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 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 RA
Breath sounds are clear bilaterally.
BGL: 108
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?
See also:
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!
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!!
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.
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
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
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?
Tom
Tom,
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.
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?
Tom
Tom,
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
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.
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.
Tom
i would be concerned, that the LVH plus the flipped T’s in many leads are often findings of Hypertrophic Cardiomyopathy..
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.
Tom,
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?
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…
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.
LVH and biatrial Hypertrophy would not cause the patient to have slurred speech and changes in mentation.
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.
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
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.
Sorry forgot to add I have seen a similar ECG in a pt in ICU with hypocalcemia secondary to citrate anticoagulation for continuous dialysis.
Any family history of early death, like Brugada?
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 ..
@ 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.
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!
Thanks,
Tom