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From the Oklahoma State University College of Osteopathic Medicine (Dr. Daniel), Tulsa, OK; and the Department of Emergency Medicine (Drs. Courtney and Kline), Carolinas Medical Center, Charlotte, NC.
Dr. Daniel is currently at the Bowman-Gray School of Medicine, Dept
of Internal Medicine, Wake Forest University, Winston-Salem, NC.
Correspondence to: Jeffrey Kline, MD, Assistant Director of Research, Department of Emergency Medicine, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232; e-mail: Jkline{at}carolinas.org
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Abstract |
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 TOP Abstract IntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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Methods: A 21-point ECG scoring system was derived (relative weights in parentheses): sinus tachycardia (2), incomplete right bundle branch block (2), complete right bundle branch block (3), T-wave inversion in leads V1 through V4 (0 to 12), S wave in lead I (0), Q wave in lead III (1), inverted T in lead III (1), and entire S1Q3T3 complex (2). ECGs obtained within 48 h prior to pulmonary arteriography were located for 60 patients (26 positive for PE, 34 negative for PE) and for 25 patients with fatal PE.
Results: Interobserver agreement (11 readers) for ECG score was good (Spearman r = 0.74). The ECG score showed significant positive relationship to systolic pulmonary arterial pressure (sPAP) in patients with PE (r = 0.387, p < 0.001), whereas no significant relationship was seen in patients without PE (r = - 0.08, p = 0.122). When patients were grouped by severity of pulmonary hypertension (low, moderate, severe), only patients with severe pulmonary hypertension from PE had a significantly higher ECG score (mean, 5.8 ± 4.9). At a cutoff of 10 points, the ECG score was 23.5% (95% confidence interval [CI], 16 to 31%) sensitive and 97.7% (95% CI, 96 to 99%) specific for the recognition of severe pulmonary hypertension (sPAP > 50 mm Hg) secondary to PE. In 25 patients with fatal PE, the ECG score was 9.5 ± 5.2.
Conclusions: The derived ECG score
increases with severity of pulmonary hypertension from PE, and a score
10 is highly suggestive of severe pulmonary hypertension from
PE.
Key Words: clinical • decision making • decision support systems • ECG • heart arrest • pulmonary embolism • pulmonary heart disease
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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The purpose of the present report was to develop a structured ECG score based on ECG criteria that have previously been associated with RV strain from PE, and to test this scoring system with multiple emergency physicians using ECGs from patients who underwent pulmonary angiography, or who died from acute PE. We sought to test two hypotheses: (1) that a structured ECG score would vary positively with the pulmonary arterial pressure in patients with PE, and (2) that a structured ECG score obtained from patients with severe pulmonary arterial hypertension induced by PE would be higher than patients without pulmonary hypertension, and higher than patients without PE.
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Materials and Methods |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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The study aim was to devise a scoring system that could be completed by primary-care physicians with reasonable accuracy within 2 min. A pilot study was therefore performed with three emergency physicians who interpreted 11 ECGs from patients with PE to examine for speed and accuracy in interpreting these criteria. Based on this pilot study, the ECG criteria were narrowed to four abnormalities (Fig 1 ). We eliminated several findings commonly associated with PE because the physicians all had difficulty interpreting the criteria, including P-pulmonale, and right-axis or left-axis deviation. ECGs were copied without the computer interpretation for the reader to see. The relative contribution of the four abnormalities to the overall score is shown in parentheses: sinus tachycardia (2); incomplete right bundle branch block (2); complete right bundle branch block (3); T-wave inversion, graded by magnitude (V1 [0 to 2], V2 [1 to 3], V3 [1 to 3], V1 through V4 all inverted > 2 mm [4]); and components of the S1Q3T3 complex (S wave in lead I [0], Q wave in lead III [1], inverted T wave in lead III [1], and the entire S1Q3T3 complex [2]). The maximum score was 21 points. The relative weight of each criterion was set on the basis of the expected importance of each abnormality in the distinction of patients with massive PE from patients with submassive PE or no PE.1 4
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/
) scan was
performed within 1 week prior to death, and the final interpretation
was high probability for PE, and a formal echocardiographic study was
also performed which demonstrated evidence of RV strain (enlarged right
ventricle, abnormal septal motion, moderate or severe tricuspid
regurgitation, or RV hypokinesis). An ECG had to be obtained after the
initial symptoms and signs of PE. If multiple ECGs were obtained prior
to death, two ECGs were copied: the one most proximate to the time of
symptom onset (eg, the ECG obtained in the emergency
department [ED]), and the last ECG obtained prior to death. Clinical data were abstracted from the chart, the ECGs were each given an identifier numeral, and clinical data from each subject were entered into a database (Excel 97; Microsoft; Seattle, WA). The ECG for each case was labeled with the identifier numeral, and ECG tracings were distributed to the ECG readers with a reading sheet (Fig 1) attached to each ECG.
Eleven physicians were selected to serve as ECG readers. These individuals were chosen to represent a diverse spectrum of primary-care emergency medicine practitioners from two academic emergency medicine residencies, including seven attending emergency physicians with an average of 6 years of postresidency experience and four postgraduate year 3 emergency medicine residents. The readers were given instructions to complete the reading of all 60 cases within 90 min. A written cover letter instructed the readers that "each ECG comes from a patient in whom you suspect pulmonary embolism." The readers were blinded to all other clinical data, including the diagnosis of each subject. A scoring sheet was completed for each ECG. Score sheets had a check box for each criterion, but did not include the relative values of the ECG findings. Data from each score sheet were entered into the computer spreadsheet for calculation of the ECG scores and for statistical analysis. ECG scores were computed using the derived scoring system as detailed above; no adjustment was made to the scoring system after the data from readers were obtained.
Statistical Analysis
The specific aim was to test if the ECG score would increase in
proportion to the pulmonary artery pressure in patients with PE.
Because the ECG scores in group A were not normally distributed,
(Kolmogorov-Smirnov distance, 0.183; p < 0.001; SigmaStat v2.0;
Jandel Scientific; San Rafael, CA), data were compared with
nonparametric statistical tests. Accordingly, a Spearman rank
correlation coefficient, r, is reported for the regression
plot of ECG score as a function of pulmonary arterial pressure.
Interobserver agreement was also examined using r values.
Cases were classified into three classes of severity based on the
systolic pulmonary arterial pressure (sPAP): low, 0 to 30 mm Hg;
moderate, 31 to 49 mm Hg; and severe, 50 mm Hg. ECG scores between
PE-negative and PE-positive categories were compared using Mann-Whitney
rank sum test or analysis of variance on ranks with Dunn’s post
hoc comparison when more than two groups were compared;
p < 0.05 was considered significant. Area under the curve for the
receiver operating characteristic (ROC) was calculated by the
trapezoidal rule, and SEM was calculated using the method of Hanley and
McNeil.10
For standard diagnostic indexes, 95% confidence
intervals (CIs) were calculated using the Confidence Interval Analysis
program.11
The ECG scores from group B were found to be
normally distributed; therefore, a paired t test was used to
compare the first ECG score to the last ECG score obtained prior to
death.
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Results |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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/ scan performed prior to the pulmonary
angiography. Prior / scans were read as low probability
for PE in 10 patients, intermediate probability in 38 patients,
indeterminate probability in 7 patients, and high probability in 3
patients. The mean ± SD time after symptom onset to the time
of the ECG used for scoring was 27.5 ± 48 h. Six patients had
symptoms that began > 1 week prior to the first ECG, but complained
of worsening symptoms within the previous 72 h. Pulmonary
angiogram findings were read as positive for PE in 26 patients and
negative for PE in 34 patients (probability of PE, 43.3%; 95% CI, 30
to 57%). In the 26 patients with PE, prior / scan
findings were read as low probability in 4 patients, moderate
probability in 12 patients, indeterminate probability in 5 patients,
and high probability in 3 patients. Two of the 26 patients with PE
underwent no / scanning prior to pulmonary angiography.
Subjects with PE did not differ from subjects without PE in age (mean,
56.9 ± 17.2 years) or in the frequency of preexisting
cardiopulmonary disease. No patient with PE had a documented history of
myocardial infarction, whereas one patient without PE had a history of
myocardial infarction. Three patients with PE had a history of COPD,
and four patients without PE had a history of COPD. Average sPAP for
subjects with PE was 46 ± 17 mm Hg vs 42 ± 16 mm Hg for subjects
without PE (p < 0.05, unpaired t test).
For group B, 25 patients (14 female patients) were found to meet
inclusion criteria (all from Carolinas Medical Center). The initial
symptoms and signs of PE included one or more of syncope or seizure,
dyspnea, hypoxemia, tachypnea, tachycardia, or overt cardiogenic shock.
Documentation indicated strong antemortem suspicion or diagnosis of PE
in 24 of 25 cases. Eighteen patients had massive bilateral PE
demonstrated on autopsy, 4 patients had massive bilateral pulmonary
arterial obstruction found on pulmonary angiography, and 3 patients had
high-probability / scan finding plus echocardiographic
evidence of RV dysfunction prior to death. The mean age in group B was
63.4 ± 18.4 years. Paired ECGs (one at the time of initial symptoms,
and the last ECG recorded prior to death) were available for 18
patients in group B. The mean time after symptom onset to the first ECG
was 9.1 ± 12.7 h. The mean time interval between these 18 ECGs was
49 ± 61 h (median, 26.6 h; range, 2 to 192 h). The mean
time interval between the last ECG obtained and death was
41.7 ± 58.6 h (median, 15.5 h; range, 45 min to 240 h).
Sixteen patients in group B initially presented with symptoms of PE to
the ED that raised enough suspicion to warrant testing for PE. Thirteen
of the 16 ED patients died within 24 h of presentation to the ED,
4 of whom experienced cardiac arrest while being transferred to have a
/ scan performed.
The ECG scores were first examined for the degree of interobserver variability among the 11 readers. In group A, 11 readers produced 60 scores, for a total of 660 scores. The mean of all 660 scores was 3.6 ± 3.4 (median score, 3; first to third interquartile range, 0 to 5). Assessment of interrater reliability was determined for all 11 readers by calculating r values for all possible reader pairs (55 unique r-value calculations). With this comparison, r values calculated for all possible pairs of observers ranged from 0.55 to 0.89 with an average r of 0.74 for all 11 observers, indicating good overall agreement.12 Table 1 shows that only two components of the ECG score were found with a significantly higher frequency in patients with PE and that no ECG component was markedly more frequent in patients with PE compared to patients without PE.
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/ scan readings: for the
six patients with normal pulmonary angiogram findings, the ECG score
was 2.7 ± 1.6 and the sPAP was 33.4 ± 9.7 mm Hg; for the four
patients with positive pulmonary angiogram findings, the ECG score was
4.4 ± 4.1 and the sPAP was 34.2 ± 12.8 mm Hg.
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50 mm Hg. Patients without PE were distributed as
follows: low (n = 13), moderate (n = 16), and severe (n = 5).
Patients with PE were distributed as follows: low (n = 7), moderate
(n = 7), and severe (n = 12). The mean ECG score of the 12 patients
with PE and severe pulmonary hypertension was 5.8 ± 4.9, which was
significantly higher than the mean ECG score (3.1 ± 2.3;
p < 0.001) from the other 48 patients. Among patients without PE,
Figure 3
, top, shows that the ECG score did not show a stepwise
increase with the severity of systolic pulmonary hypertension. In
contrast, among patients with PE, the ECG score did significantly
increase in relation to the severity of pulmonary hypertension in
subjects with PE. Figure 3
, bottom, shows that the ECG score
increased in a statistically significant stepwise fashion.
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10.
All 13 patients died within 24 h of obtaining the ECG tracing. The
most frequently observed changes between the first and second ECG were
the development of an incomplete or complete right bundle branch block
(n = 8), the progression of a partial
S1Q3T3
pattern to its complete form (n = 6), and the progression of an
incomplete right bundle branch block to complete right bundle branch
block (n = 3). Eight of 18 patients developed new anterior T-wave
inversion in more than one precordial lead. Three patients developed
preterminal bradycardia on ECG and therefore lost the points that had
been contributed by the previous presence of tachycardia. |
Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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10 points, the ECG scoring system was
highly specific for the detection of PE with severe pulmonary
hypertension, and the ECG score was 10 points in 52% of patients
with fatal PE. These data support the hypothesis that pulmonary hypertension induced by acute PE causes a set of pathophysiologic processes that alter the surface ECG in a specific pattern, which can be reasonably well modeled by an explicit ECG score. First, the regression data indicate that the ECG scoring system increases significantly in relation to the pulmonary arterial pressure in patients with PE, whereas no positive relationship was observed in patients without PE. Second, when patients were grouped according to severity of pulmonary hypertension, a clearly positive relationship was observed between the ECG score and the severity of pulmonary hypertension for patients with PE, but this finding was not evident in patients without PE. These observations suggest that when RV pressure is elevated by acute severe PE, that right-sided cardiac conduction and repolarization are affected to a greater degree than when RV pressures are chronically elevated. The present data do not allow a mechanistic explanation for this observation, but previous animal models have shown that experimental acute pulmonary hypertension can produce RV subendocardial ischemia.16 The present study included five subjects without PE who had severe elevation of pulmonary arterial pressures all secondary to chronic diseases: three patients with severe COPD, one patient with primary pulmonary hypertension, and one patient with obesity-hypoventilation syndrome. Patients with suspected chronic PE were excluded in the present study. As a point of speculation, it is possible that patients who were categorized as having severe PE were the only patients in group A who experienced rapid and severe enough increase in right-sided pressures to produce RV subendocardial ischemia.
The data also support the hypothesis that the ECG score can assist the
clinician in the rapid recognition of severe pulmonary hypertension
from PE. Toward this goal, this study primarily assessed the
performance and reproducibility of a structured ECG score, rather than
the frequency or importance of certain findings of PE on ECG. At the
central hospital for this study (Carolinas Medical Center), most fatal
PE cases were initially suspected or diagnosed by emergency physicians,
and most of these patients died rapidly. As such, emergency physicians
can play a pivotal role in the management of massive PE, especially if
they can rapidly and accurately recognize the presence of cardiac
stress from severe PE. We reasoned that if the ECG has any value in
this process, then it was more important to show that a group of
emergency physicians would all interpret ECGs in a similar way, rather
than have a specialist interpret the tracing and enumerate the specific
abnormalities. This study design therefore helps to show that a
competent primary-care provider can accurately use the derived ECG
score. In particular, an ECG score 10 was 97.7% specific and
23.5% sensitive for the presence of severe pulmonary hypertension
caused by a PE. These diagnostic indexes were derived from group A,
which had a pretest probability of PE (43%) that could be considered
typical of outpatients with / scan findings that are read
as nondiagnostic for PE (either low or intermediate probability), but
who elicit a high enough clinical suspicion to warrant pulmonary
angiography.17
Thus, a high ECG score could be
particularly useful in the ED patient in whom PE is suspected, but when
imaging procedures are either unavailable, or noninvasive imaging study
results are inconclusive. A high ECG score used together with clinical
probability assessment for PE based on other criteria18
could help drive the decision to pursue more invasive testing for PE.
The data from group B also show that the ECG scores were high in
patients with fatal PE, and that the ECG score increased as the
severity of cardiac stress intensified before cardiac arrest. In these
18 patients, the dominant ECG manifestation of impending cardiac
failure was the development of a new incomplete or complete right
bundle branch block, or the development of new anterior T-wave
inversion. These findings point out the potential importance of using
serial ECGs, together with other clinical criteria, to alter the
clinical probability of massive PE. In group B, four ED patients—all
with ECG scores 10—suffered cardiac arrest while waiting for
pulmonary vascular imaging. In all cases, physicians had already
documented a high suspicion for PE; in all four patients, heparin
infusion was the only treatment.
This study has several limitations. First, readers were not tested
prospectively to determine the accuracy of the ECG score when it is
assessed in the clinical setting. We are currently performing a
prospective study to determine the ability of a high ECG score to
predict two findings: (1) the presence of RV dysfunction on
echocardiography in patients with PE diagnosed by either
/ scan or contrast-enhanced spiral CT scan, and (2) the
frequency of PE proven by pulmonary angiography in patients with a
nondiagnostic / scan or a finding on contrast-enhanced
spiral CT that is negative for PE. This prospective phase will also
better define the best cutoff point for the ECG score, and clarify if
specific criteria should be given more or less weight in the scoring
system. Post hoc analysis of the present data suggests that
the incomplete right bundle branch block should have been given more
weight, and that isolated T-wave inversion in V1
should have been given less weight, given that the latter finding is
often a normal variant. Nevertheless, when the ECG scoring system was
adjusted in various ways post hoc, the area under the ROC
curve did not increase. Another limitation to the study is that the
subgroup without PE who had severe pulmonary hypertension was small,
and no patient had a process which would have been likely to produce a
rapid increase in pulmonary arterial pressure (eg, ARDS, air embolism,
or fat embolism syndrome). It remains possible that when the ECG
scoring system is evaluated in more subjects with severe pulmonary
hypertension, but without PE, the specificity of the ECG scoring system
may decrease.
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Conclusion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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Footnotes |
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/ = ventilation/perfusion Received for publication October 13, 2000. Accepted for publication February 1, 2001.
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References |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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This article has been cited by other articles:
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  G. Ginsburg, N. Sunder, and P. G. Harrell Acute right bundle branch block as a presenting sign of acute pulmonary embolism. Anesth. Analg., September 1, 2006; 103(3): 789 - 791. [Full Text] [PDF]
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 A. Geibel, M. Zehender, W. Kasper, M. Olschewski, C. Klima, and S. V. Konstantinides Prognostic value of the ECG on admission in patients with acute major pulmonary embolism Eur. Respir. J., May 1, 2005; 25(5): 843 - 848. [Abstract] [Full Text] [PDF]
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 U. J. Schoepf, S. Z. Goldhaber, and P. Costello Spiral Computed Tomography for Acute Pulmonary Embolism Circulation, May 11, 2004; 109(18): 2160 - 2167. [Abstract] [Full Text] [PDF]
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 S. Iles, C. J. L. Heron, G. Davies, J. G. Turner, and L. E. L. Beckert ECG Score Predicts Those With the Greatest Percentage of Perfusion Defects Due to Acute Pulmonary Thromboembolic Disease Chest, May 1, 2004; 125(5): 1651 - 1656. [Abstract] [Full Text] [PDF]
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 N. Kucher, N. Walpoth, K. Wustmann, M. Noveanu, and M. Gertsch QR in V1 - an ECG sign associated with right ventricular strain and adverse clinical outcome in pulmonary embolism Eur. Heart J., June 2, 2003; 24(12): 1113 - 1119. [Abstract] [Full Text] [PDF]
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S. Z. Goldhaber Cardiac Biomarkers in Pulmonary Embolism Chest, June 1, 2003; 123(6): 1782 - 1784. [Full Text] [PDF]
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 British Thoracic Society guidelines for the management of suspected acute pulmonary embolism Thorax, June 1, 2003; 58(6): 470 - 483. [Full Text] [PDF]
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 S M Athar, B S P Chin, and E J Flint Transient disappearance of left bundle branch block pattern: an unusual ECG presentation of acute pulmonary embolism Postgrad. Med. J., September 1, 2002; 78(923): 555 - 558. [Abstract] [Full Text] [PDF]
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