SHOCK, Vol. 49, No. 2, pp.

131–136, 2018

IDENTIFICATION OF HYPOTENSIVE EMERGENCY DEPARTMENT

PATIENTS WITH CARDIOGENIC ETIOLOGIES

Daniel J. Henning, * Kathleen E. Kearney, † Michael Kennedy Hall, *

Claudius Mahr, † Nathan I. Shapiro, ‡§ and Graham Nichol * jj
*Division of Emergency Medicine, University of Washington School of Medicine, Seattle, Washington;
†
Division of Cardiology, University of Washington School of Medicine, Seattle, Washington; ‡ Department
of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts; §The Center for
Vascular Biology Research and Division of Molecular and Vascular Medicine, Beth Israel Deaconess
Medical Center, Boston, Massachusetts; and jjUniversity of Washington-Harborview Center for
Prehospital Emergency Care, Seattle, Washington

Received 31 May 2017; first review completed 19 Jun 2017; accepted in final form 10 Jul 2017
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ABSTRACT—Objective: Identify predictors of cardiogenic etiology among emergency department (ED) patients with
hypotension, and use these predictors to create a clinical tool to discern cardiogenic etiology of hypotension. Methods: This
secondary analysis evaluated a prospective cohort of consecutive patients with hypotension in an urban, academic, tertiary
care ED from November 2012 to September 2013. We included adults with hypotension, defined as a new vasopressor
requirement, systolic blood pressure (SBP) < 90 mm Hg after at least 1 L of crystalloid or 2 units packed red blood cells, or
SBP < 90 mm Hg and fluids withheld due to concern for fluid overload. The primary outcome was cardiogenic etiology,
adjudicated by two physician chart review, with 25% paired chart review (kappa ¼ 0.92). We used multivariable logistic
regression to predict cardiogenic etiology, utilizing clinical data abstracted from the electronic medical record. We created a
prediction score from significant covariates and calculated its test characteristics for cardiogenic hypotension. Results: Of
700 patients with hypotension, 107 (15.3%, 95% CI: 12.6%–18.0%) had cardiogenic etiology. Independent predictors of
cardiogenic etiology were shortness of breath (OR 4.1, 95% CI: 2.5–6.7), troponin > 0.1 ng/mL (37.5, 7.1–198.2),
electrocardiographic ischemia (8.9, 4.0–19.8), history of heart failure (2.0, 1.1–3.3), and absence of fever (4.5,
2.3–8.7) (area under the curve [AUC] ¼ 0.83). The prediction score created from these predictors yielded 78% sensitivity
and 77% specificity for cardiogenic etiology (AUC ¼ 0.827). Conclusions: Clinical predictors offer reasonable ED screening
sensitivity for cardiogenic hypotension, while demonstrating sufficient specificity to facilitate early cardiac interventions.
KEYWORDS—Cardiogenic, emergency department, shock

INTRODUCTION emphasis placed on recognition of sepsis, the more prevalent

disease (4, 11).
Patients who present to an emergency department (ED) with
The early implementation of any intervention in cardiogenic
hypotension may have hypoperfusion indicative of shock,
shock, including MCS, is likely important to prevent irrevers-
indicating an elevated risk of mortality across etiologies
ible end-organ damage (12). Patients and future studies could
(1–4). A cardiogenic etiology is found in 15% of patients
benefit from a clinical prediction rule to identify cardiogenic
with shock in the ED setting (3, 4), and cardiogenic shock is
etiologies of hypotension in the ED. This investigation seeks to
associated with nearly 33% short-term mortality when present
identify independent predictors of cardiogenic etiology among
in the ED (3). Yet early identification can facilitate early
ED patients with persistent hypotension, and to assess the
interventions, including percutaneous coronary intervention
clinical utility of these predictors in identifying cardiogenic
or potentially mechanical circulatory support (MCS) (5, 6),
hypotension, shock, and mortality among hypotensive ED
which may reduce mortality in this population.
patients.
Identifying cardiogenic etiologies of hypotension can be
challenging in the ED due to clinical overlap with other
etiologies (7). For instance, cardiogenic shock can cause an METHODS
inflammatory state similar to that observed in septic shock, Study design
while myocardial dysfunction often complicates septic shock
This was retrospective analysis of a previous prospective, observational
(8–10). This overlap can complicate the early recognition of cohort study of consecutive patients with shock in the ED from November 11,
cardiogenic shock, especially given the current clinical 2012 to September 23, 2013 (13). The study was conducted at an urban,
academic ED that has 55,000 annual visits. This study was granted a waiver of
documented written consent under minimal risk criteria by the human subjects
Address reprint requests to Daniel J. Henning, MD, MPh, Harborview Medical
committee of the institutional review board. STROBE guidelines were used to
Center, Box 359702, 325 9th Avenue, Seattle, WA 98104. E-mail: henning2@uw.edu
report the results of this study (14).
The original study was supported by Beth Israel Deaconess Medical Center,
Department of Emergency Medicine.
The authors report no conflicts of interest. Participants
Supplemental digital content is available for this article. Direct URL citation
appears in the printed text and is provided in the HTML and PDF versions of this We included all admitted adult (age 18 or older) patients with persistent
article on the journal’s Web site (www.shockjournal.com). hypotension in the ED: systolic blood pressure < 90 mm Hg after resuscitation
DOI: 10.1097/SHK.0000000000000945 with at least 1 L intravenous fluid, hypotension with intravenous fluids
Copyright ß 2017 by the Shock Society restricted due to documented concern of fluid overload (i.e., patients with

131
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132 SHOCK VOL. 49, No. 2 HENNING ET AL.

known heart failure or hemodialysis dependent), or a vasopressor requirement. Sample size justification
We excluded patients with hypotension due to atrial fibrillation with rapid
ventricular response or supraventricular tachycardia who were discharged once This study sought to identify predictors of cardiogenic hypotension using
rate control was achieved, intoxication, and hypotension due to transient multivariable logistic regression. We estimated a priori that 15% of patients had
medication effect. We also excluded patients who had a documented baseline cardiogenic etiology, allowing up to 10 predictors to be included in the logistic
systolic blood pressure < 90 mm Hg, unless a 10 mm Hg decrease in systolic regression model using the n/10 rule to prevent over fitting.
blood pressure occurred.
ED screening and enrollment occurred using an alert preprogrammed into
clinical information technology systems. All patients with hypotension noted RESULTS
at triage, in nursing notes, or on the bedside monitors (two readings more
than 5 min apart), or who required vasopressor medications at any point Of 700 patients enrolled in the parent study, 107 of 700
during their ED stay, were prospectively identified for possible inclusion in the (15.3%) had a cardiogenic cause as the most likely etiology of
study. Eligible patients then underwent a confirmatory chart review to affirm
the presence of shock and absence of exclusion criteria. This confirmatory hypotension in the ED. Seventy-six of 700 (10.9%) met criteria
review and subsequent data abstraction typically occurred 1 month after ED for cardiogenic shock, and 68 of 700 (9.7%) were cardiogenic
arrival and was performed without subsequent knowledge of the hospital patients who died in-hospital. Cardiogenic patients had a higher
course.
prevalence of comorbidities generally associated with cardiac
Data collection disease, including coronary artery disease, heart failure, myo-
cardial infarction, and chronic obstructive pulmonary disease,
Elements of the history of present illness, initial vital signs, physical
examination, past medical history, and medications were abstracted from the while non-cardiogenic hypotension was more frequently asso-
hospital record into an a priori standardized database for each enrolled patient. ciated with alcoholism and end-stage liver disease (Table 1).
The history and physical examination came exclusively from the ED attending Cardiogenic patients had higher mean troponin concentrations,
and resident charts. Basic demographics, length of stay, disposition data, and all
laboratory values were obtained from the electronic health record. Electrocar- whereas non-cardiogenic patients demonstrated higher initial
diogram ischemia was defined as any electrocardiographic findings that temperatures and percentage of immature granulocytes
suggested ischemia according to the final cardiologist interpretation. (Table 2).
A study investigator adjudicated each patient’s underlying cause of insta-
bility using all available information (e.g., diagnostic testing results, physician The cohort had an overall mortality of 19.6% (95% CI:
notes, etc.) at the end of the hospital stay. Underlying causes were initially 16.8%–22.7%) before discharge. Patients with cardiogenic
classified as septic, cardiogenic, hemorrhagic, hypovolemic, anaphylactic,
neurogenic, or other based on previously published methods and definitions
(10, 11, 15), and then reclassified as a binary outcome: cardiogenic or non- TABLE 1. Demographics of patients with cardiogenic and
cardiogenic. Patients were systematically screened for evidence to determine a non-cardiogenic etiologies of hypotension
cause of shock, and each patient was assigned a single diagnosis that Non- P
represented the most likely cause of shock in the ED. To determine inter-
Cardiogenic cardiogenic value
rater reliability, a second physician reviewer adjudicated a 25% sample,
and the agreement between the two reviewers was found to be sufficient to n 107 593
proceed with a single adjudication for each patient (kappa ¼ 0.92, 95% CI: Age in years (16) 68.3 (18.5) 65.2 (16.6) 0.08
0.83 –1.0). Male (%) 58 (54.2) 334 (56.3) 0.68
Race (%)
Outcomes African American 15 (14.0) 61 (10.3) 0.25
Asian 5 (4.7) 23 (3.9) 0.70
The primary outcome was the adjudicated diagnosis: cardiogenic or non-
cardiogenic etiology of hypotension. Secondary outcomes included cardiogenic Hispanic 3 (2.8) 26 (4.3) 0.47
shock in the ED (patients meeting any one criteria for end-organ damage: White 66 (61.7) 410 (69.1) 0.13
altered mental status, lactate  2 mmol/L, or vasopressor requirement) (10, 16, Other 18 (16.8) 73 (12.3) 0.20
17) and in-hospital mortality. Code status in ED
Do not intubate 16 (15.0) 76 (12.8) 0.55
Data analysis Do not resuscitate 16 (15.0) 80 (13.5) 0.05
Comorbidities
Data analysis was performed using SAS v9.3 statistical software (SAS Alcoholism 2 (1.9) 46 (7.8) 0.03
Institute Inc, Cary, NC). A binary outcome variable was created for the primary Diabetes 36 (33.6) 154 (26.0) 0.10
outcome of cardiogenic etiology (i.e., cardiogenic or non-cardiogenic). A
Foley catheter 1 (0.9) 21 (3.5) 0.15
univariate assessment of the association between diagnosis and binary clinical
covariates was performed using chi-square. For continuous covariates, Student t Vascular catheter 3 (2.8) 59 (10.0) 0.02
test or Wilcoxon rank sum was used as appropriate. A multivariate logistic Heart failure 32 (29.9) 102 (17.2) <0.01
regression model was to predict cardiogenic etiology of hypotension. All Coronary artery disease 41 (38.3) 128 (21.6) <0.01
covariates from the initial univariate analysis with P < 0.1 were included in Chronic obstructive pulmonary 20 (18.7) 68 (11.5) 0.04
the logistic regression model selection process. A stepwise model selection disease
process was used, with P < 0.05 required for entry and P < 0.1 required to stay Dementia 6 (5.6) 41 (6.9) 0.62
in the model. Model discrimination was assessed using area under the curve Hypertension 56 (52.3) 250 (42.2) 0.05
(AUC). The Hosmer–Lemeshow test was used to assess model calibration. The Intravenous drug use 1 (0.9) 8 (1.4) 0.73
model was internally validated using bootstrapping techniques. The logistic
End-stage liver disease 2 (1.9) 57 (9.6) <0.01
regression analysis was repeated on 1,000 different samples of the same size
drawn with replacement from the original dataset. Median b-estimates and odds Peripheral vascular disease 11 (10.3) 39 (6.6) 0.17
ratios with 95% confidence intervals were recalculated for each model covariate Chronic renal insufficiency 13 (12.2) 38 (6.4) 0.04
using these repeated samples. Hemodialysis 7 (6.5) 54 (9.1) 0.39
b-coefficients from the initial logistic regression analysis were used to Stroke 11 (10.3) 43 (7.3) 0.28
assign weight to each independent predictor. The test characteristics for Myocardial infarction 14 (13.1) 34 (5.7) <0.01
different score thresholds were calculated to optimize sensitivity and specificity Human immunodeficiency virus 0 (0) 11 (1.9) 0.16
when predicting cardiogenic etiology for hypotension. As sensitivity analyses, Hematologic malignancy 3 (2.8) 22 (3.7) 0.64
the prediction score test characteristics were calculated in two subpopulations Solid malignancy 19 (17.8) 151 (25.5) 0.09
of cardiogenic hypotension to assess the efficacy in identifying the highest risk
Solid organ transplant 0 (0) 18 (3.0) 0.07
cardiogenic population most likely to benefit from early interventions: cardio-
genic shock in the ED and cardiogenic patients who died in hospital. ED indicates emergency department.

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SHOCK FEBRUARY 2018 CARDIOGENIC HYPOTENSION IN THE EMERGENCY DEPARTMENT 133
TABLE 2. Clinical results associated with cardiogenic and TABLE 4. Prediction scores assigned for each covariate to predict
non-cardiogenic etiologies of hypotension cardiogenic hypotension
Non- P Covariate Score
Cardiogenic cardiogenic value
Troponin  0.1 ng/mL 3
Initial vital signs (SD) Electrocardiogram ischemia 2
Temperature (8F) 97.2 (6.5) 100.2 (6.3) <0.01 Reported shortness of breath 1.5
Heart rate (beats/min) 88 (28.6) 94 (24.6) 0.02 Absence of reported or measured fever 1.5
Respiratory rate (breaths/min 21 (5.6) 20 (6.1) 0.34 History of heart failure 0.5
Systolic blood pressure (mm Hg) 92 (23.3) 87 (16.2) 0.01
A total score  2 suggests cardiogenic hypotension.
Diastolic blood pressure (mm Hg) 56 (15.7) 51 (12.6) <0.01
Oxygen saturation (%) 97 (4.3) 97 (4.5) 0.55
Laboratory results (SD) (Table 5). In the sensitivity analyses for higher-risk cardiogenic
White blood cell count (cells/mm3) 12.6 (7.3) 12.8 (9.3) 0.79
patients, a score  2 had 82% sensitivity and 75% specificity
Immature granulocytes (cells/mm3) 1.1 (1.1) 7.0 (9.2) <0.01
Hematocrit (%) 36.0 (7.7) 33.8 (7.6) <0.01 identifying cardiogenic shock in the ED and 79% sensitivity
Platelets (1,000 cells/mm3) 253 (116.2) 236 (146.1) 0.25 and 71% specificity for patients who died in-hospital. In the
Bicarbonate (mEq/L) 21.9 (21.9) 22.0 (5.6) 0.86 overall study population, 28.6% of patients with a score  2 had
Creatinine (mg/dL) 2.1 (1.8) 2.0 (1.9) 0.55 cardiogenic shock in the ED, and 10.4% of patients with a
International normalized ratio 1.8 (1.7) 1.8 (1.5) 0.83
score  2 had cardiogenic hypotension and died before dis-
Glucose (mg/dL) 159 (92.1) 148 (93.3) 0.31
Lactate (mmol/L) 3.3 (3.0) 2.8 (2.3) 0.09 charge (Fig. 1).
Troponin (ng/mL) 0.76 (1.8) 0.17 (0.3) <0.01
Cardiac specific (%)
Troponin  0.1 ng/mL 13 (12.2) 2 (0.3) <0.01 DISCUSSION
Shortness of breath 48 (44.9) 109 (18.4) <0.01
Among patients with persistent hypotension in the ED, the
Electrocardiogram ischemia 25 (23.4) 14 (2.4) <0.01
Absence of reported or 95 (88.8) 366 (61.7) <0.01 likelihood of a cardiogenic etiology can be assessed using
Measured fever simple history, physical, and laboratory information. A clinical
SD indicates standard deviation. prediction score of  2 has reasonable sensitivity and specifici-
ty for cardiogenic cause of hypotension, increasing the likeli-
hood of cardiogenic hypotension from 15.3% in the overall
hypotension had mortality of 26.2% (95% CI: 18.7%–35.3%) hypotensive population to 38.3%. Only 5% of patients with < 2
which increased to 34.2% (95% CI: 24.5%–45.4%) if evidence points had cardiogenic hypotension.
of cardiogenic shock (altered mental status, lactate  2 mmol/ The clinical prediction score identified patients within the
L, or vasopressor requirement) was observed in the ED. two higher-risk sub-populations of cardiogenic hypotension
Patients determined to have cardiogenic hypotension, but not with similar efficacy. While prospective validation and rule
meeting criteria for shock, had 6.5% (95% CI: 0.8%–21.8%) refinement to include echocardiography are necessary, this
mortality (Supplemental Table 1, http://links.lww.com/SHK/ novel prediction score demonstrated adequate sensitivity for
A618). high-risk cardiogenic patients to justify clinical implementa-
The covariates reported shortness of breath (4.1, 95% CI: tion as an ED screening tool. The specificity of 75% signifi-
2.5–6.7), history of heart failure (2.0, 95% CI: 1.1–3.3), cantly narrows the hypotensive population to one where the
absence of measured or reported fever (4.5, 95% CI: 2.3– assessment for early MCS would not overwhelm cardiology or
8.7), troponin  0.1 ng/mL (OR 37.5, 95% CI: 7.1–198.2), and system resources. Based on the low incidence of cardiogenic
ischemia on electrocardiogram (8.9, 95% CI: 4.0–19.8) (AUC shock across an already infrequent group of patients with
0.827) were independently predicted cardiogenic hypotension persistent hypotension, only one in four patients screened in
(Table 3). The bootstrapping internal validation provided simi- by the score would have cardiogenic shock. Yet, using the study
lar estimates (Supplemental Table 2, http://links.lww.com/ institution as a model, a patient would meet score threshold less
SHK/A619). than once daily. In exchange for the opportunity to initiate early
The prediction score assigned points based on the covariate cardiac interventions, the resources required to implement this
b-coefficients from the logistic regression model (Table 4). A screening may be inexpensive to the health system.
composite score of 2 or more had 78% sensitivity and 77% The logistic regression model and prediction score give
specificity for cardiogenic hypotension in this population weights to the various findings typically integrated into an

TABLE 3. Logistic regression model predicting cardiogenic hypotension among all ED patients with persistent hypotension
Covariate AOR 95% CI b-coefficient Std. error P value
Troponin  0.1 (ng/mL) 37.5 7.1–198.2 3.62 0.85 <0.01
Electrocardiogram ischemia 8.9 4.0–19.8 2.18 0.41 <0.01
Report shortness of breath 4.1 2.5–6.7 1.41 0.41 <0.01
History of heart failure 2.0 1.1–3.3 0.67 0.27 <0.01
Absence of reported or measured fever 4.5 2.3–8.7 1.50 0.34 <0.01
AUC ¼ 0.827 Hosmer–Lemeshow ¼ 0.09
AUC indicates area under the curve.

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134 SHOCK VOL. 49, No. 2 HENNING ET AL.

TABLE 5. Test characteristics of a prediction score  2 for cardiogenic hypotension, cardiogenic shock in the ED, and cardiogenic patients
who died in-hospital among overall population with persistent hypotension
Sens (%), Spec (%), PPV (%), NPV (%),
Population n Score  2 (95% CI) (95% CI) (95% CI) (95% CI)
Cardiogenic hypotension 107 83 78 (70–90) 77 (70–82) 38 (32–45) 95 (93–97)
Cardiogenic shock in the ED 76 62 82 (73–90) 75 (72–79) 29 (23–35) 97 (96–99)
Cardiogenic hypotension with mortality 28 22 79 (63–94) 71 (68–74) 26 (20–32) 98 (96–99)
ED indicates emergency department; NPV, negative predictive value; PPV, positive predictive value; Sens, sensitivity; Spec, specificity.

ED diagnosis. Notably, a history of coronary artery disease or
myocardial infarction were not significant independent predic-
tors of cardiogenic hypotension after controlling for the other
model covariates. Similarly, a history of heart failure only met
score threshold if accompanied by another independent predic-
tor. Conversely, 2 of 15 (13.3%) patients with a tropo-
nin  0.1 ng/mL and 14 of 39 (35.9%) with ischemia on
electrocardiogram had non-cardiogenic hypotension, remind-
ing clinicians to avoid basing clinical diagnoses on the presence
or absence of a single data point. Along these lines, our recent
study demonstrated that patients with suspected septic shock
often did not have measured or reported fever (18). That study
informs the application of the proposed criteria here, reminding
clinicians that while hypotensive patients without signs of fever
have a higher likelihood of cardiogenic cause, sepsis may still
be present and an assessment for infectious causes is still
necessary. Until novel diagnostic approaches improve the
identification of cardiogenic hypotension, this process provides
a reasonable approach.
Prior studies describe cardiogenic shock most frequently
occurring as the sequela of myocardial infarction (19, 20),
and typically occurring after a patient is admitted (21). Likely
reflecting the lower incidence of cardiogenic shock in the
emergency setting, expert recommendations give the vague
guidance that a ‘‘cardiogenic cause of shock should be consid-
ered for shock in the ED without an obvious cause’’ (19),
without acknowledging the diagnostic difficulty in identifying
those patients with a cardiogenic cause of shock in the absence
of an obvious ischemic event. We found that cardiogenic
hypotension accounted for nearly one of seven ED patients
with persistent hypotension. These cardiogenic patients fre-
quently met criteria for cardiogenic shock in the ED, which was
associated with a 34.2% mortality rate (20). Furthermore, the
majority of our patients with cardiogenic hypotension did not
have a troponin > 0.1 ng/mL or electrocardiogram ischemia,
suggesting that myocardial infarction is less frequently the
cause of shock in ED patients. Still, early MCS may benefit
patients with cardiogenic shock, even without myocardial
infarction, by offloading the heart to promote recovery and
maintaining cardiac output to prevent end-organ damage as a
bridge to more definitive treatment such as durable ventricular
assist devices or cardiac transplant (22, 23). An emphasis in the
current literature on managing shock in the context of acute
myocardial infarction likely reflects the inherent difficulty

FIG. 1. Demonstration of the patient populations created when stratifying ED patients with persistent hypotension using the proposed prediction
score at a threshold of two points. ED indicates emergency department.

Copyright © 2017 by the Shock Society. Unauthorized reproduction of this article is prohibited.
SHOCK FEBRUARY 2018
when identifying nonischemic presentations of cardiogenic
shock.
As the emphasis shifts to the earlier treatment of cardiogenic
shock, developing reliable methods for early identification will
allow interventions to be moved into the ED. If the strong
predictors of cardiogenic hypotension described here are pri-
oritized in the diagnostic work-up of persistent hypotension, the
ambiguity surrounding this diagnosis could decrease.
Future studies should validate our findings in an indepen-
dent, prospective ED patient population, ideally incorporating
point-of-care ultrasound, which may decrease time to diagnosis
(24, 25). Likewise, the ability of our proposed prediction score
to identify patients who may benefit from MCS should be
investigated, so that studies that attempt to move mechanical
support into the earliest stages of care can identify candidate
patients reliably.
Limitations
This is a secondary analysis of a single-center study that
prospectively identified consecutive patients with hypotension
after resuscitation. Yet, data were abstracted retrospectively, so
misclassification bias may exist as the clinical data collected
were limited to what we were able to obtain from the medical
records. Likewise, diagnoses were adjudicated by retrospective
chart review, although the strong agreement between reviewers
makes diagnostic misclassification less likely to influence
results. While a broad spectrum of clinical data was included
in our analysis, the vast majority of patients did not have formal
echocardiography performed in the ED. While myocardial
depression on echocardiography may suggest a cardiogenic
cause of hypotension, in our institution these studies are rarely
performed in the ED. Given that nearly one in three patients
with septic shock will have systolic myocardial dysfunction as
well (9), echocardiography alone cannot provide a definitive
diagnosis. Patients with atrial fibrillation who were discharged
explicitly after rate control was achieved were excluded from
the original study. While hypotension due to primary atrial
fibrillation was rare, this exclusion does remove a group of
patients with cardiogenic hypotension from the population,
although treatment of this patient group is targeted toward
resolving the arrhythmia rather than inotropic or MCS. Last,
this study was performed at a tertiary care center, to which
patients with a larger burden of disease and those with hemo-
dynamic instability are often referred. This limits the generali-
zation of our findings to smaller community hospitals and may
also affect the rates of adverse outcomes.
CONCLUSION
Cardiogenic etiologies often underlie persistent hypotension
in the ED, are frequently associated with clinical criteria for
shock, and carry a high mortality rate. Simple data that are
readily available at the bedside offer robust leverage to predict
cardiogenic etiologies of hypotension with sufficient sensitivity
and specificity to screen ED patients. Such screening would
allow the treatment of cardiogenic shock, including MCS
initiation, to be moved earlier in the course of care, potentially
improving the outcomes for this high-risk patient population.
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CARDIOGENIC HYPOTENSION IN THE EMERGENCY DEPARTMENT 135
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