Syncopal Home Runs

Last week we talked about reasons that the Quick Six ECG view sucks.  The Quick Six view only involves the frontal leads – I, II, III, aVR, aVL, and aVF.  It leaves off half of the ECG, and the ignored half has a lot of important information.  One of the scenarios last week concerned syncope.  There are three pathologies to specifically rule out when you are taking a syncope ECG.  Remember the Two Rules of EMS.  Rule Two is “Look Cool.”  Finding one of these three pathologies is an incredible way to look cool.  It is the EMS equivalent of Babe Ruth pointing to the right field bleachers and then smashing a ball there.

By Charles M Conlon, Public Domain, via Wikimedia Commons

Consider something like last week’s scenario: It is a hot summer day when you respond to a city park for a 22-year-old male soccer player who fainted.  He is in good shape, feels fine now, and doesn’t really want to make a federal case out of things.  He asks that he just rest in the shade with plenty of water.  His vital signs include a blood pressure of 116/72, heart rate of 96, and a respiratory rate of 18.  What do you need to look for and rule out on an ECG? 

First, there are the obvious points, specifically acute ischemia and arrhythmias.  Finding new-onset atrial fibrillation can easily explain syncope, as can ventricular tachycardia, supraventricular tachycardias, and bradyarrhythmias.  Ischemia and infarction should be our bread and butter and should be found when present.  Finally, anything unusual should be noted.  “Unusual” includes big-assed T waves from hyperkalemia, new bundle branch blocks in patients that shouldn’t have bundle branch blocks, and those kinds of findings.  But this post is about three ECG findings that require the precordial leads to find and diagnose.

Brugada Pattern or Brugada syndrome is the finding that I mentioned in passing last week.  It is a genetic disease that has an increased risk of ventricular tachyarrhythmias and sudden cardiac death.  I’m not going to get into all of the genetic information – if you care about that kind of thing, you’re probably the kind of person who can look up the information without my help.  The specific pathogenesis hasn’t been well-established, either.  It seems to be related to right ventricular abnormalities and/or sodium channel weirdness.

I remember that the disease is much more prevalent in men compared to women, and is more common in people of Asian descent.  I even remember being told that southeast Asian males from traditional cultures would go to bed wearing dresses so that the evil spirits that kill men in the night wouldn’t find them – but I can’t find a citation on that information.  It is probably not true, but makes things easier to remember.  The only times I have seen it in reality the dudes involved weren’t visibly Asian. 

Brugada pattern ECGs are pretty simple – right bundle branch block or incomplete RBBB patterns in the septal leads with ST elevation.  So let’s work through that.  Septal leads are V1 and V2, but this can continue into V3.  The RBBB pattern is usually RSR’ with a wide QRS, right?  An incomplete RBBB pattern is that RSR’ shape, but barely narrow – like 0.09 or 0.10 seconds.  Anytime a QRS complex is wide (or tall or deep), the ST segment tends to be pushed in the opposite direction from the terminal QRS wave.  So a wide RSR’ pattern should have ST depression; the ST segment should be pushed down, opposite from the upright R’ wave.  But the Brugada pattern doesn’t do that.  It doesn’t do what is expected.  There is an upright R’ wave with ST elevation.  That is what makes it weird, and that is what makes it noticeable.

ST elevation with terminal R waves.

There is a difference between Brugada pattern and Brugada syndrome, by the way.  The Brugada pattern is the ECG findings.  Brugada syndrome is a person with the ECG pattern that suffered a tachyarrhythmia or sudden cardiac death.  The prevalence of Brugada syndrome in patients with the Brugada pattern is not well-established (because it is rare), but a meta-analysis demonstrated a 10% rate of complication at 2.5 years.¹  That means that for every two and a half years that passes, a person has a 10% chance of kicking it.  It is not good.  

One of the coolest stories I have heard concerned two newish paramedics.  They responded to visit with a dude complaining of chronic low back pain.  Picking at the issue, they found that the man’s back hurt due to falling down a lot.  Picking at the falling down thing, they figured out that homeboy kept fainting.  That resulted in an ECG, and that resulted in them recognizing the Brugada pattern.  They took “chronic low back pain guy” to the hospital and called the Brugada.  The nurse blew them off; she even accused them of making up words.  The physician took their ECG, looked at it, slapped the medics high-five, and called cardiology.  It is flat bad-ass to call your shot like that.

The second precordial finding is hypertrophic cardiomyopathy (HCM).  Hypertrophy is thickening.  Cardio- is heart.  Myo- is muscle. And –pathy is bad.  All that means Thick Heart Muscle Badness.  HCM is how it is usually abbreviated.  It is different from more common hypertrophy like left ventricular hypertrophy (LVH) because it doesn't have an obvious cause.  It is the leading cause of sudden cardiac arrest in young athletes.²  The prevalence is 0.2-0.5% of the general population.

The ECG findings concern left ventricular hypertrophy with dagger-like lateral Q waves.  Breaking it down again, LVH involves the number 35.  Find the deepest wave in V1 or V2 and count how deep it is.  Then count the highest R wave in V5 or V6.  Add them together.  If the result is greater than 35mm (in a patient older than 35 years), be suspicious of LVH.  In a patient younger than 35, swap the height numbers to 53mm.  Lateral strain, and an R wave in aVL taller than 12mm helps to confirm LVH.  So find the LVH.  With LVH, look for narrow, sharp, needle-ish Q waves in the lateral leads (I, aVL, V4, V5, and V6).  That’s it.  If you find the LVH and the lateral Qs, speak up about your suspicions regarding hypertrophic cardiomyopathy.

Note the depth of V2 plus the height of V5 is suspicious for LVH.  In addition, the narrow/sharp/dagger-like lateral Q waves increase the suspicion of HCM.

The last syncopal finding to specifically rule out is long QT syndrome (LQTS).  LQTS is a genetic disease found in a patient with a QTc greater than 500ms in the absence of other (correctible) causes*.  There are a few ways to find the QTc.  First, measure the QT from the onset of the QRS complex to the tangent of the T wave.  Apply the Bazett formula (QT in milliseconds divided by the square root of the R-R interval in milliseconds)… Who am I kidding - square roots means there is too much math for EMS professionals in the middle of a call.  We’re busy with a patient and math is dumb.  So forget about that one.  The second method of finding the QTc is to estimate the QTc.  In heart rates under 100 per minute, the QT interval should be less than half the R-R interval.  Does the T wave end before the halfway point of the R-R? 

The final way to find the QTc is to have the computer in the monitor calculate it for you.  It calculates and prints it at the top of every 12-lead.  How’s that for handy?  In order to do that, however, it needs the precordial leads.  The monitor will not calculate intervals without all leads working.  So put the V-leads on the patient.  Normal QTc intervals are under 470ms in males and 480ms in females.  But 500ms is an easier number for me to remember.  If the number at the top of the ECG is bigger than 500, especially in the absence of other obvious causes of long QTc intervals, worry about LQTS.  Simple.  Place the V-leads and read what the monitor prints out. 

Prolonged QT intervals can be caused by a bunch of things.  The four main causes are drugs, electrolytes, CNS pathologies, and ischemia.  In the absence of those causes, congenital LQTS should be on your mind. 

Each one of these three findings needs to be specifically looked for in syncope patients.  The three pathologies are rare, but being able to find one of them would result in potentially saving the patient’s life.  Plus, it makes you look cool.  EMS Rule 2, baby.  But each of these require the precordial leads to be placed.  Do you use them?  Would you have placed the V-leads on the 22-year-old soccer player who fainted on a hot day?  If not, what findings are you missing?  How many opportunities for calling your home run shot have you missed?

1. Gehi AK, Duong TD, Metz LD, Gomes JA, Mehta D. Risk stratification of individuals with the Brugada electrocardiogram; a meta-analysis. J Cardiovasc Electrophysiol. 2006 Jun;17(6):577-583.

2. Maron BJ, Thompson PD, Puffer JC, et al. Cardiovascular preparticipation screening of competitive athletes. Circulation 1996 Aug;94(4):850–856.

*A QT interval is the flat measurement between the onset of the QRS complex and the end of the T wave.  The problem is that as heart rates increase, the QT interval should shorten – that makes sense because the heart has to repolarize and be ready for the next beat.  That has to be done faster at higher heart rates.  So the QTc is the corrected QT interval – corrected to what it would be if the heart rate was 60 beats per minute.