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THE ELECTROCARDIOGRAM IN ACUTE CORONARY SYNDROMES
315
(95% CI 1.07 to 1.85), while T-wave inversion of 1–5
mm carries a relative risk of 2.37
(95% CI 1.78 to 3.14),
and T-wave inversion ⬎5 mm carries a relative risk of
3.36 (95% CI 1.67 to 6.14).
23
Refer to Figure 22-3A–D
for examples of inverted T-waves associated with ACS.
When T-wave inversion is seen in the undifferenti-
ated ACS patient, it increases the patient’s mortality
risk because of its association with ACS. However,
in the STEMI patient, minimally inverted (⬎1 mm)
static T-wave inversion does not predict a worse
outcome.
23
One pattern of T-wave inversion deserves special
attention. In Wellens’ syndrome, a patient with a
history of anginal chest pain presents with marked
T-wave inversion in leads V2 and V3 (occasionally in
leads V1 and V4 to V6), or less commonly a bipha-
sic T-wave in leads V2-V3. These fi ndings suggest a
critical stenosis in the left anterior descending (LAD)
be seen in leads III and aVF. T-wave inversions may also
be seen in leads V1 and V2 and, more rarely, in leads
V3 and V4, particularly in younger populations.
21
In the healthy population, T-wave abnormalities
may be seen in the setting of glucose ingestion, body
positioning, deep inspiration, tachycardia, or obesity.
22
In the ill ED population, T-wave change that is new,
dynamic, ⬎1 mm, or present in ⬎1 lead in a coronary
distribution may represent myocardial ischemia in the
patient who presents with chest pain.
21
In a 2008 study
by Lin et al., the presence or absence of T-wave fl at-
tening or inversion was examined in 5,582 patients
who presented to the ED with a potential ACS. The
study concludes that there is a higher 30-day rate of
cardiovascular event (death, AMI, invasive procedure,
or positive stress test) in those patients with T-wave
abnormalities. Risk increases with the degree of T-wave
change; T-wave fl attening carries a relative risk of 1.41
Figure 22.3 T-wave inversion in acute coronary syndrome.
A–D. Typical ischemic T-wave inversions with symmetric
downsloping and upsloping confi gurations. E–F. Wellens’
syndrome T-wave inversions. (E. with the deeply inverted
T-wave pattern and F. with the biphasic T-wave pattern).
CHAPTER 22
316
digitalis effect can be associated with a “scooped”
appearance of the ST depression and can be associ-
ated with QT shortening (in contrast to the QT pro-
longation that may be present in ACS).
21
U waves
U waves are small defl ections that follow T-waves.
In general, they demonstrate the same polarity as
T waves; U-wave inversion in leads other than leads
aVR, III, and aVF can signal myocardial ischemia.
U waves may also been seen in cases of uncontrolled
hypertension, left ventricular enlargement, and valvu-
lar heart disease.
Serial electrocardiogram and continuous
ST-segment trend monitoring
A 12-lead EKG records only 10 seconds of electrical
activity; therefore, a single EKG may fail to capture
dynamic changes of early ACS. Comparison of the
new EKG to an old EKG in the medical record or a
prehospital EKG, or performing serial EKGs in the
ED, may help identify ACS earlier, which can lead to
a more rapid delivery of therapy. Fesmire et al., in a
study of 1000 patients admitted for chest pain, dem-
onstrate that serial EKGs are more sensitive (68.1%
versus 55.45%) and more specifi c (99.4% versus
97.1%) compared to a single EKG for detection
of AMI. Serial EKGs detect injury in an additional
16.2% of AMI patients. High-risk patients benefi t the
most from additional EKGS; they are 15 times more
likely to have their therapy changed when compared
to low-risk patients.
32
In a high-risk patient, the inter-
vals between EKGs may be taken 5–10 minutes apart,
versus 30 minutes to 2 hours in a lower-risk patient.
33
Serial EKG monitoring does not require extra equip-
ment, but does require additional staffi ng.
Another option for monitoring change of the
ST-segment is continuous ST-segment monitoring.
Continuous ST-segment monitoring requires spe-
cialized equipment that monitors ST-segment trends
every few seconds to minutes; alarm thresholds
typically include a change of 200 µV in one lead
or 100 µV in two contiguous leads.
34
Continuous
ST-segment monitoring is of value in distinguish-
ing dynamic change of the ST-segment in AMI from
other causes of static ST-segment elevation. A 1999
study by Moons et al. also suggests that the area
under the curve of the ST-segment has prognostic
artery. The EKG will not show Q waves or signifi -
cant ST-segment elevation, biomarkers will be nor-
mal or only slight elevated, and the patient will be
chest pain-free at the time of the EKG. However, this
patient will be at high risk for acute anterior MI and
death, and requires admission.
24
Refer to Figure 22-3
E–F for examples of inverted T-waves associated with
Wellens’ syndrome.
ST-segment depression
When T-wave inversion is combined with ST depres-
sion, it predicts a worse outcome. In a study by Larsen
et al., ST depression with T-wave inversion carries a
relative risk of 1.98 (1.21–3.26) for cardiovascular
disease mortality during a 7-year follow-up period,
while negative T-wave alone has a relative risk of
1.82 (1.35–2.45).
25
Risk of MI also increases with a
greater number of leads involved and greater degree
of ST-segment depression. Savonitto et al. conclude
that in patients with an NSTEMI, the greater the sum
of ST-segment depression in all leads, the greater the
risk of 30-day mortality.
26
ST-segment depression with T-wave inversion
accompanied by ST elevation in lead aVR signifi es left
main coronary artery involvement, and is a potential
indication for an emergent coronary angiography.
27–30
In the Savonitto et al. study, the extent of ST depres-
sion shows a highly signifi cant correlation with the
degree of three-vessel or left main coronary disease.
26
Although left main occlusion is a rare entity, because
this vessel provides the blood supply to a large portion
of the heart, it is associated with a high mortality rate.
Patients generally present catastrophically with pul-
monary edema, cardiogenic shock, or sudden death
due to ventricular dysrhythmias.
31
Medical manage-
ment of acute left main occlusion is largely ineffective.
In this situation, the presence of intercoronary collat-
erals, a dominant right coronary artery, or incomplete
occlusion increase chance of survival, but the key to
survival is the time to reperfusion by invasive meth-
ods (PCI and coronary artery bypass graft surgery).
Not all ST-segment depression is due to subendocar-
dial ischemia. The ST-segment depression of reversible
ischemia is usually fl at or downsloping, similar to the
ST-segment depression associated with hypokalemia
(typically with serum potassium level ⬍3.0 mmol/L)
or digitalis effect. Both hypokalemia and digitalis may
cause positive U waves in contrast to the new negative
U waves that can be seen in ischemia.
21
In addition,
THE ELECTROCARDIOGRAM IN ACUTE CORONARY SYNDROMES
317
in the fi rst several hours. A Q wave can develop within
the fi rst hour after coronary artery occlusion; it will
be fully developed within 8 to 12 hours postocclusion.
Over the following 2–5 days, the ST-segment eleva-
tion resolves, but with persistent T-wave inversion that
may recover over weeks to months, or last indefi nitely.
Q waves persist for months to years postinfarction.
In a subset of STEMI patients, the ST-segment eleva-
tion persists, most often resulting from left ventricular
aneurysm.
Hyperacute T waves
Although the hyperacute T wave is an early indicator
of STEMI, other clinical syndromes, such as hyper-
kalemia and benign early repolarization (BER), can
cause hyperacute T waves; these prominent T waves
are non-ischemic in origin. The hyperacute T wave in
signifi cance; in the study, a greater area under the ST
trend curve is associated with larger infarct size and
lower resultant left ventricular ejection fraction.
35
Refer to Figure 22-4 for an example of a patient with
evolving inferior wall STEMI.
Evolution of the EKG in STEMI: hyperacute T waves,
dynamic change of the ST-segment, and Q waves
The EKG in STEMI evolves in a classic progression over
a time course of minutes to months. During the fi rst
few minutes of a STEMI, the QT interval may prolong,
followed by an increasing prominence in the T wave
that is out of proportion to the preceding QRS com-
plex. This prominent, or “hyperacute,” T wave appears
within 5 to 30 minutes of AMI, but may persist for
several hours. Next, the ST-segment elevates, typically
Figure 22.4 ST-segment trend monitoring—progressive
ST-segment changes in a patient with inferior wall
ST-segment elevation myocardial infarction. Note the
progressive increase in ST-segment magnitude over a
5 minute period of observation.
CHAPTER 22
318
membranes, causing the ST-segment deviation from
its normal, isoelectric position. The Joint Task Force
of the ESC/ACC/AHA/WHF defi nes ST-segment ele-
vation according to the following criteria: new ST
elevation at the J point in two contiguous leads with
cut off points ⬎0.2 mV (2 mm) in men or ⬎0.15 mV
in women in leads V2-V3, or ⬍0.1 mV in men and
women in other leads.
5
They defi ne lead contiguity as
follows: Anterior: V1-V6; Inferior: II, III, and aVF;
Lateral: I and aVL; and Frontal: aVL, I, aVR, II, III,
and aVF. As ST-segment elevation progresses, it may
become indistinct from the T wave, resembling a
monophasic action potential: the so-called monopha-
sic R wave.
Only 15–25% of patients with ST-elevation have
AMI. The differential diagnosis for causes of ST ele-
vation other than infarction is broad, including acute
myopericarditis, Prinzmetal’s angina, left ventricular
hypertrophy, left ventricular aneurysm, bundle branch
block, ventricular paced rhythm, benign early repo-
larization, hyperkalemia, Wolff-Parkinson-White syn-
drome, and Brugada’s syndrome, among many others.
The ability to distinguish these noninfarction causes of
ST-segment elevation from AMI is important, since the
under-diagnosis of STEMI prevents timely life-saving
therapy while overdiagnosis of infarction can lead to
unnecessary, expensive, and dangerous interventions.
In a study by Brady et al., the authors describe a
technique of morphologic analysis of the ST-segment
that acts as a diagnostic aid in the patient with
ST-segment elevation suspected of STEMI.
37
By draw-
ing a line between the J point and the apex of the
ST-segment–T-wave complex, the clinician can deter-
mine if the ST-segment morphology is concave (EKG
waveform below the line) or nonconcave (EKG wave-
form above or on the line). The presence of a non-
concave ST-segment has a poor sensitivity (77%) but
a high specifi city (97%) for ruling in acute MI. This
technique is best used as an adjunct to the EKG diag-
nosis of STEMI; with its high specifi city, the clinician
can rule in STEMI. Refer to Figure 22-6 for examples
of ST-segment elevation syndromes (both STEMI and
noninfarction causes of ST-segment elevation).
In addition to ST-segment elevation, recipro-
cal ST-segment depression (Figures 22-7 and 22-8),
also known as reciprocal change, may be present in
STEMI; this is a mirroring phenomenon observed
on the ventricular wall opposite injury.
38
Yet, its
cause remains unknown, with distant ischemia and
AMI is asymmetric, broad based, rounded at the apex,
and dynamic in nature. It may be accompanied by
reciprocal ST-segment depression in the inferior leads.
The hyperkalemic T wave, in contrast, is symmetric,
narrow, peaked, and static (static in terms of altera-
tions of the serum potassium level). T waves in BER
are asymmetric, and have a “notching” or concavity
of the J point. The J point is the transition point at
the end of the QRS complex and the beginning of the
ST-segment. The amplitude of the T wave may change,
yet the T wave should not become biphasic or inverted.
In addition, the T wave of BER may be associated
with a shorter QT interval and ST-segment elevation
⬍2 mm in leads V2-V5 and ⬍0.5 mm in the limb
leads, but is unaccompanied by reciprocal ST-segment
depression in other anatomic regions. BER has a high
prevalence in young, African-American, athletic men.
Hyperacute T waves in the elderly with ACS symptoms
are unlikely to be attributed to BER, particularly when
the ST-segment elevation is limited to the limb leads.
36
Refer to Figure 22-5 for examples of prominent T waves
(“hyperacute”) associated with early STEMI.
ST-segment elevation
The hyperacute T wave in AMI may precede or
develop concurrently with ST-segment elevation. The
ST-segment elevation seen in STEMI is called a “cur-
rent of injury” because the damage done to the heart
alters the electrical charge on the myocardial cell
Figure 22.5 Hyperacute T waves of early ST-segment
elevation myocardial infarction: tall, broad-based, blunt
apex, and asymmetric.
THE ELECTROCARDIOGRAM IN ACUTE CORONARY SYNDROMES
319
Anterior STEMI will have reciprocal change in the
inferior leads 40–70% of the time; in inferior STEMI,
ST-segment depression is seen in leads I and aVL in
approximately 30% of such patients.
38
Q waves
A normal, or nonpathologic, Q wave represents the
depolarization of the septal wall between two ven-
tricles; an abnormal Q wave usually signifi es myocar-
dial necrosis, and is both wider and deeper.
19,39
The
2007 Joint Task Force of the ESC/ACC/AHA/WHF
defi nes an abnormal Q wave as any Q wave in leads
V2-V3 ⬎20 msec, a QS complex in leads V2-V3, any
Q wave ⬎30 msec and ⬎0.1 mV deep, or QS complex
in leads I, II, aVL, aVF, or V4-V6. These changes must
be present in any two contiguous leads.
5
A Q wave in
lead V1 is considered normal.
5
While Q waves usually develop within 12 hours of
infarction, they can also develop early in the course of
the infarction, at a time in which urgent reperfusion
therapy is still of benefi t; thus, the mere appearance of
pathologic Q waves does not preclude the consider-
ation for emergent reperfusion therapy. Further, early
electrophysiologic effect as likely possibilities. If
ST-segment elevation is accompanied by recipro-
cal change, the presence of the reciprocal change
improves specifi city for the EKG diagnosis of STEMI.
Figure 22.6 ST-segment elevation syndromes.
A. Benign early repolarization with concave morphology.
B. Acute myopericarditis with concave morphology.
C. Obliquely straight morphology of STEMI. D. Convex
morphology of STEMI.
Figure 22.7 Subtle ST-segment elevation myocardial
infarction of the lateral wall with ST-segment elevation
in leads I and AVL. ST-segment depression, termed
reciprocal ST-segment depression or reciprocal change, is
seen in the inferior leads. The presence of the reciprocal
change strongly supports ST-segment elevation myocardial
infarction in this patient with subtle ST-segment elevation
in the lateral leads.
CHAPTER 22
320
by the circumfl ex artery and its obtuse marginal
branches or the right coronary artery and its poste-
rior descending branch. Approximately 3–9% of all
MIs diagnosed by biomarkers are posterior infarc-
tions that present without ST-segment elevation on the
12-lead EKG.
41
Posterior MI may present as persistent
ST-segment depression in leads V1-V4; ST depression
⬎2 mm in leads V1-V3 is 90% specifi c for posterior
STEMI.
41
In the presence of inferior AMI, anterior
ST-segment depression almost always signifi es pos-
terior STEMI.
42,43
Posterior STEMI also frequently
accompanies lateral wall AMI. A posterior infarction
pattern may be more easily discernable by using the
reverse transillumination technique or the mirror
test; both techniques require inversion of the EKG
and either back-illumination by a strong light source
or viewing the EKG in a mirror. Another aid to diag-
nosing posterior wall infarction is the application of
additional EKG leads V7-V9, which should be placed
on the left back of the patient in the same horizontal
plane as leads V4-V6. Lead V7 is placed at the poste-
rior axillary line, lead V8 inferior to the scapular tip,
and lead V9 at the paravertebral border. Figure 22-9
demonstrates the classic 12-lead EKG fi ndings of pos-
terior wall STEMI; it also demonstrates ST-segment
elevation in the additional posterior leads V8 and V9.
In the majority of right ventricle (RV) infarction
presentations, the right coronary artery or one of
appearance of abnormal Q waves within 6 hours of
symptom onset in acute anterior infarction is associ-
ated with larger infarct size and increased hospital
mortality.
40
The subset of STEMI patients who never
develop Q waves has a better prognosis in terms of left
ventricular function and survival.
Role of additional EKG leads
Due to the insensitivity of the EKG, an infarct in cer-
tain anatomic segments can be missed electrocardio-
graphically; there are certain regions of the heart that
are electrographically silent (i.e., under refl ected): the
inferior wall, the lateral wall, the posterior wall, and
the right ventricle. “Electrographically silent” refers to
the 12-lead EKG’s limited ability to portray these ana-
tomic segments of the heart.
The inferior and lateral walls of the left ventricle
are refl ected, yet these regions are less than optimally
scrutinized by the standard 12-lead EKG; they are
electrocardiographically “near silent.” STEMI in these
two anatomic distributions can be subtle electrocardio-
graphically. Refer to Figures 22-7 and 22-8 for STEMI
of the lateral and inferior walls, respectively, with sub-
tle ST-segment elevation.
Electrocardiographically “silent” regions of the
heart include the posterior wall of the left ventricle
and the right ventricle. The posterior wall is supplied
Figure 22.8 Subtle inferior wall ST-segment elevation myocardial infarction with minimal ST-segment elevation and
reciprocal ST-segment depression in leads I and AVL.
THE ELECTROCARDIOGRAM IN ACUTE CORONARY SYNDROMES
321
Left bundle branch block
Left bundle branch block (LBBB) represents approxi-
mately 7% of myocardial infarctions. Patients with
LBBB in ACS have signifi cantly higher mortality, as
not only do patients with LBBB tend to be older with
more comorbid conditions, but the EKG itself is more
diffi cult to interpret correctly, leading to delays in
diagnosis and therapy.
In normal conduction of a cardiac electrical impulse,
the right ventricle and left ventricle are simultane-
ously depolarized via the right and left bundle of His.
In LBBB, normal conduction through the left bundle
of His is blocked; the left ventricle is depolarized in a
delayed fashion from impulses traveling through the
right ventricle to the interventricular septum and then
to the left ventricle. This progression is represented
on the EKG by negative QS waves in leads V1, V2, or
V3 with a large monophasic R wave (large, prolonged
QRS complex) in leads I, aVl, and V6. The sequence
of repolarization is also altered, causing ST-segment
and T-wave changes that can mimic ACS.
The patient with LBBB has a “new normal EKG.”
The ST-segment and T-wave confi gurations will
be in the opposite direction (discordant) with the
major, terminal portion of the QRS complex. For
its branches is occluded. Isolated RV infarction only
accounts for 3% of MI cases, but should be suspected
when there is ST-segment elevation in lead V1 or when
there is evidence of inferior STEMI, since 50% of those
patients will have associated RV MI.
43
Right-sided leads
V1R-V6R are placed on the anterior chest wall in a mir-
ror image to the standard chest leads. Lead V4R is the
key lead in diagnosing RV infarction; ST-segment eleva-
tion ⬎1 mm is both sensitive (90–100%) and specifi c
(68–95%). In the setting of concurrent posterior MI,
this sensitivity and specifi city decreases.
43
Identifi cation
of RV infarct patients is important because they can be
more susceptible to nitrate and diuretic-related hypoten-
sion resulting from the preload dependence.
44
Notable challenges to EKG interpretation in
presumed ACS presentations: the confounding
patterns
In addition to the presence of electrographically silent
areas of the heart, EKG interpretation can also be
obscured by patterns of new ST-segment and T-wave
abnormality seen in several common clinical sce-
narios: left bundle branch block, ventricular paced
rhythms, and left ventricular hypertrophy.
45
Figure 22.9 Posterior wall ST-segment elevation myocardial
infarction. Leads V1, V2, and V3 demonstrate horizontal
ST-segment depression with prominent R wave and upright
T wave. Additional EKG leads V8 and V9, the posterior
leads, demonstrate ST-segment elevation, consistent with
ST segment elevation myocardial infarction of the
posterior wall.
CHAPTER 22
322
ST-segment elevation of 1 mm or more concordant 1
with QRS complex (Five points; Figure 22-10a)
ST-segment depression of 1 mm or more in lead 2
V1, V2, or V3 (Three points; Figure 22-10b)
ST-segment elevation of 5 mm or more discordant 3
with QRS complex. (Two points; Figure 22-10c)
A Sgarbossa et al. EKG algorithm score of three or
greater (i.e., either of the fi rst two criteria) is highly
specifi c in diagnosing AMI in patients with LBBB. A
score of two, representing the last Sgarbossa et al. cri-
terion, is not helpful in diagnosis. However, a score of
zero cannot exclude AMI. The criteria were applied to
the American College of Emergency Physicians clini-
cal policy in modifi ed form as a decision rule for when
to initiate emergent reperfusion therapy.
48
Subsequent studies that have tested the Sgarbossa et
al. criteria have mixed conclusions about their utility,
with some studies saying that they are no better than
clinical judgment. In 2008, Tabas et al. published a
meta-analysis that reevaluated data from 11 studies
(2100 patients) since 1996; they conclude that when
one of the fi rst two Sgarbossa et al. criteria are pres-
ent, the specifi city for AMI is 98% with a positive
likelihood ratio of 7.9, but that the presence of the
instance, in the anterior leads (leads V1-V3) that
have negative QRS complexes, we expect to see
ST-segment elevation and an upright T wave. In the
lateral leads (leads I, aVl, V5, and V6) with posi-
tive QRS complexes, we expect to see ST-segment
depression and T-wave inversion. This relationship
is known as the “rule of appropriate discordance.”
46
Loss of this relationship may indicate ACS in the
appropriate patient.
Whether or not it is possible to diagnose AMI in
the patient presenting with ACS symptoms and LBBB
has been a subject of great research and clinical inter-
est. In a 1996 study, Sgarbossa et al. attempted to
establish a set of criteria for diagnosing acute infarc-
tion in the setting of LBBB.
47
The EKGs of patients
enrolled in the GUSTO-1 (Global Utilization of
Streptokinase and Tissue Plasminogen Activator for
Occluded Coronary Arteries) trial had LBBB and
AMI confi rmed by biomarkers compared to EKGs of
control patients with known, stable coronary heart
disease and LBBB taken from an outpatient database.
Sgarbossa et al. report three EKG criteria of potential
independent value in diagnosis of AMI as well as a
scoring system (0–5 points):
Figure 22.10 Sgarbossa et al. criteria for acute myocardial
infarction in left branch bundle block. A. Concordant
ST-segment elevation. B. Concordant ST-segment depression
limited to the right precordial leads. C. Excessive, discordant
ST-segment elevation.
THE ELECTROCARDIOGRAM IN ACUTE CORONARY SYNDROMES
323
Left ventricular hypertrophy
The Sokolow-Lyon Index (the S-wave amplitude
in V1 plus the R wave amplitude in lead V5 or V6
⬎35 mm) is one of many methods of diagnosing
the left ventricular hypertrophy (LVH) pattern by
EKG. LVH can produce the following EKG changes:
increased QRS voltage, widened QRS complex, poor
R-wave progression, and repolarization abnormali-
ties of the ST-segment and T wave. Importantly,
ST-segment and T-wave abnormalities are seen in
approximately 75% of LVH cases. The repolar-
ization abnormalities, which mimic AMI, can be
divided into two categories: those associated with ST
elevation and hyperacute T waves, and those associ-
ated with ST-segment depression and T-wave inver-
sion.
46
Morphologic analysis of the ST-segment can
help distinguish STEMI from LVH. The ST-segment
of LVH is typically concave (rather than the “tomb-
stone” convexity of AMI).
46
In a 2004 study by Pope et al., having LVH does not
alter the true-positive rate for ACS, but it does increase
the false-positive rate by almost 50%.
52
A feature of
LVH that may help distinguish it from AMI is the
static nature of its ST-segment and T-wave abnormali-
ties, unlikely to change during the course of ED eval-
uation. Serial EKG monitoring or ST-segment trend
analysis may assist the clinician with diagnosis.
40
Section IV: Decision making
A normal or nonspecifi cally (i.e., minimally) •
abnormal EKG does not rule out AMI.
The EKG must be interpreted within the context of •
the clinical presentation.
With regards to AMI, the EKG is most useful in •
ruling in acute myocardial infarction, but is not
particularly sensitive and should not be used alone
to rule out AMI.
Additional EKG leads, such as leads V4R, V8, •
and V9, can add diagnostic information in ACS,
particularly with a moderate to high suspicion for
AMI and a nondiagnostic EKG.
ST-segment elevation in chest pain patients does not •
always result from STEMI; sound EKG interpretation,
ST-waveform analysis, reciprocal change, and serial
monitoring, can assist in this EKG differentiation.
Confounding EKG patterns such as bundle branch •
block, LVH, and ventricular paced rhythms reduce
third criteria in isolation is not sensitive or specifi c
enough to diagnose acute MI. Although the research
of Tabas et al. lends support to the criteria, it also
reaffi rms that the lack of Sgarbossa et al. criteria does
not rule out infarction. As is true with most EKG
characteristics and AMI, the Sgarbossa et al. criteria
are specifi c and thus helpful with ruling in infarction;
the criteria are not sensitive and therefore are of little
value in ruling out MI.
Right ventricular paced rhythm
In a right ventricular paced rhythm (VPR), similar to
LBBB, the depolarization of the left ventricle is delayed
in comparison to the right ventricle. The impulse prop-
agates from the right ventricle to the interventricular
septum to the left ventricle, resulting in a greater time
of total depolarization and a wide QRS complex. The
EKG of the right ventricular paced rhythm differs from
LBBB in leads V5 and V6; in such paced rhythms, a
QS complex replaces the monophasic R wave seen
in LBBB.
The rule of appropriate discordance, however, still
applies. In right ventricular paced rhythms, the QRS
complex is positive in leads I and aVl; the ST-segment
is depressed with T-wave inversion in those leads.
Similarly, in leads with a negative QRS complex (leads
II, III, aVf, and V1-V6), the ST-segment is elevated
and the T wave is upright. Similarly to LBBB, a lack
of discordance could signify ACS, although the lack
of these fi ndings does not rule out ACS.
Sgarbossa et al.’s criteria can also be applied in the
right ventricular paced rhythm presentation. Returning
to the GUSTO-1 data, there were 17 patients with
pacemakers and AMI in the study; of the three criteria
previously discussed above, the most useful in diagnosis
of AMI and RV paced rhythm is the third: ST-segment
elevation ⱖ5 mm discordant to the QRS complex.
49
This fi nding has a specifi city of 88% and a positive like-
lihood of diagnosis of AMI of 4.41.
50
It is speculated
that the reason that the excessive discordance (the third
Sgarbossa et al. criterion) is helpful in the EKG interpre-
tation of right ventricular paced rhythms, in contrast to
the LBBB presentation, is that it results from the fact
that most such rhythms have predominantly negative
QRS complexes, so that there is more “opportunity”
to witness a discordant change in the ST-segment.
51
As
with LBBB, the Sgarbossa et al. criteria can help rule in
infarct in right ventricular paced rhythms, yet not rule
out AMI.
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