Electrocardiographic Diagnosis of Acute Coronary Syndromes (ACS): A Clinical Decision Support Tool for Optimizing Patient Management
Authors: William J. Brady, MD, FACEP, Vice Chairman of Emergency Medicine and Associate Professor of Emergency Medicine, Department of Emergency Medicine; Associate Professor of Internal Medicine and Program Director of Emergency Medicine Residency, Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville, VA; Andrew D. Perron, MD, Assistant Professor of Emergency Medicine, Department of Emergency Medicine; Medical Director, First Med, Department of Emergency Medicine, University of Virginia Health System, Charlottesville, VA; Edward Ullman, MD, Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA.
Peer reviewer: David J. Robinson, MD, MS, Research Director and Assistant Professor, Department of Emergency Medicine, The University of Texas Houston Medical Center; Director, Diagnostic Observation Center, Memorial Hermann Hospital, Houston, TX.
Perhaps no diagnostic procedure performed in emergency medicine or cardiology is as useful, predictive, complex, or as essential for guiding life-saving therapy as the electrocardiogram (ECG). The well-documented benefits of early diagnosis and rapid revascularization for acutely ischemic coronary arteries—whether it be with pharmacological or procedural interventions—in the setting of acute myocardial infarction (AMI) have served to emphasize the critical importance of competency among emergency physicians in electrocardiographic interpretation. Because the emergency physician usually is the first physician to evaluate patients with chest pain, he or she is charged with the responsibility of rapid, accurate diagnosis and appropriate, timely therapy.
Although the ECG has remained a time-honored, diagnostic modality in the practice of emergency medicine for decades, from the perspective of false-positive and false-negative results, the value of the ECG is potentially limited by a number of shortcomings. These include the myriad causes of "normal" and "nondiagnostic" interpretations, the variable manifestations of evolving AMI patterns, the non-ST-T wave elevation AMI, confounding and mimicking patterns, and the isolated acute posterior wall AMI. The presence of left bundle-branch block (LBBB), ventricular paced rhythms (VPRs), and left ventricular hypertrophy (LVH) present additional interpretative challenges.
Complicating these atypical ECG characteristics is the fact that nearly 50% of patients with AMI present to the emergency department (ED) with a normal or nondiagnostic standard 12-lead ECG, although early in the course of hospitalization, up to 20% of these patients will develop changes consistent with transmural injury. Hence, the nondiagnostic, initial ECG may inappropriately reassure the clinician who is evaluating a low-risk patient with an atypical presentation of chest pain; this may lead to discharge from the ED. Accordingly, it should be stressed that in patients with continuous chest pain and an initially unremarkable ECG, serial acquisition of a standard 12-lead ECG at frequent intervals may improve diagnostic accuracy.
With these clinical issues in focus, the authors of this landmark review present a systematic approach for ECG interpretation in the setting of acute ischemic oronary syndromes. To enhance the accuracy of diagnosis, a glossary of characteristic ECGs is included as a clinical decision support tool. Finally, because confirmation of AICS is an indication for prompt therapeutic intervention, a management supplement is included that outlines options for pharmacotherapeutic and procedural interventions for the entire range of AICS, including ST-elevation MI, non-ST elevation MI, and unstable angina.— The Editor
For a PDF copy of the ECG supplement referenced throughout this issue, click here.
Uses of the Electrocardiogram
In the chest pain patient, the electrocardiogram (ECG) is used to help establish the diagnosis of acute ischemic coronary syndrome or, alternatively, some other non-coronary ailment; to select appropriate therapy; to determine the response to ED-delivered treatments; to establish the correct inpatient disposition location; and to predict risk of both cardiovascular complication and death. In the case of AMI with ST segment elevation (STE), reperfusion treatments, such as thrombolysis or angioplasty and other therapies, urgently must be considered. Conversely, in the instance of the chest pain patient demonstrating STE resulting from a non-infarction syndrome, the correct diagnosis must be made not only to offer appropriate management for that particular illness but also to avoid the incorrect application of potentially dangerous therapies such as thrombolysis. The emergency physician also may use the ECG for monitoring response to treatment in the patient with an acute coronary syndrome. For example, thrombolytic therapy has been reported to cause more rapid resolution of STE.
The initial 12-lead ECG obtained in the ED can be a helpful guide for determination of cardiovascular risk and, as such, the choice of in-hospital admission location. Brush and colleagues have classified initial ECGs into high- and low-risk groups.1 The low-risk electrocardiographic group had absolutely normal ECGs, non-specific ST-T wave changes (NSSTTW), or no change when compared with a previous ECG. High-risk ECGs had significant abnormality or confounding pattern, such as pathologic Q waves, ischemic ST segment or T wave changes, LVH, LBBB, or VPR. Patients who have initial ECGs that are classified as low risk have a 14% incidence of AMI, 0.6% incidence of life-threatening complications, and a mortality rate of 0%.1 Patients who have initial ECGs that are classified as high risk have a 42% incidence of AMI, 14% incidence of life-threatening complications, and a mortality rate of 10%.1 Another approach to risk prediction involves a simple calculation of the number of electrocardiographic leads with ST segment deviation (elevation or depression), with an increasing number of leads being associated with higher risk.1 Along similar lines, the clinician also is able to qualitatively predict risk by a summation of the total millivolts of ST segment deviation; once again, higher totals are associated with greater risk.1
Limitations of the Electrocardiogram. From the perspective of the electrocardiographic diagnosis of AMI, the ECG has numerous shortcomings, including the "normal" and "nondiagnostic" interpretations, evolving AMI patterns, the non-STE AMI, confounding and mimicking patterns, and the isolated acute posterior wall AMI. The ECG that provides clear evidence of acute ischemia without obvious infarct—clearly not a diagnostic dilemma—is encountered in approximately 50% of patients found to have myocardial infarction. The remaining patients represent the potential electrocardiographic diagnostic dilemma group. Within this segment of patients, the ECG may be entirely normal, nonspecifically abnormal, or clearly abnormal yet without definitive pathologic STE indicative of AMI. Refer to Table 1 for a review of the electrocardiographic findings in the chest pain patient and the association with ultimate diagnosis.
| Table 1. Electrocardiographic Findings in the ED Chest Pain Patient with Respect to the Final Hospital Diagnosis2 | |||
| Interpretation | AMI | USAP* | Noncoronary Diagnoses |
| Normal | 1% | 4% | 95% |
| Nonspecific | 3% | 23% | 75% |
| Abnormal (not % diagnostic of ACS) | 4% | 21% | 75% |
| Abnormal (changes documented previously) | 7% | 48% | 45% |
| Abnormal (changes not documented previously) | 25% | 43% | 32% |
| Infarction | 73% | 13% | 14% |
| * USAP = Unstable angina pectoris | |||
The ECG may be described as "nondiagnostic" if NSSTTW changes are noted. These nonspecific changes are defined as less than 1 millimeter (mm) ST segment depression (STD), or STE with or without abnormal morphology and blunted, flattened, or biphasic T waves without obvious inversion or hyperacuity. Other electrocardiographic issues that may produce nondiagnostic changes are sinus tachycardia and bradycardia or artifactual issues such as a wandering or irregular baseline. Lee and coworkers noted that adult chest pain patients with nonspecific or other nondiagnostic electrocardiographic features had a relatively low risk of AMI ranging from 3% to 4% but a significant risk of unstable angina, which occurred in approximately one-fifth of all such cases.2 Other investigators have found that approximately 6% of patients with AMI demonstrate a "nonspecifically abnormal" ECG on presentation.
Additionally, it has been shown that over-reliance on a normal or nonspecifically abnormal ECG in a patient with anginal chest pain who currently is sensation-free—either due to spontaneous resolution or medical therapy—should be avoided. Patients with an initially nondiagnostic ECG who later develop AMI during that hospitalization more often are sensation-free or minimally uncomfortable on presentation; these patients also frequently lack a history of ischemic heart disease. Further, the total elapsed time from chest pain onset in patients with normal ECGs does not assist in "ruling out" the possibility of AMI in chest pain patients with a single electrocardiographic observation. Although the negative predictive value of the ECG is quite high, it is not 100%, even up to 12 hours after the onset of the patient’s chest symptoms.4 Once again, the patient’s history of the event is more helpful for determining ED dispostion, particularly so if they are pain-free when the ECG is obtained.
Alternatively, in a somewhat different application of the term, the nondiagnostic ECG initially is encountered in approximately 50% of patients who ultimately are found to have experienced a myocardial infarction. With this use of the descriptor "nondiagnostic," the clinician is referring to the lack of pathologic STE noted on the ECG. Significant STD and/or T wave changes may be seen in these situations—findings certainly suggestive of an active coronary ischemic event.
The electrocardiographic abnormalities associated with AMI may be masked by the altered patterns of ventricular conduction encountered in patients with confounding patterns; classically, these patterns include LBBB, VPR, and LVH. These patterns can obscure and/or mimic the typical electrocardiographic findings of AMI. Common medical opinion holds that the electrocardiographic diagnosis of AMI is at least difficult if not impossible in the presence of such findings when, in fact, this diagnosis is at times straightforward when the physician is aware of the characteristics of these patterns.
Electrocardiographic Abnormalities of Acute Ischemic Coronary Syndromes
The earliest electrocardiographic finding resulting from AMI is the hyperacute T wave (see Figure 1 in ECG supplement), which may appear minutes after the interruption of blood flow; the R wave also increases in amplitude at this stage. The hyperacute T wave, a short-lived structure that evolves rapidly into STE, often is asymmetric, with a broad base; these T waves also are not infrequently associated with reciprocal STD in other electrocardiographic leads. Such a finding on the ECG is transient in the AMI patient; progressive STE usually is the typical pattern encountered. The differential diagnosis of the hyperacute T wave includes transmural AMI, hyperkalemia, benign early repolarization (BER), acute pericarditis, and LVH. (See Figure 2 in the ECG supplement.)
As the infarction progresses, the hyperacute T wave evolves further into the giant R wave (see Figure 3 in ECG supplement), yet another transient structure. The giant R wave is best described as an intermediate electrocardiographic structure, occurring after the development of the hyperacute T wave and before the appearance of typical STE. The giant R wave is formed when the ST segment elevates and combines with the prominent R wave, particularly in the anterior distribution; the giant R wave also has been referred to as a "tombstone" on the ECG. In many instances, this structure is not seen; it usually is very transient in nature and may be missed entirely.
With continued infarction, the ST segment assumes a more typical morphology. (See Figure 4 in the ECG supplement.) The initial upsloping portion of the ST segment usually is either convex or flat; if the STE is flat, it may be either horizontally or obliquely so. An analysis of the ST segment waveform may be particularly helpful with distinguishing among the various causes of STE and identifying the AMI case. This technique (see Figure 5 in the ECG supplement) uses the morphology of the initial portion of the ST segment/T wave (defined as beginning at the J point and ending at the apex of the T wave). Patients with non-infarctional STE (i.e., with early repolarization or LVH-related changes) tend to have a concave waveform morphology. Conversely, patients with STE due to AMI have either obliquely flat or convex waveforms.5 The use of this STE waveform analysis in ED chest pain patients markedly may increase the sensitivity for the correct electrocardiographic diagnosis of AMI. This morphologic observation should be used only as a guideline. As with most guidelines, it is not perfect. The electrocardiographic differential diagnosis of STE is broad (see Figure 6 in the ECG supplement and Table 2), including AMI, bundle-branch block, LVH, VPRs, pericarditis, and left ventricular aneurysm, among many other entities.
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Table 2. Electrocardiographic Differential Diagnosis of ST Segment Elevation |
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Acute myocardial infarction (AMI) |
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Table 3. Electrocardiographic Differential Diagnosis of ST Segment Depression |
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Myocardial ischemia |
Inverted T waves (see Figure 10 in the ECG supplement) produced by myocardial ischemia classically are narrow and symmetric. T wave inversion associated with acute ischemic coronary syndrome is morphologically characterized by an isoelectric ST segment that usually is bowed upward and followed by a sharp symmetric downstroke. The terms coronary T wave and coved T wave have been used to describe these T wave inversions. Prominent, deeply inverted, and widely splayed T waves are more characteristic of noninfarctional, nonischemic conditions such as cerebrovascular accident. (See Figure 11 in the ECG supplement.) Noninfarctional causes of T wave inversion include juvenile T wave patterns, LVH, acute myocarditis, Wolff-Parkinson-White (WPW) syndrome, acute pulmonary embolism, and cerebrovascular accident.
An important subgroup of patients with unstable angina often have deep T wave inversions (see Figure 12 in the ECG supplement, upper panel) in the precordial leads (V1 through V4); the T wave also may be biphasic in this same distribution (see Figure 12 in the ECG supplement, lower panel). The syndrome is important to recognize because it is highly specific for stenosis of the left anterior descending coronary artery with anterior wall AMI as the natural history. This has been termed the left anterior descending T wave, or Wellen’s, syndrome. T wave inversion also may be caused by non-STE infarction and evolving states of STE AMI.
In general, Q waves represent established myocardial necrosis. Q waves alone rarely are the sole manifestation of AMI. Pathologic Q waves may be caused by a previously unrecognized prior infarction, or conversely, a prior myocardial infarction may mask ischemic extension in the same anatomic location. Approximately 10% of healthy young men have Q waves in the inferior leads.5 Q waves usually develop within 8-12 hours after a transmural AMI yet they may be noted as early as 1-2 hours after the onset of complete coronary occlusion. As such, the simultaneous presence of Q waves and STE (see Figure 13 in the ECG supplement) does not preclude consideration of thrombolytic therapy.
Anatomic Location of AMI. It is important to be able to identify the anatomic location of an AMI to estimate the amount of jeopardized myocardium and to determine the relative risk of morbidity and mortality. The extent of myocardial necrosis varies greatly with the site of occlusion and presence of collateral circulation. As an obvious example, a proximal occlusion of the left anterior descending (LAD) artery usually results in much more extensive anterior wall myocardial necrosis than mid-artery occlusion. See Table 4 for a listing of electrocardiographic leads, ST segment finding, and involved anatomic segment of the infarcting heart. Electrocardiographic identification of anterior wall AMI (see Figure 14 in the ECG supplement) is made using the standard precordial leads V1 to V4. If STE occurs in one or more of leads V1 to V4 only, it is termed either anterior or anteroseptal. Extension to the lateral wall (anterolateral AMI, see Figure 15 in the ECG supplement) results in additional STE located in leads I, aVL, V5, or V6.
| Table 4. Electrocardiographic Leads, ST Segment Finding, and Involved Anatomic Segment of the Infarcting Heart | ||
| Anatomic Segment Involved in AMI | Electrocardiographic Leads | ST Segment Finding |
| Anterior Wall of LV* | V1-V4 | Elevation |
| Anterolateral Walls of LV | V1-V6 (± I & AVL) | Elevation |
| Lateral Wall of LV | I & AVL and/or V5 & V6 | Elevation |
| Inferior Wall of LV | II, III, & AVF | Elevation |
| Posterior Wall of LV | V1-V3 // V8 & V9 | Depression//Elevation |
| Right Ventricle | RV4 (or RV1-RV6) | Elevation |
| * LV = Left ventricle | ||
The right coronary artery supplies the AV node and inferior wall of the left ventricle in 90% of patients. The left circumflex artery performs this function in the 10% of patients who have a dominant left coronary artery. Inferior AMIs (see Figure 17 in the ECG supplement) are characterized by STE in at least two of the inferior leads (II, III, and aVF). Patients with inferior wall AMI with electrocardiographic evidence of more extensive infarction, such as reciprocal changes in the anterior precordium, lateral extension with STE in leads V5 and V6, or right ventricular infarction identified by STE in the right precordial lead V4R are at risk of in-hospital mortality.
The term posterior myocardial infarction (PMI) refers to infarction involving the posterior wall of the left ventricle, resulting from occlusion of either the right coronary artery, its posterior descending branch, or less commonly, the circumflex artery. Posterior wall involvement occurs in 15-21% of all AMIs, usually in conjunction with inferior or lateral infarction. (See Figure 18 in the ECG supplement.) PMI can occur as an isolated phenomenon (see Figure 19 in the ECG supplement), but the incidence probably is low. Patients experiencing acute inferior wall AMI with either right precordial (leads V1, V2, and/or V3) STD or posterior lead (leads V8 and V9) STE (see Figure 20 in the ECG supplement), in general have larger-sized myocardial infarctions with lower resultant ejection fractions and higher rates of acute cardiovascular complication and death compared to patients with inferior AMIs without such changes.7
As the standard 12-lead ECG does not include posterior leads, changes associated with necrosis in this region are reflected in the anterior chest leads. These electrodes are opposite rather than adjacent to the site of damage and the changes seen are the reverse of what one would normally expect. Thus, the STE that occurs with PMI becomes STD in the right precordial leads: V1 through V3 (see Figure 20 in the ECG supplement). Abnormalities most frequently are detected in leads V1 and V2, and to a lesser extent in lead V3. Electrocardiographic abnormalities (see Figure 20 in the ECG supplement and Table 5) noted on the standard 12-lead ECG that are suggestive of acute PMI include the following (in leads V1, V2, or V3): 1) horizontal STD; 2) a tall, upright T wave; 3) a tall, wide R wave; and 4) an R/S wave ratio of 1.0 or greater. Further, the combination of horizontal STD with an upright T wave increases the diagnostic accuracy of these two separate electrocardiographic findings. It must be remembered that a dominant R wave, which is in fact an evolving Q wave, takes a number of hours to develop and, therefore, is not frequently seen on the initial ECG. The use of the additional posterior leads, V8 and V9 (see Figure 20 in the ECG supplement), may well confirm the presence of a PMI and are felt to be superior to the findings noted in leads V1 through to V3.
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Table 5. Electrocardiographic Findings of Acute Posterior Wall AMI* |
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Horizontal ST segment depression |
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* In leads V1, V2, or V3 with the exception of the posterior leads V8 and V9 |
The standard 12-lead electrocardiographic findings for right ventricular infarction include STE in the inferior distribution as well as in the right precordial chest leads, particularly lead V1 (perhaps the only lead on the standard ECG that reflects changes in the right ventricle). In the setting of inferior wall AMI, if the degree of STE is disproportionally greater in lead II relative to the other inferior leads, RV infarction also is suggested. At times, co-existing acute posterior wall AMI may obscure the STE resulting from right ventricular infarction in lead V1 as seen in the patient with the acute inferoposterior myocardial infarction with right ventricular involvement. Recordings from leads placed on the right side of the chest are much more sensitive and specific for detecting the changes of right ventricular infarction. The right-sided precordial electrodes are placed across the right side of the chest in a mirror image of the standard, left-sided leads and are labeled V1R to V6R; RV1 to RV6 is another commonly used nomenclature for this lead distribution. The clinician may use either the entire right-sided leads V1R to V6R or the single lead V4R (see Figure 21 in the ECG supplement). Lead V4R (right 5th intercostal space mid-clavicular line), is the most useful lead for detecting STE associated with right ventricular infarction and may be used solely for the evaluation of the possible right ventricular infarction. The STE that occurs in association with right ventricular infarction frequently is quite subtle, reflecting the relatively small muscle mass of the right ventricle; at other times, the STE is quite prominent, similar in appearance to the ST segment changes seen in the standard 12-lead ECG.
Serial Electrocardiography
Nearly 50% of patients with AMI come to the ED with a normal or nondiagnostic standard 12-lead ECG, yet early in the course of hospitalization, up to 20% of these patients will develop changes that are consistent with transmural injury. (See Figure 22 in the ECG supplement.) The nondiagnostic ECG can falsely reassure the emergency physician who is evaluating the low-risk patient with an atypical presentation of chest pain, leading to the release of this patient from the ED. In the patient with continuous chest pain and an initially unremarkable ECG, serial acquisition of a standard 12-lead ECG at frequent intervals may improve diagnostic accuracy. (See Figure 22 in the ECG supplement.) In particular, serial ECGs can identify the diagnostic evolution of STE, identifying a candidate for reperfusion treatment. Serial ECG also may assist the emergency physician with the patient who has both confounding and mimicking patterns (see Figures 23 [LVH], 24 [BER], and 25 [LBBB] in the ECG supplement). For example, the chest pain patient with electrocardiographic LVH will manifest STE; initial diagnostic uncertainly can be addressed using serial ECG—the patient with STE AMI will likely demonstrate progression of the elevation while the non-ischemic individual will reveal a static pattern over the short term in the ED. The serial ECG technique may be accomplished using either frequent applications of the standard 12-lead ECG or computer-assisted ST segment trend monitoring.
Potentially, serial ECGs may provide surveillance of patients coming to the ED with chest pain and a nondiagnostic ECG on presentation.9,10 In the cardiac care unit (CCU) setting, applying ST segment monitoring in the early stages of admission reportedly provided important, additional information not noted on the initial ED ECG.11 In fact, 17% of such patients demonstrated dynamic electrocardiographic change during the initial six hours of CCU monitoring. Such ST segment trend monitoring may provide the earliest evidence of coronary occlusion in patients with preinfarction angina. In addition, such evaluation may provide evidence of painless or silent ischemia. Scientific support for ST segment trend monitoring in the ED is sparse. Fesmire and colleagues applied this technique to 1000 ED chest pain patients;12 serial ST segment monitoring identified an additional 16.2% of patients with myocardial injury who were not identified on the initial ECG. The patient with the confounding ECG also may benefit from this diagnostic technique. The LBBB pattern, a classic confounder to the electrocardiographic diagnosis of AMI, may be further investigated with serial ECG. Fesmire and colleagues encountered five patients with final diagnosis of AMI in the presence of LBBB who demonstrated significant electrocardiographic change during the early phase of ED care and surveillance with frequent serial ECGs.13
Serial 12-lead ECG tracings obtained every 20 seconds, with computer interpretation and comparison, have been developed for the continuous monitoring of the ST segment in patients with AMI receiving thrombolytic therapy. Three-dimensional computer representations allow graphic images of initial occlusion in patients with AMI and subsequent reperfusion. In one series, Krucoff and associates note that angiographically proven reperfusion is detected with a sensitivity of 89% using serial ST segment trend monitoring, with a corresponding specificity of 82%.14 ST segment trend monitoring in multiple investigations has proved to be an effective method for noninvasive evaluation of reperfusion after delivery of thrombolytic therapy.
Additional Lead Electrocardiograms. It has been suggested that the sensitivity of the 12-lead ECG may be improved if three additional body surface leads are employed in selected individuals. Acute posterior and right ventricular myocardial infarctions are likely to be under diagnosed, as the standard lead placement of the 12-lead ECG does not allow these areas to be assessed directly. Additional leads frequently used include V8 and V9 which image the posterior wall of the left ventricle, and lead V4R, which reflects the status of the right ventricle. The standard ECG, coupled with these additional leads, constitutes the 15-lead ECG, the most frequently employed extra-lead ECG in clinical practice. Without doubt, a more detailed description of the extent of the myocardial injury may be obtained if additional leads are used to augment the standard 12-lead ECG in selected patients. The use of the additional leads may not only confirm the presence of AMI but also alter treatment decisions. See Figure 26 A in the ECG supplement for a representative example of a 15-lead ECG in a patient with AMI of the inferior, posterior, and lateral walls, as well as of the right ventricle.
In a study of all ED chest pain patients, one group reported that the 15-lead ECG provided a more accurate description of myocardial injury in those patients with AMI yet failed to alter rates of diagnoses, the use of reperfusion therapies, or disposition locations.15 Looking at a more select population of ED patients, Zalenski and colleageus investigated the use of the 15-lead ECG in chest pain patients with a moderate to high pretest probability of AMI who were already identified as candidates for hospital admission.16 In this 15-lead ECG study, the authors reported an 11.7% increase in sensitivity with no loss of specificity (i.e., no increase in false-positive findings for the diagnosis of STE AMI).16 They concluded that "the findings of ST elevation by use of these extra leads can strengthen the ED diagnosis of AMI on the initial tracing and may provide an indication for thrombolytic treatment."16 They further suggest that leads V8 and V9 are superior for the diagnosis of PMI to the reciprocal STD seen in leads V1 to V3.16
Additional-lead ECGs may produce valuable information about injury, necrosis, and ischemia in carefully selected cases.15,16 Indications to obtain 15-lead ECGs in patients with suspected acute ischemic heart disease include: 1) STD in leads V1 through V3 or suspicious isoelectric ST segments in leads V1 through V3; 2) borderline STE in leads V5 and V6, or borderline STE in leads II, III, and aVf; 3) all STE inferior AMIs (STE in leads II, III, and aVF); or 4) isolated STE in lead V1 or STE in leads V1 and V2. The physician must realize that these indications, despite their apparent clinical utility, remain unproven. Placement of the additional leads comprising the 15-lead ECG are demonstrated in Figure 26 B in the ECG supplement.
Confounding Electrocardiographic Patterns
Left Ventricular Hypertrophy. Electrocardiographic LVH and the related repolarization changes are not uncommonly encountered in the ED chest pain patient. Their presence on the ECG, particularly the repolarization changes that alter the morphology of the ST segment and/or the T wave, may confound the early ED evaluation of the chest pain patient. In patients with LVH, ST segment/T wave changes (see Figure 27 in ECG supplement) are encountered in approximately 70% of cases; these changes result from altered repolarization of the ventricular myocardium17 and represent the new normal for the patient with electrocardiographic LVH. These changes may mask and/or mimic the early findings consistent with acute coronary ischemia (see Figure 28 in ECG supplement); this effect, however, occurs to a lesser extent than is encountered with the LBBB and VPR situations. LVH is associated with poor R wave progression and loss of the septal R wave in the right to mid-precordial leads, most commonly producing a QS pattern. In general, these QS complexes are located in leads V1 and V2, rarely extending beyond lead V3. As predicted by the concept of appropriate discordance, STE is encountered in this distribution along with prominent, "hyperacute" T waves. The STE seen in this distribution may be greater than 5 mm in height and is difficult to distinguish from that associated with AMI. The initial, up-sloping portion of the ST segment/T wave complex frequently is concave in LVH compared to the either flattened or convex pattern observed in the AMI patient. This morphologic feature is imperfect; early AMI may reveal such a concave feature.
Left Bundle-Branch Block. LBBB markedly reduces the diagnostic power of the ECG. The associated—and expected—ST segment and T wave abnormalities of LBBB may mimic both acute and chronic ischemic change, potentially leading the uninformed physician to make an incorrect diagnosis and to institute potentially dangerous therapy. Further, the electrocardiographic abnormalities associated with AMI may be masked by the altered patterns of ventricular conduction encountered in patients with LBBB. Many emergency physicians are of the opinion that the electrocardiographic diagnosis of AMI is virtually impossible in the presence of LBBB. Others believe this diagnosis can be straightforward using established criteria.
In the patient with LBBB, the anticipated or expected ST segment/T wave configurations are discordant, directed opposite from the terminal portion of the QRS complex and called QRS complex-T wave axes discordance.5 (See Figures 29 and 30 in ECG supplement.) As such, inferior and right precordial leads with either QS or rS complexes may have markedly elevated ST segments, which mimic AMI. The lateral leads, with the large monophasic R wave, demonstrate STD. The T wave, especially in the right to mid precordial leads, has a convex upward shape or a tall, vaulting appearance, similar to the hyperacute T wave of early myocardial infarction. The T waves in leads with the monophasic R wave frequently are inverted. Loss of this normal QRS complex/T wave axes discordance in patients with LBBB may imply an acute process, such as AMI. An inspection of the ECG in patients with LBBB must be performed, looking for a loss of this QRS complex vs. ST segment/T wave axes discordance.
Sgarbossa and colleagues have developed a clinical prediction rule to assist with the ECG diagnosis of AMI in the setting of LBBB using specific electrocardiographic findings.18 They analyzed the numerous electrocardiographic abnormalities previously reported as suspicious or diagnostic for AMI in patients with LBBB and identified three criteria that are suggestive of acute infarction. This rule, developed from 131 patients with LBBB and enzymatically proven AMI who were enrolled in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial,18 reported that three specific ECG criteria were independent predictors of myocardial infarction. The ECG criteria (see Figure 31 A in the ECG supplement) suggesting a diagnosis of AMI, ranked with a scoring system based on the probability of such a diagnosis, include: 1) STE greater than 1 mm that was concordant with the QRS complex (score of 5); 2) STD greater than 1 mm in leads V1, V2, or V3 (score of 3); and 3) STE greater than 5 mm that is discordant with the QRS complex (score of 2). A total score of 3 or more suggests that the patient likely is experiencing an AMI based on the electrocardiographic criteria. With a score of less than 3, the electrocardiographic diagnosis is less assured, requiring additional evaluation. Refer to Figure 31 B in the ECG supplement for an example AMI noted in the setting of LBBB.
Subsequent literature has suggested that the Sgarbossa et al clinical prediction rules are less useful than reported.18-20 The first such investigation,19 which applied the Sgarbossa et al18 criteria to patients with chest pain and LBBB in the ED of a North American hospital, found much less promising results—a very low sensitivity coupled with poor interobserver reliability. A second study investigated the diagnostic and therapeutic effect of this criteria; none effectively distinguished the patients who had AMI from those patients with noncoronary diagnoses.20 The authors concluded that electrocardiographic criteria are poor predictors of AMI in LBBB situations and suggested that all patients suspected of AMI with LBBB should be considered for thrombolysis. A third investigation followed just this recommendation—using a thrombolytic agent in all patients with LBBB presumed to have AMI;21 they also reported an alarmingly high rate of inappropriate thrombolysis in chest pain patients with LBBB and presumed AMI (49%). The authors also retrospectively investigated the effect of the Sgarbossa et al criteria on the diagnosis and management.18,21 These investigators, in contrast to the previously noted reports, found significant accuracy using the Sgarbossa et al criteria18—noting approximately an 80% rate of correct diagnosis using the prediction rule. Had the clinical prediction rule been employed, the authors suggest that inappropriate thrombolysis would have been avoided in many instances.
Traditional criteria for administration of thrombolytic agents in the AMI patient most often involve electrocardiographic STE situated in an anatomic distribution; the presence of a new LBBB pattern represents another electrocardiographic criterion for such therapy. This second criterion suggests that appropriate patients with LBBB pattern and a history suggestive of AMI receive a thrombolytic agent if it is not otherwise contraindicated. This approach is perhaps reasonable if the physician has a high suspicion of AMI and is comfortable initiating thrombolysis based solely on clinical information—in other words, an analysis of the patient’s history and physical examination. Physicians, however, may be uncomfortable administering a thrombolytic agent under such circumstances; in fact, patients with electrocardiographic LBBB and AMI less often receive thrombolysis despite an increased risk of poor outcome18,22 and the potential for significant benefit.23 The clinician must realize that of all patients with chest pain, electrocardiographic LBBB pattern without obvious infarction, and clinically presumed AMI, only a minority actually will be experiencing AMI.18 Treating all such patients with LBBB and presumed AMI will subject a number of non-infarction patients to the significant risks and expense of thrombolysis.21
Nonetheless, even if the Sgarbossa et al clinical prediction rule is found to be less useful in the objective evaluation of the ECG in the patient with LBBB,18 the report has merit. It has forced the clinician to review the ECG in detail and cast some degree of doubt on the widely taught belief that the ECG is not useful for diagnosis of AMI in patients with LBBB.
Ventricular Paced Rhythms. As with the LBBB pattern, the right ventricular paced rhythm (VPR) pattern may both mimic and mask the manifestations of acute ischemic coronary syndrome. In VPR, the ventricular depolarization pattern is abnormal, with activation of the ventricles occurring from the right to the left, and resembling a LBBB pattern in part. In the patient with VPR, the ECG records the altered ventricular activation as it moves from right to left, producing a broad, mainly negative QS or rS complex in leads V1 to V6 with either poor R wave progression or QS complexes. A large monophasic R wave is encountered in leads I and aVL and, on occasion, in leads V5 and V6. QS complexes also may be encountered in leads II, III, and aVf. The expected ST segment/T wave configurations are discordant (see Figure 32 in the ECG supplement), directed opposite from the terminal portion of the QRS complex and are similar to the electrocardiographic principles applied in the setting of LBBB. As such, leads with QS complexes may have marked STE, mimicking AMI. Leads with large monophasic R waves demonstrate STD. The T wave, especially in the right to mid precordial and inferior leads, has a convex upward shape or a tall, vaulting appearance, similar to the hyperacute T wave of early myocardial infarction. The T waves in leads with the monophasic R wave frequently are inverted. An inspection of the ECG in patients with VPR must be performed, looking for a loss of this QRS complex/T wave axes discordance. Loss of this normal QRS complex/T wave axes discordance in patients with VPR may imply an acute process.24
Sgarbossa et al published a report detailing the electrocardiographic changes encountered in patients with VPR experiencing AMI25—a report similar to their work in patients with LBBB and AMI. Three electrocardiographic criteria were found to be useful in the early diagnosis of AMI, including: 1) discordant STE of 5 mm or greater; 2) concordant STE of 1 mm or greater; and 3) STD of 1 mm or greater in leads V1, V2, or V3.25 The physician must realize, however, that these ST segment changes are only suggestions of AMI in patients with complicated ECGs; clinical decisions must be based upon an analysis of the clinical history, electrocardiographic results, and in most cases, the results of other investigations such as serum markers, nuclear scans, and echocardiography. Conversely, their absence does not rule out the possibility of AMI. Therapeutic decisions must be made with these caveats in mind.
Figure 33 in the ECG supplement illustrates AMI in the setting of a VPR. This ECG is the second study performed in serial fashion in a chest pain patient with a pacemaker. Note the progressive change noted in the inferior leads with the development of STE.
Non-ST Segment Elevation AMI. It has been reported that total occlusion of the infarct-related artery is uncommon in the early hours after non-STE myocardial infarction (formerly the non-Q wave infarction). When total occlusion is present, perfusion is maintained by collateral vessels. These anatomic findings support the contention that the non-STE infarction often indicates an incomplete ischemic event, with additional myocardium at risk. Patients with non-STE infarction may have transient and nonspecific findings, such as STD or T wave abnormalities in any of the anatomic leads of the 12-lead ECG. Symmetric, convex, downward STD or inverted or biphasic T waves characteristically are seen. Differentiating non-STE anterior AMI from posterior AMI can be difficult. The additional leads V8 and V9 may further assist this differentiation.
Patterns that Resemble Acute Ischemic Coronary Syndromes. Unfortunately, it is not uncommon to find STE on the ECG of the ED chest pain patient; its cause rarely involves AMI.26 The occurrence of numerous other noninfarctional STE syndromes only reinforces the point that STE is an insensitive marker of AMI.27 One prehospital study of adult chest pain patients demonstrated that the majority of patients manifesting STE on the ECG did not have AMI as a final hospital diagnosis; rather, LVH and LBBB accounted for the majority of the cases.6 Further, in a review of adult ED chest pain patients with STE on the ECG, STE resulted from AMI in only 15% of this population; LVH, seen in 30% of adult chest pain patients, was the most frequent cause of this STE.27 These non-infarct STE syndromes are not infrequently misdiagnosed as acute infarction, which then may subject the patient to unnecessary and potentially dangerous therapies and procedures. For example, a report by Sharkey and coworkers noted that 11% of patients receiving a thrombolytic agent were not experiencing AMI.28 The electrocardiographic syndromes producing this pseudo-infarct STE included BER (30%), LVH (30%), and various intraventricular conduction abnormalities (30%).28
LVH, LBBB, and VPR, which also must be considered in the electrocardiographic differential diagnosis of STE, have been discussed in the section concerning confounding patterns. Other such mimicking patterns include BER, acute pericarditis, and left ventricular aneurysm.
The syndrome of BER is felt to be a normal variant, not indicative of underlying cardiac disease. The electrocardiographic definition (see Figure 34 in the ECG supplement) of BER includes the following characteristics: 1) STE; 2) upward concavity of the initial portion of the ST segment; 3) notching or slurring of the terminal QRS complex; 4) symmetric, concordant T waves of large amplitude; 5) widespread or diffuse distribution of STE on the ECG; and 6) relative temporal stability.5
The STE begins at the "J" (or junction) point—the portion of the electrocardiographic cycle where the QRS complex ends and the ST segment begins. The degree of J-point elevation usually is less than 3.5 mm. This STE morphologically appears as if the ST segment has been evenly lifted upward from the isoelectric baseline at the J point. This elevation results in a preservation of the normal concavity of the initial, up-sloping portion of the ST segment/T wave complex, a very important electrocardiographic feature used to distinguish BER-related STE from STE associated with AMI. The STE elevation encountered in BER usually is less than 2 mm but may approach 5 mm in certain individuals. Eighty to ninety percent of individuals demonstrate STE of less than 2 mm in the precordial leads and less than 0.5 mm in the limb leads; only 2% of cases of BER manifest STE of greater than 5 mm. The degree of STE related to BER usually is greatest in the mid- to left precordial leads (leads V2 to V5). The ST segments of the remaining electrocardiographic leads less often are elevated to the extent observed in leads V2 through V5. The limb leads (I, II, III, aVl, and aVf) less often are observed to demonstrate STE; one large series reported that the limb leads revealed STE in only 45% of cases of BER. "Isolated" BER in the limb leads (i.e., no precordial STE) is a very rare finding. Such "isolated" STE in the inferior (II, III, and aVf) or lateral (I and aVl) leads should prompt consideration of another explanation for the observed ST segment abnormality.
Acute pericarditis produces diffuse inflammation of the superficial epicardium, resulting in a current of injury that is manifested by electrocardiographic STE (see Figure 35 in the ECG supplement). STE usually is less than 5 mm in height, observed in numerous leads, and is characterized by a concavity to its initial upsloping portion. In some instances, the STE actually may be obliquely flat; convexity of the STE, however, strongly suggests AMI. The STE due to acute pericarditis usually is noted in the following electrocardiographic leads: I, II, III, aVl, aVf, and V2 to V6 (essentially, all leads except V1); reciprocal STD also is seen in lead aVr and occasionally in lead V1. The STE most often is seen in many leads simultaneously, though it may be limited to a specific anatomic segment. If the process is focal, the inferior wall often is involved with leads II, II and aVf commonly affected. PR-segment depression (see Figure 35 in the ECG supplement, leads II, III, and aVF) associated with pericarditis is the most helpful feature for arriving at the correct electrocardiographic diagnosis; such a finding has been described as "almost diagnostic" for acute pericarditis and is best seen in lead V6 and the inferior leads. Reciprocal PR segment elevation can be seen in lead aVr. (See Figure 35 in the ECG supplement.)
Left ventricular aneurysm is defined as a localized area of infarcted myocardium that bulges outward during both systole and diastole. Left ventricular aneurysms most often are noted after large anterior wall events but also may be encountered after post inferior and posterior wall myocardial infarctions. In most cases, the left ventricular aneurysm is manifested electrocardiographically by varying degrees of STE (see Figures 36A and B in the ECG supplement) which may be difficult to distinguish from ST segment changes due to AMI, particularly in the chest pain patient with known past myocardial infarction.5 Left ventricular aneurysm is characterized electrocardiographically by persistent STE seen several weeks after AMI. Because of the frequent, anterior location of LVA, STE most often is observed in leads I, aVl, and V1 to V6. Of course, the inferior wall LVA would be manifested on the surface ECG by STE in the inferior leads; such STE, however, usually is less pronounced than the ST segment changes seen in the anterior leads. The actual ST segment abnormality due to the LVA may present with varying morphologies, ranging from obvious, convex STE to minimal, concave elevations. The distinction from STE in the AMI patient may be difficult.
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References
1. Brush JE, Brand DA, Acampora D, et al. Use of the initial electrocardiogram to predict in-hospital complications of acute myocardial infarction. N Engl J Med 1985;312:1137-1141.
2. Lee T, Cook F, Weisberg M, et al. Acute chest pain in the emergency room: Identification and examination of low risk patients. Arch Intern Med 1985;145:65-69.
3. Rouan GW, Lee TH, Cook EF, et al. Clinical characteristics of patients with acute myocardial infarction and nonspecific electrocardiograms. Clin Res 1987;35:360A.
4. Singer AJ, Brogan GX, Valentine SM, et al. Effect of duration from symptom onset on the negative predictive value of a normal ECG for exclusion of acute myocardial infarction. Ann Emerg Med 1997;29:575-579.
5. Aufderheide TP, Brady WJ. Electrocardiography in the patient with myocardial ischemia or infarction. In: Gibler WB, Aufderheide TP, eds. Emergency Cardiac Care. 1st ed. St. Louis, MO: Mosby; 1994:169-216.
6. Otto LA, Aufderheide TP. Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis of acute myocardial infarction. Ann Emerg Med 1994;23:17-24.
7. Matetzky S, Freimark D, Chouraqui P, et al. Significance of ST segment elevations in posterior chest leads (V7 to V9) in patients with acute inferior myocardial infarction: Application for thrombolytic therapy. J Am Coll Cardiol 1998;31:506-511.
8. Zeymer U, Neuhaus KL, Wegscheider K, et al. Effects of thrombolytic therapy in acute myocardial infarction with or without right ventricular involvement. HIT-4 Trial Group. Hirudin for Improvement of Thrombolysis. J Am Coll Cardiol 1998;32:876-881.
9. Fesmire FM, Smith EE. Continuous 12-lead electrocardiograph monitoring in the emergency department. Am J Emerg Med 1993;11:54-60.
10. Gibler WB, Sayre MR, Levy RC, et al. Serial 12-lead electrocardiographic monitoring in patients presenting to the emergency department with chest pain. J Electrocardiol 1994;26(Suppl):238-243.
11. Jernberg T, Lindahl B, Wallentin L. ST-segment monitoring with continuous 12-lead EKG improves early risk stratification in patients with chest pain and EKG nondiagnostic of acute myocardial infarction. J Am Coll Cardiol 1999;34:1413-1419.
12. Fesmire FM, Percy RF, Bardoner JB, et al. Usefulness of automated serial 12-lead EKG monitoring during the initial emergency department evaluation of patients with chest pain. Ann Emerg Med 1998;31:3-11.
13. Fesmire FM. ECG diagnosis of acute myocardial infarction in the presence of left bundle branch block in patients undergoing continuous ECG monitoring. Ann Emerg Med 1995;26:69-82.
14. Krucoff MW, Green CE, Satler LF, et al. Noninvasive detection of coronary artery patency using continuous ST-segment monitoring. Am J Cardiol 1986;57:916-922.
15. Brady WJ, Hwang V, Sullivan R, et al. A comparison of the 12-lead ECG to the 15-lead ECG in emergency department chest pain patients: Impact on diagnosis, therapy, and disposition. Am J Emerg Med 2000;18:239-243.
16. Zalenski RJ, Cook D, Rydman R. Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9: The 15-lead ECG. Ann Emerg Med 1993;22:786-793.
17. Huwez FU, Pringle SD, Macfarlane FW. Variable patterns of ST-T abnormalities in patients with left ventricular hypertrophy and normal coronary arteries. Br Heart J 1992;67:304-307.
18. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle branch block. N Engl J Med 1996;334:481-487.
19. Shapiro NI, Fisher J, Zimmer GD, et al. Validation of electrocardiographic criteria for diagnosing acute myocardial infarction in the presence of left bundle branch block. Acad Emerg Med 1998;5:508.
20. Shlipak MG, Lyons WL, Go AS, et al. Should the electrocardiogram be used to guide therapy for patients with left bundle branch block and suspected acute myocardial infraction? JAMA 1999;281:714-719.
21. Edhouse JA, Sakr M, Angus J, et al. Suspected myocardial infarction and left bundle branch block: Electrocardiographic indicators of acute ischemia. J Accid Emerg Med 1999;16:331-335.
22. Rogers WJ, Bowlby LI, Chandra NC, et al. Treatment of myocardial infarction in the United States (1990 to 1993): Observations from the National Registry of Myocardial Infarction. Circulation 1994;90:2103-2114.
23. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomized trial of intravenous streptokinase, oral aspirin, both, or neither amount 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988;2:349.
24. Kozlowski FH, Brady WJ, Aufderheide TP, et al. The electrocardiographic diagnosis of acute myocardial infarction in patients with ventricular paced rhythms. Acad Emerg Med 1998;5:52-57.
25. Sgarbossa EB, Piniski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. Am J Cardiology 1996;77:423-424.
26. Rude RE, Poole WK, Muller JE, et al. Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3697 patients. Am J Cardiol 1983;52:936-942.
27. Brady WJ. ST segment elevation: Causes and diagnostic accuracy. J Emerg Med 1998;16:797.
28. Sharkey SW, Berger CR, Brunette DD, et al. Impact of the electrocardiogram on the delivery of thrombolytic therapy for acute myocardial infarction. Am J Cardiol 1994;73:550-553.
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