CONCISE DEFINITIVE REVIEW

Bram Rochwerg, MD, MSc (Epi), FRCPC, Series Editor

Advances in the Management of Cardiogenic

Shock
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy

Jacob C. Jentzer, MD1

OBJECTIVES: To review a contemporary approach to the management of Janine Pöss, MD2
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023

patients with cardiogenic shock (CS).

Hannah Schaubroeck, MD3
DATA SOURCES: We reviewed salient medical literature regarding CS. David A. Morrow, MD, MPH4
STUDY SELECTION: We included professional society scientific statements Steven M. Hollenberg, MD5
and clinical studies examining outcomes in patients with CS, with a focus on Alexandre Mebazaa, MD, PhD6
randomized clinical trials.
DATA EXTRACTION: We extracted salient study results and scientific statement
recommendations regarding the management of CS.
DATA SYNTHESIS: Professional society recommendations were integrated with
evaluated studies.
CONCLUSIONS: CS results in short-term mortality exceeding 30% despite
standard therapy. While acute myocardial infarction (AMI) has been the focus of
most CS research, heart failure-related CS now predominates at many centers.
CS can present with a wide spectrum of shock severity, including patients who
are normotensive despite ongoing hypoperfusion. The Society for Cardiovascular
Angiography and Intervention Shock Classification categorizes patients with or at
risk of CS according to shock severity, which predicts mortality. The CS population
includes a heterogeneous mix of phenotypes defined by ventricular function, he-
modynamic profile, biomarkers, and other clinical variables. Integrating the shock
severity and CS phenotype with nonmodifiable risk factors for mortality can guide
clinical decision-making and prognostication. Identifying and treating the cause of
CS is crucial for success, including early culprit vessel revascularization for AMI.
Vasopressors and inotropes titrated to restore arterial pressure and perfusion are
the cornerstone of initial medical therapy for CS. Temporary mechanical circula-
tory support (MCS) is indicated for appropriately selected patients as a bridge to
recovery, decision, durable MCS, or heart transplant. Randomized controlled trials
have not demonstrated better survival with the routine use of temporary MCS in
patients with CS. Accordingly, a multidisciplinary team-based approach should
be used to tailor the type of hemodynamic support to each individual CS patient’s
needs based on shock severity, phenotype, and exit strategy.
KEY WORDS: acute myocardial infarction; cardiogenic shock; heart failure;
mechanical circulatory support; shock

C
ardiogenic shock (CS) represents a final common pathway in which
cardiovascular disease causes circulatory failure, hypoperfusion, and
end-organ dysfunction (1, 2). Short-term mortality of adults with
CS has declined over time but still exceeds 30% during hospitalization and
increases to 40–50% after 30 days (3). Early recognition and effective treatment Copyright © 2023 by the Society of
of CS is needed to prevent the downward spiral of shock that often culminates Critical Care Medicine and Wolters
in death (4). CS management remains largely driven by expert consensus, as Kluwer Health, Inc. All Rights
few adequately powered randomized clinical trials (RCTs) have demonstrated Reserved.
improvements in survival versus standard therapies in patients with CS (5). DOI: 10.1097/CCM.0000000000005919

1222      www.ccmjournal.org September 2023 • Volume 51 • Number 9

Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

KEY POINTS
Question: What is the optimal management of
patients with cardiogenic shock (CS)?
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
Findings: Few randomized trials have demon-
strated incremental improvements in survival with
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023
tested therapies for patients with CS, particularly
for those without acute myocardial infarction (AMI).
Meaning: Contemporary management of CS
requires individualized therapy guided by a mul-
tidisciplinary team integrating shock severity,
phenotype, and risk modifiers. Reversal of the
triggering etiology is paramount (particularly early
revascularization for patients with AMI), with resto-
ration of systemic perfusion using a combination
of vasoactive drugs and temporary mechanical
circulatory support tailored to the patient’s needs
while minimizing preventable complications.
Challenges with RCTs in CS include difficulties in
obtaining consent, discomfort regarding equipoise, di-
sease heterogeneity, and lack of standardized manage-
ment across different centers and countries. Therefore,
reevaluation of the goals and execution of contempo-
rary CS research is necessary. This narrative review
summarizes the contemporary management of CS,
based on literature review and discussions held at the
2022 Critical Care Clinical Trialists’ Workshop, a gath-
ering of international CS experts focused on critically
appraising current CS management strategies, ongoing
trials, and recommendations for the design of future
RCTs.
EPIDEMIOLOGY, DEFINITION, AND
CLASSIFICATION OF CS
The Changing Epidemiology of CS
Acute myocardial infarction (AMI) has historically
been the most common etiology of CS, and nearly
all published RCTs in CS have enrolled exclusively
AMI-CS patients, with few RCTs in patients with CS
from other etiologies (5–7). Non-AMI causes of CS may
now predominate in some centers, due to a greater rel-
ative increase in non-AMI causes of CS including those
with new-onset or chronic cardiomyopathy with de-
compensated heart failure (HF) (3, 8, 9). This changing
Critical Care Medicine www.ccmjournal.org      1223
Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
Concise Definitive Review
epidemiology has implications for both therapy and
RCTs, as patients with AMI-CS and HF-related CS
(HF-CS) have divergent pathophysiology, clinical pre-
sentation, and therapeutic approaches (10). Patients
with de novo HF-CS (e.g., acute myocarditis or new
diagnosis of cardiomyopathy) may differ further from
patients with HF-CS arising from a chronic cardiomy-
opathy, with the latter able to tolerate worse ventricular
function and lower cardiac output due to chronic ad-
aptation (10, 11).
Evolving Definitions of CS
CS has been defined broadly as tissue and organ hypo-
perfusion due to ineffective cardiac output, which
may result from myocardial dysfunction or obstruc-
tive causes (e.g., cardiac tamponade) that merit spe-
cific intervention (1). Traditional clinical and research
definitions of CS include the triad of hypotension
(e.g., systolic blood pressure < 90 mm Hg), low cardiac
output despite adequate preload, and hypoperfusion
(e.g., elevated lactate, cold or mottled extremities, al-
tered mental status, oliguria) (1, 2). Hypotension may
be absent in some CS patients at an early stage with
preserved compensatory mechanisms; these patients
are labeled as normotensive CS (12). Patients who
are hypotensive due to a low cardiac output but have
preserved perfusion are classified as preshock (Fig. 1)
(12–14). Patients with preshock have a better prog-
nosis than those with normotensive CS, who in turn
have better outcomes than those with hypotensive CS,
highlighting an opportunity for early recognition and
reversal of hypoperfusion to facilitate timely stabiliza-
tion (15, 16). Recent studies emphasize the importance
of hypoperfusion (particularly an elevated serum lac-
tate level), as opposed to blood pressure or hemody-
namics, in determining outcome (13, 14, 17–20).
Classification of CS
Severity Staging in CS. Recognition of the wide
range of CS severity that may be encountered in clin-
ical practice led to development of the Society for
Cardiovascular Angiography and Intervention (SCAI)
Shock Classification, which defined five stages of esca-
lating CS severity (labeled A through E) for patients
with acute cardiovascular disease, including AMI or
decompensated HF (Fig. 2) (13). Hemodynamically
stable patients with acute cardiovascular disease are
 Jentzer et al

and those with hypoperfusion requiring an interven-

tion beyond fluid resuscitation are classified as hav-
ing shock (SCAI Shock Stages C, D, and E) (13). The
SCAI Shock Classification provides a useful tool for
characterizing CS in clinical communication and re-
search. Validation studies have consistently demon-
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy

strated that the SCAI Shock Classification correlates

with prognosis, with incrementally higher mortality at
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023

Figure 1. Conceptual model demonstrating the overlap between
different states of hemodynamic compromise. Shock is defined by
the presence of hypoperfusion; most, but not all, patients will also
be hypotensive. Patients with hemodynamic instability who do not
meet criteria for shock are labeled as preshock (13).
labeled SCAI Shock Stage A (“At Risk”), those with he-
modynamic instability without hypoperfusion are la-
beled SCAI Shock Stage B (“Beginning” or preshock),
each higher SCAI Shock Stage (14, 21, 22). The revised
SCAI Shock Classification highlights the spectrum of
CS severity and mortality risk that exists within each
SCAI Shock Stage (14). The mortality risk observed
in patients with preshock (SCAI Shock stage B) and
mild or normotensive CS (SCAI Shock Stage C) is not
trivial, emphasizing the importance of recognizing CS
early during the disease process (14, 16, 23).
Phenotypes of CS. CS is a hemodynamically diverse
condition, including different patterns of ventricular
function, filling pressures, peripheral vascular tone,
and cardiac output (1, 21). Patients with right ventric-
ular (RV) or biventricular dysfunction and congestion
have higher shock severity, more organ failure, and

Figure 2. Determination of the Society for Cardiovascular Angiography and Intervention (SCAI) Shock stage using the revised SCAI
Shock Classification. Adapted from Jentzer et al (21) with permission. Adaptations are themselves works protected by copyright. So in
order to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the
owner of copyright in the translation or adaptation. CPR = cardiopulmonary resuscitation, MCS = mechanical circulatory support.

1224      www.ccmjournal.org September 2023 • Volume 51 • Number 9

Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
 Concise Definitive Review

worse outcomes (24, 25). Congestion may be absent in
one-third of patients (“cold and dry”) (1). The etiology
of CS, particularly the presence of AMI and successful
revascularization, can influence the presentation and
clinical course (10, 11, 17, 20). AMI and CS can induce
the release of pro-inflammatory mediators, causing a
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
hemodynamics, etiology, laboratory studies, or other
clinical variables (Fig.  3) (21). Risk modifiers are in-
dependent nonmodifiable risk factors for mortality
across the spectrum of CS severity, the most notable
being older age and CA with coma (14, 21, 30, 35).
Numerous potential risk modifiers have been identified

systemic inflammatory response that can trigger im- within the context of the SCAI Shock Classification,
paired microcirculation, inappropriate vasodilation, including hemodynamic variables (e.g., right atrial
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023

and progressive organ dysfunction (1, 2, 26). Mixed pressure), echocardiographic measurements (e.g., RV
vasodilatory-CS resulting from systemic inflammation dysfunction), laboratory biomarkers (e.g., hemometa-
with or without infection has been associated with bolic CS), and clinical features (e.g., worsening shock
greater shock severity, more organ failure, and worse trajectory) (14, 21, 24, 31, 32). The presence of irre-
prognosis (8, 9, 27). As many as 30–50% of patients versible anoxic brain injury in patients who are coma-
with CS have concomitant cardiac arrest (CA), which tose after CA may preclude a favorable outcome even
is associated with myocardial dysfunction, global with reversal of shock (14, 36). Established risk factors
ischemia-reperfusion injury, systemic inflammation, for mortality in CS patients have been codified in com-
and higher mortality (5, 22, 28–30). The end stage of posite risk scores (e.g., the Intraaortic Balloon Pump in
CS characterized by severe
lactic acidosis and multiple
organ failure has been re-
cently termed “hemometa-
bolic” or “cardiometabolic”
shock and is associated
with RV congestion, greater
shock severity, and worse
outcomes (4, 19, 31–33).

PROGNOSTICATION
IN CS
The revised SCAI Shock
Classification elaborated
a three-axis model for
conceptualizing the core
domains needed for clinical
decision-making and prog-
nostication in individual
CS patients: shock severity,
phenotype, and risk modi-
fiers (14, 21). The overall
assessment of CS severity
integrates numerous factors
beyond simply assigning
the SCAI Shock Stage (Fig.
3) (34). The phenotype of
CS, although interrelated, is
Figure 3. Components to be considered when evaluating the severity and phenotype of patients
distinct from the severity of with cardiogenic shock. Markers of shock severity (bottom) are distinct from the assessment of
CS and can be defined using shock phenotype (top) (14, 21, 33). MCS = mechanical circulatory support, SCAI = Society for
echocardiography, invasive Cardiovascular Angiography and Intervention.

Critical Care Medicine www.ccmjournal.org      1225

Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
 Jentzer et al

Cardiogenic Shock II [IABP-SHOCK-II] score and CS
score) that can enhance risk stratification when com-
bined with the SCAI Shock Classification (17, 20, 37).
CONTEMPORARY STANDARD CARE
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
shock phenotype and those with severe CS or a poor
response to initial therapy where direct measurements
of cardiac output and systemic vascular resistance can
facilitate titration of vasoactive drugs (1, 12, 40, 41).
Early coronary angiography should be performed
for patients with CS and suspected AMI or an undi-

FOR CS agnosed cardiomyopathy (1, 2, 6, 38). For those with

Early Identification and Evaluation AMI-CS, randomized controlled trials have demon-
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023

strated that early successful culprit vessel revascular-

Early recognition with identification and treatment
of the underlying cause is a central goal in the initial
management of patients with CS (Supplemental Table
1, http://links.lww.com/CCM/H343) (1, 2, 6, 38, 39).
An electrocardiogram and point-of-care cardiac ultra-
sound are useful to screen for myocardial ischemia, left
ventricle (LV)/RV dysfunction, and structural heart
disease (38, 39). Invasive hemodynamic monitoring
is valuable, starting with an arterial catheter for pre-
cise blood pressure measurement and a central venous
line to administer vasoactive medications and measure
filling pressures and venous oxygen saturation (1, 2,
6). Pulmonary artery catheter monitoring can be in-
formative, particularly for patients with an uncertain
ization improves long-term survival, and nonculprit
vessel revascularization should be deferred initially
(2, 6, 20, 42, 43). Evidence-based interventions for
patients with CS based on published RCTs are shown
in Table 1 (1, 2, 5, 6). A proposed framework for man-
agement guided by the SCAI Shock Classification is
presented in Figure 4 (21).
Initial Respiratory and Hemodynamic
Stabilization
Oxygen supplementation is recommended to maintain
arterial oxygen saturation above 90% (2, 6). Noninvasive
ventilation with continuous positive airway pressure

TABLE 1.
Evidence-Based Interventions for Patients With Cardiogenic Shock Based on Randomized
Clinical Trials
Evidence-Based Strategies Source

Revascularization in AMI-CS
Early revascularization improves survival Should We Emergently Revascularize Occluded Coronaries for
Cardiogenic Shock trial
Initial multivessel revascularization is harmful Culprit Lesion Only PCI versus Multivessel PCI in Cardiogenic Shock
trial
Vasoactive drug use
 orepinephrine is safer (fewer arrhythmias)
N Sepsis Occurrence in Acutely Ill Patients-II trial and Study Comparing
than dopamine or epinephrine the Efficacy and Tolerability of Epinephrine and Norepinephrine in
Cardiogenic Shock trial
 obutamine and milrinone produce similar sur- Dobutamine Compared with Milrinone
D
vival and adverse events
Levosimendan does not improve survival Meta-analysis
Temporary mechanical circulatory support use
 outine IABP use in AMI-CS does not im-
R IABP-SHOCK-II trial
prove survival
 p-front VA-ECMO use does not improve
U Extracorporeal Membrane Oxygenation-Cardiogenic Shock trial
survival vs rescue VA-ECMO
AMI-CS = acute myocardial infarction-cardiogenic shock, IABP = intra-aortic balloon pump, VA-ECMO = venoarterial extracorporeal
membrane oxygenation.

1226      www.ccmjournal.org September 2023 • Volume 51 • Number 9

Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
 Concise Definitive Review
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023

Figure 4. Management algorithm for patients with or at risk for cardiogenic shock (CS) tailored to the Society for Cardiovascular
Angiography and Intervention (SCAI) Shock stage. Algorithm represents authors’ expert consensus regarding general approaches based
on best available evidence to date with recognition that decisions should be tailored to patient-specific factors. AMI = acute myocardial
infarction, BP = blood pressure, ECG = electrocardiogram, ECMO = extracorporeal membrane oxygenation, HTX = heart transplant,
IABP = intra-aortic balloon pump, LVAD = left ventricular assist device, MCS = mechanical circulatory support, PAC = pulmonary artery
catheter, Spo2 = pulse oximetry, STEMI = ST-segment elevation myocardial infarction.

can reduce work of breathing and improve pulmonary crystalloid bolus over 15–30 min); in case of con-
edema; high-flow nasal cannula may be useful, partic- gestion, diuretic therapy is indicated (1, 2, 38). Beta-
ularly when positive airway pressure is not desirable blockers and other blood pressure-lowering therapies
(44). When invasive mechanical ventilation is needed, should generally be withheld until CS resolves as evi-
lung-protective ventilation limiting the tidal volume denced by a lack of ongoing hypoperfusion or vaso-
and driving pressure may be considered in the absence pressor requirements (45). An IV vasodilator trial (e.g.,
of supporting evidence (1, 38, 44). While positive pres- nitroprusside or nitroglycerin) may be considered for
sure ventilation may improve LV loading conditions normotensive CS, in whom the systemic vascular re-
and ameliorate pulmonary edema, it is essential to rec- sistance (and therefore LV afterload) is expected to
ognize the potential for positive pressure ventilation be high. Despite limited evidence, vasopressor and
to potentially worsen hemodynamics depending on inotrope therapy remains standard for initial hemo-
volume status and RV function (44). dynamic support for patients with CS (1, 2, 6, 7, 46).
CS patients without signs of congestion might ben- Norepinephrine is generally the preferred first-line
efit from cautious fluid administration (e.g., 250 mL vasopressor in hypotensive patients with CS, based
Critical Care Medicine www.ccmjournal.org      1227
Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
 Jentzer et al
on a more favorable safety profile (particularly fewer
arrhythmias) in comparison to either dopamine or ep-
inephrine (2, 6, 38, 46–48). The optimal blood pressure
goal for patients with CS remains to be established and
likely varies between patients, recognizing that an av-
erage mean arterial pressure less than 65 mm Hg has
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
been associated with worse outcomes (1, 49). A goal
systolic blood pressure greater than or equal to 90 mm
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023
Hg and mean arterial pressure greater than or equal
to 65 mm Hg have been suggested based on extrapo-
lation from populations with other forms of shock (1,
2). Once arterial pressure has been restored using a va-
sopressor, an inotrope may be added to restore perfu-
sion by improving cardiac output; this often increases
arterial pressure to allow vasopressor weaning (38,
46). A recent underpowered RCT demonstrated sim-
ilar outcomes and safety profiles for dobutamine and
milrinone in a heterogeneous CS population including
one-third with AMI-CS (50). Notably, dobutamine
has a faster onset and offset of effect and may be less
likely to produce vasodilatory hypotension (38, 46).
The combination of norepinephrine and dobutamine
is useful for many patients with CS, recognizing that
certain etiologies and phenotypes of CS may respond
better to different agents (1, 2, 6, 38). Vasopressin can
increase LV afterload and reduce cardiac index and is
reserved for RV-predominant CS or mixed vasodila-
tory-CS with an adequate cardiac index (e.g., post-car-
diotomy CS) (46, 51). Toxicity from vasopressors and
inotropes is common, including excessive vasocon-
striction aggravating hypoperfusion, tachycardia caus-
ing myocardial ischemia, and tachyarrhythmias (46).
Temporary Mechanical Circulatory Support
Higher vasopressor requirements are associated with
increased mortality in patients with CS, likely reflecting
greater shock severity and an elevated risk of drug-
induced adverse effects (25, 46, 52, 53). Temporary
mechanical circulatory support (MCS) devices can pro-
vide additional hemodynamic support when vasoactive
drugs are either ineffective or associated with toxicity
(40). The IABP remains the most used temporary MCS
device in many countries due to its low cost, ease of im-
plantation, and relatively low risk of complications (7,
54, 55). The IABP failed to improve survival in patients
with AMI-CS and is therefore not recommended for
routine use in this setting (6, 56, 57). The IABP reduces
1228      www.ccmjournal.org September 2023 • Volume 51 • Number 9
Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
LV afterload and it has been speculated that this might
be useful for patients with HF-CS, particularly at lower
shock severity (58, 59). The IABP remains indicated for
mechanical complications of AMI, including papillary
muscle or ventricular septal rupture (1, 2, 6, 60).
Percutaneous left ventricular assist devices (pLVADs)
provide greater hemodynamic support than the IABP
but have not been demonstrated to improve survival
and may be associated with a higher risk of complica-
tions including bleeding, thromboembolism, and limb
ischemia (61–63). Percutaneous right ventricular assist
devices (pRVADs) can be used alone (for isolated RV
failure) or in combination with a pLVAD (for biven-
tricular failure), but have not been tested in RCTs (40).
Venoarterial extracorporeal membrane oxygenation
(VA-ECMO) is the only temporary MCS device that
can provide robust biventricular cardiac support and
pulmonary support and can be useful for severe or re-
fractory CS (SCAI Shock Stages D and E) including
patients with ongoing CA (53, 64–67). However, the re-
cent ECMO-CS trial failed to demonstrate an improve-
ment in survival with early VA-ECMO versus initial
medical therapy with rescue VA-ECMO (used in 39%)
(67). VA-ECMO can increase LV afterload potentially
resulting in elevated LV end-diastolic pressure, LV dil-
atation, and impaired aortic valve opening. Therefore,
providing LV unloading (“venting”) during VA-ECMO
may be important and can be achieved by addition of
an IABP or a pLVAD among other alternatives (64,
68). Considering that RCTs have not demonstrated
improved outcomes with any MCS device in patients
with CS, routine use of MCS devices cannot be recom-
mended in unselected patients with CS despite the po-
tential for benefit in some patients (40, 61, 67, 69).
Available evidence is insufficient to identify which
patients are likely to benefit from temporary MCS, and
many of the highest-risk patients do poorly even with
robust MCS (4, 36). Late initiation of MCS after pro-
gression to hemometabolic shock may be inadequate
to salvage the patient (4, 38). Until adequate data are
available, evaluation by a multidisciplinary shock team
using a structured approach to evaluation and stan-
dardized care protocols (potentially based on invasive
hemodynamic data) appears to be the best way to in-
dividualize advanced CS therapies (70, 71). Further in-
vestigation is necessary to understand which elements
of a multifaceted shock team response (e.g., invasive
hemodynamic assessment, rapid implementation and

escalation of temporary MCS, multidisciplinary coor-
dination, standardized protocols) are beneficial.
The general principles we use to select patients for
temporary MCS parallel the SCAI Shock Classification
three-axis model (14, 21, 40). Patients in whom hemo-
dynamics are inadequately supported with vasoactive
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
drugs (or in whom toxicity from these drugs occurs)
have a greater need for temporary MCS and would
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023
preferably have MCS initiated as soon as they are de-
termined to be eligible (40). The type of MCS that
should be used is determined by the CS phenotype,
particularly the presence of RV versus LV dysfunction
and respiratory failure which guide the decision be-
tween pRVAD/pLVAD or VA-ECMO (40). Finally, the
patient’s candidacy for temporary MCS should hinge
on their overall burden of nonmodifiable risk factors
(e.g., age, comorbidities, brain injury, organ failure)
that will ultimately determine not only their prog-
nosis but also their candidacy for destination thera-
pies. Temporary MCS should be used only with a clear
exit strategy as a bridge to potential recovery, durable
MCS, or heart transplantation; for selected patients, a
bridge to decision/candidacy strategy may be consid-
ered (64). Many patients with CS (particularly acute-
on-chronic HF-CS) will not have recovery of cardiac
function and require either durable MCS or heart
transplantation (72). Candidacy for durable MCS and
heart transplantation should be evaluated early, with
the goal of preserving end-organ function for patients
who are likely to be eligible for these therapies (1).
Patients with CS who do not have cardiac recovery and
are not candidates for durable MCS or transplant have
dismal outcomes, and early palliative care consultation
is appropriate (1).
Right Ventricular Predominant CS
Treatment of CS due to isolated or predominant RV
failure must consider the presence and etiology of pul-
monary hypertension as well as the harmful effects of
positive pressure ventilation on the right heart (44,
73). Amelioration of factors that raise pulmonary vas-
cular resistance (e.g., hypoxia, hypercarbia, acidosis,
high airway pressures) is essential, and endotra-
cheal intubation should be avoided if possible; high-
flow nasal cannula can provide oxygenation support
without excessive positive airway pressure. Inadequate
RV preload can compromise stroke volume, but high
Critical Care Medicine www.ccmjournal.org      1229
Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
Concise Definitive Review
RV filling pressures (i.e., RAP > 15–20 mm Hg) can
worsen RV performance resulting in kidney and liver
dysfunction (73). Maintaining a mean arterial pres-
sure above the mean pulmonary artery pressure is ad-
visable, and milrinone or vasopressin may have more
favorable effects on RV afterload than catecholamines
(46). Selective pulmonary vasodilators (either inhaled
or systemic) may be indicated depending on the cause
of RV failure, particularly for RV failure due to pul-
monary hypertension in the absence of pulmonary
congestion or hypoxemic lung disease (73). Where
available, pRVADs are generally reserved for refrac-
tory RV-predominant CS in the absence of severe pul-
monary hypertension, with VA-ECMO preferred for
those with pulmonary hypertension or biventricular
CS (40). For patients with CS due to RV infarction,
fluid loading and dobutamine are useful, with inhaled
nitric oxide and pRVAD used for refractory cases; loss
of atrioventricular electrical synchrony due to com-
plete heart block can compromise hemodynamics
and may be ameliorated by atrioventricular sequential
pacing (i.e., DDD pacing mode) (1, 6).
FUTURE CS RESEARCH
Numerous RCTs in patients with CS are currently on-
going and will expand the evidence base (Supplemental
Table 2, http://links.lww.com/CCM/H343), including
several that aim to compare advanced temporary MCS
devices (e.g., Impella and VA-ECMO) versus optimal
medical therapy whose proposed sample sizes exceed
the sum total of patients enrolled in published RCTs
utilizing these devices (74, 75). Integration of pheno-
typing and shock severity classification is essential for
future research to encapsulate the heterogeneity of CS
populations and understand pathophysiologic mecha-
nisms which could yield novel treatment strategies in
specific subgroups (21, 33). Implementing a more con-
sistent standard of care including a multidisciplinary
shock team with an evidence-based CS protocol has
the potential to improve the generalizability of RCTs
into clinical practice but requires additional rigorous
investigation to establish the efficacy and safety of each
proposed element (70). Involvement of governmental
and regulatory authorities coupled with patient advo-
cate input is encouraged when designing RCTs. Since
informed consent must often be delayed or deferred
due to the severity of illness at initial presentation, it is
 Jentzer et al
crucial that patient representatives are involved when
defining the intervention and control arms and utiliz-
ing the emergency exception from informed consent
process may be necessary. Adaptive trials that con-
sider dynamic changes in the patient’s presentation
and clinical evolution may be useful in this popula-
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
tion. Inclusion of key patient-centered outcomes be-
yond survival (e.g., days alive without organ failure) is
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023
encouraged.
CONCLUSIONS
Patients with CS are at high risk for mortality de-
spite contemporary therapy. Regardless of the hemo-
dynamic support strategy selected, it is essential to
reverse hypoperfusion as rapidly and completely as
possible to avoid progressive end-organ failure and
refractory CS. The marked heterogeneity observed
within the CS population precludes a one-size-fits-
all approach to the care of CS patients. Shock severity
classification in combination with a multidisciplinary
team-based strategy can enable individualized therapy.
Advances in understanding the pathophysiology and
biomarker patterns associated with specific CS pheno-
types could further facilitate personalized medicine.
Future studies are needed to not only establish the
safety and efficacy of specific treatments in CS but to
identify which patients are most likely to benefit from
certain therapies such as temporary MCS. Finally, CS
research should be harmonized in terms of shock phe-
notype and severity as well as studied outcomes to en-
able generalizability.
1 Department of Cardiovascular Medicine, Mayo Clinic,
Rochester, MN.
2 Department of Internal Medicine/Cardiology, Heart Center
Leipzig at University of Leipzig, Leipzig, Germany.
3 Department of Intensive Care Medicine, Intensive Care Unit,
Ghent University Hospital, Ghent, Belgium.
4 TIMI Study Group, Cardiovascular Division, Brigham and
Women’s Hospital, Boston, MA.
5 Division of Cardiology, Emory University School of Medicine,
Atlanta, GA.
6 Department of Anesthesia & Critical Care, Université Paris
Cité, APHP, Inserm MASCOT, FHU PROMICE, Paris,
France.
Supplemental digital content is available for this article. Direct
URL citations appear in the printed text and are provided in the
HTML and PDF versions of this article on the journal’s website
(http://journals.lww.com/ccmjournal).
1230      www.ccmjournal.org September 2023 • Volume 51 • Number 9
Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
Dr. Pöss receives research funding from the German Cardiac
Society, German Heart Research Foundation, and Dr. Rolf M.
Schwiete Foundation. Dr. Schaubroeck has received hono-
raria from Abiomed. Dr. Morrow’s institution received funding
from Abbott, Abiomed, and Amgen; he disclosed that he is a
member of the Thrombolysis in Myocardial Infarction Study
Group, which has received institutional research grant support
through Brigham and Women’s Hospital from: Abbott, Amgen,
Anthos Therapeutics, ARCA Biopharma, AstraZeneca, Bayer
HealthCare Pharmaceuticals, Daiichi-Sankyo, Eisai, Intarcia,
Ionis Pharmaceuticals, Janssen Research and Development,
LLC, Merck, Novartis, Pfizer, Quark Pharmaceuticals, Regeneron
Pharmaceuticals, Roche, Siemens Healthcare Diagnostics,
Softcell Medical Limited, and Zora Biosciences. He has received
consulting fees from Abbott Laboratories, ARCA Biopharma,
InCardia, Inflammatix, Merck & Co, Novartis, and Roche
Diagnostics. Dr. Mebazaa received grant from Roche Diagnostics,
Abbott Laboratories, 4TEEN4, and WIndtree Therapeutics; he
received honoraria for lectures from Roche Diagnostics, Bayer,
and MSD; he is a consultant for Corteria Pharmaceuticals,
S-Form Pharma, FIRE-1, Implicity, 4TEEN4, and Adrenomed;
he is coinventor of a patent on combination therapy for patients
having acute and/or persistent dyspnea; and he disclosed the
off-label product use of Vasopressors and specific mechanical
circulatory support devices may not be labeled for use in shock.
The remaining authors have disclosed that they do not have any
potential conflicts of interest.
For information regarding this article, E-mail: Jentzer.Jacob@
mayo.edu
REFERENCES
1. van Diepen S, Katz JN, Albert NM, et al; American Heart
Association Council on Clinical Cardiology; Council on
Cardiovascular and Stroke Nursing; Council on Quality of Care
and Outcomes Research; and Mission: Lifeline: Contemporary
management of cardiogenic shock: A scientific statement
from the American Heart Association. Circulation 2017;
136:e232–e268
2. Chioncel O, Parissis J, Mebazaa A, et al: Epidemiology, path-
ophysiology and contemporary management of cardiogenic
shock - a position statement from the Heart Failure Association
of the European Society of Cardiology. Eur J Heart Fail 2020;
22:1315–1341
3. Osman M, Syed M, Patibandla S, et al: Fifteen-year trends in
incidence of cardiogenic shock hospitalization and in-hospi-
tal mortality in the United States. J Am Heart Assoc 2021;
10:e021061
4. Esposito ML, Kapur NK: Acute mechanical circulatory support
for cardiogenic shock: The “door to support” time. F1000Res
2017; 6:737
5. Tyler JM, Brown C, Jentzer JC, et al: Variability in reporting of
key outcome predictors in acute myocardial infarction cardio-
genic shock trials. Catheter Cardiovasc Interv 2022; 99:19–26
6. Zeymer U, Bueno H, Granger CB, et al: Acute Cardiovascular
Care Association position statement for the diagnosis and
treatment of patients with acute myocardial infarction com-
plicated by cardiogenic shock: A document of the Acute

Cardiovascular Care Association of the European Society
of Cardiology. Eur Heart J Acute Cardiovasc Care 2020;
9:183–197
7. Tavazzi G, Rossello X, Grand J, et al: Epidemiology, monitoring,
and treatment strategy in cardiogenic shock. A multinational
cross-sectional survey of ESC-acute cardiovascular care as-
sociation research section. Eur Heart J Acute Cardiovasc Care
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
2022; 11:706–711
8. Jentzer JC, Ahmed AM, Vallabhajosyula S, et al: Shock in the
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023
cardiac intensive care unit: Changes in epidemiology and
prognosis over time. Am Heart J 2021; 232:94–104
9. Berg DD, Bohula EA, van Diepen S, et al: Epidemiology of
shock in contemporary cardiac intensive care units. Circ
Cardiovasc Qual Outcomes 2019; 12:e005618
10. Abraham J, Blumer V, Burkhoff D, et al: Heart failure-related
cardiogenic shock: Pathophysiology, evaluation and manage-
ment considerations: Review of heart failure-related cardio-
genic shock. J Card Fail 2021; 27:1126–1140
11. Bhatt AS, Berg DD, Bohula EA, et al: De Novo vs acute-on-
chronic presentations of heart failure-related cardiogenic
shock: Insights from the critical care cardiology trials network
registry. J Card Fail 2021; 27:1073–1081
12. Saxena A, Garan AR, Kapur NK, et al: Value of hemody-
namic monitoring in patients with cardiogenic shock under-
going mechanical circulatory support. Circulation 2020;
141:1184–1197
13. Baran DA, Grines CL, Bailey S, et al: SCAI clinical expert con-
sensus statement on the classification of cardiogenic shock:
This document was endorsed by the American College of
Cardiology (ACC), the American Heart Association (AHA), the
Society of Critical Care Medicine (SCCM), and the Society of
Thoracic Surgeons (STS) in April 2019. Catheter Cardiovasc
Interv 2019; 94:29–37
14. Naidu SS, Baran DA, Jentzer JC, et al: SCAI SHOCK stage
classification expert consensus update: A review and incorpo-
ration of validation studies: This statement was endorsed by
the American College of Cardiology (ACC), American College
of Emergency Physicians (ACEP), American Heart Association
(AHA), European Society of Cardiology (ESC) Association for
Acute Cardiovascular Care (ACVC), International Society for
Heart and Lung Transplantation (ISHLT), Society of Critical
Care Medicine (SCCM), and Society of Thoracic Surgeons
(STS) in December 2021. J Am Coll Cardiol 2022; 79:933–946
15. Menon V, Slater JN, White HD, et al: Acute myocardial infarc-
tion complicated by systemic hypoperfusion without hypo-
tension: Report of the SHOCK trial registry. Am J Med 2000;
108:374–380
16. Jentzer JC, Burstein B, Van Diepen S, et al: Defining shock
and preshock for mortality risk stratification in cardiac inten-
sive care unit patients. Circ Heart Fail 2021; 14:e007678
17. Harjola VP, Lassus J, Sionis A, et al; CardShock Study
Investigators: Clinical picture and risk prediction of short-
term mortality in cardiogenic shock. Eur J Heart Fail 2015;
17:501–509
18. Jentzer JC, Kashani KB, Wiley BM, et al: Laboratory markers
of acidosis and mortality in cardiogenic shock: Developing a
definition of hemometabolic shock. Shock 2022; 57:31–40
19. Jentzer JC, Schrage B, Patel PC, et al: Association between
the acidemia, lactic acidosis, and shock severity with outcomes
Critical Care Medicine www.ccmjournal.org      1231
Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
Concise Definitive Review
in patients with cardiogenic shock. J Am Heart Assoc 2022;
11:e024932
20. Poss J, Koster J, Fuernau G, et al: Risk stratification for
patients in cardiogenic shock after acute myocardial infarc-
tion. J Am Coll Cardiol 2017; 69:1913–1920
21. Jentzer JC, Rayfield C, Soussi S, et al: Advances in the staging
and phenotyping of cardiogenic shock Part 1: Clinical context.
JACC 2022; 1:1–14
22. Jentzer JC, van Diepen S, Barsness GW, et al: Cardiogenic
shock classification to predict mortality in the cardiac intensive
care unit. J Am Coll Cardiol 2019; 74:2117–2128
23. Kapur NK, Kanwar M, Sinha SS, et al: Criteria for defining
stages of cardiogenic shock severity. J Am Coll Cardiol 2022;
80:185–198
24. Burstein B, van Diepen S, Wiley BM, et al: Biventricular
function and shock severity predict mortality in cardiac ICU
patients. Chest 2022; 161:697–709
25. Thayer KL, Zweck E, Ayouty M, et al: Invasive hemodynamic
assessment and classification of in-hospital mortality risk
among patients with cardiogenic shock. Circ Heart Fail 2020;
13:e007099
26. Jentzer JC, Lawler PR, van Diepen S, et al: Systemic inflamma-
tory response syndrome is associated with increased mortality
across the spectrum of shock severity in cardiac intensive care
patients. Circ Cardiovasc Qual Outcomes 2020; 13:e006956
27. Jentzer JC, Bhat AG, Patlolla SH, et al: Concomitant sepsis
diagnoses in acute myocardial infarction-cardiogenic shock:
15-year national temporal trends, management, and out-
comes. Crit Care Explor 2022; 4:e0637
28. Ahmed AM, Tabi M, Wiley BM, et al: Outcomes associated with
cardiac arrest in patients in the cardiac intensive care unit with
cardiogenic shock. Am J Cardiol 2022; 169:1–9
29. Vallabhajosyula S, Dunlay SM, Prasad A, et al: Cardiogenic
shock and cardiac arrest complicating ST-segment eleva-
tion myocardial infarction in the United States, 2000-2017.
Resuscitation 2020; 155:55–64
30. Jentzer JC, Henry TD, Barsness GW, et al: Influence of cardiac
arrest and SCAI shock stage on cardiac intensive care unit
mortality. Catheter Cardiovasc Interv 2020; 96:1350–1359
31. Jentzer JC, Soussi S, Lawler PR, et al: Validation of cardio-
genic shock phenotypes in a mixed cardiac intensive care unit
population. Catheter Cardiovasc Interv 2022; 99:1006–1014
32. Zweck E, Thayer KL, Helgestad OKL, et al: Phenotyping car-
diogenic shock. J Am Heart Assoc 2021; 10:e020085
33. Jentzer JC, Rayfield C, Soussi S, et al: Machine learning
approaches for phenotyping in cardiogenic shock and critical
illness: Part 2 of 2. JACC 2022; 1:1–14
34. Jentzer JC: Understanding cardiogenic shock severity
and mortality risk assessment. Circ Heart Fail 2020; 13:
e007568
35. Jentzer JC, Schrage B, Holmes DR, et al: Influence of age
and shock severity on short-term survival in patients with
cardiogenic shock. Eur Heart J Acute Cardiovasc Care 2021;
10:604–612
36. Jentzer JC, van Diepen S, Henry TD: Understanding how
cardiac arrest complicates the analysis of clinical trials of
cardiogenic shock. Circ Cardiovasc Qual Outcomes 2020;
13:e006692
 Jentzer et al
37. Beer BN, Jentzer JC, Weimann J, et al: Early risk stratification
in patients with cardiogenic shock irrespective of the under-
lying cause - the cardiogenic shock score. Eur J Heart Fail
2022; 24:657–667
38. Jentzer JC, Tabi M, Burstein B: Managing the first 120 min of
cardiogenic shock: From resuscitation to diagnosis. Curr Opin
Crit Care 2021; 27:416–425
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
39. Jentzer JC, Ternus B, Eleid M, et al: Structural heart disease
emergencies. J Intensive Care Med 2021; 36:975–988
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023
40. Henry TD, Tomey MI, Tamis-Holland JE, et al; American Heart
Association Interventional Cardiovascular Care Committee of
the Council on Clinical Cardiology; Council on Arteriosclerosis,
Thrombosis and Vascular Biology; and Council on
Cardiovascular and Stroke Nursing: Invasive management of
acute myocardial infarction complicated by cardiogenic shock:
A scientific statement from the American Heart Association.
Circulation 2021; 143:e815–e829
41. Garan AR, Kanwar M, Thayer KL, et al: Complete hemody-
namic profiling with pulmonary artery catheters in cardiogenic
shock is associated with lower in-hospital mortality. JACC
Heart Fail 2020; 8:903–913
42. Hochman JS, Sleeper LA, Webb JG, et al: Early revasculariza-
tion in acute myocardial infarction complicated by cardiogenic
shock. SHOCK Investigators. Should we emergently revascu-
larize occluded coronaries for cardiogenic shock. N Engl J Med
1999; 341:625–634
43. Thiele H, Akin I, Sandri M, et al; CULPRIT-SHOCK Investigators:
PCI strategies in patients with acute myocardial infarction and
cardiogenic shock. N Engl J Med 2017; 377:2419–2432
44. Alviar CL, Miller PE, McAreavey D, et al; ACC Critical Care
Cardiology Working Group: Positive pressure ventilation
in the cardiac intensive care unit. J Am Coll Cardiol 2018;
72:1532–1553
45. van Diepen S, Reynolds HR, Stebbins A, et al: Incidence and
outcomes associated with early heart failure pharmacotherapy
in patients with ongoing cardiogenic shock. Crit Care Med
2014; 42:281–288
46. Jentzer JC, Hollenberg SM: Vasopressor and inotrope
therapy in cardiac critical care. J Intensive Care Med 2021;
36:843–856
47. Leopold V, Gayat E, Pirracchio R, et al: Epinephrine and
short-term survival in cardiogenic shock: An individual data
meta-analysis of 2583 patients. Intensive Care Med 2018;
44:847–856
48. Rui Q, Jiang Y, Chen M, et al: Dopamine versus norepinephrine
in the treatment of cardiogenic shock: A PRISMA-compliant
meta-analysis. Medicine (Baltim) 2017; 96:e8402
49. Burstein B, Tabi M, Barsness GW, et al: Association between
mean arterial pressure during the first 24 hours and hospital
mortality in patients with cardiogenic shock. Crit Care 2020;
24:513
50. Mathew R, Di Santo P, Jung RG, et al: Milrinone as compared
with dobutamine in the treatment of cardiogenic shock. N Engl
J Med 2021; 385:516–525
51. Jolly S, Newton G, Horlick E, et al: Effect of vasopressin on
hemodynamics in patients with refractory cardiogenic shock
complicating acute myocardial infarction. Am J Cardiol 2005;
96:1617–1620
1232      www.ccmjournal.org September 2023 • Volume 51 • Number 9
Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
52. Choi KH, Yang JH, Park TK, et al: Differential prognostic
implications of vasoactive inotropic score for patients with
acute myocardial infarction complicated by cardiogenic shock
according to use of mechanical circulatory support. Crit Care
Med 2021; 49:770–780
53. Jentzer JC, Baran DA, Bohman JK, et al: Cardiogenic shock
severity and mortality in patients receiving venoarterial extra-
corporeal membrane oxygenator support. Eur Heart J Acute
Cardiovasc Care 2022; 11:891–903
54. Berg DD, Barnett CF, Kenigsberg BB, et al: Clinical prac-
tice patterns in temporary mechanical circulatory support for
shock in the Critical Care Cardiology Trials Network (CCCTN)
Registry. Circ Heart Fail 2019; 12:e006635
55. Strom JB, Zhao Y, Shen C, et al: National trends, predic-
tors of use, and in-hospital outcomes in mechanical circula-
tory support for cardiogenic shock. EuroIntervention 2018;
13:e2152–e2159
56. Thiele H, Zeymer U, Neumann FJ, et al; IABP-SHOCK II
Trial Investigators: Intraaortic balloon support for myocar-
dial infarction with cardiogenic shock. N Engl J Med 2012;
367:1287–1296
57. Unverzagt S, Buerke M, de Waha A, et al: Intra-aortic balloon
pump counterpulsation (IABP) for myocardial infarction com-
plicated by cardiogenic shock. Cochrane Database Syst Rev
2015; 2015:CD007398
58. den Uil CA, Van Mieghem NM, M BB, et al: Primary intra-aortic
balloon support versus inotropes for decompensated heart
failure and low output: A randomised trial. EuroIntervention
2019; 15:586–593
59. Jentzer JC, van Diepen S, Henry TD, et al: Influence of intra-
aortic balloon pump on mortality as a function of cardiogenic
shock severity. Catheter Cardiovasc Interv 2022; 99:293–304
60. Damluji AA, van Diepen S, Katz JN, et al; American Heart
Association Council on Clinical Cardiology; Council on
Arteriosclerosis, Thrombosis and Vascular Biology; Council
on Cardiovascular Surgery and Anesthesia; and Council on
Cardiovascular and Stroke Nursing: Mechanical complications
of acute myocardial infarction: A scientific statement from the
American Heart Association. Circulation 2021; 144:e16–e35
61. Thiele H, Jobs A, Ouweneel DM, et al: Percutaneous short-
term active mechanical support devices in cardiogenic shock:
A systematic review and collaborative meta-analysis of ran-
domized trials. Eur Heart J 2017; 38:3523–3531
62. Dhruva SS, Ross JS, Mortazavi BJ, et al: Association of use
of an intravascular microaxial left ventricular assist device vs
intra-aortic balloon pump with in-hospital mortality and major
bleeding among patients with acute myocardial infarction
complicated by cardiogenic shock. JAMA 2020; 323:734–745
63. Miller PE, Bromfield SG, Ma Q, et al: Clinical outcomes and
cost associated with an intravascular microaxial left ventricular
assist device vs intra-aortic balloon pump in patients present-
ing with acute myocardial infarction complicated by cardio-
genic shock. JAMA Intern Med 2022; 182:926–933
64. Guglin M, Zucker MJ, Bazan VM, et al: Venoarterial ECMO for
adults: JACC scientific expert panel. J Am Coll Cardiol 2019;
73:698–716
65. Yannopoulos D, Bartos J, Raveendran G, et al: Advanced re-
perfusion strategies for patients with out-of-hospital cardiac
arrest and refractory ventricular fibrillation (ARREST): A phase

2, single centre, open-label, randomised controlled trial. Lancet
2020; 396:1807–1816
66. Belohlavek J, Smalcova J, Rob D, et al; Prague OHCA Study
Group: Effect of intra-arrest transport, extracorporeal cardio-
pulmonary resuscitation, and immediate invasive assessment
and treatment on functional neurologic outcome in refrac-
tory out-of-hospital cardiac arrest: A randomized clinical trial.
Downloaded from http://journals.lww.com/ccmjournal by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCy
JAMA 2022; 327:737–747
67. Ostadal P, Rokyta R, Karasek J, et al: Extracorporeal mem-
wCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 08/17/2023
brane oxygenation in the therapy of cardiogenic shock:
Results of the ECMO-CS randomized clinical trial. Circulation
2023; 147:454–464
68. Grandin EW, Nunez JI, Willar B, et al: Mechanical left ven-
tricular unloading in patients undergoing venoarterial extra-
corporeal membrane oxygenation. J Am Coll Cardiol 2022;
79:1239–1250
69. Unverzagt S, Machemer MT, Solms A, et al: Intra-aortic balloon
pump counterpulsation (IABP) for myocardial infarction com-
plicated by cardiogenic shock. Cochrane Database Syst Rev
2015; 2015:CD007398
70. Papolos AI, Kenigsberg BB, Berg DD, et al; Critical Care
Cardiology Trials Network Investigators: Management and
Critical Care Medicine www.ccmjournal.org      1233
Copyright © 2023 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
Concise Definitive Review
outcomes of cardiogenic shock in cardiac ICUs with versus
without shock teams. J Am Coll Cardiol 2021; 78:1309–1317
71. Tehrani BN, Truesdell AG, Sherwood MW, et al: Standardized
team-based care for cardiogenic shock. J Am Coll Cardiol
2019; 73:1659–1669
72. Hernandez-Montfort J, Sinha SS, Thayer KL, et al: Clinical out-
comes associated with acute mechanical circulatory support
utilization in heart failure related cardiogenic shock. Circ Heart
Fail 2021; 14:e007924
73. Kanwar MK, Everett KD, Gulati G, et al: Epidemiology and
management of right ventricular-predominant heart failure
and shock in the cardiac intensive care unit. Eur Heart J Acute
Cardiovasc Care 2022; 11:584–594
74. Thiele H, Freund A, Gimenez MR, et al; ECLS-SHOCK
Investigators: Extracorporeal life support in patients with acute
myocardial infarction complicated by cardiogenic shock - de-
sign and rationale of the ECLS-SHOCK trial. Am Heart J
2021; 234:1–11
75. Udesen NJ, Moller JE, Lindholm MG, et al; DanGer Shock
investigators: Rationale and design of DanGer shock: Danish-
German cardiogenic shock trial. Am Heart J 2019; 214:
60–68