Wednesday, April 29, 2020

Cardiac Arrest. What does the ECG show? Also see the bizarre Bigeminy.

A 60-something woman presented after a witnessed cardiac arrest. CPR was started immediately.  EMS arrived and found her in a wide complex PEA rhythm. She was given 3 mg IV epinephrine and multiple rounds of ACLS over approximately 20 minutes.

Her husband stated that she had not been feeling well in the past 2 weeks and c/o dizziness as well as diarrhea.

She was never defibrillated.

I was texted this ECG in real time, but it turns out to actually be the 2nd one recorded in the ED.

What do you think?

This is what I wrote:

This looks like pseudoSTEMI to me.  What appears to be ST elevation seems to be a wide QRS.  I am only looking on my phone though.

Indeed, if you find the end of the QRS, which is easy to see in V1, then draw a line down to lead II across the bottom, then you can find the end of the QRS in lead II.  The go to the left and find that same point under aVR/aVL/aVF and under I, II, III, and you can draw this line back up to find the end of the QRS in these leads.

Sure enough, all of what you might think is ST Elevation is really QRS:

The K returned at 2.7 mEq/L.  This is commonly found after epinephrine for cardiac arrest, but could have been pre-existing and a possible contributing factor to cardiac arrest.

A recent similar case:

A 40-something with chest pain. Is this inferior MI?

Just as interesting is EKG 1, 24 minutes before the first:

What do you think here?

There is a bigeminy with very Bizarre looking PVCs.  These are frequently found in cases of Torsades.

Below, I post 4 more examples of ECGs that were recorded from patients who had Torsades.

1 hour later, this was recorded:
Now there is a very long QT.
See especially lead V2, where the QT is 640 ms, and QTc would be about 680 ms.
Interestingly, the computer measured the QT as 245 ms!!

Of note, she's on some QT prolonging medications as well as Hydroxychloroquine for Rheumatoid Arthritis, but no other known QT prolonging medications.

This was recorded at 6 hours:
Again, bizarre bigeminy with very long QT of both native beat and of the PVC

Computerized QT = 430
QTc = 449
Verified by overreading cardiologist

Obviously much longer, or they are U-waves

Potassium level

Troponin I peaked at 0.875 ng/mL, so an angiogram was done.

--Minimal coronary atherosclerosis
--No obstructive epicardial coronary artery disease or evidence of plaque rupture noted to explain prolonged QT or ventricular fibrillation cardiacarrest, suspect nonischemic mechanism

The estimated left ventricular ejection fraction is 45 %.
No wall motion abnormality.

Clinical Course

Initially, her potassium level was low which was replaced.  Despite of replacing potassium, she continued to have ventricular ectopy with prolonged QT interval and had 2 episodes of R on T phenomena followed by torsades de pointes, which was cardioverted.

Therefore, she underwent temporary pacemaker placement and overdrive pacing at a rate of 90 bpm to keep the heart rate up in order to prevent these PVCs triggering ventricular arrhythmia.

The ultimate reason for the long QT was never definitively determined.  Hypokalemia was unlikely because she continued to have ventricular arrhythmia despite of correcting electrolytes.  Drug-induced QT interval cannot be completely ruled out, but the tox consult found the she had definitely not overdosed and did not believe that therapeutic doses would do this.

Final Diagnosis: Cardiac Arrest due to Torsades from long QT of unknown etiology.


Below, I post 4 more examples of ECGs that were recorded from patients who had Torsades, either shortly before, during, or after.

3 of the 4 have similarly bizarre PVCs.

MY Comment by KEN GRAUER, MD (4/30/2020):
Cardiac Arrest with Bizarre PVCs/Torsades de Pointes: Intriguing case with many interesting features. I’ll focus my comments on selected points that enhance those superbly presented by Dr. Smith.
  • Relevant REVIEW of the CASE: The patient was a 60-something woman who presented in PEA cardiac arrest. Initial serum K+ = 2.7 mEq/L, which later decreased to 2.0 mEq/L — before treatment that returned it to normal. The patient was on some QT-prolonging medications. Cardiac cath showed minimal disease. The patient developed Torsades de Pointes, which was converted electrically, with recurrence prevented by overdrive pacing. She recovered. Final diagnosis was cardiac arrest due to Torsades from a prolonged QTc of uncertain etiology.
  • Dr. Smith showed a total of 10 ECGs in his comments above. For clarity — I’ve numbered the 3 ECGs I discuss according to the sequence in which they appear above in Dr. Smith’s comments (Figure-1):

Figure-1: The 3 ECGs I discuss, numbered according to their sequential appearance in comments by Dr. Smith (See text).

ECG #4 — This is the 3rd ECG that was done in this case (obtained ~1 hour after arrival in the ED).

QUESTIONS Regarding ECG #4:
  • In general — WHICH of the 12 leads on an ECG should be used to measure the QT interval?
  • WHY does this matter in a case like the one discussed today?
  • For ECG #4  WHICH of the 12 leads should be used to measure the QT interval?
  • The computer measured the QTc to be 245 msec. Since computerized ECG interpretations are supposed to be accurate for measurement of intervals — HOW could the computer be so off?
  • Extra Credit: WHAT is the rhythm in ECG #4? (Feel free to look ahead to ECG #5 when checking your answer.)

ANSWERS Regarding ECG #4:
  • The BEST lead on a 12-lead ECG for measuring the QT interval — is THAT lead in which you can clearly see the beginning and end of the QT — and, in which the QT interval is longest.
  • The reason this matters in this case, is that this patient was predisposed to, and later developed Torsades.
  • Assessment of the QT interval in ECG #4 is extremely challenging! This is because none of the 12 leads really show a distinct end point for the QT interval. One might think BLUE arrows in leads II and aVF indicate the end of a normal QTc. Other leads (ie, I, III, V3-thru-V6) manifest an even less distinct end point of the QT interval. But as per Dr. Smith — the KEY lies with focusing on lead V2, with the PURPLE arrow highlighting a shallow-but-distinct negative T wave. Thus, the QTc is markedly prolonged (ie, over 600 msec). BOTTOM Line: Measure the QTc in THAT lead in which you most clearly see the end of the interval, and in which the QT is longest ( = in lead V2 in for ECG #4). Be SURE to look at all 12 leads when measuring the QTc!
  • In general — computer measurement of intervals is accurate. BUT — computer measurements depend on where the computer determines the beginning and end of the interval being measured. As emphasized in the previous bullet — the end of the QT interval in ECG #4 is indistinct, and extremely difficult to determine.
  • PEARL #1 — IF it is difficult for YOU to determine the end of the QT interval, then it will also be difficult for the computer! In such cases — Be aware that you can not trust the computer estimation, and YOU need to assess the QTc yourself!
  • Extra Credit Answer: Did YOU notice that the P wave in lead II of ECG #4 is not upright? (P wave within the PURPLE circle). This means that the rhythm in ECG #4 was not sinus! However, the P wave in this tracing was positive in leads I and aVL (P wave within the BLUE circle). This means there was a low atrial rhythm. Confirmation that the rhythm in ECG #4 was not sinus — is forthcoming from inspection of lead II in ECG #5, in which the P wave now is upright in lead II (P wave within the RED circle).

What is the Difference between PMVT and Torsades?
A useful classification of WCT (Wide-Complex Tachycardia) rhythms — separates them into those that are monomorphic (with similar QRS morphology during the tachycardia) vs those that are polymorphic (in which QRS morphology varies).
  • When QRS morphology of an obviously irregular ventricular tachycardia changes from one beat to the next — the rhythm is called PMVT (PolyMorphic Ventricular Tachycardia).
  • Torsades de Pointes — is defined as PMVT that occurs in association with a long QTc on baseline ECG. This is especially true when the rhythm in question manifests the shifting QRS polarity around the baseline (ie, “twisting of the points”) that is characteristic of Torsades.

PEARL #2 — Distinction between PMVT vs Torsades is more than academic. Both treatment and the response to therapy tends to be different with these 2 entities.
  • 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 given at high and sometimes repeated doses (even if initial serum Mg++ levels are not low). Optimal treatment of Torsades entails finding and “fixing” the cause of the long QTc. As was seen in this case — defibrillation and/or overdrive pacing may be needed.
  • 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, 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.

ECG #5 — This is the 4th ECG done on the patient in this case (obtained ~6 hours after arrival in the ED).

QUESTION Regarding ECG #5:
  • WHAT ECG findings in ECG #5 predispose to development of Torsades?

ANSWER Regarding ECG #5:
  • Among the findings in ECG #5 that predispose to development of Torsades are: i) underlying bradycardiaii) a very long QTc interval (the GRAY arrow in the long lead II rhythm strip shows the end of the QT interval, which appears to be at least 600 msec)iii) Frequent and bizarre-looking PVCs, that also manifest an extremely long QT interval (the PINK arrow showing the end of the QT for the PVC, which is beat #8).
  • PEARL #3: As per Dr. Smith — bizarre-looking PVCs are often seen in patients who go on to develop Torsades.

ECG #8 — This is an ECG obtained from another patient with known Torsades, used by Dr. Smith for illustrative purposes:
  • There is atrial pacing of narrow-complex beats #1, 3 and 8.
  • Note again the presence of bizarre-looking PVCs ( = beats #2 and 4).
  • Note how difficult it is to assess the QTc of the narrow beats — because we really do not see a distinct end point to the T wave. More than any other lead — lead I suggests the QTc to be prolonged — but, the marked dip in the baseline seen in simultaneously-recorded leads II and III suggest this may be artifact.
  • Beginning with beat #2 — a run of Torsades is triggered. Note the characteristic shifting polarity of QRS complexes from positive-to-negative-to-positive-then-negative again (ie, “twisting of the points”).
Final Learning Points — It is common in practice when PMVT is encountered not to know (or be able to identify) IF the baseline QTc is prolonged or not. This is the case in ECG #8 — as I would not be certain that the baseline QTc is prolonged from this single tracing alone. As explained above — this distinction between Torsades vs PMVT with a normal QTc is important — because IF the QTc is indeed prolonged, then the PMVT is Torsades — in which case treatment and the response to therapy may differ than if the rhythm is PMVT without QT prolongation.
  • Hopefully either a baseline ECG and/or additional monitoring of the patient will reveal more clearly if the baseline QTc is prolonged.
  • Careful assessment of clinical factors potentially predisposing to one or the other etiology (Torsades vs PMVT) may help if the only ECG available does not clearly reveal the end of the QT interval in any of the leads (ie, Was serum K+ and Mg++ low? Use of QT-prolonging drugs? Acute ischemia? etc.).


  1. Hello DR. Smith, 2 questions:

    -This blog has taught us, many times in the previous posts, that PVCs can "reveal" an ongoing AMI by showing ST anomalies which may be less evident in native QRS complexes. So, especially if I look at ECGs 1 and 4 in your final examples, i notice changes which I would for sure interpret as ischemic if I didn't know that wasn't the case. So, question is: how do we tell the difference? Maybe because there's also a long QT in native beats? Or because in native beats there is ZERO STE/STE compared to PVCs?

    -About the fourth ECG (the one which was recorded "1 hour later") QT sure looks very long if you look at leads V1 and V2, but it is kinda short looking at lead DII; plus, i can clearly see U waves in lead V4: is it possible that the long QT interval observed in leads V1 and V2 represents U waves merging with T waves? That would explain why QT in lead DII looks short. Also, I remember one post in this blog which stated that drugs may cause long QT, but NOT U waves (as in, long QU interval): if i remember right, so, tox consult was right about not accounting this on Chloroquine.
    And.. why, in the first ECG (but not in the others) QRS is WIDE too, which is not a feature of hypokalemia? Is this some conduction disturbance in the post-ROSC state, or what?

    Thank you!

    1. YES — The PVCs in the examples you mention do manifest marked ST elevation in some leads. That said — this occurs amidst a background of Torsades de Pointes and truly bizarre-looking PVCs — so I wouldn’t focus on ST segment deviations in these bizarre-morphology PVCs. Optimal treatment of Torsades (in addition to IV Mg++) includes identifying and “fixing” (if at all possible) the underlying cause — after which you can repeat the ECG to see if underlying ST elevation is still present. As to your other questions — I see QRS widening in the first 3 ECGs. Perhaps some of this is post-resuscitation related. In My Comment (above, at the bottom of the page — which I added AFTER you asked these questions) — I discuss the discrepancy between what looks to be a normal QT vs a long QT for ECG #4 in my Figure-1 (the tracing done 1 hour later). The end limit of the T wave is just not clear in virtually all leads — but I agree with Dr. Smith, that in lead V2 (PURPLE arrow in my ECG #4) — the QTc truly appears prolonged (and this is more than just addition of a U wave to the end of the T wave). I hope the above addresses your concerns — :)

  2. Is that osborn wave / j wave which looks like ST elevation?

  3. Hi. When there are 10 tracings, none of which are numbered — it is always difficult for me to know WHICH one(s) you are referring to ... But IF you are asking about the 1st ECG — NO, I do not believe that extra notching is an Osborn wave. Instead (as per Dr. Smith) — it seems to be part of the QRS complex. An Osborn wave is an accentuated J-point (occurs after the QRS) — and you should see it more consistently in more leads than we do here ... — :)


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