Mastering The Electrocardiogram: State-of-the-Art Techniques for Evaluating ST S
Mastering The Electrocardiogram: State-of-the-Art Techniques for Evaluating ST Segment Elevation in Acute Myocardial Infarction and Other Clinical Syndromes (Part I)
Author: William J. Brady, MD, Assistant Professor of Emergency Medicine and Internal Medicine, Medical Director, Chest Pain Center, Department of Emergency Medicine, University of Virginia School of Medicine, University of Virginia Health System, Charlottesville, VA.
Peer Reviewer: Raghavan Chari, MD, FACEP, Department of Emergency Medicine, Washington County Hospital, Hagerstown, MD.
The 12-lead electrocardiogram is arguably the most powerful, least invasive, most cost-effective, and predictive tool in our diagnostic armamentarium. In recent years especially, the widely recognized benefits of early diagnosis and rapid revascularization of AMI have cast into focus the urgency of clinical competence in bedside electrocardiographic (ECG) assessment. The emergency physician is frequently the first in-hospital clinician to evaluate patients with chest pain. In this regard, he or she is charged with the responsibility of making a rapid, precise diagnosis and then initiating or recommending appropriate mortality-reducing and myocardium-sparing pharmacotherapeutic and invasive interventions.
As a general rule, the clinical pathway in chest-pain patients bifurcates in two directions. In the case of documented AMI with ST segment elevation (STE) on the ECG, revascularization therapies and other interventions should be considered. In order to maximize the benefits of such therapy, pharmacotherapeutic or surgically mediated interventions to establish coronary artery patency must be delivered soon after the onset of infarction. In contrast, when patients with chest pain demonstrate STE that is associated with a noninfarction syndrome-pericarditis, bundle branch block, CNS event-a different management pathway should be followed that will not only improve outcomes in this subgroup but avoid unnecessary application of potentially dangerous and/or invasive therapies such as thrombolysis or angioplasty.
Because these are critical clinical decisions, with both financial and outcome implications, the emergency physician must become proficient in ECG interpretation, which is often pivotal to clinical management of patients with chest pain. Unfortunately, the ECG has numerous shortcomings when it is used for evaluation of the chest-pain patient. Whereas some patients with chest pain present with STE that is due to an AMI, other patients present with confounding patterns and/or masquerading syndromes. In many cases, perhaps the majority, STE caused by AMI is readily appreciated. However, confounding patterns such as left bundle branch block (LBBB), ventricular paced rhythms (VPR), and left ventricular hypertrophy (LVH) may obscure the typical electrocardiographic findings of AMI as well as produce noninfarctional STE that may lead the uninformed emergency physician astray.
With these issues in mind, the following review focuses on strategies for evaluating the chest-pain patient with STE. The differential diagnosis of these patients is reviewed in detail, and strategies for confirming a coronary ischemia-related condition are outlined. Finally, comprehensive sets of electrocardiographic tracings are provided in order to enhance the evaluation of ECGs at the bedside.
-The Editor
ECG Diagnosis: Pearls and Pitfalls
Despite the attention that is given to the diagnosis and management of AMI, fewer than 5% of ED visits are precipitated by the chief complaint of chest discomfort.1-3 However, depending upon the patient population encountered, as many as one-fifth of these patients will experience an AMI; a much higher proportion may be diagnosed with unstable angina pectoris, while the remainder will be found to have a non-coronary source of chest discomfort.4,5
To distinguish among these etiologies, the emergency physician typically relies upon three principle evaluation strategies: a complete history of the event; the 12-lead ECG; and cardiac enzyme levels and other serum markers of myocardial injury. While the clinical history of the discomfort and its associated issues are of major importance, the ECG remains a powerful clinical tool for evaluation of these patients. Moreover, the ECG is essential for directing the emergency physician toward proper therapy, especially treatments aimed at interrupting the ischemic cascade and restoring coronary perfusion as well as securing an adequate disposition.6-9
Consequently, accurate interpretation of the ECG and confirming a diagnosis of AMI among the numerous causes of STE is a mandatory skill for the emergency physician. Complicating this assessment, however, is the fact that syndromes causing non-AMI STE are frequently misdiagnosed as acute infarction. For example, one study notes that 11% of patients receiving a thrombolytic agent were not experiencing an AMI. The electrocardiographic syndromes producing this pseudo-infarct STE included benign early repolarization (30%), LVH (30%), and various intraventricular conduction abnormalities (30%).10 Incorrect electrocardiographic interpretations by emergency physicians have been noted in other reviews as well.11-13 (See Table 1 and Figure 1. Figures are included in the enclosed supplement.)
Generally speaking, ST segment elevation is the most "challenging" electrocardiographic feature encountered in the chest-pain patient-challenging because its presence must be explained and, if the clinical history suggests AMI, urgent therapeutic decisions must be made. Unfortunately, STE is also seen in other noninfarction syndromes, reinforcing the point that STE is an insensitive marker of AMI.14
Underscoring this observation is a prehospital study of adult chest pain patients that demonstrates that the majority of patients manifesting STE on the ECG did not have AMI as their final hospital diagnosis. Instead, LVH and LBBB accounted for the majority of the cases.15 Furthermore, in another review of adult ED chest-pain patients with STE on the ECG, the STE resulted from AMI in only 15% of this population; LVH, which was seen in 30% of adult chest-pain patients, was the most frequent cause of this STE in this group of patients.16 Finally, in the coronary care unit population, another study demonstrated that STE was diagnostic for acute infarct in only half of patients with a history of ischemic heart disease who had characteristic ST segment changes.17 (See Table 2.)
The ECG in AMI
Depending upon the patient population and the associated prevalence of ischemic heart disease, the ECG will be diagnostic for AMI in only 25-50% of all patients with proven infarction.5-7 Moreover, it should be stressed that AMI is not the most common diagnosis in adult chest-pain patients with STE. Consequently, a comprehensive understanding of ECG patterns in AMI-which can range from subtle and confusing to classical and unequivocal-is essential for detecting patients with suggestive historical features who can benefit from mortality-reducing interventions.
ST Segment Elevation (STE). AMI-related STE is said to occur when the ST segment is elevated at least 1 mm (0.1 mv) at a distance measured 0.08 seconds from the J point of the QRS complex. STE in AMI is caused by the electrical current of injury associated with cellular compromise and/or death. In the presence of myocyte dysfunction, leakage of predominantly negatively charged ions from the intracellular space into the extracellular space alters the electrical charge across the cellular membrane. As a result, myocardial cells are no longer able to maintain a normal resting membrane potential during electrical diastole. The relative difference in membrane potentials between injured and normal cells produces the current of injury that manifests as STE on the surface ECG.
Table 1. Syndromes that May Cause STE
MI
Variant angina
Acute pericarditis
Benign early repolarization
Left ventricular hypertrophy
Bundle branch block
Cardiomyopathy
Acute myocarditis
Left ventricular aneurysm
Pre-excitation syndromes
Hyperkalemia
Hypothermia
CNS events
Acute abdominal disorder
Temporal Evolution. The ECG undergoes a well-established temporal evolution following the onset and continuing presence of coronary artery occlusion. (See Figure 2 and Figure 3a through Figure 3c for ECGs of evolving AMI.) The earliest electrocardiographic finding associated with AMI is the hyperacute T wave, which may appear minutes after the interruption of blood flow to the myocardium; the R wave also increases in amplitude at this stage. Accordingly, the differential diagnosis of the hyperacute T wave includes both transmural AMI and hyperkalemia.
Hyperacute T Wave. In the case of AMI, the hyperacute T wave is noted as early as 30 minutes after the onset of coronary occlusion and transmural infarction. It tends to be a short-lived phenomenon that evolves rapidly to STE. The hyperacute T wave of early AMI is often asymmetric with a broad base. Not infrequently, these T waves are with reciprocal ST segment depression in other ECG leads. (See Figure 2, the left panel in Figure 3a, and Figure 4 for examples of hyperacute T waves associated with AMI.)
T waves of large magnitude are also seen in patients with hyperkalemia. Because this T wave morphology is also described as "hyperacute," it may be confused with the hyperacute T wave of early transmural myocardial infarction. In hyperkalemia, T waves tend to be tall, narrow, and peaked, with a prominent or sharp apex. Moreover, these T waves tend to be symmetric in morphology; if "split down the middle," the resulting portions should be mirror images. As the serum potassium level increases, the T waves tend to become taller, peaked, and narrowed in a symmetric fashion in the anterior distribution. (See Figure 5 for an example of a hyperacute T wave associated with hyperkalemia.)
R Wave. From a temporal perspective, a large (some refer to it as a "giant") R wave is the next ECG finding in continuing myocardial infarction. It is best described as an intermediate or transitional electrocardiographic structure, occurring after the development of the hyperacute T wave, but before the appearance of typical STE.
In fact, this structure is not often seen, inasmuch as it is very transient in nature. 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 has also been referred to as a "tombstone" on the ECG. (See Figure 3b and Figure 6 for examples of the giant R wave.)
The importance of the giant R wave is linked to its electrocardiographic differential diagnosis, which includes early AMI as well as recent electrical cardioversion of arrhythmia.18,19 In the latter case, the R wave may result from acute bundle branch dysfunction with altered, inefficient ventricular conduction. As a rule, in the absence of AMI, this transient finding resolves rapidly after restoration of spontaneous circulation. (See Figure 7 for ECG sequences demonstrating giant R waves in a patient resuscitated from cardiac arrest.) In addition, if the patient presents with sinus tachycardia in the early stage of AMI, a giant R wave configuration occurring in the setting of a rapid pulse may be misidentified as ventricular tachycardia. (See Figure 8 for an example of a patient with sinus tachycardia and inferior wall AMI who was misdiagnosed initially as having ventricular tachycardia.)
ST Segment Elevation. As myocardial infarction progresses, the STE assumes a more typical morphology. The initial upsloping portion of the ST segment usually is either convex or flat; if the ST segment is flat, it may be either horizontally or oblique to baseline. (See Figure 9 for examples of STE morphologies in encountered in AMI.)
Not infrequently, an analysis of the ST segment waveform may help distinguish among the various causes of STE and, therefore, assist in identifying the patient with the AMI. This technique evaluates the morphology of the initial portion of the ST segment/T wave. This portion of the cardiac electrical cycle is defined as beginning at the J point and ending at the apex of the T wave. The waveform of patients with non-infarctional STE tends to be concave. (See Figures 1c through 1g for examples of STE with a concave initial ST segment morphology, representing non-infarction syndromes.) Conversely, patients with STE due to AMI have either obliquely flat or convex waveforms. Use of this STE waveform analysis in ED chest-pain patients increases the sensitivity and positive predictive value for correct electrocardiographic diagnosis of AMI markedly.16
It should be emphasized that these morphologic distinctions should only be used as a general guideline. As with most guidelines, it is not infallible. Patients with ST segment elevation due to AMI may demonstrate concavity of this portion of the waveform.20 (See Figure 10a through Figure 10c for examples of patients with documented AMI and concave ST segment waveforms.) On the other hand, patients with acute pericarditis may present with STE characterized as obliquely flat. (See Figure 1d.) The total height of the STE is usually greater in the anterior leads compared to all others; the evolution of the electrocardiographic features noted above also occurs more rapidly in anatomic segments other than the anterior wall. Following maximum STE, the ST segment gradually returns to its baseline location over 12-24 hours.21-23 This is accompanied by T wave inversion.
Q Wave. Eventually, the R wave diminishes and may disappear entirely with the development of the Q wave. In general, Q waves represent myocardial necrosis and completed infarction. Although Q waves may be encountered in the initial, early stages of transmural AMI, they usually are not fully developed until 12 hours after infarction ensues. In patients who present to the ED with an ECG demonstrating characteristic Q waves, the benefits of thrombolytic therapy are uncertain. In this regard, it should be noted that a small percentage of patients with AMI will develop Q waves as early as two hours after the onset of transmural AMI.21-23 (See Figure 2 [middle panel], Figure 3b, and Figure 11.) Consequently, an accurate history confirming two hours of chest discomfort in a patient with STE accompanied by prominent, simultaneous Q waves in the same anatomic distribution does not preclude the patient from being considered for acute revascularization therapy.20
Reciprocal ST Segment Depression. Reciprocal ST segment depression (STD), also known as reciprocal change, is defined as STD in leads that are separate and distinct from leads manifesting STE. The STD is either horizontal (see Figure 12, upper panel) or downward-sloping (see Figure 12, lower panel). The cause(s) of reciprocal change remain(s) unknown but may involve displacement of the injury current vector away from the infarcting myocardium, co-existing distant ischemia, and/or it may be a manifestation of infarct extension.
Regardless of its cause, reciprocal changes in the setting of transmural AMI identify a subset of patient with an increased chance of poor outcome and, therefore, an individual who may benefit from a more aggressive approach in the ED. Furthermore, its presence on the ECG supports the diagnosis of AMI with very high sensitivity and positive predictive values greater than 90%.15,16
The use of reciprocal change in both prehospital and ED chest-pain patients retrospectively increased the diagnostic accuracy in the electrocardiographic recognition of AMI.15,16 It is perhaps most useful in patients with chest pain and STE of uncertain etiology. The presence of reciprocal STD in these cases strongly suggests AMI. Its absence, unfortunately, cannot be used to rule-out AMI in that reciprocal change is not encountered in all patients with acute infarction. Patients with inferior wall AMI manifest reciprocal changes in approximately 75% of cases, whereas anterior wall myocardial infarcts demonstrate such STD in no more than one-third of patients. Moreover, the combination of ST segment waveform analysis and reciprocal changes in ED chest-pain patients does not appear to increase the diagnostic accuracy of the ECG for AMI beyond the use of each strategy independently.16
Table 2. Causes of STE Among Chest Pain Patients in the ED
Causes of ST segment elevation among ED chest-pain patients. 902 patients presented with chest pain; 202 (22%) patients demonstrated STE on ECG; the responsible etiologies are listed below.12
| Syndrome | % of Patients |
| LVH | 25 |
| LBBB | 15 |
| AMI | 15 |
| BER | 12 |
| RBBB | 5 |
| IVCD* | 5 |
| Aneurysm | 3 |
| Pericarditis | 2 |
| Undefined | 18 |
* IVCD = Intraventricular conduction delay
Premature Ventricular Contractions (PVCs). Premature ventricular contractions (PVCs) occur frequently in patients with acute coronary ischemia. In most cases of PVC, the "rule of appropriate discordance" describes the normal and benign relationship of the terminal portion of the QRS complex to the ST segment/T wave. The same principles that are applied in the LBBB and VPR situations may be used. For example, the observation of a PVC with a concordant ST segment may suggest AMI. In most cases, other sinus beats on the ECG should support such a diagnosis. Certain cases, however, may involve questionable STE, in which case confirmation of AMI may be made by observing a PVC with concordant ST segment changes. (See Figure 13, which shows a series of PVCs in the right precordial leads V1 top to V3 bottom.) The PVCs in leads V1 and V2 demonstrate concordant STE that is not the expected waveform morphology; the correct waveform morphologic relationship is seen in lead V3 -it is one of discordance with the terminal portion of the QRS complex.
Additional Leads. Additional lead ECGs are used to better define the extent of myocardial injury, particularly in cases involving the right ventricle (RV) and the posterior wall of the left ventricle. The 15-lead ECG technique uses three additional leads to investigate the right ventricle (lead RV4) and the posterior wall (leads V8 and V9). The standard 12-lead ECG does not define either area well. Right ventricular infarction complicates approximately 25% of inferior wall AMI. Patients with inferior wall infarction present with hypotension resulting from acute right-sided heart failure and reduced preload from either pre-existing volume depletion or nitrate-induced venodilation.
Right Ventricular Infarction (RV). In right ventricular infarction, the 12-lead ECG reveals typical STE in the inferior leads as well as STE in the right precordial leads, especially lead V1. In contrast to the anteroseptal AMI, which is characterized by increasing STE as one moves from right to mid-precordial leads, in RV AMI, decreasing magnitude of ST segment elevation in the V1 to V4 distribution is noted. Additional lead applications can be used to define RV injury, including a complete reversal of the standard left-sided precordial leads (resulting in RV1 through RV6, see Figure 14) or a simplified approach, using only RV4. (See Figure 15.) In either case, the degree of STE in the right-sided leads may be of smaller magnitude than that observed in anterior MI due to the relatively smaller RV muscle mass.
Posterior Infarction. Posterior AMI refers to infarction of the dorsal area of the heart and, in most cases, involves occlusion of either the left circumflex or the right coronary artery and its posterior descending branch. As predicted from the coronary anatomy, posterior AMI most often occurs in conjunction with acute inferior or lateral myocardial infarction. Although true, isolated posterior AMI does occur, it is rare.24
The emergency physician may employ additional-lead ECGs in select cases, looking for involvement of the posterior wall in patients with co-existing inferior or lateral acute infarct. Alternatively, in a chest-pain patient with a high clinical suspicion for AMI, but in whom only STD is noted in the right precordial leads, an additional-lead ECG may reveal posterior AMI. Identification of a larger infarct, as with the case of extension to posterior MI, may not have an impact on therapy. On the other hand, identifying a patient with an isolated posterior AMI, however uncommon, which may have escaped detection using standard electrocardiography, may alter therapeutic decisions and clinical outcome.
Additional Lead ECG. Using additional-lead ECGs in all adult chest pain patients encountered in the ED does not appear to have therapeutic or diagnostic benefits.25 However, when considering a high-risk population of patients, such as coronary care unit admissions, additional lead ECGs have been shown to improve the rate of diagnosis of posterior AMI.26
Because the endocardial surface of the posterior wall faces the precordial leads, the electrocardiographic changes resulting from AMI will be reversed. An R wave with increased voltage in the right precordial leads (V1 to V3) is the major electrocardiographic feature associated with posterior AMI. An R/S wave ratio greater than 1.0 in leads V1 or V2 is another suggestive finding.24 (See Figure 15.) Moreover, ST segment depression with a prominent, upright T wave in a similar distribution are highly correlated with posterior AMI.
If one considers the "reverse nature" of these electrocardiographic abnormalities when applied to the posterior wall, the findings assume a more recognizable, ominous meaning. The tall R wave is actually a significant Q wave while the ST segment/T wave abnormalities represent ST segment elevation with inverted T wave. When interpreting the ECG in an appropriate patient, the finding of STD in the right precordial leads should suggest either anterior wall ischemia or acute posterior wall myocardial infarction. Greater than 1 mm ST segment elevation in the posterior leads, V8 and V9, confirms the presence of posterior AMI and are felt to be more accurate in confirming the diagnosis as compared to the findings noted in leads V1 through V3.26 (See Figure 15 for an example of an infero-latero-posterior AMI diagnosed via a 15-lead ECG.)
Variant Angina. Prinzmetal's angina, also known as variant angina, presents with chest discomfort and ST segment abnormalities; the basic pathophysiologic lesion is felt to be vasospasm. The actual ST waveform encountered in such cases depends upon the size of the vessel involved-large vessel involvement produces STE while smaller caliber vessels in spasm cause STD. Most commonly, the electrocardiographic manifestation is STE. Classically, the chest discomfort occurs at rest and resolves with traditional antianginal therapy or calcium antagonist treatment. If the episode is prolonged, AMI may occur. The ST segment elevation in variant angina is difficult, if not impossible, to distinguish from that associated with AMI.
Non-Infarction Cardiac Syndromes Producing ST Segment Elevation
Right Bundle Branch Block. Right bundle branch block (RBBB), which is accompanied by predictable depolarization-repolarization changes, can produce marked ST segment/T wave changes.20 In fact, RBBB is responsible for about 5% of non-infarctional STE in chest pain patients.16 In general, unlike the potential AMI-masking effect of a LBBB, the presence of a RBBB on the ECG should not obscure the electrocardiographic diagnosis of AMI, although can suggest an incorrect diagnosis to the uniformed observer. False-positive diagnoses will not occur if the clinician is well versed in the electrocardiographic characteristics-including variations and morphologies-of RBBB and its associated ST segment/T wave abnormalities.
In RBBB, the deflection representing right ventricular activation is delayed and becomes very prominent, resulting in a broad R wave in lead V1. This broadened R wave may take any of the following morphologies: monophasic R, biphasic RSR, or qR formation. In lead V6, early intrinsicoid deflection and either a wide S or RS complex wave are seen. QS complexes are encountered in the inferior leads. The QRS complex duration is prolonged (i.e., it is usually greater than 0.12 seconds).
In addition, pronounced ST segment changes are seen and, in fact, are the "norm" in the patient with RBBB.21 The right precordial leads, which reflect predominantly positive forces, are usually associated with STE and T-wave inversion. The ST segment in the inferior and left precordial leads is frequently elevated with an upright T wave; the degree of STE is usually greater in the inferior distribution. As predicted by the rule of appropriate discordance, the ST segment/T wave structure is directed opposite the terminal portion of the QRS complex.
The ST segment/T wave changes noted above are the expected consequences of a depolarization-repolarization disturbance produced by the bundle branch block. Accordingly, the RBBB pattern may resemble either lateral, inferior, or posterior wall AMI. (See Figure 16 for an example of RBBB with the expected ST segment/T wave morphologies.) Figure 17a shows a single electrocardiographic complex (lead V1) in a patient with enzyme-proven AMI. In this figure, the ST segment is concordant with the terminal portion of the QRS complex-a violation of the rule of appropriate discordance and, therefore, strong electrocardiographic evidence of AMI. Figure 17b represents a 12-lead ECG in a patient with RBBB and AMI; again, the STE is concordant in the right precordial leads, which is strongly suggestive of AMI.
Left Bundle Branch Block (LBBB). In contrast to RBBB, LBBB markedly reduces the diagnostic power of the ECG. With this finding, the associated and expected ST segment-T wave abnormalities of LBBB can mimic both acute and chronic ischemic changes.20,24,27,28 Of special concern is the fact that these morphological abnormalities have the potential of suggesting an incorrect diagnosis of MI. Furthermore, such changes can also mask the classic electrocardiographic findings of AMI. One recent study of out-of-hospital chest pain patients undergoing 12-lead ECG analysis revealed that 51% of patients with 1 mm or greater ST segment elevation in two anatomically contiguous leads (i.e., electrocardiographic thrombolytic agent criteria) had non-myocardial infarction conditions for their final hospital diagnosis.15 LBBB was the second most frequently encountered electrocardiographic pattern responsible for this non-infarction ST segment elevation.
If one considers the ED chest pain population, LBBB was responsible for 15% of STE syndromes; as in the prehospital chest pain population, LBBB represents the second most often seen pattern causing non-AMI STE in the ED.16 The ST segment/T wave abnormalities encountered with LBBB are the most frequently misinterpreted pseudoinfarct pattern in practice today.24
As every physician knows, the electrocardiographic abnormalities associated with AMI may be masked by altered patterns of ventricular conduction observed in patients with LBBB. This situation, however, is far from hopeless. Although common medical opinion holds that the electrocardiographic diagnosis of AMI is virtually impossible in the presence of LBBB, in fact, the diagnosis of MI, even in the presence of LBBB, is often straightforward and considered "disarmingly easy" by several authorities.29 In this regard, a recent study by Sgarbossa and his group30 successfully addresses this clinical misconception. Their approach has been to develop a clinical prediction rule that can be used quickly and easily in ED patients with suspected acute myocardial infarction and concomitant LBBB.
In the patient with LBBB,20,29 the 12-lead ECG records abnormal ventricular activation as it moves from right to left, producing a broad, mainly negative QS or rS complex in lead V1. In lead V6, late intrinsicoid deflection is noted, resulting in a positive, monophasic R wave; similar structures are frequently found in leads I and aVl. Poor R wave progression or QS complexes are noted in the right to mid precordial leads, rarely extending beyond leads V4 or V5. QS complexes may also be encountered in leads III and aVf. The anticipated or expected ST segment-T wave configurations are discordant (i.e., they are directed opposite from the terminal portion of the QRS complex); this is called QRS complex-T wave axis discordance. As such, leads with either QS or rS complexes may have markedly elevated ST segments, mimicking acute myocardial infarction. Leads with a large monophasic R wave demonstrate ST segment depression. 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 waves of early myocardial infarction. The T waves in leads with the monophasic R wave are frequently inverted. (See Figure 18 for an electrocardiographic example of a LBBB with expected ST segment/T wave morphologies.) Loss of this normal QRS complex-T wave axis discordance in patients with LBBB may imply an acute process, such as acute myocardial infarction.
Using specific electrocardiographic findings, the Sgarbossa group has developed a clinical prediction rule to assist in the ECG diagnosis of AMI in patients with LBBB.30 In formulating their prediction rule, they analyzed numerous electrocardiographic abnormalities previously reported to be suspicious or diagnostic for AMI in patients with LBBB.
The rule, developed from 131 patients with LBBB and enzymatically proven AMI who were enrolled in the GUSTO-I trial, states that three ECG criteria are independent predictors of myocardial infarction. Specifically, the ECG criteria suggesting a diagnosis of AMI, ranked with a scoring system based on the probability of such a diagnosis, include: ST segment elevation greater than 1 mm that is concordant with the QRS complex (score of 5) (See Figure 19- leads I, aVl, V5, and V6 ); ST segment depression greater than 1 mm in leads V1, V2, or V3 (score of 3); and ST segment elevation greater than 5 mm that is discordant with the QRS complex (score of 2). (See Figure 19-leads V2 through V4.)
A total score of three or more suggests that the patient is likely to have an AMI, based on the ECG criteria. In chest pain patients with a score less than three, the electrocardiographic diagnosis is less assured, and the patient will require additional clinical evaluation. (Please refer to Figure 20 for elucidation of these criteria and an accompanying ECG supporting the electrocardiographic diagnosis of AMI.)The usefulness of this clinical prediction instrument emphasizes the importance of becoming familiar with associated, or anticipated, ST segment/T wave changes caused by abnormal ventricular conduction patterns observed in LBBB.
Ventricular Paced Rhythms (VPR). In right ventricular-paced rhythms, the ventricular depolarization pattern is abnormal (i.e., activation of the ventricles proceeds from the right to the left which, in most cases, resembles a LBBB pattern). This produces 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 may also be encountered in leads II, III, and aVf. The anticipated ST segment-T wave configurations are discordant (i.e., they are directed opposite of the terminal portion of the QRS complex). This illustrates the rule of appropriate discordance and is similar to the electrocardiographic principles applied in the setting of LBBB.20,27 (See Figure 21a for the appropriate discordant QRS complex-ST segment/T wave relationship.)
As a result, leads with QS complexes may have marked STE, mimicking AMI. Leads with a large monophasic R wave 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 are frequently inverted. The ECGs in patients with VPR should be inspected 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, such as AMI.31,32
In a report similar to one they published on LBBB, the Sgarbossa group published a report detailing the electrocardiographic changes encountered in patients with VPR with confirmed AMI.30,33 Of 41,021 patients with enzymatically confirmed AMI entered in the GUSTO trial, 32 patients with VPR (0.1%) were encountered and enrolled in this study. Fifteen patients were excluded due to the presence of native rhythm or other non-right ventricular paced rhythms, leaving 17 cases (6 single- and 11 dual-chamber ventricular pacemakers) that were used for analysis.1,10 These study patients were compared to a similar number of randomly selected, age-matched control subjects with known, stable coronary artery disease and permanent right-ventricular pacing.
Classic ECG criteria for myocardial infarction in the setting of ventricular pacing were assessed between the two groups.34-36 Three ECG criteria were found to be useful in the early diagnosis of AMI, including: discordant STE greater than or equal to 5 mm (see Figure 21b); concordant STE greater than or equal to 1 mm (see Figure 21c); and ST segment depression greater than or equal to 1 mm in leads V1, V2, or V3.32,33 (See Figure 21d.) Interestingly, no criteria involving QRS-complex or T-wave morphologies alone were found to be useful. This article, in contrast to much of the existing cardiology literature, distinguishes between past myocardial infarction and AMI; it furthers provides electrocardiographic, interpretative tools for making the early electrocardiographic diagnosis of AMI.34,36 It should be stressed that these ST segment changes are only suggestive of AMI in patients with complicated ECGs; they are not diagnostic of AMI. Furthermore, their absence does not rule out the possibility of AMI.
Another strategy is also available for improving accuracy of interpretation of the ECG in patients with permanent ventricular pacemakers-the clinician may perform an analysis of the native, underlying rhythm. In this case, the pacemaker may be deactivated temporarily, but only if the underlying rhythm is able to sustain adequate perfusion and the emergency physician has the equipment and expertise for such a maneuver. Alternatively, some patients may experience intermittent periods of the native rhythm. Assuming that the focus is supraventricular in origin and the intraventricular conduction is normal, information may be obtained from this brief glimpse.37 Unfortunately, this approach will not be useful in most patients with AMI and VPR.
Summary
Patients who have chest pain and ST segment elevation (STE) on the 12-lead electrocardiogram and are experiencing AMI may be candidates for urgent coronary revascularization, with either thrombolysis or primary angioplasty. Other chest-pain patients with electrocardiographic STE may be suffering from a non-coronary chest discomfort syndrome. Correct identification of these patients is required to offer the most appropriate treatments and to avoid potentially dangerous therapies.
References
1. Hedges JR, Kobernick MS. Detection of myocardial ischemia/infarction in the emergency department patient with chest discomfort. Emerg Med Clin North Am 1988;6:317-340.
2. Hedges JR, Rouan GW, Toltzis R, et al. Use of cardiac enzymes identifies patients with acute myocardial infarction otherwise unrecognized in the emergency department. Ann Emerg Med 1987;16:248-253.
3. Rouan GW, Hedges JR, Toltzis R, et al. A chest pain clinic to improve the follow-up of patients released from an urban university teaching hospital emergency department. Ann Emerg Med 1987;16:1145-1150.
4. Aufderheide TP, Hendley GE, Woo J, et al. A prospective evaluation of prehospital 12-lead ECG application in chest pain patients. J Electrocardiol 1992;24(suppl):8-13.
5. Aufderheide TP, Keelan MH, Hendley GH, et al. Milwaukee prehospital chest pain project: Phase I. Feasibility and accuracy of prehospital thrombolytic candidate selection. Am J Cardiol 1992; 69:991-996.
6. Muller DW, Topol EJ. Selection of patients with acute myocardial infarction for thrombolytic therapy. Ann Intern Med 1990;113:949-960.
7. Kleiman NS, White HD, Ohman EM, et al. Mortality within 24 hours of thrombolysis for myocardial infarction: The importance of early reperfusion. Circulation 1994;90:2658-2665.
8. Lee TH, Weisberg MC, Brand DA, et al. Candidates for thrombolysis among emergency room patients with acute chest pain: Potential true-and false-positive rates. Ann Intern Med 1989;110:957-962.
9. The GUSTO Investigators: An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. N Engl J Med 1993;329:673-682.
10. 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.
11. Chapman GD, Ohman M, Topol EJ, et al. Minimizing the risk of inappropriately administering thrombolytic therapy (Thrombolysis and angioplastly in myocardial infarction [TAMI] study group). Am J Cardiol 1993;71:783-787.
12. Blankenship JC, Almquist AK. Cardiovascular complications of thrombolytic therapy in patients with a mistaken diagnosis of acute myocardial infarction. J Am Coll Cardiol 1989;14: 1579-1582.
13. Larsen GC, Griffith JL, Beshansky JR, et al. Electrocardiographic left ventricular hypertrophy in patients with suspected acute cardiac ischemia-Its influence on diagnosis, treatment, and short-term prognosis. J Gen Intern Med 1994;9:666-673.
14. Rude RE, Poole WK, Muller JE, et al. Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3,697 patients. Am J Cardiol 1983;52: 936-942.
15. 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.
16. Brady WJ. Causes of ST segment elevation in emergency department chest pain patients. Abstract presented at the International Emergency Medicine Conference, Vancouver, British Columbia, March 26, 1998.
17. Miller DH, Kligfield P, Schreiber TL, et al. Relationship of prior myocardial infarction to false-positive electrocardiographic diagnosis of acute injury in patIents with chest pain. Arch Int Med 1987;147:257-261.
18. Van Gelder IC, Crijns HJ, Van Der Laarse A, et al. Incidence and clinical significance of ST segment elevation after electrical cardioversion of atrial fibrillation and atrial flutter. Am Heart J 1991;12:51-56.
19. Madias JE, Krikelis EN. Transient giant R waves in the early phase of acute myocardial infarction: Association with ventricular fibrillation. Clin Cardiol 1981;4:339-349.
20. 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: Mosby; 1994:169-216.
21. Fesmire FM, Percy RF, Wears RL, et al. Risk stratification according to the initial electrocardiogram in patients with suspected acute myocardial infarction. Arch Intern Med 1989;149:1294-1299.
22. Hackworthy RA, Vogel MB, Harris PJ. Relationship between changes in ST-segment elevation and patency of the infarct-related coronary artery in acute myocardial infarction. Am Heart J 1986;112:279-288.
23. Cohen M, Hawkins L, Greenberg S, et al. Usefulness of ST-segment changes in >/= leads on emergency room electrocardiogram in either unstable angina pectoris or non-Q-wave myocardial infarction in predicting outcome. Am J Cardiol 1991;67: 1368-1377.
24. Goldberger A. Myocardial Infarction: Electrocardiographic Differential Diagnosis. 4th ed, St. Louis: Mosby; 1991.
25. Brady WJ, Chang N, Hwang V, et al. The 15-lead electrocardiogram in emergency department chest pain patients: Comparison to the 12-lead electrocardiogram. Ann Emerg Med 1997;30:281.
26. 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;22:786-791.
27. Brady WJ, Aufderheide TP: Left Bundle Block Pattern Complicating the Evaluation of Acute Myocardial Infarction. Acad Emerg Med 1997;4:56-62.
28. Rosner MH, Brady WJ. The electrocardiographic diagnosis of acute myocardial infarction in the presence of left bundle branch block: A report of two illustrative cases. Am J Emerg Med (1998 accepted/publication pending).
29. Marriott HJL. Myocardial infarction. In: Marriott HJL, ed. Practical Electrocardiography. 8th ed. Baltimore, MD: Williams and Wilkins; 1988:419-450.
30. 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.
31. 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.
32. Rosner MH, Brady WJ. The electrocardiographic diagnosis of acute myocardial infarction in patients with ventricular paced rhythms. Am J Emerg Med (1998 accepted/publication pending).
33. Sgarbossa EB, Piniski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular-paced rhythm. Am J Cardiol 1996;77:423-424.
34. Barold SS, Falkolff MD, Ong LS et al. Electrocardiographic diagnosis of myocardial infarction during ventricular pacing. Cardiol Clin 1987;5:403-417.
35. Barold SS, Wallace WA, Ong LS, et al. Primary ST and T wave abnormalities in the diagnosis of acute anterior myocardial infarction during permanent ventricular pacing. J Electrocardiol 1976;9:387-390.
36. Niremberg V, Amikam S, Roguin N, et al. Primary ST changes. diagnostic aid in patients with acute myocardial infarction. Br Heart J 1977;39:502-507.
37. Brady WJ. Cases in electrocardiography-The electrocardiographic diagnosis of acute myocardial infarction in patients with ventricular-paced rhythms: Value of the native rhythm. Am J Emerg Med 1998;16:85-86.
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