Sunday, June 28, 2020

Repost: 63 minutes of ventricular fibrillation, followed by shock. What is going on?

This was published back on Sept 19, 2014 and I came across it again.  It is very instructive, so I am reposting today. 

A middle-aged patient presented in continued ventricular fibrillation after 5 minutes of down time and 45 minutes of prehospital resuscitation by medics, using King Airway, LUCAS, Inspiratory Threshold Device (ITD, ResQPod), defibrillation 4 times, and epinephrine x 3 through an intraosseous line.  The patient had continued to swallow and breathe while being resuscitated (suggesting effective chest compressions).

There was no other clinical history available at that time.

In the ED, we found that ventilations were effective with the King airway.  LUCAS compressions were continued, and end-tidal CO2 was 26 mm Hg (supporting evidence that chest compressions were effective and supporting the possibility of a good neurologic prognosis). 

We administered ventilations slowly at 10 per minute, following the indicator light on the ITD.  After 300 mg of amiodarone, 100 mg of lidocaine, and 500 mcg/kg of esmolol + 50 mcg/kg/min drip, plus more epinephrine and also bicarbonate, and another defibrillation, a rhythm check at 18 minutes after arrival revealed an organized, mostly narrow complex, but slow, rhythm.  We could not feel a pulse.  A bedside cardiac ultrasound, subcostal view, showed the following:

This is reverse orientation: ventricles are right upper and atria left lower.  The RV is closest to the transducer and is very small (essentially excluding pulmonary embolism as etiology).  The LV has extremely thick walls and a very small LV chamber (there is very little blood to pump)

I  interpreted this as hypertrophic cardiomyopathy (HOCM), and was suspicious of HOCM as the etiology of arrest, as it is well known to cause ventricular fibrillation.

I put the vascular transducer on the right carotid artery, with power Doppler, and this showed good flow in the carotid, corresponding to the cardiac contractions.

Thus, we did not restart chest compressions.

An ECG was recorded:
The first 5 seconds appears to be an irregular wide complex tachycardia, with multiform QRS.  However, there are many beats which are clearly narrow complex but only appear to be wide due to ST segment shifts.  This is best seen in lead II across the bottom.
The next 5 seconds appear to be an irregularly irregular, polymorphic wide complex tachycardia.  This is reminiscent of Atrial Fib with WPW, except that the rate is not as fast as is usually seen with that entity.

The exact rhythm here is uncertain.

It is not unusual to have very bizarre ECGs immediately after resuscitation, especially if there is underlying cardiomyopathy, as suspected here.
Case continued:

The patient remained very hypotensive.  Due to the very small LV volume and the need for volume loading in patients with very thick-walled ventricles and slit-like LV [as one sees in HOCM (See this very instructive case)], we began volume loading.

Another ECG was recorded 5 minutes after the first:
There is an uncertain supraventricular rhythm, sinus vs. accelerated junctional, with a narrow QRS.  There appear to be delta waves.  There is bizarre ST elevation in V1-V3 and aVR that does not look like STEMI.
V2 and V3 resemble the Spiked Helmet Sign.
My opinion was that this was not a STEMI and we did not activate the cath lab.  

As the patient was bradycardic and hypotensive, we gave the patient push dose epinephrine, and a norepinephrine drip was started.   The esmolol was stopped.  Fluids were continued.  The BP and pulse rose.

The venous pH was 7.16, pCO2 48, bicarb 17, and lactate 6.8.  K = 3.6 mEq/L.  

The King airway was removed and he was endotracheally intubated.  A third ECG was recorded another 20 minutes later:

Now there is clearly sinus tachycardia.  There is an incomplete RBBB.  There is unusual ST elevation in V1-V3 which does not look like STEMI.
Lead V3 still resembles the spiked helmet sign

No charts had yet been found.  

At this point in time, the cardiologist was called and he recognized the patient and stated that he has HOCM.  He was in favor of assessing the coronary arteries, and so the cath lab was activated.

The patient became more hemodynamically stable.  Another bedside echo was done:

This is a parasternal short axis, and shows very thick concentric hypertrophy, but better LV filling now, with much more effective cardiac output

Here is the parasternal long axis view:

An arterial line was placed, and the BP by arterial line was 190/120, with a heart rate of 130.  O2 saturations fell and the chest x-ray revealed pulmonary edema.  

Comment: Esmolol, a beta-1 blocker with half life of 9 minutes: When ventricular filling is extremely limited, as with this severe Hypertrophic cardiomyopathy, tachycardia may be more detrimental than usual.  In addition, low end-systolic volume can lead to outflow obstruction.  Therefore, we restarted the esmolol.   Esmolol is a particularly good choice because if the hypothesis is wrong (and tachycardia is important for cardiac output because of low stroke volume), it can be stopped and its effect rapidly diminishes due to short half life.

Case continued:

Fluids were stopped and esmolol was rebolused and the infusion restarted.  The BP improved at 130/80 with a pulse of 90-120

As access for a cooling catheter was difficult, it was decided to delay targeted temperature management until after the angiogram.

Shortly before transfer to the cath lab, this ECG was recorded:
Sinus tachycardia with narrow complex, with delta waves.  ST elevation largely resolved.

The patient was identified and medical records were accessed: 

It was learned that the patient had a history of HOCM and WPW, and also a history of severe embolic ischemic stroke due to paroxysmal atrial fibrillation, with hemorrhagic transformation.  Because of this bleeding danger, and also because the physician did not believe that the patient was having acute coronary syndrome, no aspirin or Plavix or heparin was given.  The possibility was also considered that this was all initiated by a cerebral hemorrhage that caused stress cardiomyopathy.  He therefore underwent a CT scan of the head prior to angiography. This had no new findings, only the previous ischemic stroke (encephalomalacia).

The angiogram showed normal coronaries.  

Peak troponin I was 51 ng/mL (very large Type 2 MI -- this troponin level is typical of a moderately large STEMI -- most NSTEMI are less than 10 ng/mL)

Formal echo showed HOCM with no outflow obstruction.

Cooling: The patient underwent targeted temperature management.

By 72 hours, the patient showed no signs of awakening, but by 96 hours was intermittently following commands.  By 7 days, the patient was "very interactive."

Learning Points:

1.   With excellent CPR technique, patients in ventricular fibrillation can be resuscitated even after a very long down time.  In this case, even with a left ventricle that could barely fill, the CPR was effective enough to have adequate perfusion.  Good chest compressions, at the right rate (no more, and no less, than 100) and depth (at least 5 cm, or 2 inches), decompression, ITD (ResQPod), slow ventilations (10/min), are among the many critical interventions that may lead to successful resuscitation.  Whether co-incidental or not in this case, we have had good rates of conversion of VF when esmolol is given.  After the initial publication on esmolol for ventricular fibrillation by Dr. Brian Driver and Smith (me), there have been multiple other reports.

See this case of 68 minutes of cardiac arrest in a paramedic, plus recommendation from a 5 member expert panel on CPR.

2.  Not all cardiac arrest, even with pathologic ST elevation, is due to STEMI.   Cardiomyopathies, combined with cardiac arrest, can result in bizarre ECGs.  Stress cardiomyopathy may cause VF and ST elevation, and other PseudoSTEMI patterns may be present but unrelated to the VF.

3.   ECGs may be very bizarre immediately after defibrillation. Give a few minutes to record another before coming to conclusions.

4.  Bedside ultrasound is incredibly valuable in cardiac arrest, both for assessing cardiac function and for assessing carotid blood flow.  We have been routinely using Transesophageal Echo (TEE) for all cardiac arrests for the last 3 years.  Here are 2 such cases.

5.  Pulses may be absent when there is good perfusion through the carotid.  Use Doppler carotid ultrasound to assess carotid flow.  To my knowledge, there is no human literature on this.  Cerebral oxygenation monitor can also be used.

6.  End Tidal CO2 is a good indicator of effectiveness of chest compressions. 
--By this systematic review in Resuscitation 2013, a value less than 10 mmHg (1.33 kPa) is associated with a very low return of spontaneous circulation.    
--In this systematic review from J Int Care Med 2014, the mean etCO2 in patients with return of spontaneous circulation (ROSC) was 26 mm Hg (3.5 kPa)

7.  Do not do any adverse neurologic prognostication prior to 72 hours after arrest, and it is preferable to wait even longer.  Here is one article from 2014 on this topic by Keith Lurie's group from HCMC and the U of Minnesota, and another (on which I am a co-author) from HCMC this summer of 2014.

8.  When a cardiac arrest victim has a history of "clots" and is on coumadin, one must entertain the diagnosis of pulmonary embolism.  However, ventricular fibrillation is an unusual presenting rhythm in pulmonary embolism:
--In this study, 5% of VF arrest was due to PE: V fib is initial rhythm in PE in 3 of 60 cases.  On the other hand, if the presenting rhythm is PEA, then pulmonary embolism is likely.  When there is VF in PE, it is not the initial rhythm, but occurs after prolonged PEA renders the myocardium ischemic.
--Another study by Courtney and Kline found that, of cases of arrest that had autopsy and found that a presenting rhythm of VF/VT had an odds ratio of 0.02 for massive pulmonary embolism as the etiology, vs 41.9 for PEA.      

MY Comment by KEN GRAUER, MD (6/27/2020):
As I reviewed the above series of 4 tracings in active search for insightful commentary about the various cardiac rhythms — I found myself continually returning to Dr. Smith’s 3rd Learning Point cited above = “ECGs may be very bizarre immediately after defibrillation. Give it a few minutes to record another before drawing conclusions.” As motivated as I was to devise some new, definitive interpretation for the rhythms in this case — it didn’t happen for me. Instead — I’ll simply add this 9th Learning Point:
  • Accept that your peri-resuscitation patient may not show you an easy-to-interpret tracing. When this happens — Be content with the basics. VFib and malignant VT rhythms need to be shocked. In contrast — rhythms such as seen in the 2nd tracing above do not need to be shocked — because even though there is much I can’t explain on this 2nd ECG — the rhythm is regular (at ~70/minute) — with a distinct supraventricular look to the tracing (albeit P waves are not to be seen).

Rhythms such as seen in the 1st tracing above may defy interpretation. For example, the initial part of the QRS complex is narrow and irregularly irregular during the first half of this 1st tracing. This looks like rapid AFib. But as per Dr. Smith — the widened, much more amorphous and irregularly irregular QRS complexes in the second half of this 1st tracing look much more like PMVT (PolyMorphic VT). If this rhythm that we see in the second half of this 1st tracing were to sustain and be accompanied by hemodynamic instability — then it would become “a rhythm to be shocked”.
  • NOTE: Osborn waves are not only seen with hypothermia. They may also be seen during cardiac arrest from VFib (See My Comment in the November 22, 2019 post). I believe the notching we see in lead V3 (and possibly in V2) in the 2nd and 3rd tracings above may be the result of Osborn waves — that may contribute to the bizarre ECG appearance.
  • Finally — serial tracings obtained during resuscitation (and ideally finding a prior tracing on the patient for comparison) — can go a long way toward putting together a cohesive picture. In this case — learning that this patient in cardiac arrest did have a history of hypertrophic cardiomyopathy and WPW, was instrumental in clarifying some of the changes in QRS morphology being seen. For example, sinus tachycardia is definitely seen in the 3rd tracing above. With regard to this 3rd, and then the 4th tracing that follows it — looking at these 2 ECGs in succession reveals as the main change, a new initial slurring of the QRS complex in multiple leads in the 4th tracing that was not seen in the 3rd tracing. This initial slurring in multiple leads can now be recognized as representing delta waves in this patient who we have learned has WPW (even though the PR interval does not look as short in many leads as it is usually does with WPW).

BOTTOM LINE: Through superb efforts by the resuscitation team — this patient was saved despite less than definitive arrhythmia diagnosis. Definitive arrhythmia diagnosis simply wasn't possible early on during resuscitation — but it wasn't needed, because the patient was saved. ECGs may look bizarre for a while after defibrillation ...

ADDENDUM (6/28/2020): After taking another look at the serial tracings in this case — I’d add the following to my thoughts on what I wrote yesterday:

I agree completely with Dr. Smith — that the 2nd and 3rd ECGs shown above manifest several leads showing the Spiked Helmet Sign.
  • First described by Littman in 2011 (Letter to Mayo Clin Proc86 (12): 1245, 2011) — the Spiked Helmet Sign ( = SHS) is an uncommon and unique electrocardiographic finding, that is seen in patients with acute critical illness (such as the prolonged cardiac arrest, as occurred in this case). The sign is typically associated with a high mortality. In addition to extensive acute MI, Takotsubo Cardiomyopathy, and cardiac arrest — other conditions that have been associated with SHS include intracranial hemorrhage, sepsis, severe metabolic disorders. Many other critical care conditions will doubtlessly be added to this list — as recognition of this important ECG sign becomes more widespread.
  • As shown in the insert of Figure-1 — the name of this “dome-and-spike” pattern is derived from the Pickelhaube, a spiked helmet worn in the 19th and 20th centuries by Prussian and German soldiers, as well as by policemen and firemen. (The literal translation of “Pickelhaube” in German = “pointe” or “pickaxe” for Pickel — and “bonnet” for Haube.).
  • As described by Crinion, Abdollah & Baranchuk (Circulation 141:2106  June 23, 2020) — the QRS-ST segment with the Spiked Helmet Sign may show 3 specific components; i) Some elevation of the isoelectric line that begins before the QRS complex (ie, making up the first half of the helmet); ii) Then sharp ascent of the R wave (ie, the “spike” in the helmet); and finally; iii) Coved ST elevation of varying degree, that may mimic an acute ST elevation MI (ie, the second half of the helmet).
  • One, two, or all 3 of these components may be seen in one or more leads on the ECG. Although initial reports limited the occurrence of this finding to the inferior leads — any of the 12 leads on an ECG may be affected!
  • The proposed mechanism is fascinating — namely, a hyperadrenergic state with adrenergically mediated prolongation of repolarization. The reason for elevation of the isoelectric line beginning before the QRS complex — may result from similar pathophysiology as is seen in conditions with marked QT (and/or QU) prolongation — with the late and enlarged T and U waves being superimposed on the initial portion of the QRS. Other features shared with excessive endogenous catecholamine states such as long QT syndrome and Takotsubo Cardiomyopathy — include Torsades de Pointes, T wave alternans, and pseudo-infarct ST elevation.
  • PEARL — As noted above, SHS may produce ST elevation that might easily be mistaken for acute infarction. However, distinction from a STEMI can usually be made by recognizing the upward shift of the isoelectric line that begins before the QRS complex — and which often comes close to “lining up” with the ST elevation seen after the QRS. This distinguishing feature is best illustrated within the PURPLE rectangle in the SHS insert in Figure-1. Further support that the ST elevation pattern of SHS is not the result of acute infarction may be forthcoming from atypical distribution of the QRS-ST segment changes on the 12-lead ECG — and lack of the typical evolutionary pattern of ECG changes seen with true STEMI.

Figure-1: Spiked Helmet Sign that is seen in several leads in the 2nd and 3rd ECGs. The insert with the spiked helmet is from Laszlo Littmann’s 2011 Letter to Mayo Clinic Proceedings (See text).

Returning to Figure-1 — a combination of ECG findings may be contributing to the unusual picture we see here, especially in the anterior chest leads of ECG #2 and ECG #3. These include:
  • The Spiked Helmet Sign in leads V2 and V3 of ECG #2 — and in lead V3 of ECG #3. As I outlined in RED — all 3 components of SHS appear to be present in leads V2 and V3 of ECG #2. As outlined in PURPLE — elevation of the isoelectric baseline before the QRS no longer appears to be present in lead V3 of ECG #3 (which was obtained 20 minutes after ECG #2).
  • Other potential contributing factors complicate interpretation of what we are seeing in ECGs #2 and #3. Perhaps some of the ST elevation we see in lead V1 of ECG #2 might be the result of Brugada phenocopy (which is a common transient cause of a Brugada-1 ECG pattern after cardiac arrest). As I alluded to yesterday in my initial commentary — Osborn waves may produce J-point notching in patients with cardiac arrest. As we later learn — the patient in this case does have WPW — and the 4th ECG that was done (shown above) does reveal definite delta wavesHow much of the elevation before the QRS complex in ECG #2 can be attributed to being a delta wave vs the initial component of SHS is uncertain. I suspect we are seeing a combination of the two. Finally — I suspect the coved ST elevation that we see in all 3 anterior leads (V1, V2, V3) in both ECG #2 and ECG #3 is at least in part the result of the Spiked Helmet Sign — which is resolving in ECG #3 (done 20 minutes after ECG #2), and which is essentially gone by the time the 4th ECG (shown above) is done, which was some time after ECG #3, and just before transfer to the cath lab.

My Final Thought — I won’t overlook the Spiked Helmet Sign again. Given the extended resuscitation efforts described above by Dr. Smith — recognition of this ECG sign was not needed to tell the providers that the patient was “critical” in this case. That said — Awareness and prompt recognition of SHS may be important in selected cases to: i) Alert you to the high probability of mortality unless underlying predisposing factors can be corrected; andii) Explain the bizarre ECG findings on your patient’s tracing.


  1. In your post on the SHS there is a reference to the Circulation article. This states that it is thought to be due to hyperadrenergic tone but then states that there are reports of SHS occuring with stellate ganglion blockade. This doesn't make sense to me - stellate ganglion blockade will decrease sympathetic tone and so I would think that if anything this would get rid of a SHS. Am I interpreting this wrong? Thanks again for posting, as always.

    1. Thanks for your comment. Please take a look at the Addendum that I just now wrote on the Spiked Helmet Sign = SHS (I wrote this today, which was after you had submitted your question). I tried to synthesize my understanding of the proposed pathophysiology for SHS. That said — I agree with your comment. I also don't understand why persistence of Spiked Helmet Sign after stellate block (that should reduce sympathetic tone) would support a hyperadrenergic mechanism for causing SHS. I’ve referred your question to Dr. Adrian Baranchuk (corresponding author of the Circulation article), as well as to Dr. Smith. I’ll let you know their response.

    2. I have just heard back from Dr. Adrian Baranchuk, who co-authored the Circulation manuscript that you reference. He consulted lead author Dr. Derek Crinion. From Dr. Crinion — “Authors of Ref. #2 explain that immediately after the ablation, the patient developed non-sustained PMVT and SHS. They hypothesized that the ablation itself caused acute central sympathetic activation. Within hours the ECG normalized, and the patient had NO further VT or SHS. In the longterm sympathetic blockade would reduce the QT, risk of VA and SHS.” — From Dr. Baranchuk — “Even when counterintuitive, ANS ablation can produce ANS storm.” BOTTOM LINE ( = My Synthesis of the above Comments by Drs. Crinion and Baranchuk) — The fact that stellate ganglion ablation may initially (within the first few hours) precipitate sympathetic “storm”, and that this WAS accompanied by brief appearance right after the ablation of the Spiked Helmet Sign DOES support the theory that a “hyperadrenergic state” IS associated with SHS. But long-term — there is sympathetic blockade which reduces the risk of subsequent PMVT (and hopefully results in improved longterm outcome.


DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

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