Journal of Cardiovascular Nursing

Vol. 31, No. 3, pp 267Y273 x Copyright B 2016 Wolters Kluwer Health, Inc. All rights reserved.

Relationship Between Physiological

Parameters and Acute Coronary Syndrome in
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Patients Presenting to the Emergency

Department With Undifferentiated Chest Pain
Jaimi H. Greenslade, BPsych (Hons), PhD; Daniel Beamish, BSc (Hons);
William Parsonage, DM, MRCP, FRACP; Tracey Hawkins, BNursing, GradDip Emerg Nursing;
Jessica Schluter, BNursing, PhD; Emily Dalton, BSc, BNursing;
Kate Parker, BNursing, BHltSc(Psych); Martin Than, MBBS;
Christopher Hammett, MB ChB, FRACP; Arvin Lamanna, MBBS, FRACP; Louise Cullen, MBBS

Objective: The investigators of this study sought to examine whether abnormal physiological parameters are
associated with increased risk for acute coronary syndrome (ACS) in patients presenting to the emergency
department (ED) with chest pain. Methods: We used prospectively collected data on adult patients presenting
with suspected ACS in 2 EDs in Australia and New Zealand. Trained research nurses collected physiological data
including temperature, respiratory rate, heart rate, and systolic blood pressure (SBP) on presentation to the ED.
The primary endpoint was ACS within 30 days of presentation, as adjudicated by cardiologists using standardized
guidelines. The prognostic utility of physiological parameters for ACS was examined using risk ratios.
Louise Cullen, MBBS
Emergency Physician, Department of Emergency Medicine, Royal
Jaimi H. Greenslade, BPsych (Hons), PhD Brisbane and Women’s Hospital; School of Medicine, University of
Research Fellow, Department of Emergency Medicine, Royal Brisbane and Queensland; and School of Public Health, Queensland University of
Women’s Hospital; School of Medicine, University of Queensland; and Technology, Brisbane, Queensland, Australia.
School of Public Health, Queensland University of Technology, Brisbane,
Queensland, Australia. All authors contributed significantly to the research. JHG, DB, LC, WP, and MT
contributed to study design. DB, ED, TH, JS, KP, and AL were responsible
Daniel Beamish, BSc (Hons) for data collection. JHG and LC analyzed and interpreted the data. JHG and
Research Assistant, School of Medicine, University of Queensland,
LC wrote the report, and all authors made critical intellectual contribution.
Brisbane, Queensland, Australia.
All authors have read and approved the manuscript.
William Parsonage, DM, MRCP, FRACP This study was funded by the Queensland Emergency Medicine
Cardiologist, Department of Cardiology, Royal Brisbane and Women’s Research Foundation (QEMRF).
Hospital; School of Medicine, University of Queensland; and School
Jaimi H. Greenslade is a coinvestigator on research grants from Roche
of Public Health, Queensland University of Technology, Brisbane,
and Siemens. William Parsonage received research grants from Genzyme
Queensland, Australia.
Corp and Inverness Medical as well as consultancy fees from Abbott,
Tracey Hawkins, BNursing, GradDip Emerg Nursing AstraZeneca, and Hospira; is a coinvestigator on research grants from
Research Nurse, Department of Emergency Medicine, Royal Brisbane Roche Diagnostics and Siemens; and received support to attend
and Women’s Hospital, Brisbane, Queensland, Australia. meetings/conferences from Abbott, Sanofi-Aventis, and AstraZeneca.
Jessica Schluter, BNursing, PhD Martin Than received funds from Alere, Beckman Coulter, Roche, and
Research Nurse, Department of Emergency Medicine, Royal Brisbane Abbott for research support, speaking, and travel reimbursement.
and Women’s Hospital, Brisbane, Queensland, Australia. Christopher Hammett is a coinvestigator on a research grant from Roche
Emily Dalton, BSc, BNursing Diagnostics. Louise Cullen received research grants from Alere (formerly
Research Nurse, Department of Emergency Medicine, Royal Brisbane Inverness Medical), Radiometer Pacific, Abbott Diagnostics, Roche, and
and Women’s Hospital, Brisbane, Queensland, Australia. Siemens; consultancy fees from Abbott Diagnostics and Novartis; as well
Kate Parker, BNursing, BHltSc(Psych) as support to attend meetings/conferences from Abbott Diagnostics,
Research Nurse, Department of Emergency Medicine, Royal Brisbane Alere, AstraZeneca, Novartis, Radiometer Pacific, Pfizer, and Boehringer
and Women’s Hospital, Brisbane, Queensland, Australia. Ingelheim. Daniel Beamish, Tracey Hawkins, Jessica Schluter, Emily Dalton,
Kate Parker, and Arvin Lamanna have no conflicts of interest to disclose.
Martin Than, MBBS
Emergency Physician, Department of Emergency Medicine, Christchurch Although some of the authors have been in receipt of funding from different
Hospital, Christchurch, New Zealand. commercial sources, at no time has there been any external influence on
the study design, data collection, data analysis, data interpretation, the
Christopher Hammett, MB ChB, FRACP
writing of the report, or the decision to submit the paper.
Cardiologist, Department of Cardiology, Royal Brisbane and Women’s
Hospital, and School of Public Health, Queensland University of Correspondence
Technology, Brisbane, Queensland, Australia. Jaimi H. Greenslade, BPsych (Hons), PhD, Department of Emergency
Arvin Lamanna, MBBS, FRACP Medicine, Royal Brisbane and Women’s Hospital, Butterfield St, Herston,
Cardiology Registrar, Department of Cardiology, Royal Brisbane and Queensland 4029, Australia (jaimi.greenslade@health.qld.gov.au).
Women’s Hospital, Brisbane, Queensland, Australia. DOI: 10.1097/JCN.0000000000000228

267

Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

268 Journal of Cardiovascular Nursing x May/June 2016

Results: Acute coronary syndrome was diagnosed in 384 of the 1951 patients (20%) recruited. Compared with
patients whose SBP was between 100 and 140 mm Hg, patients with an SBP of lower than 100 mm Hg or higher
than 140 mm Hg were 1.4 times (95% confidence interval, 1.2Y1.7) more likely to have ACS. Similarly, compared with
patients whose temperature was between 36.5-C and 37.5-C, patients with temperature of lower than 36.5-C
or higher than 37.5-C were 1.4 times (95% confidence interval, 1.1Y1.6) more likely to have ACS. Heart rate and
respiratory rate were not predictors of ACS. Conclusions: Patients with abnormal temperature or SBP were slightly
more likely to have ACS, but such risk was of too small a magnitude to be useful in clinical decision making.
Other physiological parameters (heart rate and respiratory rate) had no prognostic value. The use of physiological
parameters cannot reliably confirm or rule out ACS.
KEY WORD: acute coronary syndrome

R apid assessment of patients with chest pain is cru-

cial because mortality after acute myocardial infarc-
tion is directly related to time taken to receive treatment.1
Cardiac causes of pain, such as acute coronary syndrome
(ACS), represent one of the most immediate risks to
human life; however, a cardiac cause for chest pain is
found only in approximately 15% of chest pain
patients.2Y4 The formal investigation of ACS requires
serial blood tests and electrocardiograms within 6 to
24 hours followed by further imaging or provocative
testing.5Y7 These investigations are time consuming, are
expensive, and may not be available in all healthcare
facilities.8 An important role for nurses is to rapidly and
accurately identify those patients who require formal in-
vestigation for their chest pain. Finding a clear set of
physiological parameters that identify patients at higher
risk for ACS would allow nurses to initiate appropriate
plans of care and promptly escalate patients requiring
formal investigation for ACS.
A number of authors have found that abnormal phys-
iological parameters on hospital admission may portend
poor prognosis for patients with diagnosed acute myocar-
dial infarction. For instance, abnormal blood pressure,9Y12
respiratory rate,13 and heart rate14 are predictors of in-
hospital mortality and reinfarction in patients with acute
myocardial infarction. It has also been found in initial
research of patients presenting with undifferentiated chest
pain that systolic blood pressure (SBP), respiratory rate,
and heart rate are predictors of cardiac complications
within 72 hours.15 However, additional larger studies
have not been conducted to corroborate these results.
If abnormal physiological parameters were indicative
of increased ACS risk, these may be used to assist nurs-
ing staff to risk-stratify the large number of patients who
present to the ED with symptoms suggestive of ACS.
Patients with abnormal parameters could be flagged as
requiring immediate intensive investigation for ACS, thus
avoiding excess mortality that is associated with delays
to treatment in ACS patients. This would be of partic-
ular benefit for nurses in rural and remote settings, where
access to immediate blood results and objective testing
is limited and decisions need to be made about whether
to transfer patients for further investigation. In busy met-
ropolitan hospitals, it is usually the nursing staff members
who initiate care for patients; being able to quickly iden-
tify physiological parameters as potential markers for ACS
places these nurses in a better position to escalate their
concerns and advocate for their patients. Thus, the goal
of this analysis was to determine the utility of physiolog-
ical parameters in predicting ACS for patients presenting
to the hospital with chest pain. In this present study, the
investigators examine the relationship between a range
of physiological parameters (respiratory rate, SBP, heart
rate, and temperature) and ACS.
Methods
Setting and Design
This is an analysis of data from a prospective observa-
tional study conducted on adult emergency department
(ED) patients requiring evaluation for potential ACS. The
study was performed in the EDs of 2 large university teach-
ing hospitals and has been described in detail elsewhere.16,17
Human Research and Ethics Committees at both hos-
pitals approved the study protocol.
Participants
Adult patients were eligible for inclusion if they presented
to the ED with chest pain of at least 5 minutes’ duration,
suggestive of ACS. Features suggestive of ACS included
acute chest, epigastric, neck, jaw, or arm pain, discom-
fort, or pressure or breathlessness without an obvious
noncardiac source.18 Patients were excluded if they had a
clear alternate cause for the symptoms (eg, findings of
pneumonia), were unable or unwilling to provide informed
consent or be contacted after discharge, were transferred
from another hospital, or were pregnant. Patients with
ST-elevation MI on presentation were also excluded from
this study because these individuals have a definitive diag-
nosis and do not undergo risk stratification and investi-
gation in the ED. Trained research nurses worked with
senior clinicians and consecutively screened and enrolled
eligible patients during office hours (8:00 AM to 5:00 PM).
Treatment of patients was at the discretion of the treating
physician and independent of study enrollment.
Data Collection
Trained research nurses collected data during office hours
using standardized reporting guidelines.19 Data on

Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

 Relationship Between Physiological Parameters and ACS 269

temperature, heart rate, respiratory rate, and SBP were
taken on presentation. Blood samples were taken on
presentation (0 hours) and at least 6 hours later. Troponin
was measured by the Beckman Coulter second-generation
AccuTnI assay (Beckman Coulter, Chaska, Minnesota)
at 1 hospital. The Abbott ARCHITECT cardiac troponin
I assay (Abbott, Inc, Chicago, Illinois) was used for the
second. These troponin results were used for clinical de-
cision making and as part of outcome adjudication to
determine ACS versus no ACS.
Thirty days after initial attendance, trained research
nurses conducted telephone follow-up and medical record
review for the diagnosis of ACS. Information was ob-
tained from the patient and from hospital databases about
whether there had been any cardiac events, investigations,
or contact with any healthcare providers during the
30-day period. All follow-up information was verified
through contact with the healthcare provider, and original
copies of medical records and cardiac investigations were
obtained. Exercise stress testing, stress echocardiography,
myocardial perfusion scanning, coronary computed tomo-
graphy angiography, and coronary angiography were in-
cluded in relevant investigations.
Outcome Measures
The primary endpoint for this study was diagnosis of
ACS. Individuals were categorized as having ACS if they
were diagnosed with acute myocardial infarction or defi-
nite unstable angina pectoris on presentation or within
30 days of admission. All final diagnoses were adjudi-
cated independently by 1 of 2 cardiologists. A second
cardiologist reviewed all patients with an adjudicated
diagnosis of ACS and 10% of patients with a non-ACS
adjudicated diagnosis. Endpoint agreement was reached
in all instances. The criterion for acute myocardial infarc-
tion was according to the universal definition,6 namely,
evidence of myocardial necrosis with evidence of ische-
mia. Electrocardiogram changes or positive provocative
or imaging results including exercise tolerance testing,
myocardial perfusion scan, stress echocardiography, com-
puted tomography coronary angiography, and coronary
angiography during catheterization are included as evi-
dence of ischemia. Necrosis was diagnosed on the basis
of a rise or fall of cardiac troponin concentration for at
least 6 hours with at least 1 value higher than the 99th
percentile of the reference range at a level of assay im-
precision near 10%. If the troponin was greater than the
reference range but no rise or fall was recorded, other
causes of raised troponin were considered. If no alter-
native cause for the troponin rise was apparent and if the
clinical presentation was suggestive of ACS, an adjudi-
cated diagnosis of acute myocardial infarction was made.
Diagnosis of unstable angina pectoris was given for
patients with negative serial troponin results; ischemic
symptoms; and objective evidence of ischemia on the
exercise stress testing, stress echocardiography, myocar-
dial perfusion scanning, coronary computed tomography
angiography, or coronary angiography.
Data Analysis
Data were analyzed using Stata version 12 (StataCorp,
College Station, Texas). Descriptive statistics were used
to compare the baseline characteristics of the sample
across ACS and non-ACS groups. The data for each of
the physiological parameters were displayed graphically
by ACS group (positive vs negative). Continuous data
(respiratory rate, heart rate, temperature, and SBP) were
analyzed 2 ways. First, because previous research has
examined physiological parameters as linear predictors
of ACS, the mean values of these parameters were com-
pared across patients with and without ACS. Because the
data were mildly skewed, log values were taken and back-
transformed means (geometric means) were compared
across groups. Second, because a J-shaped relationship

TABLE 1 Baseline Characteristics of the Sample by Diagnosis (N = 1951)

No Acute Coronary Syndrome Acute Coronary Syndrome
Baseline Characteristic (n = 1567) (n = 384) P
Age, mean (SD) 58.30 (14.98) 68.15 (12.67) G.01
Male gender 903 (57.63) 260 (67.71) G.01
Risk factors
Dyslipidemia 838 (53.48) 274 (71.35) G.01
Diabetes 200 (12.76) 82 (21.35) G.01
Hypertension 755 (48.18) 257 (66.93) G.01
Smoking 304 (19.40) 61 (15.89) .11
Family history of coronary artery disease 853 (54.44) 260 (67.71) G.01
Medical history
Angina 522 (33.31) 190 (49.48) G.01
Acute myocardial infarction 337 (21.51) 135 (35.16) G.01
Congestive heart failure 114 (7.28) 39 (10.16) .06
Coronary artery bypass graft 114 (7.28) 56 (14.58) G.01
Prior angioplasty 262 (16.62) 96 (25.0) G.01
Stroke 163 (10.4) 54 (14.06) .04

With the exception of age, data are number (percentage within ACS category).

Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

270 Journal of Cardiovascular Nursing x May/June 2016

FIGURE. Distribution of physiological parameters by ACS category.

has also been postulated in which high or low values
are associated with ACS, continuous physiological param-
eters were then categorized into normal or abnormal
and linked to ACS. The following values were considered
abnormal: heart rate less than 60 or greater than 100, SBP
lower than 100 mm Hg or higher than 140 mm Hg,
temperature lower than 36.5-C or higher than 37.5-C,
and respiratory rate less than 12 or greater than 20. All
categorizations were determined a priori. The number
and percentage of patients in the ACS and non-ACS
groups with abnormal parameters were reported. Risk
ratios (with 95% confidence intervals) were then cal-
culated to identify the prognostic utility of abnormal phy-
siological parameters for 30-day ACS. Because risk ratios
are a relative measure, risk differences were also reported
to provide information on absolute ACS risk reduction.
For the analyses in which normal or abnormal values
were considered, missing physiological parameters were
considered normal. Analyses were repeated with missing
data excluded. In all cases, the result was of similar mag-
nitude and the same interpretation was yielded. Thus,
only data with missing cases included are reported here.
Patients categorized as ST-elevated myocardial infarction
on admission were excluded from all analyses because
these patients are routinely transferred for immediate
treatment rather than undergoing risk stratification.
Results
Data were available for 1951 patients, with a mean age
of 60.23 (SD, 15.07). There were 384 patients (19.68 %)
with ACS at 30 days. Baseline characteristics of the
sample by outcome are provided in Table 1. The ACS
patients were older, were more likely to have risk fac-
tors, and were more likely to have a history of cardiac
disease than the patients without ACS.
Distribution of physiological parameters by ACS cate-
gory is shown in Figure 1. There was substantial overlap

TABLE 2 Geometric Mean (95% Confidence Interval) for Physiological Parameters by Diagnosis
(N = 1951)
Variable No Acute Coronary Syndrome (n = 1567) Acute Coronary Syndrome (n = 384) P
Heart rate 75.19 (74.34Y76.06) 72.96 (71.20Y74.77) .02
Respiratory rate 17.68 (17.51Y17.85) 17.87 (17.52Y18.22) .34
Systolic blood pressure 139.47 (138.32Y140.64) 145.86 (143.14Y148.62) G.01
Temperature 36.33 (36.30Y36.36) 36.23 (36.17Y36.28) G.01

A geometric mean is the back-transformed (exponentiated) average of log-transformed values. P values are from independent group t tests. Data
were missing for heart rate (4), respiratory rate (24), systolic blood pressure (4), and temperature (247).

Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

 Relationship Between Physiological Parameters and ACS 271

TABLE 3 Number of Patients With Abnormal Physiological Parameters by Outcome, Risk Ratio, and
Risk Difference (N = 1951)
No Acute Coronary Acute Coronary Risk Ratio (95% % Risk Difference (95%
Variable Syndromea (n = 1567) Syndromea (n = 384) Confidence Interval) Confidence Interval)
Heart rate 375 (23.9) 110 (28.6) 1.2 (1.0 to 1.5) 3.9 (j0.2 to 8.2)
Respiratory rate 262 (16.7) 81 (21.1) 1.3 (1.0 to 1.6) 4.8 (j0.1 to 9.7)
Systolic blood 753 (48.1) 223 (58.1) 1.4 (1.2 to 1.7) 6.3 (2.8 to 9.9)
pressure
Temperature 807 (51.5) 233 (60.7) 1.4 (1.1 to 1.6) 5.8 (2.3 to 9.3)
a
Data are number (percentage of patients within ACS category). Abnormal values are less than 60 or greater than 100 for heart rate, less than 12 or
greater than 20 for respiratory rate, lower than 100 mm Hg or higher than 140 mm Hg for systolic blood pressure, and lower than 36.5-C or
higher than 37.5-C for temperature.

of the values in the ACS and non-ACS groups, and few
clear differences were evident on visual inspection. The
exception was SBP, which appeared to be slightly higher
in the ACS group.
The mean values of each parameter in the ACS and
non-ACS groups are provided in Table 2. The patients
with ACS had a higher mean SBP than the patients without
ACS. Mean temperature and heart rate were lower in
the patients with ACS. In all instances, the magnitude
of these differences was small.
The number of patients with abnormal physiological
parameters in the ACS and non-ACS groups is provided
in Table 3. These findings largely supported those of
Table 2; the patients with abnormal SBP or temperature
were at slightly higher risk for ACS than the patients with
normal parameters.
Further post hoc analyses were conducted on respira-
tory rate, temperature, SBP, and heart rate because these
variables had displayed mean differences in the ACS and
non-ACS groups. Specifically, to ensure that combining
high and low abnormal values did not obscure the results,
we examined whether classification of respiratory rate
and SBP into abnormal high values versus all other values
as well as classification of temperature and heart rate into
abnormal low versus all other values would influence the
risk ratios (Table 4). Reassuringly, the risk ratios for high
SBP, high respiratory rate, low temperature, and low heart
rate were similar to those looking at any abnormal value.
The risk ratio for low heart rate just reached significance
but this result was interpreted with caution given the post
hoc nature of the testing. Risk ratios in which low SBP,
low respiratory rate, high temperature, and high heart
rate were compared with all other values were not signif-
icantly different from 1.
Discussion
This is one of the first large studies in which investi-
gators examined whether abnormal physiological param-
eters are indicative of increased ACS risk in patients
presenting with chest pain. The investigators of this study
found that, although a number of physiological param-
eters on admission have associations with ACS, none
could be used to reliably confirm or exclude ACS. Patients
with abnormal temperature or SBP were slightly more
likely to have ACS, but such risk was of too small a mag-
nitude to be useful in clinical decision making. Other phy-
siological parameters (heart rate and respiratory rate) had
no prognostic value.
The finding that abnormal temperature and blood
pressure were prognostic for ACS is in line with pre-
vious research on patients with acute myocardial infarc-
tion.9Y12,14,15 However, the finding that patients with
ACS had higher SBP and lower temperature than patients
without ACS is contrary to these previous studies. It has
been found in research that low blood pressure is
associated with cardiac complications,9Y12,14,15 with low
blood pressure postulated to be a measure of poor sys-
tolic ventricular function and greater myocardial injury.20
Elevations in body temperature have also been observed
after acute myocardial infarction21 and are linked to size
of infarct and circulating biomarker levels.21,22 One

TABLE 4 Post hoc Analyses of Patients With Abnormal Physiological Parameters by Outcome, Risk
Ratio, and Risk Difference (N = 1951)
Variable Risk Ratio (95% Confidence Interval) % Risk Difference (95% Confidence Interval)
Heart rate G 60 beats per minute 1.4 (1.1 to 1.7) 7.1 (1.9 to 12.4)
Heart rate 9 100 beats per minute 0.87 (0.6 to 1.2) j2.5 (j8.4 to 3.3)
Respiratory rate G 12 breaths per minute 1.4 (0.8 to 2.5) 7.7 (j0.8 to 2.5)
Respiratory rate 9 20 breaths per minute 1.2 (1.0 to 1.5) 4.2 (j0.9 to 9.3)
Systolic blood pressure G 100 mm Hg 0.8 (0.38 to 1.9) j3.1 (j16.5 to 10.4)
Systolic blood pressure 9 140 mm Hg 1.4 (1.2 to 1.7) 6.5 (2.9 to 10.1)
Temperature G 36.5-C 1.4 (1.1 to 1.6) 6.1 (2.6 to 9.6)
Temperature 9 37.5-C 0.6 (0.2 to 2.1) j8.7 (j23.3 to 6.0)

Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

272 Journal of Cardiovascular Nursing x May/June 2016
What’s New and Important
h Patients with a SBP G100mmHg or 9140mmHg were
1.4 times more likely to have ACS compared with
patients whose SBP was between 100 and 140mmHg.
h Patients with temperature G36.5-C or 937.5-C were
1.4 times more likely to have ACS compared to patients
whose temperature was between 36.5-C and 37.5-C.
h Heart rate and respiratory rate did not predict ACS.
possible explanation for our inconsistent direction of
results is that, in our population of patients with undif-
ferentiated chest pain, abnormal temperature and blood
pressure may not be specific signs of ischemia but instead
may reflect poor general health, advanced age, and car-
diac risk factors. Consequently, these abnormal values
are predictors of ACS only because they co-occur with
risk factors predisposing patients to ACS.
Further, there were few patients in our cohort with
notably low SBP or notably high temperature. Therefore,
we are unable to adequately test whether low blood pres-
sure and high temperature also predict ACS. Further
research in which larger numbers of individuals with a
wider range of values are enrolled would be required to
provide a more complete assessment of the prognostic
utility of these physiological parameters. Even with a larger
trial, it is unlikely that these parameters will significantly
influence clinical decision making. They may prove useful
as red flags, thereby empowering nurses to escalate their
concerns with objective data.
The investigators found that abnormal respiratory
rate and heart rate did not increase the risk of being di-
agnosed with ACS; a finding that is in contrast to the
significance of abnormalities in these parameters in pa-
tients with proven ACS. Through past research, heart
rate has emerged as a predictor of poor prognosis in those
patients with proven ACS,23,24 with heart rate reduction
therapies purportedly resulting in improved myocardial
perfusion,25 reduced myocardial oxygen consumption,
and increased mechanical efficiency of the left ventricle.24
Similarly, abnormalities in respiratory rate are likely to
occur after acute myocardial infarction because circu-
latory failure alters both ventilatory control and pulmo-
nary perfusion.13 An abnormal respiratory rate is a
predictor of acute myocardial infarction13 because it is
an indicator of the presence of left ventricular failure as-
sociated with significant compromise of contractility
after acute myocardial infarction.
As noted above, one explanation for the failure to
link physiological parameters to ACS in this study may
be that there were few cases in which such parameters
were notably abnormal. Mildly abnormal physiological
parameters occur for a variety of reasons in the popu-
lation of patients presenting with chest pain and may be
a result of a patient’s pain experience or anxiety related
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.
to symptoms. As such, they do not appear useful for dis-
tinguishing cardiac and noncardiac causes of chest pain.
There are a number of limitations of this study. We
used only a single measure of each physiological para-
meter on presentation. The use of a single measurement
is problematic because observations are dynamic and can
be influenced by many factors including medications and
the hospital environment. The use of multiple measure-
ments, both on admission and across the ED stay, would
provide a more accurate estimate of the patient’s true
value. Further, a significant number of patients with ACS
may present atypically or without pain, and this cohort
was not included in this study. There were a large num-
ber of patients with missing data on temperature, but this
number did not differ by diagnosis (ACS vs non-ACS).
Finally, recruitment was done during times when research
staff was available, and thus, patients presenting out of
hours were not included. Data are not available on the
number of patients presenting after hours or the cohort
that met exclusion criteria in this study; thus, the extent
of potential selection bias is unable to be quantified.
Conclusions
In a cohort of patients presenting to the hospital with
chest pain, a number of physiological parameters are prog-
nostic for ACS. However, none could be used to reliably
confirm or exclude ACS.
Acknowledgments
The authors thank the patients who participated in the
study as well as the research staff, emergency department
staff, and laboratory technicians of all participating sites
for their invaluable efforts.
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