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 into the left anterior descending artery (LAD) and left circumflex artery (LCX). The LAD runs down the anterior aspect of the heart and provides the main blood supply to the anterior left ventricle and ventricular septum, whereas the LCX runs in the atrioventricular (AV) sulcus between the left atrium and left ventricle and provides blood to the lateral and posterior regions of the heart. The right coronary artery (RCA) also arises directly from the aortic root. It runs in the AV sulcus between the right atrium and right ventricle and provides blood to the right side of the heart and inferior portion of the left ventricle. The sinoatrial node is perfused by the RCA, whereas the AV node is perfused by a combination of the RCA and LAD in most patients.
Risk factors predictive of underlying coronary artery disease (CAD) have been identified and include age >40 years, male patients or postmenopausal females, hypertension, dyslipidemia, diabetes mellitus, smoking, family history of CAD, truncal obesity, and a sedentary lifestyle. It is important to remember that these risk factors are based on large demographic analyses and cannot be used to predict the presence or absence of CAD in a given patient. Approx-imately half of all patients presenting with ACS have no identifiable risk factors outside of age and sex.
A thorough history is the most sensitive tool for the detection of ACS, and an experienced clinician will always be wary of its variable presentation. Chest pain is the most common presenting complaint. Myocardial ischemia is classically described as pressure-like or squeezing sensation located in the retrosternal area or left side of the chest. Inquire about the quality, duration, frequency, and intensity of the pain. Determine whether there is radiation of pain, associated symptoms, and provoking and palliating factors. Symptoms commonly associated with myocardial ischemia include nausea, diaphoresis, shortness of breath, and palpitations. Anginal pain can radiate in almost any direction depending on the individual patient and the affected region of the heart, but radiation to the shoulder, arm, neck, and jaw is most common. It should be noted that the intensity of pain is not predictive of the overall severity of the myocardial insult, and even minimal symptoms can correlate with significant mortality.
Up to a third of patients with ACS will present with symptoms other than chest pain. Also known as “anginal equivalents,” these presentations further complicate the accurate diagnosis of ACS. Possible complaints include dyspnea, vomiting, altered mental status, abdominal pain, and syncope. Patients at an increased risk of atypical presentations include the elderly, women, diabetics, polysubstance abusers, psychiatric patients, and nonwhite minorities. These patients have a near 4-fold increase in mortality owing to inherent delays in their diagnosis, treatment, and disposition. Always obtain a detailed social history and inquire about any recent and chronic substance abuse. Habitual tobacco use has been proven to be an independent risk factor for CAD, whereas cocaine use can not only induce significant coronary spasm in the acute setting, but also accelerate the atherosclerotic process when chronically abused.
There are no physical findings specific for ACS, and the exam is frequently normal. Obtain a complete set of vital signs and closely monitor unstable patients. Bradycardia is common with inferior wall ischemia owing to an increase in vagal tone, whereas tachycardia may represent compensation for a reduction in stroke volume. Concurrent hypertension increases the myocardial O2 demand and may exacerbate the underlying ischemia, whereas acute cardiogenic shock has an extremely poor prognosis.
Carefully auscultate the heart for any abnormal sounds. Acute changes in ventricular compliance may result in an S3, S4, or paradoxically split S2. The presence of a new systolic murmur may signify either papillary muscle infarction with secondary mitral valve insufficiency or ventricular septal infarction with secondary perforation. Look for signs of acute congestive heart failure (CHF), including jugular venous distension, hepatojugular reflux, and inspiratory crackles. Perform a rectal exam to look for evidence of gastrointestinal bleeding, and document a thorough neurologic exam in patients who may require treatment with anticoagulant or thrombolytic medications.
Obtain a 12-lead ECG immediately on presentation for patients with symptoms concerning for ACS. The emergent identification of a STEMI ensures that definitive therapy can be arranged as quickly as possible to limit further myocardial loss. The use of prehospital ECG analysis has further reduced any delays in appropriate therapy. Keep in mind that a single ECG provides only an isolated snapshot of myocardial electrical activity, and as such, any changes in clinical status should prompt repeat testing. In addition, fewer than half of all AMIs are of the STEMI variety, and ECG interpretation may be completely normal in the setting of NSTEMI or UA. ST-segment elevations suggest the presence of an acute transmural infarction, whereas ST-segment depressions suggest active myocardial ischemia. The morphology of the ST-segment elevations with AMI is typically straight or convex upward (“tombstone”) in appearance, whereas concave ST-segment elevations generally indicate a more benign etiology (left ventricular hypertrophy, benign early repolarization, pericarditis). Concerning ST-segment changes with ACS, whether elevations or depressions, should be seen in a distinct anatomical region with corresponding reciprocal changes (Table 14-1). Additional findings concerning for cardiac ischemia include inverted and hyperacute T-waves (wide-based asymmetric high-amplitude T-waves). Q waves indicative of myocardial necrosis generally appear late in the course of patients with ACS and cannot be relied on in the acute decision-making process.
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