Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android

Key Points

  • Consider acute coronary syndrome (ACS) in the initial assessment of all patients presenting with chest pain and/or difficulty breathing.

  • Atypical presentations are common, especially in women, the elderly, and diabetics.

  • Obtain an emergent electrocardiogram in all patients with concern for ACS to rapidly identify ST-segment elevation myocardial infarctions (STEMI).

  • Patients with STEMI require immediate reperfusion therapy with either thrombolytics or percutaneous coronary intervention to salvage the maximum amount of viable myocardium.


Acute coronary syndrome (ACS) encompasses a spectrum of disease that includes unstable angina (UA), non–ST-segment elevation myocardial infarctions (NSTEMI), and ST-segment elevation myocardial infarctions (STEMI). The distinction between the 3 is based on historical factors, electrocardiogram (ECG) analysis, and cardiac biomarker measurements. ACS is the leading cause of mortality in the industrialized world and accounts for more than 25% of all deaths in the United States. More than 5 million patients per year present to U.S. emergency departments with symptoms concerning for ACS, although fewer than 10% will be diagnosed with acute myocardial infarctions (AMI). That said, between 2% and 4% of all patients with ACS are initially misdiagnosed and improperly discharged from the ED, resulting in significant morbidity and mortality and accounting for the leading source of malpractice payouts in the United States.

The pathophysiology of myocardial ischemia can be broken down into a simple imbalance in the supply and demand of coronary perfusion. Atherosclerosis is responsible for almost all cases of ACS. This insidious process begins with the deposition of fatty streaks in the coronary arteries of adolescent patients and progresses by early adulthood to the formation of organized fibro-fatty plaques. As plaques enlarge throughout adulthood, they progressively limit coronary blood flow and may eventually induce the development of anginal symptoms with exertion. In time, plaques can rupture, causing secondary intraluminal thrombus formation and a sudden reduction in coronary perfusion (ie, AMI).

UA is a clinical diagnosis that has no pathognomonic ECG findings or confirmatory elevations in cardiac biomarkers. Patients with classic anginal symptoms that are either new, accelerating in frequency or severity, or that occur without exertion are considered to have UA. UA and NSTEMI are very similar from a pathophysiologic standpoint with the latter being distinguished by the presence of elevated cardiac biomarkers. Both conditions arise from the non-complete occlusion of coronary blood flow with the secondary development of ischemia and infarction, respectively. Complete occlusions of the coronary arteries typically result in transmural infarctions of the myocardium with associated ST segment elevation (STEMI) on the ECG and increased biomarker levels. Of note, the mortality rates of patients with NSTEMI and STEMI are identical at the 6-month follow-up point.

It is very important to understand the basic anatomy of the coronary arteries to identify concerning ECG patterns and predict clinical complications. The left coronary artery (ie, left mainstem artery) arises from the aortic root and branches almost immediately ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.