Syncope, History of Coronary Disease, and ST Elevation: Should Medics Activate the Cath Lab?
Limb leads
Precordial Leads
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There is ST Elevation in V1-V3, and in aVL, with reciprocal ST depression in II, III, and aVF. There is also some ST depression in V5 and V6, and ST elevation in aVR. What do you think? |
The medics interpreted the ST elevation, with reciprocal ST depression, as STEMI, and activated the cath lab.
Note that you cannot see the entire QRS on the prehospital ECG. The R-waves in leads II and III are cut off. The S-waves in V1-V3 are cut off. There is likely to be very high voltage that is cut off.
It is important to remember that not all ST elevation with reciprocal ST depression is a manifestation of STEMI. LVH, LBBB, and WPW can all have ST Elevation with reciprocal ST depression. Especially LVH.
On arrival, I looked at the ECG and immediately knew it was a false positive due to LVH.
An ECG was recorded in the ED:
This ECG has similarities to Left Bundle Branch Block (LBBB), but it is NOT LBBB because the QRS is not long enough and there is not enough delay from onset of the QRS to peak of R-wave in lateral leads. Q-waves in V5 and V6, and absence of monophasic R-wave in aVL also argue against LBBB. See more on LBBB and LVH at the bottom of the post.
The cath lab was de-activated.
There was further history:
The patient had not anything to eat or drink all day long and felt subjectively dehydrated. He had been walking much of the day, then went to the bathroom and after urinating became light headed and fell w/ brief loss of consciousness.
There was never any chest pain or dyspnea.
He had a history of CABG and ischemic cardiomyopathy.
A repeat ECG 3 hours later was not different.
Outcome:
The troponins were slightly positive, peaking at 0.52 ng/mL (not consistent with STEMI). Cr. was elevated, consistent with dehydration.
Echo showed:
Thus, there is echo evidence of myocardial infarction (new or old), thought to be old. Syncope could have been vasovagal (neurocardiogenic, triggered by dehydration), but with poor LV function, it could also have been due to ventricular tachycardia. Acute type I MI is much less likely. Troponin elevation is probably due to type II MI: underperfusion in the setting of chronic coronary disease.
The patient refused further investigations and was discharged.
Learning Points:
1. Syncope alone is an uncommon presentation of STEMI. Any ECG finding with ST elevation should be approached with skepticism if there is no chest pain or chest discomfort.
Corollary: It should be very unusual for medics to activate the cath lab for syncope alone, without chest pain, as any associated ST Elevation is likely to be a false positive.
2. LVH is a common cause of false positive ST elevation, and often has reciprocal ST depression.
LBBB has recently been re-defined:
Strauss DG, Selvester RH, Wagner GS. Defining left bundle branch block in the era of cardiac resynchronization therapy. Am J Cardiol. 2011;107(6):927–34.
Here is a quote from the abstract:
“Three key studies over the past 65 years have suggested that 1/3 of patients diagnosed with LBBB by conventional electrocardiographic criteria may not have true complete LBBB, but likely have a combination of left ventricular hypertrophy and left anterior fascicular block. On the basis of additional insights from computer simulations, the investigators propose stricter criteria for complete LBBB that include a QRS duration ≥140 ms for men and ≥130 ms for women, along with mid-QRS notching or slurring in ≥2 contiguous leads. Further studies are needed to reinvestigate the electrocardiographic criteria for complete LBBB and the implications of these criteria for selecting patients for CRT.”
One more very short article with full text:
Int Cardiovasc Res J. 7(2):39-40.LBBB: State of the Art Criteria.
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