ECG Blog #233 — Why Did the Patient Die?

The ECG shown in Figure-1 was obtained from a previously healthy 70-year old man, who presented to the ED (Emergency Department) with new-onset dyspnea.

• Does the anterior T wave inversion represent acute ischemia from Wellens’ Syndrome?
• If not — What is YOUR diagnosis?

 

Figure-1: ECG obtained from a previously healthy 70-year old man with new-onset dyspnea.

 

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NOTE #1: Some readers may prefer at this point to listen to the 7:40 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-49).

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Today’s ECG Media PEARL #49 (7:40 minutes Audio) — Reviews the ECG finding of Anterior T Wave Inversion (with emphasis on not overlooking acute PE as the cause!).

• NOTE #2: Among the topics discussed in this Audio Pearl are the ECG findings with acute PE (See Figure-3 and Figure-4 in the ADDENDUM below) — Wellens' Syndrome (reviewed in ECG Blog #209) — and — Giant T Wave Syndrome (reviewed in ECG Blog #59).

 

 

 

My THOUGHTS on the ECG in Figure-1:

The rhythm is sinus tachycardia at ~115/minute. The PR interval is normal. The QRS is not prolonged. The QTc appears to be no more than minimally prolonged (though this is difficult to assess given the tachycardia). The frontal plane axis is relatively vertical (almost +90 degrees) — but not quite rightward (since the S wave in lead I is not predominantly negative). There is no chamber enlargement.

 

Regarding Q-R-S-T Changes:

• There is a Q wave in lead III — and perhaps a tiny q wave in lead aVF. There is a QS complex in lead V1.
• Regarding R Wave Progression — a tiny initial r wave (positive deflection) is seen in lead V2 — with this R wave gradually increasing in size, until transition finally occurs between leads V5-to-V6.
• ST segments are coved, with moderate symmetric T wave inversion in leads III, aVF and leads V1-thru-V4. A smaller effect on ST-T waves is seen in leads II, V5 and V6.

 

Additional ECG Findings Relevant to Today’s Case:

• An S1Q3T3 pattern is present!
• S waves persist across all chest leads (with a significant S wave still present in lateral lead V6).
• Slight ST elevation is seen in lead aVR.

 

IMPRESSION:

The History is KEY in today’s case: This previously healthy 70-year old man presented with new-onset dyspnea. There is no mention of chest pain. As a result — acute coronary disease would seem to be much less likely. In contrast — acute PE (Pulmonary Embolism) is perfectly consistent with this history! 

• In association with the history in today’s case — several of the ECG findings noted above in Figure-1 place acute PE as the presumed diagnosis until proven otherwise.

 

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The ECG Diagnosis of Acute PE:

The ECG is far from optimal as an investigative tool for the diagnosis of acute PE. That said — there are times when the ECG, in conjunction with the clinical history — can be extremely helpful in suggesting the diagnosis even before additional testing can be accomplished. The ECG in Figure-1 provides an excellent example of this situation.

• PEARL #1: The ECG is unlikely to identify patients with smaller PEs. Do not expect to see anything on the ECG of these patients (This may be a “blessing in disguise” — as longterm benefits of anticoagulating such patients are debatable). Sensitivity of the ECG for suggesting the possibility of acute PE is clearly better with large (especially submassive) PEs.

 

PEARL #2: One of the problems with using the ECG as a diagnostic tool for detecting acute PE — is that there is no single ECG finding definitive for this diagnosis. Instead, acute PE may be suggested by a combination of several supportive ECG findings that occur in association with the “right” clinical scenario (ie, recent onset of unexplained dyspnea, syncope and/or shock, especially in a patient predisposed or with a prior history of venous thromboembolism).

• We list the ECG findings to look for when considering the diagnosis of acute PE in Figure-2. 
• We expand upon these ECG findings in the Addendum below (See Figure-3 and Figure-4).

 

Figure-2: ECG findings associated with acute PE. There is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis may be suggested by the presence of at least several of these ECG findings when they occur in the “right” clinical setting (See text).

 

WHAT are the ECG Findings in Today's Case?

We list below positive and negative ECG findings from Figure-2 that are relevant to today's case:

• Sinus Tachycardia — While not absolutely essential for the diagnosis, a rapid heart rate (usually to at least 90/minute) is a common and expected finding in patients with hemodynamically significant acute PE. The heart rate in Figure-1 is over 100/minute.
• Acute RV “Strain” — Awareness of ECG evidence of RV (Right Ventricular) Strain is one of the most important ECG indicators of acute hemodynamically significant PE. Unfortunately, this sign remains all-to-often unappreciated and misinterpreted as coronary ischemia. RV “strain” manifests as ST depression and/or T wave inversion that typically occurs in anterior leads (V1,2,3) — and/or — in inferior leads (II,III,aVF). Abnormal ST-T wave changes consistent with acute PE are seen in both of these lead areas in Figure-1.
• S1Q3T3 — Whereas the diagnostic value of this pattern is minimal at best, when seen as an isolated finding — a definite S1Q3T3 pattern can be extremely helpful IF seen in association with other ECG evidence of acute PE. Such is the case here.
• There is no RAA.
• The frontal plane axis is relatively vertical — but not rightward.
• Neither complete nor incomplete RBBB is present.
• There is no tall R wave in lead V1.
• Persistent Precordial S Waves — Poor R wave progression with persistence of S waves across the chest leads (through to lead V6) — is another ECG sign seen here that is consistent with new or chronic pulmonary disease.
• ST Elevation in Lead aVR — Among the unappreciated benefits of lead aVR in ECG interpretation, is awareness that acute right heart “strain” (as seen with large acute PE) may often produce ST elevation in right-sided lead aVR. Although subtle — there is ST elevation in lead aVR in Figure-1.
• Atrial fibrillation is not present.

 

Putting It All Together: The one unifying diagosis that explains all of the ECG findings noted above in Figure-1, in this 70-year old man who presented to the ED with new-onset dyspnea (but no mention of chest discomfort) — is acute PE.

 

 

CASE FOLLOW-UP: A presumed diagnosis of acute PE was rapidly made by the treating clinicians. They promptly initiated thrombolytic therapy. Unfortunately, the patient’s condition deteriorated as treatment was being started. Resuscitation was unsuccessful. Although confirmatory testing was not completed (made impossible by the patient’s unstable and rapidly deteriorating condition) — I believe the circumstances of cardiac arrest within minutes of arrival in the ED, in association with the combination of ECG findings shown in Figure-1 is consistent with massive acute PE as by far the most likely etiology for explaining this patient's rapid demise.

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Acknowledgment: My appreciation to Ismail Mahmood (from Babil, Iraq) for making me aware of this case and allowing me to use this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
• ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
• ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”. 
• ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome (What it is — and what it is not! ).
• ECG Blog #59 — Reviews the causes of Giant T Wave Inversion.

 

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ADDENDUM (6/12/2021): I've excerpted below in Figure-3 and Figure-4 — several pages from my ECG-2014-ePub — that summarize the ECG findings of acute PE (Pulmonary Embolus).

 

 

Figure-3: Summary of KEY findings in the ECG diagnosis of acute PE.

Figure-4: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE.

ECG Blog #232 (47) — What is Bigeminy?

You are given the ECG shown in Figure-1 — but without the benefit of any history.

• What is the cause of the paired beats in the long lead II rhythm strip?

 

Figure-1: You are asked to interpret this ECG without the benefit of any history (See text).

 

MY Sequential APPROACH to this CASE:

Rate & Rhythm: The QRS complex is narrow in all 12 leads — so the rhythm is supraventricular. 

• NOTE #1: The long lead II rhythm strip at the bottom of the tracing is not continuous with the 12-lead above it. This long lead II rhythm strip encompasses a total of 14 consecutive beats — and shows a “bigeminal” rhythm (ie, there are 7 pairs of beats that occur in a repetitive pattern of alternating shorter and longer R-R intervals). 
• We KNOW that there is at least some conduction — as it appears that each of the QRS complexes at the end of each longer R-R interval is preceded by an upright P wave with a constant (albeit prolonged) PR interval.

 

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NOTE #2: At this point in my assessment — I was not certain of the etiology of the rhythm. That said, from a clinical perspective — I thought determining the precise rhythm diagnosis was not yet essential because: i) With regard to initial management of this patient — What counts most is recognition that there is a supraventricular rhythm at a reasonable ventricular rate, with at least a number of beats being sinus-conducted; and, ii) I could not help but notice the marked ST-T wave changes on the 12-lead that demanded more immediate attention!

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PEARL #1: As stated above — the rhythm in Figure-1 is “bigeminal”, supraventricular, and notable in that the 1st beat in each of the 7 pairs of beats is sinus conducted (albeit with a prolonged PR interval). It’s helpful to be aware of the Differential Diagnosis for a bigeminal supraventricular rhythm when there is sinus conduction of the 1st beat in each pair. This differential diagnosis includes:

• 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).
• SA ( = Sino-Atrial) Block.
• Mobitz I, 2nd-Degree AV Block ( = AV Wenckebach) with 3:2 AV conduction.
• Mobitz II, 2nd-Degree AV Block.

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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: Although the diagnosis of Mobitz II, 2nd-Degree AV Block would be of immediate concern (because of the need for cardiac pacing) — Mobitz II is highly unlikely in Figure-1 because: i) Among the forms of 2nd-Degree AV Block — Mobitz II is extremely uncommon (ie, In my experience — at least 90-95% of 2nd-Degree AV Blocks are of the Mobitz I type); and, ii) The QRS is almost always wide with Mobitz II (but the QRS is narrow in Figure-1).

 

The NEXT Steps in My Assessment:

The limb leads in Figure-1 suggest there has been recent inferior MI:

• There are Q waves in each of the 3 inferior leads. The largest Q wave is seen in lead III, which manifests a QS complex (ie, all negative QRS). Considering how tiny the QRS complex in lead aVF is — the Q wave in this lead is both deep and wide. In contrast — the q wave in lead II is small and narrow — but the fact that all 3 inferior leads manifest Q waves (with these Q waves being very large in 2 of the 3 leads) confirms that inferior MI has occurred at some point in time.
• All 3 of the inferior leads manifest at least some degree of ST elevation. ST segments look hyperacute in leads II and aVF (straight ST segment takeoff in lead II; T waves and ST segments being more “voluminous” in both II and aVF). Relatively speaking — the amount of ST elevation in lead III is less, and it is accompanied by fairly deep T wave inversion that is consistent with “reperfusion T waves”.
• The ST-T wave picture in high-lateral leads I and aVL is almost the “mirror-image” opposite of the ST-T wave in lead III. That is — the ST segment in both of these leads is straightened (albeit not depressed) — and the tall, peaked T waves are almost the “opposite” of the deep T wave inversion seen in lead III.

 

IMPRESSION: There has been a recent Inferior MI. It is difficult to “date” this infarction in the absence of any history. My “guess” would be “recent” (ie, perhaps 6-to-12 hours ago, up to 1-to-2 days ago) — but probably not so acute as occurring within the past 1-to-4 hours or so.

• I based this “date estimation” on the finding of established Q waves (which are very large in leads III and aVF) + deep reperfusion T waves in lead III (which suggest that at least some time has passed) — yet withpersistence of some ST elevation in all 3 inferior leads (with hyperacute-looking ST-T waves in leads II and aVF).
• CAVEAT: Anything is possible. On occasion — surprisingly deep Q waves can form in as little as 1-2 hours! Moreover, the course of evolving infarction is not always immediate — but sometimes can be “stuttering” — with spontaneous reopening, followed by re-closure, with this reopening and/or re-closure sometimes occurring a number of times until a final disposition develops. 

 

The CHEST LEADS in ECG #1

The chest leads in ECG #1 are consistent with recent Posterior MI — which is a common accompaniment of inferior MI. This is easiest to appreciate with use of the “Mirror Test” that I illustrate in Figure-2 (See ECG Blog #193 — for more on the “Mirror” Test).

• The mirror-image view of leads V2 and V3 (within the RED border in Figure-2) — looks similar (albeit even more dramatic) to what we see in lead III in ECG #1 — namely, a modest amount of ST elevation in association with deep, symmetric T wave inversion. This is consistent with reperfusion T waves in the left ventricular posterior wall location.
• Application of the Mirror Test in Figure-2 also provides insight into a disproportionate increase in anteriorlead R wave amplitude (that is seen in leads V2 and V3 of ECG #1). When viewed in its mirror-image — this disproportionate increase in R wave amplitude in leads V2 and V3 is seen as deepening Q waves (within the RED border in Figure-2).

  

Figure-2: To illustrate the Mirror Test — I’ve enlarged anterior leads V1, V2, V3 — and have placed them next to a mirror-image ( = vertically flipped) view of these leads.

 

A Closer LOOK at the RHYTHM:

Now that we know this patient has had a recent infero-postero MI — it becomes EASIER to interpret the long lead II rhythm strip in ECG #1. For clarity — I have numbered the beats in Figure-3. 

Figure-3: For clarity — I have numbered the beats in the long lead II rhythm strip. WHAT is the cardiac rhythm?

 

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NOTE: Some readers may prefer at this point to listen to the 5:45 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-3. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-47).

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Today’s ECG Media PEARL #47 (5:45 minutes Audio) — Reviews the concept of Bigeminy (which may be due to Atrial or Ventricular Bigeminy, Wenckebach conduction — or other causes).

 

MY Sequential APPROACH to Interpreting the RHYTHM:

In addition to recognition of recent infero-postero MI — We have already made some observations about the rhythm:

• The QRS complex is narrow in all 12 leads — so we know that the rhythm is supraventricular.
• There is group beating, in the form of a “bigeminal” rhythm (ie, there are 7 pairs of beats that occur in a repetitive pattern of alternating shorter and longer R-R intervals).
• PEARL #3: Recognition of recent or acute inferior MI in association with group beating — should immediately make you suspect AV Wenckebach ( = 2nd-degree AV block, Mobitz Type I). This is especially true when each of the relatively longer R-R intervals ends with a conducted sinus P wave that manifests a fixed PR interval (RED arrows in the long lead II rhythm strip in Figure-4).
• PEARL #4: AV Wenckebach that occurs in association with acute inferior MI is often associated with 1st-Degree AV Block. Therefore, the finding that the PR interval is prolonged for each of the P waves highlighted by RED arrows in the long lead II rhythm strip in Figure-4 further favors the likelihood of Mobitz I as the etiology of this rhythm.
• PEARL #5: The atrial rhythm should be regular (or at least, almost regular) — IF there is some type of AV block. Therefore, in order to prove that the rhythm in Figure-4 is AV Wenckebach — we need to establish that the underlying atrial rhythm is regular. Use of calipers and looking in other leads facilitates accomplishing this. NOTE: Most of the time when there is AV Wenckebach — those P waves that are not readily visible can be found hiding within elevated ST segments and T waves. For example — YELLOW arrows in lead V1 highlight where P waves within the T wave of the 1st beat in each pair are hiding.

 

Figure-4: I’ve added arrows to Figure-3 to highlight P waves. The RED arrows indicate obvious sinus P waves that conduct with 1st-degree AV block. The YELLOW arrows in lead V1 clue us into the fact that P waves are hiding within the T wave of the 1st beat in each of the 2-beat groups.

 

PEARL #6: Common things are common! Admittedly — I can not clearly see indication that a sinus P wave is hiding within the T wave under each of the WHITE arrows in Figure-5. That said, these T waves do appear to be “extra” peaked and, by far — the most logical assumption based on precise “walking out” of my calipers — is that another P wave is hiding within the T waves of beats #2, 4, 6, 8, 10, 12 and 14. 

 

Figure-5: Using calipers suggests that the most logical assumption to make — is that the WHITE arrows I have added to Figure-4 highlight another hidden P wave.

 

For clarity — I’ve colored all arrows in RED to highlight the location of regular sinus P waves I believe are occurring throughout the long lead II rhythm strip (Figure-6).

• Isn’t it now easier to appreciate Wenckebach periodicity?

Figure-6: I’ve colored all arrows in RED to highlight where I believe regular sinus P waves occur throughout the long lead II rhythm strip. 

 

LADDERGRAM:

The easiest way to illustrate the mechanism in today’s rhythm — is by drawing a laddergram (Figure-7). 

• NOTE: For review on how to read (and draw) laddergrams — See ECG Blog #188.   

Figure-7: My proposed Laddergram illustration of the Mobitz I, 2nd-degree AV block with 3:2 AV conduction, as described above in today’s case (See text).

 

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Acknowledgment: My appreciation to Bashiruddin Sayeem (from Chittagong, Bangladesh) for the case and these tracings.

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RELATED BLOG POSTS Regarding the INFARCT:

• ECG Blog #218 — Reviews when a T wave is Hyperacute (including the 5:20 minute Audio Pearl in this blog post). 
• ECG Blog #194 — Reviews how to tell IF the “culprit” artery has Reperfused, using clinical and ECG Criteria (including the 6 minutes Audio Pearl in this blog post). 
• ECG Blog #184 — Reviews the “magical” mirror-image opposite relationship with acute ischemia between lead III and lead aVL (including the 2:15 minutes Audio Pearl in this blog post). 
• ECG Blog #224 — Reviews this important picture to recognize (which resembles in many ways today's tracing = HOW to quickly recognize Mobitz I with Acute Inferior MI). 
• ECG Blog #193 — Reviews a case of an acute infero-postero MI that illustrates use of the “Mirror” Test.

 

RELATED BLOG POSTS Regarding the RHYTHM:

• ECG Blog #186 — The AV Blocks (including a 4:30 minute Audio Pearl on When to suspect Mobitz I, 2nd-Degree AV Block). 
• ECG Blog #78 — Shows a case of Atrial Bigeminy, in which every-other-P wave is a PAC that is either blocked or conducted with aberration. 
• ECG Blog #140 — Another case study of Atrial Bigeminy, showing various forms of aberrant conduction. 
• ECG Blog #57 — Atrial Bigeminy with blocked PACs that mimics AV block. 
• ECG Blog #228 — Shows a case of Ventricular Bigeminy (including the challenge of assessing ST-T wave changes with this rhythm). 
• ECG Blog #206 — A bigeminal rhythm due to a complicated AV Block.
• ECG Blog #163 — A case if Escape-Capture Bigeminy (possibly with SA Block).
• ECG Blog #188 — How to Read (and Draw) Laddergrams.
• ECG Blog #206 — For review of a fascinating case of a Bigeminal Rhythm due to 3:2 AV Wenckebach with alternating Hemiblock.
• ECG Blog #144 — Escape-Capture Bigeminy with 2nd-Degree AV Block of indeterminate severity (at least 2:1 AV block, but possible higher grade).

ECG Blog #231 — A Bizarre, Irregular Tachycardia ...

The 12-lead ECG shown in Figure-1 was obtained from a previously healthy 55-year old man who presented to the ED (Emergency Department) with shortness of breath, altered sensorium and hemodynamic instability.

• WHAT are the diagnostic possibilities for the rhythm?
• What do you feel is the most likely rhythm diagnosis?

 

Figure-1: Presenting ECG from a 55-year old man with shortness of breath, altered sensorium and hemodynamic instability (See text).

 

 

MY THOUGHTS on ECG #1:

My initial impression on looking at the ECG in Figure-1 — was that this irregular, wide rhythm was probably rapid AFib (Atrial Fibrillation), with a mixture of PVCs (Premature Ventricular Contractions) and aberrant conduction of supraventricular impulses.

 

I Changed My Mind on taking a 2nd Look at this tracing:

• I saw no sign of atrial activity.
• I thought all 25 QRS complexes on this tracing were probably ventricular in etiology (Figure-2). Although the QRS does not look overly wide in some leads — as you follow each of these 25 beats down the page from lead I at the top (looking in each of the 11 simultaneously-recorded leads below lead I) — the QRS is revealed to be either definitely wide in other leads — or — to manifest a QRS morphology strongly suggestive of a ventricular etiology (ie, the all-negative, widened complexes in lead V6 for beats #4,5; 8; 11, 12; 14,15; and 21 are ~99% likely to be ventricular in etiology).
• While I can't rule out the possibility that there might be a few supraventricular "capture" beats in Figure-2 — I believe it fair to say that more than 20 of the 25 beats in this tracing are ventricular in etiology.
• Unlike AFib — there does appear to be a "pattern" to the rhythm in Figure-2 (Doesn't the shape and relative timing of beats within the 2 YELLOW and 2 WHITE rectangles in Figure-2 look surprisingly similar?).
• BOTTOM Line: Despite irregularity of the rhythm and variability in QRS morphology — I thought the rhythm in Figure-2 had to represent some form of VT (Ventricular Tachycardia).

 

Figure-2: I have numbered the beats in ECG #1. Doesn't it look like there is some kind of repetitive group pattern in successive beats? (Look within the 2 YELLOW and 2 WHITE rectangles at sequential beats in the long lead V6).

 

 

VT Terminology:

Before going further — it may help to review a number of terms that have been used to describe the morphologic appearance of various forms of VT. These include:

• Monomorphic VT — in which there is a similar (if not identical) QRS appearance throughout the episode of VT.
• PolyMorphic VT (PMVT) — in which QRS morphology and/or axis continuously changes from one beat-to-the-next throughout the episode of VT. PMVT is not a regular rhythm — and it is often quite irregular. When PMVT is associated with a long QT interval — the rhythm is then defined as Torsades de Pointes (See ECG Blog #36 for more on distinction between Torsades vs PMVT).
• Pleomorphic VT — in which more than a single QRS morphology is seen during an episode of VT. Pleomorphic VT differs from PMVT — because QRS morphology is not changing from one beat-to-the-next. Instead, one QRS morphology will be seen for a number of beats — and then another morphology may take over and continue for another series of beats. Several different morphologies may be seen. (For more on Pleomorphic VT — Please SEE My Comment in the June 1, 2020 post in Dr. Smith’s ECG Blog).
• Bidirectional VT — in which there is beat-to-beat alternation of the QRS axis. This unique and very uncommon form of VT distinguishes itself from PMVT and pleomorphic VT — because a consistent pattern (ie, 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. (CLICK HERE — for this case report Review by Femenia et al on BiDirectional VT in a patient with CPVT = Catecholaminergic Polymorphic VT).

 

 

WHY CARE about QRS Morphology with VT?

Classification of the morphologic type of VT may provide clues to etiology, outcome and treatment.

• Monomorphic VT may occur in patients with or without underlying structural heart disease. Because the ventricular activation sequence is constant in monomorphic VT (which is why all beats look the same) — successful treatment (either by medication or cardioversion) is generally easier to accomplish. 
• The occurrence of monomorphic VT in a patient without underlying structural heart disease (and without QT prolongation or metabolic/electrolyte abnormalities) — is known as Idiopathic VT. The “good news” — is that long-term prognosis of patients with idiopathic VT tends to be excellent (See ECG Blog #197 for more on Idiopathic VT).
• As noted earlier — Bidirectional VT is extremely uncommon. Think of digitalis toxicity and catecholaminergic polymorphic VT as potential etiologies in which you are more likely to see bidirectional VT.
• Pleomorphic VT is also uncommon, and less well known than the other morphologic forms of VT. Patients with pleomorphic VT generally have significant underlying structural heart disease. A number of mechanisms have been proposed to explain the pattern of pleomorphic VT, in which there may be one or more runs of VT with a given similar QRS morphology — that is then punctuated by runs of VT with 1 or more other QRS morphologies. Potential mechanisms for explaining pleomorphic VT are complex — and include the possibility of: i) a single VT circuit with more than a single exit site; ii) the presence of more than a single VT circuit; and/or, iii) shifting conduction properties that alter the activation sequence (Liu & Josephson — Circ Arrhythm Electrophyiol 4:2-4 2011). 

 

PolyMorphic VT (PMVT) — is divided into 2 groups, depending on whether the preexisting QT interval is prolonged. 

• The occurrence of PMVT in association with baseline QTc prolongation — is defined as Torsades de Pointes. Torsades often has a multifactorial etiology (ie, drug-induced, electrolyte depletion, CNS disturbance and/or other underlying disorder that may predispose to QT lengthening). KEY aspects of treatment include IV Mg++ (often at high dose) + finding and “fixing” the cause of the long QTc.
• In contrast — PMVT without QT lengthening most often has an ischemic etiology. Although IV Mg++ is also indicated as initial treatment of PMVT with a normal QT — it is clearly less likely to respond to IV Mg++, than when the QT interval is prolonged. Instead, antiarrhythmic drugs such as amiodarone or ß-blockers may be needed — and/or treatment targeted to correcting ischemia.

 

COMMENT on Today's Case:

What I found especially interesting about the rhythm in Figure-2, is that unlike the complete variability in QRS morphology and R-R intervals that is usually seen with PMVT — there seemed to be a distinct, repetitive pattern in several parts of this tracing.

• That said, given lack of atrial activity and numerous different ventricular QRS morphologies — I thought the rhythm in today's case to be most consistent with Polymorphic VT.
• Clinical details on this patient were scarce — but there was no history of medication use or toxic ingestion.

 

My thoughts as to why there may be a repetitive pattern in parts of the rhythm in from today's case — are illustrated in Figure-3, which I adapted from the September 23, 2011 post in Dr. Venkatesan's Cardiology Blog.

• Although one might expect PMVT to originate from multiple sites in the ventricles — much (if not most) of the time — this is not what happens. Instead — it is more common for PMVT to originate from a single ventricular focus (despite significant variation in QRS morphology that may sometimes be seen from one beat-to-the-next).
• As suggested in Figure-3 — the physiologic explanation for why this may happen, is that the polymorphic VT focus may travel over a different path in its exit from the myocardium.
• Irregularity of PMVT may be explained by variation in conduction times for the various exit paths.
• The "repetitive pattern" that I suggest is present (within the YELLOW and WHITE rectangles drawn in Figure-2) — may be the result of a somewhat organized "rotation" over a series of potential exit paths.
• PEARL: As one might imagine — most PMVT rhythms are hemodynamically unstable, with tendency toward rapid deterioration to VFib. That said — Dr. Venkatesan makes the clinically important point that on occasion — some PMVT rhythms are surprisingly well tolerated! This could be the result of a "competition" between the different foci and/or exit sites that serve to prevent any one malignant focus from predominating and precipitating deterioration to VFib. To paraphrase Dr. Venkatesan, "One VT focus may act like a natural anti-tachycardia pacing device, that serves to terminate a VT from another focus".

 

Figure-3: I have adapted this figure from the September 23, 2011 post in Dr. Venkatesan's Cardiology Blog. It explains how "polymorphic" VT might arise from a single ventricular focus, rather than from multiple sites in the ventricles (See text).

 

FOLLOW-UP to Today's Case:

Unfortunately — the rhythm in Figure-2 deteriorated, and cardiac arrest was called. The patient could not be resuscitated. I believe this unfortunate clinical course supports our presumption of PMVT as the etiology of the rhythm in today's case. Further information on the case was not available — so we never learned the cause of this malignant rhythm.

 

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Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #36 — Reviews some irregular wide tachycardia rhythms (with distinction between Torsades de Pointes vs Polymorphic VT discussed in Figure-3 on this post). 
• See My Comment in the June 1, 2020 post in Dr. Smith's ECG Blog — for review of Pleomorphic VT.
• Pleomorphic VT and Sudden Cardiac Death — Editorial by Liu and Josephson on potential mechanisms to explain the ECG appearance of Pleomorphic VT. 
• Case Report on BiDirectional VT — by Femenia et al on this patient with BiDirectional VT from CPVT (Catecholaminergic Polymorphic VT).
• ECG Blog #197 — Reviews the concept of Idiopathic VT (including recognition and treatment of Fascicular VT and RVOT VT).
• Multifocal vs Polymorphic VT — September 23, 2011 post from Dr. S. Venkatesan's insightful and user-friendly Cardiology Blog (from which I adapted his figures to derive my Figure-3).

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ADDENDUM (6/5/2021 - 8pm):

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Today’s ECG Media PEARL #48 (5:00 minutes Audio) — Reviews the ECG and clinical distinction between PolyMorphic VT (PMVT) vs Torsades de Pointes.