ST-elevation myocardial infarction (STEMI) is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent electrocardiographic (ECG) ST elevation and subsequent release of biomarkers of myocardial necrosis (O’Gara). The most important intervention to improve early survival for patients with STEMI presenting within 12 hours of symptom onset is prompt myocardial reperfusion, with a 20% to 25% relative risk reduction with fibrinolytic therapy (FTT). There is a 30% additional relative risk reduction with primary percutaneous coronary intervention (PCI) (Keeley).
The symptoms of myocardial infarction (MI) are varied, with some patients having one symptom and others having multiple. Those presenting with MI, but without chest pain, constitute between 33 to 58% of all MI presentations (Canto). Along with chest pain, other symptoms can include the following:
The presence of atypical symptoms such as shortness of breath, sweating, back pain, fatigue, and nausea make symptom interpretation difficult for those experiencing them (McKee).
Diagnostic ST elevation in the absence of left ventricular (LV) hypertrophy or left bundle-branch block (LBBB) is defined as new ST elevation at the J point in at least 2 contiguous leads of ≥2 mm (0.2 mV) in men, or ≥1.5 mm (0.15 mV) in women in leads V2–V3 and/or of ≥1 mm (0.1 mV) in other contiguous chest leads or the limb leads (Thygesen). The majority of patients will evolve ECG evidence of Q-wave infarction, and ST depression in ≥2 precordial leads (V1–V4) may indicate transmural posterior injury (O’Gara). Transthoracic echocardiography may provide evidence of focal wall motion abnormalities and facilitate triage in patients with ECG findings that are difficult to interpret (O’Gara).
The universal definition of MI includes an elevated level of cardiac troponin (cTn), with signs or symptoms consistent with myocardial ischemia (Thygesen).
In 1965, a new protein constituent of the cardiac myofibrillar apparatus was discovered, which subsequently came to be known as troponin (Ebashi), and in the late 1990s, a sensitive and reliable radioimmunoassay was developed to detect it in the serum (Katus). Since then, the role of cardiac troponins as diagnostic biomarkers of myocardial injury in the context of acute coronary syndrome (ACS) has been well established (Garg). Troponin levels appear in the serum 4 to 10 hours after the onset of AMI (Jaffe), peak at 12 to 48 hours, and remain elevated for 4 to 10 days (Garg).
Cardiac troponin (cTn) is a complex comprising three subunits (Garg):
Troponin I and T isoforms are highly specific and sensitive to cardiac myocytes and, therefore, are known as cardiac troponins (cTn) (Garg). The detection of cTn-I or cTn-T in the bloodstream is, therefore, a highly specific marker for cardiac damage (Ooi).
Even though increased cTn-T levels are highly indicative of a cardiac event, it is still not 100% specific. There are six mechanisms that have been proposed to explain the release of troponin into the bloodstream: normal cell turnover, myocyte necrosis, apoptosis or programmed cell death, proteolytic fragmentation, increased cell membrane permeability and membranous blebs (Garg).
Cardiac biomarkers for diagnosis of AMI have become more and more sensitive in recent decades, but there is still not a perfect test to diagnose AMI. Clinicians need to use every option given to them to quickly and accurately determine what is happening with their patient. Clinical assessment, 12-lead ECG, and cardiac troponin (cTn) I or T form the diagnostic cornerstones of patients with acute onset chest pain (Garg).
Relevant class I recommendations from the 2013 American College of Cardiology Foundation/AHA STEMI guidelines include (1) a 12-lead ECG by EMS personnel at the site of first medical contact (FMC) in patients with symptoms consistent with STEMI; (2) EMS transport directly to a PCI-capable hospital for primary PCI with an ideal FMC-to-device time system goal of 90 minutes or less; (3) for patients initially presenting to a non–PCI-capable hospital, immediate transfer to a PCI-capable hospital for primary PCI, with a FMC-to-device time system goal of 120 minutes or less; and (4) in the absence of contraindications, fibrinolytic therapy for patients at non–PCI-capable hospitals when the anticipated FMC-to-device time at a PCI-capable hospital exceeds 120 minutes because of unavoidable delays (O’Gara).
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Dan Bunker DNAP, MSNA, CRNA—Dan has worked in the healthcare industry for nearly 30 years. He worked as a registered nurse in the Coronary Care ICU for 7 years and was a flight nurse with Intermountain’s Life Flight for nearly 10 years. He has been a Certified Registered Nurse Anesthetist (CRNA) for 11 years working in the hospital settings as well as maintaining his own private practice. In addition, he is a professor in the nurse anesthesia program at Westminster College in Salt Lake City, Utah. He has served in various leadership roles within the Utah Association of Nurse Anesthetists (UANA) and current president-elect.