ECG Monitoring - ST Segment Monitoring - AJCC 1999

CONSENSUS STATEMENT FOR PRACTICE http://www.aacn.org/AACN/jrnlajcc.nsf/GetArticle/ArticleFour86?Ope...
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American Journal of Critical Care American Journal of Critical Care Home
NOVEMBER 1999 - VOLUME 8 - NUMBER 6wew
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CONSENSUS STATEMENT FOR PRACTICE
Multilead ST-Segment Monitoring in Patients With Acute
Coronary Syndromes: A Consensus Statement for Healthcare
Professionals
Barbara J. Drew and the ST-Segment Monitoring Practice Guideline Working Group
About the Authors
By Barbara J. Drew, RN, PhD, (Chair) and Mitchell W. Krucoff, MD, (Co-chair) for the
ST-Segment Monitoring Practice Guideline International Working Group.* From the School
of Nursing, University of California, San Francisco, Calif (BJ D). All members of the
ST-Segment Monitoring Practice Guideline International Working Group are listed in the
Acknowledgments. This article originally appeared in the November 1999 issue of the
American Journal of Critical Care, Vol 8, No. 6, pp372-386.
Reprint requests: InnoVision Communications, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800)
899-1712 or (949) 362-2050 (ext 515); fax, (949) 362-2022; e-mail, ivcReprint@aol.com.
In patients with acute coronary syndromes (unstable angina, ST elevation and nonST
elevation myocardial infarction), the goal of pharmacological and catheter-based
interventions is to reverse ongoing ischemia and to prevent or interrupt myocardial cell
death. For patients with acute myocardial infarction, early reperfusion and sustained
patency of the culprit artery are important determinants of survival.
1
Thus, continuous monitoring of the status of the culprit artery is mandatory to tailor
appropriate therapy for each patient.
2
Although coronary angiography reveals vessel
anatomy at a brief moment in time, electrocardiographic (ECG) monitoring reflects
myocardial physiology continuously, both during normal periods and during ischemia. Thus,
the ECG provides a more accurate assessment of the myocardium than does angiography
in situations in which vessel patency has been restored but ischemia persists because of
no reflow or reperfusion injury. Moreover, currently, ECG monitoring is the only practical
way to detect recurrent or transient ischemic events over time.
ECG monitoring is more sensitive than patients symptoms for detecting transient
myocardial ischemia because 80% to 90% of ECG-detected episodes are clinically
silent.
3-10
Asymptomatic changes in the ST segment in a patient with known coronary
artery disease are a well-established and highly specific indication that the patient is
experiencing transient myocardial ischemia. Moreover, compelling data from independent
cohorts of patients consistently indicate unfavorable outcomes among patients who have
such ST changes during continuous ECG monitoring after episodes of unstable
angina
4,5,7,11-14
or myocardial infarction.
15-21
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To date, no large-scale, well-controlled clinical trial has been done to prove that hospital
treatment based on the results of ST-segment monitoring improves outcomes in patients
with acute coronary syndromes. However, because of the prognostic importance of
ischemic events detected with ST-segment monitoring, patients with acute coronary
syndromes most likely would benefit from early detection and treatment of ischemia.
Accurate detection of ischemic events is especially important in current clinical practice
because a variety of recently developed treatment options are available, including new
reperfusion strategies, new anticoagulant and antiplatelet agents, and innovative
catheter-based techniques.
Although software for ST-segment monitoring is widely available in commercial bedside
cardiac monitors, it is not often activated by healthcare professionals for patients with acute
coronary syndromes treated in emergency departments, cardiac catheterization
laboratories, intensive cardiac care units, or step-down telemetry units. Underuse of
ST-segment monitoring appears to stem from 2 general sources: (1) technical problems
with noise levels and lack of adequate equipment for accurate ST-segment analysis; and (2)
a lack of clarity about how information about changes in the ST segment, especially in
asymptomatic patients, should be used to determine clinical therapy.
This report provides consensus guidelines for the optimal application of ST-segment
monitoring in patients with acute coronary syndromes. Although ST-segment monitoring has
been used in children,
22
this discussion focuses on adults, who make up the vast majority
of patients with acute ischemic coronary syndromes. The following specific questions are
addressed:
1. Who should have ST-segment monitoring?
2. What are the goals and recommended time frames for ST-segment monitoring in various
diagnostic groups?
3. Who should not have ST-segment monitoring?
4. What ECG leads should be monitored?
5. What equipment requirements are necessary for accurate ST-segment monitoring?
6. What strategies improve the accuracy and clinical usefulness of ST-segment monitoring?
7. What knowledge and skills should clinicians have for safe and effective ST-segment
monitoring of patients in a hospital unit?
8. What are priorities for future research and development?
Development of the Guidelines
A literature search was used to determine key nurse and physician scientists who had
published articles on ST-segment monitoring of patients in acute care hospital units. These
scientists were invited to participate in a working group that met in Dallas, Tex, in November
1998. Additional members were added to the working group as recommended by the initial
key scientists. The final group included 10 physicians, 10 nurses, and 1 cardiac monitoring
engineering expert.
The 10 nurses included 5 nurse scientists with doctoral degrees and 5 doctoral students
involved in research on ischemia. Eleven members of the working group were from various
locations throughout the United States; 9 were from other countries, including Denmark,
Sweden, the Netherlands, Australia, and Scotland.
At the initial meeting, consensus was reached on each of the 8 substantive areas
mentioned earlier. The chair of the working group drafted an initial guideline that was
critiqued by all members of the group via telephone calls and e-mail messages. The
guideline was revised according to the critiques, and a second draft was circulated. This
article includes the final, revised consensus document.
Who Should Have ST-Segment Monitoring?
Unstable angina and ST elevation or nonST elevation myocardial infarction most often
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occur in patients with significant coronary artery disease who have disruption of an
atherosclerotic plaque and a subsequent dynamic coronary occlusive process that involves
cycles of plaque rupture, platelet stimulation, coronary vasospasm, and thrombus
formation.
23-30
For this reason, these patients should be considered the highest priority for
ST-segment monitoring, which provides uninterrupted real-time information about the
occurrence, frequency, and severity of ischemic episodes over the course of the dynamic
occlusive process.
In addition to unstable angina and acute myocardial infarction, a number of other acute
situations occur in which ST-segment monitoring may be useful, although these conditions
should not take priority over monitoring of patients with acute coronary syndromes. The
Table is a summary of potential benefits of ST-segment monitoring in patients with various
diagnoses.
x
What Are the Goals and Recommended Time Frames for ST-Segment
Monitoring?
Acute Coronary Syndromes
Patients with acute myocardial infarction or unstable angina should be monitored for a
minimum of 24 to 48 hours, or until they remain event-free for 12 to 24 hours. For patients
with acute ST elevation myocardial infarction, 2 periods of ST-segment monitoring are
important: an early period (within the first 6 hours after therapy) to assess patency of the
infarct-related artery after thrombolytic therapy
26,29-31
or primary angioplasty
32
and a late
period (6-48 hours after therapy) to detect recurrent ischemia.
Patients who experience recurrent (especially silent) ischemia should be monitored after
bed-rest restrictions have been discontinued, preferably with real-time telemetry for
ST-segment monitoring; however, retrospective Holter monitoring may also be useful in
patients with less acute problems. Absence of ischemic events with increasing activity (eg,
bathing, toileting) may provide the clinical justification for transfer from the intensive care
unit (ICU) and early discharge from the hospital. If chest pain or anginal-equivalent
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symptoms develop after ST-segment monitoring has been discontinued, monitoring should
be reinstituted for 12 to 24 hours.
Chest Pain That Prompts a Visit to an Emergency Department
A total of 8 to 12 hours of ST-segment monitoring in combination with determinations of
serum biochemical markers of injury is a cost-effective way to triage patients who come to
the emergency department because of chest pain.
33-36
Because a substantial proportion
of these patients do not have unstable coronary syndromes, ST-segment monitoring of
patients in the emergency department is less costly than is admitting all patients with
possible myocardial infarction to an ICU. Figure 1 is an example of a risk-stratification
algorithm for use in patients who come to the emergency department because of chest
pain.
37
x
Catheter-Based Interventions
Ideally, ST-segment monitoring with radiolucent electrodes and lead wires should be started
in the cardiac catheterization laboratory during catheter-based interventions (eg, coronary
angioplasty, stent placement, atherectomy). This practice provides the opportunity to
document the patient-specific, coronary sitespecific ST-segment deviation fingerprint
associated with transient occlusion during catheter balloon inflation.
38
It also indicates
patients in whom a coronary artery can be occluded without ECG changes, in whom
monitoring for abrupt coronary reocclusion cannot rely on ST-segment monitoring.
Because of current techniques for immediately sealing groin puncture sites, patients in
stable condition who have more elective catheter-based interventions are typically
mobilized early after the intervention and are discharged from the hospital the same day
without the need for ST-segment monitoring. However, for patients with unstable conditions
or patients with less definitive catheter-based interventional outcomes who require
monitoring in an ICU or an intermediate care unit, ST-segment monitoring for 6 to 12 hours
is recommended. Figure 2 is an example of a clinical flow diagram for postprocedural
management based on ST-segment monitoring.
5 of 20 4/10/2006 9:33 AM
x
Postprocedural monitoring in patients undergoing catheter-based interventions has 2 goals:
to detect abrupt reocclusion at the intervention site due to vessel dissection or thrombosis
38
and to distinguish ischemic from nonischemic chest pain. In terms of the first goal, abrupt
reocclusion is most likely to occur early after the procedure, either before the patient has left
the cardiac catheterization laboratory or within the first several hours after transfer to
another hospital unit.
39
In terms of the second goal, nearly 50% of patients who have
placement of a stent and about 12% of patients who have angioplasty experience chest
pain after the interventional procedure.
40

This type of chest pain either requires urgent recatheterization/revascularization for
treatment of abrupt reocclusion or is benign and requires no intervention. Benign chest pain
can be caused by stretching of the coronary vessel during high-pressure balloon inflations
or stent deployment.
Benign chest pain, nausea, and other nonspecific symptoms can also be due to
gastrointestinal distress brought on by fasting or by esophageal reflux after eating in the
supine position. The absence of ST-segment deviation during these situations may provide
reassurance that such symptoms are not related to ischemia. A potential cost benefit of
ST-segment monitoring is that it may reduce the number of unnecessary repeat cardiac
catheterizations by distinguishing between ischemic and benign causes of postprocedural
6 of 20 4/10/2006 9:33 AM
symptoms.
However, the absence of ST-segment deviation during chest pain can be considered
reassuring only if ST-segment deviation was detected during coronary occlusion in the
catheterization laboratory. For example, if a circumflex coronary artery is stented, and no
changes in the ST segment are observed on ECGs obtained during balloon inflation, then
the absence of ST-segment deviation when chest pain recurs does not rule out ischemia or
a problem at the intervention site (eg, an occlusive thrombus).
Cardiac transplant patients who undergo catheter-based interventions are a higher priority
than are other patients for postprocedural ST-segment monitoring because the former are
vulnerable to silent reocclusion due to altered sensory discrimination.
Cardiac or Noncardiac Surgery
Experience with ST-segment monitoring of patients after cardiac or noncardiac surgery is
limited. However, Mangano and coworkers
42-45
detected a high-risk period immediately
after surgery when patients emerge from anesthesia and experience pain. Such arousal of
the sympathetic nervous system is accompanied by an increase in heart rate, and therefore
ischemia in the early postoperative period often occurs because myocardial oxygen
demand exceeds blood flow capabilities, rather than because of coronary occlusion
processes.
Postoperative myocardial ischemia may also develop because of fluid shifts and
hypercoagulability, which tend to occur somewhat later in the 24 to 48 hours after surgery.
Therefore, ST-segment monitoring of surgical patients with coronary heart disease or
cardiac risk factors should begin immediately after surgery when the patient is being
monitored in a postanesthesia recovery unit and should continue in the ICU for
approximately 24 to 48 hours.
Who Should Not Have ST-Segment Monitoring?
Certain subgroups of patients with acute coronary syndromes may not be candidates for
currently available ST-segment monitoring technologies. In general, these are patients in
whom interpretation of evidence of ischemic changes on the static ECG is confounded by
conduction abnormalities, left ventricular hypertrophy, or excessive artifact. If a static ECG
is unsuitable for detection of ischemia, use of ST-segment monitoring most likely will lead to
false alarms, staff fatigue, and disenchantment with the technology, and potentially even to
unnecessary therapy, curtailment of patients activities, or delay in discharge from the
hospital.
Patients who may not be candidates for ST-segment monitoring include those who have (1)
left bundle branch block, (2) intermittent right or left bundle branch block, (3) ventricular
pacing rhythm, (4) an excessively noisy signal because of restlessness or confusion, or (5)
wound dressings over the precordium.
Few current ST-segment monitors automatically change the point at which the ST segment
is measured when the heart rate changes, and they do not correct measurements of ST
amplitude when changes occur in the QRS amplitude. This situation means that patients
with steeply upsloping ST-T waves, such as patients who have left bundle branch block
may be plagued with false-positive ST alarms when there is a change in heart rate. In
addition, patients who have large changes in QRS amplitude when changing body position
also may be plagued with false alarms that confound interpretation of data from
ST-segment monitoring.
What ECG Leads Should Be Monitored?
Monitoring ST-segment changes in all 12 ECG leads is recommended for accurate
detection of myocardial ischemia in patients with acute coronary syndromes because
7 of 20 4/10/2006 9:33 AM
ischemia may be due to more than one mechanism and cause changes in different leads at
different times.
10,46,47
For example, Klootwijk et al
47
found that ST changes dispersed
and shifted among different leads over time in at least 31% of patients with unstable angina
who had more than a single episode of ST-segment deviation during a 48-hour monitoring
period.
47

Likewise, Drew et al
10
found that 42% of recurrent ischemic events detected with full
12-lead ST-segment monitoring were not detected by monitoring the single ECG lead that
had maximal ST-segment deviation at the onset of acute myocardial infarction or during
catheter balloon inflation. Similarly, Krucoff et al
48
reported that of 524 angioplasty patients
who had ST-segment monitoring after the coronary intervention, 92 (18%) had episodes of
ST deviation; 43% of the episodes were elevations in the ST segment, and 57% were
depressions.
48

Thus, patients with acute coronary syndromes differ from patients with stable coronary
artery disease who have transient myocardial ischemia; the latter typically have only ST
depressions, which are reliably visualized on ECG tracings obtained with lead V
5
during
exercise or ambulatory monitoring. For this reason, single-lead ST-segment monitoring is
insufficient for patients with acute coronary syndromes.
10,47,49,50
Leads Valuable for Detecting Coronary Occlusion
Myocardial ischemia due to coronary occlusion has a variety of causes in patients with
acute coronary syndromes: (1) occlusive thrombus with acute myocardial infarction, (2)
balloon inflation during catheter-based interventions, (3) rethrombosis of the infarct-related
artery after thrombolytic therapy, (4) reocclusion of the treated artery after catheter-based
procedures, and (5) coronary vasospasm. The classic ECG pattern produced by coronary
occlusion is ST-segment elevation detected by a restricted number of leads that lie directly
over the ischemic myocardial zone.
Right Coronary Artery Occlusion. The lead that most often shows maximal ST-segment
elevation during occlusion of the right coronary artery and ischemia of the inferior wall of the
heart is lead III; next, in order, are lead aVF and lead II.
51-53
Interestingly, lead II is the
lead most often selected for monitoring in ICUs.
54
However, during injury of the inferior
wall, the ECG tracing obtained with lead II typically displays the least ST-segment elevation
of the tracings obtained with the 3 available inferior leads.
Left Coronary Artery Occlusion. Maximal ST-segment elevation during occlusion of the
left anterior descending coronary artery and injury of the anterior wall of the heart typically is
observed on the mid precordial ECG leads V
2
and V
3
, and less often lead V
4
.
49,51-53
Occlusion of the left circumflex artery produces no visible changes in the ST segment on
the standard 12-lead ECG in about one third of patients. Patients who have visible changes
in the ST segment during occlusion of the circumflex artery may have ischemia of the
inferior, lateral, or posterior wall of the heart, and thus a variety of patterns may be observed
in patients in whom no ECG lead is indicated as being far superior to other leads.
49,51-53
ECGs obtained with additional posterior leads, V
7
, V
8
, and V
9
, may show ST-segment
elevation in these extra leads during injury of the posterior wall. However, because of the
distance of the posterior part of the thorax from the left ventricle, the amplitude of ST
elevation is low, often less than 1 mm, which is difficult for the human eye to discern.
Reciprocal ST-segment depression during injury of the posterior wall is best observed in
one of the rightward standard precordial leads, V
1
, V
2
, and/or V
3
. Because the heart is
situated in the chest more anteriorly than posteriorly, the amplitude of these reciprocal ST
8 of 20 4/10/2006 9:33 AM
depressions may be greater than the amplitude of ST elevations recorded with posterior
leads.
Summary. In summary, the most valuable leads for detecting occlusion of the 3 major
epicardial coronary arteries encompass 9 of the 12 standard ECG leads. The arteries and
the leads are as follows: right coronary artery, leads III, aVF, and II; left anterior descending
artery, leads V
2
, V
3
, and V
4
. For the left circumflex artery, a variety of leads may be
involved, depending on the myocardial zone affected (lateral, inferior, and/or posterior), as
follows: leads V
5
and V
6
(lateral), leads III, aVF, and II (inferior), and leads V
1
, V
2
, and V
3
(posterior).
Leads Valuable for Detecting Demand-Related Ischemia
In addition to coronary occlusion, patients with acute coronary syndromes may have global,
subendocardial ischemia due to an increase in myocardial oxygen demand beyond the flow
limits of stenotic coronary vessels. Although patients with these demand-related ischemic
events may not require urgent interventions such as thrombolytic therapy or immediate
angioplasty, their prognosis is worse than that of patients without such events.
3-9

Thus, detection of demand-related ischemia with ST-segment monitoring is important.
Ischemic events related to an increase in myocardial oxygen demand may occur during a
tachyarrhythmia or, in patients with severe coronary artery disease, may be elicited by only
a slight increase in heart rate. The classic ECG pattern of demand-related ischemia is 1 to 2
mm of horizontal or down-sloping ST-segment depression on the tracings from several
leads, with maximal ST depression typically recorded by leads lying over the left ventricular
apex (eg, lead V
5
).
55
Monitoring a Patients ST Fingerprint
Krucoff et al
38
introduced the concept of the ST fingerprint, which is defined as the
12-lead ECG pattern of ST-segment elevations and depressions that is unique to a
particular patient and is based on the anatomic site of coronary occlusion.
38
During acute
myocardial infarction, a patients ST-fingerprint ECG is ideally recorded at peak ST-segment
deviation, before thrombolytic or primary angioplasty therapy is started. Subsequent
duplication of this patient-specific ECG pattern can be used to diagnose reocclusion of the
infarct-related artery.
2,24,26,56-58
When 12-lead ST-segment monitoring is not available, evidence of rapid ST-segment
recovery (normalization) in the single lead with peak ST-segment elevation is useful for
predicting patency of the infarct-related artery.
29,59,60
However, single-lead monitoring is
not sensitive for diagnosing ischemia related to other mechanisms (eg, ischemia of
myocardial zones that do not get their blood supply from the infarct-related artery).
10
Therefore, 12-lead ECG monitoring, rather than single-lead monitoring, is recommended
because the former covers more of the bases for detecting both coronary artery occlusion
and demand-related ischemia in anterior, inferior, lateral, and often, posterior myocardial
zones.
In patients undergoing catheter-based interventions, the ST-fingerprint ECG is ideally
recorded during inflation of the catheter balloon. Subsequent duplication of this
patient-specific ECG pattern can be used to diagnose abrupt reocclusion of the treated
artery, which requires urgent recatheterization/revascularization.
38
A partial reocclusion of
the treated artery may not reproduce the patients ST-fingerprint ECG pattern and thus may
be impossible to distinguish from other ischemic mechanisms. Partial reocclusion, however,
is less of an emergency than is abrupt, total reocclusion, and the latter should never go
undetected in clinical practice.
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12-Lead ECG Options
Three 12-lead ECG configurations have been investigated for ST-segment monitoring
(Figure 3).
The Modified Standard 12-Lead ECG. The modified standard 12-lead ECG in which limb
leads are placed on the body torso (Mason-Likar lead configuration)
61
requires 10
electrodes to record 8 channels of ECG information (leads I and II and the 6 precordial
leads). The remaining 4 limb leads (III, aVR, aVL, aVF) are derived from leads I and II.
62
This torso-positioned electrode configuration was developed for exercise testing to reduce
noise levels.
x
This configuration is recommended over standard limb-lead positioning for ST-segment
monitoring because the torso-positioned configuration reduces false alarms due to a noisy
signal when the patient moves the extremities. Differences in ECG findings between
standard and modified standard 12-lead ECGs have been studied by a number of
investigators.
63-67
Reported differences between the 2 configurations include appearance
or disappearance of inferior Q waves,
66,67
changes in the amplitude of QRS and T
waves,
64
a change in slope of the ST segment,
64
and a rightward axis shift with the
torso-positioned configuration.
63-67
Differences between the standard and the modified
standard lead configurations can be minimized by placing the arm electrodes as close to the
shoulders as possible.
63
The modified standard 12-lead ECG system has been used extensively for research studies
with the portable Mortara ELI 100 ST monitor (Mortara Instrument, Milwaukee, Wis).
56
In
addition, a growing number of manufacturers of cardiac bedside monitors make monitors
that accommodate use of this 10-electrode approach for 12-lead ECG monitoring.
Unfortunately, however, not all of these bedside monitors include full 12-lead ST-segment
analysis or storage of information from all 12 leads in a full disclosure format.
Derived 12-Lead ECG. A second 12-lead ECG method uses the Frank vectorcardiographic
lead configuration,68 which requires 8 electrodes to record 3 channels of ECG information
(X, Y, and Z leads). A derived 12-lead ECG has been developed for this system by taking
part of each of the 3 mother leads to construct 12 daughter leads similar in waveform
morphology to the 12 standard leads.
69
Advocates of the vectorcardiographically derived
12-lead ECG emphasize that the standard ECG contains redundant information in
contiguous leads and that 3 channels of information are enough to diagnose ischemia in
various myocardial zones.
10 of 20 4/10/2006 9:33 AM
They assert that all important clinical information is contained within the 3 orthogonal X, Y,
and Z leads and that ischemia can be readily recognized by clinicians when the 3-lead
format is translated into the more familiar 12-lead ECG format.
70
Importantly, the Frank
lead configuration includes electrodes on the patients back and an electrode under the right
axilla, so this system may be more sensitive than the standard ECG for detecting injury of
the posterior wall of the heart and of the right ventricle. The Frank lead system has been
used extensively in research studies with the MIDA system (Ortivus Medical, Tby,
Sweden) to analyze both ST-segment and QRS changes during ischemia.
14,27,31,71-77
The EASI 12-Lead ECG. A third 12-lead ECG method uses a modified Frank lead
configuration and requires 5 electrodes to record 3 channels of ECG information. A 12-lead
ECG has also been derived for this lead configuration by Dower et al
78
and is referred to as
the EASI 12-lead ECG (Zymed Inc, Camarillo, Calif). Investigations with the EASI 12-lead
ECG indicate that it is comparable to the standard 12-lead ECG for detection of
arrhythmia
79,80
and ischemia.
81-83
Future research and development are required to
make available use of the EASI 12-lead ECG in commercial bedside monitors having
12-lead ST-segment analysis and full-disclosure capabilities.
Summary. Sound scientific evidence indicates that all three 12-lead ECG configurations are
valuable for ST-segment monitoring. However, all 3 lead configurations, Mason-Likar,
63-67
Frank vectorcardiographic, and EASI, differ from the standard extremity lead configuration,
and thus clinicians should be cautious when making serial ECG comparisons recorded with
2 different lead configurations in a given patient. In addition, clinicians should be cautious
when comparing snapshot 12-lead ECGs, which are obtained with patients supine, with
ECGs printed from an ST monitor, because the latter may involve a different body position
and associated alterations in ST-T wave morphology.
Most Valuable Leads When 12-Lead ECG Monitoring Is Unavailable
If only 2 leads are available for ST-segment monitoring, use of leads III and V
3
is
recommended for patients with acute coronary syndromes, unless available information
from a patients prior 12-lead ECG recorded during an ischemic event indicates that another
lead is more sensitive.
10,51-53
The best 3-lead combination is leads III, V
3
, and V
5
;
however, many bedside cardiac monitors are capable of monitoring only a single precordial
(V) lead because the monitors provide only a single chest electrode. In addition, these 2-
and 3-lead combinations for ischemia exclude lead V
1
, which is considered the best lead to
monitor for detection of cardiac arrhythmias.
What Equipment Requirements Are Necessary for Accurate ST-Segment
Monitoring?
Bedside cardiac monitors used to detect cardiac arrhythmias in real time in hospital units
are often not suitable for ST-segment monitoring, although the displayed ECG lead may
show ST abnormalities when ST-segment deviation is striking. Often distortions of the
low-frequency content of the signal due to inadequate filtering techniques and baseline
wander correction may result in distortions of the ST segment.
84,85

In addition, typically, information from only 1 to 2 ECG leads is displayed at the patients
bedside and from only 1 lead at the central monitoring station, although many systems
record information from 2 to 3 leads simultaneously. Therefore, the sensitivity for detecting
episodes of ST deviation in areas not covered by the lead(s) being monitored is decreased.
Moreover, in current ICUs selection of ECG leads typically focuses on detection of
arrhythmias, and the usual selection is lead V1 and/or lead II, neither of which is highly
sensitive for detection of ischemia.
53,54

11 of 20 4/10/2006 9:33 AM
Finally, fatigue of the person watching the monitor, partly due to the display of tracings for
multiple patients, results in underdetection of changes in the ST segment, especially when
no ST analysis software and alarm notification are available to augment human
observation.
86
In summary, ST-segment monitoring devices can only be used reliably for
detection of ischemia in the following situations: (1) filtering techniques result in an
adequate low-frequency response; (2) full 12-lead or vectorcardiographic lead capability is
available; (3) proper algorithms for detection of ischemia are integrated, including storage of
complexes and measurements for comparison in full-disclosure format and trending of the
ST deviations over time.
84
What Strategies Improve the Accuracy and Clinical Usefulness of
ST-Segment Monitoring?
Proper Application of Electrodes
Because the amplitude of clinically significant ST-segment deviations is typically as small as
1 mm, a noisy signal is a problem for accurate diagnosis. Careful preparation of the skin
that includes shaving areas where the electrodes will be placed and removing skin oils and
cutaneous debris with alcohol and abrasion is imperative and will substantially reduce false
alarms.
Consistent Placement of Leads
Marking the locations of the electrodes with indelible ink is advantageous so that electrodes
that are removed for any reason (eg, leads V
2
and V
3
are typically removed during
recording of echocardiograms) can be replaced in their original locations. ECG information
obtained from electrodes located close to the heart (ie, the precordial leads) is especially
prone to waveform changes when the electrodes are relocated as little as 1 cm away from
the original locations. Figure 4 shows ECG tracings that resulted in misdiagnosis and a
subsequent unnecessary cardiac catheterization in a patient with inconsistent lead
placement.
12 of 20 4/10/2006 9:33 AM
x
Selection of the ST-Segment Measurement Point
Many monitors offer a choice of points, such as J +60 ms or J +80 ms, for measuring the
ST segment. Most experts program monitors to measure the ST segment at the earlier J +
60 ms point because this point is less likely to coincide with the upslope of the T wave in
patients in whom sinus tachycardia develops.
Measurement of Delta ST in the Diagnosis of Transient Ischemia
A widely accepted definition of transient myocardial ischemia, developed for use with
ambulatory Holter monitoring, is ST-segment deviation of 0.1 mV or greater (1 mm with
normal standardization of 1 mV =10 mm) that lasts at least 1 minute.
87
Although the same
definition has been applied to 12-lead ST-segment monitoring, clinicians must recognize
that the 12-lead configuration has more redundancy than does the 1- to 3-lead Holter
system because electrodes are placed closer to each other (especially the 6 precordial
leads) in the 12-lead configuration.
Therefore, changes in the ST segment during an ischemic event are typically visible on
tracings from more than 1 of the 12 ECG leads, and if just 1 mm of ST change is observed
with just 1 lead, the ST episode should be considered questionable, especially in
asymptomatic patients. Although patients may have ST-segment deviation for less than 1
minute during a brief inflation of an angioplasty balloon, spontaneous ischemia typically
lasts 1 to 30 minutes. When ST-segment deviation lasts for more than 30 minutes without a
return to the baseline ST value, the probability of cell death and myocardial infarction
increases.
For diagnosis of transient myocardial ischemia, the baseline ST level must first be
13 of 20 4/10/2006 9:33 AM
established at a time when the patient is not experiencing ischemia.
47,88
In patients
without acute infarction, the baseline ST level is usually established upon initiation of
ST-segment monitoring. The baseline measurement is often not isoelectric (ie, identical to
the TP or PR segments) because patients may have chronic repolarization abnormalities
due to conditions such as left ventricular hypertrophy, digitalis therapy, or normal early
repolarization.
88
When an acute change occurs in the ST level on a tracing obtained with a particular ECG
lead, the baseline ST value for this lead should be subtracted from the new ST value to
obtain a change score or delta ST measurement. Delta ST values that are at least 1 mm
indicate an ischemic event. Thus, an ischemic event may produce a normal-looking
isoelectric ST segment in a patient whose baseline ST level is depressed due to left
ventricular hypertrophy or digitalis therapy. This situation is called pseudonormalization of
the ST segment, and if pseudonormalization is not recognized, an ischemic event may not
be detected.
Setting ST Alarm Parameters Appropriately
For research studies, the alarms for 12-lead ST-segment monitoring are often programmed
to trigger an audible alarm if 1 mm of ST-segment deviation occurs on tracings from 2 ECG
leads or 2 mm of deviation occurs on a tracing from a single lead and either deviation lasts
more than 1 minute. For bedside cardiac monitoring, the alarm thresholds should be set 1 to
2 mm above and below the patients baseline ST level (rather than the isoelectric level),
because the patients baseline level is rarely isoelectric.
88
Recognition of Good and Bad ST Alarms
Current technology for ST-segment monitoring is generally configured to detect a change in
the ST segment but does not include any interpretative function that characterizes the
change as clinically good or bad for the patient. The interpretative function is fulfilled by the
bedside healthcare professional who assesses whether the new deviation from a previous
ST value represents improvement or worsening. The ST-segment monitor simply records
the degree, extent, and timing of the ST change.
In the early stages of myocardial infarction, rapid ST-segment recovery is predictive of
patency of the infarct-related artery
.29,59,60
For example, a reduction of 50% or more in
the peak ST elevation within 1 hour of thrombolytic therapy is predictive of a patent
vessel.
59
Such rapid changes in the ST segment will trigger alarms that should be
considered good alarms. Conversely, a silent ST monitor during thrombolytic therapy
suggests no change in the ST segment, and a more aggressive approach (eg, rescue
angioplasty) may be warranted.
89
In the later stages of acute myocardial infarction, when
ST recovery is complete (ie, the ST segments have returned to baseline levels), a ST alarm
should be considered a bad alarm, signifying recurrent ischemia.
Recognition of False Alarms Due to Changes in Body Position
Until the advent of continuous 12-lead ST-segment monitoring, ECG changes related to
changes in body position were not a concern because snapshot 12-lead ECGs were
always recorded with the patient supine. However, when patients are monitored over time,
they assume multiple body positions, such as lying on their right or left side, sitting upright,
or even standing.
Echocardiographic data indicate that the heart moves closer to the chest wall when a
patient moves from the supine to the left-lying position.
90
Such a positional change often
produces greater amplitude QRS waveforms and exaggerated amplitudes in ST-segment
deviations, which can be mistaken for evidence of an ischemic event.
88,91
14 of 20 4/10/2006 9:33 AM
One way to ascertain whether a patient will have false alarms due to positional changes is
to compare changes in the ST-T wave that occur when the patient moves from supine, to
right-lying, to left-lying positions at the initiation of ST-segment monitoring. These positional
templates can be used subsequently to distinguish ST changes due to ischemia from those
due to changes in body position.
A second approach is to consider that all changes in the ST segment that occur
instantaneously over 1 to 2 cardiac cycles and that are accompanied by a change in the
QRS waveform are due to changes in body position rather than to true ischemia. When the
patients body position during an alarm condition is not clearly known (eg, the monitor
watcher at the central nursing station cannot see the patient), a 12-lead ECG should be
recorded with the patient supine to verify that observed ST changes are also present when
the patient is supine.
Confirmation of ST-Segment Monitoring Trends With 12-Lead ECG Printouts
Most computer-assisted ST monitors have graphic representations of the ST-segment trend
detected with a single lead or summated leads. Although trend information is convenient for
quickly detecting potential ischemic events, the ECG findings in question should be printed
out to confirm that the changes in the ST segment are due to ischemia rather than to a
transient arrhythmia such as an accelerated ventricular rhythm. In addition, if the ST monitor
indicates an ischemic event but ST deviation is not visually detected on the printed out
ECG, the accuracy of the ST monitor should be questioned, because the human eye is
capable of observing 1 mm of ST-segment deviation.
92
What Knowledge and Skills Should Clinicians Have for Safe and Effective
ST-Segment Monitoring of Patients in a Hospital Unit?
Ideally, each hospital unit should develop a protocol for ST-segment monitoring that is
relevant to the types of patients cared for in that unit. For example, the goals and lengths of
monitoring differ among various hospital units, such as emergency department areas for
observation of chest pain, cardiac care units, cardiac surgical ICUs, and step-down
telemetry units.
The best education for learning about ST-segment monitoring is hands-on clinical
experience, because expertise is developed over time by experiencing numerous clinical
scenarios. Accurate ST-segment monitoring requires expertise in interpreting 12-lead
ECGs, an understanding of the patients clinical situation, and knowledge of the functions
and limitations of the ST-segment monitoring system.
At a minimum, clinicians should be able to do the following:
1. accurately place and consistently maintain ECG leads;
2. identify the lead that shows peak ST elevation and recognize rapid ST recovery versus
sustained ST elevation in acute myocardial infarction;
3. recognize abrupt reocclusion during monitoring of patients after angioplasty;
4. recognize false alarms that are due to a noisy signal or to transient arrhythmia; and
5. assess a patients cardiac symptoms and hemodynamic status to determine the clinical
importance of changes in the ST segment.
What Are Priorities for Future Research and Development?
Research and Development by Manufacturers
Future cardiac monitors should incorporate analysis of the ST segment in all 12 leads plus
arrhythmia analysis. Monitors should provide full disclosure of data from all 12 leads for at
least 24 hours to ensure accurate diagnosis and documentation of transient ischemic and
arrhythmic events. Seamless ST-segment monitoring should be available from the
emergency department to the cardiac catheterization laboratory to the cardiac care unit to
the step-down telemetry unit, and the system should be portable, for use during
intrahospital transport between units. In addition, better noise-reduction strategies should be
15 of 20 4/10/2006 9:33 AM
developed to reduce the number of false alarms.
Advancing the Science for Patients With Acute Coronary Syndromes
The notion that early detection and suppression of myocardial ischemia (especially silent
ischemia) benefit patients with acute coronary syndromes by improving the poor prognosis
associated with ST-deviation episodes should be investigated in a large-scale,
well-controlled clinical trial. Such a trial should include only hard clinical end points such
as death or (re)infarction because soft end points such as urgent recatheterization or
revascularization may be affected by events observed with ST-segment monitoring.
Future research is also needed to sort out the value of leads other than the standard
12-lead set that are recorded directly or are derived from other leads. In addition, the value
of ST-segment monitoring in the prehospital phase is unknown. Finally, the clinical
importance and independent contribution of QRS and T-wave abnormalities and changes
are unclear and require further investigation.
Acknowledgments
The members of the ST-Segment Monitoring Practice Guideline International Working Group were as
follows: Mary G. Adams, RN, MS, University of California, San Francisco, Calif; Kathy J . Booker, RN, MS,
Millikin University, Decatur, Ill; Mary Caldwell, RN, PhD, University of California, San Francisco, Calif; Peter
Clemmensen, MD, DSc, the Rigshospital Copenhagen and University Hospital, Copenhagen, Denmark;
Mikael Dellborg, MD, PhD, Sahlgrenska University Hospital/stra, Gteborg, Sweden; Barbara J . Drew, RN,
PhD, chair of writing group and panel of experts, School of Nursing, University of California, San Francisco,
Calif; Denis W. Drew, MD, Alameda Hospital, Alameda, Calif; Sven V. Eriksson, MD, PhD, Danderyd
Hospital, Karolinska Institutet, Daneryd, Sweden; Marjorie Funk, RN, PhD, Yale University School of
Nursing, New Haven, Conn; W. Brian Gibler, MD, University of Cincinnati Hospital, Cincinnati, Ohio; Brigid
Ide, RN, MS, University of California, San Francisco Stanford Health Care, San Francisco, Calif; Peter
Klootwijk, MD, PhD, University Hospital Rotterdam Dijkzigt, Rotterdam, the Netherlands; Mitchell W. Krucoff,
MD, cochair, Veterans Affairs Medical Center, Durham, NC; Angela Kucia, RN, MA, The Queen Elizabeth
Hospital, Woodville, South Australia; Arthur C. Maas, MD, Duke Clinical Research Center, Durham, NC;
Anders Melcher, MD, PhD, Danderyd Hospital, Karolinska Institutet, Danderyd, Sweden; Simon Meij, MSc,
University Hospital Rotterdam Dijkzigt, Rotterdam, the Netherlands; Michele M. Pelter, RN, MS, University of
California, San Francisco, Calif; Simon Stewart, RN, PhD, Department of Public Health, Glasgow, Scotland;
Rolf F. Veldkamp, MD, PhD, University Hospital Rotterdam Dijkzigt, Rotterdam, the Netherlands; and
Shu-Fen Wung, RN, PhD, University of Illinois at Chicago, Chicago, Ill.
References
1. Simoons ML, Vos J , Tijssen J GP, et al. Long-term benefit of early thrombolytic therapy in
patients with acute myocardial infarction: 5 year follow-up of a trial conducted by the
Interuniversity Cardiology Institute of the Netherlands. J Am Coll Cardiol.
1989;14:1609-1615.
2. Klootwijk P, Cobbaert C, Fioretti P, Kint PP, Simoons ML. Noninvasive assessment of
reperfusion and reocclusion after thrombolysis in acute myocardial infarction. Am J Cardiol.
1993;72:75G-84G.
3. Gottlieb SO, Weisfeldt ML, Ouyang P, Mellits DE, Gerstenblith G. Silent ischemia as a
marker for early unfavorable outcomes in patients with unstable angina. N Engl J Med.
1986;314:1214-1219.
4. Gottlieb SO, Weisfeldt ML, Ouyang P, Mellits DE, Gerstenblith G. Silent ischemia
predicts infarction and death during 2 year follow-up of unstable angina. J Am Coll Cardiol.
1987;10:756-760.
5. Nademanee K, Intarachot V, J osephson MA, Rieders D, Mody FV, Singh BN. Prognostic
significance of silent myocardial ischemia in patients with unstable angina. J Am Coll
Cardiol. 1987;10:1-9.
6. Krucoff M. Identification of high-risk patients with silent myocardial ischemia after
percutaneous transluminal coronary angioplasty by multilead monitoring. Am J Cardiol.
1988;61:29F-34F.
7. Langer A, Freeman MR, Armstrong PW. ST segment shift in unstable angina:
pathophysiology and association with coronary anatomy and hospital outcome. J Am Coll
Cardiol. 1989;13:1495-1502.
8. Larsson H, J onasson T, Ringqvist I, Fellenius C, Wallentin L. Diagnostic and prognostic
16 of 20 4/10/2006 9:33 AM
importance of ST recording after an episode of unstable angina or non-Q-wave myocardial
infarction. Eur Heart J. 1992;13:207-212.
9. Amanullah AM, Lindvall K. Prevalence and significance of transientpredominantly
asymptomaticmyocardial ischemia on Holter monitoring in unstable angina pectoris, and
correlation with exercise test and thallium-201 myocardial perfusion imaging. Am J Cardiol.
1993;72:144-148.
10. Drew BJ , Pelter MM, Adams MG, Wung SF, Chou TM, Wolfe CL. 12-Lead ST-segment
monitoring vs single-lead maximum ST-segment monitoring for detecting ongoing ischemia
in patients with unstable coronary syndromes. Am J Crit Care. 1998;7:355-363.
11. von Arnim T, Gerbig HW, Krawietz W, Hofling B. Prognostic implications of
transientpredominantly silentischaemia in patients with unstable angina pectoris. Eur
Heart J. 1988;9:435-440.
12. J ohnson SM, Mauritson DR, Winniford MD, et al. Continuous electrocardiographic
monitoring in patients with unstable angina pectoris: identification of high-risk subgroup with
severe coronary disease, variant angina, and/or impaired early prognosis. Am Heart J.
1982;103:4-12.
13. Langer A, Singh N, Freeman MR, Tibshirani R, Armstrong PW. Detection of silent
ischemia adds to the prognostic value of coronary anatomy and left ventricular function in
predicting outcome in unstable angina patients. Can J Cardiol. 1995;11:117-122.
14. Holmvang L, Andersen K, Dellborg M, et al. Relative contributions of a single-admission
12-lead electrocardiogram and early 24-hour continuous electrocardiographic monitoring for
early risk stratification in patients with unstable coronary artery disease. Am J Cardiol.
1999;83:667-674.
15. Ouyang P, Chandra NC, Gottlieb SO. Frequency and importance of silent myocardial
ischemia identified with ambulatory electrocardiographic monitoring in the early in-hospital
period after acute myocardial infarction. Am J Cardiol. 1990;65:267-270.
16. Gottlieb SO, Gottlieb SH, Achuff SE, et al. Silent ischemia on Holter monitoring predicts
mortality in high-risk postinfarction patients. JAMA. 1988;259:1030-1035.
17. Tzivoni D, Gavish A, Zin D, et al. Prognostic significance of ischemic episodes in
patients with previous myocardial infarction. Am J Cardiol. 1988;62:661-664.
18. Langer A, Minkowitz J , Dorian P, et al for the Tissue Plasminogen Activator: Toronto
(T-PAT) Study Group. Pathophysiology and prognostic significance of Holter-detected ST
segment depression after myocardial infarction. J Am Coll Cardiol. 1992;20:1313-1317.
19. Solimene MC, Ramires J A, Gruppi CJ , et al. Prognostic significance of silent myocardial
ischemia after a first uncomplicated myocardial infarction. Int J Cardiol. 1993;38:41-47.
20. Silva P, Galli M, Campolo L. Prognostic significance of early ischemia after acute
myocardial infarction in low-risk patients. IRES (Ischemia Residua) Study Group. Am J
Cardiol. 1993;71:1142-1147.
21. Gill J B, Cairns J A, Roberts RS, et al. Prognostic importance of myocardial ischemia
detected by ambulatory monitoring early after acute myocardial infarction. N Engl J Med.
1996;334:65-70.
22. McCulley ME, Bennett RL. ST segment monitoring in the pediatric ICU: detecting
myocardial ischemia in children. Crit Care Nurse. April 1997;17:81-92.
23. DeWood MA, Spores J , Notske R, et al. Prevalence of total coronary occlusion during
the early hours of transmural myocardial infarction. N Engl J Med. 1980;303:897-902.
24. 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.
25. 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.
26. Krucoff MW, Croll MA, Pope J E, et al. Continuously updated 12-lead ST-segment
recovery analysis for myocardial infarct artery patency assessment and its correlation with
multiple simultaneous early angiographic observations. Am J Cardiol. 1993;71:145-151.
27. 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.
28. Davies GJ , Chierchia S, Maseri A. Prevention of myocardial infarction by very early
17 of 20 4/10/2006 9:33 AM
treatment with intracoronary streptokinase: some clinical observations. N Engl J Med.
1984;311:1488-1492.
29. Veldkamp RF, Green CL, Wilkins ML, et al. Comparison of continuous ST-segment
recovery analysis with methods using static electrocardiograms for noninvasive patency
assessment during acute myocardial infarction. Thrombolysis and Angioplasty in Myocardial
Infarction (TAMI) 7 Study Group. Am J Cardiol. 1994;73:1069-1074.
30. Langer A, Krucoff MW, Klootwijk P, et al. Noninvasive assessment of speed and stability
of infarct-related artery reperfusion: results of the GUSTO ST-segment monitoring study. J
Am Coll Cardiol. 1995;25:1522-1557.
31. Dellborg M, Topol EJ , Swedberg K. Dynamic QRS complex and ST-segment
vectorcardiographic monitoring can identify vessel patency in patients with acute myocardial
infarction treated with reperfusion therapy. Am Heart J. 1991;122:943-948.
32. Santoro GM, Valenti R, Buonamici P, et al. Relation between ST-segment changes and
myocardial perfusion evaluated by myocardial contrast echocardiography in patients with
acute myocardial infarction treated with direct angioplasty. Am J Cardiol. 1998;82:932-937.
33. Gomez M, Anderson J L, Karagounis LA, Mulhestein J B, Mooers FB. An emergency
department-based protocol for rapidly ruling out myocardial ischemia reduces hospital time
and expense: results of a randomized study (ROMIO). J Am Coll Cardiol. 1996;28:25-33.
34. DeLeon AC, Farmer CA, King G, Manternach J , Ritter D. Chest pain evaluation unit: a
cost-effective approach for ruling out acute myocardial infarction. South Med J.
1989;82:1083-1089.
35. Gaspov J M, Lee TH, Cook EF, Weisberg MC, Goldman L. Outcome of rule-out
myocardial infarction patients admitted to a new short stay unit. Am J Cardiol.
1991;68:145-149.
36. Gibler WB, Walsh RA, Levy RC, Runyon J P. Rapid diagnostic and treatment center for
patients with chest pain in the emergency department. Ann Emerg Med. 1995;25:1-8.
37. Klootwijk P, Hamm C. Acute Coronary Syndromes: Diagnosis. Lancet. 1999;353, Suppl
II:10-15
38. Krucoff MW, Parente AR, Bottner RK, et al. Stability of multilead ST-segment
fingerprints over time after percutaneous transluminal coronary angioplasty and its
usefulness in detecting reocclusion. Am J Cardiol. 1988;61:1232-1237.
39. Detre K, Holubkov R, Kelsey S, et al. One-year follow-up results of the 1985-1986
National Heart, Lung, and Blood Institutes Percutaneous Transluminal Coronary
Angioplasty Registry. Circulation. 1989;80:421-428.
40. J eremias A, Kutscher S, Haude M, et al. Nonischemic chest pain induced by coronary
interventions: a prospective study comparing coronary angioplasty and stent implantation.
Circulation. 1998;98:2656-2658.
41. Tomai J , Crea F, Gaspardone A, et al. Mechanisms of cardiac pain during coronary
angioplasty. J Am Coll Cardiol. 1993;22:1892-1896.
42. Mangano DT, Browner WS, Hollenberg M, London MJ , Tubau J F, Tateo IM. Association
of perioperative myocardial ischemia with cardiac morbidity and mortality in men undergoing
noncardiac surgery. The Study of Perioperative Ischemia Research Group. N Engl J Med.
1990;323:1781-1788.
43. Mangano DT, Hollenberg M, Fegert G, et al. Perioperative myocardial ischemia in
patients undergoing noncardiac surgery, I: incidence and severity during the four-day
perioperative period. The Study of Perioperative Ischemia (SPI) Research Group. J Am Coll
Cardiol. 1991;17:843-850.
44. Mangano DT, Wong MG, London MJ , Tubau J F, Rapp J A. Perioperative myocardial
ischemia in patients undergoing noncardiac surgery, II: incidence and severity during the
first week following surgery. The Study of Perioperative Ischemia (SPI) Research Group. J
Am Coll Cardiol. 1991;17:851-857.
45. Hollenberg M, Mangano DT, Browner WS, London MJ , Tubau J F, Tateo IM. Predictors
of postoperative myocardial ischemia in patients undergoing noncardiac surgery. The Study
of Perioperative Ischemia Research Group. JAMA. 1992;268:205-209.
46. Krucoff MW, Sawchak ST, Pope J E, Veldkamp RF. Rethinking classical ECG patterns
of ischemia and infarction: insights from investigations with continuous ECG monitoring.
Newspaper Cardiol. December 1992:8-17.
47. Klootwijk P, Meij S, von Es GA, et al. Comparison of usefulness of computer assisted
18 of 20 4/10/2006 9:33 AM
continuous 48-h 3-lead with 12-lead ECG ischaemia monitoring for detection and
quantitation of ischaemia in patients with unstable angina. Eur Heart J. 1997;18:931-940.
48. Krucoff MW, J ackson YR, Stark KS, Kent KM. Electrocardiographic patterns of
impending coronary closure independent of unstable anginal symptoms. In: von Arnim Th,
Maseri A, eds. Predisposing Condition for Acute Ischemic Syndromes. Darmstadt,
Germany: Steinkopff Verlag; 1989:96-106.
49. Veldkamp RF, Pope J E, Wilderman NM, Trollinger KM, et al. ST segment deviation on
the 12-lead electrocardiogram during acute myocardial infarction: Optimal leads for
continuous ST segment monitoring. In: Veldkamp RF. Continuous Digital 12-Lead ST
Segment Monitoring in Acute Myocardial Infarction [doctoral thesis]. Delft, The Netherlands:
Eburon; 1995: 54-66.
50. Krucoff MW. Poor performance of lead V5 in single- and dual-channel ST-segment
monitoring during coronary occlusion. J Electrocardiol. 1988;21(suppl):S30-S34.
51. Aldrich HR, Hindman NB, Hinohara T, et al. Identification of the optimal
electrocardiographic leads for detecting acute epicardial injury in acute myocardial
infarction. Am J Cardiol. 1987;59:20-23.
52. Bush HS, Ferguson J J , Angelini P, Willerson J T. Twelve-lead electrocardiographic
evaluation of ischemia during percutaneous transluminal coronary angioplasty and its
correlation with acute reocclusion. Am Heart J. 1991;121:1591-1599.
53. Drew BJ , Tisdale LA. ST-segment monitoring for coronary artery reocclusion following
thrombolytic therapy and coronary angioplasty: identification of optimal bedside monitoring
leads. Am J Crit Care. 1993;2:280-292.
54. Drew BJ , Ide B, Sparacino PSA. Accuracy of bedside electrocardiographic monitoring: a
report on current practices of critical care nurses. Heart Lung. 1991;20:597-609.
55. Quyyumi AA, Crake T, Mockus LJ , Wright CA, Frickards A, Fox KM. Value of the bipolar
lead CM5 in electrocardiography. Br Heart J. 1986;56:372-376.
56. Krucoff MW, Wagner NB, Pope J E, et al. The portable programmable
microprocessor-driven real-time 12-lead electrocardiographic monitor: a preliminary report
of a new device for the noninvasive detection of successful reperfusion or silent coronary
reocclusion. Am J Cardiol. 1990;65:143-148.
57. Krucoff MW, Green CE, Satler LF, et al. Noninvasive detection of coronary artery
patency using continuous ST-segment monitoring. Am J Cardiol. 1986;57:916-922.
58. Krucoff MW, Pope J E, Bottner RK, Renzi RH, Wagner GS, Kent KM. Computer-assisted
ST-segment monitoring: experience during and after brief coronary occlusion. J
Electrocardiol. 1987;20(suppl):15-21.
59. Fernandez AR, Sequeira RF, Chakko S, et al. ST-segment tracking for rapid
determination of patency of the infarct-related artery in acute myocardial infarction. J Am
Coll Cardiol. 1995;26:675-683.
60. Klootwijk P, Langer A, Meij S, et al. Non-invasive prediction of reperfusion and coronary
artery patency by continuous ST segment monitoring in the GUSTO-I trial. Eur Heart J.
1996;17:689-698.
61. Mason RE, Likar I. A new system of multiple-lead exercise electrocardiography. Am
Heart J. 1966;71:196-204.
62. Macfarlane PW. Lead systems. In: Macfarlane PW, Lawrie TDV, eds. Comprehensive
Electrocardiology. New York, NY: Pergamon Press Inc; 1989:315-352.
63. Gamble P, McManu H, J ensen D, Froelicher V. A comparison of the standard 12-lead
electrocardiogram to exercise electrode placements. Chest. 1984;85:616-622.
64. Rautaharju PM, Prineas RJ , Crow RS, Seale D, Furberg C. The effect of modified limb
electrode positions on electrocardiographic wave amplitudes. J Electrocardiol.
1980;13:109-113.
65. Papouchado M, Walker PR, J ames MA, Clarke LM. Fundamental differences between
the standard 12-lead electrocardiograph and the modified (Mason-Likar) exercise lead
system. Eur Heart J. 1987;8:725-733.
66. Sevilla DC, Dohrmann ML, Somelofski CA, Wawrzynski RP, Wagner NB, Wagner GS.
Invalidation of the resting electrocardiogram obtained via exercise electrode sites as a
standard 12-lead recording. Am J Cardiol. 1989;63:35-39.
67. Pahlm O, Haisty WK, Edenbrandt L, et al. Evaluation of changes in standard
electrocardiographic QRS waveforms recorded from activity-compatible proximal limb lead
19 of 20 4/10/2006 9:33 AM
positions. Am J Cardiol. 1992;69:253-257.
68. Frank E. An accurate, clinically practical system for spatial vectorcardiography.
Circulation. 1956;13:737-749.
69. Dower GE, Machado HB, Osborne J A. On deriving the electrocardiogram from
vectorcardiographic leads. Clin Cardiol. 1980;3:87-95.
70. Pipberger HV, Bialek SM, Perloff J K, Schnaper HW. Correlation of clinical information in
the standard 12-lead ECG and in a corrected orthogonal 3-lead ECG. Am Heart J.
1961;61:34-43.
71. Dellborg M, Riha M, Swedberg K. Dynamic QRS and ST segment changes in
myocardial infarction monitored by continuous on-line vectorcardiography. J Electrocardiol.
1991;23(suppl):1-9.
72. Lundin P, Eriksson SV, Erhardt L, Strandberg LE, Rehnqvist N. Continuous
vectorcardiography in patients with chest pain indicative of acute ischemic heart disease.
Cardiology. 1992;81:145-156.
73. J ensen SM, J ohansson G, Osterman G, Reiz S, Nslund U. On-line computerized
vectorcardiography monitoring of myocardial ischemia during coronary angioplasty:
comparison with 12-lead electrocardiography. Coron Artery Dis. 1994;5:507-514.
74. Lundin P, Eriksson SV, Strandberg LE, Rehnqvist N. Prognostic informa tion from
on-line vectorcardiography in acute myocardial infarction. Am J Cardiol.
1994;74:1103-1108.
75. Lundin P, Eriksson SV, Fredrikson M, Rehnqvist N. Prognostic information from on-line
vectorcardiography in unstable angina pectoris. Cardiology. 1995;86:60-66.
76. Dellborg M, Steg PG, Simoons M, et al. Vectorcardiographic monitoring to assess early
vessel patency after reperfusion therapy for acute myocardial infarction. Eur Heart J.
1995;16:21-29.
77. Klootwijk P, Meij S, Melkert R, Lenderink T, Simoons ML. Reduction of recurrent
ischemia with abciximab during continuous ECG-ischemia monitoring in patients with
unstable angina refractory to standard treatment (CAPTURE). Circulation.
1998;98:1358-1364.
78. Dower GE, Yakush A, Nazzal SB, J utzy RV, Ruiz CE. Deriving the 12-lead
electrocardiogram from four (EASI) electrodes. J Electrocardiol. 1988;21(suppl):S182-S187.
79. Drew BJ , Scheinman MM, Evans GT. Comparison of a vectorcardiographically derived
12-lead electrocardiogram with the conventional electrocardiogram during wide QRS
complex tachycardia and its potential application for continuous bedside monitoring. Am J
Cardiol. 1992;69:612-618.
80. Denes P. The importance of derived 12-lead electrocardiography in the interpretation of
arrhythmias detected by Holter recording. Am Heart J. 1992;124:905-911.
81. Drew BJ , Adams MG, Pelter MM, Wung SF. ST-segment monitoring with a derived
12-lead electrocardiogram is superior to routine CCU monitoring. Am J Crit Care.
1996;5:198-206.
82. Drew BJ , Adams MG, Pelter MM, Wung SF, Caldwell MA. Comparison of standard and
derived 12-lead electrocardiograms for diagnosis of coronary angioplasty-induced
myocardial ischemia. Am J Cardiol. 1997;79:639-644.
83. Drew BJ , Pelter MM, Wung SF, et al. Accuracy of the EASI 12-lead electrocardiogram
compared to the standard 12-lead electrocardiogram for diagnosing multiple cardiac
abnormalities. J Electrocardiol. In press.
84. Veldkamp RF. Chapter 10, Discussion. In: Continuous Digital 12-Lead ST Segment
Monitoring in Acute Myocardial Infarction [doctoral thesis]. Delft, The Netherlands: Eburon;
1995: 92-128.
85. Mirvis DM, Berson AS, Goldberger AL, et al. Instrumentation and practice standards for
electrocardiographic monitoring in special care units: a report for health professionals by a
task force of the Council on Clinical Cardiology, American Heart Association. Circulation.
1989;79:464-471.
86. Biagini A, LAbbate A, Testa R, et al. Unreliability of conventional visual
electrocardiographic monitoring for detection of transient ST segment changes in a
coronary care unit. Eur Heart J. 1984;5:784-791.
87. Pepine C, Singh B, Gibson R, Kent K. Report of Group IV: management options. In:
Cohn PF, Kannel WB, eds. Recognition, Pathogenesis, and Management Options in Silent
20 of 20 4/10/2006 9:33 AM
Coronary Artery Disease. Circulation Monograph No. 2. 1987;75(3):II52-II53.
88. Drew BJ , Wung SF, Adams MG, Pelter MM. Bedside diagnosis of myocardial ischemia
with ST-segment monitoring technology: measurement issues for real-time clinical decision
making and trial designs. J Electrocardiol. 1998;30(suppl):174-182.
89. Schrder R, Dissmann R, Brggemann T, et al. Extent of early ST-segment elevation
resolution: a simple but strong predictor of outcome in patients with acute myocardial
infarction. J Am Coll Cardiol. 1994;
24:384-391.
90. Feldman T, Borow K, Neumann A, Lang RM, Childers RW. Relation of
electrocardiographic R wave amplitude to changes in left ventricular chamber size and
position in normal subjects. Am J Cardiol. 1985;55:1168-1174.
91. Adams MG, Drew BJ . Body position effects on the ECG. J Electrocardiol.
1997;30:285-291.
92. Pelter MM, Adams MG, Drew BJ . Computer versus manual measurement of
ST-segment deviation. J Electrocardiol. 1997;30:151-156.
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ECG Monitoring - ST Segment Monitoring - AJCC 1999

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CONSENSUS STATEMENT FOR PRACTICE http://www.aacn.org/AACN/jrnlajcc.nsf/GetArticle/ArticleFour86?Ope...

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