Friday, October 29, 2021

A deadly alcohol binge: a man in his 30s with chest pain and initial high sensitivity troponin I within normal limits

Submitted and written by Emergency Physician Dr. Arjun J V, with some minimal edits by Smith and Meyers

A man in his 30s was rushed into our ED on a Sunday morning with continuous chest pain for 2 hours. The patient was drowsy but following simple commands and was pointing to his left chest where it hurt with a single finger. He said the pain started after he tried to vomit forcefully. He also had the odor of alcohol to his breath. The patient voluntarily told the team he had half a bottle of whiskey the previous night and he was uncomfortable ever since he woke up. He did, however, consume alcohol on a regular basis but never at such high amounts.

The information about the binge drinking made the whole team take a non-urgent approach towards the patient. We took our time to settle the patient into bed, secure IV access and by the time we had a cardiac tracing on the monitor, we had the following vitals: HR - 120 bpm; BP - 100/60 mm Hg; SpO2 - 95% on RA. The patient was given antacids, started on IV fluids including thiamine before getting a 12-lead ECG within 10 minutes of arrival. Our differentials included: ACS, Boerhaave syndrome, Pneumothorax, Pancreatitis & GERD.

The monitor showed upsloping ST segments in II. A 12-lead ECG was immediately obtained: 

Here is the same image processed by "PMcardio" app, which so far seems quite good at improving image quality and resolution:

Interpretation: Sinus tachycardia, with RBBB and LAFB. Concordant STE in V2, V3, I, and aVL. The QRS in V4 is isoelectric, with excessive STE. This pattern in ACS is diagnostic of proximal LAD or even left main occlusion. We have shown perhaps 10-20 cases of this ECG pattern on this blog (see links at bottom)!

The cath lab was activated.

ECG POCUS showed anterolateral hypokinesia with an EF of ~40%. It took a while for the team to understand the gravity of this new information and to expedite the further process.

The patient had HTN and DM but was not taking medications; he also smoked cigarettes for many years.

Meanwhile, the patient dropped his saturation and his SBP tanked to 70. Cardiology was also a bit late as it was a Sunday. The patient was taken to the cath lab approximately 60 minutes after arrival and was found to have a 100% occlusion of LMCA (see image below). Patient’s initial high sensitivity Troponin-I was found to be "negative": 17 pg/mL = 17 ng/L (the reported reference range for this assay is apparently 0-50 pg/mL or ng/L).


The above angiogram shows a 100% occlusion of the LMCA. There appears to be possible minimal flow or reconstitution of the LAD and LCX. 

RCA angiogram (above), showing a grossly patent proximal and mid RCA, but which appears to have some distal obstruction.

After PCI of the LM and IABP, the patient coded in the cath lab and was reverted after 2 DC shocks. After another 3 hours in the ICU, the patient had another cardiac arrest and could not be revived. ECMO was not attempted for unclear reasons.


Young patients and atypical presentations are important reasons for a delay or missed diagnosis of deadly ACS.

ACS with RBBB and LAFB, usually with some LAD distribution ST Elevation, is diagnostic of proximal LAD or even left main occlusion until proven otherwise. The mortality of such an ECG is very high even before arriving at the cath lab. This is perhaps the highest mortality OMI ECG of all.

You cannot simply hope that an initial high sensitivity troponin will help you realize which patients are high risk ACS and which aren't. A small but important percentage of OMI patients arriving soon after onset of symptoms will have an initial high sensitivity troponin within the normal range. When the troponin is negative or minimal, the benefit of reperfusion is maximal.

Follow up your cases, review their angiograms and clinical outcomes.

See 7 more cases of true total Left main occlusion here:

Here is a post on RBBB + LAFB and its significance, with links to many more such cases:

Here is another case of massive OMI in which binge drinking obscured the judgment of some:

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