Electrocardiographic Evidence

Acute coronary syndromes are classified by the initial electrocardiogram (ECG), and patients are divided into three groups: those with ST-elevation myocardial infarction (STEMI), those without ST elevation but with enzyme evidence of myocardial damage (non–ST-elevation myocardial infarction, or NSTEMI), and those with unstable angina. Classification according to the presenting ECG coincides with current treatment strategies, since patients presenting with ST elevation benefit from immediate reperfusion. An ECG in patients with suspected acute coronary syndrome (ACS) should be obtained and interpreted within 10 minutes of presentation.²

Criteria for the diagnosis of STEMI include^1–3:

A number of potential pitfalls can contribute to misinterpretation of the ECG. Many conditions can mimic STEMI and lead to false positives. An early repolarization pattern with ≤ 3 mm ST elevation in leads V₁ to V₃ can be seen in healthy individuals, usually young men. Preexcitation, bundle branch block, pericarditis, pulmonary embolism, subarachnoid hemorrhage, metabolic disturbances such as hyperkalemia, hypothermia, and left ventricular (LV) aneurysm can be associated with ST elevation in the absence of acute myocardial ischemia. On the other hand, some conditions can lead to false negatives, including prior myocardial infarction (MI), paced rhythm, and LBBB when acute ischemia is not recognized. These pitfalls are common in the real world and in large clinical trials. For example, when ECGs from the GUSTO IIB trial were reviewed by expert readers at a core laboratory, 15% of patients with STEMI were found to have been misclassified as NSTEMI, and these patients had a 21% higher mortality rate.⁴

“Nondiagnostic” ECGs are common in the setting of acute MI. Up to 18% of patients subsequently determined to have MI have a normal ECG, and an additional 25% have nonspecific changes. These nondiagnostic ECG findings may be due to occlusion of small vessels only or to insensitivity of the 12-lead ECG to ischemia in the lateral or posterior LV territory. Visualization in the horizontal plane can be extended laterally and posteriorly by the addition of leads V₇ to V₉ and rightward by the addition of V_4R and V_5R. Systematic 15-lead ECG to include V_4R, V₈, and V₉ has been suggested to increase the sensitivity of diagnosing ST elevation from 47% to 59% without decreasing specificity.⁵ In fact, an 80-lead body surface mapping system has been shown to increase sensitivity and specificity of ECG diagnosis of ischemia, but challenges with rapid application at the bedside remain.⁶ If ischemia is strongly suspected, but changes are not seen on standard leads, obtaining an ECG with additional leads should be considered.³

ST-segment depression on ECG identifies patients with ACS at high risk. In the TIMI risk score, which has been shown to predict the likelihood of death and ischemic events, ST-segment changes, along with advanced age and prior coronary artery disease, show the strongest association with severe epicardial disease.⁷

The significance of T-wave changes is directly related to the pretest probability of disease. Large studies in asymptomatic patients show that most T-wave changes are nonspecific. In the coronary care unit, however, 87% of patients with only T-wave inversions across the precordium will have a significant left anterior descending (LAD) coronary artery stenosis by angiography. Among patients presenting to the emergency department with ACS, those with isolated T-wave changes have lower risk than those with ST depression but higher risk than those with a normal ECG.⁸

Cardiac Biomarkers

With cardiac cell death, proteins are released into the blood, and detection of these proteins has played a key role in establishing the diagnosis of ACS, risk stratification, and prediction of outcome. Beginning early in the 1970s, creatine kinase (CK) and its isoenzyme, MB, became the biomarkers of choice to establish myocardial injury and infarction. The sensitivity of CK-MB for diagnosis of MI at 6 hours is 91%, but at 2 and 4 hours, sensitivity is only 21% and 46%.⁹ The poor performance of CK-MB early in the course of MI led to the continued search for biomarkers that could diagnose MI early. Myoglobin was a contender for just such a role, because serum levels increase earlier than CK-MB, but the degree to which early sensitivity is increased is uncertain, and myoglobin lacks specificity.¹⁰

These biomarkers have now been superseded by troponin T and I, parts of the troponin-tropomyosin complex in cardiac myocytes. Troponin elevations are highly specific for myocardial cellular injury, except for infrequent false positives due to fibrin interference or cross-reacting antibodies.¹¹ Troponin is also much more sensitive than CK-MB because of its higher concentration in cardiac muscle; minor cardiac injury can elevate levels.¹¹ Even small increases in circulating troponin values correlate with adverse outcomes in the short and long term.¹¹ In non–ST-elevation ACS, elevated troponin levels not only predict increased risk but also identify the patients most likely to benefit from more aggressive antiplatelet strategies using IIb/IIIa inhibitors, use of low-molecular-weight heparin, and an early invasive strategy with coronary angiography and revascularization when appropriate.³

The challenge for the clinician, and in particular the intensivist, is that while elevation of serum troponin concentration is highly specific for myocardial cell damage, not all of that damage is a consequence of rupture of an atherosclerotic plaque. Other causes of elevated troponin, many of which are common in the intensive care unit (ICU), are listed in Table 28-2.

TABLE 28-2 Nonischemic Conditions Commonly Associated with Elevated Cardiac Troponin

Myocarditis < div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Low Systemic Arterial Blood Pressure Very High Systemic Arterial Blood Pressure Thrombocytopenia Coagulopathy Selective Decontamination of the Digestive Tract Weaning from Mechanical Ventilation Stay updated, free articles. Join our Telegram channel Join Tags: SPEC - Textbook of Critical Care 12 Month Subscription Jul 7, 2016 | Posted by admin in CRITICAL CARE | Comments Off on Biochemical or Electrocardiographic Evidence of Acute Myocardial Injury Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access