominently present in lead V4.
• There is no reciprocal ST-T wave depression, as is commonly seen with acute infarction (ie, The inverted T waves in leads V1 and V2 are likely to either be positional or a normal variant).
• The QTc is not prolonged (whereas with acute OMI — the QTc is more likely to be longer).
• R wave progression is entirely normal — and if anything, QRS amplitude is generous in the mid-chest leads (whereas with acute anterior OMI — there is often reduction, if not loss of the initial R wave in anterior leads).
• Finally — Taking a step "back" to look at the tracing in Figure-1 as a "whole" — ST-T wave morphology just "looks" benign!

BOTTOM Line: Need for Transfer to a PCI-capable Center?

Considering that the history in today’s case is of a previously healthy 30-ish year old man with an episode of vasovagal syncope, but no chest pain (ie, a “low prevalence likelihood” for acute Occlusion MI) — the above description of ECG findings is my best attempt at explaining why my brain immediately recognized the pattern in ECG #1 as a non-OMI repolarization variant. 

• I saw no need for transfer of the patient to a PCI-capable facility on the basis of this history and the initial ECG.
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• For more on “My Take” regarding the ECG entity of Repolarization Variants — Please check out My Comment at the bottom of the page in the May 23, 2022 post in Dr. Smith’s ECG Blog.

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Factors Against a Diagnosis of Acute Pericarditis:

As stated above — this patient was discharged from the hospital with a diagnosis of acute pericarditis. As a result he was treated with potent medications (that each have potential for side effects) — and told not to work for 4 weeks — as well as being given a medical diagnosis that will stay on his chart. From the information provided — I would not make the diagnosis of acute pericarditis.

• In my experience — acute pericarditis is greatly overdiagnosed! There is a tendency once acute MI is ruled out, to attribute chest pain in a patient with ST elevation to acute pericarditis. Follow-up of many (most) of these patients eventually reveals that they did not have acute pericarditis. To quote Dr. Stephen Smith, "You diagnose pericarditis at your peril" — meaning, that most patients seen in an ED who are given this diagnosis do not have pericarditis.
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• The clinical reality is — Diagnosis of acute pericarditis in an acute setting is often difficult. Inflammatory markers tend to be nonspecific. Assessment of the history for chest pain is subjective — and symptoms are not always pleuritic and positional in nature. Many patients with acute viral pericarditis do not have Echo abnormalitiy (ie, pericardial effusion is often not present). Finally — ECGs in the acute setting are often misinterpreted. (See the Audio Pearl — and Figures 4-thru-8 in the ADDENDUM below for more on the ECG and clinical diagnosis of acute Pericarditis).
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• Cardiac MRI has been increasingly used to assist in diagnosis — although this modality is not always available in the acute setting (Aldweib et al — Curr Cardiol Rev 14(3):200-212, 2018).

PEARL #1: In making the diagnosis — It's important to consider the clinical setting (ie, 80-85% of acute pericarditis in the developed world is idiopathic from presumed acute viral infection). In the "right clinical setting", the one finding that is diagnostic of acute pericarditis — is a pericardial friction rub:

• In my experience over years of consulting on countless internet cases in which the diagnosis of acute pericarditis was put forth — in the overwhelming majority of these cases, no mention of ever having listened for a pericardial friction rub was either made on the chart or included in oral presentation. In my opinion — IF there is no specific mention that "a rub was present (or absent)" — this should be taken as indication that no rub was listened for. And, since short of MRI — a rub is essentially the only clinical finding that may be definitive — Not to carefully listen for a pericardial friction rub is to overlook the best possibility for making the diagnosis (See material in the ADDENDUM below).

Acute Pericarditis: What To Look For on ECG

Distinction between acute Pericarditis vs acute MI vs a Repolarization variant can be challenging! The characteristic ECG finding of acute pericarditis is diffuse ST elevation. While ST elevation with acute MI tends to “localize” (ie, to 1 or more ECG areas — with reciprocal ST depression elsewhere) — the ST elevation with repolarization variants may at times resemble pericarditis when ST elevation is more generalized. That said — consider the following:

• PEARL #2: The History is important. Knowing that your patient was previously healthy, but developed a recent viral infection — and now has distinctly pleuritic and positional chest pain (ie, worse on lying down — and improved on sitting up and leaning forward, so as to “relieve stretch” of the pericardium) — at least increases the likelihood that acute pericarditis might be present. Hearing a “walking on snow” pericardial friction rub in such a patient could confirm your diagnosis, even before you look at the ECG.
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• Regarding Today's CASE: This previously healthy 30-ish year old man presented with syncope — without mention of recent viral infection; pleuritic or positional chest pain; or of the clinician having carefully listened to the chest for a pericardial friction rub. Thus, the clinical setting in today’s case is not really suggestive of acute pericarditis.

As noted earlier — the ECG in Figure-1 does show ST elevation in 9/12 leads. That said — the distribution and nature of this ST elevation is a bit atypical for acute pericarditis (See ADDENDUM below for details):

• PEARL #3: With acute pericarditis — the 3 leads that do not typically show ST elevation are the “right-sided” leads (ie, leads III, aVR and V1). However, in Figure-1 — it is lead aVL instead of lead III that shows T wave inversion. (NOTE: Because today’s ECG is recorded with the Cabrera format — the negative aVR lead that shows ST elevation would correspond to ST depression and T wave inversion in a positive aVR lead).
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• PEARL #4: With acute pericarditis —  the shape of the ST-T wave in lead II tends to look much more like the ST-T wave shape in lead I (instead of like ST-T wave shape in lead III — as is seen in Figure-1).
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• PEARL #5: The RATIO of the amount of ST elevation to T wave amplitude in lead V6 should be less than 0.25 (ie, height of the ST elevation, as measured from the end of the PR segment to the J-point — should be less than 1/4 of the height of the T wave in lead V6). I illustrate HOW this RATIO is arrived at in Figure-2, which I have adapted from the 3/10/21 post in Life-In-The-Fast-Lane. Applying this measurement technique in Figure-3 to today’s tracing — the ST/T Wave Ratio = 0.20. This is less than the 0.25 ratio cutoff point — and therefore not suggestive of acute pericarditis.
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• PEARL #6: There is virtually no PR depression at all in ECG #1. While significant PR depression is not a specific ECG finding with acute pericarditis — the lack of any PR segment deviation at all is a factor against the likelihood of acute pericarditis.

Figure-2: Illustration of how the ST segment to T wave ratio is calculated — adapted from Life-In-The-Fast-Lane (See text).

Figure-3: Calculation of the ST/T wave ratio in lead V6 from today's case. The ratio is 0.20 — which is not suggestive of pericarditis.

Putting It All Together:

To Emphasize — Nothing is perfect. There are always exceptions to clinical generalities (ie, A patient with baseline ST-T wave repolarization changes may on top of this, develop a case of acute pericarditis). That said — taking all factors from today’s case into account, my thoughts are the following:

• The clinical presentation of this previously healthy 30-ish year old man does not suggest a likelihood of either acute OMI or acute pericarditis.
• The initial ECG looks like a benign repolarization variant. Transfer to a PCI-capable Center seems unnecessary.
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• CASE Follow-Up: Serial troponins from today's patient were negative. Echo was completely normal, and without pericardial effusion. CT Coronary Angiogram showed no sign of underlying coronary disease. In the absence of a history of positional and/or pleuritic chest pain — and in the absence of a pericardial friction rub — evidence in support of a diagnosis of acute pericarditis is lacking. The patient was seen in follow-up and told that his initial diagnosis was mistaken. He gladly returned to work the next day. 

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) 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 #215 — Reviews the Cabrera Format (and explores potential advantages of this more logical anatomical sequencing).
• ECG Blog #114 — Reviews another case using the Cabrera format.
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• ECG Blog #208 — Reviews the ECG Diagnosis of Acute Pericarditis.
• My Comment (at the bottom of the page in the December, 13, 2019 post in Dr. Smith's ECG Blog) — regarding potential use with pericarditis of the ST/T Wave Ratio in Lead V6.
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• My Comment (at the bottom of the page in the May 23, 2022 post in Dr. Smith's ECG Blog) — regarding Repolarization Variant Patterns.
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• ECG Blog #193 — for review of the concept of “OMI” ( = Occlusion-based Myocardial Infarction) — and why this term should replaced the outdated STEMI paradigm. 
• ECG Blog #337 and ECG Blog #294 — relevant related Blog posts on the importance of the OMI paradigm (in preference to the outdated STEMI paradigm).

 

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ADDENDUM (2/24/2023):

• The Audio Pearl below reviews the Cabrera Lead Format ...

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ECG Media PEARL #32 (7:30 minutes Audio) — reviews the Cabrera ECG Format — and doing ECGs at a recording speed of 50 mm/second.

 

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ECG Media PEARL #25 (9:50 minutes Audio) — Pearls & Pitfalls regarding the ECG diagnosis of Acute Pericarditis.

In the following 5 Figures — I post written summary from my ECG-2014-ePub on the ECG diagnosis of Acute Pericarditis.

• CLICK HERE — for a PDF of this 9-page file on Pericarditis that appears in Figures-4-thru-8.
• An additional criterion that has sometimes been cited as helpful for making the diagnosis of acute Pericarditis — is the ST/T Wave Ratio in Lead V6 (Please see My Comment at the BOTTOM of the page in the December 13, 2019 post of Dr. Smith's ECG Blog).

Figure-4: How to make the diagnosis of acute Pericarditis (ie, use of the History and Physical Exam).

Figure-5: ECG findings (4 Stages of acute pericarditis — with attention on diagnostic Stage I). How helpful is PR depression?

 

Figure-6: PR depression (Continued). Spodick’s sign. Acute MI vs Pericarditis vs Repolarization variants?

 

Figure-7: Acute MI vs Pericarditis. ECG findings with acute Myocarditis. Pericarditis vs Early Repolarization?

 

Figure-8: Pericarditis vs Early Repolarization? (Continued).

ECG Blog #364 — VT in Need of Cardioversion?

The ECG in Figure-1 was obtained from a 60ish year old man on arrival to the ED (Emergency Department). The presenting complaint was chest pain — and the patient collapsed soon after arrival in the ED.

QUESTION:

A cardiologist interpreted the rhythm in Figure-1 as VT (Ventricular Tachycardia). 

• Do YOU agree with this cardiologist?

Figure-1: The initial ECG in today's case — obtained from a 60ish year old man who collapsed in the ED shortly after this tracing was recorded. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

There are a number of reasons why the ECG in Figure-1 is difficult to interpret:

• The rhythm is fast — and the QRS looks to be very wide. More than QRS widening — the shape of QRS complexes varies from one-beat-to-the-next (Seen best in the long lead II rhythm strip at the bottom of the tracing).
• The rhythm looks fairly regular — and atrial activity is absent. The finding of a fairly regular, wide tachycardia without clear sign of atrial activity (especially when seen in an acutely symptomatic patient) — should immediately prompt a diagnosis of VT until proven otherwise.

Rebuttal to the above Initial Diagnosis:

I initially thought that the rhythm in ECG #1 was likely to be VT. That said — I changed my mind after looking closer because of the following findings:

• The rhythm in the long lead II rhythm strip is not regular. Instead, close inspection reveals that there is slight-but-real R-R interval variation from 1 beat to the next. 
• The overall rate for the rhythm in Figure-1 is fast (ie, probably ~110-115/minute) — but not nearly as fast as expected with a hemodynamically significant VT (that almost always is at least 130/minute).
• There appears to be “Shark-Fin” ST elevation for beats #3,4,5,6 in the inferior leads — and for beats #8,9,10,11 and #15,16 in the long lead II rhythm strip.
• There is “shark-fin” ST depression in leads I, aVL and V2.
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• Putting These ECG Findings Together: I have described an irregularly irregular rhythm without P waves — at an overall rate of ~110/115/minute. These findings suggest that instead of VT — the rhythm in Figure-1 is AFib with a fairly rapid ventricular response. 
• This leaves us with having to explain why the QRS is wide. Since the rhythm is supraventricular (ie, AFib) — we can accurately assess QRS morphology. The upright R wave in lead V1 — together with the wide terminal S waves in lateral leads I and V6 — is consistent with RBBB (Right Bundle Branch Block). Predominant negativity of the QRS in lead I — with predominant positivity in the inferior leads suggests LPHB (Left Posterior HemiBlock). Thus, there appears to be bifascicular block (ie, RBBB/LPHB).
• That said — a significant component of the QRS widening that we see in Figure-1 is probably the result of “shark-fin” ST segment deviation (elevation and depression). Looking at the location of ST elevation (ie, in the inferior leads — and in V4,5,6) — and the location of ST depression (ie, in leads I,aVL; V1,V2) — this ECG picture suggests an ongoing acute infero-postero-lateral STEMI.

What is Shark Fin Morphology?

It's important to be aware of the pattern of "Shark Fin" ST segment elevation — in which the QRS complex looks wide, because it blends in with ST segments that show extreme ST elevation in multiple leads. As a result — the boundary between the end of the QRS complex and the ST segment becomes indistinguishable in those leads showing marked ST elevation or depression.

• "Shark Fin" ST segment elevation is most often a sign of severe transmural ischemia that results from acute coronary occlusion. Consideration of prompt cardiac cath is essential for clarifying the anatomy — since in many (most) cases, prognosis is likely to be poor unless there is prompt reperfusion. (For more on "Shark Fin" ST elevation — See the Audio Pearl in the ADDENDUM below — as well as ECG Blog #265 for an example of a case with even more dramatic "shark fin" ST elevation).
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• PEARL #1: The KEY for confirming that "Shark Fin" morphology is the cause of the striking ECG picture this produces — is to find 1 or 2 leads in which you can clearly define the limits (end point) of the QRS complex. The most helpful leads for doing this in today's case are leads II and III — in which in Figure-2, I've drawn in a RED line parallel to the heavy ECG grid line in simultaneously-recorded leads I,II,III. Note that I've extended this line down to the corresponding complex in the long lead II rhythm strip at the bottom of the tracing.
• The reason for continuing the RED line all the way down to the corresponding beat in the long lead II rhythm strip — is that this tells you where the QRS complex ends and the ST segment begins in the long lead II rhythm strip.
• Knowing this landmark for the complexes in the long lead II rhythm strip — allows us to draw in and extend upward the PURPLE lines parallel to the heavy ECG grid line in the other 3 sets of simultaneously-recorded leads (PURPLE lines in Figure-2).
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• CONCLUSION: The ECG in Figure-2 shows AFib with a fairly rapid ventricular response with "Shark Fin" ST elevation that is most marked for certain complexes in the inferior leads. Reciprocal "shark fin" ST depression is seen for certain complexes in leads I and aVL — and ST depression indicative of posterior infarction is seen in lead V2.

Figure-2: I've labeled the end point of the QRS complex selected leads to facilitate defining "shark fin" ST segment elevation or depression (See text).

CASE Follow-Up:

As noted in today’s case presentation — this patient presented with chest pain, and then collapsed soon after the ECG in Figure-1 was obtained. Cardiopulmonary resuscitation was promptly started — but was unsuccessful.

• Given the rapid rate of AFib — the new bifascicular block ( = RBBB/LPHB) — and the obvious extensive acute STEMI — it is unfortunate but not surprising that this patient could not be resuscitated.
• Given a lack of prior history — I don’t know if the AFib on ECG #1 is (or is not) a new finding. If this is a new finding — then it’s important to be aware of the adverse prognostic significance of seeing new AFib in association with acute MI.
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• Final PEARL: In my experience — it is not common that new AFib must urgently be cardioverted in the ED. That said — today’s case provides an exception to this generality, in that the patient is symptomatic (ie, with new chest pain) — the rate of the AFib is relatively rapid (almost all R-R intervals between 2-3 large boxes — therefore the overall heart rate is clearly over 100/minute) — and — the initial ECG shows a bifascicular block with an extensive ongoing STEMI. Even if providers initially thought that the rhythm was VT — prompt synchronized cardioversion might still be the treatment of choice for today's arrhythmia given the patient's instability in this clinical scenario. 

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Acknowledgment: My appreciation to 黄建成 and 罗莉莲 (from Malaysia) for the case and this tracing.

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ADDENDUM (2/19/2023):

• The Audio Pearl below reviews the concept of "shark fin" ST elevation. 

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ECG Media PEARL #73 (5:40 minutes Audio) — Reviews the concept of "Shark Fin" ST elevation and depression as a sign of extensive acute infarction.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
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• ECG Blog #265 — Reviews a case of Shark-Fin ST Elevation.

ECG Blog #363 — How Many Directions?

The ECG in Figure-1 was obtained from an older woman — who presented with chest pain and palpitations over the previous hour. She had a history of hypertension, and was on medication for this — but she was otherwise healthy. BP = 140/90 mm Hg in association with the rhythm in Figure-1.

• How would YOU interpret the rhythm in Figure-1?
• Is this Ventricular Bigeminy?

Figure-1: ECG obtained from an older woman with palpitations. Is there Ventricular Bigeminy? (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

This is a challenging tracing! As always — I favor starting by first assessing the cardiac rhythm.

• Although there is a long lead II rhythm strip at the bottom of the tracing in Figure-1 — this is a bit confusing, because of marked overlap between this long lead II rhythm strip and the bottom portion of QRS complexes in simultaneously-recorded leads V2 and V3 above it. That said — it looks as if the bigeminal pattern of alternating QRS morphology every-other-beat continues throughout the tracing!
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• The QRS complex is wide for all beats on this tracing. This is best seen in lead I.
• I do not see P waves anywhere on this tracing.
• The Rate of the rhythm is fast. The problem assessing the heart rate — is uncertainty IF we should calculate the rate of similar-looking complexes — or — the total rate of all QRS complexes in this tracing. I favor the latter — which suggests an overall heart rate of ~180-190/minute.
• A similar problem arises when trying to assess for Regularity of the rhythm in Figure-1. There clearly is a "bigeminal" pattern, albeit with changing QRS morphology every-other-beat. Assessment for "regularity" of the rhythm is made difficult — because the R-R interval between beats is virtually constant, even though QRS morphology is constantly changing. This differs from the "usual" bigeminal rhythm — in which we typically see a "regular regularity" in the form of alternating shorter-then-longer R-R intervals.
• NOTE: I found it easiest to evaluate the overall regularity of today's rhythm by selecting a lead in which there are all positive complexes (such as lead I or lead V6) — and measuring the R-R interval from the onset of the R wave upstroke from one beat — to the onset of the R wave upstroke of the next beat (ie, In Figure-2 — Doesn't the R-R interval between the RED arrows in lead I look regular?).
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• PEARL #1: One of my favorite quotes in teaching ECG interpretation is, "12 leads are better than one". For example, in Figure-1 — Doesn't QRST morphology for all beats in lead I look similar? However, when we look at simultaneously-recorded leads II and III — it becomes obvious that QRS morphology is very different for alternate beats!

The Rhythm in Today's Case: Putting It All Together

As I stated at the onset of today's case — This is a challenging tracing! 

• I initially thought that the rhythm in Figure-1 was ventricular bigeminy (ie, that every-other-beat was a PVC). That said — reasons why today's rhythm is not ventricular bigeminy are: i) There is no sign of sinus P waves anywhere on today's initial tracing (ie, For there to be ventricular bigeminy — there should be an underlying sinus rhythm, in which every sinus-conducted beat is then followed by a PVC); and, ii) At 180-190/minute — the overall heart rate in today's initial rhythm is much faster than is usually seen with a sinus tachycardia, making ventricular bigeminy highly unlikely. (Contrast today's rhythm with true ventricular bigeminy — that was seen in ECG Blog #343).
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• I next considered the possibility of some type of alternating bundle branch block. That said, on closer inspection — this seemed unlikely because: i) As was the reasoning against ventricular bigeminy — there is no underlying sinus rhythm; and, ii) Both QRS morphologies in Figure-2 manifest QRS widening — instead of alternate beats being narrow. Neither QRS morphology resembles RBBB conduction — so this would not be alternating RBBB with LBBB. (Contrast  today's rhythm with true alternating bundle branch block — that was seen in ECG Blog #306).
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• Therefore: Summarizing our findings up to this point — we have a bigeminal rhythm with alternating QRS morphology in which all QRS complexes are wide, but without any P waves. This leaves us with the diagnosis of BiDirectional VT (BDVT).

Figure2: I've labeled the initial tracing. The RED arrows in lead I reveal a surprisingly regular rhythm. To facilitate assessment of the 2 different QRS morphologies — I've placed one set of even-numbered beats in each of the 4 lead groups within a dotted RED-YELLOW rectangle. Although both even- and odd-numbered beats resemble lbbb morphology — the frontal plane axis for these 2 QRS morphologies is markedly different! (See text).

CASE Follow-Up:

Additional history revealed no digoxin use — and no herbal or new medications. Troponin was slightly positive (felt unlikely to represent acute MI). Electrolytes were normal.

• The patient was treated with IV Amiodarone. The result is shown in ECG #2 — which I have put together with the initial ECG in Figure-3 to facilitate comparison.

Figure-3: Comparison of the initial tracing — with the ECG obtained after treatment with IV Amiodarone. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Figure-3:

Treatment with IV Amiodarone resulted in successful conversion to sinus rhythm ( = ECG #2). Of note — the QRS complex with after conversion to sinus rhythm is indeed wide.

• Lead-to-lead comparison of QRS morphology in ECG #2 — with the lead-to-lead appearance of the 2 different QRS morphologies seen in even- and odd-numbered beats in ECG #1 — suggest that this patient's QRS morphology during sinus rhythm is different in enough leads to strongly suggest that ECG #1 did in fact represent BiDirectional VT!

What is BiDirectional VT?

There are 4 basic types of VT (Ventricular Tachycardia) morphology: i) Monomorphic VT; ii) Polymorphic VT (PMVT) — which includes Torsades de Pointes; iii) Pleomorphic VT; and, iv) BiDirectional VT (BDVT). I review these terms in the June 1, 2020 post of Dr. Smith's ECG Blog — and limit my comments here to BDVT:

• BiDirectional VT — is by far the least common form of morphologic VT. This rhythm is characterized by beat-to-beat alternation of the QRS axis. It distinguishes itself from PMVT and pleomorphic VT — because a consistent pattern (alternating long-short cycles) is usually seen throughout the VT episode. As implied in its name, there are 2 QRS morphologies in BiDirectional VT — and they alternate every-other-beat.

PEARL #2: It's helpful to appreciate that BiDirectional VT is difficult to recognize. This is because the rhythm is not common — the rate is usually rapid (so not easy to determine if P waves might be hiding within T waves or the wide QRS complexes) — and the rhythm can easily be mistaken for ventricular bigeminy or alternating bundle branch block. NOTE: When contemplating the diagnosis of BDVT — Consider one of the following conditions which are known to predispose to this arrhythmia:

• Digitalis toxicity
• Acute myocarditis
• Acute MI
• Hypokalemic periodic paralysis
• CPVT (Catecholaminergic PolyMorphic VT )
• Metastatic cardiac tumors
• Some types of Long QT Syndrome
• Herbal aconite poisoning

NOTE: In view of reduced use of Digoxin in recent years — CPVT is probably the most common cause of BiDirectional VT. This familial cardiac arrhythmia is the result of gene mutation. 

• The heart is structurally normal in patients with CPVT. As a result — the resting ECG tends to be normal.
• These patients are at high risk for malignant arrhythmias. Typically — these arrhythmias are induced by exercise or intense emotional states (ie, associated with increased catecholamine discharge). As a result — ETT (Exercise Treadmill Testing) can be used to elicit BDVT, and therefore help to diagnosie CPVT.
• The mechanism for malignant arrhythmias with CPVT is a result of gene mutation. This leads to an increase in intracellular Ca++ concentration — which facilitates after-depolarizations and triggered arrhythmic activity — often beginning with multiple PVCs that evolve to BiDirectional VT. When persistent — BDVT may deteriorate to VFib.
• Treatment of CPVT is aimed at suppressing excess adrenergic activity — which is why ß-blockers are the drug of choice for both acute and longterm treatment. If this fails to control episodes — an ICD is indicated.  

FINAL Note on Today's CASE:

Unfortunately — I lack details on what happened in today's case. To the best of my knowledge — today's patient had none of the predisposing causes of BDVT — and it was not discovered why she had this arrhythmia. 

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Acknowledgment: My appreciation to Sadiq Ameen (from Sana's City, Yemen) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Arrhythmia Interpretation.
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• ECG Blog #343 — Reviews a case of Ventricular Bigeminy.
• ECG Blog #306 — Reviews a case of Alternating Bundle Branch Block (with an underlying sinus rhythm — and every-other-beat with LBBB conduction).
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• NOTE: References I used for my above discussion of BiDirectional VT were — Ali et al (J Coll Phys and Surgeons Pakistan 23(5):347-349, 2013) — and — Femenia, Baranchuk et al (Indian Pacing Electrophysiol J 12(2):65-68, 2012).
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• The June 1, 2020 post in Dr. Smith's ECG Blog — Reviews the entity of pleomorphic VT (and the other morphologic types of VT).