Wide Complex Tachycardia -- VT, SVT, or A Fib with RVR? If SVT, is it AVNRT or AVRT?

A 69 y.o. male with pertinent past medical history including Atrial fibrillation, atrial flutter, cardiomyopathy, Pulmonary Embolism, and hypertension presented to the Emergency Department via ambulance for respiratory distress and tachycardia. 

Per EMS report, patient believes he has been in atrial fibrillation for 5 days, since coming down with flu-like illness with rhinorrhea, productive cough, SOB. Patient is on rivaroxaben, carvedilol, and dofetilide (to suppress atrial fib -- rhythm control).  He states that he maybe missed a dose or two during recent illness. On EMS arrival, patient's oxygen saturation was in the high 80s and improved on 4L O2 via nasal cannula. 

He was noted to have irregular heart rhythm with rates 120-170s. BG 248. 

Bedside ultrasound showed volume depletion and no pulmonary edema.

Here is the prehospital ECG:

First ED ECG

What do you think?

Description: Regular Wide Complex Tachycardia at a rate of about 160.  VT?  SVT with aberrancy?  If SVT, is it AVRT or AVNRT?  It appears too regular to be atrial fib with RVR

I inspected this carefully and it is very regular.  Thus, it really cannot be atrial fibrillation

Is it Ventricular Tachycardia, which is usually a regular rhythm?

Smith opinion: I at first thought this was VT and would have electrically cardioverted.  But I changed my mind after seeing the old ECG (below)

I later sent it to Ken Grauer, who annotated as below with the red Xs:

The "Y" in lead II across the bottom appears to be a PVC.  

Thus is it almost impossible that this is VT, even without the old ECG.  Since it is regular, it must be PSVT (AVNRT or AVRT).    

Thus, adenosine is very likely to work here.

 

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If you want to know more detail (skip if you do not need so much detail), especially if it is AVNRT or AVRT, Ken writes the below, where he also agrees that it cannot be atrial fibrillation:

There are 2 places with this otherwise very regular WCT is “interrupted”. The 1st place ( = X) is kind of bizarre, in that QRS morphology look very similar in leads I,II,III — but a little earlier and narrower (almost like this beat may have occurred during the “supernormal conduction” period ( = a truly RARE phenomenon).

But the 2nd interruption = Y — looks to be a PVC — which is why, even before seeing the prior tracing, I suspected this initial ECG was supraventricular (and not VT).  

Smith: this is because it is almost impossible to have a PVC in the midst of VT

I measured intervals with calipers on my big screen — and other than these 2 interruptions, find the rhythm VERY regular. I don’t see evidence of retrograde atrial activity during the WCT — but usually with the “almost regular AFib rhythms” — you can when you measure pick up some slight differences — so my hunch is that the initial ECG is a REENTRY SVT rhythm, that then breaks down to AFib.

Now you CAN on occasion see PVCs during reentry SVTs that do not convert the SVT. Theoretically  — this can occur with BOTH AVNRT and AVRT. In theory, a PVC is more likely to convert AVRT — because part of the reentry pathway is OUTSIDE of the AV Node (ie, passing thru the AP) — and therefore a PVC would be more likely to “run into” the reentry pathway, and convert the rhythm.

In theory, with AVNRT — the reentry pathway is completely contained WITHIN the AV node — so a PVC would seem LESS likely to convert AVNRT, because it “can’t get to” the reentry pathway that is entirely within the AV node — so my hunch is this initial ECG was AVNRT ________________________

The patient was stable enough to look for a previous ECG.  Here it is:

Slow atrial fibrillation, rate controlled with carvedilol presumably

This shows the same QRS morphology (RBBB + LPFB), proving that the rhythm above is supraventricular, and NOT VT (as suspected by the PVC)

The providers realized it was not VT, but did not recognized it as SVT with RBBB/LPFB.  Instead they diagnosed it as Atrial Fib with RVR.

Thus, they did not give adenosine.

A patient who has atrial fib and is on dofetilde is on a "rhythm control" strategy for AF.  Dofetilide is used for atrial fib rhythm control, not for rate control.

The appropriate management would be to give IV fluids first to restore volume in this patient whom they believed had pneumonia as the initiating factor.  I'm not sure if they started with this, but let's assume that they did.

If you think this is atrial fibrillation with RVR, then because the patient is anticoagularted, one could safely sedate and cardiovert.  Of course, this is NOT atrial fib, but rather PSVT, and so adenosine should work. (Some are now advocating for calcium channel blockers, but that discussion is for another day).

The patient did not want to be electrically cardioverted, so they gave metoprolol.

t = 14 minutes, after giving IV metoprolol

Now there is atrial fibrillation with a much slower rate and PVCs.

Metoprolol can sometimes convert SVT, and sometimes the rhythm can change to atrial fibrillation.

t = 16 minutes

Further Care in the ED:

1. Patient hemodynamically stable, discussed options with patient, would prefer medications before attempting cardioversion
2. Patient given metoprolol 5 mg IV with improvement in HR to 110-120s, repeated ~q5 mins x3. Patient also given metoprolol PO 50 mg. 
3. Mag 2g administered 
4. Appeared mildly hypovolemic on US, LV function grossly preserved, reports decreased PO intake, given gentle 500 cc bolus
5. CXR with likely infiltrates vs edema, blood cultures collected, started ceftriaxone and azithromycin
6. Given patient reports not having taken home meds today, given home dofetilide, coreg and xarelto
7. Labs notable for mild Acute Kidney Injury (Cr 1.5). pH 7.4. 
8. CT noncon prelim consistent with pneumonia, final read pending
9. Patient's HR 110s, respiratory effort improved, reported symptomatic improvement

Later in afternoon

After a brief hospital stay, the patient was discharge, still in atrial fibrillation.

On a visit 2 months later, he was cardioverted.

A wide complex tachycardia

Submitted by Van Wall M.D., Written by Pendell Meyers

Let's go back to the basics for a common and classic scenario.

A middle-aged patient presents with shortness of breath and palpitations. The patient was stable without signs of low cardiac output or distress. Her ECG is shown below (first see what you think without using the baseline): 

What do you think?

There is a (minimally) wide complex, regular monomorphic tachycardia at a little faster than 150 bpm. I measure the QRS duration at almost exactly 120 ms. The differential would include ventricular tachycardia, any cause of narrow complex regular tachycardia plus added conduction aberrancy (such as a bundle branch block), or other causes of QRS widening like hyperkalemia or sodium channel blockade. Of course, the interpreter should always start by assuming that a wide complex monomorphic tachycardia is due to ventricular tachycardia and/or life threatening hyperkalemia, until proven otherwise.

This demonstrates why it is so important to be able to recognize RBBB, LBBB, and paced rhythms (pacer spikes) so quickly. This ECG has perfect RBBB morphology, one of the rare times that we can be confident that a regular wide complex rhythm is not classic ventricular tachycardia. 

For more discussion on features of SVT vs. VT, see these prior posts:

Wide Complex Tachycardia: Ventricular Tachycardia or Supraventricular Tachycardia with Aberrancy?

Wide Complex Tachycardia and Cyanosis

A prior baseline showing identical RBBB morphology during sinus rhythm would prove this definitively. 


Here is the prior baseline ECG on file:

This shows the same RBBB morphology in sinus rhythm.

They applied Lewis leads to see if they could get a better look at the atrial rhythm:

I can't say that I see clear atrial activity.

They gave 12 mg adenosine (a perfectly reasonable and guideline-endorsed option for any rhythm that is regular and monomorphic, regardless of QRS width):

Flutter waves are revealed.

The rhythm soon returned to 2:1 atrial flutter, of course. The patient was then rate controlled and did well.

Learning Points:

Assume that wide complex regular tachycardia is VT and/or hyperkalemia. Then work backwards and prove that assumption false, if possible. VT is more likely statistically, and the likelihood of VT increases further with age, cardiac pathology, and QRS duration.

Recognizing classic RBBB or LBBB morphology may enable the diagnosis of SVT with aberrancy. This can be basically definite if the morphology is shown to be identical to prior known RBBB or LBBB morphology on baseline ECG.

Adenosine is contraindicated in irregular or polymorphic QRS complex rhythms. It is not contraindicated for wide complex regular monomorphic tachycardia, and is very reasonable in this scenario.

Young Man with a Heart Rate of 257. What is it and how to manage?

A 30-something was in the ED for some minor trauma when he was noted to have a fast heart rate.  He acknowledged that he had palpitations. but only when asked.  He had a history heavy alcohol use.  Blood pressure was normal (109/83).

Here is his 12-lead:

There is a wide complex tachycardia with a rate of 257, with RBBB and LPFB (right axis deviation) morphology.

The Differential Diagnosis is: 
SVT with aberrancy(#) 
      [AVNRT vs. WPW (also called AVRT*)]
      Atrial flutter with 1:1 conduction, with aberrancy
      VT coming from the anterior fascicle (fascicular VT)@


*AVRT = AV Reciprocating Tachycardia (Tachycardic loop that uses both the AV node and an accessory pathway.  Depending on whether the accessory pathway is unidirectional or bidirectional, this can go down the AV node and up the accessory pathway (orthodromic), or down the pathway and up the AV node (antidromic).

#Aberrancy means that the impulse coming from (AVNRT) or through (Orthodromic AVRT) the AV node is too rapid to allow for repolarization of all the conducting fibers.   In this case, the right bundle and the posterior fascicle are unable to repolarize, but the anterior fascicle is. The impulse goes through the (left) anterior fascicle (which is superior) and then goes from this superior left location through non-conducting fibers to the inferior and right.  Hence the latter part of the QRS is to the right and inferior (RBBB morphology and right and inferior axis).

@Read about Fascicular VT here: 

Idiopathic Ventricular Tachycardias for the EM Physician

Case Continued

He was completely stable, so adenosine was administered.

This resulted in conversion to sinus rhythm:

Sinus rhythm

Aside: Now that we know the rhythm converts with adenosine, the differential diagnosis is narrowed.  See Learning point 1 below.

Case continued

The patient reverted to tachycardia.  This confirms SVT, either AVNRT or WPW.  Right ventricular outflow tract VT also converts with adenosine, and it also has an inferior axis, but it does not have a right bundle branch block morphology

He was given adenosine again.

What do you think of this management?















Comment on management: If adenosine converts, and then the patient reverts, there is no point in going to adenosine without some other therapy to prevent reversion.  Adenosine has a very short half life.  This patient proved that he will go back into SVT after the adenosine is gone.

Management options for continuously reverting SVT are of several kinds:

1) longer acting AV node blockade (most commonly calcium channel blockers, but could be a beta blocker)
2) suppression of the PACs that initiate SVT (beta blockers, which also block the AV node)
3) Also, a type 1a antidysrhythmic (such as procainamide) to slow depolarization might work.

First: try giving 2-4 g of Magnesium, then adenosine again.
Next: try verapamil, which will convert it as well as adenosine does, but has a much longer duration of action and so will maintain sinus rhythm.
Never give verapamil to someone with poor LV function.


Dosing: 

Verapamil 
Dosed at 2.5-5 mg IV over 2 min (over 3 min in elderly patients).
A follow-up dose of 5-10 mg (0.15 mg/kg) IV is administered 15-30 min later if the SVT persists and no adverse reaction occurs. The maximum dose is 20-30 mg. may be followed by an infusion of 0.005 mg/kg/min.

Diltiazem 
Dosed at 0.25 mg/kg IV over 2 min.
A subsequent dose of 0.35 mg/kg IV is administered if no response is seen and no significant drug-induced adverse event occurs.
Infusion is 5-15 mg/hr

Other options include beta blockers.

Case continued:

Adenosine was given again and the patient converted, then reverted.
The patient was cardioverted, then reverted.
The patient was cardioverted again, then reverted.
Magnesium and procainamide were given and the patient did not revert.  

Procainamide is another reasonable solution to the problem.  It does not block the AV node but does slow phase 0 of depolarization, which will also frequently break the re-entrant cycle.  In this pediatric study, it was 71% successful and better than amiodarone.  
https://www.ahajournals.org/doi/full/10.1161/CIRCEP.109.901629

Aside on Procainamide: it also has the very theoretical benefit of not blocking the AV node if this is WPW with an anterograde conducting pathway AND the patient converts to atrial fib.  The fact that we saw no delta wave in the 12-lead is good evidence that, if there is an accessory pathway, it does not conduct in the anterograde direction.]

Follow up

Later history revealed that he had been having palpitations with rapid ventricular rate for several years, about 2 episodes per year.  These episodes start with sudden onset tachycardia.  He is uncertain whether his rhythm is regular or not and he is uncertain about the rate but thinks it's "extremely fast and it is like the heart is beating in my neck". 

Most of the times he thought that these were panic attacks and he was trying to just relax for the episodes to go away.  They usually lasted anywhere between 1-2 hours.

The patient was found to have a "concealed" posteroseptal pathway (WPW without delta waves) confirmed to have SVT at EP study and was ablated.

Here is the Electrophysilogist's note:

"Only 1 pathway attachment could be ablated, the second one deep within the CS could not be ablated with high power.  Sustained SVT could not be induced after that."

"Due to some difficulty maneuvering the catheters, and with accessory pathway being noted on the EP study, it would be important to rule out any structural abnormalities that could be associated with accessory pathway like Ebstein's anomaly.  I have ordered an echocardiogram which will be done today, after that patient can be discharged to home with follow-up in 2 to 3 months." 

The echo was normal.

Learning points

1. In this regular wide complex tachycardia, since the rhythm converted w adenosine, it is almost certainly SVT w aberrancy, which can be either: 
            A. AVNRT w aberrancy, or 
            B. Orthodromic AV Reciprocating Tachycardia (WPW), also with aberrancy

You might also consider these, but they don't fit: 

     B. Antidromic AV Reciprocating Tachycardia (WPW) -- very unlikely given the morphology  
     C. RV outflow tract tachycardia (but this will have LBBB morphology -- so it is not RVOT)

2. If the rhythm converts and then reverts to tachycardia with either adenosine or electricity, Neither one of those modalities should be attempted until some longer acting pharmacological solution is given.

3.  WPW does not always have delta waves on the baseline ECG. This is called "Concealed conduction".  It may happen because the accessory pathway can only conduct in a retrograde direction (hence, orthodromic SVT).  It can also happen if the accessory pathway is so far away from the sinus node that the impulse goes through the AV node before it can pre-excite the bypass tract.

4.  Many people experience SVT as a "Panic Attack." (see below: SVT misdiagnosed as panic disorder)

5.  The AV node in young people can sometimes conduct at extremely fast rates.  In this case, it was able to conduct at a rate of 257 (down the AV node, then up the bypass tract)

6.  These tachydysrhythmias are so fast that they can degenerate into ventricular fibrillation. Admission and referral to electrophysiology is always indicated.


SVT misdiagnosed as panic disorder
Lessmeier TJ, Gamperling D, Johnson-Liddon V, et al. Unrecognized paroxysmal supraventricular tachycardia. Potential for misdiagnosis as panic disorder. Arch Intern Med. 1997;157(5):537–543.
Lessmeier et al. performed a retrospective survey in 107 patients with reentrant PSVT and found that 67% had symptoms fulfilling the DSM-IV criteria for panic disorder.※ Only 48 (45%) patients were correctly diagnosed upon initial evaluation; 55% were undiagnosed for a mean of 3.3 y following initial presentation, including 13 patients with apparent pre-excitation on resting ECG. Physicians initially attributed symptoms to “panic, anxiety or stress” in half of these patients, with women more likely than men to have their symptoms attributed to psychiatric causes (65% vs. 32%; P <.04).

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MY Comment by KEN GRAUER, MD (9/7/2020):

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Interesting case with thorough discussion by Dr. Smith on arrhythmia management. As a result — I’ll limit my comments to a few additional points.

• The patient in today’s case is a 30-something man admitted for minor trauma. The patient had a history of heavy alcohol use. He was mildly symptomatic with palpitations — but was felt to be completely stable at the time his initial ECG was obtained. For clarity — I have put the 2 ECGs in today’s case together in Figure-1.

Figure-1: The 2 ECGs in today’s case (See text).

Looking at ECG #1: As per Dr. Smith — the differential diagnosis of the extremely rapid SVT rhythm (at ~255/minute) seen in ECG #1, in which there is no clear sign of atrial activity — includes: i) A reentry SVT rhythm (ie, AVNRT vs orthodromic AVRT); ii) AFlutter with 1:1 AV conduction; and, iii) VT.

IF the rhythm in ECG #1 was VT — it would almost certainly be a form of Idiopathic VT — since there is no indication from the history that this 30-something man has underlying ischemic heart disease. As a result — it’s worth briefly reviewing this entity of “Idiopathic” VT.

• Drs. Meyers, Smith; Weingart wrote an extensive review on Idiopathic VT in the September 14, 2018 post of Dr. Smith’s ECG Blog.
• My Comment at the bottom of this Sept. 14, 2018 post adds a series of PEARLS on “My Take” regarding this subject.
• I’ll add here 2 more reference links on the subject — by Brugada; Diez — and — by Tondo et al.

WHAT is Idiopathic VT?

• The vast majority of VTs are associated with underlying structural heart disease.
• PEARL #1: It is important to remember that ~10% of patients who present with VT do not have ischemic or underlying structural heart disease — nor do they have a metabolic or electrolyte disturbance — nor do they have QTc prolongation. The importance of recognizing these patients with Idiopathic VT who have a structurally normal heart — is that the presentation, clinical course, and both short- and long-term management differ greatly compared to the ~90% of patients with the “usual” ischemic or structural forms of VT.
• Although exceptions exist — the “good news” regarding patients who present with idiopathic VT — is that this rhythm is generally seen in an otherwise healthy, younger adult population (often <40yo). Long-term prognosis tends to be surprisingly good! Suspect an idiopathic form of VT when a younger adult without known coronary or structural heart disease develops a regular WCT (Wide-Complex Tachycardia) rhythm during exercise or other strenuous effort — and despite this, seems to tolerate the WCT rhythm surprisingly well.
• Not all forms of idiopathic VT are predictable based on their ECG appearance (Anderson et al, 2019). That said — many of them are, which is important for management considerations since (as per Dr. Smith above) — Adenosine and/or Verapamil may be treatments of choice for idiopathic VT. In contrast, Adenosine and Verapamil are ill-advised (if not, contraindicated) for treatment of ischemic VT.

By far, the most common form of idiopathic VT are the OT VTs ( = Outflow Tract VTs). The other frequently encountered form of idiopathic VT is Fascicular VT.

• Among the Fascicular VTs — the most common type by far (over 90% of cases) is Left Posterior Fascicular VT — in which the ECG shows a RBBB/LAHB pattern (VT exit near the posterior hemifascicle). Much less commonly there may be Left Anterior Fascicular VT (RBBB/LPHB pattern) — and rarely Septal Fascicular VT (RBBB with a normal axis).
• Among the OT VTs — Most attention is given to RVOT VT (Right-Ventricular Outflow Tract VT) — because RVOT VT makes up ~80-90% of all OT VTs.
• But in ~10-20% of cases — there may be LVOT VT (Left-Ventricular Outflow Tract VT). This is important to appreciate, because initial management of OT VTs (ie, Adenosine, Verapamil) is similar for RVOT and LVOT VT — but ECG recognition of RVOT and LVOT is different!
• RVOT VT is usually fairly easy to recognize on ECG — because chest leads show a LBBB pattern, with an inferior axis in the limb leads (ie, much greater positivity of the QRS complex in inferior leads compared to lead I).
• LVOT VT may be more challenging to recognize on ECG. You may also see a LBBB pattern in the chest leads with LVOT VT (as well as the inferior axis in limb leads). Although many complicated variations in QRS morphology are possible (that extend way beyond our scope! — Anderson et al, 2019) — the chest lead LBBB pattern characteristic of LVOT (as distinguished from RVOT) — is that transition tends to occur earlier (ie, by V1-V2 for LVOT vs after V3 or V4 for RVOT).
• The other reason recognition of LVOT VT is so challenging — is that it sometimes presents with a RBBB pattern in the chest leads (in the form of wide, prominent R waves in leads V1,V2) + the inferior axis in limb leads. This could resemble the Left Anterior form of Fascicular VT.

BOTTOM Line SIMPLIFICATION: Initial use of Adenosine for treatment of a previously healthy, hemodynamically stable patient who presents with presumed idiopathic VT is completely appropriate, and a treatment of choice. Adenosine is especially likely to work IF the patient has an OT VT (ie, either RVOT or LVOT). That said, the clinical reality is — that you will not always be able to recognize all forms of idiopathic VT that are likely to be Adenosine-responsive based on ECG appearance.

• IV Verapamil (or Diltiazem) is an effective, alternative treatment for idiopathic VT. And, IF you know that the WCT rhythm is indeed Fascicular VT — then IV Verapamil is the drug of choice.
• Be aware that there are case reports of Adenosine working for Fascicular VT. That said — most of the time Adenosine won’t work for this rhythm (Reviriego) — which is why IF you knew the WCT rhythm was Fascicular VT, then you might decide not to start treatment with Adenosine.
• KEY Point: Do not use Adenosine or Verapamil/Diltiazem if you know that the WCT rhythm is ischemic VT. These drugs are not effective for this indication — and, risk of adverse effects significantly increases (with real risk of deterioration to VFib if Verapamil/Diltiazem is used to treat ischemic VT).

PEARL #2 — Did YOU see the Electrical Alternans in ECG #1? The fascinating but uncommon phenomenon of electrical alternans is frequently misunderstood — and, it is often overlooked when it does occur. Electrical alternans can be subtle.

• Although most commonly associated with pericardial tamponade — electrical alternans has also been associated with an expanding array of other clinical conditions.
• In its simplest form — electrical alternans is a beat-to-beat variation in any one or more parts of the ECG recording. It may occur with every-other-beat — or with some other recurring ratio (3:1; 4:1; etc.). Amplitude or direction of the P wave, QRS complex, ST segment and/or T wave may all be affected. Alternating interval duration (of PR, QRS or QT intervals) may also be seen.
• NOTE: There are 3 of the 12 leads in ECG #1 that show clear evidence of electrical alternans. To facilitate identifying this — I have enclosed these 3 leads within a RED rectangle in Figure-2. Isn’t the every-other-beat alternation of R wave amplitude now obvious in leads V3, V4 and V5? More subtle, but still readily identifiable — is the every-other-beat alternation in T wave amplitude seen in leads V3 and V4 in Figure-2.
• In addition to pericardial tamponade — one of the most helpful insights that recognition of electrical alternans provides, is that it suggests a reentry mechanism for a regular SVT rhythm. In this setting — QRS alternans during a regular SVT rhythm (as we see in Figure-2) often indicates retrograde conduction over an AP (Accessory Pathway). That said — because QRS alternans can occasionally also be seen with simple AVNRT (in which the reentry pathway is contained entirely within the AV node) — recognizing this form of electrical alternans does not prove the existence of a participating AP — but it is suggestive. (And, a reentry SVT with a participating AP was found in today’s case!).

BOTTOM Line SIMPLIFICATION: Even if recognizing electrical alternans in a regular SVT does not prove the existence of a participating AP — knowing that the mechanism of this SVT is almost certain to be reentry may help in clinical decision-making regarding optimal management. In Today's Case — Recognition of electrical alternans provides yet one more reason in support of initially trying Adenosine.

• NOTE #1: Although not common — Be aware that electrical alternans may occasionally be seen with monomorphic VT.
• NOTE #2: Among the list of other Clinical Conditions in which electrical alternans has been described include the following: — long QT syndrome — severe electrolyte disturbance (low Ca++; low K+/Mg++) — alcoholic or hypertrophic cardiomyopathy — acute PE — subarachnoid hemorrhage — cardiac arrest or the post-resuscitation period — and various forms of ischemia (spontaneous or induced by exercise; severe LV dysfunction).
• NOTE #3: In the context of a long QTc or ischemia — the finding of ST segment and/or T wave alternans may predict the occurrence of malignant ventricular arrhythmias.
• For MORE on Electrical Alternans — CLICK HERE.

P.S.: The BEST way not to overlook electrical alternans — is to remember to LOOK for it whenever you have a regular narrow or wide tachycardia of uncertain etiology. Doing so may provide an important clue to the etiology of the rhythm.

Figure-2: I’ve enclosed within a RED rectangle the 3 leads in ECG #1 in which there is clear evidence of electrical alternans. (See text).

Is it VT or SVT with Aberrancy?

Here is a classic ECG, presented and analyzed by Ken Grauer:

Figure-1: The initial ECG in this case, obtained by the EMS team (See text).

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MY Comment by KEN GRAUER, MD (5/5/2020):

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The 12-lead ECG in Figure-1 was obtained from a woman in her 80s who was seen by EMS for symptoms of new confusion and hypotension. She had a history of an MI in the past.

• WHAT is the rhythm in ECG #1?
• How certain are you of your diagnosis?

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Smith's comment on management:

First, what do you want to do?

The patient has confusion and hypotension, so she is in shock.  And she has a regular wide complex tachycardia that cannot be sinus (because it is rate 180 and she is 80 years old).

Therefore, cardiovert immediately.

Assuming this works, then you can proceed to analyze the 12-lead

--If it is SVT with aberrancy or VT, electrical cardioversion should do the job.
--Consider etomidate or ketamine sedation, depending on how "confused" or awake she is.
--Adenosine is not contraindicated when there is reasonable probability that SVT is the etiology; that is not reasonable here, as Ken will tell you below.

--If cardioversion does not work (or the rhythm recurs after successful conversion), then an anti-dysrhythmic to treat (or prevent) needs to be given, and/or the underlying etiology needs to be reversed (e.g., acute coronary syndrome).   

Choice of anti-dysrhythmic for recurrent refractory or recurrent VT is beyond the scope of this blog post, but you can start by looking at the Procamio study for stable VT: procainamide was better than amiodarone.  In short, the literature on pharmacologic therapy for VT is terrible, whether using it for stable VT, refractory VT, or recurrent VT.

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Ken Grauer on the ECG:

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MY Comment by KEN GRAUER, MD (5/5/2020):

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MY THOUGHTS on ECG #1: The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) Rhythm at ~220/minute, without clear sign of atrial activity.

• PEARL #1: Even before you look any further at this ECG — statistical odds that a regular WCT rhythm without atrial activity is VT (especially given that this is an older patient with known history of coronary disease) — are at least 90%. This emphasizes the point that you have to prove that this rhythm is not VT — rather than the other way around. AVOID starting from the assumption that there is aberrant conduction ... (SEE the April 15, 2020 post in Dr. Smith’s ECG Blog for another case in which I review my initial approach to a regular WCT rhythm).

Among the ECG Features I look to first for rapid distinction between an SVT rhythm (with QRS widening due to either preexisting BBB or aberrant conduction) vs VT are: i) Frontal plane axis during the WCT rhythm; ii) Resemblance to any known form of BBB or hemiblock; and, iii) Is there relative “delay” in the initial QRS deflection? Applying these features to ECG #1:

• Is there “extreme” Axis deviation? By this I mean — is the QRS complex during the WCT all negative in either lead I or lead aVF? To emphasize that this criterion is of no benefit in distinguishing between VT vs SVT if there is any positivity at all for the QRS complex in both of these leads. In ECG #1 — We see a fragmented, but all negative QRS complex in lead I! This means there is extreme axis deviation during the WCT rhythm (in this case, extreme right axis) — which allows you within a few seconds to increase statistical odds to ≥95% that this regular WCT rhythm without P waves is VT.
• Is there resemblance to any known form of conduction block? In ECG #1 — the QRS complex in lead V1 resembles RBBB morphology. That said — lack of any R wave in lead I, and lack of a wide terminal S wave in lead V6 negate the possibility of RBBB conduction. The nearly monophasic upright QRS complex in lateral lead V6 resembles LBBB morphology. But lack of a monophasic upright QRS in other lateral leads (I and aVL), and lack of predominant negativity in anterior leads negates the possibility of LBBB conduction. This means QRS morphology in ECG #1 does not resemble any form of known conduction defect! NOTE: Exceptions to this QRS morphology rule do exist — in that some patients may have an extremely abnormal baseline QRS morphology during sinus rhythm (and therefore an equally abnormal QRS morphology during tachycardia). That said — the overall bizarre QRS morphology we see in ECG #1 further increases statistical odds above the already high likelihood we previously established.
• Is there relative “delay” in the initial QRS deflection? SVT rhythms tend to manifest more rapid initial depolarization vectors — because supraventricular depolarization generally begins its path toward the ventricles by travel over established conduction pathways. A notable exception to this generality is when there is an AP (accessory pathway) that bypasses the AV node (ie, in a patient with WPW). That said — “relative delay” in the initial portion of the QRS complex in multiple leads favors VT. Although sophisticated research studies cite a number of indices with precise initial deflection time limits as “accurate” criteria for VT — in practice, making precise millimeter measurements of initial QRS deflections at the bedside of a crashing patient is both time-consuming, and extremely difficult to accomplish. Subjective measurements often suffice! In ECG #1 — Note the presence of relatively wide Q waves at the onset of the QRS complex in leads V1-thru-V5. Note that for each of these Q waves — the initial downsloping portion of these Q waves is angled instead of straight (ie, suggesting delay). This is consistent with VT.
• BOTTOM Line: The rhythm in ECG #1 is almost-certain-to-be VT. Treat the patient accordingly.

FOLLOW-UP: The patient was electrically cardioverted. The result appears in Figure-2, with the post-cardioversion ECG shown below the initial tracing.

• Does the post-cardioversion tracing confirm that the regular WCT rhythm from ECG #1 was VT?
• HINT: Are all of the beats in ECG #2 the same?

Figure-2: Comparison between the initial ECG and the post-cardioversion tracing. Does the post-cardioversion tracing confirm that the rhythm in the initial ECG was VT? (See text).

ANSWER: Unfortunately — there is no simultaneous long lead II rhythm strip for either ECG #1 or ECG #2. This would have been especially helpful for interpretation of ECG #2 (ie, EMS 12-lead ECGs often do not display a simultaneous long lead rhythm strip). That said — we still see enough in ECG #2 to confirm the diagnosis of VT in ECG #1 (I’ve labeled KEY findings in Figure-3 below).

• There are a total of 12 beats in ECG #2 — with beats #1, 2, 3 displayed in leads I, II, III — beats #4, 5, 6 in leads aVR, aVL, aVF — beats #7, 8, 9 in leads V1, V2, V3 — and beats #10, 11, 12 in leads V4, V5, V6 (See Figure-3 below).
• Electrical cardioversion has resulted in conversion of the rhythm to sinus (RED arrows highlighting sinus P waves in selected leads).

The KEY to the Answer lies with realization that beats #1 and #4 in Figure-3 look different from normally sinus-conducted beats in their respective leads.

• Looking first at beat #1 in each of the 3 simultaneously-obtained leads (ie, leads I, II, III) — QRS morphology is clearly different than the appearance of beats #2 and 3 in these leads.
• Note that the PR interval preceding beat #1 is slightly shorter than the PR interval preceding beats #2 and 3 (This is best seen in lead II).
• Finally — Note that QRS morphology of beat #1 in lead I of the post-cardioversion tracing looks very much like the QRS morphology we see in lead I during the regular WCT rhythm. This is because beat #1 in ECG #2 is a Fusion Beat (ie, QRS and ST-T wave morphology of beat #1 looks intermediate between QRS and ST-T wave morphology during VT, and after conversion to sinus rhythm). Realizing that beat #1 in ECG #2 is a fusion beat (ie, “F” in Figure-3) — explains why the PR interval of beat #1 is slightly shorter than the PR interval of normally-conducted sinus beats #2 and 3 (ie, before the P wave preceding beat #1 was able to fully conduct — a late-cycle PVC arose from the ventricles). Seeing a fusion beat with QRS morphology that at least in lead I of ECG #2 looks virtually identical to QRS morphology in lead I during the WCT rhythm — all but confirms that the WCT rhythm was VT (For more on fusion beats — CLICK HERE).

Beat #4 in the post-cardioversion tracing is slightly early! Beat #4 is a ventricular beat (ie, “V” in Figure-3). We explain this as follows:

• Using calipers — we can establish that the underlying sinus rhythm continues throughout the 12 beats seen in ECG #2. RED arrows in this Figure highlight the first 3 sinus P waves. Although the 4th P wave could be easy to overlook — the slanted BLUE lines in lead aVL show that regular occurrence of sinus P waves continues. That the notch that occurs right after the QRS of beat #4 in lead aVL is a sinus P wave — is established because it occurs right-on-time with respect to the 3 preceding RED arrows, and the next 2 sinus beats (ie, the 2nd and 3rd slanted BLUE lines in lead aVL).
• The fact that beat #4 is wide and occurs early — is not preceded by any P wave — and, the underlying sinus rhythm continues throughout (3 RED arrows, followed by the 3 slanted BLUE lines) — means that beat #4 has to be coming from the ventricles. Beat #4 is a late-cycle PVC. The fact that QRS morphology of beat #4 in ECG #2, at least in lead aVL — looks so very much like QRS morphology in lead aVL during the regular WCT — adds further support that the regular WCT rhythm was VT.
• PEARL #2: The finding of an identical QRS morphology for ventricular beats that occur during sinus rhythm — compared to QRS morphology during the regular WCT rhythm — confirms that the WCT was VT. While I fully acknowledge that QRS morphology of the fusion beat and the late-cycle PVC in ECG #2 is not quite identical in all 3 leads compared to QRS morphology in these leads during the WCT rhythm — I thought QRS morphology of the unique shape of the fusion beat ( = beat #1) in lead I, and of the late-cycle PVC ( = beat #4) in lead aVL was close enough to QRS morphology in these leads during the WCT to be unlikely the result of chance. BOTTOM Line: I thought QRS morphology of beat #1 in lead I and of beat #4 in lead aVL provided strong additional support that ECG #1 was VT.

Figure-3: Key findings from Figure-2 have been labeled (See text).

WHAT ELSE does the Post-Cardioversion ECG Show?

Now that we’ve determined the rhythm and identified the etiology of beats #1 and 4 in ECG #2 — We can interpret the rest of the tracing:

• The rhythm in ECG #2 is sinus with occasional late-cycle ventricular beats (including a fusion beat). The PR, QRS and QTc intervals are normal. There is marked left axis deviation with an almost null complex for the QRS in lead II. In view of predominant negativity in leads III and aVF — this probably qualifies as LAHB.
• There is no chamber enlargement (I didn’t perceive the P was in lead V1 as having a deep enough negative component to qualify for LAA).
• Deep Q waves are seen in the normally-conducted sinus beats in the high-lateral leads (ie, leads I and aVL).
• R wave progression is lacking in the chest leads. A QS complex is seen in lead V1. A tiny initial r wave appears in leads V2 and V3 — but then disappears in leads V4-thru-V6, which manifest tiny, fragmented complexes.
• Hyperacute T waves (ie, T waves that are larger-and-fatter-than-they-should-be with respect to the QRS complex) are present in multiple leads.

BOTTOM Line: The post-cardioversion ECG of this elderly woman clearly shows evidence of extensive prior infarction. ST-T waves in ECG #2 are markedly abnormal in multiple leads.

• The above said — I feel it impossible to be certain from this single post-conversion tracing whether anything acute is going on (ie, this could be a “memory” effect, that sometimes follows an episode of sustained VT — in which marked ST-T wave abnormalities not due to infarction are seen and persist for hours, or even days).
• Given that there really is no J-point ST elevation in ECG #2 — no reciprocal ST depression — and given nearly uniform presence of similar-looking prominent T waves in almost all leads on this tracing — my hunch is that the ST-T wave changes in ECG #2 are not new!
• The fact that this elderly patient woke up; was normotensive, alert and oriented without chest pain soon after conversion to sinus rhythm — supported my hunch that the abnormal ST-T wave changes in ECG #2 were unlikely to be acute.
• Repeating the ECG after the patient arrived in the ED would have been insightful.

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NOTE: My sincere THANKS to Emmanuel Reisman (from Monsey, NY) for sharing this case with us!

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