A 20-something woman with cardiac arrest.

The patient is a 20 something female. She is healthy with no known cardiac disease. She was admitted to the neurology department due to headache and vomiting. She was found to have a viral CNS infection. 

A few days into her hospital stay she developed chest discomfort and the following ECG was recorded. 

What do you think? Why such large T-waves?  Are these hyperacute T-waves? Are these ECG changes related to the CNS infection perhaps? What disease processes would you put on your list of differential diagnoses?

When I saw the ECG of this patient I saw that there was definitely something "off". I didn't get the OMI feeling, but I did worry about the T waves. It was hard for me to precisely explain why it did not "feel" like an OMI. 

The ECG below was on file and was taken a few days earlier, on the day of admission to the hospital.

This ECG is relatively normal

Thus, the first ECG above shows clear change from the ECG on admission, with more wide based T-waves inferiorly and laterally. The wider base of the T waves results in QTc prolongation. There is no ST-elevation. There is a massive inverted T wave in lead aVL. The T-waves have more area under the curve than baseline, but don't appear like typical hyperacute T waves. Are you worried about OMI in this case? Is this an inferior OMI with reciprocal T wave inversion i aVL? The chest pain quickly subsided. A troponin was drawn and the patient was put on telemetry monitoring.

I sent the top ECG to Dr Smith with no information and without the baseline ECG. 

His response was:  "I would not call it OMI.  The T-waves have a very wide base, but not a lot of 'bulk.'  This is what T-waves look like when there is a long QT."

During the night, while on telemetry, the patient became bradycardic, with periods of isorhythmic AV dissociation (nodal escape rhythm alternating with sinus bradycardia), and there were sporadic PVCs. In the early morning an increase in PVC frequency was observed and then a sudden tachyarrhythmia appeared. Below are two ECGs from the telemetry monitoring.

The above ECGs show the initiation and continuation of a polymorphic ventricular tachycardia. Polymorphic ventricular tachycardia can be ischemic, catecholaminergic or related to QT prolongation. Polymorphic VT in the setting of long QTc is called Torsades de Pointes, and this again can be acquired or based on inherited long QT syndromes. Common  causes of acquired long QT is electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia) and side effect of certain medications. 

Cardiac arrest was called and advanced life support was undertaken for this patient. The patient was given chest compressions while waiting for the cardiac arrest team to arrive. After about 90 seconds of chest compressions she awoke.  She spontaneously converted (Defibrillation was not performed).  

Smith aside: from morphology alone, it is imposible to diffentiate ventricular fibrillation from Torsades.  In my experience, most interpreters think Torsades when what they are seeing is really VF.  

One of the hallmark difference between the two is that TdP usually is self limited (will convert back to sinus) and VF almost never does so.  The most important difference is that the QT interval on the baseline ECG must be long in order to diagnose TdP. 

Most such rhythms in the setting of ischemia are VF and will not convert without defibrillation.

Case continued

The tachyarrhythmia terminated on its own. At this time the following blood test were available. Troponin I 205ng/L and N-terminal proBNP 2243ng/L

The hand held echo showed a septal and anterior wall motion abnormality. The patient was referred for coronary angiography which did not reveal any atherosclerotic changes. Troponin I peaked at 769 ng/L.  NT-pro-BNP peaked at 4831, consistent with heart failure. A formal echo at the PCI center after coronary angiography revealed a large septal and apical WMA. There was hyperkinesis of the basal segments and findings were interpreted as typical of takotsubo cardiomyopathy. An MRI was deemed unnecessary at the diagnosis of stress cardiomyopathy was concidered certain. The echocardiographic findings normalized within 3 days as did N-terminal proBNP. 

Smith: it is likely that this was myocarditis in this young patient with a serious viral infection. Without an MRI, it is impossible to know.

The morning before the cardiac arrest potassium was 4,3.mmol, magnesium 0,79mmol (laboratory ref value 0,71-0,94) The patient was given magnesium sulfate 10 mmol (2,4g) iv infusion over 10 minutes post ROSC, due to TdP arrest.  A repeat magnesium level was not drawn prior to coronary angiography. Calcium level was normal. There were no clinical reasons to suspect the electrolyte levels to be significantly different at the time of cardiac arrest compared to the measured values

So, this patient experienced a cardiac arrest based on acquired long QT in the setting of takotsubo cardiomyopathy. Electrolytes were normal and she was not given any medications that are known to cause QT prolongation. Even in patients with genetically verified long QT syndrome, the QTc is not always prolonged. Due to the dramatic circumstances with cardiac arrest in the setting of stress cardiomyopathy decision was made to test the patient for long QT syndrome. This was done to rule occult LQTS as a contributing cause of cardiac arrest. She did not carry any mutation know to cause long QT syndrome. The patient did well. Below is the ECG one month after discharge. Echo revealed normalized function. 

 

Learning points: 

1. To the uninitiated, long QT T-waves may appear like hyperacute T-waves 

2. Takotsubo cardiomyopathy is not a completely benign disorder. 

3. Long QT syndrome may have normal QTc on the ECG. 

See this comprehensive post on PMVT:

Polymorphic Ventricular Tachycardia

https://www.sciencedirect.com/science/article/pii/S1109966623001033

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MY Comment, by KEN GRAUER, MD (10/18/2023):

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Truly fascinating case by Dr. Nossen! — that I believe raises more questions than it answers. That said — I focus my comment on the development of Torsades de Pointes.

• In Figure-1 — I've labeled the 1st telemetry monitoring tracing in today's case.

Figure-1: The telemetry monitoring tachyarrhythmia ...

MY Thoughts on Today's CASE:

My interpretation of the 1st ECG shown in today's case (knowing only that the patient was a 20-year old, previously healthy woman who was admitted to the hospital for headache and vomiting attributed to a "viral CNS infection") — was that the highly unusual hypervoluminous deeply inverted T waves seen only in leads I and aVL — in association with QTc prolongation (both new findings compared to this patient's admission ECG) — were most likely the result of acute viral myocarditis:

• QTc prolongation was indeed present in this 1st ECG we were shown — though not as marked as is commonly seen with Takotsubo Cardiomyopathy. And localization of the T wave inversion seen to only the high-lateral leads is clearly not the usual picture seen with Takotsubo Cardiomyopathy.
• The above said, as emphasized by Dr. Nossen — Echo and cardiac catheterization were felt sufficiently definitive of the diagnosis of Takotsubo (such that cardiac MRI was not deemed necessary).

The Telemetry Monitoring Tachyarrhythmia in Figure-1:

The above said — regardless of the etiology, the tachyarrhythmia seen in Figure-1 is a picture that must be "ingrained" in the mind of every emergency care provider. A picture tells 1,000 words — and this 3rd ECG that we were shown ( = the first telemetry monitoring rhythm that I show above in Figure-1) is definitive for Torsades de Pointes!

• NOTE: The monitoring system used shows the same beats in both limb leads and chest leads (which is why I used the same numbering in both sets of leads — in which I stopped after beat #10, because the rhythm was deteriorating).
• 
  
• There are 2 sinus beats in Figure-1 — with the rhythm starting only after a presumed P wave in front of beat #1. But we clearly see the sinus P wave in front of beat #3 (RED arrow).
• The definitive diagnosis of Torsades de Pointes is made in Figure-1 — because we see: i) QTc prolongation of sinus-conducted beat #3; ii) Bradycardia (ie, the long R-R interval preceding sinus beat #3) — with bradycardia further predisposing to QTc prolongation of subsequent beats; and, iii) A polymorphic form of VT, here with clear "twisting of the points" (alternating negative — then positive — then negative QRS polarity, depending on which leads you are looking at).

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 #1: It is important to distinguish between PMVT (PolyMorphic Ventricular Tachycardia) vs Torsades de Pointes. This distinction is more than academic — because both treatment and the response to therapy tend 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 — which in today's case was presumably the acute viral infection.
• 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.

PEARL #2: The fact that the patient in today's case is a previously healthy 20-year old woman admitted for an acute viral infection makes an ischemic etiology highly unlikely. Demonstration of a prolonged QTc with sinus-conducted beats confirms the diagnosis of Torsades.

PEARL #3: The clinical reality when one encounters PMVT in practice — is how common it is not to know (or be able to identify) IF the baseline QTc is prolonged or not. It's important to appreciate the above described differences in treatment and outcome between PMVT vs Torsades — because IF the QTc is indeed prolonged, then the PMVT rhythm is Torsades — in which case treatment and the response to therapy may differ than if the rhythm is PMVT without QT prolongation.

• Hopefully, in such cases in which we never get to see if the QTc during the tachyarrhythmia is normal or prolonged — either a baseline ECG and/or additional monitoring of the patient will more clearly reveal QTc duration.
• 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.).
• 
  
• Fortunately in today's case — the patient's episodes of Torsades did not persist after the initial 2.4 g IV dose of Magnesium. Whether resolution of her cardiac issues — recovery from her acute viral CNS infection (ie, CNS disorders may lead to QTc prolongation) — or other factors — account for resolution of the patient's episodes of Torsades is unknown. As per Dr. Nossen — Echo after discharge showed normalization of LV function — and the final post-discharge ECG in today's case (that was shown above) showed normalization of the QTc.