cardiovascular disorders
Overview of Acute Coronary Syndromes (ACS)
Diagnosis of Acute Coronary Syndromes
Serial ECGs Serial cardiac markers Immediate coronary angiography for patients with STEMI or complications (eg, persistent chest pain, hypotension, markedly elevated cardiac markers, unstable arrhythmias) Delayed angiography (24 to 48 hours) for patients with NSTEMI or unstable angina without complications noted above 40 years (younger in patients with diabetes), whose main symptom is chest pain or discomfort. Pain must be differentiated from the pain of disorders such as Overview of Pneumonia , The approach is the same when any ACS is suspected: initial and serial ECG and serial cardiac marker measurements, which distinguish among unstable angina, NSTEMI, and STEMI. Every emergency department should have a triage system to immediately identify patients with chest pain for rapid assessment and ECG. Pulse oximetry and chest x-ray (particularly to look for mediastinal widening, which suggests aortic dissection) is also done. ECG is the most important test and should be done as soon as possible (eg, within 10 minutes of presentation). It is the center of the decision pathway because fibrinolytics benefit patients with STEMI but may increase risk for those with NSTEMI. Also, urgent cardiac catheterization is indicated for patients with acute STEMI but not for those with NSTEMI. 1 mm in 2 or more contiguous leads subtending the damaged area (see figure Acute lateral left ventricular infarction (tracing obtained within a few hours of onset of illness) ). There is striking hyperacute ST-segment elevation in leads I, aVL, V4, and V6and reciprocal depression in other leads. Pathologic Q waves are not necessary for the diagnosis. The ECG must be read carefully because ST-segment elevation may be subtle, particularly in the inferior leads (II, III, aVF); sometimes the reader’s attention is mistakenly focused on leads with ST-segment depression. If symptoms are characteristic, ST-segment elevation on ECG has a specificity of 90% and a sensitivity of 45% for diagnosing MI. Serial tracings (obtained every 8 hours for 1 day, then daily) showing a gradual evolution toward a stable, more normal pattern or development of abnormal Q waves over a few days (see figure Inferior (diaphragmatic) left ventricular infarction (after the first 24 hours) ) tends to confirm the diagnosis. Significant Q waves develop with decreasing ST-segment elevation in leads II, III, and aVF. Because nontransmural (non–Q wave) infarcts are usually in the subendocardial or midmyocardial layers, they do not produce diagnostic Q waves or distinct ST-segment elevation on the ECG. Instead, they commonly produce only varying degrees of ST-T abnormalities that are less striking, variable, or nonspecific and sometimes difficult to interpret (NSTEMI). If such abnormalities resolve (or worsen) on repeat ECGs, ischemia is very likely. However, when repeat ECGs are unchanged, acute MI is unlikely and, if still suspected clinically, requires other evidence to make the diagnosis. A normal ECG taken when a patient is pain free does not rule out unstable angina; a normal ECG taken during pain, although it does not rule out angina, suggests that the pain is not ischemic. If right ventricular (RV) infarction is suspected, a 15-lead ECG is usually recorded; additional leads are placed at V4R, and, to detect posterior infarction, V8 and V9. ECG diagnosis of myocardial infarction is more difficult when a left bundle branch block configuration is present because the ECG changes resemble changes due to STEMI (see figure Left bundle branch block ). ST-segment elevation concordant with the QRS complex strongly suggests MI as does Cardiac markers (serum markers of myocardial cell injury) are Cardiac enzymes (eg, CK-MB [creatine kinase MB isoenzyme]) Cell contents (eg, troponin I, troponin T, myoglobin) These markers are released into the bloodstream after myocardial cell necrosis. The markers appear at different times after injury, and levels decrease at different rates. Sensitivity and specificity for myocardial cell injury vary significantly among these markers, but the troponins (cTn) are the most sensitive and specific and are now the markers of choice. Recently, several new, highly sensitive assays of cardiac troponin (hs-cTn) that are also very precise have become available. These assays can reliably measure troponin levels (T or I) as low as 0.003 to 0.006 ng/mL (3 to 6 pg/mL); some research assays go as low as 0.001 ng/mL (1 pg/mL). Previous, less sensitive cTn tests were unlikely to detect cTn except in patients who had an acute cardiac disorder. Thus, a "positive" cTn test (ie, above the limit of detection) was very specific. However, the newer hs-cTn tests can detect small amounts of cTn in many healthy people. Thus, troponin levels detected with hs-cTn tests need to be referenced to the normal range, and are defined as "elevated" only when higher than 99% of the reference population. Furthermore, although an elevated troponin level indicates myocardial cell injury, it does not indicate the cause of the damage (although any troponin elevation increases the risk of adverse outcomes in many disorders). In addition to acute coronary syndromes, many other cardiac and non-cardiac disorders can elevate cTn levels (see table Causes of Elevated Troponin Levels ); not all elevated levels detected with hs-cTn represent myocardial infarction, and not all myocardial necrosis results from an acute coronary syndrome event even when the etiology is ischemic. However, by detecting lower levels of troponin, hs-cTn assays enable earlier identification of MI than other assays, and have replaced other cardiac marker tests in many centers. Patients suspected of having an ACS should have an hs-cTn assay done on presentation and again 2 to 3 hours later. Troponin should be measured at 0 and 6 hours if a standard cTn assay is used. An hs-cTn level must be interpreted based on the patient's pre-test probability of disease, which is estimated clinically based on Risk factors for ACS Symptoms ECG findings A high pre-test probability plus an elevated level detected with an hs-cTn assay is highly suggestive of ACS, whereas a low pre-test probability plus a normal hs-cTn assay result is unlikely to represent ACS. Diagnosis is more challenging when test results are discordant with pre-test probability, in which case serial hs-cTn assays often help. A patient with low pre-test probability and an initially slightly elevated troponin level detected with hs-cTn that remains stable on repeat testing probably has non-ACS cardiac disease (eg, Heart Failure (HF) , stable coronary artery disease). However, if the repeat level rises significantly (ie, > 20 to 50%) the likelihood of ACS becomes much higher. If a patient with high pre-test probability has a normal troponin level detected with hs-cTn and that rises > 50% on repeat testing, ACS is likely; continued normal levels (often including at 6 hours and beyond when suspicion is high) suggest need to pursue an alternate diagnosis. Coronary Angiography most often combines diagnosis with percutaneous coronary intervention (PCI—ie, angioplasty, stent placement). When possible, emergency coronary angiography and PCI are done as soon as possible after the onset of acute myocardial infarction (primary PCI). In many tertiary centers, this approach has significantly lowered morbidity and mortality and improved long-term outcomes. Frequently, the infarction is actually aborted when the time from pain to PCI is short (< 3 to 4 hours). Angiography is obtained urgently for patients with STEMI, patients with persistent chest pain despite maximal medical therapy, and patients with complications (eg, markedly elevated cardiac markers, presence of Cardiogenic and obstructive shock , acute After initial evaluation and therapy, coronary angiography may be used in patients with evidence of ongoing ischemia (ECG findings or symptoms), hemodynamic instability, recurrent ventricular tachyarrhythmias, and other abnormalities that suggest recurrence of ischemic events. Some experts also recommend that angiography be done before hospital discharge in patients with STEMI who have not yet had angiography who have inducible ischemia on stress imaging or an ejection fraction<40%. Routine laboratory tests are nondiagnostic but, if obtained, show nonspecific abnormalities compatible with tissue necrosis (eg, increased erythrocyte sedimentation rate, moderately elevated white blood cell count with a shift to the left). A fasting lipid profile should be obtained within the first 24 hours for all patients hospitalized with ACS. Cardiac Imaging Tests None using a balloon-tipped Pulmonary Artery Catheter (PAC) Monitoring can be used to measure right heart, pulmonary artery, and pulmonary artery occlusion pressures and cardiac output. This test is not routinely recommended and should be done only if patients have significant complications (eg, severe heart failure, hypoxia, hypotension) and by doctors experienced with catheter placement and management protocols. 