JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY VOL. 73, NO.

13, 2019

ª 2019 THE AUTHORS. PUBLISHED BY ELSEVIER ON BEHALF OF THE AMERICAN

COLLEGE OF CARDIOLOGY FOUNDATION. THIS IS AN OPEN ACCESS ARTICLE UNDER

THE CC BY-NC-ND LICENSE (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Standardized Team-Based Care for

Cardiogenic Shock
Behnam N. Tehrani, MD,a Alexander G. Truesdell, MD,a,b Matthew W. Sherwood, MD,a Shashank Desai, MD,a
Henry A. Tran, MD,a Kelly C. Epps, MD,a Ramesh Singh, MD,a Mitchell Psotka, MD, PHD,a Palak Shah, MD,a
Lauren B. Cooper, MD,a Carolyn Rosner, NP,a Anika Raja, BS,a Scott D. Barnett, PHD,a Patricia Saulino, RN, MPA,a
Christopher R. deFilippi, MD,a Paul A. Gurbel, MD,a Charles E. Murphy, MD,a Christopher M. O’Connor, MDa

ABSTRACT

BACKGROUND Cardiogenic shock (CS) is a multifactorial, hemodynamically complex syndrome associated with high
mortality. Despite advances in reperfusion and mechanical circulatory support, management remains highly variable and
outcomes poor.

OBJECTIVES This study investigated whether a standardized team-based approach can improve outcomes in CS and
whether a risk score can guide clinical decision making.

METHODS A total of 204 consecutive patients with CS were identified. CS etiology, patient demographic characteristics,
right heart catheterization, mechanical circulatory support use, and survival were determined. Cardiac power output
(CPO) and pulmonary arterial pulsatility index (PAPi) were measured at baseline and 24 h after the CS diagnosis.
Thresholds at 24 h for lactate (<3.0 mg/dl), CPO (>0.6 W), and PAPi (>1.0) were determined. Using logistic regression
analysis, a validated risk stratification score was developed.

RESULTS Compared with 30-day survival of 47% in 2016, 30-day survival in 2017 and 2018 increased to 57.9% and
76.6%, respectively (p < 0.01). Independent predictors of 30-day mortality were age $71 years, diabetes mellitus,
dialysis, $36 h of vasopressor use at time of diagnosis, lactate levels $3.0 mg/dl, CPO <0.6 W, and PAPi <1.0 at 24 h
after diagnosis and implementation of therapies. Either 1 or 2 points were assigned to each variable, and a 3-category risk
score was determined: 0 to 1 (low), 2 to 4 (moderate), and $5 (high).

CONCLUSIONS This observational study suggests that a standardized team-based approach may improve CS out-
comes. A score incorporating demographic, laboratory, and hemodynamic data may be used to quantify risk and guide
clinical decision-making for all phenotypes of CS. (J Am Coll Cardiol 2019;73:1659–69) © 2019 The Authors.
Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

D espite advances in early

cardiogenic shock (CS) remains the most
common cause of in-hospital mortality af-
ter acute myocardial infarction (AMI), with rates
reperfusion,
exceeding 50% for nearly 2 decades (1–4). Several rea-
sons account for these poor outcomes. The short-term
stabilizing effects of vasopressors and inotropes are
counterbalanced by their adverse effects on afterload
and oxygen demand, resulting in end-organ hypoper-
fusion, lactic acidosis, and refractory shock (5). The
intra-aortic balloon pump (IABP) offers minimal he-
modynamic benefit and does not improve outcomes

Listen to this manuscript’s
audio summary by
Editor-in-Chief
Dr. Valentin Fuster on
JACC.org.
From the aINOVA Heart and Vascular Institute, Falls Church, Virginia; and bVirginia Heart, Falls Church, Virginia. Dr. Tehrani has
served as a consultant for Medtronic and Abiomed. Dr. Truesdell has served as a consultant and is a member of the Speakers
Bureau for Abiomed. Dr. Desai is a member of the Speakers Bureau for Abbott and Medtronic; and is a consultant for Abiomed. Dr.
Singh is an advisory board member for Baxter; and a speaker for Baxter and Abbott. Dr. Psotka has served as a consultant for
Amgen, Cytokinetics, and Roivant. Dr. Shah has received grant support from Merck, Medtronic, American Heart Association/
Enduring Hearts; and has served as a consultant for NuPulse CV 5 and Ortho Clinical Diagnostics. Dr. Cooper has received grant
support from Abbott. Dr. deFilippi has received research grants from Roche Diagnostics; has received consulting fees from Abbott
Diagnostics, FujiRebio, Metabolomics, Ortho Diagnostics, Roche Diagnostics, and Siemens Healthcare; has received honoraria
from WebMD; and has received royalties from UpToDate. Dr. Gurbel has received research grants from Amgen, Bayer, Duke
Cardiovascular Research Institute, Haemonetics, Idorsia Inois, Janssen, Merck, and the National Institutes of Health; and has
served as a consultant for Boehringer Ingelheim, Janssen Pharmaceuticals, Bayer, and Merck. All other authors have reported that
they have no relationships relevant to the contents of this paper to disclose. This study was presented as an oral presentation at
the Transcatheter Cardiovascular Therapeutics 30th Annual Scientific Session, September 21 to 25, San Diego, California. William
W. O’Neill, M.D. served as guest associate editor on this paper.

Manuscript received November 29, 2018; revised manuscript received December 12, 2018, accepted December 21, 2018.

ISSN 0735-1097 https://doi.org/10.1016/j.jacc.2018.12.084

1660 Tehrani et al. JACC VOL. 73, NO. 13, 2019

Standardized Team-Based Care in Cardiogenic Shock APRIL 9, 2019:1659–69

ABBREVIATIONS (6). The limitations of these conventional for the management of patients with CS. This task
AND ACRONYMS therapies inspired the development of force performed a comprehensive review of the
rapidly deployable percutaneous axial and current state of CS management (16) and devel-
ADHF = acute decompensated
heart failure
centrifugal flow mechanical circulatory sup- oped a new diagnostic and therapeutic algorithm
port (MCS) devices for use not only in CS (Central Illustration). This algorithm emphasized 5
AMI = acute myocardial
infarction but also in high-risk percutaneous coronary clinical goals: rapid identification of the shock
CPO = cardiac power output intervention (PCI), and acute and chronic state, mandatory invasive hemodynamics, mini-
CS = cardiogenic shock
decompensated heart failure. Although these mizing use of vasopressors and inotropes, early
devices provide superior hemodynamic sup- mechanical support of the left ventricle and/or
IABP = intra-aortic balloon
pump port compared with IABP, clinical trials to right ventricle as appropriate, and, finally, cardiac
MCS = mechanical circulatory date have failed to report any mortality recovery. The protocol was drafted and formalized
support benefit (7). during a 6-month period from July through
PAPi = pulmonary arterial Significant variation also exists in the uti- December 2016.
pulsatility index lization of invasive hemodynamic variables to
pVAD = percutaneous guide therapy. Although clinical trials have DEPLOYMENT OF THE SHOCK TEAM. From January
ventricular assist device
not shown a survival benefit for the empiric 3, 2017, to June 30, 2018, a total of 204 consecutive
RAP = right atrial pressure
use of right heart catheterization (RHC) in an patients admitted to our institution with a diagnosis
RHC = right heart all-comer population, more recent single- of CS were identified and evaluated prospectively.
catheterization
center observational data have reported ben- The clinical and hemodynamic criteria used to di-
RV = right ventricular
efits in the setting of AMI and acute decom- agnose CS were the same as previously defined in the
VA-ECMO = veno-arterial
pensated heart failure (ADHF) CS (8,9). The SHOCK (Should We Emergently Revascularize
extracorporeal membrane
oxygenation most recent scientific statement by the Occluded Coronaries for Cardiogenic Shock) trial (1).
American Heart Association suggests that Clinical criteria included systolic blood
RHC may play an important role in the diagnosis and pressure <90 mm Hg for $30 min (or vasopressors to
management of CS by providing objective hemody- maintain systolic blood pressure $90 mm Hg) and
namic data to complement traditional laboratory evidence of end-organ hypoperfusion. Hemodynamic
markers assessing end-organ perfusion (10). Addi- criteria were Fick cardiac index #1.8 l/min/m 2
tional data suggest that centralizing care of patients without vasopressors (or #2.2 l/min/m 2 with vaso-
with high-acuity cardiovascular conditions such as CS pressors) and a pulmonary capillary wedge
to tertiary care centers with cardiac intensive care pressure $15 mm Hg. Lactic acid levels were
units staffed by multidisciplinary physician teams measured as surrogate markers of end-organ perfu-
may reduce in-hospital mortality (10–13). sion at baseline and 24 h after implementation of
therapies. Patients with both AMI-CS and ADHF-CS
SEE PAGE 1670
were evaluated.
When a patient was suspected to be in CS, the
Despite the growing body of evidence supporting
shock team was activated through a 1-call “shock
timely recognition of CS, hemodynamic monitoring,
line” to gather on-call physicians from 4 different
tailored escalation to MCS, and centralized care,
service lines (interventional cardiology, cardiovas-
variations in practice patterns in CS management
cular surgery, advanced heart failure, and critical
endure and may contribute to persistently high mor-
care) for multidisciplinary consultation and
tality rates (14,15). We hypothesized that the
decision making (16) (Central Illustration). In pa-
deployment of a multidisciplinary “shock team”
tients presenting from out-of-hospital with AMI-CS,
providing timely diagnosis and utilizing standardized
the emergency department physician activated the
protocols would reduce practice variations and
shock team so that they had ample time to mobi-
improve clinical outcomes. We derived a validated
lize the resources. The interventional team pro-
score based on clinical, laboratory, and hemodynamic
ceeded with emergent coronary angiography,
criteria to guide clinical decision making. We further
comprehensive hemodynamic assessment, and pe-
present the longitudinal outcomes of our single-
ripheral vascular evaluation for large-bore MCS
center, high-volume CS program after implementa-
access. The process for shock team activation was
tion of our innovative care model.
the same for non-ACS patients presenting with CS.
METHODS After shock team activation, non-ACS patients were
transferred to the cardiac intensive care unit or
DEVELOPMENT OF A SHOCK TEAM PROTOCOL. In cardiac catheterization laboratory for emergent
2016, we formed a task force to develop a protocol transthoracic echocardiography and RHC to
JACC VOL. 73, NO. 13, 2019 Tehrani et al. 1661
APRIL 9, 2019:1659–69 Standardized Team-Based Care in Cardiogenic Shock

C ENTR AL I LL U STRA T I O N Cardiogenic Shock Algorithm

Patient with suspected cardiogenic shock (CS)

Clinical criteria to rapidly identify shock state:

Systolic blood pressure (SBP) <90 mm Hg for >30 minutes

(or use of inotropes/vasopressors to maintain SBP)
Evidence of end-organ hypoperfusion

Lactate level >2 mmol/l

Activate Shock Team through a one-call line for multidisciplinary discussion:

Interventional Cardiology; Cardiac Surgery; Advanced Heart Failure; Critical Care

Transfer patient to cardiac catheterization lab or cardiac intensive care unit (CICU) for evaluation

If acute decompensated heart failure If acute myocardial infarction cardiogenic

cardiogenic shock (ADHF-CS) suspected: shock (AMI-CS) suspected:
Right heart catheterization Right heart catheterization
Echo Coronary angiography + revascularization
Assessment of peripheral vascular anatomy

Hemodynamic Criteria for Cardiogenic Shock:

Fick cardiac index <1.8 l/min/m2 without inotropes/vasopressors

(or <2.2 l/min/m2 with inotropes/vasopressors)

Pulmonary capillary wedge pressure >15 mm Hg

Cardiac power output (CPO) <0.6 W

PAPi <1.0

If Hemodynamic Criteria are met, consider Percutaneous Mechanical Circulatory Support (PMCS)

Admit Patient to CICU

Daily bedside echocardiograms for patients with PMCS

Frequent neurovascular assessments for patients with PMCS
Serial assessment of end-organ perfusion and hemodynamics: CPO, PAPi and lactate

Evaluation for weaning vs. escalation of support

Tehrani, B.N. et al. J Am Coll Cardiol. 2019;73(13):1659–69.

Schematic representation of the care pathways in the upstream and critical care management of patients with acute myocardial infarction (AMI) and acute
decompensated heart failure (ADHF) cardiogenic shock at the INOVA Heart and Vascular Institute. CPO ¼ [mean arterial pressure x cardiac output]/451;
PAPi ¼ [systolic pulmonary arterial pressure - diastolic pulmonary arterial pressure]/right atrial pressure.
1662 Tehrani et al. JACC VOL. 73, NO. 13, 2019

Standardized Team-Based Care in Cardiogenic Shock APRIL 9, 2019:1659–69

F I G U R E 1 30-Day Survival According to Group and Time Period

100%

82%
80%
62% 72%
Survival Percent 60%
60%
63%

40%
44%

20%
ADHF, β = 6.0, P < 0.2329
AMI, β = 19.0, P < 0.0001
0%
Jan-June, 2017 Jul-Dec, 2017 Jan-Jun, 2018
AMI ADHF

ADHF ¼ acute decompensated heart failure; AMI ¼ acute myocardial infarction.

guide multidisciplinary decision making regarding

pharmacological therapies and percutaneous MCS
T A B L E 1 Clinical and Demographic Characteristics
options.
Acute MI Acute Decompensated In all patients who underwent MCS device im-
(n ¼ 82) HF (n ¼ 122)
plantation, contemporary arterial access techniques
Age, yrs 64.0  11.0 58.4  14.0
were used (17). Based on operator discretion,
Male 58 (70.7) 84 (68.9)
different closure strategies were employed: either
Race
White 47 (57.3) 68 (55.7) dual ProGlide (Abbott Inc., Chicago, Illinois) suture-
African American 8 (9.8) 33 (27.1) based pre-closure followed later by return to the
Other 27 (32.9) 21 (17.2) catheterization laboratory for a crossover balloon
Hispanic 6 (7.3) 7 (5.7) occlusion technique removal, or manual compression
Diabetes mellitus 46 (56.1) 47 (38.5) in patients not undergoing suture-based pre-closure
Index GFR <60 ml/min 46 (56.1) 73 (59.8)
(18,19). After device implantation, a final ipsilateral
Cerebrovascular disease 15 (18.3) 33 (27.0)
femoral run-off angiogram was performed, and if any
Previous MI/PCI/CABG/valve surgery 13 (15.9) 35 (28.7)
Outside transfer 50 (61.0) 56 (45.9)
evidence of compromised limb perfusion was noted,
Pressors at index diagnosis 64 (78.0) 80 (65.6) an ipsilateral antegrade distal perfusion catheter was
Pressors at 24 h 49 (59.8) 64 (52.5) placed. In patients with contraindications to con-
Out-of-hospital cardiac arrest 9 (11.0) 6 (4.9) ventional transfemoral axial-flow MCS placement
In-hospital cardiac arrest 10 (12.2) 5 (4.1) (e.g., left ventricular [LV] thrombus, mechanical
Right heart catheterization 60 (73.2) 107 (87.7)
aortic valve, critical aortic stenosis with valve
Baseline lactate level, mg/dl 4.9  4.3 4.3  3.8
area <0.6 cm 2, moderate to severe aortic insuffi-
Baseline CPO, W 0.5  0.1 0.5  0.2
ciency, severe peripheral arterial disease), the shock
Baseline PAPi 1.2  1.4 1.6  1.3
Lactate at 24 h, mg/dl 3.7  5.5 3.5  5.0
team assessed their candidacy for alternative access
CPO at 24 h, W 0.8  0.2 0.8  0.3 (e.g., percutaneous axillary artery or transcaval ac-
PAPi at 24 h 2.2  1.4 2.2  1.4 cess) or alternate MCS devices such as veno-arterial
Lactate at 24 h $3.0 mg/dl 13 (15.9) 23 (18.9) extracorporeal membrane oxygenation (VA-ECMO)
CPO at 24 h <0.6 W 36 (43.9) 45 (36.9) or IABP as appropriate. Patients with CS supported
PAPi at 24 h <1.0 8 (9.8) 11 (9.0)
with VA-ECMO were also evaluated for concomitant
Values are mean  SD or n (%).
implantation of the percutaneous ventricular assist
CABG ¼ coronary artery bypass grafting; CPO ¼ cardiac power output; HF ¼ heart failure; device (pVAD) Impella CP (Abiomed, Danvers, Massa-
GFR ¼ glomerular filtration rate; MI ¼ myocardial infarction; PAPi ¼ pulmonary arterial pulsatility
index; PCI ¼ percutaneous coronary intervention.
chusetts) to decompress the left ventricle and reduce
afterload (20).
JACC VOL. 73, NO. 13, 2019 Tehrani et al. 1663
APRIL 9, 2019:1659–69 Standardized Team-Based Care in Cardiogenic Shock

T A B L E 2 Clinical Course and Outcomes T A B L E 3 Univariate Odds Ratios and 95% Confidence Intervals for
30-Day Mortality
Acute MI Acute Decompensated
(n ¼ 82) HF (n ¼ 122) Odds Ratio Wald
IABP 35 (42.7) 20 (16.4) (95% Confidence Chi-Square
Interval) Test p Value
Escalation from IABP 17 (48.6) 7 (35.0)
Male 0.85 (0.46–1.58) 0.23 0.61
pVAD only 41 (50.0) 29 (23.8)
Age $71 yrs 3.17 (1.59–6.34) 10.68 <0.01
Impella 2.5 0 (0.0) 1 (3.4)
Index creatinine >2.3 mg/dl 1.96 (1.37–2.80) 13.48 <0.01
Impella CP 40 (97.6) 22 (75.9)
Diabetes mellitus 8.75 (4.51–17.01) 41.01 <0.01
Impella 5.0 0 (0.0) 5 (17.2)
Outside transfer 0.83 (0.47–1.46) 0.51 0.51
Impella RP 1 (2.4) 1 (3.4)
Out-of-hospital cardiac arrest 4.59 (0.55–4.56) 0.75 0.39
VA-ECMO only 3 (3.7) 7 (5.7)
In-hospital cardiac arrest 1.34 (0.45–4.04) 0.28 0.60
pVAD þ VA-ECMO 7 (8.5) 14 (11.5)
Right heart catheterization 0.19 (0.09–0.40) 18.52 <0.01
Impella CP þ VA-ECMO 6 (85.7) 13 (92.9)
pVAD only 1.53 (0.85–2.78) 1.99 0.16
Impella 5.0 þ VA-ECMO 1 (14.3) 1 (7.1)
pVAD þ VA-ECMO 1.37 (0.55–3.43) 0.44 0.50
Dialysis 27 (32.9) 34 (27.9)
VA-ECMO Only 4.42 (1.11–17.65) 4.43 0.04
LVAD or Transplant
IABP 0.64 (0.33–1.27) 1.67 0.20
LVAD 3 (3.7) 13 (10.7)
Escalation from IABP 1.06 (0.44–2.56) 0.02 0.89
Transplant 0 (0.0) 5 (4.1)
Dialysis 19.45 (9.05–41.75) 57.51 <0.01
Stroke 2 (2.4) 4 (3.3)
Pressors at diagnosis >36 h 12.05 (6.02–24.09) 24.58 <0.01
30-day survival 52 (63.4) 78 (63.9)
Previous MI/PCI/CABG/valve surgery 2.65 (1.37–5.15) 8.35 <0.01
Cause of death
Lactate at 24 h $3.0 mg/dl 54.81 (12.61–238.23) 28.41 <0.01
Multiorgan failure 24 (80.0) 35 (79.5)
CPO at 24 h <0.6 W 42.45 (18.55–98.45) 76.73 <0.01
Anoxic brain injury 4 (13.3) 0 (0.0)
PAPi at 24 h <1.0 14.4 (6.96–29.90) 51.47 <0.01
ICH 0 (0.0) 1 (2.3)
RA/PCWP at 24 h >0.63 8.55(3.88–18.85 28.34 <0.01
Other 2 (6.7) 8 (18.2)
RAP at 24 h >15 mm Hg 6.88 (2.89–16.39) 18.94 <0.01
Values are n (%).
IABP ¼ intra-aortic balloon pump; ICH ¼ intracranial hemorrhage; LVAD ¼ left RAP/PCWP ¼ right atrial pressure/pulmonary capillary wedge pressure; other abbreviations as in
ventricular assist device; pVAD ¼ percutaneous ventricular assist device; Tables 1 and 2.
VA-ECMO ¼ veno-arterial extracorporeal membrane oxygenation; other
abbreviations as in Table 1.

undergoing RHC, serum lactate, CPO, and PAPi mea-

In addition to conventional hemodynamic mea-
surements (Online Table 1) and lactate level de-
terminations, cardiac power output
pulmonary arterial pulsatility index (PAPi) were
measured serially. If the patient was determined to
have biventricular failure while supported by the
pVAD, evaluation for right ventricular (RV) support
was undertaken, using either concomitant pVAD or
VA-ECMO. Our team also used algorithms for man-
agement and weaning of VA-ECMO support (Online
Figure 1). Bedside echocardiograms were performed
daily to evaluate heart function and ventricular
assist device positioning. The cardiac intensive care
unit team communicated daily with shock team
members, and recommendations
regarding weaning or escalation of support. In
consultation with the advanced heart failure team,
patients with refractory CS despite
referred for consideration of destination LV assist
device and/or heart transplantation. All patients
were evaluated for survival to 30 days from hospital
discharge.
STATISTICAL ANALYSIS. Data are presented as mean
 SD or frequency and percent. Comparisons were
made by using chi-square analysis. In patients
surements were analyzed at baseline and 24 h after
the CS diagnosis and implementation of therapies.
(CPO) and Cutpoints were determined at 24 h for lactate
(<3.0 mg/dl), CPO (>0.6 W), and PAPi (>1.0) using
individual receiver-operator characteristic curves
with the Youden J statistic.
Given the small number of deaths after discharge
(n ¼ 3), we decided to develop the risk model using a
binary 30-day survival classification rather than a
time-to-event analysis. Using logistic regression,
terms were considered for model inclusion based on
clinical and historical relevance, with the outcome of
interest the probability of 30-day mortality. Parame-
ters for consideration were first assessed at the uni-
were made variate level with a p value criterion of # 0.10. Odds
ratios (ORs) and 95% confidence intervals (CIs) are
presented.
MCS were A multivariate model was run to assess the joint
impact of all statistically significant parameters at the
univariate level. The model was run again after the
exclusion of parameters failing to meet our initial
exclusion criterion; 6 parameters met a similar crite-
rion of 0.10, resulting in a final risk score model of 7
parameters. Age $71 years was included despite a lack
of statistical significance given its large OR and
1664 Tehrani et al. JACC VOL. 73, NO. 13, 2019

Standardized Team-Based Care in Cardiogenic Shock APRIL 9, 2019:1659–69

institutions, and 71% required vasopressor support at

T A B L E 4 Odds Ratios and 95% Confidence Intervals for 30-Day Mortality
the time of diagnosis. At time of presentation, 27% of
Odds Ratio (95% Wald Chi-Square patients were on IABP support, and 44% of those ul-
Confidence Interval) Test p Value Points
timately proceeded to escalation of MCS. CS threshold
Lactate threshold at 79.51 (5.568–*) 10.82 <0.01 2
24 h $3.0 mg/dl markers at 24 h were lactate levels <3.0 mg/dl
Pressors duration from 16.80 (3.03–93.21) 10.42 <0.01 2 (n ¼ 168 [82.4%]), CPO >0.6 W (n ¼ 123 [60.3%]), and
diagnosis >36 h
PAPi >1.0 (n ¼ 185 [90.7%]).
CPO at 24 h <0.6 10.17 (1.70–60.81) 6.45 0.01 2
Diabetes mellitus 8.23 (2.17–31.87) 9.60 <0.01 1 MORTALITY AT 30 DAYS. Before implementation of
Dialysis 5.91 (1.49–23.45) 6.39 0.01 1 the shock team, our baseline survival to 30 days’
PAPi at 24 h <1.0 7.82 (0.97–62.85) 3.74 0.05 1
post-discharge for all CS was 47%. During 2017 and
Age $71 yrs 2.98 (0.75–11.90) 2.38 0.12 1
2018, this rate increased to 58% and 77%, respectively
Total – – 10
(p < 0.001) (Figure 1). The vital status of all patients
Age $71 years was included given clinical relevance. *Upper limit exceeds 999. was confirmed at 30 days from hospital discharge,
Abbreviations as in Table 1. and none was lost to follow-up. Use of RHC was
associated with a 39% absolute increase in survival
clinical relevance. Risk scores were assigned as such: (71% vs. 32.0%; p < 0.01). The most common primary
rounded ORs #10, 1 point; >10, 2 points; and a final cause of death was multi-organ failure (n ¼ 59 [80%])
summary risk score calculated by summing points (Table 2). Among patients experiencing either in-
assigned to the 7 parameters. A final risk score for 30- hospital (n ¼ 15) or out-of-hospital (n ¼ 15) cardiac
day survival was derived with a range of 0 to 10. arrest, survivors had significantly shorter times to
Finally, we compared the discriminant ability of our return of spontaneous circulation compared with
risk prediction model versus the established Card- nonsurvivors (10.7  2.5 min vs. 32.3  3.9 min; p <
Shock risk score (21) using the Spearman rank corre- 0.01). In patients requiring MCS, every 1-h delay in
lation coefficients, receiver-operator characteristic escalation of therapy was associated with a 9.9%
curves, and area under the curve statistics. increased risk of death. The use of VA-ECMO for cir-
culatory support was associated with a significant
RESULTS risk of increased mortality (OR: 4.42; 95% CI: 1.11 to
17.65).
PATIENT CHARACTERISTICS. A total of 204 patients
presented with CS over an 18-month period (Table 1). RISK SCORE. Univariate OR and 95% CIs are pre-

Their mean age was 61  13 years, 70% were male, sented in Table 3. Twelve parameters were statisti-
46% had diabetes mellitus, 58% had renal insuffi- cally associated with 30-day mortality with p < 0.10:
ciency, and 30% required dialysis. Fifty-two age $71 years, index creatinine >2.3 mg/dl, diabetes
percent of patients were transferred from outside mellitus, VA-ECMO, dialysis, vasopressor duration
>36 h at the time of index CS diagnosis, previous
F I G U R E 2 Estimated Probability of 30-Day Mortality cardiac intervention, right atrial pressure (RAP)
>15 mm Hg at 24 h, RAP/pulmonary capillary wedge
1.0 pressure >0.63 at 24 h, and all 3 CS threshold markers
(lactate, CPO, and PAPi) at 24 h after diagnosis and
0.8 implementation of therapies. Following multivariate
Probability of Death

testing, only 7 parameters remained in the model.

0.6 Although age $71 years was not statistically signifi-
cant in the multivariate model, age was included for
0.4 its clinical relevance. Lactate threshold >3.0 mg/dl at
24 h was the most predictive, followed by >36 h of
0.2 pressor duration at the time of index diagnosis,
CPO <0.6 W, and PAPi <1.0 at 24 h.
After assignment of points to significant parame-
0.0
0 1 2 3 4 5 6 7 8 9 10 ters, the 30-day risk of mortality score ranged from
30-Day Mortality Risk Score 0 to 10 (3.4  3.2; median 3.0) (Table 4). The final
multivariate model had a C-statistic of 0.97 (95% CI:
Predicted risk scores are based on unconditional logistic regression model 0.95 to 0.99) and an optimal risk score cutpoint of
predicting 30-day mortality. 3 to 4 as calculated by using the Youden index. A
median risk score of 3 was associated with a 15.0%
JACC VOL. 73, NO. 13, 2019 Tehrani et al. 1665
APRIL 9, 2019:1659–69 Standardized Team-Based Care in Cardiogenic Shock

F I G U R E 3 IHVI Cardiogenic Shock Risk Score

Integer 30-Day
Risk Factor Risk Score
Score Mortality Risk

Lactate, mmol/L @24 hrs ≥3.0 2

‘Low’ risk score:
Pressors duration from diagnosis >36 hours 2 0.0%
0-1
CPO @24 hrs <0.6 W 2
‘Moderate’ risk score:
Diabetes Mellitus 1 17.6%
2-4
Dialysis 1
‘High’ risk score:
PAPi @24 hrs <1.0 1 82.4%
5+

Age ≥71 years 1

A multivariate model was run to assess the joint impact of all statistically significant parameters at the univariate level. The model was run
again following exclusion of parameters failing to meet the initial exclusion criterion, with 6 parameters meeting a similar criterion of 0.10,
resulting in a final risk score model of 7 parameters. Age $71 years was included despite a lack of statistical significance given its large odds
ratio (OR) and clinical relevance. Risk scores were assigned as such: rounded odds ratio #10, 1 point; >10, 2 points; and a final summary risk
score calculated by summing points assigned to the 7 parameters. A final risk score for 30-day mortality was derived with a range of 0 to 10.
CPO ¼ cardiac power output; IHVI ¼ Inova Heart and Vascular Institute; PAPi ¼ pulmonary arterial pulsatility index.

risk of death at 30 days. Risk scores $6 were associ-
ated with at least a 91% risk of 30-day mortality
(Figure 2). Risk categories of low (risk score: 0 to 1
[38.2%]), moderate (risk score: 2 to 4 [29.4%]), and
high (risk score: $5 [32.4%]) were created based on
approximate 33rd and 66th percentiles (Figure 3).
Observed to predicted probabilities of 30-day mor-
tality with 95% CIs are presented in Online Figure 2.
Finally, we compared the discriminant ability of
our derived risk score versus the CardShock risk
score. Both risk scores were highly correlated
(r ¼ 0.75, p < 0.0001) and exhibited high discriminant
ability (Inova Heart and Vascular Institute area under
the curve 0.97 [95% CI: 0.95 to 0.99] vs. CardShock
area under the curve 0.97 [95% CI: 0.94 to 0.99])
(Figure 4).

F I G U R E 4 Receiver Operating Characteristic Curve Comparing IHVI Cardiogenic Shock Versus CardShock Risk Prediction Models for
30-Day Mortality

1.0

0.8
Sensitivity

0.6

0.4

0.2
IHVI: AUC = 0.97; 95% CI: 0.95-0.99
CardShock: AUC = 0.97; 95% CI: 0.94-0.99
0.0
0.0 0.2 0.4 0.6 0.8 1.0
1 - Specificity

IHVI CardShock

Both risk scores showed excellent discriminant ability with area under the curve (AUC) statistics >90.0%. CI ¼ confidence interval;
IHVI ¼ Inova Heart and Vascular Institute.
1666 Tehrani et al.
Standardized Team-Based Care in Cardiogenic Shock
DISCUSSION
Several single-center reports have suggested the
feasibility of a standardized team-based approach to
managing CS; however, limited outcomes data have
been published using this care model (22,23).
Although most previous studies focused on AMI-CS,
few included patients with ADHF-CS. The subset of
nonischemic heart failure often accounts for up to
30% of CS (10). Whether due to medication non-
adherence, or long-term changes in their neurohor-
monal milieu resulting in low output and vasoplegic
states, these patients also present acutely ill with an
elevated risk for short-term mortality (24). The med-
ical complexities of these patients highlight the
importance of having cross-collaborative interven-
tional cardiology, cardiac surgery, critical care, and
advanced heart failure shock teams. This published
series is the first to highlight not only the feasibility of
a multidisciplinary shock team for both phenotypes
of CS but also clinical outcomes using this innovative
approach.
Key to formulating a reliable CS algorithm is un-
derstanding the importance of hemodynamic data to
guide clinical decision making. Esposito et al. (25)
suggested 3 primary treatment objectives for man-
aging AMI-CS: 1) coronary perfusion via revasculari-
zation; 2) circulatory support to achieve a viable
mean arterial pressure; and 3) ventricular unloading
to mitigate the deleterious effects of afterload and
oxygen demand. Our findings suggest that the
empiric use of RHC is important to solving this
hemodynamic support equation in patients with CS.
Lactate was identified as an important surrogate
marker of clinical outcomes. A lactate level $3 mg/dl
at 24 h had a sensitivity of 45.9%, false-positive rate
of 1.5%, and positive predictive value of 94.4% for
mortality, similar to what has been reported in the
National Cardiogenic Shock Initiative (26). We also
identified CPO and PAPi as 2 significant hemodynamic
variables to assess response to therapy. CPO has been
validated as a hemodynamic marker strongly associ-
ated with in-hospital mortality, and PAPi is a surro-
gate marker of RV function (27,28). Both are included
in our risk score, highlighting the complementary role
of hemodynamics and laboratory markers in tailoring
therapies. This approach contrasts with other scoring
systems, which have not been validated for all CS
phenotypes and do not incorporate hemodynamic
variables (29–31).
Persistent RV dysfunction at 24 h was also associ-
ated with increased mortality. Of the 19 patients with
RV dysfunction, 6 were supported with the pVAD, 2
JACC VOL. 73, NO. 13, 2019
APRIL 9, 2019:1659–69
with VA-ECMO alone, and 6 with VA-ECMO and
concomitant LV venting with Impella CP or Impella
5.0. The 6 patients who received only pVAD support
required no RV support due to early improvement in
RV function. Two patients received Impella RP sup-
port at the onset of CS diagnosis due to clear evi-
dence of primary RV failure (post–LV assist device RV
failure and acute inferior ST-segment myocardial
infarction with RV failure). All these decisions arose
from continuous and longitudinal reassessment by
the shock team throughout each patient’s dynamic
hospital course.
Our experience showed that patients requiring
stand-alone VA-ECMO for MCS had the highest 30-
day mortality (OR: 4.46; 95% CI: 1.12 to 17.79;
p ¼ 0.03). We believe several factors contributed to
this finding: impaired LV unloading due to increased
afterload, acute kidney injury requiring dialysis, and
bleeding and vascular complications (Online Table 2).
These factors have been previously identified as
predictors of mortality in patients receiving VA-
ECMO (32,33). Our study also included patients who
had VA-ECMO and either Impella CP or Impella 5.0 as
an LV vent. Although the study was not powered to
detect differences such as renal failure between VA-
ECMO and VA-ECMO plus Impella, our study does
highlight the higher degree of critical illness in pa-
tients who required VA-ECMO for circulatory support.
Therefore, the observed high rates of acute kidney
injury in these patients was likely multifactorial, not
only due to inadequate renal perfusion from
myocardial dysfunction but also potentially due to
device-related factors. Diligent surveillance for
optimal device functioning by using daily echocar-
diograms and serial assessment of lactate dehydro-
genase, plasma free hemoglobin, and haptoglobin
levels revealed an overall incidence of hemolysis in
47.5% of patients with the pVAD. The rate of clinically
significant hemolysis, however, defined as anemia
requiring blood transfusion or renal failure requiring
dialysis, was 9.8% in patients with the pVAD, 40% in
patients with stand-alone VA-ECMO, and 52% in pa-
tients with VA-ECMO plus Impella. In addition, con-
version of MCS to VA-ECMO was higher in the ADHF
patient population (n ¼ 21) compared with the AMI-CS
group (n ¼ 10). We believe that the increased severity
of biventricular dysfunction in the patients with
ADHF (RAP 22.1  6.8 mm Hg vs. 16.4  4.6 mm Hg) at
the time of MCS escalation was partly responsible.
Given the observational nature of these findings,
further research with randomized clinical trials using
standardized protocols, consistent shock severity
definitions, and uniform device indications are
JACC VOL. 73, NO. 13, 2019
APRIL 9, 2019:1659–69
needed to better understand the relationship be-
tween critical illness and circulatory support devices
not only with acute kidney injury and hemolysis, but
also with respect to the hemodynamic changes seen
in both AMI-CS and ADHF.
Finally, >50% of our patients with CS were
transferred from outside institutions, both inside
and outside of our health system. To minimize
practice variation, we disseminated our management
algorithm to cardiologists, intensivists, and emer-
gency department physicians at these facilities.
Physicians at any of our spoke hospitals are
encouraged to access our CS call line and engage the
shock team regarding patients who warrant timely
transfer to our tertiary hub center. In our analysis,
out-of-hospital transfer was not associated with
increased mortality. There is precedent for imple-
menting regionalized care systems resulting in
improved survival for other time-sensitive cardio-
vascular conditions such as cardiac arrest, ST-
segment elevation myocardial infarction, aortic
dissection, and stroke (34–36). Pilot studies have
shown the feasibility of mobile CS teams that travel
to spoke hospitals to initiate MCS, stabilize patients,
and then transport them back to the hub institution
(37,38). Although different hypothetical models have
been proposed to develop CS hub-and-spoke sys-
tems, we believe it is critically important to imple-
ment coordinated regionalized systems of care to
reduce practice variation and centralize the care of
the patient with CS to high-volume tertiary medical
centers able to offer early escalation of therapy and
full-spectrum, multidisciplinary care (13).
STUDY LIMITATIONS. First, this was a single-center
prospective registry with a limited number of pa-
tients who were followed up only to 30 days’ post–
hospital discharge. The observational and under-
powered nature of this study resulted in wide CIs
observed with several variables during univariate
and multivariate analyses, which can attenuate
their prognostic significance. However, the vari-
ables included were those most associated with
increased mortality in our study and the current
literature (26–31).
Second, this study evaluated all patients with a
primary diagnosis of CS and was not limited to the
AMI phenotype. Our heterogeneous patient popu-
lation also included those with ADHF-CS. Given the
presence of multiple comorbidities and the dynamic
nature of their hospital courses, some of these pa-
tients also developed concomitant septic shock, for
which there is unclear benefit from MCS. Despite
this limitation, our study population may be best
Tehrani et al. 1667
Standardized Team-Based Care in Cardiogenic Shock
representative of patients in real-world clinical
practice. Although this study was limited by power
to identify signals affecting the efficacy of our al-
gorithm and risk score in the 2 patient populations,
we believe that these findings have cross-
applicability to both CS phenotypes. We also
believe that these findings may serve as a roadmap
for future large-scale studies evaluating care path-
ways aimed at improving outcomes in patients with
both AMI and ADHF-CS.
Third, our registry also included patients who were
ineligible for MCS for reasons other than cardiovas-
cular and anatomic contraindications (superseding
medical comorbidities, life expectancy <6 months,
and patient/family preferences based on discussions
regarding goals of care). Such patients have been
excluded from other registries (39). We also identified
patients with irreversible multiorgan failure who
received MCS and ultimately died. This outcome
highlights the fact that CS encompasses a wide spec-
trum of clinical presentations, including patients in
end-stage hemometabolic shock in whom invasive
therapies have not been shown to positively affect
survival. Little is known regarding the manner to best
identify medical futility in the spectrum of CS, and
further studies are therefore needed to develop
schema to risk-stratify these potentially “non-
salvageable” patients.
CONCLUSIONS
Our observational study suggests that the imple-
mentation of a shock team predicated on a multidis-
ciplinary standardized team-based approach
emphasizing timely diagnosis, mandatory invasive
hemodynamics, and appropriate use of MCS is not
only feasible but may result in improved survival in
all-comer patients with CS. In addition, a validated
score that uses demographic, laboratory, and hemo-
dynamic markers can help to stratify risk and guide
clinical decision-making in patients with all pheno-
types of CS. We believe that concerted efforts to apply
standardized multidisciplinary care in a coordinated
regionalized approach may not only reduce practice
variation and improve patient outcomes but may also
facilitate pragmatic trial designs evaluating current
and future novel therapies for a clinical syndrome
that for too long has been marked by excessive
morbidity and mortality.
ACKNOWLEDGMENTS The authors would like to
acknowledge the Dudley Family for their continued
contributions and support of the INOVA Dudley
Family Center for Cardiovascular Innovation. The
1668 Tehrani et al. JACC VOL. 73, NO. 13, 2019

Standardized Team-Based Care in Cardiogenic Shock APRIL 9, 2019:1659–69

authors would also like to acknowledge Abdulla PERSPECTIVES

Damluji, MD, FACC, from the Johns Hopkins Uni-
versity, Division of Cardiology, and Shashank
COMPETENCY IN SYSTEMS BASED PRACTICE:
Sinha, MD, MSc, from the University of Michigan,
A multidisciplinary team–based approach that incor-
Division of Cardiology, for providing editorial
porates timely diagnosis, structured protocols, he-
assistance with this manuscript.
modynamic guidance, validated risk stratification, and
centralized care can improve outcomes for patients
ADDRESS FOR CORRESPONDENCE: Dr. Behnam N.
with CS.
Tehrani, Cardiac Catheterization Laboratory, INOVA
Heart and Vascular Institute, 3300 Gallows Road,
TRANSLATIONAL OUTLOOK: Pragmatic clinical
Falls Church, Virginia 22042. E-mail: behnam.
trials are required to evaluate current and innovative
tehrani@inova.org. Twitter: @behnam_tehrani. OR
therapies and establish evidence-based treatment
Dr. Christopher M. O’Connor, Inova Heart and
protocols to improve clinical outcomes for patients
Vascular Institute, Duke University, 3300 Gallows
with various types of CS.
Road, Falls Church, Virginia 22042. E-mail: christopher.
oconnor@inova.org. Twitter: @coconnormd.

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KEY WORDS cardiogenic shock, mechanical
circulatory support, multidisciplinary care,
shock team
A PP END IX For supplemental figures and
tables, please see the online version of this
paper.