September 21, 2017

Background: Each year approximately 790,000 Americans suffer an acute myocardial infarction (AMI) (Benjamin 2017). Traditional treatment for an acute myocardial infarction has included morphine, oxygen, nitroglycerine and aspirin (MONA) with interventions such as percutaneous coronary intervention providing more definitive management. There has been little data from randomized control studies that supports the use of oxygen in AMI. Recent studies such as the AVOID trial suggest that hyperoxia results in harm while a 2016 Cochrane Review suggest no benefit in supplemental oxygen. (Stub 2015, Cabello 2016). There has, however, not been a large randomized control study comparing supplemental O2 to ambient air with patient centered outcomes until the DETO2X-AMI trial.

November 23, 2015

Background: We have already discussed the value of a good history in assessing patients with chest pain on REBEL EM. What is known about chest pain is that it is a common complaint presenting to EDs all over the world, but only a small percentage of these patients will be ultimately diagnosed with Acute Coronary Syndrome (ACS). This complaint leads to prolonged ED length of stays, provocative testing, potentially invasive testing, and stress for the patient and the physician. For simplicity sake, we will say that, looking at the ECG can make the diagnosis of STEMI. What becomes more difficult is making a distinction between non-ST-Elevation ACS (NSTEMI/UA) vs non-cardiac chest pain. ED physicians have different levels of tolerance for missing ACS with many surveys showing that a miss rate of <1% is the acceptable miss rate, but some have an even lower threshold, as low as a 0% miss rate. Over testing however, can lead to false positives, which can lead to increased harms for patients. In November 2015, a new systematic review was published reviewing what factors could help accurately estimate the probability of ACS.

February 6, 2014

Troponin testing is an important component of the diagnostic workup and management of acute coronary syndromes (ACS). The increasing sensitivity of troponin assays has lowered the number of potentially missed ACS diagnoses, but this has also created a diagnostic challenge due to a decrease in the specificity of the test. From 1995 to 2007, the limit of troponin detection fell from 0.5 ng/mL to 0.006 ng/mL (see below graph). Robert Jesse summed up this frustration with the following quote:
When troponin was a lousy assay it was a great test, but now that it's becoming a great assay, it's getting to be a lousy test.
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