Acute Coronary Ischemia and Infarction
Figures
Figure 6-16.
Right ventricular ischemia with inferior wall infarction. A: ST-segment elevations in leads II, III, and aVF are
accompanied by ST-segment elevations in V1. B: The right-sided ECG confirms ST-segment elevation in the
right ventricle (V4R).
A
B
91
ElEctrocardiography in EmErgEncy mEdicinE
Figures
Figure 6-17.
Anterior wall aneurysm. This patient presented after 2 hours of chest pain. He had a history of myocardial
infarction, but no previous ECG was available. The prominent QS waves in leads V1 through V5 and the ST-
segment elevations in these leads without significant T-wave abnormalities suggest aneurysm. Reciprocal
changes in the inferior leads are absent. Emergent angiogram for presumed STEMI revealed an apical
aneurysm with impending rupture and thrombus. No significant LAD lesions were detected. The persistence
of ST-segment elevations more than 2 to 3 weeks after infarction suggests a ventricular aneurysm. A followup
ECG was not available in this case.
Figure 6-18.
Anterolateral STEMI and the RBBB pattern. RBBB primarily affects the terminal phase of ventricular
depolarization, producing a wide R wave in the right chest leads (V1 through V2) and a wide S wave in the left
chest leads (V3 through V6). A pattern of acute anterior lateral wall infarction is indicated by the ST-segment
elevations in leads V1 through V6.
92
Acute Coronary Ischemia and Infarction
Figures
Figure 6-19.
A: Typical LBBB pattern. Note the poor R-wave progression in the right precordial leads and the discordance
of QRS and ST/T vectors reflected by ST-segment elevations in the right precordial leads and ST-segment
depressions with T-wave inversions in the left precordial leads. B: A subsequent ECG from this patient showed
the development of ST-segment elevation of more than 1 mm in lead V3 (5 points in the Sgarbossa criteria).
There are also terminal T-wave inversions in leads V2 and V3 caused by anterior ischemia. An angiogram
showed 100% occlusion of the proximal LAD coronary artery.
A
B
93
ElEctrocardiography in EmErgEncy mEdicinE
Figures
Figure 6-20.
AMI in the setting of a paced rhythm. This ECG has ST-segment depression of 1 mm or more in lead V1, V2, or
V3 concordant to (in same direction as) the QRS complex and ST-segment elevation of 5 mm or more that was
discordant with (in the opposite direction from) the QRS complex. ST-segment elevation or 5 mm or more in
predominantly negative QRS complexes is the best marker, with a sensitivity of 53% and specificity of 88%.
94
C h apter s eve n
Additional-Lead Testing in
Electrocardiography
Andrew D. Perron, MD, and William J. Brady, MD
The standard 12-lead ECG is a useful infarction. These two entities are at risk of
but clearly limited tool in the search for the being underdiagnosed, because placement for
emergency department patient at risk for acute the standard 12-lead ECG does not allow these
coronary syndrome. For example, one study1 areas of myocardium to be assessed directly.6
examined the initial ECG in a group of adult Additional leads that can be used to examine
patients with chest pain, all of whom were these “silent” areas include the right-sided lead
subsequently proved to have had an AMI. V4R (also termed RV4), which reflects electrical
Less than 50% of these patients demonstrated current changes in the right ventricle,7 and
ST-segment elevation on their initial ECG; the posterior leads V8 and V9, which image
the remaining patients manifested a variety the posterior wall of the left ventricle.6
of ischemic changes, including ST-segment
depression and T-wave inversion. Perhaps of The Right Ventricular Leads
greatest concern to the emergency clinician is
that, in 30% of patients, the initial ECG was Cohn et al8 were the first to describe right
normal or showed nonspecific changes only. This ventricular infarction as the clinical syndrome of
same study also demonstrated that ST-segment hypotension, elevated jugular venous pressure,
depression was a relatively poor indicator of AMI; and shock in the presence of clear lung fields. The
less than 50% of patients who presented with true incidence of right ventricular infarction is
isolated precordial ST-segment depression were uncertain. Reported rates vary depending on the
subsequently determined to have had an AMI. method of detection used, eg, autopsy, invasive
studies, or noninvasive imaging, including
Some authors have suggested that the electrocardiography.7 Although isolated right
sensitivity of the 12-lead ECG can be improved ventricular infarction is presumably a rare
if additional body surface leads are used for the phenomenon, ECG studies have consistently
evaluation of chest pain in selected individuals.2–5 shown that right ventricular infarction will
The two coronary syndromes that could be accompany approximately one third of inferior
more easily identified by such a strategy are wall AMIs.9–11 The anatomic reason for this
acute posterior and right ventricular myocardial association with inferior ischemia is that most
95
Electrocardiography in Emergency Medicine
right ventricular infarctions result from occlusion ST-segment elevation is correspondingly less.
of the right coronary artery proximal to the right In comparing the diagnostic performance of six
ventricular branch. The left circumflex artery right-sided leads (V1R through V6R) with a single-
supplies the right ventricle in approximately lead V4R, the literature has demonstrated similar
10% of patients and, in this situation, right rates of right ventricular infarction diagnosis.4
ventricular infarction can present in the setting
of a lateral wall AMI, as opposed to inferior MI. Identifying right ventricular involvement
can be important, because patients with
A number of findings on the standard 12-lead coexisting inferior infarction have a larger
ECG are suggestive of right ventricular AMI, amount of jeopardized myocardium than do
including ST-segment elevation in the inferior patients without right ventricular involvement.
leads (II, III, and aVF)12 or in the right precordial As a result, they are at increased risk for life-
chest leads, particularly V1, the only one of threatening complications, including high-grade
the standard 12 leads that reflects the right AV blocks,10 atrial fibrillation, symptomatic
ventricle.10,13–15 On occasion, coexisting AMI of the sinus bradycardia, atrial infarction, cardiogenic
left ventricle’s posterior wall can obscure the ST- shock, cardiopulmonary arrest, and death.7
segment elevation resulting from right ventricular In fact, the complication rate for this type of
infarction in lead V .1 16–18 A pattern of the relative infarction is similar to that expected of anterior
magnitudes of the ST-segment elevation in the AMIs.23 Aggressive therapy is warranted to limit
inferior leads could indicate right ventricular adverse events. Zehender et al24 showed that
AMI—when ST-segment elevation is greatest in patients with right ventricular AMI diagnosed
lead III compared with the other inferior leads, by ST-segment elevation in V4R had significantly
then right ventricular infarction is suggested. reduced mortality rates and in-hospital
Other findings suggestive of right ventricular complications if they received thrombolysis.
AMI in the presence of inferior wall MI include
the presence of a right bundle-branch block,19,20 Because patients with right ventricular AMI
second- and third-degree atrioventricular are pre-load dependent for left ventricular
(AV) blocks,21 and ST-segment elevation in filling, they are vulnerable to nitrate-induced
lead V2 50% greater than the magnitude hypotension. Under these circumstances, the
of ST-segment depression in lead aVF.22 usual treatment for AMI can induce potentially
dangerous hypotension. ST-segment elevation in
The addition of lead V4R provides objective lead V4R should prompt the physician to avoid the
evidence of right ventricular involvement that can use of nitrates and other vasodilating agents and
be noted on the 12-lead ECG. Right ventricular to administer crystalloid infusions judiciously to
infarction can be diagnosed with 80% to 100% avoid systemic hypotension. Negative inotropes
sensitivity by ST-segment elevation of more (such as -blockers) should be used extremely
than 1 mm in lead V R.4 7,10,11 Robalino et al20 cautiously in patients identified as having right
found that ST-segment evaluation above 1 mm ventricular AMI, because administration of
in V4R has 100% sensitivity, 87% specificity, these drugs could lead to severe hypotension.
and 92% predictive accuracy in detecting acute
infarction of the right ventricle resulting from The Posterior Leads
occlusion of the right coronary artery above its
first ventricular branch.20 As shown in Figure The term posterior myocardial infarction
7-1, the magnitude of the ST-segment elevation refers to AMI of the posterior wall of the left
can be less pronounced than is usually seen in ventricle. This region is supplied by either
the standard 12 leads of the ECG. This finding the left circumflex artery or, less frequently, a
results from the fact that the right ventricle is dominant right coronary artery with prominent
composed of considerably less muscle mass posterolateral or posterior descending branches.
than is the left ventricle; with less myocardium Consequently, infarctions involving the posterior
manifesting a current of injury, the degree of wall usually occur in conjunction with inferior
or lateral AMIs and are estimated to occur in
96
Additional-Lead Testing in Electrocardiography
15% to 20% of all infarctions.25 Isolated posterior Evaluating the posterior wall through the
myocardial infarctions occur less commonly. 15-lead ECG is often more rewarding than
The rapid recognition of posterior myocardial the 12-lead evaluation. ST-segment elevation
infarction is important for several reasons. greater than 1 mm in V8 and V9 confirms the
Patients with inferior or lateral wall AMI with diagnosis of posterior myocardial infarction;
concomitant posterior myocardial infarction are such a finding is more indicative of AMI than
experiencing a larger infarction; in essence, two the anterior lead findings described above.3,4,16
walls of the left ventricle are involved. The risks In fact, the sensitivity could be as high as
of dysrhythmia, left ventricular dysfunction, and 90% for identifying posterior AMIs,31 with a
death increase proportionally with the size of the predictive accuracy up to 93.8%.6 Notably,
infarct. Therefore, the combination of inferior or false-positive ST-segment elevation in V8 and
lateral AMI with posterior myocardial infarction V9 occurs at the same frequency encountered
is a factor for less favorable prognosis.26–29 In a in the 12-lead ECG.25 However, the degree of
recent survey, many cardiologists and emergency ST-segment elevation could be significantly less
physicians indicated they would be more likely in the posterior leads than in the anterior leads
to administer thrombolytic agents if they saw because of the greater distance between the
ECG evidence suggestive of posterior myocardial epicardial surface and the surface leads as well
infarction.30 However, current protocols for the as the amount of interposed tissues (Figure 7-3).
thrombolytic treatment of AMI do not specifically
address isolated posterior myocardial infarction. A recent increase in the use of posterior
chest leads has indicated that the incidence of
Using the standard 12-lead ECG to identify posterior myocardial infarction is higher than
posterior myocardial infarction can be once thought. Posterior myocardial infarction
challenging. ECG changes occur primarily in was thought to be very rare, but it can be present
V1 and V2, occasionally extending to V3. These in as many as 11% of cases of AMI.2,3,7,32 Similar
include 1) horizontal ST-segment depression, to right ventricular AMIs and V4R, ECG changes
2) a tall, upright T wave, 3) a tall, wide R wave, in V8 and V9 might provide information about
and 4) an R/S wave ratio greater than 1.25 These the amount of myocardium involved and the
changes seem more familiar when thought of potential complications for isolated posterior
as a reversal of the ECG findings indicative of myocardial infarction and posterior myocardial
transmural AMI. They are reversed for posterior infarction associated with inferior and/or lateral
myocardial infarction because the endocardial AMI. Oraii et al32 observed that patients with
surface of the posterior wall faces the anterior posterior myocardial infarction who exhibit
precordial leads. In other words, “when reversed,” posterior-lead ST-segment elevation had more
the ST-segment depression, prominent R waves, frequent in-hospital complications than did
and tall, upright T waves in leads V1 to V3 matched control subjects (odds ratio of 7).
represent the ST-segment elevation, prominent
Q waves, and T-wave inversions of posterior Recently, valuable information regarding
myocardial infarction (Figure 7-2). When viewed the pathophysiology and natural history of
in this manner, the ECG changes on the 12- posterior myocardial infarction has been
lead ECG in posterior myocardial infarction revealed through ECG studies performed during
assume a more familiar, ominous significance. coronary angiography. Khaw et al33 demonstrated
Indications of coexisting infarctions on the improved detection of posterior myocardial
inferior or lateral walls of the left ventricle infarction using the 15-lead ECG during single-
are other ECG features that should stimulate vessel percutaneous transluminal coronary
consideration of acute posterior myocardial angioplasty of the right, circumflex, and left
infarction, particularly if these findings are anterior descending coronary arteries. Overall
accompanied by ST-segment depression or sensitivity during circumflex occlusion was 32%
prominent R waves in leads V1 to V3. for the 12-lead ECG versus 69% for the 15-lead
ECG when maximal ST-segment depression
97
Electrocardiography in Emergency Medicine
in leads V2 to V3 was considered secondary to 15-lead ECG should be obtained when there is
posterior wall injury. In a similar study, Wung et evidence of inferior AMI, lateral AMI, or ST-
al34 showed that adjusting the ischemic threshold segment depression in V1, V2, or V318,35 (Table
from 1 to 0.5 mm of ST-segment elevation in 7-1). Although the following indications are less
leads V7 to V9 improved sensitivity for diagnosing clearly established as emergency department
posterior myocardial infarction from 49% with indications, clinicians may consider using a
the 12-lead ECG to 94% with the 15-lead ECG. 15-lead ECG in the following situations: right
Future use of this lower criterion could increase bundle-branch block, second- and third-degree
the reported incidence of posterior myocardial AV blocks, and ST-segment elevation in lead
infarction from the 11% mentioned above.2,3,7,32 V2 less than 50% the magnitude of ST-segment
Correale et al19 suggested that higher in-hospital depression in aVF. Additionally, inferior AMI
mortality and complication rates found with presenting with hypotension is a strong indicator
right ventricular involvement are actually related of coexistent right ventricular infarction,
more to posterior extension masked by right although hemodynamic instability presents in
ventricular involvement than to right ventricular the minority of right ventricular AMI cases.7
involvement itself. This study evaluated patients
with inferior AMI using extra-lead ECGs (V3R Limitations of Additional-Lead
to V5R and V8 and V9), cardiac enzymes, cardiac Electrocardiography
catheterization, and other methods. Comparing
ECG markers, enzyme peaks, ejection fractions, In a few situations, additional-lead
and coronary scores, they concluded that the electrocardiography might not yield an accurate
masking of markers of posterior extension by diagnosis. Regarding right ventricular infarction,
right ventricular involvement is likely the result ST-segment elevation in lead V4R is represented
of electrical balancing. All these studies affirm by a rightward and anteriorly oriented vector.
the usefulness of the 15-lead ECG for diagnosing Consequently, leftward ST-segment deviation,
posterior myocardial infarction and predicting as seen in V5 and V6 during a lateral AMI, could
prognosis for patients in whom it develops. cancel the right-lead ST-segment elevation
and obscure the diagnosis. Additionally, if
Indications for Using ST-segment elevation is not prominent in the
Additional Leads inferior leads, it will be less prominent in V4R.
It is important to maintain a high index There are also cases of inferior wall AMI
of suspicion for right ventricular or posterior with simultaneous right ventricular infarction
wall involvement when evaluating emergency but false-negative ST-segment elevation in lead
department patients at risk for acute coronary V4R. A study by Kosuge et al36 suggests that this
syndrome with the 12-lead ECG, particularly phenomenon results from concomitant posterior
when only subtle abnormalities are present. A wall ischemia with a resultant current of injury
that attenuates ST-segment elevation otherwise
Table 7-1. observed in the right precordial leads. This study
Indications for obtaining additional-lead ECGs in involved patients with first-time inferior wall AMI
emergency department patients and total occlusion of the right coronary artery
proximal to its first ventricular branch. Patients
1. ST-segment depression or suspicious isoelectric ST without ST-segment elevation of more than 1
segments in leads V1 to V3 mm in V4R had a higher frequency of dominant
right coronary arteries in addition to greater
2. Borderline ST-segment elevation in leads V5 and V6 or levels of ST-segment elevation in V7, V8, and V9.
in leads II, III, and aVF
Several studies have suggested that the 15-
3. ST-segment elevation inferior AMIs (ST-segment lead ECG has greater sensitivity for identifying
elevation in leads II, III, and aVF) AMIs than the standard 12-lead ECG.2,3,6,16,17
Two of them are particularly noteworthy.
4. ST-segment elevation in leads V1 and V2 or isolated
ST-segment elevation in lead V1
98
Additional-Lead Testing in Electrocardiography
Zalenski et al16 compared 12- and 15-lead ECGs Agarwal et al38 used posterior chest leads
in a prospective study that demonstrated an (V7 through V9) on patients with chest pain
increase in sensitivity (from 47.1% to 58.5%) considered to have a cardiac cause but without
for the diagnosis of AMI by ST-segment ST-segment elevation on the 12-lead ECG. Of
elevation with the use of additional leads. 58 such patients (the authors did not mention
Specificity remained unchanged, and the odds the total number of patients screened), 18 had
of meeting ECG thrombolytic therapy criteria posterior-lead ST-segment elevation of more than
increased 6-fold. Later work by Zelenski et al17 1 mm or Q waves, and all 18 were confirmed to
revealed that additional-lead analysis increased have had AMI by creatine phosphokinase criteria
diagnostic accuracy modestly and influenced or cardiac catheterization. The investigators
therapy by increasing the administration of concluded that all patients with suspected AMI
fibrinolytic agents. These results, obtained but nondiagnostic 12-lead results should receive
in a patient population with a high suspicion posterior lead analysis. This conclusion can be
for acute coronary disease, are promising. extrapolated to suggest that strong consideration
be given to the use of 15-lead ECGs for suspected
More recent work by Brady et al37 involved AMI despite a nondiagnostic 12-lead ECG.4
emergency department patients with general
chest pain, not just those with suspected AMI Obtaining a 15-Lead ECG
or unstable angina, and therefore with a lower
pretest probability for AMI.37 This prospective A 15-lead ECG can be obtained by moving the
study with a real-time physician survey showed leads on a standard 12-lead machine or using
that the 15-lead ECG did not alter diagnostic a specialized 15-lead ECG machine. The least
and management decisions related to acute expensive method involves manipulating the
coronary ischemic syndromes (AMI and leads on a 12-lead machine to image additional
unstable angina). However, physicians thought areas of the heart. After a standard 12-lead ECG
the 15-lead ECG provided a more complete is obtained, the leads are moved as follows:
anatomic picture of the ischemic events than the right ventricular (right-sided) lead V4R is
did 12-lead ECGs. The authors concluded that moved to the right side of the chest in a position
all patients with chest pain in the emergency analogous to the left-sided lead V4 seen in Figure
department do not require a 15-lead ECG and 7-4, and the posterior leads V8 and V9 are moved
that more studies are needed to identify the to the patient’s left back at the tip of the scapula
patients who will truly benefit from 15-lead (V8) and half the distance between lead V8 and
analysis. These are likely to be patients with the paraspinal muscles (V9) (Figure 7-5).
right precordial lead ST-segment depression
and inferior or lateral AMIs, particularly those
with hypotension, as discussed above.
Key Facts
• The right ventricle and posterior wall of the left ventricle are not well visualized on the standard 12-
lead ECG.
• The additional lead (15-lead) ECG can be obtained using a standard 12-lead ECG machine.
• ST-segment elevation in lead V4R is indicative of a right ventricular infarction. Patients with
this entity are at increased risk for morbidity and mortality from the MI, and preload-reducing
medications should be used with caution, if at all.
• ST-segment elevation in leads V8 and V9 is indicative of a posterior left ventricular infarct. Patients
with this entity are also at increased risk for morbidity and mortality from the MI.
99
Electrocardiography in Emergency Medicine
Conclusions 8. Cohn JN, Guiha NH, Broder MI, et al. Right
ventricular infarction: clinical and hemodynamic
The 15-lead ECG is a potentially valuable tool features. Am J Cardiol. 1974;44:209-214.
used to identify right ventricular and posterior
wall infarctions, particularly if the diagnosis is 9. Zeymer U, Heuhaus KL, Wegscheider W, et al.
obscure on a routine 12-lead ECG. Its primary Effects of fibrinolytic therapy in acute myocardial
benefit is in providing information about the infarction with or without right ventricular
extent, severity, and potential complications involvement. J Am Coll Cardiol. 1998;32:876-881.
of some AMIs, particularly in areas that might
be missed by the standard 12-lead ECG. This 10. Braat SJ, Brugada P, DeZwaam C, et al. Value of the
can result in the identification of patients electrocardiogram in diagnosing right ventricular
who would benefit from more aggressive involvement in patients with acute inferior wall
therapeutic regimens. It could also prevent myocardial infarction. Br Heart J. 1983;49:368-372.
the deleterious administration of nitrates
to a patient with right ventricular AMI. 11. Klein HO, Tordjman T, Ninio R, et al. The early recognition
of right ventricular infarction: diagnostic accuracy of the
The 15-lead ECG is easily obtained and readily electrocardiographic V4R lead. Circulation. 1983;67:558-565.
available in most emergency departments. The
generally accepted indications for a 15-lead 12. Andersen HR, Nielsen D, Falk E. Right ventricular infarction:
ECG are inferior wall AMI, lateral wall AMI, diagnostic value of ST elevation in lead III greater than that of
and ST-segment depression in leads V1 to V3. lead II during inferior/posterior infarction, and comparison
Other 12-lead ECG findings suggestive of right with right chest leads V3R to V7R. Am Heart J. 1989;117:82-85.
ventricular AMI (ie, right bundle-branch block,
second- and third-degree AV blocks, and lead 13. Lopez-Sendon J, Coma-Canella I, Alcasena S, et al.
V2 ST-segment elevation of more than 50% Electrocardiographic findings in acute right ventricular
of the magnitude of ST-segment depression infarction: sensitivity and specificity of electrocardiographic
in lead aVF) might also prompt a 15-lead alterations in right precordial leads V4R, V3R, V1, V2,
investigation. Further clinical research is needed and V3. J Am Coll Cardiol. 1985;6:1273-1279.
to define the ultimate role of the 15-lead ECG
in routine emergency department practice. 14. Croft C, Nicord P, Corbett JR, et al. Detection of
acute right ventricular infarction by precordial
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26. Brush JE, Brand DA, Acamparo D, et al. Use of the initial 33. Khaw K, Moreyra A, Tannenbaum A, et al. Improved
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29 Matetzky S, Freimark D, Chouraqui P, et al. Significance of and body surface mapping. Ann Emerg Med. 1997;29:28-33.
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patients with acute inferior myocardial infarction: application 36. Kosuge M, Kimura K, Ishikawa T, et al. Implications of the
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have inferior wall acute myocardial infarction with right
30. Novak PG, Davies C, Ken GG. Survey of British Columbia ventricular involvement. Clin Cardiol. 2001;24:225-230.
cardiologists’ and emergency physicians’ practice of
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in the diagnosis and treatment of acute myocardial 15-lead ECGs in ED chest pain patients: impact on diagnosis,
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31. Perloff JK. The recognition of strictly posterior 38. Agarwal J, Khaw K, Aurignac F, et al. Importance
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electrocardiography. Circulation. 1964;30:706-718. myocardial infarction, but nondiagnostic routine 12-lead
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32. Oraii S, Maleki M, Tavakolian AA, et al. Prevalence
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101
Electrocardiography in Emergency Medicine
Figures
Figure 7-1.
V4R lead in a patient with inferior MI identified on a standard 12-lead ECG. Note the Q wave preceding the ST
complex and the marked ST-segment elevation in this lead.
Figure 7-2.
The ECG relationship between leads V1 and V2 and their posterior correlates (V8 and V9). A posterior wall MI will
have a “reversal” of the findings typical for transmural MI in leads V1 and V2. Specifically, the standard ECG will
demonstrate ST-segment depression, a prominent R wave, and upright T waves in these leads. When viewed
with leads V8 and V9, these same findings are recognized as a typical transmural AMI pattern, with ST-segment
elevation, pathologic Q waves, and T-wave inversions. Reprinted from: Brady WJ, Erling B, Pollack M, et al.
Electrocardiographic manifestations: acute posterior wall myocardial infarction. J Emerg Med. 2001;20(4):397.
With permission from Elsevier.
102
Additional-Lead Testing in Electrocardiography
Figures
Figure 7-3.
A: Standard 12-lead ECG from a patient experiencing a lateral AMI. Note ST-segment depression in leads V1
through V3 and ST-segment elevation in leads V5 and V6. B: Posterior leads (V8 and V9) from the same patient
as in Figure 7-3A. Note the subtle but definite ST-segment elevation in these leads, confirming posterior wall
MI. Reprinted from: Brady WJ, Erling B, Pollack M, et al, Electrocardiographic manifestations: acute posterior
wall myocardial infarction. J Emerg Med. 2001;20(4):393. With permission from Elsevier.
A
B
103
Electrocardiography in Emergency Medicine
Figures
Figure 7-4.
Axial depiction of the standard precordial leads as well as additional leads (V4R, V8, and V9) and their relation
to the myocardium. Note that lead V1 shows only a small portion of the right ventricular muscle mass, whereas
V4R is positioned directly over this area to better identify the right ventricular infarct. Similarly, V8 and V9
directly show the posterior wall of the left ventricle. Reprinted from: Somers MP, Brady WJ, Bateman DC, et al.
Additional electrocardiographic leads in the ED chest pain patient: right ventricular and posterior leads. Am J
Emerg Med. 2003;21:569. With permission from Elsevier.
Figure 7-5.
Proper placement of V4R (A) and V8 and V9 (B) leads. V4R is placed as a mirror image of the standard V4
location. V8 is placed on the patient’s left back at the tip of the scapula, and V9 is placed half the distance
between lead V8 and the paraspinal muscles. Reprinted from: Somers MP, Brady WJ, Bateman DC, et al.
Additional electrocardiographic leads in the ED chest pain patient: right ventricular and posterior leads. Am J
Emerg Med. 2003;21:572. With permission from Elsevier.
104
C h apter e i g h t
New ECG Technologies for Detection
of Acute Myocardial Ischemia
and Infarction in the Emergency
Department
Barbara J. Drew, RN, PhD, and William J. Brady, MD
For patients who present to the emergency depression criterion is nonspecific (sensitivity
department with chest pain or anginal equivalent about 80%; specificity about 25%).2 Isolated T-
symptoms, the standard 12-lead ECG is the wave inversion is the least sensitive and specific
initial tool used for triage and clinical decision- criterion for ischemia that progresses to MI.2
making. Unlike serum biomarkers that require
myocardial cell death to become positive, the One reason ECG criteria have limited
ECG may be positive with ST/T-wave changes diagnostic accuracy for acute MI is that
of acute ischemia before myocardial infarction nonischemic causes of ST/T-wave changes
(MI) has occurred. Initiating early reperfusion can confound the diagnosis. Ischemic and
therapy for acute MI at a time when the ECG nonischemic causes of ST-segment elevation,
shows ST-segment elevation and biomarkers are ST-segment depression, and T-wave inversion
still negative provides the greatest potential for are summarized in Figures 8-1 and 8-2. Most of
myocardial salvage and optimal patient outcomes. the ECG confounders of ischemia cause long-
term ST/T-wave alterations that do not change
ECG criteria for ischemia that is likely to dynamically while a patient is being evaluated in
progress to MI include any of the following an emergency department. For example, patients
in two or more contiguous leads: ST-segment with left ventricular hypertrophy (LVH), bundle-
elevation at the J point with cut-off points of at branch block, early repolarization, or digitalis
least 0.2 mV (2 mm) in leads V1, V2, or V3 and at therapy have fixed ST/T-wave abnormalities
least 0.1 mV (1 mm) in other leads; ST-segment that do not worsen or resolve during the
depression; and symmetric T-wave inversion emergency department evaluation period.
with T nadir at least 1 mm below the isoelectric However, if the ST/T-wave changes are caused
line.1 Unfortunately, these criteria fail to identify by acute myocardial ischemia in a patient with
many patients presenting to an emergency evolving MI or unstable angina, they typically
department who are later confirmed to have ACS. vary in magnitude over minutes or hours.
For example, the ST-segment elevation criteria
are insensitive for acute MI (sensitivity about A second reason ECG criteria have limited
57%; specificity about 91%) and the ST-segment diagnostic accuracy is that ischemia and
infarction are localized phenomena that produce
105
Electrocardiography in Emergency Medicine
ST/T-wave changes only in leads facing the occlusion and spontaneous reperfusion in early
ischemic zone. Although the standard 12-lead infarction. Seven studies have documented
ECG quite accurately depicts anterior and the frequency of intermittent reperfusion
inferior wall MIs, it often misses injury to other in acute MI, as measured by continuous ST-
areas of the heart such as the right ventricle segment monitoring.4–10 Meta-analysis of these
and left ventricular apical and posterior walls. studies indicates an overall prevalence of
34% to 40% (95% confidence interval).11
Two new noninvasive ECG technologies
have recently been introduced to augment the Detection of myocardial ischemia in patients
standard 12-lead ECG diagnosis of ischemia with unstable angina is even more elusive
and infarction: continuous ST-segment than identifying acute MI, because ST-segment
monitoring and body surface mapping. ST- deviation can last just minutes and is frequently
segment monitoring aims to differentiate the not accompanied by classic anginal pain. In
dynamic changes of evolving MI from fixed ECG a study of 12-lead ST-segment monitoring of
confounders and to detect transient (often silent) patients with ACS, Drew et al12 reported that,
ischemia in patients with unstable angina. Body of 574 transient ST events, 441 (77%) were
surface mapping aims to provide leads facing all asymptomatic. Figure 8-4 illustrates how ST-
myocardial zones of the right and left ventricle. segment monitoring in the emergency department
prevented inappropriate discharge of a patient
ST-Segment Monitoring with presumed noncardiac chest pain who, in
reality, had unstable angina related to a critical
Clinical Application stenosis of the left main coronary artery.
The best method for identifying the dynamic ST-Segment Monitoring Technology
ST-segment changes of ACS is to monitor the
12-lead ECG continuously. When attempting Computer algorithms for continuous ST-
to distinguish confounders such as LVH segment monitoring were introduced as
from acute ischemia, it is helpful to retrieve a software options in hospital cardiac monitoring
patient’s prior ECG for comparison. However, equipment in the late 1980s. Although most
prior ECGs are often unavailable. Moreover, current cardiac monitors come equipped with
observed ST/T-wave changes between a current computerized ST-segment monitoring capability,
and prior ECG could be caused by slightly clinicians must activate the software for it to
different electrode placement at the two time work. The reason ST-segment algorithms are
points rather than by ischemia. An advantage not automatic, like computerized arrhythmia
of ST-segment monitoring is that electrodes algorithms, is that ischemia monitoring is
remain in fixed locations during the emergency inappropriate for patients without risk of
department evaluation period, so one can be ischemia/infarction. If ST-segment monitoring
confident that observed ST/T-wave changes are is not available with an existing hospital
not related to different electrode positions. monitoring system, the cardiac monitoring
manufacturer can be contacted to determine
Patients with ST-segment elevation MI whether it can be added as a software upgrade.
(STEMI) can have dynamic changes that are
missed by a standard (10-second) 12-lead ECG. Most computerized ST-segment monitoring
Figure 8-3 illustrates how five standard ECG algorithms continuously analyze ST amplitudes
recordings taken 20 minutes apart in a patient in all available ECG leads, even if only one lead
evaluated in an emergency department failed is displayed on the bedside or central monitoring
to show signs of acute inferior MI because all station. For example, if a standard five-electrode
five missed the periods of ST-segment elevation. configuration is used, with electrodes on the
This pattern of dynamic ST-segment elevation limbs plus one on the chest, seven leads are
has been termed “intermittent reperfusion” and actually available (I, II, III, aVR, aVL, aVF, and
is thought to represent cycles of thrombotic a “V” lead). Because most monitoring systems
106
New ECG Technologies
have a “full disclosure” feature that allows fluctuations is a slight change in heart position
retrieval of the past 24 hours of ECG data, ST relative to the monitoring electrode.20 Patients
events can be printed from multiple leads, even with positional ST-segment amplitude changes
if only one lead has been displayed. Ideally, typically have positional QRS amplitude changes
all 12 leads should be recorded, but if that is as well (Figure 8-5). Therefore, a good strategy
impractical, displaying an “inferior” lead such for identifying a false ST alarm caused by body
as the routinely monitored lead II along with an position change is to note an associated QRS
“anterior” lead such as lead V3 will increase the change. To minimize possible overtreatment in
sensitivity for detecting acute occlusion of the left these patients, health care professionals should
anterior descending and right coronary arteries. be taught to evaluate the ST segment in the
supine state. When an ST alarm sounds and the
Underutilization of ST-Segment patient is in a side-lying position, the patient
Monitoring in Emergency Department should be returned to the supine position. If
Settings the ST-segment deviation disappears in the
supine state, it is likely to be a false alarm.
Continuous 12-lead ST-segment monitoring
in the emergency department is a Class I Summary of ST-Segment Monitoring
recommendation in the latest STEMI guidelines14
as well as the American Heart Association’s ST-segment monitoring can be a valuable
practice standards for ECG monitoring in hospital adjunct to the standard 12-lead ECG for
settings.15 Despite these recommendations, ST- identifying patients with ACS in the emergency
segment monitoring is rarely used in emergency department. This monitoring is noninvasive
departments. A major reason for this lack of and inexpensive and can be implemented with
use is the problem of false ST alarms. Common standard hospital bedside equipment. The same
causes of false alarms include technical factors skills are used to analyze ST-segment monitoring
such as a noisy signal or failure to select data as are used to interpret the standard
appropriate alarm parameters. Because most 12-lead ECG. Future studies are required to
patients’ normal baseline ST level is not perfectly determine whether clinical decision-making
isoelectric, failure to tailor alarm settings to the guided by continuous ST-segment monitoring
individual patient can result in excessive false will lead to more accurate and timely diagnosis
ST alarms. False alarms can also be triggered and treatment of patients presenting to the
by an arrhythmia that has secondary ST/T- emergency department with chest pain.
wave abnormalities such as the development of
bundle-branch block or ventricular rhythms. Body Surface Mapping
The most problematic false alarms are those Body surface mapping is an ECG technique
caused by body position changes. Sizable changes that uses numerous leads, allowing more
in ST-segment amplitudes can occur when a complete visualization of cardiac electrical
patient changes position (eg, rolls from supine activity than the standard 12-lead ECG. This
to a side-lying position).16,17 Such fluctuations enhanced visualization allows more complete
are more difficult to distinguish from ischemia imaging of the heart and greater sensitivity
than the fixed ST-segment abnormalities of for detecting STEMI, potentially resulting in
common ECG confounders because they, like more appropriate and timely therapy. Although
ischemic episodes, are transient. Drew et al18 many studies compare body surface mapping
reported that a change in body position is with 12-lead electrocardiography, body surface
the most common cause of false ST alarms. mapping is not designed to replace standard
Positional ST-segment changes have also been electrocardiography.21-23 Rather, the body surface
a cause of unnecessary cardiac catheterizations mapping ECG is an extension of the standard
and percutaneous coronary interventions.19 The 12-lead ECG; it can be considered a second tier
most likely explanation for these ST-segment evaluation tool to identify ACS-related injury.
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Electrocardiography in Emergency Medicine
Currently, a chest pain patient is evaluated poor sensitivity of the 12-lead ECG is the
with a combination of a focused history, physical application of additional leads. It has been
examination, serum biomarkers, and a 12-lead suggested that the diagnostic power of the ECG
ECG. The ECG assists in the diagnosis of STEMI, can be increased if additional body surface
as well as in selecting appropriate therapies leads (eg, leads V4R [right ventricular lead] as
and inpatient disposition. Although the ECG well as leads V7 through V9 [left ventricular
is an invaluable tool in this evaluation, it is a posterior wall leads]) are employed in selected
less-than-perfect indicator of acute MI because individuals.26 Body surface mapping is simply
of the existence of “electrocardiographically a natural extension of the “additional-lead”
silent” areas of the heart, such as the right concept with the application of 20 to 240 leads,
ventricle and portions of the left ventricular depending on the system employed. The most
apical, lateral, and posterior walls. established technology at present is the 80-lead
body surface mapping system, which uses 64
The sensitivity of a single 12-lead ECG for anterior and 16 posterior leads (Figure 8-6).
the diagnosis of acute MI is relatively poor.
Fesmire and Percy24 noted that the initial 12- Body Surface Mapping Data Display
lead ECG demonstrated a sensitivity of only
55% in patients ultimately diagnosed with acute Clinical information is displayed in three
MI. Rude and colleagues25 examined the initial basic formats: a standard 12-lead ECG (Figure
ECG in a group of adult chest pain patients, 8-7A), an 80-lead ECG (Figure 8-7B), and color
all of whom were subsequently proved to contour maps (Figure 8-7C). Color coding
have had an acute MI. Less than 50% of these (Figure 8-8) is used to depict the direction of
patients demonstrated ST-segment elevation the waveforms (Table 8-1): green represents an
on their initial ECG; the remaining patients isoelectric position, red represents a positive
manifested a variety of ischemic changes, deflection above the isoelectric line, and blue
including ST-segment depression, T-wave represents a negative deflection below the
inversion, and nonspecific ST/T-wave changes. isoelectric line. Four torso maps are provided,
each analogous to a component of the cardiac
One strategy used to overcome this initially
Table 8-1.
Color coding on torso contour maps
QRS isointegral map A measure of ventricular depolarization; represents the area under the curve for the QRS
complex
Green Isoelectric QRS complex (positive and negative deflections are equal)
Red R wave greater than the sum of Q and S waves (predominantly positive QRS complex)
Blue Predominant Q or S wave (predominantly negative QRS complex)
STT isointegral map Represents ventricular repolarization; displays the total area under the ST segment and T
wave
Deep red Prominent, hyperacute T waves
Blue Inverted T waves
ST0 isopotential map Measures the voltage at the beginning of the ST segment (the J point)
Red J-point elevation
Blue J-point depression
Green Isoelectric J point (no ST-segment elevation or depression)
ST60 isopotential map Shows the voltage 60 msec after the J point
Like the ST0 map, used to visualize ST-segment elevation and depression
108
New ECG Technologies
cycle: QRS isointegral map, STT isointegral map, no further ECG testing is appropriate, and
ST0 isopotential map, and ST60 isopotential the priority becomes timely transport of the
map. The QRS isointegral map represents the patient to the cardiac catheterization laboratory.
area under the curve for the QRS complex; this However, if the treatment decision is fibrinolytic
map is a measure of ventricular depolarization. therapy, a body surface mapping may be recorded
Green on the QRS isointegral map indicates an after the initiation of fibrinolytic therapy to
isoelectric QRS complex in which positive and more completely investigate the extent of the
negative deflections are equal. Red indicates STEMI. Menown and colleagues27 investigated
an R wave greater than the sum of the Q and S the ability of body surface mapping to detect
waves; ie, a predominantly positive QRS complex. both posterior and right ventricular wall
Blue indicates a predominant Q or S wave, ie, a infarction in patients diagnosed with inferior-
predominantly negative QRS complex. The STT wall STEMI. They compared the body surface
isointegral map displays the total area under mapping with an additional-lead ECG, using
the ST segment and T wave; this represents V2R, V4R, V7, and V9 in addition to the standard
ventricular repolarization. Prominent, hyperacute 12 leads. ST-segment elevation over the right
T waves are seen as deep red. Inverted T waves ventricle and posterior wall was detected in
are blue. The ST0 and ST60 isointegral maps significantly more patients with body surface
measure voltage at a single time point relative mapping than with an additional-lead ECG.
to the J point, displayed in millimeters. The The investigators concluded that body surface
ST0 isopotential map measures the voltage at mapping more directly visualized the right
the beginning of the ST segment (ie, the J point ventricle and posterior wall of the left ventricle,
itself). J-point elevation is seen as red on ST0 increasing the diagnostic rate of STEMI in
maps; J-point depression is represented by blue, these poorly imaged regions of the heart.
and green indicates an isoelectric J point (ie, no
ST segment elevation or depression). The ST60 In a slightly different application of body
isopotential shows the voltage at a single point on surface mapping, the 80-lead ECG can be
the ST segment 60 msec after the J point. Similar performed to further evaluate the patient with
to the ST0 map, the ST60 color map is used to a nondiagnostic 12-lead ECG (“nondiagnostic”
visualize ST segment elevation and depression. in the sense that a STEMI is not noted). If the
12-lead ECG is nondiagnostic, then one of several
Clinical Application of Body Surface ECG patterns is possible: normal, nonspecific
Mapping ST/T-wave changes, ST-segment depression, T-
wave inversion, or a confounding abnormality (eg,
Body surface mapping can be used in ACS left bundle-branch block). If clinical suspicion
patients to detect unanticipated STEMI (from remains for ACS, then body surface mapping can
the 12-lead ECG perspective) and to define the be valuable. In this situation, the clinician might
total extent of myocardial injury. The technique observe ST-segment elevation in leads outside
is useful for clinical decision-making to select the standard precordial electrode sites. Menown
appropriate therapies and to evaluate the response et al28 used body surface mapping to further
to these treatments. Body surface mapping should evaluate patients with suspected ACS and only
not necessarily be the initial ECG diagnostic ST-segment depression on their initial 12-lead
test performed in a chest pain patient suspected ECG. Numerous patients with serum-marker–
of ACS. Rather, the typical evaluation should confirmed acute MI demonstrated ST-segment
occur, including the standard 12-lead ECG. elevation on body map regions not imaged by
If the standard ECG demonstrates a STEMI, the standard 12-lead ECG, including the inferior,
then further evaluation is unwarranted and the lateral, posterior, and right ventricular regions.
clinician should focus on urgent management
decisions. If the treatment decision involves 109
primary percutaneous coronary intervention,
Electrocardiography in Emergency Medicine
Summary of Body Surface Mapping References
Body surface mapping is a potentially 1. Alpert JS, Thygesen K, Antman E, et al. Myocardial
valuable clinical tool. Its value lies in its infarction redefined: a consensus document of the Joint
ability to image areas of the heart that are European Society of Cardiology/American College of
electrocardiographically silent from the Cardiology Committee for the redefinition of myocardial
perspective of the standard 12-lead ECG. infarction. J Am Coll Cardiol. 2000;36(3):959-969.
The body surface mapping ECG does not
replace the traditional 12-lead ECG; rather, it 2. Menown IBA, MacKenzie G, Adgey AAJ. Optimizing the
complements it, providing the clinician with initial 12-lead electrocardiographic diagnosis of acute
another noninvasive imaging modality that myocardial infarction. Eur Heart J. 2000;21:275-283.
can be performed at the bedside safely, easily,
and accurately. The body surface mapping ECG 3. Drew BJ, Pelter MM, Wung SF, et al. Accuracy of the EASI
provides a more complete depiction of injury 12-lead electrocardiogram compared to the standard 12-
currents related to the inferior, lateral, posterior, lead electrocardiogram for diagnosing multiple cardiac
and right ventricular areas of the heart, which abnormalities. J Electrocardiol. 1999;32 Suppl:38-47.
has potential to influence therapeutic decisions.
4. Krucoff MW, Croll MA, Pope JE, et al. Continuously
Conclusions updated 12-lead ST-segment recovery analysis for
myocardial infarct artery patency assessment and its
ST-segment monitoring and body surface correlation with multiple simultaneous early angiographic
mapping are new technologies that can be observations. Am J Cardiol. 1993;71(2):145-151.
implemented in the emergency department to
improve the ECG diagnosis of acute myocardial 5. Veldkamp RF, Green CL, Wilkins ML, et al. Comparison
ischemia and infarction. ST-segment monitoring of continuous ST-segment recovery analysis with
is valuable to detect transient (and often silent) methods using static electrocardiograms for noninvasive
myocardial ischemia in patients with unstable patency assessment during acute myocardial infarction.
angina and to detect the dynamic ST-segment Thrombolysis and Angioplasty in Myocardial Infarction
changes with evolving STEMI and to differentiate (TAMI) 7 Study Group. Am J Cardiol. 1994;73:1069-1074.
these from the fixed ST deviations observed in
patients with LVH, early repolarization, bundle- 6. Langer A, Krucoff MW, Klootwijk P, et al. Noninvasive
branch block, and digitalis therapy. Body surface assessment of speed and stability of infarct-related
mapping provides leads that face areas of the artery reperfusion: results of the GUSTO ST segment
myocardial wall such as the posterior, right monitoring study. Global Utilization of Streptokinase and
ventricular, apical, and sections of the infero- Tissue Plasminogen Activator for Occluded Coronary
lateral wall that are not well depicted by the Arteries. J Am Coll Cardiol. 1995;25:1552-1557.
standard 12-lead ECG. In addition, a body surface
mapping ECG provides information on the extent 7. Davies GJ, Chierchia S, Maseri A. Prevention of
of the injury pattern, aiding in risk stratification. myocardial infarction by very early treatment
with intracoronary streptokinase: some clinical
observations. N Engl J Med. 1984;311:1488-1492.
8. Hackett D, Davies G, Chierchia S, Maseri A. Intermittent
coronary occlusion in acute myocardial infarction:
value of combined thrombolytic and vasodilator
therapy. N Engl J Med. 1987;317:1055-1059.
9. Dellborg M, Riha M, Swedberg K. Dynamic QRS-
complex and ST-segment monitoring in acute myocardial
infarction during recombinant tissue-type plasminogen
activator therapy. Am J Cardiol. 1991;67:343-349.
10. Kwon K, Freedman SB, Wilcox I, et al. The unstable ST
segment early after thrombolysis for acute infarction
and its usefulness as a marker of recurrent coronary
occlusion. Am J Cardiol. 1991;67:109-115.
11. Veldkamp RF, Simoons ML, Pope JE, Krucoff MW. Continuous
multilead ST-segment monitoring in acute myocardial infarction.
In: Clements IP, ed. The Electrocardiogram in Acute Myocardial
Infarction. Armonk, NY: Futura Publishing Co; 1998:1-30.
Key Facts
• During continuous ST-segment monitoring, body position changes (eg, supine to left-side-lying
position) can cause ST-segment changes mimicking ischemia and triggering false ST monitor
alarms.
• Body surface mapping depicts a “snapshot” of time and thus does not depict dynamic ECG
changes over time, as does continuous ECG monitoring.
• When troubleshooting possible false ST monitor alarms, the clinician should move the patient to the
supine position to avoid serial comparisons between supine and side-lying (or other) positions.
110
New ECG Technologies
12. Drew BJ, Pelter MM, Adams MG. Frequency, characteristics, and 21. Menown IBA, Allen J, Anderson JM, Adgey AA. Early
clinical significance of transient ST segment elevation in patients diagnosis of right ventricular or posterior infarction
with acute coronary syndromes. Eur Heart J. 2002;23:941-947. associated with inferior wall left ventricular acute
myocardial infarction. Am J Cardiol. 2000;85:934-938.
13. Yamaji H, Iwasaki K, Kusachi S, et al. Prediction of acute left
main coronary artery obstruction by 12-lead electrocardiography: 22. Ornato JP, Menown IBA, Riddell JW, et al. 80-
ST segment elevation in lead aVR with less ST segment lead body map detects acute ST segment elevation
elevation in lead V1. J Am Coll Cardiol. 2001;38:1348-1354. myocardial infarction missed by standard 12-lead
electrocardiography. J Am Coll Cardiol. 2002;39:332A.
14. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA
guidelines for the management of patients with ST-elevation 23. McClelland AJJ, Owens CG, Menown IBA, et al.
myocardial infarction. Dallas, TX: American Heart Association; Comparison of the 80-lead body surface map to physician
July 2004. Available at: http://www.americanheart.org/presenter. and to 12-lead electrocardiogram in detection of acute
jhtml?identifier=3023467. Accessed on March 19, 2007. myocardial infarction. Am J Cardiol. 2003;92:252-257.
15. Drew BJ, Califf RM, Funk M, et al. Practice standards 24. Fesmire FM, Percy RF. Usefulness of automated
for electrocardiographic monitoring in hospital serial 12-lead ECG monitoring during the initial
settings. Circulation. 2004;110:2721-2746. emergency department evaluation of patients with
chest pain. Ann Emerg Med. 1998;31:3-11.
16. August T, Mazzeleni A, Wolff L. Positional and respiratory
changes in precordial lead patterns simulating acute 25. Rude RE, Poole WK, Muller JE, et al. Electrocardiographic
myocardial infarction. Am Heart J. 1958;55:706-714. and clinical criteria for recognition of acute
myocardial infarction based on analysis of 3,697
17. Adams MG, Drew BJ. Body position effects on patients. Am J Cardiol. 1983;52:936-942.
the ECG: implication for ischemia monitoring.
J Electrocardiol. 1997;30:285-291. 26. Melendez LJ, Jones DT, Salcedo JR. Usefulness of
three additional electrocardiographic chest leads
18. Drew BJ, Wung SF, Adams MG, Pelter MM. Bedside diagnosis of (V7, V8 and V9) in the diagnosis of acute myocardial
myocardial ischemia with ST-segment monitoring technology: infarction. Can Med Assoc J. 1978;119:745-748.
measurement issues for real-time clinical decision-making
and trial designs. J Electrocardiol. 1998;30:157-165. 27. Menown IBA, Allen J, Anderson JM, Adgey AA. Early
diagnosis of right ventricular or posterior infarction
19. Drew BJ, Adams MG. Clinical consequences of ST- associated with inferior wall left ventricular acute
segment changes caused by body position mimicking myocardial infarction. Am J Cardiol. 2000;85:934-938.
transient myocardial ischemia: hazards of ST-segment
monitoring? J Electrocardiol. 2001;34:261-264. 28. Menown IBA, Allen J, Anderson JM, Adgey AAJ. ST segment
depression only on initial 12-lead ECG: early diagnosis of
20. Feldman T, Borow K, Neumann A, et al. Relation of acute myocardial infarction. Eur Heart J. 2001;22:218-227.
electrocardiographic R-wave amplitude to changes in
left ventricular chamber size and position in normal
subjects. Am J Cardiol. 1985;55:1168-1174.
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Electrocardiography in Emergency Medicine
Figures
Figure 8-1.
Ischemic and nonischemic causes of ST-segment elevation.
Figure 8-2.
Ischemic and nonischemic causes of ST-segment depression and/or T-wave inversion.
112
New ECG Technologies
Figures
Figure 8-3.
A: Initial ECG in a 76-year-old woman presenting to the emergency department with chest pain. ST-segment
depression is present in leads V1 through V4 and slight ST elevation in leads III and aVF. The patient was
enrolled in a research study involving continuous 12-lead ST-segment monitoring.3 However, in this patient,
clinical decision-making was based on the routine method of recording standard “snapshot” 12-lead ECGs
every 20 minutes. B: Eight minutes after the initial ECG, an ST alarm showed striking ST-segment changes
indicative of acute inferior MI. C: ST trends over a 1-hour period in the emergency department showed
dynamic ST-segment elevation. Representative waveforms in lead III are shown at three time points above
the trend. Five standard ECGs were recorded (upright arrows), and all 5 missed the periods of ST-segment
elevation. This patient developed positive biomarkers of infarction and was diagnosed as having acute inferior
ST-elevation MI. However, this diagnosis would not have been made without the continuous ST-segment
monitoring data because all five standard 12-lead ECGs showed normal isoelectric ST segments.
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Electrocardiography in Emergency Medicine
Figures
Figure 8-4.
A: Initial ECG in a 46-year-old woman presenting to the emergency department with a history of intermittent
chest pain relieved by nitroglycerin. She was enrolled in a study involving continuous 12-lead ST-segment
monitoring. Her initial ECG was normal. After two negative troponin values and 6 hours of observation, plans
were made to discharge the patient. B: While the patient was walking to the bathroom, an ST alarm sounded
and a transient ST-segment depression event occurred, accompanied by chest discomfort. The ST event
lasted only several minutes; however, the diagnosis of unstable angina was now confirmed because her
accelerating chest pain episodes were clearly caused by myocardial ischemia. This ST event met criteria for
critical stenosis of the left main coronary artery, ie, ST elevation in lead aVR with less ST elevation in lead V1.13
Cardiac catheterization revealed 99% stenosis of the left main coronary artery. The patient was taken directly
from the cardiac catheterization laboratory to the operating room for coronary bypass surgery. Without the ST
alarm, this patient would have been discharged with an unstable high-risk coronary lesion.
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New ECG Technologies
Figures
Figure 8-5.
A: Left lateral precordial leads recorded with the patient in a supine position. B: Same patient in the left
side-lying position shows down-sloping ST-segment depression in leads V5 and V6. This ST-segment change
triggered an ST monitor alarm. On closer inspection, however, the accompanying changes in QRS amplitude
indicate it is a false ST alarm caused by body position change. These changes could be reproduced by turning
the patient back and forth between supine and left side-lying positions.
AB
115
Electrocardiography in Emergency Medicine
Figures
Figure 8-6.
Lead configuration for the 80-lead ECG: 64 anterior and 16 posterior.
116
New ECG Technologies
Figures
Figure 8-7.
Acute, isolated, posterior wall myocardial infarction. A: Minimally abnormal standard 12-lead ECG with
nonspecific ST/T-wave changes. B: Abnormal 80-lead ECG with anterior ST-segment depression and posterior
ST-segment elevation.
A
B
117
Electrocardiography in Emergency Medicine
Figures
Figure 8-7, continued.
C: Abnormal color contour maps with ST0 isopotential (left) and ST60 isopotential (right), indicating an acute,
isolated posterior wall myocardial infarction with blue in the anterior region (ST-segment depression) and red
in the posterior region (ST-segment elevation).
C
Figure 8-8.
Color coding used to depict QRS complex, ST-segment, and T-wave characteristics.
118
C h apter N i n e
ACS Mimics: Non–AMI Causes of
ST-Segment Elevation
Fredrick M. Abrahamian, DO
ST-segment elevation is an important ECG differential diagnosis of ST-segment elevation
criterion for the diagnosis of AMI. In patients and of ways to differentiate noninfarction
suspected of having an acute coronary ischemic syndromes from true infarction are imperative.
event, in addition to basing therapeutic decisions
such as emergent angioplasty and thrombolysis Prinzmetal Angina
on the patient’s history, decisions are also
heavily based on the presence of ST-segment The ST-segment elevation associated with
elevation on the ECG.1,2 Although AMI is an Prinzmetal angina is impossible to differentiate
important cause of ST-segment elevation, other from that associated with AMI. The underlying
conditions can also cause elevation of the ST process resulting in the elevation is identical in
segment (Table 9-1).3,4 In fact, compared with
noninfarction syndromes such as left ventricular Table 9-1.
hypertrophy (LVH), AMI is a less common Differential diagnosis of ST-segment elevation
cause of ST-segment elevation in patients with
chest pain.5,6 Other common causes include Acute myocardial infarction
early repolarization, left bundle-branch block Acute pericarditis or myocarditis
(LBBB), and left ventricular aneurysm (LVA).3 Brugada syndrome
Cardioversion
Commonly misdiagnosed conditions as Early repolarization
well as leading diagnoses associated with ST- Hyperkalemia
segment elevation for which thrombolytic Left bundle-branch block
agents are given inappropriately include LVA, Left ventricular aneurysm
LVH, early repolarization, and pericarditis.7–9 Left ventricular hypertrophy
In addition, there is considerable interobserver Normal ST-segment elevation
disagreement over the extent and cause of Prinzmetal angina
ST-segment elevation.10 Because the clinical Pulmonary embolism
consequences of misinterpretation could be ST-segment elevation of normal variant
deleterious, a thorough knowledge of the Miscellaneous causes (see text)
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Electrocardiography in Emergency Medicine
both conditions (ie, occlusion of an epicardial the ST segment are uncommon with LVA; if
artery). In Prinzmetal angina, the occlusion present, they should raise suspicion for AMI.
results from a brief spasm of an epicardial artery
with temporary transmural ischemia. However, There is no direct relationship between
because the spasm is brief, there is often no the extent of ST-segment elevation and the
associated myocardial infarction and, after a short size of the aneurysm. The QRS duration
time, with the resolution of symptoms, the ST increases with increasing age of the aneurysm.17
segments return to normal. Certainly, infarction Patients who have undergone left ventricular
can ensue if the occlusion lasts long, especially in aneurysmectomy will have diminished ST-
patients with underlying coronary artery disease. segment elevations compared with preoperative
ECGs. In a small study of patients following
Left Ventricular Aneurysm left ventricular aneurysmectomy, none had
complete normalization of the ST segment.18
LVA is most commonly associated with a
transmural myocardial infarction and is more Because LVA is commonly associated with
predominant in men than in women. Other an old transmural myocardial infarction, other
conditions that could result in LVA include blunt ECG features of LVA include the presence of large
chest trauma, Chagas disease, and sarcoidosis.11 Q waves and loss of R waves (or poor R-wave
LVA is most often related anatomically to a progression) in the same distribution as the ST-
complete occlusion of the left anterior descending segment elevation (Figure 9-1). Although most
(LAD) artery; hence, it is frequently observed at Q waves develop within 8 hours after AMI, in
the anterior wall of the left ventricle. Aneurysms a minority of patients they can develop within
located at the inferior or posterior aspect of the 2 hours.11 Hence, distinguishing between AMI
left ventricle are uncommon. The myocardium and LVA based on the presence of Q waves is
at the aneurysm is thinner compared with the somewhat difficult and could be misleading.
surrounding muscle and is characterized by a
full-thickness scar. On echocardiography, which LVA by itself does not result in reciprocal
is an excellent diagnostic tool for demonstrating ST-segment depressions. In the absence of
LVA, the aneurysm appears as a convex conditions that alter intraventricular conduction
protrusion during both systole and diastole.11 (eg, LVH), the presence of reciprocal changes
should heighten suspicion for AMI.19 In
A clue to the presence of LVA on the ECG addition, the absence of reciprocal changes
is ST-segment elevation of 1 mm or more does not exclude AMI. For instance, anterior
persisting for 4 or more weeks after AMI in wall myocardial infarctions resulting from
the corresponding areas of infarction (ie, leads occlusion of the LAD artery distal to the origin
with abnormal Q waves) (Figure 9-1). However, of the first diagonal branch result in precordial
persistent ST-segment elevation does not always ST-segment elevations but can also result in
imply the presence of an aneurysm.12,13 ECG minimal (≤1 mm) elevations of the ST segment
and radionuclide imaging studies have shown in the inferior leads (although reciprocal ST-
that persistent ST-segment elevation is more an segment depressions should still be absent).20,21
indicator of dyskinesia and asynergy than of an
aneurysm.14,15 The exact mechanism responsible Serial ECGs can help differentiate between
for the persistent ST-segment elevation AMI and LVA. Patients with LVA will have
associated with aneurysm is not well known.4,11 no dynamic changes in their ECGs and,
when the current ECG is compared with
The elevated ST segment associated with previous ECGs, there should be no new
LVA often assumes a concave morphology. A findings. Patients with AMI often have
nonconcave (especially a convex) morphology dynamic changes on ECG and reveal new
should strongly be suspected as AMI, although findings not seen on older ECG records.
it is occasionally encountered with LVA.16 In
addition, significant elevations (≥5 mm) of
120
Non–AMI Causes of ST-Segment Elevation
Acute Pericarditis and should also raise suspicion for AMI.3,4
Myocarditis In pericarditis, the junction of the QRS
In most patients with acute pericarditis, the complex and the ST segment (J point) is clearly
initial ECG changes include diffuse ST-segment discernible, whereas in AMI, the J point is often
elevations and PR-segment depressions (stage obliterated.4 Abnormal Q waves do not develop
1) (see Chapter 11). ECG changes associated with pericarditis, unless it is complicated by
with stage 1 pericarditis must be differentiated infarction.23 The ST-segment and T-wave changes
from those associated with other conditions with pericarditis occur more slowly than those
causing similar findings such as myocardial of AMI. In AMI or myopericarditis, T-wave
infarction, early repolarization, and myocarditis. inversions become visible before the ST segments
return to baseline, whereas, in pericarditis, the T
In acute pericarditis, with the exception of waves stay upright until the ST segments return
lead aVR, the ECG demonstrates widespread ST- to baseline.4,22,23 The T waves in pericarditis are
segment elevations with a concave morphology.4,22 often incompletely and less deeply inverted
With pericarditis, the ST segment in aVR is than are the T waves associated with AMI.4
usually depressed. An elevated ST segment in this
lead can exclude pericarditis. Frequently, lead Diffuse PR-segment depression, an early ECG
V1 and, rarely, lead V2 as well exhibit depressed sign of pericarditis, is almost never associated
or isoelectric ST segments.23 The ST segments in with AMI.23 PR-segment depression is not specific
AMI, unlike those associated with pericarditis, for acute pericarditis. The differential diagnosis
are elevated regionally following a specific includes myopericarditis, early repolarization
arterial distribution and often assume a convex- (localized to either limb leads or precordial
upward morphology.16 Patients with postoperative leads), atrial infarction (a rare condition), and
pericarditis or those with pericardial adhesions pericardial effusion/cardiac tamponade.3,23–26
from previous surgery or injury can exhibit Using the TP segment as a reference, in
localized ST-segment elevations. However, pericarditis the PR segment is often elevated in
even these patients are not expected to lead aVR and can occasionally be elevated in lead
demonstrate reciprocal ST-segment depression V .1 4,23 In addition, in pericarditis, the PR-segment
in the inferior, anterior, or lateral leads. deviation is often absent in a single limb lead.23
Close inspection of the ST segments in The ST-segment elevation in early
the limb leads can also provide clues to help repolarization is often confined to the precordial
distinguish between AMI and acute pericarditis. leads (most marked in V4), with an associated
When the ST-segment elevation in lead II is notch at the J point. In acute pericarditis, the
greater in magnitude than the ST-segment ST segment is elevated diffusely both in limb
elevation in lead III, acute pericarditis is the and precordial leads, and there is usually no
likely diagnosis. The reverse is true in cases associated notch at the J point.4 A reliable
of acute inferior MI. Another useful feature to means of differentiating pericarditis from early
differentiate AMI from acute pericarditis or repolarization is to measure (in millimeters) the
early repolarization is the relationship of the ST ratio of the ST-segment elevation to the T-wave
segments in leads III and aVL. A depressed ST amplitude in lead V6. A ratio of 0.25 or more
segment in lead aVL associated with an elevated is strongly associated with acute pericarditis
ST segment in lead III suggests infarction (Figure (or AMI), while a ratio of less than 0.25 favors
9-2). This reciprocal relationship is not present early repolarization. If lead V6 is not available,
with acute pericarditis or early repolarization.3 In an ST/T ratio of 0.25 or more in lead V5, V4,
acute pericarditis or when the early repolarization or I is also suggestive of acute pericarditis.27
pattern involves the limb leads, the ST segment
is depressed in aVR but not in aVL.3 Significant PR-segment depression can also be seen in
elevations (>5 mm) of the ST segment are patients with early repolarization. Unlike the
uncommon with pericarditis; if present, they diffuse pattern associated with acute pericarditis,
in early repolarization the distribution of
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Electrocardiography in Emergency Medicine
the PR-segment depression is more confined atrioventricular or interventricular block or any
to either the limb or precordial leads.4,23 In significant arrhythmia, especially ventricular, in
comparison with T waves related to pericarditis, the absence of heart disease.23 Unlike pericarditis,
T waves in early repolarization are often taller in myopericarditis, T-wave inversions become
and more peaked. In acute pericarditis, the visible before the ST segments return to baseline,
tallest precordial R wave is usually seen in whereas, in pericarditis, the T waves stay upright
lead V5; in contrast, in early repolarization the until the ST segment returns to baseline.23
tallest precordial R wave is usually observed
in lead V4.23 Unlike with pericarditis, the ECG Left Bundle-Branch Block
associated with early repolarization does
not display dynamic changes and remains The ECG changes associated with LBBB
unchanged over a period of observation.4 include prolonged, abnormal QRS complexes
and ST-segment and T-wave abnormalities
The ECG diagnosis of concomitant localized (see Chapter 2). The abnormal ventricular
(regional) pericarditis complicating AMI (ie, depolarization as well as secondary ST/T changes
infarct pericarditis) is difficult.28 There are no make the diagnosis of concomitant AMI in the
standard ECG criteria, and those that have presence of LBBB difficult. Normally, in LBBB the
been proposed require serial evaluations of T- ST segment and the T wave act in a discordant
wave changes for days, making it less valuable fashion with the main QRS complex. If the main
for emergency physicians in the acute setting. QRS complex is positive (eg, in leads I, aVL,
Oliva and colleagues noted that patients with V5, and V6), then the expected secondary ST/T
postinfarction regional pericarditis have a changes will be ST-segment depression with
different pattern of T-wave evolution than do T-wave inversion. If the main QRS complex
those without pericarditis.29–31 They found that, is negative (eg, in leads V1 and V2), then the
in the absence of reinfarction or very small expected secondary ST/T changes will be concave
infarcts, the atypical T-wave evolution that ST-segment elevation with upright T waves. This
suggested postinfarction regional pericarditis relationship between the direction of the QRS
included either T waves that remain positive complex and the ST changes is often referred
for more than 48 hours after infarction or to as the “rule of appropriate discordance.”32–34
a premature, gradual reversal of inverted T
waves in positive deflections. The sensitivity In LBBB, the presence of concordant changes
and specificity of these T-wave alterations were (ie, ST-segment elevation ≥1 mm in leads with
100% and 77%, respectively.29,30 Similar T-wave a positive QRS complex such as lead V5, or
changes can also be seen with postinfarction ST-segment depression ≥1 mm in leads with a
pericardial effusion without pericarditis.30 negative QRS complex such as leads V1 through
V3, II, III, aVF) is abnormal and considered highly
Acute myocarditis can also result in diffuse specific and predictive for acute myocardial
ST-segment elevation.3 Other findings can include ischemia or infarction.32–37 However, the
diffuse T-wave inversions (the most common limitation of these findings lies with their low
finding) and ST-segment depression.4 The ECG sensitivity and poor negative likelihood ratio;
changes of acute myocarditis can resemble those hence, the absence of these features cannot be
of AMI. The distinction is often difficult to used to exclude AMI.34–36 Another ECG feature
make based on a single ECG. The evolutionary suggestive of AMI in the presence of LBBB
changes of the ECG in acute myocarditis are is extreme (≥5 mm) discordant ST-segment
more gradual than those associated with AMI. deviation (Figures 9-3A and 9-3B).33 Similarly, this
feature also exhibits low sensitivity and might
Myocarditis and pericarditis often coexist. be found in the absence of acute infarction.3,37,38
ECG clues to myopericarditis include those
seen with pericarditis, as well as any acute Additional features suggestive of myocardial
QRS-complex change, QT prolongation, or infarction with LBBB include replacement of the
convex ST-segment elevation and the presence of secondary concave ST-segment elevations with
122
Non–AMI Causes of ST-Segment Elevation
a convex ST segment; deep T-wave inversion in and V1, and significant Q waves can be present
leads V1 to V3; the presence of Q waves in at least in leads III, aVF, or both.4,22 Significant ST-
two of leads I, aVL, V5, and V6; and Q waves in II, segment elevation is uncommon with PE; most
III, and aVF, especially if associated with T-wave often the amplitude is less than 1 mm.4,43
inversions.3,4,32,39 Clues to previous myocardial
infarction also include notching of the upstroke Left Ventricular Hypertrophy
part of a wide S wave in at least two of leads
V3, V4, and V5 (the Cabrera sign) or notching LVH is among the most common causes of ST-
of the R-wave upstroke in leads I, aVL, V5, and segment elevation and is frequently mistaken for
V6 (the Chapman sign).4,39,40 Obtaining serial AMI.3,5,6 It produces changes in the QRS complex,
ECGs to look for dynamic changes as well as to the ST segment, and the T wave. Similar to LBBB,
compare them with previous ECGs is invaluable abnormal repolarization associated with LVH
in identifying patients with acute pathology. is also reflected by secondary ST/T changes. In
LVH, the ST segment and the T wave deviate
The ECG diagnosis of infarction-related LVA in the opposite direction from the major QRS
in the presence of LBBB is also problematic. A complex. The ST-segment elevation associated
suggested feature for the detection of LVA with with LVH has a concave contour and is generally
LBBB is the presence of stable isoelectric or limited to leads V1 through V3 (Figure 9-4). The
elevated (≥1 mm) ST segments in left precordial amount of ST-segment elevation depends on how
leads (V4 through V6) with predominantly deep the S wave extends (eg, the deeper the S
positive QRS complexes (opposite the discordant wave, the greater the ST-segment elevation).3
changes normally seen with uncomplicated
LBBB).41,42 However, the proposed feature has low Patients with fully developed LVH commonly
sensitivity, and it can also be observed in patients have ST-segment depression with T-wave
with AMI and LBBB.42 Changes associated with inversion in leads I, aVL, V5, and V6. The ST-
AMI tend to be more dynamic with fluctuating segment depression is often minimal and has a
amplitude of the ST segments, and those downsloping contour (hockey stick shape). The
associated with LVA are more likely to be stable.42 T waves are not deep and are asymmetrically
inverted (slow downward phase with fast upward
Pulmonary Embolism wave) (Figure 9-4). Significant and/or horizontal
ST-segment depressions and deep symmetric
Numerous ECG findings have been described inverted T waves are atypical and should raise
with pulmonary embolism (PE) (see Chapter suspicion for an ischemic process (Figure 9-5).4
16). The incidence and severity of the changes Similarly, T-wave inversions in leads other than
associated with PE depend on the severity of the lateral leads suggest myocardial ischemia
the pulmonary vasculature obstruction.4 Most (Figure 9-5). Prominent asymmetric deep T-
ECG changes are transient and nonspecific. wave inversion (ie, giant negative T waves) in
With moderate to severe PE, the most commonly association with other ECG findings of LVH
observed pattern is sinus tachycardia with can also be seen with apical hypertrophic
nonspecific ST-segment and T-wave changes.43 cardiomyopathy (Yamaguchi syndrome).39
A common ST/T change encountered with a Additional clues to a myocardial ischemic
moderate-to-large PE is ST-segment depression process associated with LVH include ST-segment
and T-wave inversion in leads V1 through V .3 43-45 depression and T-wave inversions in leads V1
and V2, as well as dynamic ECG changes.
ST-segment elevation with or without T-wave
inversion can also be encountered with PE. As in patients with AMI, the presence of LBBB
These changes at times resemble inferior and, might obscure the diagnosis of LVH. Although
to a lesser degree, anteroseptal infarction (ie, there is no formal consensus, suggested criteria
“pseudoinfarction” pattern) and the distinction for the ECG diagnosis of LVH in the presence
can be difficult to make.3,4,46 The ST-segment of LBBB have included S-wave amplitude in V2
elevations are often limited to leads III, aVF, plus R-wave amplitude in V6 of more than 45
123
Electrocardiography in Emergency Medicine
mm or a QRS complex duration longer than diagnosis is made during electrophysiologic
160 msec with left atrial enlargement.47–50 studies or with the aid of a pharmacologic
challenge of a type IA antiarrhythmic.
Hyperkalemia Arrhythmogenic right ventricular
cardiomyopathy (see Chapter 13) has an ECG
ST-segment deviations, either depressions or pattern similar to that of Brugada syndrome,
elevations, can also be seen with moderate to so the distinction is difficult to make. A drug
severe hyperkalemia. The ST-segment elevation challenge with sodium channel blockers could
related to hyperkalemia is uncommon and can be help in differentiating these two conditions.58,59
diffuse or localized, resembling that associated
with AMI.51,52 Elevations could be observed in The ST-segment elevation associated with
leads V1 and V2.39 Unlike the typical plateau or Brugada syndrome is limited to leads V1 and
upsloping ST segment associated with AMI, the V2 or V3. Typically, it has a saddleback or coved
ST-segment elevation in hyperkalemia often appearance with a gradual downslope, ending
displays a downsloping appearance. In addition, with an inverted T wave. The terminal portion
other ECG features suggestive of hyperkalemia of the QRS complex and the beginning of the
are often present (see Chapter 15), and the ST ST segment are indistinct. In contrast, the ST
segment returns to baseline with treatment.3,4 segment associated with anteroseptal infarction
complicated by RBBB has a distinct transition
Cardioversion from the QRS complex to the ST segment,
demonstrating a horizontal or upsloping
Transient ST-segment deviations, either (convex-upward), rather than a downsloping,
depressions or elevations, can be encountered morphology.3,58 An additional distinguishing
when transthoracic and epicardial electrical point is that Brugada syndrome is not usually
shocks are used to convert unstable associated with reciprocal ST changes, which
tachyarrhythmias.53–56 The ST-segment elevation are normally found in patients with AMI.
at times could be significant (>5 mm), but it lasts
only 1 to 3 minutes after the cardioversion. In Normal ST-Segment Elevation,
comparison with patients without ST-segment Early Repolarization (Normal
elevation, patients with ST-segment elevation Variant), ST-Segment
often have a lower conversion rate and are Elevation of Normal Variant
less likely to remain in sinus rhythm.55 The
mechanism of ST-segment elevation associated Most healthy men display ST-segment
with cardioversion is not well understood and elevation in the precordial leads V1 through
has not been linked to myocardial damage.54–57 V4. This so-called male pattern of ST-segment
elevation is very common and is considered
Brugada Syndrome a normal finding. It is highest in men aged
of 17 to 24 years and declines gradually with
A distinct ECG feature of Brugada syndrome advancing age. The amplitude of the ST-
(see Chapter 13) is ST-segment elevation in the segment elevation ranges from 1 to 3 mm (most
right precordial leads (V1 through V3) in the marked in V2), with a concave morphology
absence of ischemia, electrolyte abnormalities, (Figure 9-6). There are no associated T-wave
and structural heart disease. The high take- abnormalities or reciprocal changes. Similar
off ST segment in V1 to V2 resembles the rSR' ST-segment elevation is observed less frequently
pattern seen with right bundle-branch block in women. If present, the “female pattern”
(RBBB); however, the wide S wave in leads I, elevation is most commonly less than 1 mm.3
aVL, and V6 that are associated with RBBB might
be absent in Brugada syndrome. Most often A commonly observed normal variant, often
the QT interval is within normal limits.3,4,58 referred to as early repolarization or benign
early repolarization, is also associated with ST-
Although ECG findings can be highly
suggestive of Brugada syndrome, the definitive
124
Non–AMI Causes of ST-Segment Elevation
segment elevation in the precordial leads (most QRS voltage.3 Differentiating this variant from
commonly leads V2 through V5). The amplitude AMI can be difficult. Helpful clues favoring
of the ST-segment elevation ranges from 1 to myocardial ischemia include convex-upward
4 mm (most marked in V4), with a concave- ST-segment elevations, a prolonged QT interval,
upward morphology. Associated findings include and deep, symmetric T-wave inversion.
a notch at the J point and tall, upright T waves
(Figure 9-7). There are no reciprocal changes. Miscellaneous Causes
Less commonly, early repolarization involves the
limb leads. In this case, the associated findings Numerous other conditions have been
include ST-segment elevation in the limb leads described in case reports as causing ST-segment
(commonly observed in the inferior leads II, III, elevation: cardiac and mediastinal tumors,
and aVF, with the elevation in lead II greater acute aortic dissection, mitral valvuloplasty,
than that in lead III) and reciprocal ST-segment pancreatitis, gallbladder disease, septic shock,
depression in aVR.3 Early repolarization can also anaphylactic reaction, drugs (eg, antidepressant
involve the atrial tissue, which manifests as PR- drug overdose or class IC antiarrhythmia drugs),
segment depression. The ECG changes associated thiamine deficiency, hypercalcemia (usually
with early repolarization can be confused with associated with extreme levels and localized to
the ECG changes of stage 1 pericarditis. The leads V1 and V2), cocaine intoxication, cardiac
differentiating features of these two conditions trauma, C5 and C6 spinal cord injury, and
are described earlier in this chapter. various central and autonomic central nervous
system disorders.3,4,39,58 Although the mechanism
Midprecordial (leads V3 to V5) ST-segment for the ST-segment elevation in these conditions
elevation with terminal T-wave inversion can is not well understood, for most (eg, aortic
also be a normal finding. This “ST elevation dissection, intracranial pathology, septic shock)
of the normal variant” is often seen in young it is most likely a reflection of concomitant
black men. The morphology of the ST segment transient myocardial injury or dysfunction,
tends to be concave-upward. Other associated rather than the primary process itself.60,61
findings include a short QT interval and high
Hypothermia is another condition often
Key Facts
• A history of AMI with large Q waves in association with concave ST-segment elevation less than 5
mm in anterior leads should raise suspicion for LVA.
• In pericarditis, leads aVR and V1 frequently exhibit depressed ST segments; however, the presence
of ST-segment depression in any other leads virtually excludes pericarditis in favor of AMI.
• ST-segment elevation in lead II exceeding the elevation in lead III is highly suggestive of acute
pericarditis or early repolarization rather than AMI.
• A depressed ST segment in lead aVL associated with an elevated ST segment in lead III suggests
infarction. This reciprocal relationship is not present with acute pericarditis or early repolarization.
• LBBB is associated with discordance between the direction of the QRS complexes and the ST
segments. Absence of this expected relationship is highly specific for acute myocardial ischemia or
infarction.
• Large pulmonary emboli can produce ST-segment elevation, most commonly in leads V1 to V2 and
III; however, reciprocal ST-segment changes should be absent.
• Horizontal ST-segment depressions and symmetric T-wave inversions are atypical of the normal
secondary ST/T changes associated with LVH and should raise suspicion for an ischemic process.
• Brugada syndrome can be distinguished from AMI by the absence of reciprocal ST-segment
changes.
125
Electrocardiography in Emergency Medicine
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ST-segment elevation: the diagnosis of acute
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ST segment. Acad Emerg Med. 2001;8:961-967.
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of ST-segment elevation after healing of acute block. J Electrocardiol. 2000;33(suppl):87-92.
myocardial infarction to the presence of left ventricular
aneurysm. Am J Cardiol. 1984;54:84-86. 35. Li SF, Walden PL, Marcilla O, et al. Electrocardiographic
diagnosis of myocardial infarction in patients with left
bundle branch block. Ann Emerg Med. 2000;36:561-565.
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36. Kontos MC, McQueen RH, Jesse RL, et al. Can 49. Noble LM, Humphrey SB, Monaghan GB. Left
myocardial infarction be rapidly identified in ventricular hypertrophy in left bundle branch
emergency department patients who have left bundle- block. J Electrocardiol. 1984;17:157-160.
branch block? Ann Emerg Med. 2001;37:431-438.
50. Fragola PV, Autore C, Ruscitti G, et al. Electrocardiographic
37. Madias JE, Sinha A, Ashtiani R, et al. A critique of diagnosis of left ventricular hypertrophy in the
the new ST-segment criteria for the diagnosis of acute presence of left bundle branch block: a wasted
myocardial infarction in patients with left bundle- effort. Int J Cardiol. 1990;28:215-221.
branch block. Clin Cardiol. 2001;24:652-655.
51. Chawla KK, Cruz J, Kramer NE, et al. Electrocardiographic
38. Madias JE, Sinha A, Agarwal H, et al. ST-segment elevation in changes simulating acute myocardial infarction caused
leads V1-V3 in patients with LBBB. J Electrocardiol. 2001;34:87-88. by hyperkalemia: report of a patient with normal
coronary arteriograms. Am Heart J. 1978;95:637-640.
39. Mirvis DM, Goldberger AL. In: Zipes DP, Libby P, Bonow RO,
et al, eds. Heart Disease: A Textbook of Cardiovascular Medicine. 52. Simon BC. Pseudomyocardial infarction and hyperkalemia: a
7th ed. Philadelphia, PA: Elsevier Saunders; 2005:107-151. case report and subject review. J Emerg Med. 1988;6:511-515.
40. Chapman MG, Pearce ML. Electrocardiographic diagnosis 53. Gurevitz O, Lipchenca I, Yaacoby E, et al. ST-segment
of myocardial infarction in the presence of left bundle- deviation following implantable cardioverter defibrillator
branch block. Circulation. 1957;16:558-571. shocks: incidence, timing, and clinical significance.
Pacing Clin Electrophysiol. 2002;25:1429-1432.
41. Madias JE, Kaminetsky A, Solanki N. Myocardial infarction-
induced ventricular aneurysm in the presence of complete 54. Kok LC, Mitchell MA, Haines DE, et al. Transient
left bundle branch block: a case report suggesting a new ST elevation after transthoracic cardioversion in
electrocardiographic diagnostic criterion. J Electrocardiol. patients with hemodynamically unstable ventricular
1999;32:179-183. [Erratum in: J Electrocardiol. 1999;32:373-375]. tachyarrhythmia. Am J Cardiol. 2000;85:878-881.
42. Madias JE, Ashtiani R, Agarwal H, et al. Diagnosis 55. Van Gelder IC, Crijns HJ, Van der Laarse A, et al.
of myocardial infarction-induced ventricular Incidence and clinical significance of ST-segment elevation
aneurysm in the presence of complete left bundle after electrical cardioversion of atrial fibrillation and
branch block. J Electrocardiol. 2001;34:147-154. atrial flutter. Am Heart J. 1991;121(1 Pt 1):51-56.
43. Ullman E, Brady WJ, Perron AD, et al. 56. Chun PK, Davia JE, Donohue DJ, et al. ST-segment elevation
Electrocardiographic manifestations of pulmonary with elective DC cardioversion. Circulation. 1981;63:220-224.
embolism. Am J Emerg Med. 2001;19:514-519.
57. Ben-Dov IZ, Leibowitz D, Weiss T. ST-segment
44. Petruzzelli S, Palla A, Pieraccini F, et al. Routine elevation post cardioversion: a current of injury
electrocardiography in screening for pulmonary without injury. Int J Cardiol. 2006;106:255-256.
embolism. Respiration. 1986;50:233-243.
58. Wilde AA, Antzelevitch C, Borggrefe M, et al. Proposed
45. Ferrari E, Imbert A, Chevalier T, et al. The ECG in pulmonary diagnostic criteria for the Brugada syndrome: consensus
embolism: predictive value of negative T waves in precordial report. Circulation. 2002;106:2514-2519.
leads—80 case reports. Chest. 1997;111:537-543.
59. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome:
46. Falterman TJ, Martinez JA, Daberkow D, et al. Pulmonary report of the second consensus conference. Circulation.
embolism with ST-segment elevation in leads V1 to 2005;111:659-670. [Erratum in: Circulation. 2005;112:e74].
V4: case report and review of the literature regarding
electrocardiographic changes in acute pulmonary 60. Kuroiwa T, Morita H, Tanabe H, et al. Significance of ST segment
embolism. J Emerg Med. 2001;21:255-261. elevation in electrocardiograms in patients with ruptured
cerebral aneurysms. Acta Neurochir. 1995;133:141-146.
47. Klein RC, Vera Z, DeMaria AN, et al. Electrocardiographic
diagnosis of left ventricular hypertrophy in the presence of left 61. Wang K, Asinger RW, Marriott HJ. ST-segment
bundle branch block. Am Heart J. 1984;108(3 Pt 1):502-506. elevation in conditions other than acute myocardial
infarction. N Engl J Med. 2003;349(22):2128-2135.
48. Haskell RJ, Ginzton LE, Laks MM. Electrocardiographic
diagnosis of left ventricular hypertrophy in the presence of 62. Mattu A, Brady WJ, Perron AD. Electrocardiographic
left bundle branch block. J Electrocardiol. 1987;20:227-232. manifestations of hypothermia. Am J
Emerg Med. 2002;20:314-326.
127
ElEctrocardiography in EmErgEncy mEdicinE
Figures
Figure 9-1.
LVA (localized to the anterior wall of the left ventricle) diagnosed as an acute anterior myocardial infarction.
Clues to the presence of LVA on this ECG include large Q waves in association with ST-segment elevations
<5 mm in the anterior leads, poor R-wave progression, and absence of reciprocal changes. The patient had
experienced one previous AMI. Serial ECGs did not demonstrate dynamic changes and, compared with
previous ECGs, showed no new findings. Echocardiogram confirmed the presence of LVA.
Figure 9-2.
Acute inferior myocardial infarction misdiagnosed as pericarditis. Clues to the presence of acute inferior
myocardial infarction in this ECG include ST-segment elevation in the inferior leads and reciprocal ST-segment
depression in lead aVL. Reciprocal changes are not present with acute pericarditis. Note the associated convex
ST-segment elevation in lead V1, which, when found with inferior myocardial infarction, suggests a right
ventricular infarction.21 Coronary angiogram revealed 100% occlusion of the proximal segment of the right
coronary artery. The remaining vessels were patent. The ST-segment elevation in the precordial leads was
present in a baseline ECG and most likely was caused by an early repolarization (normal variant) pattern.
128
Non–AMI Causes of ST-Segment Elevation
Figures
Figure 9-3.
A. LBBB with AMI. Note the presence of discordant ST-segment deviation >5 mm in leads V2 and V3.
B. Baseline ECG from the same patient, obtained 6 months before. Images courtesy of Jeffrey A. Tabas, MD.
A
B
129
ElEctrocardiography in EmErgEncy mEdicinE
Figures
Figure 9-4.
ST-segment elevation (leads V1 and V2) associated with LVH. In LVH, the ST segment has a concave
morphology and is limited to leads V1 to V3. Note the mild ST-segment depression and asymmetrically
inverted T waves in the lateral leads (I, aVL, V5, and V6), commonly seen with fully developed LVH.
Figure 9-5.
LVH with concurrent ischemic changes. The observed ST-segment depression and T-wave changes on this
ECG were misattributed to secondary ST/T changes associated with LVH. The presence of symmetric, deep
T-wave inversions, however, is consistent with cardiac ischemia.
130
Non–AMI Causes of ST-Segment Elevation
Figures
Figure 9-6.
Normal “male pattern” ST-segment elevation, commonly seen in young healthy men. The ST-segment
elevation is frequently observed in the precordial leads V1 to V4 (most marked in lead V2). It has a concave
morphology, with an amplitude ranging from 1 to 3 mm.
Figure 9-7.
Early repolarization. An isolated view of lead V6 demonstrates the classic notch at the J-point (arrow) and tall
upright T-wave that is found in many cases of early repolarization.
131
Electrocardiography in Emergency Medicine
132
C h apter te n
ACS Mimics: Non–ACS Causes of
ST-Segment Depression and T-Wave
Abnormalities
Douglas D. Mayo, MD
ST-segment depression and T-wave ischemia or ACS (Table 10-1). In addition, ST-
inversions are indications of ACS. This chapter segment depression can be seen in patients
focuses on the non-ACS causes of those ECG with left ventricular hypertrophy (LVH) and
abnormalities. Certain treatments that are left bundle-branch block (LBBB) and in those
beneficial to patients with cardiac ischemia taking digitalis therapeutically (Figure 10-1).
related to ACS could be harmful to patients with Because patients with these three usually less-
ECG abnormalities caused by conditions other acute conditions can present complaining of
than ACS. Therefore, emergency physicians chest pain or an anginal equivalent, it becomes
must be able to differentiate a potentially important to recognize the differences.
life-threatening condition from a possibly
benign cause of abnormalities on the ECG. Left Ventricular Hypertrophy
ST-Segment Depression LVH refers to enlargement of the muscle
fibers of the left ventricle. This condition usually
ST-segment depression is associated with occurs from chronic pressure or volume overload
conditions less acute than acute myocardial over a period of months to years; LVH is not an
acute phenomenon. The ECG is an imperfect,
Table 10-1. but inexpensive and widely available, tool for
Causes of ST-segment depression on ECG diagnosing LVH. Several scoring systems have
been developed to diagnose LVH by ECG; the
Digitalis effect Estes and Scott criteria are most widely used.1
Hyperkalemia Unfortunately, the ECG lacks sensitivity for
Hypokalemia diagnosing LVH (range, 12% - 29%), but it does
Left bundle-branch block have adequate specificity.1 Because it can be
Left ventricular hypertrophy difficult to make the diagnosis of LVH in the
Myocardial ischemia/infarction first place, it becomes even harder to determine
Pulmonary embolism whether the ST-segment or T-wave changes are
related to LVH or possibly to acute ischemia.
133
Electrocardiography in Emergency Medicine
LVH produces five major ECG changes: QRS complex. Accordingly, leads with either
increased QRS voltage, increased QRS duration, QS or RS complexes have elevated ST segments
left axis deviation, left atrial abnormality, and and thus mimic ACS. In a similar fashion,
depolarization (ST/T) changes.2 The first four large monophasic R waves have ST-segment
features can be helpful in diagnosing LVH, but depression, which can also mimic ACS. In
this discussion focuses on the repolarization addition, T waves following large monophasic R
changes, because they can easily be confused waves are usually inverted. Loss of this normal
with signs of ACS. Pressure and volume overload discordance suggests ACS. In other words, ST-
in LVH lead to prolonged repolarization and segment depression that is concordant (in the
thus negative forces on both the ST segment same direction) with the major, terminal portion
and T wave (a “strain pattern”). In a review of the QRS complex is suggestive of ACS.5
of 886 patients with LVH, Okin et al3 found
these ST/T-wave changes to be more common Sgarbossa et al used data from the GUSTO-
in patients with heart disease and in those 1 trial to identify three ECG criteria that can
with greater left ventricular mass. The LVH predict acute infarction in patients with LBBB.6
strain pattern produces a downsloping ST- The first independent predictor was ST-segment
segment depression with abnormal T wave in elevation of 1 mm or more that was concordant
leads with tall R waves (I, aVl, V4 to V6). The with the QRS complex. The second was ST-
downsloping ST-segment depression, which segment depression of 1 mm or more in lead
usually lacks J-point depression, is usually V1, V2, or V3. The final independent predictor
followed by an inverted T wave (Figure 10-1A). was ST-segment elevation of 5 mm or more
The T-wave morphology is asymmetric and (in other words, too much elevation) that
characterized by a gradual downsloping followed was discordant with the QRS complex. The
by a rapid return to baseline. The terminal authors used these three criteria to develop a
portion of the T wave often becomes positive, scoring system, which they found to be highly
thus “overshooting” the baseline.1,4 Given the specific for the diagnosis of acute myocardial
chronicity of LVH, these ST/T-waves should not infarction. More recent studies have called the
vary with serial ECGs. As with all the topics usefulness of these criteria into question.7,8
discussed in this chapter, dynamic changes on Nevertheless, this approach dispels the
serial ECGs should raise suspicion for ACS. myth that it is impossible to diagnose acute
myocardial infarction in the setting of LBBB.
Left Bundle-Branch Block
Digitalis Effect
LBBB occurs as a result of interruption of
conduction through the left bundle of His. Even at therapeutic levels, digitalis causes
In LBBB, left ventricular activation occurs ECG changes that can mimic ACS. These
in a delayed fashion from rami off the right effects include prolongation of the PR interval
bundle branch. The asynchronous activation (vagal effect), flattening or inversion of the T
of LBBB manifests as loss of the normal early waves, shortening of the QT interval, and ST-
septal forces (negative QS waves in V1, V2) segment depression.9,10 These changes need to
and large, prolonged QRS complexes (≥0.12 be differentiated from those of digitalis toxicity,
sec) in the leftward leads (I, aVl, and V6). The which manifests primarily as arrhythmia.
altered activation of the ventricles also leads to The J point is usually not depressed, but the
altered repolarization and thus ST- and T-wave ST segment appears to be “sagging,” with a
changes that can mimic ACS (Figure 10-1B). concave upward appearance. This “scooped”
appearance has also been dubbed the “Salvador
The “rule of appropriate discordance” Dali effect,” after the famous painter with the
indicates that in the setting of LBBB, ST- characteristic moustache (Figure 10-1C).10
segment and T-wave configurations are directed
opposite the major, terminal portion of the These changes are more noticeable in the
inferolateral precordial leads. On occasion, the
134
Non–ACS Causes of ST-Segment Depression and T-Wave abnormalities
J point is depressed, which can mimic ACS, 180° away from the left ventricle are negative and
but this usually occurs only in leads with tall hence inverted. The position of the patient can
R waves.9 In patients with baseline ST-segment also affect whether T waves are inverted. In some
depression or T-wave inversion, those effects patients in a ventral position, T waves in leads II,
are magnified by digitalis treatment; patients III, aVL, and aVF may be inverted, but these leads
with normally upright T waves might show normalize or become upright when the patient
T-wave inversion when treated with digitalis.1 changes to the horizontal position. T waves in
Although it could be difficult to distinguish lead III can be either upright or inverted without
ST-segment depression related to digitalis from an underlying problem. This has led some
that caused by ACS, the appearance usually can clinicians to say that a “flipped T in III is free.”
help. Digitalis can cause a “sagging” or “scooped
out” appearance, whereas ischemia causes the The causes of T-wave inversions range from
typical horizontal or downsloping depression. benign, normal variants to life-threatening
emergencies (Table 10-2). The more serious
T-Wave Inversion causes include ACS, PE, and intracranial
lesions. The causes of the inversions can be
T-wave inversions on ECGs frequently have
both ACS and non–ACS causes. Inversions caused Table 10-2.
by ACS are usually narrow and symmetric, Causes of T-wave inversion on ECG11
whereas those that are asymmetric, deeply
inverted, and widely splayed are more typical Primary T-wave inversions
of non–ACS causes.11 As noted above, LVH, Myocardial ischemia/infarction
LBBB, and digitalis effect can result in ST- Intracranial abnormalities (T-wave inversion may be
segment depression as well as T-wave inversion. massive)
In addition, acute myocarditis, juvenile T- Post-tachycardia T-wave pattern
wave patterns, preexcitation syndromes, acute Left or right ventricular overload
pulmonary embolism (PE), cerebrovascular Apical hypertrophic cardiomyopathy (Yamaguchi
accident, and later stages of pericarditis have also syndrome)
been shown to cause inversions (Figure 10-2). Digitalis effect
Other heart diseases
Within the cardiac electrical cycle, the T wave hypertrophic cardiomyopathy
reflects ventricular repolarization. The T wave dilated cardiomyopathy
results from the spontaneous repolarization arrhythmogenic right ventricular dysplasia
of myocytes, with epicardial cells repolarizing myocardial tumor
before endocardial cells. With an electrically pericarditis
negative epicardium relative to the rest of the Subjunctional rhythms
heart, the repolarization wave runs opposite Metabolic abnormalities
to that of depolarization, producing a T-wave Normal variants
deflection of positive voltage.11 T waves are juvenile T-wave pattern
normally upright in leads I, II, and V3 to V6 and early repolarization
normally inverted in aVR, with the other leads Secondary T-wave inversions
being variable.9 The normal T wave usually Left bundle-branch block
has a gradual upstroke with a more abrupt Right bundle-branch block
down stroke, which results in characteristic Ventricular ectopic beats
asymmetry. Furthermore, symmetry of T waves Ventricular pacing (memory T wave)
can indicate an underlying abnormality. However, Idiopathic global T-wave inversions
women and the elderly can have symmetric T- Acute pericarditis/myocarditis
wave without an explainable cardiac cause.11 Wolff-Parkinson-White preexcitation syndrome and
variants
In general, leads over the left ventricle remain Acute pulmonary embolism
positive. In contrast, leads positioned more than
135
Electrocardiography in Emergency Medicine
classified as primary or secondary changes. abnormality and possibly due to underlying
Primary changes occur from alterations in ACS. This distinction can be difficult given
the duration or morphology of the action the coexistence of cardiovascular and
potential, without simultaneous changes in the cerebrovascular disease in these patients.
sequence of activation.11 When forces arise that
interfere with the normal inverse relationship ECG abnormalities are common in patients
between endocardial activation time and action with intracranial lesions, occurring in 92%
potential duration, a T-wave inversion occurs. of patients with acute strokes in one study.15
In contrast, secondary T-wave inversions Repolarization abnormalities are particularly
occur from aberrant ventricular activation in important because they probably serve as
the setting of a normal action potential.11 harbingers for the increased number of
arrhythmias and sudden death associated with
Pulmonary Embolism acute intracranial lesions.16,17 Prominent upright
T waves as well as T-wave inversions have been
The ECG is usually abnormal in patients with seen in acute presentations of intracranial lesions.
PE, although a normal ECG does not rule out First described in patients with subarachnoid
this condition. According to the PIOPED data, hemorrhage, these “cerebral T waves” have also
the ECG is abnormal in about 70% of patients been noted in patients who have experienced
with PE and with no preexisting cardiovascular ischemic strokes, transient ischemic attacks, and
disease.12 However, the findings for PE on ECG nonvascular intracranial lesions.17,18 Although it
are both insensitive and nonspecific. Although was previously thought that these ECG changes
the classic S1Q3T3 pattern is fairly common on were related to underlying, preexisting heart
board and training examinations, it occurs only disease, case-control studies comparing ECGs
about 12% of the time in patients with acute obtained during acute stroke with previously
PE, and often it is seen in patients without PE obtained ECGs show that these changes did
(Figure 10-2A).13 Abnormalities attributable to not predate the acute cerebrovascular event.15,16
PE include tachyarrhythmias, right bundle- Cardiac enzyme concentrations are elevated
branch block, inferior Q waves, ST-segment in about 10% of patients with acute stroke and
changes, and T-wave changes, including frank tend to occur in a delayed manner.19 Underlying
inversion. The T-wave changes often include coronary artery disease is probably not the
shallow inversions in the inferior leads. Deeper only explanation for these elevated cardiac
T-wave inversions in the midprecordial leads enzyme levels, especially because they have
can be related to right ventricular strain and been noted in young patients with subarachnoid
can be seen in massive PE.13 Although the hemorrhages and no underlying coronary artery
exact mechanism for T-wave inversion from PE disease.16 In addition, the rapid appearance
remains debated, several possibilities have been and then resolution of ECG abnormalities
proposed. The theories include mechanisms of also favor a neural cause of cardiovascular
ischemia, strain, and cardiac memory, as seen disease.19,20 When an intracranial lesion leads to
in pacing, LVH, and bundle-branch block.14 hypoperfusion of the posterior hypothalamus,
this causes release of catecholamines, which
Intracranial Lesions causes myocardial injury. The myocardial
injury is manifested by ECG changes and
Cardiac abnormalities are commonly seen cardiac enzyme elevations.19,20 However, some
in patients with intracranial abnormalities. patients have isolated ECG changes related to
Cerebrovascular disease increases one’s intracranial abnormalities without myocardial
likelihood of cardiovascular disease and injury and thus no cardiac enzyme elevation.
vice versa. For the treating physician, it
becomes important to distinguish cardiac The T-wave inversions from a primary
abnormalities caused by an intracranial lesion intracranial lesion have a distinct morphology.
from those unrelated to the intracranial The waves are widely splayed and very deep,
136
Non–ACS Causes of ST-Segment Depression and T-Wave abnormalities
with an outward bulge of the ascending limb ACS in patients with preexcitation syndromes.
and a remarkable asymmetry (Figure 10-2B).11 Tall R waves in the right precordial leads could
Intracranial lesions can also induce larger, be mistaken for a posterior wall myocardial
more prominent T waves or flatten the waves. infarction. Q waves in II, III, and aVF might
ST-segment changes, depression and elevation, mimic an inferior wall myocardial infarction.
have been caused by intracranial lesions. In addition, the inferior Q waves are often
Sometimes these changes are nonspecific. These seen with ST-segment changes similar to those
ST-segment changes can appear more often in associated with LVH and bundle-branch block.11
patients with ischemic strokes than in those
with intracranial hemorrhage.21 ST changes Juvenile T-Wave Pattern and Early
usually occur in the precordial and lateral leads Repolarization
and often resolve quickly.19 Because patients
with acute central nervous system lesions Some patients without an underlying
can also develop ACS, it becomes important pathologic cause have ECGs that generate
to consider this possibility when evaluating concern for ACS at first glimpse. These
these ECG changes. ST-segment changes are physiologic variants include ST-segment changes
more likely to represent actual ACS in diabetic and T-wave inversions in otherwise normal
patients and in individuals older than 65.21,22 patients. In children, the T-wave vector can be
directed posteriorly, which results in T-wave
Preexcitation Syndromes inversions in the right precordial leads of V1 to
V3. As patients age, this vector becomes more
Preexcitation syndromes often present anterior and the inversions become upright. In a
with evidence of ventricular preexcitation small number of patients, the T-wave inversions
or arrhythmias. Wolff-Parkinson-White in V1 to V3 continue into adulthood in a condition
(WPW) syndrome is probably the best known known as persistent juvenile T-wave pattern,
preexcitation syndrome. The classic triad of a benign physiologic variant (Figure 10-2D).
preexcitation seen in WPW syndrome consists
of a short PR interval (<0.12 sec), a delta wave, Early repolarization is another benign
and a wide QRS (>0.12 sec). The abnormal physiologic variant that can manifest as T-
sequence of activation can lead to repolarization wave inversions as well as ST-segment changes.
abnormalities, which manifest as ST/T-wave Although it can be diffusely present, the early
changes. These changes are usually opposite repolarization pattern is most often noted in the
the delta wave and QRS complex and can be mid to lateral precordial leads of V3 to V6. J-point
mistaken for ischemic changes. T-wave inversions elevation is the hallmark of early repolarization
can be seen in leads with tall R waves (Figure and, unlike myocardial ischemia, the ST segment
10-2C). Other ECG changes also might mimic maintains a normal or only slightly concave
appearance. Patients with early repolarization
Key Facts
• In addition to acute ischemia, LVH, LBBB, and digitalis can cause ST-segment depression and T-
wave inversions.
• In addition to acute ischemia, acute myocarditis/pericarditis, juvenile T-wave pattern, preexcitation
syndrome, PE, and intracranial abnormalities can cause T-wave inversions.
• Large voltages together with ST-segment and T-wave changes should prompt consideration of LVH.
• Scooped-out ST-segment depression should prompt consideration of digitalis.
• Widely splayed and very deep T-wave inversions should prompt consideration of an intracranial
lesion.
137
Electrocardiography in Emergency Medicine
can also have prominent or biphasic T-wave 6. Sgarbossa EB, Pinski SL, Barbagelata A, et al.
inversion. The early repolarization pattern is Electrocardiographic diagnosis of evolving acute
often seen in athletes and young black men. myocardial infarction in the presence of left bundle-
In many cases, the ST-segment changes and branch block. N Engl J Med. 1996;334:481-487.
T-wave inversions normalize with exercise.13
7. Shapiro NI, Fisher J, Zimmer GD, et al. Validation
Pericarditis of electrocardiographic criteria for diagnosing acute
myocardial infarction in the presence of left bundle
Pericarditis can produce both ST-segment branch block [abstract]. Acad Emerg Med. 1998;5:508.
changes and T-wave inversions (Figure 10-
2E). These changes are usually seen diffusely 8. Shlipack MG, Lyons WL, Go AS, et al. Should the
throughout all limb and precordial leads, electrocardiogram be used to guide therapy for
although occasionally the changes are limited patients with left bundle branch block and suspected
to fewer leads. Unlike ischemia, there are no myocardial infarction? JAMA. 1999;281:714-719.
reciprocal changes. Depression of the PR segment
further supports the diagnosis of pericarditis. PR- 9. Wagner GS. Marriott’s Practical Electrocardiography. 9th ed.
segment elevation in aVR is a reliable indicator of Baltimore, MD: Lippincott Williams & Wilkins; 1999.
pericarditis. The four stages of pericarditis can be
summarized as 1) diffuse ST-segment elevation, 10. Dubin D. Rapid Interpretation of EKGs. 6th ed.
often with PR-segment depression (elevation Tampa, FL: Cover Publishing, 2000.
in aVR), 2) return of ST segments and PR
segments to baseline and flattening of T waves, 11. Hayden GE, Brady WJ, Perron AD, et al. Electrocardiographic
3) inversion of T waves, and 4) resolution of T-wave inversion: differential diagnosis in the chest
abnormalities or permanence of T-wave inversion. pain patient. Am J Emerg Med. 2002;20:252-262.
References 12. Rodger M, Makropoulos D, Turek M, et al. Diagnostic
value of the electrocardiogram in suspected pulmonary
1. Pollehn T, Brady WJ, Perron AD. Electrocardiographic ST embolism. Am J Cardiol. 2000;86:807-809.
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13. Goldberger AL. Myocardial Infarction:
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Approach. 7th ed. St Louis, MO: Mosby; 2006. St Louis, MO: Mosby-Yearbook; 1991.
3. Okin PM, Devereux RB, Nieminen MS, et al. Relationship of the 14. Nikolic G. T-wave inversion in pulmonary
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4. Brady WJ, Chan TC, Pollack M. Electrocardiographic with prior tracings. Stroke. 1979;10:253-259.
manifestations: patterns that confound EKG diagnosis
of acute myocardial infarction—left bundle branch 16. Yamour BJ, Sridharan MR, Rice JF, et al.
block, ventricular paced rhythm, and left ventricular Electrocardiographic changes in cerebrovascular
hypertrophy. J Emerg Med. 2000;18:71-78. hemorrhage. Am Heart J. 1980;99:294-300.
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accuracy [abstract]. J Emerg Med. 1998;16:797-798. cardiac arrhythmias: cerebral electrocardiographic influences
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18. Dimant J, Grob D. Electrocardiographic changes
and myocardial damage in patients with acute
cerebrovascular accidents. Stroke. 1977;8:448-455.
19. Oppenheimer S, Norris JW. Cardiac manifestations
of acute neurological lesions. In: Aminoff MJ, ed.
Neurology and General Medicine. 3rd ed. Philadelphia,
PA: Churchill-Livingstone; 2001:171-185.
20. Chua HC, Sen S, Cosgriff RF, et al. Neurogenic ST depression
in stroke. Clin Neurol Neurosurg. 1999;101:44-48.
21. Lavy S, Yaar I, Melamed E, et al. The effect of acute
stroke on cardiac functions as observed in an intensive
stroke care unit. Stroke. 1974;5:775-780.
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cardiac monitoring and echocardiography in TIA
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138
Non–ACS Causes of ST-Segment Depression and T-Wave abnormalities
Figures
Figure 10-1.
Causes of ST depression. A: Left ventricular hypertrophy. B: Left bundle-branch block. C: Digitalis effect.
Images courtesy of Amal Mattu, MD.
AB
C
139
Electrocardiography in Emergency Medicine
Figures
Figure 10-2.
Causes of T-wave inversion. A: Pulmonary embolism. B: Intracranial hemorrhage. C: WPW syndrome. D:
Juvenile T-wave pattern. E: Stage 3 pericarditis. Images courtesy of Amal Mattu, MD.
ABC
DE
140
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