JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
17, 2019
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VOL. 74, NO.
ª 2019 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
PUBLISHED BY ELSEVIER
ORIGINAL INVESTIGATIONS
Cardiogenic Shock Classification
to Predict Mortality in the
Cardiac Intensive Care Unit
Jacob C. Jentzer, MD,a,b Sean van Diepen, MD, MSC,c Gregory W. Barsness, MD,a Timothy D. Henry, MD,d
Venu Menon, MD,e Charanjit S. Rihal, MD, MBA,a Srihari S. Naidu, MD,f David A. Baran, MDg
ABSTRACT
BACKGROUND A new 5-stage cardiogenic shock (CS) classification scheme was recently proposed by the Society for
Cardiovascular Angiography and Intervention (SCAI) for the purpose of risk stratification.
OBJECTIVES This study sought to apply the SCAI shock classification in a cardiac intensive care unit (CICU) population.
METHODS The study retrospectively analyzed Mayo Clinic CICU patients admitted between 2007 and 2015. SCAI CS
stages A through E were classified retrospectively using CICU admission data based on the presence of hypotension or
tachycardia, hypoperfusion, deterioration, and refractory shock. Hospital mortality in each SCAI shock stage was stratified
by cardiac arrest (CA).
RESULTS Among the 10,004 unique patients, 43.1% had acute coronary syndrome, 46.1% had heart failure, and 12.1%
had CA. The proportion of patients in SCAI CS stages A through E was 46.0%, 30.0%, 15.7%, 7.3%, and 1.0% and
unadjusted hospital mortality in these stages was 3.0%, 7.1%, 12.4%, 40.4%, and 67.0% (p < 0.001), respectively. After
multivariable adjustment, each higher SCAI shock stage was associated with increased hospital mortality (adjusted odds
ratio: 1.53 to 6.80; all p < 0.001) compared with SCAI shock stage A, as was CA (adjusted odds ratio: 3.99; 95%
confidence interval: 3.27 to 4.86; p < 0.001). Results were consistent in the subset of patients with acute coronary
syndrome or heart failure.
CONCLUSIONS When assessed at the time of CICU admission, the SCAI CS classification, including presence or absence
of CA, provided robust hospital mortality risk stratification. This classification system could be implemented as a clinical
and research tool to identify, communicate, and predict the risk of death in patients with, and at risk for, CS.
(J Am Coll Cardiol 2019;74:2117–28) © 2019 by the American College of Cardiology Foundation.
C ardiogenic shock (CS) continues to be associ-
ated with high rates of morbidity and
mortality, posing a therapeutic challenge
for clinicians (1–4). Although the mortality among
patients with CS may be decreasing over time,
short-term mortality rates remain 35% to 40% in
recent studies (1–9). Other than culprit vessel revas-
cularization for patients with acute myocardial
From the aDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota; bDivision of Pulmonary and Critical Care
Medicine, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota; cDepartment of Critical Care Medicine and
Division of Cardiology, Department of Medicine, University of Alberta Hospital, Edmonton, Alberta, Canada; dCarl and Edyth
Lindner Center for Research and Education, Christ Hospital Health Network, Cincinnati, Ohio; eDepartment of Cardiovascular
Medicine, Cleveland Clinic, Cleveland, Ohio; fWestchester Heart and Vascular Institute, Westchester Medical Center and New York
Medical College, Valhalla, New York; and the gSentara Heart Hospital, Advanced Heart Failure Center and Eastern Virginia Medical
School, Norfolk, Virginia. Dr. Baran has served as a consultant for Abiomed, Abbott, Getinge, and LivaNova; and has served as a
speaker for Novartis. All other authors have reported that they have no relationships relevant to the contents of this paper to
disclose.
Manuscript received May 22, 2019; revised manuscript received July 5, 2019, accepted July 7, 2019.
ISSN 0735-1097/$36.00 https://doi.org/10.1016/j.jacc.2019.07.077
2118 Jentzer et al.
Shock Classification Stratifies Mortality Risk
ABBREVIATIONS infarction (MI), no other intervention has
AND ACRONYMS
demonstrated an improvement in short-
term survival among patients with CS, and
ACS = acute coronary
syndrome
no established beneficial therapies exist for
patients with non-MI etiologies
AKI = acute kidney injury
(1,5–9). A recent scientific statement from
APACHE = Acute Physiology
the American Heart Association highlighted
and Chronic Health Evaluation
BP = blood pressure
several potential priorities for the future of
CS research, to address the limited therapeu-
CA = cardiac arrest
tic options and uncertainty about the efficacy
CCI = Charlson Comorbidity
of standard treatment modalities in CS (1).
Index
CI = confidence interval SEE PAGE 2129
CICU = cardiac intensive care
unit Although diagnostic criteria for CS have
CS = cardiogenic shock been clearly defined in the literature, a major
gap in the field of CS research has been the
ECMO = extracorporeal
membrane oxygenation lack of a standard schema to uniformly
HF = heart failure characterize CS severity across
MCS = mechanical circulatory protocols and individual centers (1). CS pop-
support ulations encompass a broad spectrum of he-
MI = myocardial infarction modynamic derangement ranging
OR = odds ratio isolated hypoperfusion that is easily reversed
with initial therapies to refractory shock with
SCAI = Society for
Cardiovascular Angiography multiorgan failure and hemodynamic
and Intervention
collapse (1). Patients with differing degrees of
VIS = vasoactive-inotropic shock severity may have varying respon-
score
siveness to therapeutic interventions and
different clinical outcomes, yet they are considered
the same for the purposes of clinical trial and registry
enrollment, leading to substantial heterogeneity in
CS study populations. Multiple risk scores exist to
predict mortality in patients with CS, but these apply
primarily to CS complicating acute MI and the need
for multiple input variables reduces their clinical
applicability (10,11). Although these scores can pro-
vide mortality risk stratification, they fail to provide
meaningful characterization of the severity of CS in a
way that can be easily communicated between pro-
viders and inform treatment and transfer decisions.
Prior studies have failed to determine the effects that
overall illness severity may have on the risk-benefit
profile of available therapeutic interventions (7–11).
To overcome these limitations, the Society for
Cardiovascular Angiography and Intervention (SCAI)
developed an expert consensus statement, endorsed
by multiple relevant societies, proposing a novel CS
classification scheme, which categorizes patients
with or at risk of CS into worsening stages of hemo-
dynamic compromise for the purposes of facilitating
patient care and research (12). The SCAI CS classifi-
cation consensus statement describes 5 stages of CS,
each of which may have an “A” modifier signifying
the occurrence of cardiac arrest (CA) (12). This clas-
sification schema was developed based on expert
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JACC VOL. 74, NO. 17, 2019
OCTOBER 29, 2019:2117–28
T A B L E 1 Study Definitions of Hypotension, Tachycardia,
Hypoperfusion, Deterioration, and Refractory Shock
Term Definition
of CS Hypotension/ Presence of any of the following criteria:
tachycardia
Admission systolic BP <90 mm Hg

Minimum systolic BP <90 mm Hg during
first 1 h

Admission MAP <60 mm Hg

Minimum MAP <60 mm Hg during first 1 h

Admission HR >100 beats/min

Maximum HR >100 beats/min during first 1 h

Admission HR > admission systolic BP

Mean HR > mean systolic BP during first 1 h
Hypoperfusion Presence of any of the following criteria:

Admission lactate >2 mmol/l

Urine output <720 ml during first 24 h

Creatinine increased by $0.3 mg/dl during
first 24 h
Deterioration Presence of any of the following criteria:

Maximum lactate > admission lactate

Number of vasoactives during first 24 h
> number of vasoactives during first 1 h
research
Maximum VIS during first 24 h > VIS during
first 1 h

Maximum NEE during first 24 h > NEE during
first 1 h
Refractory shock Presence of any of the following criteria:
from

Mean systolic BP during first 1 h <80 and on
vasoactives

Mean systolic MAP during first 1 h <50 and on
vasoactives

Number of vasoactives during first 1 h >2

Number of vasoactives during first 1 h >1 and
IABP during first 24 h

Admission lactate $10 mmol/l
VIS is calculated as using vasoactive drug doses (in mg/kg/min), as follows:
VIS ¼ dobutamine þ dopamine þ (10 * phenylephrine þ milrinone) þ
(100 * [epinephrine þ norepinephrine]) þ (10,000 * units/kg/min vasopressin).
NEE is calculated using the dose equivalency as follows: 0.1 mg/kg/min
norepinephrine ¼ 0.1 mg/kg/min epinephrine ¼ 15 mg/kg/min dopamine ¼ 1 mg/kg/min
phenylephrine ¼ 0.04 U/min vasopressin.
BP ¼ blood pressure; HR ¼ heart rate; IABP ¼ intra-aortic balloon pump;
MAP ¼ mean arterial pressure; NEE ¼ norepinephrine-equivalent vasopressor
dose; VIS ¼ vasoactive-inotropic score.
consensus opinion and its ability to discriminate
among levels of mortality risk in critically ill patients
remains to be established. The goal of this study was
to examine the construct validity of the SCAI CS
staging schema by demonstrating the ability of a
simple functional classification of SCAI shock stages
at the time of cardiac intensive care unit (CICU)
admission to predict mortality in unselected CICU
patients.
METHODS
STUDY POPULATION. The Institutional Review
Board of the Mayo Clinic (IRB # 16-000722) approved
the study as posing minimal risk to patients, and it
was performed under a waiver of informed consent.
We analyzed a database of consecutive unique adult
patients $18 years of age admitted to the CICU at
Mayo Clinic Hospital St. Mary’s Campus between
January 1, 2007, and December 31, 2015 (13–15). The
JACC VOL. 74, NO. 17, 2019 Jentzer et al. 2119
OCTOBER 29, 2019:2117–28 Shock Classification Stratifies Mortality Risk

C ENTR AL I LL U STRA T I O N Definitions of SCAI Shock Stages A Through E, With Associated Cardiac Intensive Care
Unit and Hospital Mortality in Each SCAI Shock Stage

Cardiogenic Shock Stage Study Definition Observed Mortality in Overall Cohort

Stage A (”At risk”) Neither hypotension/tachycardia nor

hypoperfusion
Stage B (”Beginning”) Hypotension/tachycardia
WITHOUT hypoperfusion
Stage C (”Classic”) Hypoperfusion WITHOUT
deterioration
Stage D (”Deteriorating)” Hypoperfusion WITH deterioration
NOT refractory shock

0%

%
10

20

30

40

50

60

70
Stage E (”Extremis“) Hypoperfusion WITH deterioration
Cardiac Intensive Care Unit Mortality
AND refractory shock Hospital Mortality

Jentzer, J.C. et al. J Am Coll Cardiol. 2019;74(17):2117–28.

Cardiac intensive care unit and hospital mortality increased as a function of higher Society for Cardiovascular Angiography and Intervention shock stage.

Mayo Clinic CICU is a closed, 16-bed unit serving
critically ill cardiac medical patients. Post-operative
cardiac surgery patients and patients receiving
extracorporeal membrane oxygenation (ECMO) sup-
port are cared for in a separate cardiovascular surgical
intensive care unit. To minimize the risk of survival
and treatment biases associated with CICU read-
mission, only data from each patient’s first CICU
admission were analyzed. According to Minnesota
state law statute 144.295, patients may decline
authorization for inclusion in observational research
studies; patients who declined Minnesota Research
Authorization were excluded from the study.
DATA SOURCES. We recorded demographic, vital
sign, laboratory, clinical, and outcome data, as well
as procedures and therapies performed during the
CICU and hospital stay, as previously described;
radiographic, invasive hemodynamic, and physical
examination data were not available (13–15). All rele-
vant data were extracted electronically from the
medical record using the Multidisciplinary Epidemi-
ology and Translational Research in Intensive Care
Data Mart, a repository storing clinical data from all
intensive care unit admissions at the Mayo Clinic
Rochester (16). The admission value of all vital signs,
clinical measurements, and laboratory values was
defined as either the first value recorded after CICU
admission or the value recorded closest to CICU
admission. In addition, vital signs were recorded
every 15 min during the first hour after CICU admis-
sion. Peak vasoactive medication (vasopressor and
inotrope) doses were used to calculate the vasoactive-
inotropic score and norepinephrine-equivalent vaso-
pressor dose (17–19). Admission diagnoses included
all International Classification of Diseases-9th

T A B L E 2 Definition of CS Stages Used in this Study, Based on the SCAI Consensus Statement Classification

CS Stage SCAI Definition

Stage A (“at risk”)
Stage B (“beginning”)
Stage C (“classic”)
Stage D (“deteriorating)”
Stage E (“extremis”)
Patients without CS who are hemodynamically stable but have acute cardiovascular disease putting them at risk of developing CS
Patients without CS who display hemodynamic instability, including hypotension and/or tachycardia, but with normal perfusion
Patients with CS, manifested by hypoperfusion (lactic acidosis, oliguria, cool/clammy periphery, or altered mentation) requiring
intervention
Patients with CS whose hemodynamic instability and/or hypoperfusion fails to respond to initial interventions
Patients with CS and overt or impending circulatory collapse, including CA with ongoing resuscitation

Adapted with permission from Baran et al. (12).

CA ¼ cardiac arrest; CS ¼ cardiogenic shock; SCAI ¼ Society for Cardiovascular Angiography and Intervention.

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2120 Jentzer et al. JACC VOL. 74, NO. 17, 2019

Shock Classification Stratifies Mortality Risk OCTOBER 29, 2019:2117–28

F I G U R E 1 Study Inclusion and Exclusion Criteria and Distribution of SCAI Shock Stages

All CICU admissions

between January 1, 2007
and April 30, 2018
(n = 12,904)

Excluded 2,900 admissions:

• 1,877 readmissions
• 755 no research authorization
• 268 admitted outside the study period

Final study population

(n = 10,004)

Stage A Stage B Stage C Stage D Stage E

(n = 4,602) (n = 2,998) (n = 1,575) (n = 732) (n = 97)

The final study population included 10,004 unique patients. CICU ¼ cardiac intensive care unit; SCAI ¼ Society for Cardiovascular Angiography
and Intervention.

Revision diagnostic codes recorded on the day of
CICU admission and the day before or after CICU
admission; these admission diagnoses were not
mutually exclusive, and the primary admission diag-
nosis could not be determined. Admission diagnoses
of interest included acute coronary
(ACS), heart failure (HF), supraventricular tachy-
cardia, atrial fibrillation, ventricular
ventricular tachycardia, shock, CA,
failure, and sepsis.
The APACHE (Acute Physiology and Chronic Health
Evaluation)-III score, APACHE-IV predicted hospital
mortality, and Sequential Organ Failure Assessment
score were automatically calculated for all patients
using data from the first 24 h of CICU admission using
previously validated electronic algorithms,
missing variables imputed as normal as the default
(13–15,20–22). The Charlson Comorbidity Index (CCI)
and individual comorbidities were determined from
the medical record using a previously validated elec-
tronic algorithm (23). Severe acute kidney injury (AKI)
during the CICU stay was defined as doubling of serum
creatinine from baseline, increase in serum creatinine
to $4.0 mg/dl, or new dialysis initiation; patients with
a prior history of dialysis were excluded from this
analysis (14).
DEFINITION OF SHOCK STAGES. We defined hypo-
tension or tachycardia, hypoperfusion, deterioration,
and refractory shock using data from CICU admission
through the first 24 h in the CICU (Table 1). Hypo-
tension and tachycardia were defined within the first
syndrome 1 h of CICU admission. The definition of hypo-
perfusion included an elevated lactate level on
fibrillation, admission or AKI developing within 24 h after
respiratory admission. Deterioration was defined as increasing
vasoactive drug requirements after the first hour or a
rising lactate level after admission. We used prag-
matic and simplified definitions to divide patients
into the 5 SCAI shock stages with increasing severity
(A through E) using combinations of these variables
(Central Illustration). Importantly, the SCAI shock
with classification system (Table 2) involves details such as
rapid escalation of inotropes or addition of temporary
mechanical circulatory support (MCS) devices, which
were not available in the database (12) Late deterio-
ration was defined as increasing vasopressor re-
quirements after 24 h.
STATISTICAL ANALYSIS. The primary endpoint was
all-cause hospital mortality; secondary endpoints
included CICU mortality. Hospital disposition and all-
cause mortality were determined using electronic
review of medical records. Categorical variables are

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JACC VOL. 74, NO. 17, 2019 Jentzer et al. 2121
OCTOBER 29, 2019:2117–28 Shock Classification Stratifies Mortality Risk

T A B L E 3 Baseline Characteristics, Comorbidities, Admission Diagnoses, and Therapies of Patients According to SCAI Shock Stage

With Data, % Stage A (n ¼ 4,602) Stage B (n ¼ 2,998) Stage C (n ¼ 1,575) Stage D (n ¼ 732) Stage E (n ¼ 97) p Value

Demographics
Age, yrs 100.0 67.1  14.7 66.4  15.7 69.9  16.0 68.7  14.1 68.3  14.7 <0.001
Female 100.0 1,562 (33.9) 1,216 (40.6) 654 (41.5) 278 (38.0) 36 (37.1) <0.001
White 100.0 4,289 (93.2) 2,779 (92.7) 1,430 (90.8) 659 (90.0) 79 (81.4) <0.001
Comorbidities
Charlson Comorbidity Index 99.8 2.1  2.5 2.5  2.6 2.8  2.8 3.0  2.8 2.1  2.6 <0.001
History of MI 99.8 914 (19.9) 581 (19.4) 311 (19.8) 160 (21.9) 14 (14.4) 0.79
History of HF 99.8 746 (16.2) 638 (21.3) 339 (21.6) 212 (29.0) 18 (18.6) <0.001
History of diabetes mellitus 99.8 1,222 (26.6) 851 (28.5) 483 (30.8) 257 (35.2) 24 (24.7) <0.001
History of CKD 99.8 770 (16.8) 604 (20.2) 418 (26.6) 221 (30.2) 18 (20.4) <0.001
Prior dialysis 100.0 131 (2.8) 130 (4.3) 192 (12.2) 107 (14.6) 11 (11.3) <0.001
Admission ICD-9 diagnoses*
ACS 99.0 2,111 (46.4) 1,172 (39.4) 634 (40.7) 300 (41.3) 50 (52.6) <0.001
HF 99.0 1,675 (36.8) 1,562 (52.5) 758 (48.7) 513 (70.7) 56 (59.0) <0.001
Cardiac arrest 99.0 330 (7.3) 311 (10.5) 219 (14.1) 280 (38.6) 53 (55.8) <0.001
Shock 99.0 217 (4.8) 449 (15.1) 166 (10.7) 429 (59.1) 88 (92.6) <0.001
Respiratory failure 99.0 506 (11.1) 660 (22.2) 389 (25.0) 460 (63.4) 64 (67.4) <0.001
Sepsis 99.0 102 (2.2) 205 (6.9) 100 (6.4) 163 (22.4) 35 (36.8) <0.001
AF/SVT 99.0 1,165 (25.6) 1,150 (38.7) 571 (36.7) 304 (41.9) 30 (31.6) <0.001
VT/VF 99.0 665 (14.6) 516 (17.4) 247 (15.9) 158 (21.8) 22 (23.2) <0.001
Therapies and procedures
Vasoactives first 1 h 100.0 126 (2.7) 339 (11.3) 90 (5.7) 249 (34.0) 81 (83.5) <0.001
Number of vasoactives first 1 h 100.0 0.0  0.2 0.1  0.4 0.1  0.3 0.4  0.6 1.4  1.0 <0.001
VIS first 1 h 99.1 0.2  1.6 1.3  10.5 1.4  12.1 5.4  15.3 30.1  46.7 <0.001
NEE first 1 h 100.0 0.00  0.01 0.01  0.10 0.01  0.12 0.05  0.15 0.29  0.47 <0.001
Invasive ventilator first 24 h 100.0 257 (5.6) 419 (14.0) 232 (14.7) 417 (57.0) 73 (75.3) <0.001
Dialysis 100.0 119 (2.6) 138 (4.6) 72 (4.6) 137 (18.7) 21 (21.6) <0.001
CRRT 100.0 9 (0.2) 30 (1.0) 23 (1.5) 94 (12.8) 11 (11.3) <0.001
IABP during hospitalization 100.0 266 (5.8) 330 (11.0) 69 (4.4) 162 (22.1) 38 (39.2) <0.001
Impella 100.0 5 (0.1) 7 (0.2) 4 (0.2) 3 (0.4) 2 (2.1) 0.004
ECMO 100.0 15 (0.3) 28 (0.9) 8 (0.5) 16 (2.2) 5 (5.2) 0.02
PAC 100.0 239 (5.2) 245 (8.2) 49 (3.1) 163 (22.3) 25 (25.8) <0.001
Coronary angiogram 100.0 2,694 (58.5) 1,471 (49.1) 720 (45.7) 349 (47.7) 50 (51.6) <0.001
PCI 100.0 1,834 (39.8) 932 (31.1) 430 (27.3) 205 (28.0) 26 (26.8) <0.001
RBC transfusion 100.0 308 (6.7) 403 (13.4) 197 (12.5) 228 (31.2) 37 (28.1) <0.001

Values are mean  SD or n (%), unless otherwise indicated. The p value is for the trend across SCAI shock stages A to E. *Admission diagnoses are not mutually exclusive and sum to >100%.
ACS ¼ acute coronary syndrome; AF ¼ atrial fibrillation; CICU ¼ cardiac intensive care unit; CKD ¼ chronic kidney disease; CRRT ¼ continuous renal-replacement therapy; ECMO ¼ extracorporeal membrane
oxygenation; HF ¼ heart failure; ICD-9 ¼ International Classification of Diseases-9th Revision; MI ¼ myocardial infarction; PAC ¼ pulmonary artery catheter; PCI ¼ percutaneous coronary intervention;
RBC ¼ red blood cell; SVT ¼ supraventricular tachycardia; VF ¼ ventricular fibrillation; VT ¼ ventricular tachycardia; other abbreviations as in Tables 1 and 2.

reported as number and percentage and the Pearson
chi-square test was used to compare groups. Contin-
uous variables are reported as mean  SD. Trends
across the SCAI shock stages were determined using
linear regression. Logistic regression was used to
determine the association between the SCAI shock
stages and hospital mortality before and after adjust-
ing for age, sex, CCI, APACHE-IV predicted hospital
mortality, admission diagnosis of CA, and the use of
vasoactive medications, intra-aortic balloon pump,
coronary angiography, percutaneous coronary inter-
vention, and mechanical ventilation. Discrimination
was assessed using the area under the receiver-
operating characteristic curve (C-statistic) value.
Two-tailed p values <0.05 were considered statisti-
cally significant. Statistical analyses were performed
using JMP Pro version 14.1.0 (SAS Institute, Cary,
North Carolina).
RESULTS
STUDY POPULATION. We screened 12,904 adult ad-
missions to the CICU during the study period and
excluded 2,900 patients (1,877 readmissions, 755 pa-
tients without Minnesota Research Authorization,
and 268 patients whose admission did not occur
entirely within the study period), as demonstrated in
Figure 1 (13–15). The final study population of 10,004

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2122 Jentzer et al. JACC VOL. 74, NO. 17, 2019

Shock Classification Stratifies Mortality Risk OCTOBER 29, 2019:2117–28

T A B L E 4 Severity of Illness Scores, Vital Signs, and Laboratory Data of Patients According to SCAI Shock Stage

With Data, % Stage A (n ¼ 4,602) Stage B (n ¼ 2,998) Stage C (n ¼ 1,575) Stage D (n ¼ 732) Stage E (n ¼ 97) p Value

Severity of illness
APACHE-III score 100.0 51.3  18.2 60.8  20.4 69.5  24.4 97.4  31.5 118.5  38.8 <0.001
APACHE-IV predicted hospital mortality, % 100.0 9.9  11.6 15.8  16.7 22.0  20.7 48.4  28.1 64.8  27.8 <0.001
Day 1 SOFA score 99.9 2.3  2.0 3.4  2.7 4.4  2.9 9.1  3.9 11.4  3.9 <0.001
Severe AKI 89.2 257 (6.1) 333 (12.4) 233 (17.8) 269 (44.2) 40 (49.4) <0.001
Late deterioration 100.0 188 (4.1) 190 (6.3) 108 (6.9) 205 (28.0) 17 (17.5) <0.001
Admission vital sign data
Systolic blood pressure, mm Hg 99.4 130.8  22.9 114.4  26.1 123.0  27.7 113.8  27.9 99.8  25.3 <0.001
Diastolic blood pressure, mm Hg 96.2 72.1  14.5 67.1  18.6 68.8  17.8 65.7  19.5 57.6  19.4 <0.001
Mean arterial pressure, mm Hg 96.2 87.2  15.1 79.6  19.6 83.1  18.9 79.9  20.9 70.1  20.9 <0.001
Heart rate, beats/min 99.4 72.4  13.9 93.1  26.8 84.8  25.5 89.4  24.7 95.5  27.9 <0.001
Shock index* 99.4 0.57  0.15 0.84  0.29 0.72  0.28 0.83  0.29 1.04  0.38 <0.001
Respiratory rate, breaths/min 95.9 17.3  5.2 19.1  6.0 19.3  5.9 20.2  5.9 21.8  6.5 <0.001
Pulse oximetry, % 99.4 96.6  4.2 95.6  5.6 95.2  7.3 93.2  9.0 86.5  16.8 <0.001
Glasgow Coma Scale 97.3 14.5  2.0 13.9  2.9 13.6  3.3 9.8  5.1 8.3  5.1 <0.001
Urine output first 24 h, l 97.0 2.16  1.10 2.26  1.42 1.02  1.12 1.25  1.33 1.41  2.41 <0.001
Admission laboratory data
Creatinine, mg/dl 96.3 1.2  0.8 1.3  1.0 1.7  1.7 1.9  1.4 1.9  1.2 <0.001
BUN, mg/dl 96.0 23.5  16.4 27.0  18.9 30.0  20.4 36.0  23.1 34.6  20.5 <0.001
ALT, U/ml 46.5 51.9  139.5 76.2  222.2 127.3  529.8 270.8  675.0 644.5  1211.5 <0.001
Peak troponin T, mg/dl 63.3 1.8  3.3 1.7  3.2 1.8  3.4 3.3  6.9 4.0  6.5 <0.001
Hemoglobin, g/l 96.4 12.5  2.0 11.9  2.2 11.9  2.3 11.8  2.5 11.6  2.5 <0.001
Arterial pH 32.3 7.39  0.08 7.36  0.10 7.36  0.10 7.30  0.11 7.20  0.15 <0.001
Bicarbonate, mEq/l 96.9 24.6  3.7 23.9  4.4 23.4  4.6 21.2  5.3 16.7  6.5 <0.001
Anion gap, mEq/l 89.3 11.0  2.9 11.5  3.2 12.6  3.8 14.4  4.3 20.6  8.7 <0.001
Lactate, mmol/l 21.3 1.2  0.4 1.3  0.4 3.0  2.3 3.6  2.3 10.6  5.1 <0.001

Values are mean  SD or n (%), unless otherwise indicated. The p value is for the trend across SCAI shock stages A to E. *Shock index is defined as the ratio of heart rate to systolic blood pressure.
AKI ¼ acute kidney injury; ALT ¼ alanine aminotransferase; APACHE ¼ Acute Physiology and Chronic Health Evaluation; BUN ¼ blood urea nitrogen; SCAI ¼ Society for Cardiovascular Angiography and
Intervention; SOFA ¼ Sequential Organ Failure Assessment.

unique patients had a mean age of 67.4  15.2 years,
including 3,746 (37.4%) women. The mean CCI was
2.4  2.6 and the mean APACHE-IV predicted hospital
mortality was 16.9  20.0% overall. Admission di-
agnoses (not mutually exclusive) included ACS in
4,267 (43.1%) patients, HF in 4,564 (46.1%) patients,
and CA in 1,193 (12.1%) patients; 2,704 (27.3%) pa-
tients had neither ACS nor HF as an admis-
sion diagnosis.
A total of 2,468 (24.7%) patients received vasoac-
tive drugs during the CICU stay, including vasopres-
sors in 2,090 (20.9%) and inotropes in 928 (9.3%).
Among patients receiving vasoactive drugs, 1,182
(47.9%) received >1 vasoactive drug. An intra-aortic
balloon pump was placed during the CICU stay in
865 (8.6%) patients and Impella (Abiomed, Danvers,
Massachusetts) or ECMO support was used during the
hospitalization in 21 (0.2%) and 72 (0.7%) patients,
respectively.
Hypotension or tachycardia during the first hour in
the CICU was present in 4,367 (43.7%) patients,
including 2,545 (25.4%) who
hypotension and 2,956 (29.5%) who met criteria for
tachycardia; 1,134 (11.3%) patients met criteria for
both hypotension and tachycardia. Hypoperfusion
was present in 2,404 (24.0%) patients, including an
admission lactate level >2 mmol/l in 888 (41.6%) of
2,135 patients with available data. Deterioration
within 24 h of admission occurred in 2,075 (20.7%)
patients, and refractory shock was identified in 153
(1.5%) patients. Late deterioration after 24 h occurred
in 708 (7.1%) patients.
The proportion of patients with SCAI shock stages
A through E were 46.0%, 30.0%, 15.7%, 7.3%, and
1.0%, respectively (Figure 1). Baseline demographics,
comorbidities, admission diagnoses, and critical care
therapies varied significantly across the SCAI shock
stages (Table 3). The prevalence of CA increased
across the SCAI shock stages, from 7.3% in stage A to
55.8% in stage E. As the SCAI shock stage increased,
there were more extensive vital sign and laboratory
abnormalities, higher severity of illness scores, and
more frequent AKI (Table 4). The use and dosage of
met criteria for vasoactive medications and supportive therapies

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JACC VOL. 74, NO. 17, 2019 Jentzer et al. 2123
OCTOBER 29, 2019:2117–28 Shock Classification Stratifies Mortality Risk

F I G U R E 2 Hospital Mortality as a Function of SCAI Shock Stage Among Patients With and Without an Admission Diagnosis of CA

80%

70%
Observed Hospital Mortality (%)

60%

50%

40%

30%

20%

10%

0%
Stage A Stage B Stage C Stage D Stage E
SCAI Shock Stage

No Admission Diagnosis of CA Admission Diagnosis of CA

Hospital mortality was higher among patients with an admission diagnosis of cardiac arrest (CA) in each Society for Cardiovascular
Angiography and Intervention (SCAI) shock stage (all p < 0.001).

including mechanical ventilation, MCS, and dialysis
increased across the SCAI shock stages (Table 4). The
prevalence of late deterioration increased as a func-
tion of SCAI shock stage, being highest in SCAI shock
stage D (Table 4).
CICU AND HOSPITAL MORTALITY. There was a step-
wise increase in unadjusted CICU and hospital mor-
tality with each higher SCAI shock stage in the overall
population, with hospital mortality rising from 3.0%
in SCAI shock stage A to 67.0% in SCAI shock stage E
(p < 0.001) (Central Illustration). Unadjusted hospital
mortality was higher among patients with CA at each
SCAI shock stage (Figure 2) (all p < 0.001). The same
stepwise increase in hospital mortality was seen in
patients with ACS and HF and in patients without a
diagnosis of either ACS or HF (Figure 3). Patients with
late deterioration had higher mortality overall (31.4%
vs. 7.4%; p < 0.001), and in each SCAI shock stage
except stage E (Figure 4).
Compared with SCAI shock stage A, the unadjusted
odds ratio (OR) values for hospital mortality in SCAI
shock stages B through E were 2.44, 4.56, 21.80, and
65.22, respectively. The unadjusted OR value for
hospital mortality was 12.17 (95% confidence interval
[CI]: 10.34 to 14.31; p < 0.001) in patients meeting
criteria for SCAI shock stage D or E, compared with
SCAI shock stages A through C. The SCAI shock clas-
sification itself had an area under the receiver-
operating characteristic curve value of 0.765 for
hospital mortality overall, 0.775 among patients with
ACS, and 0.732 among patients with HF.
After multivariable adjustment, each higher SCAI
shock stage was associated with increased hospital
mortality compared with SCAI shock stage A (all
p < 0.001), as was CA (adjusted OR: 3.99; 95% CI: 3.27
to 4.86, 95% CI; p < 0.001); the final multivariable
model area under the receiver-operating character-
istic curve value was 0.883 in the overall population.
Compared with SCAI shock stage A, the adjusted OR
values for hospital mortality in SCAI shock stages B
through E were 1.53, 2.62, 3.07, and 6.80, respectively
(Figure 5). Each higher SCAI shock stage was associ-
ated with higher adjusted hospital mortality

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2124 Jentzer et al.
Shock Classification Stratifies Mortality Risk
F I G U R E 3 Hospital Mortality as a Function of SCAI Shock Stage
80%
70%
Observed Hospital Mortality
60%
50%
40%
30%
20%
10%
0%
ACS
(n = 4,267)
Stage A
Hospital mortality as a function of Society for Cardiovascular Angiography and Intervention (SCAI) shock stage among patients with acute
coronary syndrome (ACS) (left), heart failure (HF) (middle), or neither ACS nor HF (right). Hospital mortality increased as a function of higher
SCAI shock stage in patients with ACS or HF.
compared with SCAI shock stage A among patients
with ACS (all p < 0.001), HF (all p < 0.001), and
neither ACS nor HF (all p < 0.001). Likewise, CA was
associated with higher adjusted hospital mortality in
each of these subgroups (all p < 0.001).
DISCUSSION
Using a large cohort of unselected CICU patients, we
validated the association between the
described SCAI shock classification and hospital
mortality. We stratified patients into 5 SCAI shock
stages at the time of CICU admission, reflecting a
continuum of increasing shock severity using a
simplified definition based on hypotension or tachy-
cardia, hypoperfusion, deterioration, and refractory
shock, which can be easily applied in clinical practice.
This functional SCAI shock stages classification
effectively stratified mortality risk and performed
similarly in patients with admission diagnoses of ACS
and HF, even when adjusting for the higher illness
severity and greater use of hemodynamic support at
higher shock stages. Patients with refractory shock
(SCAI shock stage E) had >20-fold higher crude
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JACC VOL. 74, NO. 17, 2019
OCTOBER 29, 2019:2117–28
HF Neither ACS nor HF
(n = 4,564) (n = 2,704)
Stage B Stage C Stage D Stage E
hospital mortality than hemodynamically stable pa-
tients without shock (SCAI shock stage A). An
admission diagnosis of CA increased the risk of hos-
pital mortality among patients with each SCAI shock
stage, supporting its inclusion as an effect modifier in
the SCAI shock classification schema. These data
support the validity of the recent SCAI classification
of CS stages for mortality risk stratification as a
framework for future CS clinical practice and
recently research. Our examination of a mixed CICU cohort
allowed us to demonstrate the predictive ability of
this classification system in patients with diagnoses
of ACS and HF, which are the dominant causes of CS,
as well as in patients without these diagnoses. The
strong association between SCAI shock stages and
mortality in a heterogeneous CICU population, even
after adjustment for known predictors of mortality,
emphasizes the robustness of this classification sys-
tem and its potential to be applied in other critically
ill patient cohorts.
The SCAI shock classification was developed using
expert consensus for the purpose of describing CS
severity to clarify communication of patient status
between providers in different care settings to
JACC VOL. 74, NO. 17, 2019
OCTOBER 29, 2019:2117–28
facilitate patient triage and selection for advanced
therapies (12). In addition, the SCAI classification of
CS stages was designed to facilitate clinical research
by simplifying the heterogeneity inherent to CS
populations and help determine whether treatment
interactions exist as a function of CS severity. A
similar classification problem was addressed by the
development of the INTERMACS (Interagency Regis-
try for Mechanically Assisted Circulatory Support)
profiles, which subdivided patients with advanced
HF into clinically relevant groups to determine their
need for durable MCS (24). In essence, most patients
with CS would typically be classified as INTERMACS
profile 1 (“crash and burn”) or 2 (“sliding on ino-
tropes”), and the SCAI classification provides further
granularity by dividing these patients into stages C,
D, and E (12,24). In addition, the INTERMACS profiles
are intended for application at the single time
point of implantation of a durable MCS device and
do not have a construct to assess deterioration of
status.
Nearly one-half of this CICU population was clas-
sified as SCAI shock stage A (“at risk”) and the 3%
observed hospital mortality in this group suggests
that patients without hypotension, tachycardia, or
hypoperfusion at the time of CICU admission have a
favorable prognosis. Crude hospital mortality more
than doubled among patients with evidence of he-
modynamic instability (SCAI shock stage B [“begin-
ning”]), and nearly doubled again among patients
with hypoperfusion (SCAI shock stage C [“classic
shock”]). Crude hospital mortality rose to 40% among
patients with deterioration (SCAI shock stage D
[“deteriorating”]), similar to that observed in recent
randomized controlled trials and observational
studies of CS (2–4,6–9). This suggests that patients
with CS who respond to initial stabilization measures
(SCAI shock stage C) have a relatively favorable
prognosis, while the majority of patients included in
published studies of CS likely meet criteria for SCAI
shock stage D. The marked step-up in short-term
mortality risk among patients with SCAI shock stage
D and E (“extremis”) suggests a potential role for
advanced hemodynamic support options including
MCS in patients demonstrating evidence of deterio-
ration. More than two-thirds of patients classified as
SCAI shock stage E died in the hospital, emphasizing
the need to identify improved therapies for these
highest-risk patients. The prevalence of hemody-
namic deterioration after 24 h increased with higher
SCAI shock stages and was associated with higher
hospital mortality.
CA is common in CS populations and has been
associated with an increased risk of death, yet the
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Jentzer et al. 2125
Shock Classification Stratifies Mortality Risk
F I G U R E 4 Hospital Mortality and SCAI Shock Stage in Patients With and Without Late
Deterioration, Defined as Rising Vasopressor Requirements After 24 h
80%
70%
Observed Hospital Mortality
60%
50%
40%
30%
20%
10%
0%
Stage A Stage B Stage C Stage D Stage E
SCAI Shock Stage
Late Deterioration (n = 708)
No Late Deterioration (n = 9,296)
Hospital mortality was higher among patients with late deterioration in each Society for
Cardiovascular Angiography and Intervention (SCAI) shock stage, except stage E
(all other p < 0.001).
influence of this major risk modifier on therapeutic
responses has not been well studied (7,9,25,26). The
SCAI statement authors clearly emphasize the added
hazard posed by the presence of CA occurring in pa-
tients with or at risk of CS (12). In this cohort, the
prevalence of CA increased substantially with
increasing shock stage, highlighting the correlation
between CA and severe shock in CICU patients. In our
analysis, we clearly demonstrate the added mortality
hazard posed by CA at all levels of shock severity,
validating CA as a prognostically important modifier
in the SCAI shock classification. Shock severity
demonstrated a stepwise association with mortality
in patients with CA, emphasizing the synergistic
mortality effects of concomitant CS and CA in CICU
patients, as previously demonstrated in patients with
acute MI (25). The relative effect of CA on mortality
appeared to be greater among patients with mild or
no shock (SCAI shock stages A through C). Although it
remains clear that the presence of CA among CS pa-
tients is associated with worse outcomes, it is un-
likely that all such events carry the same hazard and
2126 Jentzer et al. JACC VOL. 74, NO. 17, 2019

Shock Classification Stratifies Mortality Risk OCTOBER 29, 2019:2117–28

F I G U R E 5 Adjusted OR Plot for Hospital Mortality

Stage A
(Referent)

Stage B
SCAI Shock Stage

Stage C

Stage D

Stage E

0 1 2 3 4 5 6 7 8 9 10 11 12
Adjusted OR for Hospital Mortality

Adjusted odds ratios (ORs) and 95% confidence intervals for hospital mortality with each Society for Cardiovascular Angiography and
Intervention (SCAI) shock stage derived from multivariable logistic regression, using stage A as referent. Higher SCAI shock stages had
incrementally higher adjusted odds for hospital mortality.

future studies should address whether brief CA epi-
sodes have any prognostic importance and whether
the presence of brain injury from CA modifies the
response to CS therapies (26).
Van Diepen et al. (1) have proposed a “hub-and-
spoke” care model involving transfer to tertiary cen-
ters for patients with CS, as has been instituted for
other high-acuity medical conditions such as trauma.
Uncertainty remains regarding when transfer to a
higher level of care is warranted, and ideally this
should be determined early in the course if a patient
is not responding as expected to initial therapy.
Based on the high risk of mortality after the onset of
hemodynamic deterioration (SCAI shock stage D), we
propose that patients with hypoperfusion (SCAI shock
stage C) who do not rapidly stabilize (i.e., progression
to SCAI shock stage D) should be considered for
transfer to a higher level of care before development
of overt deterioration. The simple functional defini-
tions used in this study could be leveraged by an
electronic medical record system to identify patients
with new onset or increasing severity of shock
or clinical deterioration, to highlight their escalating
mortality risk in real time and facilitate early
transfer or involvement of palliative care services if
indicated (1).
We propose that the relative efficacy of various
therapeutic interventions at each CS stage should be
further explored, as CS severity might determine the
need for and clinical response to specific therapies.
For example, temporary MCS devices can effectively
increase cardiac output in CS, yet none of these
temporary MCS devices has resulted in a proven
improvement in survival in published randomized
clinical trials of CS patients (1,8,9,27). Notwith-
standing their established hemodynamic benefits, the
invasive nature and acquisition costs of temporary
MCS devices emphasize the need to evaluate when
and in whom these devices may be most effective for
improving patient-centered outcomes (1,8,27). We
suspect that each temporary MCS device will have a
different risk-benefit profile at a given CS stage, but
this hypothesis will need to be tested in future
studies.

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JACC VOL. 74, NO. 17, 2019
OCTOBER 29, 2019:2117–28
STUDY LIMITATIONS. Despite its large sample size
and granular data, this study has a number of limi-
tations that are inherent to all retrospective cohort
studies, including the need for prospective validation
and the potential for unmeasured confounders and
missing data to have influenced the results. Owing to
lack of available invasive hemodynamic data, we
cannot be sure to what extent the shock states in this
cohort were cardiogenic in nature. The inclusion of a
mixed CICU population implies that some patients
meeting criteria for shock had noncardiogenic or
mixed shock states, similar to a recent multicenter
CICU registry (4). To focus on the presence of shock
on admission, we defined the shock stages using
variables from within 1 to 24 h of CICU admission,
recognizing that many patients develop CS after
hospital admission; owing to data availability, our
limited definition of late deterioration only included
vasopressor dosage and not worsening SCAI shock
stage (3). We were unable to include prognostically
relevant physical examination findings such as cool
or clammy extremities or altered mental status in our
definition of hypoperfusion; the inclusion of oliguria
and rising creatinine in the definition of hypo-
perfusion is less relevant among patients with end-
stage renal disease (28). In addition, the definition
for SCAI shock stage C includes the requirement for
an intervention to treat hypoperfusion, a criterion we
did not include in our definition of stage C for ease of
application (12). The infrequent use of advanced
temporary MCS devices (e.g., Impella or ECMO) in this
cohort could have influenced the observed mortality,
particularly among patients with higher
severity; nonetheless, the overall utilization of MCS
devices in this population is consistent with national
utilization among patients with CS (29). By using
International Classification of Diseases-Ninth Revi-
sion codes to define admission diagnoses, we were
unable to define the primary admission diagnoses
and could not distinguish in-hospital CA from out-
of-hospital CA. Data regarding timing,
rhythm, and neurologic status of patients with CA
were not available. We grouped patients based on
the presence of ACS without distinguishing between
ACS subtypes, limiting our ability to draw conclu-
sions about CS caused by acute MI. Data regarding
resuscitation status and limitations of therapies were
not available.
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Jentzer et al. 2127
Shock Classification Stratifies Mortality Risk
CONCLUSIONS
In a large, heterogeneous CICU cohort, we demon-
strated the feasibility of classifying patients into 5
shock stages (SCAI shock stages A to E) reflecting
progressively increasing levels of illness severity.
This pragmatic SCAI shock stages classification pro-
vided robust mortality risk stratification in the overall
cohort including patients with ACS and HF, in a
manner that was amplified by the presence of CA.
Despite its limitations, the functional adaptation of
the SCAI shock classification described herein had
very good discrimination for mortality, emphasizing
its validity and practical utility with the potential for
improved risk stratification when rigorously applied.
The simple, intuitive SCAI shock stage definitions we
report herein could be easily applied in clinical
practice by providers with different levels of exper-
tise. We suggest that future CS clinical trials consider
stratifying patients according to SCAI shock stage and
the presence of CA, to ensure consistent outcomes
reporting and to assess whether the effects of the
tested intervention vary by CS stage.
ADDRESS FOR CORRESPONDENCE: Dr. Jacob C.
Jentzer, Department of Cardiovascular Medicine and
Division of Pulmonary and Critical Care Medicine,
Department of Internal Medicine, The Mayo Clinic, 200
First Street SW, Rochester, Minnesota 55905. E-mail:
jentzer.jacob@mayo.edu. Twitter: @davebaran.
shock PERSPECTIVES
COMPETENCY IN PATIENT CARE AND PROCEDURAL
SKILLS: A CS classification system developed by the SCAI can
effectively stratify patients in a CICU, including those with an
ACS or HF, for risk of mortality. Patients with SCAI cardiogenic
shock stages D and E are at higher risk and may benefit from
early transfer to specialized centers offering advanced modalities
arrest
for circulatory support.
TRANSLATIONAL OUTLOOK: Prospective studies using a
systematic approach to shock assessment and management are
needed to determine if the efficacy of various advanced
modalities is related to disease severity.
2128 Jentzer et al.
Shock Classification Stratifies Mortality Risk
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KEY WORDS cardiac intensive care unit,
cardiogenic shock, critical care, mortality,
shock