A patient with a ventricular paced rhythm and chest pain

One of my residents who just graduated saw this patient and sent the case:

This 80-something patient presented with chest pain.  He had recently had a pacer placed for complete heart block and had not had an angiogram at that time.  Ischemia had not been suspected.

He had this ECG recorded:
There is sinus rhythm.  There is clearly a DDD pacer that detects the sinus activity and then paces the ventricle (necessary when there is complete AV block).  The pacing is in the right ventricle (all QRS negative in V1-V6, showing that the lead is in the apex of the RV).
There is some concordant ST elevation in aVL (but not 1 mm).  

There is reciprocal ST depression in II, III, aVF.
There is discordant ST elevation [opposite to a negative QRS (i.e. S-wave)] in V1-V5.
The cardiologist interpretation was "concerning for ischemia."
Is it excessively discordant ST elevation?
In V1, the J-point is 4 mm above the PQ Junction and the S-wave is 14 mm:

The ratio is 28%

We do not know for certain what excessive is in paced rhythm.

The Smith-modified Sgarbossa criteria were derived and validated in Left Bundle Branch Block, which is similar to, but not the same as, ventricular paced rhythm.  For LBBB, an ST/S ratio greater than 25% is very specific and sensitive for acute coronary occlusion. 

Can we apply the rule to paced rhythm?

I don't know for sure, but I do it and we are in the middle of a large multi-center study to try to figure it out.

Here it isPaced Electrocardiogram Requiring Fast Emergent Coronary Therapy (PERFECT) Study.   https://clinicaltrials.gov/ct2/show/NCT02765477

Importantly, 50% of physicians who care for patients with chest pain believe that you cannot diagnose STEMI in the presence of paced rhythm. This is definitely not true and an old teaching that should be thrown away.

The emergency physician activated the cath lab.  He writes that "Cardiologist thought you could not see the ischemic changes on paced ECG."

In the meantime, an old ECG was found:
The change is obvious and makes the first ECG diagnostic.
The discordant ST elevation in V1-V3 in this old ECG is proportional.
The patient had an acute 100% LAD occlusion.

Smith EKG lectures next year (2017)…..Schedule

I will be speaking at these conferences next year:

1.  Oregon ACEP's 2017 Annual Conference in SunRiver will be January 28th- February 1st.  https://oregonacep.org/

2. Rocky Mountain Winter Conference on Emergency Medicine:  Please Join Us at the 2017 Rocky Mountain Winter Conference at the Copper Mountain Resort, February 25 to March 1, 2017

3. EM conference in Boise, ID.  June 22, 2017.  Details to be announced.

4. DasSMACC (invited, not yet confirmed): Berlin, Germany, EKG workshop half day.  June 26, 2017.  Social Media and Critical Care.

5. 2017 Controversies and Consensus in Emergency Medicine, September 20-21, Northampton, MA

Non-Vagal Syncope and Saddleback Morphology in V2

This is another case provided by Mustafa Alwan, an internist from Jordan and very talented ECG enthusiast.  He posted it on Facebook EKG Club, and I am reposting with his permission.

This is a 26 year old male who presented after having had 2 episodes of syncope in 1 day.  Both episodes started with palpitations, then dizziness.  He had no family history of sudden death.    

Vital signs: normal 

Initial ECG :
This is suggestive of Type 2 Brugada morphology because of the Saddleback in lead V2
At first glance, the beta angle looks wide.
See this post for a review of Type 2 Brugada.
The method is to draw a line from the peak of the R'-wave down along the downslope of the R'-wave, as shown.  At a point which is 5 mm below the peak, you draw a line across and if the distance to the S-wave is greater than 3.5 mm, it is a wide beta angle.   This is equivalent to a 35 degree angle, or 0.61 radians (calculated as the inverse tangent of 3.5/5, or 0.7).

Dr. Ken Grauer, the ECG master who runs this site: http://ecg-interpretation.blogspot.com/, measured the beta angle here: 

So the beta angle is not wide enough to meet type 2 Brugada morphology criteria

For those wanting more — go to minute 21:19 in Ken's ECG Video on Brugada Syndrome. Here is the link to this specific point in the video — https://youtu.be/h1MhtLMF-7M?t=21m19s 

Type 2 Brugada morphology (in contrast to syndrome) is really quite common, and if you rely on the morphology alone, without the other criteria for syndrome (see below), you will have a lot of false positives.

Diagnosis of Brugada Syndrome requires both:

1. Brugada pattern ECG (either Brugada Type 1, or the newly defined Brugada Type 2 morphology)
Findings may be dynamic and are sometimes concealed; findings may be observed only in certain circumstances such as fever, intoxication, electrolyte imbalance, presence of sodium channel medications/drugs, or vagal stimulation.
2. At least one of the following:
(a) survivor of cardiac arrest,
(b) witnessed/recorded polymorphic ventricular tachycardia (VT),
(c) history of nonvagal syncope,
(d) familial antecedents of sudden death in patients younger than 45 years without acute coronary
(e) Type 1 Brugada pattern in relatives.

This patient only had (c), and no other criteria.

So this ECG did not even meet the criteria for Type 2 Brugada morphology (because the beta angle was too small).  These criteria were developed in a comparison of Brugada syndrome patients with athletes who have an Rsr' saddleback, and they were about 90% sensitive and 90% specific, so they weren't perfect.  

Presumably because this patient had 2 episodes of non-vagal syncope, he was admitted for observation and the admitting cardiologist referred him for Ajmaline challenge test (a sodium channel blocker) in the electrophysiology (EP) lab.

Here is the resulting ECG:
Now there is clearly Brugada morphology.


Does this establish Brugada syndrome?  

One cannot clearly state that there is, or is not, Brugada syndrome due to response to Ajmaline or other Na channel blockers.  One can only risk stratify for future arrhythmic events.

The considerations for ICD implantation are far beyond the scope of this article and all such patients should be evaulated by an electrophysiologist.

Not all emergency and primary care physicians, and even some general cardiologists, recognize these important issues:

This paper (full text) discusses the risk of arrhythmia in patients who have spontaneous vs. drug induced (e.g. ajmaline) type 1 morphology.  If the patient only has a history of syncope (like our patient), the risk of future arrhythmic events is 0.6%-1.9%.  If the patient with only drug-induced Brugada morphology is asymptomatic (unlike this patient), the risk of future arrhythmia is extremely low.

They reference this paper which shows that ICD implantation has a high rate of inappropriate shock and that the ICD's record a low annual rate of dysrhythmia.  

Moreover, the authors of this study, (Outcome After Implantation of a Cardioverter-Defibrillator in Patients With Brugada Syndrome) found that the best cutoff for the beta angle is wider than 35 degrees.  It is 58 degrees, which corresponds to a triangle base width of 8 mm (not 3.5 mm!!).

Here are the latest recommendations from this 2014 publication (full text: HRS/EHRA/APHRS Expert Consensus Statement on the Diagnosis and Management of Patients with Inherited Primary Arrhythmia Syndromes): 

Unfortunately, the situation of our patient is not reflected here:
Symptomatic with drug induced Type 1 ECG, but no family history

Here are the full recommendations:
Class I
  • 1.
    The following lifestyle changes are recommended in all patients with diagnosis of BrS:
    • (a)
      Avoidance of drugs that may induce or aggravate ST-segment elevation in right precordial leads (for example, visit Brugadadrugs.org),
    • (b)
      Avoidance of excessive alcohol intake.
    • (c)
      Immediate treatment of fever with antipyretic drugs.
  • 2.
    ICD implantation is recommended in patients with a diagnosis of BrS who:
    • (a)
      Are survivors of a cardiac arrest and/or
    • (b)
      Have documented spontaneous sustained VT with or without syncope.
Class IIa
  • 3.
    ICD implantation can be useful in patients with a spontaneous diagnostic type I ECG who have a history of syncope judged to be likely caused by ventricular arrhythmias.
  • 4.
    Quinidine can be useful in patients with a diagnosis of BrS and history of arrhythmic storms defined as more than two episodes of VT/VF in 24 hours.
  • 5.
    Quinidine can be useful in patients with a diagnosis of BrS:
    • (a)
      Who qualify for an ICD but present a contraindication to the ICD or refuse it and/or
    • (b)
      Have a history of documented supraventricular arrhythmias that require treatment.
  • 6.
    Isoproterenol infusion can be useful in suppressing arrhythmic storms in BrS patients.
Class IIb
  • 7.
    ICD implantation may be considered in patients with a diagnosis of BrS who develop VF during programmed electrical stimulation (inducible patients).
  • 8.
    Quinidine may be considered in asymptomatic patients with a diagnosis of BrS with a spontaneous type 1 ECG.
  • 9.
    Catheter ablation may be considered in patients with a diagnosis of BrS and history of arrhythmic storms or repeated appropriate ICD shocks.
Class III
  • 10.
    ICD implantation is not indicated in asymptomatic BrS patients with a drug-induced type 1 ECG and on the basis of a family history of SCD alone.
     But what about symptomatic patients with drug-induced type 1 ECG??

A Patient with Vomiting and Abdominal Pain

This patient complained of prolonged vomiting and abdominal pain.
With this history, the ECG is pathognomonic.
What is it?

First, there are narrow J-waves that are similar to Osborn waves.  The temperature was normal.  I am not certain, but I believe these are just exaggerated J-waves with nonspecific etiology.

More importantly, there are large U-waves best seen in leads V3 and V4.    You can also see that lead II has no visible T-wave but only a large U-wave.  (If you look at V3 directly above lead II, you see both a T-wave and U-wave.  If you follow that down to lead II below, you see no T-wave corresponding to the T-wave in V3, only a large U-wave.  This is also true for V5 and V6.)  Thus, what appears to be a long QT interval in these leads is really the QU interval.

This is nearly pathognomonic for hypokalemia.  The K was 2.4 mEq/L.  Magnesium was normal.

An Alcoholic Patient with Syncope

A middle-aged male had sudden syncope.  There was head injury and he was intoxicated with alcohol, but he stated "I've been way more intoxicated than this; I have no idea why I passed out."

He denied any kind of chest discomfort or dyspnea or jaw or shoulder pain or epigastric discomfort.

He was completely asymptomatic.

He had a head CT that was normal, a breath alcohol of 0.10% and had this ECG recorded:

What do you think?

As is very common, the computer did not adequately measure the QT interval.  The computer did find a long QT, but greatly underestimated it.
(See this post, which also links to others: Syncope and Bradycardia)

I showed this ECG to the residents and they could not identify the abnormality.  To me, it shouts in my face "long QT!"  This demonstrates how important experience is to Gestalt, and how, if one does not have that experience, one must force oneself to systematically read the ECG.

You must look at every ECG, and if the QT looks long, then measure it yourself.  A good rule of thumb is that if the QT is more than half the RR interval, then measure it and correct for heart rate.  Importantly, at high heart rates (short RR interval), the half-the-RR rule of thumb tends to label too many QT’s as abnormal. At low heart rates (long RR interval), the rule of thumb tends to label too many as normal.

I measured the QT at 530 ms, which results in a Bazett corrected QTc of 620 ms, and that is how I interpreted the ECG at the time:

Here is the old ECG for comparison:

Since the patient is alcoholic and has a long QT, one must consider hypomagnesemia and hypokalemia.  One must also consider medications, and as it turns out, the patient was on 2 psychiatric drugs which can prolong the QT.

Also, I always give any alcoholic 2 g of Mg if they are sick enough to get an IV, so we administered 2 g Mg.

He was also given IV fluids for possible dehydration.

Another ECG was recorded before the Mg was administered:

Again the QT is not correctly measured by the computer
I get 500 ms, not 467.
The correct QTc would then be approximately 610 ms.

There are also very large inferior T-waves, consistent with inferior hyperacute T-waves.
The patient continued, however, to be asymptomatic, serial ECGs showed no change, and bedside echocardiography showed no wall motion abnormality.
Therefore, I attributed these T-waves to the long QT and not to ischemia

The Mg level returned at 1.3 mEq/L (low but not terribly low, reference 1.4 mEq/L)) and K returned at 3.4 mEq/L (low but not terribly low).  2 g of Mg were administered, and then the patient was admitted, after which he received another 2 g of Mg.

The next AM, the Mg was 2.2 mEq/L and this ECG was recorded:
Near normal QTc

The patient was taken off the QT prolonging medications.

The next AM (1.5 days later) a final ECG was recorded:
The patient still has large T-waves, but the QT is normal


Whether this patient had Torsades de Pointes (due to long QT) as the etiology of his syncope is uncertain, but such a prolonged QTc certainly puts him at high risk.  The longer the QTc, the higher the risk, and that risk gets significant when the QTc is greater than 500 ms and becomes very high risk at 600 ms.

Neither the ED treating resident, nor the inpatient team, saw this long QT.  The inpatient team was skeptical of my manual measurement.  They were going to attribute the syncope entirely to dehydration and alcohol intoxication.  I had to personally consult the cardiologists to redirect the evaluation, even though my formal interpretation stated that the QTc was 620 ms.

Physicians want to believe the computer's inaccurate measurements!

Learning Points:

1.  The computer will not consistently accurately measure a very long QT.
2. Look at every ECG and visually estimate the QTc by using the half the RR interval rule of thumb.
                    --If it appears long, manually measure it yourself!  
3. Correct for heart rate using Bazett’s formula: QTc = QT / √RR  (QT divided by square root of the preceding RR interval)
4. A prolonged QT can make T-waves look very large and unusual
5. Check for QT prolonging medications or drugs.  See these two posts.
6. Check Mg and K, and give Mg to patients who drink ethanol daily.
7. Even obvious very long QT may go unrecognized without systematic interpretation.