Tuesday, July 17, 2018

Syncope in a 20-something woman

A 20-something was outside exerting herself.  She states that  it was hot outside and that she was probably dehydrated. At one point, she felt lightheaded and then can't remember anything until waking up in the ambulance.  Her friends saw her lose consciousness and fall on the ground.  She regained consciousness spontaneously before responders arrived. Fire department was on scene first, who noted a cyanotic color to the patient's face.  EMS arrived and also noted cyanotic color which improved en route to HCMC. She denies head pain, neck pain, back pain, abdominal pain or any pain at this time.  There was no nausea or vomiting.

In the ED her exam was normal.  All vital signs were normal, with a pulse of 65.

Here is her ECG:
Computer interpretation: borderline long QT interval
What do you think?

Physician assessment (who apparently took the computer read as truth): "ECG had borderline prolonged QT interval, but otherwise did not have signs of arrhythmia or RH strain (Pulmonary embolism) that would be underlying cause of syncope."

Should we believe the computer's assessment?  Never!  When you have ANY suspicion that the QT is prolonged on visualizing the ECG, you must measure it.  The computer is often wrong.

Here I measure the QT:

One should measure the longest QT of the 12 leads.
I did not do that, but just chose one that looked long
See the 2 black lines at the beginning of the QRS and end of the T-wave.
This measures about 580 ms.
The heart rate is barely above 60, so correction will not change it much.
So this is a dangerously long QT (any corrected QT above 480 - 500 ms is associated with a significant risk of Torsades de Pointes--TdP)

There is actually a second hump on many of the T-waves.  Are these large U-waves?  Perhaps, but either way, it is very abnormal and puts the patients at risk for TdP.

See this post on QT correction: 

QT Correction Formulas Compared to The Rule of Thumb ("Half the RR")

Final physician assessment: dehydration.  The patient was discharged.


Another Emergency physician was later reading the ECGs on the system and putting in final interpretations.  She immediately recognized long QT.  She called the patient back.  The patient was admitted.  

She was on no medications that would prolong the QT.  Her K was 3.4 but the ECG findings persisted after correction.  

Thus, she was diagnosed with long QT syndrome.  The electrophysiologist diagnosed it as "probable type 2" long QT (beyond the scope of this blog post and of my understanding).

Genetic testing was undertaken, results pending.

Nadolol 20 mg prescribed.  It is typical to prescribe beta blockers for congenital long QT, though that depends on the type of congenital long QT.

For more on syncope:  

Emergency Department Syncope Workup: After H and P, ECG is the Only Test Required for Every Patient.....

Comment by KEN GRAUER, MD (7/17/2018):
The KEY to optimal ECG interpretation is to routinely use a Systematic Approach. This case is a perfect example of how easy it is to miss a seemingly obvious finding if one fails to systematically assess each and every tracing encountered. This happened in this case. The computer did not detect QT prolongation. The initial treating physician believed the computer report — and failed to independently assess the QT interval. Perhaps because T waves were indistinct in most leads — it wasn’t until a second physician overread the tracing (after the patient had already been discharged …) that marked QTc prolongation was finally picked up.
  • The 6 key parameters to assess in interpretation of any 12-lead ECG include Rate – Rhythm – Intervals (PR-QRS-QT– Axis – Chamber Enlargement – and QRST Changes for Ischemia/Infarction. Sequentially assessing every ECG for these 6 parameters organizes your approach — speeds up your interpretation (because you are organized) — and avoids missing important findings.
  • As a quick estimate — the QTc is prolonged if the QT interval is clearly more than half the R-R interval. One selects a lead where the limits of the QT interval are clearly defined — and the interval looks to be longest. Ignoring the leads in which the ST-T wave is fairly flat and amorphous — one could select any of the lateral chest leads (we favor lead V4) — which clearly shows marked QT prolongation.
  • In view of this patient’s presentation (ie, exertional syncope), and the fact that mild hypokalemia was not the cause of her ECG abnormalities — the diagnosis of LQTS (Long QT Syndromewas made. Referral to EP Cardiology was appropriate given potential for arrhythmic sudden death if not treated.
As per Dr. Smith — specifics of the diagnosis of LQTS are complex, and beyond the scope of most non-cardiologists. That said, I’ll make the following points:
  • Congenital LQTS is not a common disorder. Yet it is an important entity to be aware of — because it is a potentially lethal disorder that may occur in otherwise healthy young individuals. Think of this possibility in the setting of unexplained syncope. These patients are susceptible to episodes of Torsades de Pointes that are often precipitated by adrenergic stimulation (as occurs with physical exertion or mental or emotional stress).
  • There are a number of forms of congenital LQTS, which are thought to be caused by different ion channel mutations. Clinical and ECG manifestations may differ among the various forms — with the common denominator being QT prolongation not due to other cause. That said, the amount of QT prolongation will not always be marked. In such cases, a high index of suspicion may be needed to make the diagnosis.
  • ECG features may suggest one of the more common types of LQTS. To illustrate this — I have excerpted the picture in Figure-1 from Michael Crawford’s Cardiology Text. My purpose in doing so is not to imply that the non-cardiologist needs to know what the ECG features of LQT1 vs LQT2 vs LQT3 are — but rather that awareness of an ususual QTc morphology may clue you in to the possibility that the patient in front of you may have a form of LQTS.
  • Take another look at the admission ECG for the 20-year old woman in this case (Figure-2, which I’ve placed just below Figure-1). The ECG in Figure-2 lacks the ST depression and usually distinct U wave humps of hypokalemia. Instead, the T wave is almost amorphous in the 6 limb leads — marked by a distinct (and unusual) notch in lead V3 — and a bizarrely-shaped ST-T wave in leads V4, V5, V6. Comparing this ECG with the examples in Figure-1 — I can see why the referring EP Cardiologist thought, “probable Type 2 LQTS”. 
Figure-1: Excerpted from Crawford MH: Current Diagnosis & Treatment Cardiology (4th Edition): McGraw Hill, New York, 2014.  (See text).
Figure-2: Admission ECG for the 20yo woman in this case. (See text).

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