Please enjoy our first entry in a series of clinical topics of importance submitted by EPPA’s Director of Quality; Dr. Peter Currie. In these posts, we’ll unpack a particular clinical topic in detail. Our first post focuses on one of the most common, often complex and always tense situations in the emergency department – chest pain. In particular, we’ll discuss cardiac enzyme tests and their somewhat confusing interpretation. We hope this series will illuminate topics our scribes work with every day and help other readers better understand the complexities of medical discourse. Enjoy.
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When we are evaluating a patient with chest pain, there is a “trifecta” of deadly conditions that we are primarily concerned with: acute coronary syndrome (compromised blood flow to the heart), pulmonary embolism (blood clot in the lung), and aortic dissection (tear in the wall of the aorta). The heart is a large muscular pump and it requires blood flow from coronary arteries to feed its work. Acute coronary syndrome (ACS) is a constellation of conditions resulting from complete, partial, intermittent, or threatened disruption in coronary artery blood flow. The most immediate and life-threatening is ST-elevation myocardial infarction (STEMI); this is the “big one” that is diagnosed by EKG and results in the patient going immediately to the cath lab (angiography suite) with an interventional cardiologist for an angiogram and, often, a stent. Another immediately concerning category of ACS is Non-ST elevation myocardial infarction (NSTEMI), essentially when there is cardiac damage but a normal or non-diagnostic (no ST-elevation) EKG. NSTEMI is diagnosed, or excluded, with the use of cardiac enzymes which are blood tests looking for proteins indicative of cardiac cell death.
Over the years there have been many versions of cardiac enzymes that have come and gone. One after another fell out of favor because they weren’t cardiac specific, meaning that they could be elevated/abnormal for reasons other than ACS, or they weren’t very sensitive in that they took hours/days to become positive or didn’t detect small amounts of cell death. Troponin is a cardiac specific protein but even amongst troponins, all is not equal. Variations of troponins exist and, over the years, the different iterations have become increasingly sensitive which has allowed us to discharge more patients, sooner from the Emergency Department (ED). With modern troponin, we can be confident within hours that NSTEMI is excluded and discharge appropriate patients for follow-up. If enough time has elapsed between the onset of the pain and the patient’s arrival in the ED, a single troponin is often adequate. The idea of “serial enzymes” or “delta troponin” is to check one and then another troponin to increase sensitivity.
But nothing is straight-forward; every positive troponin doesn’t necessarily indicate a primary cardiac problem. There is a concept called “demand ischemia” wherein a non-cardiac condition (sepsis, trauma, etc.) stresses the heart and, often due to underlying but not “obstructive”, coronary artery disease or just a “weak” heart, there is a “leakage” of troponin. As troponin assays have gotten more and more sensitive over the years, the number of these non-cardiac elevations has and will continue to increase. For instance, there is a new generation of high-sensitive troponin in use in Europe, but not yet FDA-approved for use in the United States, that has the promise of incredible sensitivity, potentially allowing us to discharge patients in minutes instead of hours, but also the threat of more and more positive troponins of undetermined significance. So, as with many things in medicine, the landscape is constantly changing with troponins.
Peter T. Currie, MD, FACEP, FAAEM
Medical Director of Quality, EPPA