Endurance athlete presents to EMS with syncope. Is the 12-lead ECG abnormal?

EMS is called to evaluate an unconscious 37 year old male.

En route to the scene dispatch advises paramedics that the patient is now conscious and may have experienced a syncopal episode and seizure-like activity. The spouse believes that the patient may be having a stroke.

On arrival the patient is found lying in bed. He is alert and oriented to person, place and time, but not event.

He appears to be in excellent shape.

The spouse informs the EMS crew that the patient is an endurance athlete who has recently undergone chelation therapy to “clean out his system.” It’s clear this has been a controversial topic their relationship. The spouse is not pleased about it.

She is clearly shaken by what has happened and is particularly concerned that the patient slurred his speech immediately after re-gaining consciousness.

The patient states that he was “worked up for chest pain” about 3 months ago and all tests came back negative. Otherwise he states that he has been healthy. He takes no meds.

Vital signs are assessed.

  • RR: 18
  • HR: 80 R
  • BP: 140/90
  • SpO2: 98% on room air
  • BGL: 108

Breath sounds are clear bilaterally.

The cardiac monitor is attached.


A 12-lead ECG is captured.


The paramedics sit the patient up to check orthostatics. The patient’s eye contact becomes less focused and his speech becomes slurred. He seems weak.

What are your concerns? Is this a normal ECG for an endurance athlete?


There are a few difficulties involved with this case.

First, we have the syncopal episode with possible seizure-like activity and slurred speech.

Second, we have an abormal ECG.

Third, there is a recent history of chelation therapy which may or may not be playing a role in what’s happening.

For any patient who experiences a syncopal episode the ECG should be reviewed for cardiac arrhythmias, ischemia, long or short QT interval, Brugada, ARVD, WPW, and hypertrophic cardiomyopathy.

In the endurance athlete it can be difficult to distinguish between an “athlete’s heart” and hypertrophic cardiomyopathy without the aid of an echocardiogram to examine the exact dimensions and shape of the left ventricle.

To me, this ECG shows atypical left ventricular hypertrophy with a “strain pattern” (or secondary ST-T wave abnormality).

Consider the following graphics.

Leads V1 and V2 show an unusual rSr’ pattern. ST-elevation is present and the degree of ST-elevation appears to be proportional to the depth of the S-wave. Note that the S-wave is “cropped” in lead V3 by the bottom of the ECG graph paper.

Now let’s look at the lateral leads.

Here again we see “T-wave discordance”. In other words, the T-waves are deflected opposite the main deflection of the QRS complex. In addition, the degree of the ST-T wave abnormality is proportional to the size of the QRS complex.

Finally, take a look at the T-waves in the precordial leads.

As the QRS complexes transition from negative to positive in leads V1-V6 the T-waves transition from positive to negative.

If you look at the QRS and T axis at the top of the ECG the QRS axis is 43 and the T axis is 144 which makes the QRS/T angle 101. When the QRS/T angle is ≥ 100 it’s a mathematical representation that, generally speaking, the T-waves are deflected opposite the majority of the QRS complex.

So it’s clear we’re dealing with left ventricular hypertrophy and a strain pattern.

Is it “normal” for an endurance athlete? 


The patient ended up receiving a CT scan of the head at the receiving hospital. A slow venous bleed was discovered. He was transferred to a tertiary care center for more advanced care. The ED physician did not seem particularly concerned about the 12-lead ECG.

Does that mean it was normal for him?

Here’s what electrophysiologist and cyclist Dr. John M had to say:

That ECG is very abnormal. Agree with strain diagnosis. Not only that, but the QRS is notched and fragmented. V1’s pattern along with the prominent p-wave voltage suggests the possibility of an ASD. I would agree with you entirely about the non-benignness of this patient’s syncope, and I would be very interested in the ECHO report.

The best thing the EMS crew did for this patient was take him to the hospital. 

Further Reading

Interpretation of the Electrocardiogram of Young Athletes

Electrocardiographic interpretation in athletes: the ‘Seattle Criteria’ (PDF)

Recommendations for interpretation of 12-lead electrocardiogram in the athlete



  • Christopher says:

    3L shows NSR w/o ectopy. 12L shows early repol and is unsurprising for a 37yo endurance runner. I put the PRi at 0.12 rather than 0.138. It looks short in some of the leads yet normal in some of the others.

    However, I’m most suspicious of an electrolyte abnormality, potentially hyponatremia/hypocalcemia/hypomagnesemia/hypokalemia. The normal BP says he probably isn’t hypovolemic, but instead unable to compensate properly due to electrolyte problems. He hasn’t said anything about palpitations, nor C/P or SOB. I’m still considering a cardiac event though.

    Interesting indeed!

  • Terry says:

    Lay him back down(-: Would like to know what the cardiac monitor looked like when they sat him up? He has peaked p waves–pulmonary HTN?? He has st changes all over the place and an incomplete LBBB and left ventricular hypertrophy. I think he needs his electrolytes checked and to quit the endurance athlete stuff. See what being a workout maniac gets you. Denver 1/2 marathon Oct 17th I’m in anyone else? I will skip the chelation therapy thou!!

  • RoseD says:

    I am seeing right atrial hypertrophy (peaked P waves)and some T wave inversion. I also see ST elevation in V2-V3. I am wondering what type of minerals was used for the infusion during the chelation therapy and perhaps if this is causing an problem.

  • Tom B says:

    Christopher –

    By “early repolarization” do you mean benign early repolarization? Why would that be more common with endurance athletes, just out of curiosity?

    You are wise to consider an electrolyte derangement!


  • Tom B says:

    Terry –

    There was no significant change on the cardiac monitor when the patient was sat up. Pulse rate remained approximately the same although the BP timed out.

    The patient was laid back down! 🙂 Now why would I run a marathon when I own a perfectly good car?


  • Tom B says:

    RoseD –

    You’re right! The P-waves in lead II are classic for right atrial enlargement. In addition, the second half of the P-wave is large and inverted in lead V1, which makes this bi-atrial enlargement.

    Is that significant? Could it help explain the ST-depression and ST-elevation?


  • Christopher says:


    I’d read in a few places that BER was found in higher percentages in athletes and military recruits than in the general populace. Also ECG criteria for LVH and atrial enlargement. A little Googling–now in Real Time(tm)–found some papers on the subject:

    Brady W. Benign early repolarization: Electrocardiographic manifestations and differentiation from other ST segment elevation syndromes. Amer J Emerg Med 1998; 16(6): 592-597.

    Hanne-Paparo N, Drory Y, Schoenfeld Y. Common ECG changes in athletes. Cardiol 1976;61:267.

  • Tom B says:

    Christopher –

    BER is more common in young men, and young men are more likely to be military recruits, that’s for certain!

    Most young men have at least 1 mm of ST-elevation in leads V1-V3. I myself have 2 mm of ST-elevation in leads V2 and V3!

    But is the ST-elevation of BER the same as the ST-elevation of LVH?


  • Christopher says:


    They have different shapes and concordance, it almost looks like he has both variants (right precordials vs left precordials). Although in retrospect the incomplete RBBB riding into the STE in V1-V2 may be what I’m seeing as BER, esp considering the inverted T’s in V5-V6 (which look more LVH). Fun 🙂

  • Bryan L says:

    Are those U waves I see in V2-V4? I suspect hypokalemia. I agree with LVH and atrial enlargement. The STE is most likely a result of the LVH re STEMI mimic.

  • Tom B says:

    Now we’re getting somewhere! LVH is different from BER in that ST-elevation is deflected opposite the main deflection of the QRS complex. Remember that atrial enlargement and ventricular hypertrophy (both right and left) often go together.

    As for the incomplete RBBB, I thought that was interesting as well.


  • Dave B says:

    i would be concerned, that the LVH plus the flipped T’s in many leads are often findings of Hypertrophic Cardiomyopathy..

  • Dave B says:

    just to add, the symptoms could also fit HCM, which affects seemingly young healthy athletes. couple with ecg findings for HCM, i would be very suspicious for this.

  • Dave B says:

    question… i am not sure about this, but i thought that the sharp narrow Q’s in the lateral leads (more so in V5 and V6) are important in distinguishing HCM from LVH with strain… am i off the mark on this?

  • Richard says:

    Electrolyte imbalance would be a a problem, but the enlargement could be from the remodeling in his ventricles and atria from his athletic training.

  • lvh strain pattern-ish in right precordials but no such proportionality in left precordials…

  • Balsac says:

    Now what if you were to transport this patient to the hospital and his ST elevation was found to be an acute MI despite all the LVH and BER Ect… could the physician be upset that the patient was not called in as a STEMI?

  • Chris beat me to it, electrolyte abnormality seems very likely in an otherwise healthy, asymtomatic male.

  • RoseD says:

    LVH and biatrial Hypertrophy would not cause the patient to have slurred speech and changes in mentation.

  • Ian says:

    Hypertrophy is not all that uncommon in athletes especially males. It does look as if there may be a bundle branch block. There also seems to be a rise in incidence from SCD in athletes.

  • gordon says:

    slurred speach could be from ventrical tacicardia i seen a few cases wre the electrolites were low and caused the same simptoms if he sat up n had no problem has to lie in the form of heat exhaustion and electrolite reduction requiring electrolite therapy both oraly and interneinus

  • Curse says:

    This ECG, coupled with the particularly pertinent history of chelation therapy are highly suggestive of hypocalcemia – plus or minus hypo other key electrolytes. The ST changes and evolving LBBB are the two key factors for me here. There is definite R atrial enlargement and probable L atrial enlargement as suggested by the notched P waves – although they are not overly widened. There is also definite LVH. The biatrial enlargement and LVH would not particularly concern me in an obviously fit pt with a history of endurance athletics as it is probably due to a heart as big and muscular as the rest of him. This is all semantics though until in hospital blood results are obtained.

    Prehospital treatment should be symptomatic. I would however have a lower than normal threshold for administering calcium and possibly potassium and magnesium early if this pt went into cardiac arrest as per ALS guidelines.

  • Curse says:

    Sorry forgot to add I have seen a similar ECG in a pt in ICU with hypocalcemia secondary to citrate anticoagulation for continuous dialysis.

  • Mark says:

    Any family history of early death, like Brugada?

  • Hillis says:

    The 12 lead ECG shows sinus rythm , but the peak of P wave is larger than normal, theoretically could be due to right atrial hypertrophy .. Left axis deviation with signs of left ventricualr hypertrophy, the T wave inversion in the lateral leads in normal finding in LVH. QT/Qtc is within the normal ranges , PR also seems not to be prolonged..
    I would suggest to perform ECHO as soon as possible to check the severity of LVH and to estimate the LVEF which could be the reason of his complain.. Of course i can’t rule out electrolyte abnormality thu is not so evidence in his ECG !!
    Interesting case ..

  • Curse says:

    @ Hillis. How do you get left axis from that? Axis appears normal to me. I do agree though that the ST changes do fit with LVF with strain pattern.

  • Tom B says:

    I appreciate everyone’s comments and I apologize that I don’t have the time to address all of them individually at the moment.

    The conclusion to the case is now posted!



  • Chris says:

    By the patient’s clinical history (aposidirosis treatment) And ECG (sokolow crtiteria -LVH and Pwaves in II lead -atrial hypertrophy)conclude that the patient could be suffering from “myocardiopathy” from excesive FE that could result in ‘VENTRICULAR ARRYTHMIA’

  • Interesting case by Tom from 2010, that I am only now seeing — because it has been posted on the EKG Club. VERY interesting case as described above! I will make a few comments that provide a somewhat different perspective than comments made above. I would think it unlikely that this ECG had a direct effect on this 37yo man’s syncope — but it definitely IS possible — for example, this ECG is clearly potentially consistent with HCM ( = Hypertrophic CardioMyopathy) — and when marked and obstructive in form, HCM may be associated with syncope.

    I would interpret this ECG a bit differently …. There is ECG evidence of biatrial abnormality (tall, peaked and pointed P waves in each of the inferior leads — with P wave amplitude >2.5mm = RAA — and deep negative component to the P wave in lead V1 consistent with LAA). QRS amplitude is markedly increased. It’s hard to determine the exact measurement — but R wave amplitude in V5,V6 looks to be >25-30mm — and the deep S in V3 is cut off from the bottom of the paper. There is an rSr’ in V1,V2. While possible that these leads could have been placed a bit high on the chest — I suspect lead placement is appropriate. Of note, the r’ in both V1 and V2 descends VERY steeply — which is common and normal for athletically inclined individuals. This is therefore NOT a saddleback Brugada-2 pattern. One should also note the presence of septal q waves in all lateral leads, as well as a bit more of an initial r wave in V1,V2 than is typically seen — findings which CAN be consistent (though definitely not diagnostic) with HCM.

    Finally — the ST-T waves are clearly abnormal. But the point I would emphasize is that the shape of the ST-T depression that we see in lateral leads is NOT “typical” for LV “strain”. Instead, we lack the slowly gradual down sloping of the ST segment in V5,V6 — AND — the T wave inversion is symmetric inV5,V6. In addition, shape of the J-point junction with the beginning of the ST segment is just atypical for what one usually sees when there is pure strain. This is not to say that this 37yo man might not have marked LV thickening — but it IS to say that this is not a typical pattern for simple LVH and strain. In support of this atypical appearance for simple LV “strain” — is shape of the ST-T wave in all limb leads, and the unusual “take-off” appearance in V1,V2,V3 as well as in V4,V5 … Possible reasons that might account for the findings on this ECG include: i) HCM (as mentioned above); ii) ST-T wave Repolarization abnormality (which is my guess!); iii) cardiac ischemia (less likely I think, but there IS ST elevation in V1-thru-V4); and/or iv) Some combination of any or all of these, quite possibly with associated increased LV dimensions. While ASD should always be considered whenever you see an rSr’ pattern in V1,V2 — my guess is that other entities are responsible for these ECG findings. BOTTOM LINE: It’s good that this patient got to the hospital. Clinical correlation plus Echo should prove invaluable for rapidly telling us what this ECG is most likely to represent. Great ECG for discussion! — 🙂

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