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.      

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MY Comment by KEN GRAUER, MD (6/27/2020):

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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 Proc: 86 (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 waves. How 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; and, ii) Explain the bizarre ECG findings on your patient’s tracing.

Intermittent QRS Widening Without Any History

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MY Comment by KEN GRAUER, MD (6/25/2020):

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I’ve labeled the ECG in Figure-1 as, “The initial ECG in this Case” — as I found this tracing fascinating. Imagine you knew nothing about this patient.

• HOW would you interpret this tracing?
• Is there bundle branch block?
• Are there acute changes?

Figure-1: The initial ECG in this case (See text).

First Impression: The 12-lead ECG and long lead II rhythm strip shown in Figure-1 is difficult to interpret for several reasons:

• There is much baseline artifact (especially for the first few beats in the tracing).
• Some beats are wide — and other beats are narrow.
• Despite marked variation in QRS morphology in several leads — there is only minimal change in QRS morphology in the long lead II rhythm strip.

MY THOUGHTS on ECG #1: To facilitate discussion of the rhythm and 12-lead ECG in Figure-1 — I’ve labeled key findings (Figure-2):

• The underlying rhythm is sinus at ~85/minute. I believe the slight variation in P wave morphology in the long lead II is the result of artifact. The beauty of simultaneous leads — is that P waves marred by artifact in one lead, will often be clearly visible in other leads. Thus, despite not seeing any atrial activity in the long lead II rhythm strip before beats #1-through-5, and before beat #9 — clear presence of normal sinus P waves is seen for all 14 beats on this tracing in other simultaneously-obtained leads (RED arrows in Figure-2).

Figure-2: I’ve labeled key findings from Figure-1 (See text).

The change that occurs in QRS morphology is easiest to appreciate in lead V1 (Figure-2):

Beat #8 in lead V1 is narrow and sinus-conducted.

• Beats #9 and 10 in lead V1 manifest a wide QRS complex, consistent with RBBB (Right Bundle Branch Block) morphology. RBBB produces a “terminal delay” in the sequence of ventricular activation — in which the last part of the heart to be activated is the right ventricle. This results in a terminal R’ deflection in the QRS complex in lead V1, due to travel of the depolarizing waveform to the right.
• Beat #11 in lead V1 is conducted with a normal (narrow) QRS complex.
• PEARL #1: The reason we know that QRS widening of beats #9 and 10 in lead V1 is the result of intermittent RBBB — is that the PR interval remains the same before all 4 beats in lead V1. We’d expect the PR interval prior to the wide beats to be different if the wide beats were PVCs.

It’s a bit more challenging to identify the beats that conduct with intermittent RBBB in other leads.

• PEARL #2: I like to look next at lateral leads. Because RBBB produces a “terminal delay” (ie, of the last part of ventricular activation) — lateral leads I and V6 should show a wide terminal S wave when there is RBBB. Note that a wide terminal S wave is clearly seen for beats #1, 2 and 3 in lead I. In contrast, despite a virtually identical initial QRS deflection for beat #4 in lead I (ie, tiny initial q wave, followed by a slender upright R wave) — beat #4 has no wide terminal S wave. Therefore — beats #1, 2 and 3 in Figure-2 are conducted with RBBB — but beat #4 is conducted normally.
• PEARL #3: Awareness that the initial portion of the QRS complex with RBBB is virtually identical to the initial portion of the QRS complex in sinus-conducted beats without RBBB — is the BEST clue I know to confirm that the reason for QRS widening in Figure-2 is intermittent RBBB conduction.
• Beat #5 is conducted normally. This is easiest to see by looking at lead aVL. Note that the QRS complex of beat #5 in lead aVL is clearly narrow, and lacks a wide terminal S wave. In contrast — the QRS of beats #6 and 7 in lead aVL is wide with a wide terminal S wave — because beats #6 and 7 again conduct with RBBB.
• Finally — beats #12 and 13 are narrow and conducted normally — whereas the last beat in this tracing ( = beat #14) manifests a subtle-but-widened terminal S wave deflection.
• BOTTOM LINE: The underlying rhythm in Figure-2 is sinus. There is intermittent RBBB conduction. Beats #4, 5, 8, 11, 12 and 13 all conduct normally (ie, with a narrow QRS complex). In contrast — beats #1, 2, 3, 6, 7, 9, 10 and 14 are all wide, and conduct with RBBB.
• P.S.: I have seen many cases of intermittent RBBB, in which the conduction defect was seen every-other- or every-third or -forth beat. In such cases, there is a "fixed" interval of time between beats that conduct normally, and those that conduct with RBBB. This allows some predictable amount of time for recovery of right bundle branch conduction properties. In my experience — it is far less common to see random alternation between normal and impaired conduction as we see here (perhaps a result of acute ischemia ...).

WHY is this tracing so challenging to interpret?

As alluded to earlier — QRS morphology in the long lead II rhythm strip does not appreciably change from one beat-to-the-next. The reason for this, is that RBBB is a terminal delay in ventricular conduction — and the terminal portion of the QRS complex in the long lead II rhythm strip is isoelectric!

• The thin, vertical BLUE line in Figure-2 marks the onset of the QRS complex in simultaneously-obtained leads V1, V2, V3 — and in the long lead II rhythm strip below the 12-lead.
• The thin, vertical RED line in Figure-2 marks the end of the QRS complex in these leads. Note in the long lead II rhythm strip how the last part of the QRS complex of beat #10 lies on the baseline. We simply can not reliably determine by looking at lead II alone which beats are narrow and which beats are wide!
• PEARL #4: Comfort in using simultaneously-obtained leads is of invaluable assistance for assessing complex arrhythmias!

Are there any Acute Changes on this ECG?

I thought assessment of QRS morphology of the narrow beats in Figure-2 was unimpressive — and not indicative of acute coronary disease.

• In contrast — the ST segments in leads V2 and V3 are clearly more coved than should be expected with simple RBBB (curved PURPLE lines in these leads). The J-point after the wide S wave in lead I for beats #1, 2 and 3 that conduct with RBBB also appears elevated. This patient had positive troponin values — with high-grade stenosis of the proximal LAD, as well as significant circumflex disease. I thought it of interest that the most suspicious ECG findings for acute coronary disease were found in beats that conducted with RBBB — but not in normally conducted beats.
• NOTE: If interested in review on assessing RBBB for potential ischemic changes — Please check out My Comment in the April 13, 2020 post in Dr. Smith's ECG Blog.

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ACKNOWLEDGMENT: My sincere THANKS to 유영준 (from Seoul, South Korea) for sharing this case with us!

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Diffuse T-wave inversions and a very long QT

This ECG was texted to me and I read it while mountain biking. 

My response was "takotsubo".

ECG 1

There are diffuse T-wave inversions and a bizarre QT interval, very long.
This is very typical of takotsubo.

Aside: I classify takotsubo ECGs into 2 broad categories:
1) ST Elevation which often mimics STEMI
2) T-wave inversion: does not mimic STEMI, but rather mimics NonSTEMI or reperfused STEMI

The next day I texted back to ask what the clinical presentation was, what the echo showed, and what the outcome was.

It turned out that this patient had severe alcoholism, alcohol withdrawal, and seemed to have had an alcohol withdrawal seizure prior to arrival.  His chief complaint was weakness.

Just days before, he had been in the hospital for alcohol withdrawal and had had this ECG:

ECG 2 (this is the first chronological ECG, 3 days before)

This shows both a very long QT and very prominent U-waves.

The patient at that time had suffered several episodes of torsades de pointes.  It turned out that he had a K of 2.5 and Mg of 1.3.  After these were replenished, another ECG was recorded:

ECG 3 (2nd chronological ECG, 2 days before)

Normalized

Case continued:

Electrolytes were normal.

He had a bedside echo with normal function.

His peak troponin was barely elevated at 0.035 ng/mL (99th %-ile URL = 0.030)

So this was not takotsubo.  It was very unlikely to be acute MI.

Here is the final ECG:

ECG 4 (final chronologically)

T-wave inversions still present but not as pronounced.

The etiology of the T-wave inversions was not established.  Perhaps a transient occurrence after a seizure?  Or perhaps this was indeed Wellens' syndrome without a very elevated troponin.  Only an angiogram would show for certain.

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MY Comment by KEN GRAUER, MD (6/22/2020):

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I LOVE this case presented by Dr. Smith — as it touches on a number of important entities in emergency ECG interpretation. I focus My Comment on taking a closer look at these phenomena.

• For clarity — I’ve preserved the numbering of tracings in this case in the sequence in which they are presented.
• The case begins with ECG #1 — that was texted to Dr. Smith (Figure-1).

Figure-1: The initial ECG that was presented in today’s case (See text).

MY THOUGHTS on ECG #1: The rhythm is sinus at ~90/minute. The PR interval and QRS duration are normal. The frontal plane axis is slightly leftward (about -10 degrees). The rest of the tracing is replete with abnormalities!

• As per Dr. Smith — the QT interval is markedly prolonged (it takes up more than 2/3 of the R-R interval).
• There is voltage for LVH — satisfied by Peguero Criteria (ie, sum of deepest S in any chest lead + S in V4 ≥23 [female] or ≥28 [male]). In ECG #1 — the S wave in lead V3 (18) + the S in V4 (13) = 31.
• NOTE: For review of the voltage criteria I favor for the ECG diagnosis of LVH — Please see the Table at the bottom of My Comment in the June 20, 2020 post in Dr. Smith’s ECG Blog.

But the most remarkable finding in ECG #1 is the presence of “Giant” T wave inversion. T wave inversion is seen in every lead except for leads aVR and V1.

• Although some T wave inversion is common in many conditions — the term “giant T waves” is reserved for a select number of clinical entities that produce truly deep (ie, >5-10 mm amplitude) T wave inversion. Depth of the inverted T waves in leads V3 and V4 of ECG #1 exceeds 15 mm!
• PEARL #1 — Truly “giant” T waves are not overly common. When you see them — it is worthwhile to consider the diagnostic entities listed in Figure-2. Without any history — it is impossible to know WHICH of the entities in this list is most likely. Once you know the history — Simply consider these diagnostic possibilities!
• PEARL #2 — It is tempting on seeing the biphasic T wave with steep downsloping terminal component in lead V2 of ECG #1, to think of Wellens’ Syndrome. Wellens’ Syndrome is most probably not present in this case. While an acute ischemic coronary syndrome is a diagnostic possibility (ie, acute ischemia is included among the entities listed in Figure-2) — it is well to remember that there are other causes of the ST-T wave picture that we see in lead V2 of ECG #1. These include (among others) — LVH, cardiomyopathy, coronary reperfusion. In ECG #1 — I suspect the reason for the biphasic T wave in V2 is simply the reflection of the increased QRS and ST-T wave amplitude that we see, with lead V2 representing a “transition lead” placed between the tall positive T wave in lead V1 and the very deep negative T wave in lead V3.

Figure-2: List of diagnostic entities to consider when giant T wave inversion is seen (See text).

The 2nd half of this case covers an equally important series of Learning Points.

• For clarity — I’ve placed the 2nd and 3rd tracings shown in this case together in Figure-3.
• ECG #2 (that is shown in Figure-3) — was obtained during this patient’s previous recent hospitalization, which was for alcohol withdrawal. ECG #2 was obtained 3 days before ECG #1 — and at the time ECG #2 was obtained, the patient had severe electrolyte disturbance (serum K+ = 2.5 mEq/L and serum Mg++ = 1.3 mg/dl).
• Among the other complications of this patient’s alcohol withdrawal during his recent hospitalization — were episodes of Torsades de Pointes and an alcohol withdrawal seizure.
• ECG #3 (in Figure-3) — was obtained 1 day after ECG #2, at which time serum electrolytes had been corrected.

Figure-3: The 2 ECGs shown in this case from this patient’s recent hospitalization (See text).

MY THOUGHTS on ECG #2: As per Dr. Smith — ECG #2 manifests a number of findings characteristic of significant hypokalemia and hypomagnesemia. These include:

• Marked sinus bradycardia and arrhythmia + a PVC (beat #8).
• ST segment flattening in multiple leads, with subtle hint of ST depression in some of these leads.
• Very prominent U waves in multiple leads (colored ARROWS in ECG #2).
• A very long QT interval, that is seemingly further prolonged by prominent U waves that blend in with the terminal portion of the T wave in several leads.
• PEARL #3 — We are told that this patient had several episodes of Torsades that occurred around the time that ECG #2 was obtained. This should not be surprising — since predisposing factors for developing Torsades include: i) Hypokalemia and hypomagnesemia; ii) Marked QT prolongation; and, iii) Marked bradycardia. Each of these factors were probably operative in this patient.
• DID YOU NOTE? — that the U wave that occurs just before the PVC (beat #8) is clearly larger (PURPLE arrows) than all other U waves (BLUE arrows). I have no idea why this is so — but thought it interesting to point out.

MY THOUGHTS on ECG #3: As per Dr. Smith — ECG #3 was obtained after correction of the electrolyte disturbance that was present when ECG #2 was obtained a day earlier. Be SURE to note on comparing ECG #2 with ECG #3 that:

• The rate of the rhythm in ECG #3 is now more appropriate — the rhythm is now regular — and there are now no PVCs.
• The QT interval now looks normal.
• There is now no more than minimal suggestion of tiny U waves (perhaps in leads V3, V4) — but there has clearly been marked reduction in U wave amplitude compared to ECG #2.
• ST segment flattening remains in a number of leads — but the hint of ST depression we previously saw in a few leads has resolved.
• PEARL #4 — The BEST way to get good at recognizing ECG signs of low K+ (and low Mg++) — is to profit from every opportunity you have when you know precisely what the low serum values of these 2 cations were on the initial ECG (in this case, in ECG #2) — WHEN you compare that initial tracing (when serum electrolytes were abnormal) to the ECG obtained after correction of the electrolyte disturbance (as we do in Figure-3).

PUTTING IT ALL TOGETHER in this Case:

The original question posed by assessment of ECG #1 in this case, was WHAT is the likely cause of the “giant” T waves that we see?

• Figure-2 suggests the diagnostic entities to consider.
• Of note — ECGs #2 and #3 (which were done 3 and 2 days before ECG #1) — did not show the picture of “giant” T waves that we see in ECG #1. Therefore — the likely cause would seem to be something that happened during the 2-day interim between when ECG #3 and ECG #1 was done.
• Bedside Echo was normal, and peak troponin was barely elevated — which rules out Takotsubo cardiomyopathy, apical cardiomyopathy and acute ischemia from the list of potential causes in Figure-3.
• I see nothing in the history suggestive of massive acute pulmonary embolism or Stokes-Adams attacks.

By the process of elimination — this leaves us with post-tachycardia syndrome and/or a severe CNS disorder — as the most likely cause(s) of these giant T waves.

• This patient had a number of documented episodes of Torsades during his previous hospitalization. We are told that electrolytes were corrected at the time of his discharge — but I don’t see indication as to what repeat serum electrolytes were at the time ECG #1 was obtained. It would therefore seem possible that serum K+ and Mg++ may have dropped during the 2 days since ECG #3 was done — leading to additional episodes of Torsades that might have been prolonged enough to produce a post-tachycardia “memory” effect after spontaneous resolution.
• We are told this patient had at least one alcohol withdrawal seizure. Severe CNS disorders are notorious for producing markedly abnormal (sometimes bizarre) ST-T wave changes.
• A remarkable feature of the “giant” T waves seen in ECG #1 — is how markedly prolonged the QTc is. Both post-tachycardia syndrome and CNS catastrophes are known for producing this degree of marked QTc prolongation — so either (and/or both) of these disorders may be responsible for the ECG picture we see in ECG #1.