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
Received 31 May 2017; first review completed 19 Jun 2017; accepted in final
form 10 Jul 2017
Gemmy Sistarina
 Introduction
Patients who present to an Emergency department (ED) with hypotension may have
hypoperfusion indicative of shock, indicating an elevated risk of mortality across etiologies

Identifying cardiogenic etiologies of hypotension can be challengeing in the ED due to clinical

overlap with other etiologies

The early implementation of any intervention in cardiogenic shock, including mechanical

circulatory support (MCS), is likely important to prevent irreversible end organ damage.
 Method
• Study Design : This was retrospective analysis of a previous prospective,
observational cohort study of consecutive patients with shock in the ED from
November 11 , 2012 to September 23, 2013

• Participant : We included all admitted adult (age 18 or older) patients with persistent
hypotension in the ED: systolic blood pressure<90mm Hg after resuscitation with
at least 1 L intravenous fluid, hypotension with intravenous fluids restricted due to
documented concern of fluid overload (i.e., patients with known heart failure or
hemodialysis dependent), or a vasopressor requirement.
 Methods
• Data Collection : Elements of the history of present illness, initial vital signs,
physical examination, past medical history, and medications were abstracted from
the hospital record into an a priori standardized database for each enrolled patient.

• Outcomes : The primary outcome was the adjudicated diagnosis: cardiogenic or

noncardiogenic etiology of hypotension. Secondary outcomes included cardiogenic
shock in the ED (patients meeting any one criteria for end-organ damage: altered
mental status, lactate 2mmol/L, or vasopressor requirement) and in-hospital
mortality.
 Results
• TABLE 1. Demographics of patients with cardiogenic and non-cardiogenic etiologies of hypotension
Cardiogenic Non-Cardiogenic P-Value
n 107 593
Age in years 68,3 (18,5) 65,2 (16,6) 0,08
Male (%) 58 (54,2) 334 (56,3) 0,68
Race (%)
African American 15 (14,0) 61 (10,3) 0,25
Asian 5 (4,7) 23 (3,9) 0,70
Hispanic 3 (2,8) 26 (4,3) 0,47
White 66 (61,7) 410 (69,1) 0,13
 Results
Code status in ED
Do not intubate 16 (15,0) 76 (12,8) 0,55
Do not resusitate 16 (15,0) 80 (13,5) 0,05
Comorbidities
Alcoholism 2 (1,9) 46 (7,8) 0,03
Diabetes 36 (33,6) 154 (26,0) 0,10
Foley Catheter 1 (0,9) 21 (3,5) 0,15
Vascular Catheter 3 (2,8) 59 (10,0) 0,02
Heart Failure 32 (29,9) 102 (17,2) <0,01
Coronary artery disease 41 (38,3) 128 (21,6) < 0,01
 Result
Chronic obstrutive 20 (18,7) 68 (11,5) 0,04
pulmonary disease
Dementia 6 (5,6) 41 (6,9) 0,62
Hypertension 56 (52,3) 250 (42,2) 0,05
Intravenous drug use 1 (0,9) 8 (1,4) 0,73
End-stage liver 2 (1,9) 57 (9,6) <0,01
disease
Peripheral vascular 11 (10,3) 39 (6,6) 0,17
disease
Chronic renal 13 (12,2) 38 (6,4) 0,04
insufficiency
Hemodialysis 7 (6,5) 54 (9,1) 0,39
 Result
• TABLE 2. Clinical results associated with cardiogenic and non-cardiogenic etiologies of hypotension
Cardiogenic Non Cardiogenic P-value
Initial vital signs
(SD)
Temperature (F) 97,2 (6,5) 100,2 (6,3) < 0,01
Heart Rate 88 (28,6) 94 (24,6) 0,02
(beats/min)
Respiratory rate 21 (5,6) 20 (6,1) 0,34
(breaths/min)
Systolic blood 92 (23,3) 87 (16,2) 0,01
pressure (mmHg)
 Results
Cardiogenic Non Cardiogenic P value
Laboratory results (SD)
White blood Cell Count 12,6(7,3) 12,8 (9,3) 0,79
(cells/mm3)
Immature granulocytes 1,1 (1,1) 7,0 (9,2) < 0,01
(cells/mm3)
Hematocrit(%) 36,0 (7,7) 33,8 (7,6) < 0,01
Platelets (1000 253 (116,2) 236 (141,6) 0,25
cells/mm3)
Creatinine(mg/dL) 2,1 (1,8) 2,0 (1,9) 0,55
 Results
Cardiogenic Non Cardiogenic P value
Cardiac specific (%)
Troponin ≥0,1 ng/mL 13 (12,2) 2 (0,3) < 0,01
Shortness of breath 48 (44,9) 109 (18,4) < 0,01
Electrocardiogram 25 (23,4) 14 (2,4) < 0,01
ischemia
Absence of reported or 95 (88,8) 366 (61,7) < 0,01
Measured fever
 Results
Table 4. Prediction scores assigned for each covariate to predict cardiogenic hypotension
Covariate Score
Troponin ≥ 1 ng/mL 3
Electrocardiogram ischemia 2
Reported shortness breath 1,5
Absence of reported or measured fever 1,5
History of heart failure 0,5

A total score ≥ 2 suggests cardiogenic hypotension

 Results
• 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
Population n Score ≥ 2 Sens (%) Spec (%) PPV (%) NPV (%)
Cardiogenic 107 83 78 77 38 95
hypotension
Cardiogenic 76 62 82 75 29 97
shock in the
ED
Cardiogenic 28 22 79 71 26 98
hypotension
with mortality
 Discussion
• Among patients with persistent hypotension in the ED, the likelihood of a
cardiogenic etiology can be assessed using simple history, physical, and
laboratory information.
• The clinical prediction score identified patients within the two higher-risk
sub-populations of cardiogenic hypotension with similar efficacy.
• 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.
 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.
 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.
TERIMAKASIH