Mastering the Electrocardiogram: State-of-the-Art Techniques for Evaluating ST Segment Elevation in Acute Myocardial Infarction and Other Clinical Syndromes (Part II)
Author: William J. Brady, MD, FACEP, 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 differential diagnosis of ST elevation (STE) frequently presents a diagnostic challenge in patients who present to the ED with chest pain. Part I of this two-part series on "Mastering the Electrocardiogram" discussed primarily ischemic changes that can produce alterations in the ST segments as well as isolated changes such as hyperacute T waves.
Part II continues with detailed discussions of STE and its associated features in a wide range of cardiovascular conditions, including left ventricular hypertrophy, benign early repolarization, and left ventricular aneurysm. A comprehensive glossary of ECG strips is provided to assist in morphological identification.
-The Editor
ECG Changes Associated with Non-MI Syndromes
Left Ventricular Hypertrophy (LVH). Electrocardiographic changes consistent with LVH and associated repolarization changes are commonly encountered in the ED chest-pain patient. LVH is seen frequently in prehospital chest-pain patients and is the leading cause of noninfarctional ST segment change.1 Among ED patients with the chief complaint of chest discomfort, LVH is responsible for approximately 25% of noninfarctional ST segment elevation (STE).2 Its presence on the ECG, especially the repolarization changes that alter the morphology of the ST segment and/or the T wave, may complicate early ED evaluation of the chest pain patient.
One group has shown that the electrocardiographic pattern consistent with LVH is encountered in approximately 10% of adult chest pain patients initially diagnosed in the ED with acute ischemic heart disease.3 After hospital admission and more extensive evaluation, only 26% of these patients were found to have unstable angina or AMI. Of the remainder of the patients, the vast majority were ultimately diagnosed with non-ischemic syndromes. The physicians caring for the patients in this study incorrectly interpreted the ECG more than 70% of the time. In particular, they frequently failed to identify the LVH pattern and, therefore, attributed the ST segment/T wave changes to ischemia or infarction. In fact, the observed ST segment/T wave changes resulted from repolarization abnormality associated with LVH.3
In patients with LVH, ST segment/T wave changes result from altered repolarization of the ventricular myocardium.4 These ST segment/T wave abnormalities are the new "norm" in many patients with LVH and may mask and/or mimic findings that are consistent with early AMI. These effects, however, occur less often than they do in LBBB and VPR situations.5 In particular, 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 rule of appropriate discordance (that is, the terminal portion of the QRS complex and ST segment/T wave are located on opposites sides of the iso-electric baseline), ST segment elevation is encountered in this distribution along with prominent, "hyperacute" T waves. The ST segment elevation seen in this distribution may be greater than 5 mL in height (See Figure 22 and Figure 23) and is difficult to distinguish from that associated with AMI. The initial, up-sloping portion of the ST segment-T wave complex is frequently concave in LVH compared to either the flattened or convex pattern observed in the AMI patient.5 However, this morphologic feature is imperfect; early AMI may reveal such a concave feature.
Another feature of LVH-related ST segment/T wave change is its relative permanence. The electrocardiographic changes resulting from acute coronary ischemia are dynamic in nature; they are likely to change over the short-term in the early phase of evaluation in the ED. Conversely, the ST segment/T wave abnormalities related to LVH are relatively constant or fixed; these changes are unlikely to change during initial ED evaluation. This difference in the longevity of the ST segment/T wave changes in the two syndromes lends itself to differentiation using either serial electrocardiographic monitoring or ST segment trend analysis.
One last point should be emphasized. LVH with the related repolarization changes represents a particular patient's "normal" or baseline electrocardiographic pattern. Its presence, like the normal or nondiagnostic ECG in the case without LVH, does not rule out the possibility of an early acute coronary ischemic event in a patient experiencing chest pain or other anginal equivalent complaints.5,6
Acute Pericarditis. Acute pericarditis, which may be caused by a number of infectious agents, various rheumatologic and malignant syndromes, and uremia, produces diffuse inflammation of the superficial epicardium. Ventricular inflammation produces a current of injury that is manifested, initially, by STE on the ECG, while PR segment depression is indicative of similar irritation of the atrial epicardium. The electrocardiographic changes caused by pericarditis evolve through four classic stages. The first stage is characterized by STE, which is followed by resolution of the elevation in the second stage. The third stage is characterized by T wave inversion, which is followed by normalization and a return to the baseline ECG in stage four. Q waves are not encountered in patients with pericarditis. (Table 1.)
Table 1. Four Stages of ECG Findings in Pericarditis
STAGE 1
Characterized by STE
STAGE 2
Resolution of STE
STAGE 3
T wave inversion
STAGE 4
Normalization and a return to the baseline ECG
The temporal evolution of these electrocardiographic stages occurs in a very unpredictable manner when compared to AMI. In general, stages one through three are seen over hours to days, while stage four may not be observed for several weeks. Furthermore, patients may not manifest all characteristic electrocardiographic features of pericarditis (i.e., the chest pain patient may present with stage 1 findings and progress directly to stage 4).
STE seen in patients with stage 1 pericarditis is usually less than 5 mm in height, it is observed in numerous leads, and is characterized by a concavity in its initial upsloping portion. (See Figures 24 and 25, upper and middle panels, for examples of acute pericarditis.) In some cases, the STE may be obliquely flat; convexity of the ST segment elevation, however, strongly suggests AMI. The STE due to acute pericarditis is usually noted in the following electrocardiographic leads: I, II, III, aVl, aVf, and V2-V6-essentially, all leads except V1; reciprocal ST segment depression (STD) is also seen in lead aVr and occasionally in lead V1. (See Figure 24 in lead aVr and Figure 25-lower panel.) The STE is most often seen in many leads simultaneously, though it may be limited to a specific anatomic segment. If the process is focal, the inferior wall is often involved, in which case leads II, II and aVf, are most often affected.
Several electrocardiographic features will help identify pericarditis-related STE. The absence of Q waves in the setting of STE is not particularly helpful. Conversely, the presence of Q waves suggests an alternative diagnosis of either myocarditis or AMI. However, an inflammatory process producing pericarditis may also affect the myocardium, hence, myopericarditis can develop. Patients with acute myopericarditis, therefore, may present with electrocardiographic features involving both processes, including STE, prominent Q waves, and other findings as described in the "acute myocarditis" section below.
Reciprocal STD strongly supports the electrocardiographic diagnosis of AMI; in fact, the presence of reciprocal STD on the ECG has a positive predictive value for the diagnosis of AMI in the 90-95% range.1,2 Reciprocal changes noted in AMI are usually observed in the inferior, lateral, and right precordial leads. Recall that reciprocal STD may be seen in leads aVr and V1 in acute pericarditis. The relatively static nature of STE in patients with pericarditis may also help distinguish ST segment changes from AMI; the use of either ST segment trend monitoring or serial ECGs as well as a comparison with past electrocardiograms also can be useful in these settings.
Table 2. ECG Features of Acute Pericarditis
STE
Prominent Q waves
PR segment depression
PR segment-ST segment discordant ratio greater than 0.25
PR segment depression associated with pericarditis is perhaps the most useful feature for suggesting this diagnosis. This finding has been described by some authors as "almost diagnostic" for acute pericarditis. (See Figure 24, leads II and V3 to V6, and Figure 25, middle panel.)5 Reciprocal PR segment elevation is seen in lead aVr. (See Figure 24 in, lead aVr, and Figure 25, lower panel.) For unknown reasons, PR segment abnormalities are best seen in leads V5 and V6, followed by the inferior leads.
This PR segment-ST segment discordant relationship may also be helpful in discriminating between the STE caused by acute pericarditis and benign early repolarization (BER). This can be assessed by comparing the heights of the ST segment and T wave in lead V6: the ST segment/T wave magnitude ratio. Using the PR segment as the baseline for the ST segment and the J point as the beginning of the T wave, the heights are measured. If the ratio is greater than 0.25, pericarditis is the likely diagnosis; a ratio less than 0.25 suggests BER.
This ratio may be calculated in electrocardiographic leads other than V6, including V5, V4, and I. In essence, this ratio reflects the conduction differences in the two syndromes. In BER, the J point is elevated minimally with a prominent T wave. In pericarditis, the J point is elevated to a significantly greater extent, with a less prominent T wave; furthermore, PR segment depression only increases the STE contribution to this ratio. (See Figure 26, in which this discordance ratio is used to distinguish BER from acute pericarditis.)5,7,8
Pericardial effusion may also be seen in patients with pericarditis. Electrocardiographic observations suggestive of this diagnosis include widespread low voltage (resulting from increased resistance to current flow with the accumulated fluid) and electrical alternans (a beat-to-beat alteration in QRS complex size due to shifting fluid in the pericardium).
Benign Early Repolarization. The syndrome of benign early repolarization, first described in 1936 by Shipley and Hallaran,9 is felt to be a normal variant and is not indicative of underlying cardiac disease. BER has been reported in men and women of all age groups and in people of varying ethnic background. About 1% of the general population will have early repolarization on their ECG, with an increased incidence among younger individuals. Among adult ED chest pain patients, BER is seen at an increased frequency and is encountered in 12% of such cases.2 BER is seen on the ECG in 23-48% of adult ED chest pain patients who have used cocaine.10
In a large population-based study of BER, the mean age of patients with this ECG finding was 39 years, with an age range of 16-80. The syndrome was seen predominantly in patients younger than 50 years of age and was rarely encountered in individuals over 70 (3.5%).11 Men manifest BER significantly more often than women. And, for unknown reasons, BER is more often encountered in black males between the ages of 20-40 years,12 although some authors dispute this observation.11
Recall that the ST segment of the cardiac electrical cycle represents the period between depolarization and repolarization of the left ventricle. Characteristically, the ST segment is isoelectric, meaning that it is neither elevated nor depressed relative to the TP segment. The electrocardiographic definition of BER includes the following characteristics: ST segment elevation; upward concavity of the initial portion of the ST segment; notching or slurring of the terminal QRS complex; symmetric, concordant T waves of large amplitude; widespread or diffuse distribution of STE on the ECG; and relative temporal stability.13,14
The STE begins at the "J" (or junction) point (i.e., the portion of the electrocardiographic cycle where the QRS complex ends and the ST segment begins). The degree of J-point elevation is usually less than 3.5 mm.13 Morphologically, the STE appears as if the ST segment has been evenly lifted upwards from the isoelectric baseline at the J point.42 This elevation results in a preservation of the normal concavity of the initial, up-sloping portion of the ST segment-T wave complex. This is an important electrocardiographic feature that is used to distinguish between BER-related STE from STE associated with AMI.
The STE elevation encountered in BER is usually less than 2 mm, but may approach 5 mm in certain individuals. Overall, 80-90% percent of individuals demonstrate STE that is 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 greater than 5 mm.13,15 The greatest degree of STE related to BER is usually observed in the mid- to left precordial leads (leads V2 to V5). The ST segments in other electrocardiographic leads tend to be less elevated than those in leads V2 through V5. The limb leads (I, II, III, aVl, and aVf) demonstrate STE even less frequently. In one large series, limb leads revealed STE in only 45% of cases with BER.13-15 In this regard, "isolated" BER in the limb leads (i.e., with no precordial STE) is a very rare find. In addition, the presence of "isolated" STE in the inferior (II, III, and aVf) or lateral (I and aVl) leads should prompt consideration of another explanation.
Finally, the chronicity of STE in BER can help confirm the diagnosis (i.e., patients tend to demonstrate a consistent pattern of STE over time). Exceptions to this statement, however, should be noted. For example, some individuals who are monitored over prolonged periods demonstrate magnitude changes in their STE. The magnitude of BER may also diminish as the patient ages. In 25-30% of patients with BER noted on their ECG, electrocardiographic analysis many years later will demonstrate complete disappearance of the pattern.11,13,15
The J point itself is frequently notched or irregular in contour and is considered highly suggestive, but not diagnostic, of BER.16,11,15 Prominent T waves of large amplitude and slightly asymmetric morphology are also encountered; the T waves may appear "peaked," whch is suggestive of the hyperacute T wave encountered in patients with AMI. The T waves are concordant with the QRS complex and are usually found in the precordial leads. The height of the T waves in BER ranges from approximately 6.5 mm in the precordial distribution to 5 mm in the limb leads.5,11,13 (See Figures 27 and 28 for examples of BER.)
In the setting of STE, several electrocardiographic features help distinguish BER from AMI. Especially useful for making this distinction is analysis of the ST segment/T wave complex waveform, the presence of reciprocal changes, and evolutionary changes. At times, however, making this distinction can be difficult, as suggested by one study noting that 30% of patients who incorrectly received thrombolytic therapy for presumed AMI actually had BER (a non-infarction chest pain syndrome) on the ECG.17 (Table 3.)
Table 3. ECG Features Distinguishing AMI from BER
BER
Initial, up-sloping portion of the ST segment/T wave complex is concave
Absence of Reciprocal changes
AMI
Initial, up-sloping portion of the ST segment/T wave complex is convex or
flattened
Presence of reciprocal changes
Presence of Q waves
First, the initial, up-sloping portion of the ST segment/T wave complex is concave in BER, as compared to being either flattened or convex in the AMI patient. This morphologic observation should only be used as a guideline. Reciprocal changes, defined as ST segment depression in leads distant from the area of acute infarction, is a very useful electrocardiographic finding suggestive of MI.1 Reciprocal changes are not encountered in patients with BER; the electrocardiographic finding of ST segment depression greater than 1 mm in a patient with STE on the ECG should suggest the possibility of AMI.7 The combined findings of ST segment elevation greater than 1 mm in two anatomically contiguous leads and reciprocal ST segment depression increase diagnostic accuracy for AMI to 90%.1,2 The addition of Q waves to the findings of reciprocal change and STE also strongly suggests the possibility of AMI.7
Left Ventricular Aneurysm. Left ventricular aneurysm (LVA), also described as dyskinetic ventricular segment, is defined as a localized area of infarcted myocardium that bulges outward during both systole and diastole. LVA is most often noted after large anterior wall infarction, but it may also be encountered after inferior and posterior wall myocardial injury. In most cases, LVA is manifested electrocardiographically by varying degrees of STE, which may be difficult to distinguish from ST segment changes due to AMI.5,18 STE associated with LVA probably results from either an injury current originating from viable-but ischemic-myocytes in the aneurysm, or, alternatively, from mechanical wall stress caused by traction on the normal, adjacent myocardium.
Electrocardiographically, LVA is characterized by persistent STE that develops several weeks after AMI. Because LVA is frequently anterior in location, STE is usually observed in leads I, aVl, and V1-V6. As would be expected, the surface ECG of inferior wall LVA is characterized by STE in the inferior leads; in these locations, STE is usually 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. Consequently, distinguishing LVA-mediated STE from AMI may be difficult.5
When present, reciprocal change-an electrocardiographic feature of AMI-strongly suggests that ST segment changes, at least in part, are the result of acute infarction. Patients with LVA, which is usually the result of extensive anterior wall infarction, may also have significant Q waves. In contrast, the simultaneous appearance of a Q wave is not a feature that unquestionably supports the electrocardiographic diagnosis of LVA. The dynamic nature of AMI-related STE compared to the often static ST segment character in LVA means that a review of previous ECGs, serial ECGs, or ST segment trend monitoring can be of considerable diagnostic value. (See Figures 3c, 29, and 30 for examples of LVA. Figure 3c is in the supplement to Emergency Medicine Reports, Vol. 19, No. 8, April 13, 1998.)
Cardiomyopathies. Cardiomyopathies also can produce electrocardiographic patterns that simulate findings associated with ischemic heart disease.5,18 These findings include significant Q waves, ST segment changes, and T wave abnormalities; moreover, these patients may also present with LVH and bundle branch block patterns.
Underlying anatomic lesions producing these ECG changes are diverse, but generally reflect focal and global hypertrophy, ventricular dilation, and wall thinning. The end result is altered myocardial mass and configuration, which can produce electrocardiographic pseudoinfarction patterns. For example, noninfarctional Q waves may appear in the right precordial and inferior leads of patients with hypertrophic cardiomyopathy due to massive septal hypertrophy and associated altered depolarization vector. Altered ventricular activation, which is seen in patients with both hypertrophic and idiopathic cardiomyopathies, may produce marked ST segment/T waves changes that, at times, can mimic AMI.
Cardiomyopathies also may produce significant Q waves in the inferior and right precordial distributions; in some cases, these Q waves may be seen across the precordium and involve the entire anterolateral region of ECG. As is true with LBBB, VPR, and LVH, those leads with Q waves may display STE with prominent T waves. Once again, the rule of appropriate QRS complex-ST segment/T wave discordance is a useful guide for predicting expected morphologies. The STE seen in these leads is usually less than 5 mm in height; the initial upsloping portion of the ST segment/T wave complex is concave in appearance compared to the either obliquely flat or convex structure of AMI.
In most cases of cardiomyopathy with noninfarctional STE, the STE is atypical in appearance for AMI. Certain examples of STE seen in patients with cardiomyopathy may be impossible to distinguish from AMI. In other instances, the ED physician must realize that such patterns are the new normal electrocardiographic findings for patients with cardiomyopathy; as such, actual ischemic change will be superimposed upon these "baseline" abnormalities. (See Figures 31a-31c for examples of hypertrophic and idiopathic cardiomyopathies with STE.)
Table 4. ECG Signs of Hyperkalemia
Presence of tall, symmetric T waves
Shortened QTinterval
Prolonged PR interval
Widening QRS complex
Acute Myocarditis. Acute myocarditis can be caused by a range of infectious agents and it frequently presents with acute pulmonary edema, high-grade atrioventricular block, ventricular arrhythmia, and significant ST segment/T wave abnormalities. The acute inflammatory process can lead to myocardial necrosis and marked, permanent ventricular dysfunction. The ST segment/T wave abnormalities include ST segment changes-both elevation and depression-as well as numerous T wave morphologies. These changes may reflect an associated bundle branch block. Q waves may also be encountered.
Although acute myocarditis may be found in patients of all ages, this clinical entity may be difficult to distinguish from AMI complicated by ventricular arrhythmia and pulmonary edema.5,18 Figure 32 presents the ECG of a 45-year-old male who presented with ventricular tachycardia and pulmonary edema. Although the patient's initial presentation and electrocardiographic findings suggested anterolateral AMI, the entire picture resulted from acute myocarditis.
Table 5. ECG Signs of Hypothermia
J point and the adjacent ST segment that appear to
have lifted off the iso-electric baseline
Bradycardia
Tremor artifact
Prolongation of the PR and QT intervals
T wave inversions in leads with pre-eminent J waves
Other Syndromes Producing STE
Hyperkalemia. The earliest sign of potassium intoxication (i.e., hyperkalemia) is the appearance of tall, symmetric T waves. Typically, this T wave morphology is described as "hyperacute" and may be confused with the hyperacute T wave of early transmural myocardial infarction.5 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 in supplement to the April 13, 1998, issue.) The QT interval may also become shortened at this point. With additional increases in serum potassium concentration, the PR interval is prolonged and eventually is followed by QRS complex widening, an ominous sign. (See Figure 33.)
In early stages of QRS complex widening, the ST segment may appear elevated, a source of possible confusion. In general, this pseudo-STE associated with hyperkalemia is characterized by J point elevation and prominent, hyperacute T waves. The initial, upsloping portion of the ST segment is concave rather than the flat or convex patterns seen in the AMI patient with STE. (See Figure 33 for an example of sinus rhythm with a markedly widened QRS complex.) (Table 4.)
Pre-excitation Syndromes. Pre-excitation syndromes, which usually involve Wolff-Parkinson-White syndrome (WPW), frequently present with either evidence of ventricular pre-excitation or arrhythmias. Evidence of pre-excitation includes the classic electrocardiographic triad of PR interval shortening, a Delta wave, and QRS complex widening. The patient may present with "typically appearing" paroxysmal supraventricular tachycardia, rapid, bizarre atrial fibrillation, broad-complex tachycardia, or sudden cardiac death. Regardless of the presentation, the classic triad may be apparent following stabilization and restoration of sinus rhythm.
Also of concern are various pseudo-infarction findings that, if not recognized, may lead to the wrong diagnosis and inappropriate therapy.5 For instance, Q waves may be seen in leads II, III, and aVf, which may mimic previous inferior myocardial infarction; tall R waves in the right precordial leads are suggestive of a posterior wall AMI. The ED physician must not only recognize the pseudo-infarction pattern of the WPW but also realize that such patterns may initially conceal early findings of AMI. Figure 34 demonstrates STE in the inferior leads in a patient with the classic triad of WPW findings, including PR interval shortening, a Delta wave, and QRS complex widening.
Hypothermia. When core body temperature approaches 32°C, hypothermia produces alterations in the ECG that might be mistaken for AMI. Most often, hypothermia-related electrocardiographic changes are observed at the junction between the terminal portion of the QRS complex and the initial ST segment (i.e., the J point). The J point and the adjacent ST segment appears to have lifted off the iso-electric baseline. Unlike the J point elevation seen in BER, in which the J point and ST segment are uniformly lifted upward, the J point and adjoining ST segment in hypothermia are unevenly elevated off the baseline. The resulting configuration produces the J wave, also know as the Osborn wave, or the Osborn J wave. (See Figure 35 for an example of an ECG depicting the J wave in a hypothermic patient.) (Table 5.)
In the typical situation, the J wave and related STE are most prominent in the mid-precordial and lateral precordial leads; it is seen to a lesser extent in the limb leads. In general, the amplitude of the J wave is inversely proportional to the degree of hypothermia; the J wave will increase in amplitude as the core temperature continues to drop and, conversely, will lessen as successful rewarming progresses. Other electrocardiographic features associated with hypothermia include: bradycardia; tremor artifact; prolongation of the PR and QT intervals; T wave inversions in leads with prominent J waves; and arrhythmias such as atrial fibrillation and ventricular fibrillation.5
Table 6. ECG Signs of CNS Disorders
Diffuse, deep inversion of T wave
Prominent U waves of either polarity
QT prolongation that can exceed 60% of normal value
Central Nervous System (CNS) Disorders. Certain intracranial disasters may produce significant ST segment-T wave changes.5 Most often, these alterations involve the T wave with diffuse, deep inversion. In the setting of a CNS event, relatively minor degrees of STE have been reported in leads with obviously abnormal T waves. The amplitude of the T wave inversion is impressive, approaching 15 mm in some cases. Morphologically, the T wave is asymmetric with a characteristic outward bulge in its ascending portion.
STE frequently is less noticeable than the T wave changes-usually, it is less than 3 mm. Other electrocardiogaphic features associated with acute CNS injury include prominent U waves of either polarity and QT prolongation often exceeding 60% of its normal value. The T wave inversions with associated STE are most pronounced in the mid-precordial and lateral precordial leads; such findings are also noted to a less extent in the limb leads. Figure 36 presents the ECG of a patient with a subarrachnoid hemorrhage; note the STE with T wave inversions in the anterolateral leads, suggestive of AMI. (Table 6.)
Although these ST segment/T wave abnormalities usually are encountered in patients with subarrachnoid bleed, other acute CNS events may also present with these electrocardiographic findings. Other conditions causing ECG changes include intraparenchymal hemorrhage, thromboembolism with infarction, cerebral artery occlusion, and CNS mass lesion with edema. Overall, 60% of patients with subarrachnoid hemorrhage will manifest an electrocardiographic abnormality. The pathophysiologic explanation for such electrocardiographic findings is controversial but may involve either CNS-mediated increases in sympathetic and vagal tone as well as actual myocardial damage called, "contraction band necrosis."
Acute Abdominal Disease. Acute abdominal disorders (e.g., pancreatitis, cholecystitis, hepatitis, and peritonitis) have been reported to cause electrocardiographic abnormalities ranging from Q waves to ST segment abnormalities.19 STE, which has been observed in patients with gastrointestinal emergencies, may be difficult to distinguish from from AMI. For example, the elderly diabetic patient presenting with epigastric pain and emesis who manifests STE on the ECG will almost certainly be diagnosed with AMI.
The majority of such patients will, in fact, have AMI while a minority will experience non-cardiac discomfort with an abdominal etiology. The pathophysiologic mechanism for ECG changes in abdominal disease is poorly understood but may involve direct transdiaphragmatic epicardial irritation or electrocardiographic detection of the visceral inflammatory process; either process can generate a current of injury manifested by STE. The STE may take many forms, ranging from minimal and concave to pronounced and convex.
Clinical Strategies for ECG Diagnosis: A Summary
Several strategies are available to facilitate accurate interpretation of electrocardiographic patterns in patients with chest pain. First, a knowledge of the associated, or anticipated, ST segment/T wave changes resulting from the confounding and mimicking patterns is a prerequisite for clinical management. Abnormalities of the ST segment/T wave complex that are not consistent with the altered patterns should alert the physician to the possibility of acute ischemic electrocardiographic change.5,22 Use of the rule of appropriate discordance is of considerable use in patients with LBBB, VPR, and other situations.
In other cases, serial ECGs may demonstrate the dynamic electrocardiographic changes usually encountered in acutely ischemic patients.20,21 For example, refer to Figures 37a and 37b for two examples of the serial ECG technique-both in lead V3. In the first example (Figure 37a), a 40-year-old male presented to the ED with chest discomfort after using cocaine. The ECG revealed STE in the anterior leads which was suggestive of BER and also worrisome for AMI. Serial ECGs were performed while the patient received appropriate medical therapy. The ECGs did not reveal change of the STE, suggesting a nonischemic etiology for electrocardiographic abnormality. His pain resolved without further change; the STE was felt to be due to BER.
The second example in Figure 37b was encountered in a patient with chest pain and known electrocardiographic LVH on past ECGs. The current ECG demonstrated STE which was felt to represent LVH-related change. Continued chest pain prompted the application of serial ECGs which revealed dynamic change with progressive STE indicative of AMI. The patient received a thrombolytic agent with good clinical results; elevated troponin I confirmed the diagnosis of AMI.
References
1. 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.
2. 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.
3. Larsen GC, Griffith JL, Beshansky JR, et al. Electrocardiographic left ventricular hypertrophy in patients with suspected acute cardiac ischemia-It's influence on diagnosis, treatment, and short-term prognosis. J Gen Intern Med 1994;9:666-673.
4. Huwez FU, Pringle SD, Macfarlane FW. Variable patterns of ST-T abnormalities in patients with left ventricular hypertrophy and normal coronary arteries. Brit Heart J 1992;67:304-347.
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: Mosby; 1994:169-216.
6. Brady WJ. Electrocardiographic left ventricular hypertrophy in chest pain patients: Differentiation from acute coronary ischemic events. Am J Emerg Med (1998 accepted/pending).
7. Spodick DH. Differential diagnosis of the electrocardiogram in early repolarization and acute pericarditis. N Engl J Med 1976;295:523-526.
8. Glinzton LE, Laks MM. The differential diagnosis of acute pericarditis from the normal variant: New electrocardiographic criteria. Circulation 1982;65:1004-1009.
9. Shipley RA, Hallaran WR. The four-lead electrocardiogram in two hundred normal men and women. Am Heart J 1936;11:325-45.
10. Hollander JE, Lozano M, Fairweather P, et al. "Abnormal" electrocardiograms in patients with cocaine-associated chest pain are due to "normal" variants. J Emerg Med 1994;12:199-205.
11. Mehta MC, Jain AC. Early repolarization on scalar electrocardiogram. Am J Med Sci 1995;309:305-311.
12. Thomas J, Harris E, Lassiter G. Observations on the T wave and S-T segment changes in the precordial electrocardiogram of 320 young negro adults. Am J Cardiol 1960;5:468-474.
13. Wasserburger RM, Alt WJ, Lloyd C. The normal RS-T segment elevation variant. Am J Cardiol 1961;8:184-192.
14. Brady W. Benign early repolarization: Electrocardiographic manifestations and differentiation from other ST segment elevation syndromes. Am J Emerg Med (1998 accepted/pending).
15. Kabara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38:157-161.
16. 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.
17. 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.
18. 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.
19. Ryan ET, Pak PH, DeSanctis RW. Myocardial infarction mimicked by acute cholecystitis. Ann Int Med 1992;116:218-220.
20. 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.
21. Fesmire FM, Percy RF, Bardoner JB, et al. Usefulness of automated serial 12-lead ECG monitoring during the initial emergency department evaluation of patients with chest pain. Ann Emerg Med 1998;31:3-11.
22. Brady WJ, Aufderheide TP: Left Bundle Block Pattern Complicating the Evaluation of Acute Myocardial Infarction. Acad Emerg Med 1997;4:56-62.
++++Physician CME Questions
All of the following statements regarding electrocardiographic LVH and associated ST/T wave changes are true except:
A. the rule of appropriate discordance applies.
B. they are frequently not recognized and therefore misdiagnosed as ischemic change in chest pain patients.
C. ST segment elevation is always seen in all leads with prominent QRS complexes due to LVH.
D. LVH-related ST segment changes are relatively permanent.
::::Electrocardiographic features of LVH include all of the following except:
A. poor R wave progression in the right- to mid-precordial leads.
B. prominent ST segment depression in the right precordial leads.
C. QS complexes are usually seen in leads V1 and V2.
D. associated STE frequently has a concave morphology.
::::In acute pericarditis, all of the following electrocardiographic findings are correctly matched with the ECG stage except:
A. resolution - stage 4.
B. STE - stage 1.
C. T wave inversion - stage 3.
D. Q wave formation - stage 2
::::Electrocardiographic features of acute pericarditis include all of the following except:
A. ST segment elevation.
B. T wave inversion.
C. QRS complex widening.
D. PR segment depression.
::::Benign early repolarization is characterized electrocardiographically by all of the following except:
A. prominent T waves.
B. poor R wave progression.
C. ST segment elevation with J point elevation.
D. peaked T waves similar to the hyperacute T wave of hyperkalemia.
::::Features useful in distinguishing between acute pericarditis and benign early repolarization include all of the following except:
A. the presence of q waves in BER .
B. the PR/ST discordant ratio.
C. PR segment depression in acute pericarditis.
D. None of the above
::::WPW syndrome is characterized on the ECG by all of the following except:
A. PR segment depression.
B. QRS widening.
C. Delta wave.
D. PR interval shortening.
::::STE on the ECG is characterized by all of the following except:
A. LVH and LBBB are common causes.
B. is noted in only 25 to 50% of all patients with AMI initially.
C. AMI is the most frequent cause in chest pain patients.
D. may be caused by CNS or abdominal events.
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