Standardized Team-Based Care For Cardiogenic Shock: Background
Standardized Team-Based Care For Cardiogenic Shock: Background
Standardized Team-Based Care For Cardiogenic Shock: Background
13, 2019
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/).
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/
Listen to this manuscript’s Enduring Hearts; and has served as a consultant for NuPulse CV 5 and Ortho Clinical Diagnostics. Dr. Cooper has received grant
audio summary by support from Abbott. Dr. deFilippi has received research grants from Roche Diagnostics; has received consulting fees from Abbott
Editor-in-Chief Diagnostics, FujiRebio, Metabolomics, Ortho Diagnostics, Roche Diagnostics, and Siemens Healthcare; has received honoraria
Dr. Valentin Fuster on from WebMD; and has received royalties from UpToDate. Dr. Gurbel has received research grants from Amgen, Bayer, Duke
JACC.org. 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.
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
Transfer patient to cardiac catheterization lab or cardiac intensive care unit (CICU) for evaluation
If Hemodynamic Criteria are met, consider Percutaneous Mechanical Circulatory Support (PMCS)
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
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
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.
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
Integer 30-Day
Risk Factor Risk Score
Score Mortality Risk
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- Finally, we compared the discriminant ability of
ated with at least a 91% risk of 30-day mortality our derived risk score versus the CardShock risk
(Figure 2). Risk categories of low (risk score: 0 to 1 score. Both risk scores were highly correlated
[38.2%]), moderate (risk score: 2 to 4 [29.4%]), and (r ¼ 0.75, p < 0.0001) and exhibited high discriminant
high (risk score: $5 [32.4%]) were created based on ability (Inova Heart and Vascular Institute area under
approximate 33rd and 66th percentiles (Figure 3). the curve 0.97 [95% CI: 0.95 to 0.99] vs. CardShock
Observed to predicted probabilities of 30-day mor- area under the curve 0.97 [95% CI: 0.94 to 0.99])
tality with 95% CIs are presented in Online Figure 2. (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. JACC VOL. 73, NO. 13, 2019
better understand the relationship between critical representative of patients in real-world clinical
illness and circulatory support devices not only with practice. Although this study was limited by power
acute kidney injury and hemolysis, but also with to identify signals affecting the efficacy of our al-
respect to the hemodynamic changes seen in both gorithm and risk score in the 2 patient populations,
AMI-CS and ADHF. we believe that these findings have cross-
Finally, >50% of our patients with CS were applicability to both CS phenotypes. We also
transferred from outside institutions, both inside believe that these findings may serve as a roadmap
and outside of our health system. To minimize for future large-scale studies evaluating care path-
practice variation, we disseminated our management ways aimed at improving outcomes in patients with
algorithm to cardiologists, intensivists, and emer- both AMI and ADHF-CS.
gency department physicians at these facilities. Third, our registry also included patients who were
Physicians at any of our spoke hospitals are ineligible for MCS for reasons other than cardiovas-
encouraged to access our CS call line and engage the cular and anatomic contraindications (superseding
shock team regarding patients who warrant timely medical comorbidities, life expectancy <6 months,
transfer to our tertiary hub center. In our analysis, and patient/family preferences based on discussions
out-of-hospital transfer was not associated with regarding goals of care). Such patients have been
increased mortality. There is precedent for imple- excluded from other registries (39). We also identified
menting regionalized care systems resulting in patients with irreversible multiorgan failure who
improved survival for other time-sensitive cardio- received MCS and ultimately died. This outcome
vascular conditions such as cardiac arrest, ST- highlights the fact that CS encompasses a wide spec-
segment elevation myocardial infarction, aortic trum of clinical presentations, including patients in
dissection, and stroke (34–36). Pilot studies have end-stage hemometabolic shock in whom invasive
shown the feasibility of mobile CS teams that travel therapies have not been shown to positively affect
to spoke hospitals to initiate MCS, stabilize patients, survival. Little is known regarding the manner to best
and then transport them back to the hub institution identify medical futility in the spectrum of CS, and
(37,38). Although different hypothetical models have further studies are therefore needed to develop
been proposed to develop CS hub-and-spoke sys- schema to risk-stratify these potentially “non-
tems, we believe it is critically important to imple- salvageable” patients.
ment coordinated regionalized systems of care to
reduce practice variation and centralize the care of CONCLUSIONS
the patient with CS to high-volume tertiary medical
centers able to offer early escalation of therapy and Our observational study suggests that the imple-
full-spectrum, multidisciplinary care (13). mentation of a shock team predicated on a multidis-
STUDY LIMITATIONS. First, this was a single-center ciplinary standardized team-based approach
prospective registry with a limited number of pa- emphasizing timely diagnosis, mandatory invasive
tients who were followed up only to 30 days’ post– hemodynamics, and appropriate use of MCS is not
hospital discharge. The observational and under- only feasible but may result in improved survival in
powered nature of this study resulted in wide CIs all-comer patients with CS. In addition, a validated
observed with several variables during univariate score that uses demographic, laboratory, and hemo-
and multivariate analyses, which can attenuate dynamic markers can help to stratify risk and guide
their prognostic significance. However, the vari- clinical decision-making in patients with all pheno-
ables included were those most associated with types of CS. We believe that concerted efforts to apply
increased mortality in our study and the current standardized multidisciplinary care in a coordinated
literature (26–31). regionalized approach may not only reduce practice
Second, this study evaluated all patients with a variation and improve patient outcomes but may also
primary diagnosis of CS and was not limited to the facilitate pragmatic trial designs evaluating current
AMI phenotype. Our heterogeneous patient popu- and future novel therapies for a clinical syndrome
lation also included those with ADHF-CS. Given the that for too long has been marked by excessive
presence of multiple comorbidities and the dynamic morbidity and mortality.
nature of their hospital courses, some of these pa- ACKNOWLEDGMENTS The authors would like to
tients also developed concomitant septic shock, for acknowledge the Dudley Family for their continued
which there is unclear benefit from MCS. Despite contributions and support of the INOVA Dudley
this limitation, our study population may be best Family Center for Cardiovascular Innovation. The
1668 Tehrani et al. JACC VOL. 73, NO. 13, 2019
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tion. Eur J Heart Fail 2017;19 Suppl 2:104–9. Emergency circulatory support in refractory paper.