ECG Blog #533 — A Wide Tachycardia - ME_to_DO

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ECG Blog #533 — A Wide Tachycardia ... 

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The ECG in Figure-1 was obtained from a previously healthy 60-something year old man — who sought medical care for the abrupt onset of “palpitations”. The patient was hemdynamically stable at the time this ECG was recorded.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• What would you do? 

Figure-1: The initial ECG in today's case — obtained from 60-something year old patient. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts:

The “good news” — is that the patient is hemodynamically stable at the time this ECG was recorded. As a result — We have at least a moment in time to assess the tracing before we would need to begin treatment. 

• As always, I like to start with assessment of the rhythm — for which I favor the P’s,Q’s,3R Approach for optimal time-efficient rhythm interpretation (See ECG Blog #185 — for review of the Ps,Qs,3R Approach).
• The ECG in Figure-1 lacks a long lead rhythm strip. That said, we can still interpret the rhythm — beginning with whichever of the 5 KEY parameters is easiest to assess.
• The rhythm in today’s ECG is Regular. 
• The Rate is fast, at about 170/minute.
• The QRS is wide (ie, clearly more than half a large box in duration — and probably ~0.12 second in duration).
• With regard to P waves — there is no clearly upright P wave deflection in lead II — and in general, the fast rate and large ST-T waves seem capable of “hiding” atrial activity within them. 

My Impression from the Ps,Qs,3Rs: 

In this 60-something year old man with palpitations (about whom we do not yet know anything regarding his medical history) — The rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~170/minute, but without clear sign of sinus P waves.

The differential diagnosis includes the following:  

• i) VT (Ventricular Tachycardia) — which always needs to be assumed for any regular WCT rhythm without sinus P waves until proven otherwise.
• ii) Sinus Tachycardia (with sinus P waves being hidden within the giant T waves that precede each QRS complex).
• iii) An SVT (SupraVentricular Tachycardia) reentry rhythm (ie, most commonly AVNRT or AVRT). 
• iv) AFlutter (Atrial Flutter).
• v) ATach (Atrial Tachycardia).

PEARL #1: To emphasize that although I've described my above assessment in “slow motion” — With practice, all that I’ve written above should be noted and considered within less than 1 minute!

• Because this patient is hemodynamically stable — We can take a few extra moments to see what additional clues might be present to help us narrow down our differential diagnosis.
• Statistically — in an unselected adult population of a "certain age" — at least 80% of regular WCT rhythms without clear sign of sinus P waves will turn out to be VT. 
• That said — 80% is not 100%. Therefore, if your patient is hemodynamically stable — this means that we still have a moment to look for additional clues to the etiology of the rhythm. Two of my “favorite potential clues” to look for are: 
• i) Is there any sign of atrial activity? — and, 
• ii) QRS morphology.

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Is there any sign of Atrial Activity?

Take another LOOK at the ECG in Figure-1.

• Keep in mind that sinus P waves should be upright in lead II — whereas retrograde P waves are almost always negative in one or more of the inferior leads.
• 
  
• What do YOU see? 

ANSWER:

It turns out that there is atrial activity in today's ECG — in the form of 1:1 V-A (retrograde) conduction (YELLOW arrows in Figure-2).

• Although this retrograde atrial activity is only seen in one of the inferior leads — it's hard to imagine what else this slender spike that occurs toward the end of the QRS in lead II could be other than a retrograde P wave.
• As suggested by the parallel RED timeline — these retrograde P waves clearly fall within the QRS complex, which explains why retrograde P waves might not be seen in other leads.
• P.S.: We now have an answer to the 5th parameter of the Ps,Qs,3Rs — which is the 3rd "R" = Related. So there is atrial activity, in the form of retrograde P waves that manifest a constant relationship ( = Related by a fixed RP' interval) to neighboring QRS complexes = 1:1 retrograde conduction.

PEARL #2: It's important to appreciate that the finding of 1:1 VA conduction does not distinguish between VT vs an SVT rhythm. This is because both reentry SVTs and VT may manifest 1:1 retrograde conduction.

• But IF today's rhythm is supraventricular — then it is almost certain to represent AVNRT (AV Nodal Reentrant Tachycardia) because:
• These P waves are not upright in lead II — so assuming no lead reversal, the rhythm cannot be sinus tachycardia.
• There is no sign of 2:1 AV conduction — so this is not AFlutter.
• It seems unlikely that ATach would manifest a negative P wave in only lead II with such a long RP interval.
• The other form of reentry SVT, which is AVRT ( = AtrioVentricular Reciprocating Tachycardia) generally has a longer RP' interval — with the retrograde P wave occurring later in the ST segment because of the greater amount of time needed to complete a reentry circuit that includes an AP (Accessory Pathway) that lies outside the AV Node (as I illustrate and discuss in ECG Blog #240).

Figure-2: I've labeled the retrograde P waves in today's ECG.

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Does QRS Morphology provide any Clue?

Practically speaking — aberrant conduction is most likely to take the form of some type of bundle branch block and/or hemiblock pattern. As discussed in ECG Blog #211 — although RBBB (Right Bundle Branch Block) aberration is the most common form — you can also see rate-related aberrant conduction that manifests LBBB and/or either pattern of hemiblock conduction (LAHB or LPHB — with or without RBBB).

• As emphasized in ECG Blog #204 — the 3 KEY leads for the ECG diagnosis of the bundle branch blocks are right-sided lead V1 — and left-sided leads I and V6.
• Assessment of these 3 KEY leads during the WCT rhythm in today's case is consistent with LBBB morphology — because we do see an all upright QRS in lateral leads I and V6 — and the QRS is predominantly negative in right-sided lead V1, with a steep S wave downslope in the anterior leads (as discussed in ECG Blog #346).

PEARL #3: While I was in no way certain of the diagnosis — as soon as I appreciated that QRS morphology in Figure-2 is perfectly consistent with LBBB conduction — I suspected that this regular WCT rhythm was probably supraventricular!

• KEY Point: We often need to begin treatment of the patient in front of us before we are 100% certain of the etiology of the rhythm. So although we still could not rule out the possibility of VT on the basis of this single ECG — since the patient was hemodynamically stable, using Adenosine as a diagnostic-therapeutic trial would seem an excellent option (ie, Adenosine should convert the rhythm if it is AVNRT or AVRT — and it may facilitate diagnosis of AFlutter or ATach by momentarily slowing the rate) — being ready to cardiovert if at any time the patient were to become unstable.
• 
  
• PEARL #4: The most common form of VT that manifests a QRS morphology resembling LBBB conduction in the chest leads — is RVOT VT (Right Ventricular Outflow Track VT). That said — strongly against RVOT VT in today's case is the lack of an inferior frontal plane axis (See ECG Blog #525 — for review of RVOT VT).

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CASE Follow-Up:

I subsequently learned of this patient's history:

• There was no history of coronary disease.
• Instead — the patient had a long history of arrhythmias, having undergone an ablation for a resistant SVT rhythm a number of years earlier.
• He was now being admitted to the hospital for a recurrence of his symptoms — and was scheduled for elective ablation the next day — when he developed the rhythm in Figure-1. This tachycardia easily converted to sinus rhythm following an initial 6 mg IV dose of Adenosine.
• EP study then revealed a concealed AP (Accessory Pathway) — but no inducible tachycardia. Instead — a "fast-slow" AVNRT was induced and ablated (this AVNRT rhythm being consistent with the short RP' interval highlighted by the YELLOW arrows in Figure-2).
• The LBBB morphology seen in Figure-2 was found to be the result of rate-related LBBB aberrant conduction. Conduction with a normal QRS complex resumed once the heart rate slowed following ablation.

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Acknowledgment: My appreciation to @PrecordialSwirl for submission of today's case with these tracings.

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ECG Blog #532 — A Surprise Diagnosis ...

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ECG Blog #532 — A Surprise Diagnosis ... 

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The ECG in Figure-1 was obtained from a middle-aged man — who presented to the ED (Emergency Department) with a 1-week history of intermittent "burning chest pain" — with some "shortness of breath".

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?
•   — Should you do anything else at the bedside?

Figure-1: The initial ECG ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts:

The ECG in Figure-1 was sent to me with the above history. I wrote back that my initial interpretation of this tracing was the following:

• This is a very worrisome ECG!
• There is sinus tachycardia — which of itself is a worrisome sign, since sinus tach tends to be an uncommon finding with acute MI — unless "something else" is going on (ie, heart failure, shock, etc.).
• There are inferior Q waves in a "qRS" pattern — which in the inferior leads usually means that an inferior MI has occurred at some point in time.
• At the least — there is DSI (Diffuse Subendocardial Ischemia) — as indicated by ST elevation in lead aVR, with ST depression in the other 5 limb leads (as well as in the lateral chest leads).
• I suspect there is a Precordial "Swirl" pattern — with clearly abnormal ST elevation and T wave inversion in lead V1 — and ST segment straightening with ST elevation in leads V2,V3 — and what looks to be some J-point depression in lead V6 (A "Swirl" pattern is typically seen with acute or recent proximal LAD occlusion — and the loss of R wave from V2-to-V3 suggests anterior infarction).

The difficult question is what is "new" vs "old" — and, if "new" (as I suspect) — How "new" given the 1 week history of intermittent CP?

• I asked the following: i) Any prior history of heart disease in this patient? — and, ii) Any prior ECGs available?
• I suggested that, "The patient needs prompt cath" — with my suspicion of an LAD "culprit" artery.

QUESTION:

• BUT — What did I not mention in my above comments? 

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CASE Follow-Up:

• The patient was admitted to the Intensive Care Unit with a diagnosis of acute ACS (Acute Coronary Syndrome).
• While contemplating the best approach to management — bedside Echo was done. Surprisingly — bedside Echo showed a markedly dilated RV with a "D-shaped" septum.
• CTPA (CT Scan Pulmonary Angioram) was then performed — which confirmed the diagnosis of massive acute PE (Pulmnary Embolism).
• The patient was treated with injection of low molecular weight heparin (Enoxaparin) — and rapidly improved.

PEARL #1: Bedside Echo is a non-invasive, amazingly helpful diagnostic tool in emergency medicine — that with training, can be performed within minutes (and without which — the correct diagnosis in this otherwise puzzling case would have been delayed for hours!).

• Bedside Echo can be extremely helpful in confirming acute MI when ECGs are equivocal — IF — Echo shows a localized wall motion defect.
• The caveat is that if the patient is no longer having CP (Chest Pain) at the time that Echo is done — then nothing is ruled out if the Echo is normal. But if CP persists and the Echo shows perfectly normal LV function — this makes an acute MI much less likely.
• Bedside Echo may suggest Takotsubo Cardiomyopathy if there is "apical ballooning" due to apical akinesis or hypokinesis with preserved or hypercontractile basal segments (Izumo and Akashi — Cardiovasc Diagn Ther 8(1):90-100, 2018).

BOTTOM Line: Bedside Echo can provide invaluable assistance for strongly suggesting acute PE as the cause of your patient's symptoms — and it does so in a matter of minutes! 

• In today's case — Echo was the KEY Clue that led providers away from the diagnosis of ACS (Acute Coronary Syndrome) — and to the correct clue of massive acute PE! (See ECG Blog #443 — for a case in which I review the findings of Bedside Echo and CTPA in a patient with a large acute PE). 

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What Did We Miss?

In cases like this one — I find it helpful to "soul-search" and GO BACK to try and learn from any clinical clues that may have been missed.

• "Some shortness of breath" was mentioned in the brief history we were given. It's hard to know how significant the symptom of dyspnea was in today's case from words on the printed page. Sometimes — "Ya just gotta be there!" ( = at the bedside!).
• PEARL #2: In my experience — by far, the most commonly overlooked vital sign is the respiratory rate! Much of the time — the clinician at the bedside simply does not take the time to COUNT the respiratory rate. 
• Nurses also (in my experience) do not always count the respiratory rate. Instead — they sometimes just put down 12 or 15/minute if the patient "seems OK".
• Clinical Reality: Unless you spend a conscious moment in which you truly LOOK at the patient — it is all-too-easy to miss a patient taking small but rapid breaths — unless you actually COUNT the breaths per minute. And if the patient was breathing 25-30/minute at rest ==> that's tachypnea, which should serve as an important clue that an acute pulmonary problem may be the cause!

Taking Another Look at Today's ECG ...

In addition to the history of CP (described as a "burning" chest pain in today's case) — the ST elevation in the anterior leads in the initial ECG (in Figure-1) led me to suspect an acute cardiac event as my primary diagnosis.

• PEARL #3: Instead of the anterior ST depression or T wave inversion of RV "strain" — anterior lead ST elevation may sometimes be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016). 
• Right-sided leads such as leads III, aVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2,V3 in today's initial ECG).

What I also found confusing about the initial ECG in today's case — was the question of whether there is (or is not) ST depression in multiple leads.

• The answer to this question depends on how you define the ST segment baseline — which sometimes is not an easy task.
• As review — I include below in Figure-2 my approach for determining the ST segment baseline in any given tracing.

   

Figure-2: "My Take" on defining the ST segment baseline (from Grauer K: ECG Pocket Brain-2014 ePub).

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With PEARL #3 and Figure-2 in mind — I'll add Figure-3 below, which is my summarizing chart of the ECG Findings associated with acute PE — which I then reapply to today's initial ECG in Figure-4.

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Figure-3: ECG Findings associated with acute PE (updated since ECG Blog #443).

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Figure-4: Another Look at Today's Initial ECG ...

 

Figure-4: I've labeled today's initial ECG.

KEY Point: With the above information in mind — Today's ECG (that I've labeled in Figure-4) — could be consistent with the diagnosis of acute PE, albeit without the typical appearance of RV "strain", in which T wave inversion is seen in anterior and/or inferior leads. Among the ECG findings in Figure-4 potentially consistent with acute PE are the following:

• Sinus tachycardia (Here at a rate of ~115/minute).
• S waves in multiple leads (ie, Leads I,II,III; aVF; V4,5,6).
• ST elevation in lead aVR.
• RV "strain" (Here in the form of ST depression in the inferior leads — assuming one uses the TP baseline for judging if there is ST elevation or depression).
• Anterior lead ST elevation — which as noted in PEARL #3, can be a sign of acute PE.
• ST depression in the remaining chest leads (V4,V5,V6) — again assuming one uses the TP baseline for judging if there is ST depression.

PEARL #4: ECG findings in Figure-4 against acute PE are: i) Q waves in each of the inferior leads (YELLOW arrows in leads II,III,aVF); — and, ii) Loss of r wave between lead V2-to-V3, with a QS wave in lead V3.

• In this patient who presented with a 1-week history of "burning" CP and some "shortness of breath" — this ECG leaves us with trying to distinguish between acute LAD occlusion vs acute PE (with the additional possibility of Takotsubo Cardiomyopathy — given diffuse ST-T wave abnormalities, and what appears to be a prolonged QT interval).
• KEY Point: Until bedside Echo was done in today's case — I strongly suspected acute proximal LAD occlusion as the diagnosis.

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"Take Home" Message:

On occasion — acute PE may present with a "pseudo-infarction pattern, as it did in today's case.

• Bedside Echo made the diagnosis in a matter of minutes.

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Acknowledgment: My appreciation to Mohammed Elsisi (from Cairo, Egypt) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #443 and ECG Blog #496 — Review challenging cases on the ECG diagnosis of acute PE.
• ECG Blog #313 and ECG Blog #435 — Review more cases on the ECG diagnosis of acute PE.
• ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
• ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
• My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
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• 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”. 
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• ECG Blog #380 — Reviews the concept of Precordial "Swirl".
• ECG Blog #483 — Reviews the concept of DSI (Diffuse Subendocardial Ischemia) in Pearl #1 of this blog post.

ECG Blog #531 — WCT: What to Do?

I was sent the ECG in Figure-1 — with the question, "VT or SVT"?

• The sender wanted to know, "Adenosine or Amiodarone"?
• The patient was hemodynamically stable at the time the ECG in Figure-1 was recorded, so although synchronized cardioversion could be perfectly appropriate — it would seem reasonable to try medical therapy.

QUESTION:

• How would YOU interpret the ECG in Figure-1?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~135/minute, without clear sign of sinus P waves.

• As always when confronted with a regular WCT without clear sign of sinus P waves — the principal differential is between VT (Ventricular Tachycardia) — vs some form of SVT (SupraVentricular Tachycardia) with QRS widening from either preexisting bundle branch block or rate-related aberrant conduction.

I looked more closely at the rhythm in Figure-1:

• KEY Point #1: Statistically — at least 80-90% of regular WCT rhythms without clear sign of sinus P waves will turn out to be VT (with this figure increasing to over 90% if the patient is "older" and has underlying heart disease). This of course means that sometimes (ie, 10-20% of the time) — the WCT rhythm in front of you will be supraventricular. But it especially means that we should assume VT until proven otherwise (especially if your patient is "older" and known to have underlying heart disease). — (See ECG Blog #361 — for more on assessment of the regular WCT).
• 
  
• KEY Point #2: QRS morphology in Figure-1 is perfectly consistent with LBBB conduction (ie, Monophasic upright QRS complex in left-sided leads I and V6 — and predominantly negative QRS in lead V1, as well as in other anterior leads that all manifest a very steep S wave downslope). So, although we still need to assume VT until proven otherwise — this perfectly consistent QRS morphology for LBBB conduction clearly reduces the likelihood of VT (See ECG Blog #204 — for more on the QRS morphology of LBBB conduction).
• 
  
• KEY Point #3: There does appear to be sign of some form of atrial activity — as the narrow, pointed peak to the T waves in lead aVF looks too pointed for a naturally occurring T wave — which makes me suspicious that an underlying P wave is peaking the T wave (RED arrows in Figure-2). And if these RED arrows are P waves — they are upright, and therefore not the negative P waves of retrograde conduction that are seen with reentry SVT rhythms. Instead — these upright P waves would have a surprisingly long PR interval for this tachycardia rhythm, which suggests the Bix Rule discussed in ECG Blog #227, in which when a P wave is seen near the middle of the R-R interval, tihs often means there is 2:1 AV conduction.
• 
  
• KEY Point #4: The most commonly overlooked arrhythmia (by far!) — is AFlutter (Atrial Flutter) with 2:1 AV conduction — especially when the ventricular rate is close to 150/minute (range between 130-160/minute). As a result, the BEST way to avoid overlooking AFlutter — is to always think AFlutter until proven otherwise whenever you have a regular SVT without clear sign of sinus P waves, when the ventricular rate falls within the above rate range (See ECG Blog #287 — for review of why AFlutter is so commonly overlooked) — (And for another Step-by-Step example of my "Thought Process" for uncovering AFlutter — See my discussion in the November 12, 2019 post in Dr. Smith's ECG Blog).

Figure-2: In today's case — the lead that most made me suspect underlying atrial activity was lead aVF (RED arrows).

KEY Point #5: My "Go-To" leads when I am trying to identify subtle (partially hidden) atrial activity — are leads II, III, aVF; lead aVR; and lead V1. IF none of the above leads suggest atrial activity — then I’ll survey the remaining 7 leads as I look for atrial activity. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.

• KEY Point #6: The BEST way to quickly find partially hidden atrial activity is to use calipers. Calipers instantly make you smarter! (and in my experience those clinicians who do not use calipers will commonly miss the diagnosis of complex rhythms).
• Since the most common conduction ratio of untreated AFlutter is 2:1 — the way in which I look for hidden flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the regular SVT rhythm.

I illustrate this approach in Figure-3 — in which I've added colored arrows to 4 additional leads:

• PINK arrows in lead II highlight where I strongly suspect flutter waves are hiding.
• YELLOW arrows in leads III and aVR ( = 2 more of my "Go-To" leads) highlight even more subtle atrial activity (ie, I suspect the tiny upright deflection at the beginning of some QRS complexes in lead III is the beginning of a flutter wave — as I suspect the slow upslope of the last part of the QRS in lead aVR reveals where the 2nd negative flutter wave in this lead is hiding).
• To Emphasize: Flutter waves are very subtle in leads III and aVR — but it is the perfect regularity of 2:1 AFlutter in lead aVF with the strong suggestion of supraventricular LBBB conduction that makes me all-but-certain that the underlying rhythm in Figure-3 is 2:1 AFlutter.
• P.S.: I fully admit that I do not see flutter waves in lead I — but the YELLOW arrows clearly show where 2:1 flutter waves might be hiding.

Figure-3: It is the RED arrows in lead aVF that convinced me the underlying rhythm in today's case is AFutter with 2:1 AV conduction. Less obvious in leads II,III,aVF — I strongly suspect the colored arrows in those leads highlight where flutter waves are hiding.

 

= = = = = = = = = = = = = = 

Final Point #7: A deceptively easy but all-too-commonly-forgotten way to demonstrate hidden atrial activity is to use a Lewis Lead. Once familiar with the technique (that is described in Figure-4) — it should take no more than seconds to apply a Lewis Lead for assistance with the problematic arrhythmia you are working with.

Figure-4: How to record a Lewis Lead.

CASE Conclusion:

To return to the 2nd question I was asked by the sender of today's case:

• Since today's patient was hemodynamically stable — I thought an initial attempt at medical treatment was reasonable.
• For the reasons discussed above — I was virtually certain the rhythm in today's ECG was AFlutter with 2:1 AV conduction (If uncertain about the rhythm — a vagal maneuver could be tried to bring out flutter waves or a Lewis Lead may have made flutter waves more visible).
• While Adenosine could have been used — this drug is not effective for cardioverting AFlutter (Instead — IV Adenosine would act as a "chemical Valsalva" to slow the ventricular response, which most likely would have revealed underlying flutter waves).
• I would have instead favored IV Amiodarone — which may be effective for both VT and SVT rhythms.

Providers treated this patient with IV Amiodarone. The patient remained hemodynamically stable — and within 2 hours sinus rhythm was restored. The diagnosis of AFlutter was confirmed.

• Unfortunately — the patient was an older man with significant underlying comorbidities. He did not survive the hospitalization.

= = = = = = = = = = = = = = 

Extra Credit:

Return for a moment to the ECG in Figure-3. Did you notice the markedly coved, hyperacute-appearing ST-T waves in leads V4,V5?

• My initial concern on seeing the ST-T wave appearance in leads V4,V5 — was that whatever the etiology of the regular WCT rhythm, the "cause" of this rhythm might be an ongoing acute MI.
• That said — both QRS widening and tachycardia are notorious for affecting ST-T wave appearance (ie, In today's case — underlying flutter waves might be superimposed, thereby producing the "picture" we see in Figure-3).
• I did not think the markedly peaked ST-T waves in leads V1,V2,V3 of Figure-3 looked abnormal — as they appeared to be "proportional" given how deep the anterior S waves are. But the shape of the ST-T waves in leads V4,V5 clearly suggested the possibility of an underlying ongoing MI.
• 
  
• Bottom Line: First priority in today's patient was to determine the etiology and treat the WCT rhythm — and then repeat the ECG once converted to sinus rhythm to rule out the possibility of an ongoing infarction. This was done — and by Troponins and follow-up tracings an acute MI was ruled out (and the peaked ST coving in leads V4,V5 resolved once sinus rhythm at a controlled rate was restored). An acute infarction was not the reason for this patient's unfortunate demise. 

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Acknowledgment: My appreciation for the anonymous contribution of this case.

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Relevant ECG Blog Posts to Today’s Post: 

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #204 — Reviews a user-friendly approach to the ECG Diagnosis of conduction defects (ie, LBBB — RBBB — IVCD).
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• ECG Blog #287 — Working through the diagnosis of AFlutter (with Audio Pearls, PDF, Lewis Lead).
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.