JACC: HEART FAILURE VOL. 8, NO.

11, 2020

ª 2020 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION

PUBLISHED BY ELSEVIER

MINI-FOCUS: HEART FAILURE AND CARDIOGENIC SHOCK

STATE-OF-THE-ART REVIEW

A Standardized and Comprehensive

Approach to the Management of
Cardiogenic Shock
Behnam N. Tehrani, MD,a Alexander G. Truesdell, MD,a,b Mitchell A. Psotka, MD, PHD,a Carolyn Rosner, NP,a
Ramesh Singh, MD,a Shashank S. Sinha, MD, MSC,a Abdulla A. Damluji, MD, PHD, MPH,a
Wayne B. Batchelor, MD, MHSa

HIGHLIGHTS

Cardiogenic shock is a hemodynamically complex multisystem syndrome associated with
persistently high morbidity and mortality.

We propose a multidisciplinary approach to diagnosis and management, utilizing stan-
dardized protocols that emphasize early invasive hemodynamics and team-based care.

Development of shock networks with regionalized systems of care may improve clinical
outcomes on a large scale.

ABSTRACT

Cardiogenic shock is a hemodynamically complex syndrome characterized by a low cardiac output that often culminates
in multiorgan system failure and death. Despite recent advances, clinical outcomes remain poor, with mortality rates
exceeding 40%. In the absence of adequately powered randomized controlled trials to guide therapy, best practices for
shock management remain nonuniform. Emerging data from North American registries, however, support the use of
standardized protocols focused on rapid diagnosis, early intervention, ongoing hemodynamic assessment, and multi-
disciplinary longitudinal care. In this review, the authors examine the pathophysiology and phenotypes of cardiogenic
shock, benefits and limitations of current therapies, and they propose a standardized and team-based treatment algo-
rithm. Lastly, they discuss future research opportunities to address current gaps in clinical knowledge.
(J Am Coll Cardiol HF 2020;8:879–91) © 2020 by the American College of Cardiology Foundation.

I n 1967, Drs. Killip and Kimball reported a nearly

4-fold decline in acute myocardial infarction
(AMI) mortality utilizing continuous monitoring
for post-infarction arrhythmias (1). Unfortunately, pa-
tients who developed cardiogenic shock (CS) still
fared poorly, with in-hospital mortality of 81%. It
was not until 1999 that the landmark SHOCK (Should
We Emergently Revascularize Occluded Arteries in
Cardiogenic Shock) trial demonstrated improvement
in AMI-CS survival (2). More than 2 decades later,
short-term mortality from CS still remains >40% (3).
Recent North American registries, however, suggest

From the aInova Heart and Vascular Institute, Falls Church, Virginia; and bVirginia Heart, Falls Church, Virginia. John Teerlink,
MD, served as Guest Editor for this paper.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’
institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information,
visit the JACC: Heart Failure author instructions page.

Manuscript received June 23, 2020; revised manuscript received August 25, 2020, accepted September 8, 2020.

ISSN 2213-1779/$36.00 https://doi.org/10.1016/j.jchf.2020.09.005

880 Tehrani et al. JACC: HEART FAILURE VOL. 8, NO. 11, 2020

Standardized Management of Cardiogenic Shock NOVEMBER 2020:879–91

ABBREVIATIONS that outcomes may be improved through volume overload, often culminating in multiorgan
AND ACRONYMS early shock recognition and standardized system failure and death (Figure 1) (3,15). The initial
treatment algorithms (4–6). In this review, cardiac insult may stem from various etiologies
ADHF = acute decompensated
heart failure
we discuss the pathophysiology and classifi- (Table 1). Impaired CO and progressive diastolic
cation of CS and propose a standardized dysfunction raise ventricular end-diastolic pressures,
AMI = acute myocardial
infarction approach to care, from diagnosis to discharge which reduce coronary perfusion pressure, myocar-
CICU = cardiac intensive care (Central Illustration). dial contractility, and stroke volume (3). In response
unit to tissue ischemia and necrosis, released inflamma-
EPIDEMIOLOGY AND
CO = cardiac output tory mediators further impair tissue metabolism and
ECONOMIC IMPACT
CS = cardiogenic shock induce nitric oxide production, which causes sys-
LV = left ventricle/ventricular temic vasodilation and exacerbates hypotension (16),
CS is estimated to complicate 5% to 12% of
MCS = mechanical circulatory
stressing an already dysfunctional myocardium (3).
AMIs (3). With an aging population, CS inci-
support This maladaptive response may be acute, as occurs in
dence is on the rise, and patients are
PAC = pulmonary artery AMI-CS, or superimposed on chronic neurohormonal
increasingly complex, with more associated
catheter activations that accompany ADHF-CS. Hypoxia and
comorbidities (7). Although even small
PCI = percutaneous coronary pulmonary inflammation induce pulmonary vaso-
intervention ischemic insults may precipitate shock in
constriction, increasing biventricular afterload and
RV = right ventricle/ventricular
patients with pre-existing myocardial
myocardial oxygen demand. The renal response to
dysfunction, AMI-CS is typically associated
SCAI = Society for impaired glomerular perfusion increases tubular so-
Cardiovascular Angiography with >40% loss of left ventricular (LV)
dium reabsorption and activation of the renin-
and Interventions myocardium (8). Mechanical complications
angiotensin-aldosterone axis, resulting in further
such as free wall rupture, ventricular septal defect,
volume overload and compromised diuretic effec-
and papillary muscle rupture may also precipitate
tiveness. Sympathetically mediated splanchnic vaso-
AMI-CS (9). CS may additionally occur in patients
constriction further worsens volume overload by
with heart failure due to longstanding ventricular
redistributing 50% of total blood volume back to the
dysfunction (acute decompensated heart failure with
circulation (17). Augmented ventricular filling pres-
CS [ADHF-CS]). This form of CS often follows an
sures further worsen myocardial efficiency and
indolent clinical course and is more likely to require a
ischemia, especially within the right ventricle (RV)
biventricular hemodynamic support compared with
(18). Left unabated, this maladaptive cycle often
AMI-CS (10). Post-cardiotomy CS complicates 0.1% to
progresses to death.
0.5% of cardiac surgeries, because of pre-existing
myocardial dysfunction or intraoperative complica-
DEFINITION AND CLASSIFICATION
tions, including inadequate myocardial protection,
acute bypass graft failure, prosthetic valve dysfunc-
Clinical trials and societal guidelines have employed
tion, pericardial effusion, or aortic dissection (11).
a variety of definitions of CS (2,19–23). Patient eligi-
The economic impact of CS is substantial, espe-
bility for the SHOCK trial (2) was based on both clin-
cially when accompanied by multiorgan system fail-
ical and hemodynamic criteria, whereas other trials
ure, which is associated with nearly 50% in-hospital
relied on clinical criteria, including sustained hypo-
mortality, longer lengths of stay, and greater resource
tension and evidence of end-organ malperfusion
utilization (12). Analysis of 444,253 AMI-CS admis-
(Table 2). Building on the Diamond-Forrester classi-
sions from the National (Nationwide) Inpatient Sam-
fication system using cardiac index and pulmonary
ple from 2000 to 2014 observed a 4.3-fold increased
capillary wedge pressure, CS profiles initially focused
risk of developing multiorgan system failure. Overall,
on pulmonary congestion and systemic perfusion
the annual cost of CS exceeds $65 million (12,13), and
(24). Modern CS phenotyping is more nuanced,
survivors face impaired quality of life with higher
encompassing a broader spectrum of clinical and he-
rates of immobility, depression, and chronic anxiety
modynamic presentations beyond the classic “cold
(14).
and wet” construct. Phenotypes of CS may include
PATHOPHYSIOLOGY LV-dominant, RV-dominant, and biventricular pro-
files, each with its own unique hemometabolic char-
The central pathophysiologic derangement in CS is acteristics (25). Patients may also present in pre-
diminished cardiac output (CO) (3), leading to sys- shock, in which compensatory vasoconstriction may
temic hypoperfusion and maladaptive cycles of maintain a near-normal systolic blood pressure
ischemia, inflammation, vasoconstriction, and despite malperfusion, sometimes falsely reassuring
JACC: HEART FAILURE VOL. 8, NO. 11, 2020 Tehrani et al. 881
NOVEMBER 2020:879–91 Standardized Management of Cardiogenic Shock

C ENTR AL I LL U STRA T I O N Proposed Pathway for Contemporary Shock Care

Tehrani, B.N. et al. J Am Coll Cardiol HF. 2020;8(11):879–91.

Schematic representation of a proposed pathway for cardiogenic shock (CS) management. Key components include timely recognition, early invasive hemodynamics
and selective and tailored circulatory support. Regionalized systems of care with multidisciplinary CS teams can aid in the triage and transfer of these patients to
dedicated Level 1 CS centers for full spectrum and longitudinal care. ADHF-CS ¼ acute decompensated heart failure complicated by cardiogenic shock; AMI-CS ¼ acute
myocardial infarction complicated by cardiogenic shock; CI ¼ cardiac index; CICU ¼ cardiac intensive care unit; CPO ¼ cardiac power output; IABP ¼ intra-aortic
balloon pump; PAPi ¼ pulmonary arterial pulsatility index; PCWP ¼ pulmonary capillary wedge pressure; SBP ¼ systolic blood pressure; VA-ECMO ¼ venoarterial
extracorporeal membrane oxygenation.

physicians (25,26). Although comprising only 5.2% of
the SHOCK trial registry, these normotensive and
hypoperfused patients represented a high-risk cohort
with lower average CO compared with hypotensive
patients with CS and a 43% in-hospital mortality (27).
In search of a common language for defining disease
severity, the Society for Cardiovascular Angiography
and Interventions (SCAI) recently put forth a 5-stage
(A–E) classification system for CS (26). This nomen-
clature system has been retrospectively validated and
correlated to in-hospital and cardiac intensive care
unit (CICU) mortality (28).
882 Tehrani et al.
Standardized Management of Cardiogenic Shock
F I G U R E 1 Pathophysiology of Cardiogenic Shock
Cardiogenic shock is a low-output state stemming from primary cardiac dysfunction, resulting in hypotension and systemic hypoperfusion. This maladaptive syndrome is
perpetuated by physiologic cycles of inflammation, ischemia, vasoconstriction, and volume overload.
MANAGEMENT OF CS
EMERGENCY DEPARTMENT CARE. Effective emer-
gency department triage is key to the early recogni-
tion and treatment of CS. In AMI-CS, this means
timely acquisition and interpretation of a 12-lead
electrocardiogram by emergency medical personnel
and immediate transfer to a percutaneous coronary
intervention (PCI)–capable facility. In the emergency
department, CS diagnosis can be facilitated by phys-
ical examination, electrocardiography, laboratory
evaluation, and (when available) point-of-care echo-
cardiography (29). Although patients with pre-shock
may proceed directly to the cardiac catheterization
laboratory, those with SCAI stage C or D CS may first
necessitate initial stabilization using vasopressor
therapy and mechanical ventilation, albeit without
significantly delaying reperfusion (30–32). In patients
with SCAI stage E or end-stage CS in whom aggressive
therapies may be futile, palliative care consultation
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and discussions with health care surrogates regarding
goals of care may be warranted (33).
INVASIVE HEMODYNAMIC MONITORING. Despite an
absence of benefit of routine pulmonary artery cath-
eter (PAC) use for heart failure (34), growing evidence
supports the benefit of early invasive hemodynamic
assessment in patients with CS (4–6). PAC use may
lead to earlier and more accurate identification of the
CS phenotype so that medical and device-based
therapies may be applied in a tailored fashion.
Given these considerations, the routine use of early
invasive hemodynamics has been advocated as the
standard of care in contemporary CS manage-
ment (25,31).
VASOACTIVE THERAPIES. Intravenous inotropes
and vasopressors remain fundamental to the acute
management of CS. These agents may increase ven-
tricular contractility and CO, reduce filling pressures,
and preserve end-organ perfusion (3,15). Existing
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NOVEMBER 2020:879–91 Standardized Management of Cardiogenic Shock

inotropes exert their physiological effects through the

T A B L E 1 Common Etiologies of Cardiogenic Shock
modulation of cardiomyocyte calcium fluxes. Avail-
Left ventricular failure Arrhythmia
able intravenous inotropic and vasopressor drugs

Acute myocardial infarction
Atrial fibrillation or flutter
include adrenergic agents (norepinephrine, epineph-

Hypertrophic obstructive
Ventricular tachycardia or
rine), congeners (dobutamine, dopamine), phospho- cardiomyopathy fibrillation

Bradycardia or heart block
diesterase inhibitors (milrinone), and levosimendan,

Myocarditis
which modulates positive inotropic effects through a

Myocardial contusion
combination of calcium sensitization and selective

Peripartum cardiomyopathy Pericardial disease
phosphodiesterase-3 inhibition (35,36). Limited data
Post-cardiotomy
Tamponade
support the use of norepinephrine as the preferred
Progressive cardiomyopathy
Progressive pericardial constriction
first-line agent, and retrospective analyses suggest
Septic cardiomyopathy
similar outcomes with dobutamine and milrinone
Stress cardiomyopathy (takotsubo) Chemotherapeutic, toxic, metabolic

(30,37). With mechanisms of action independent of
Ventricular outflow obstruction
Calcium-channel antagonists

Adrenergic receptor antagonists
the beta-adrenergic receptor, milrinone and levosi-
Right ventricular failure
Thyroid disorders
mendan may be considered to augment CO, especially

Acute myocardial infarction
in patients treated with beta-blockers. Temporizing
Myocarditis Valvular or mechanical dysfunction
inotropic support in acute CS has a Class IC indication
Post-cardiotomy
Aortic regurgitation—acute bacterial
(38). However, given their propensity to increase
Progressive cardiomyopathy endocarditis

Pulmonary embolism
Mechanical valve dysfunction or thrombosis
myocardial oxygen demand, ischemic burden, and
Septic cardiomyopathy
Mitral regurgitation—myocardial ischemia or
malignant arrhythmias, these agents should be used
Worsening pulmonary hypertension infarction

Progressive mitral stenosis
in the lowest possible doses for the shortest dura-
Progressive aortic stenosis
tion (5).
Ventricular septal defect or free wall rupture

MANAGING CARDIAC ARREST IN CS. More than 50%

of AMI-CS patients suffer concomitant cardiac arrest
(CA), either preceding or as a consequence of CS
(20,23). The presence of CA increases in-hospital
mortality, particularly in the absence of underlying
shockable rhythm (39). Given that anoxic brain injury
remains the leading cause of mortality in out-of-
hospital patients with CA, treatment algorithms
based on electrocardiogram findings and the presence
or absence of unfavorable clinical features have been
proposed to identify patients who might benefit from
early angiography (40). In the setting of dynamic and
time-dependent complexities associated with AMI-CS
complicated by CA, a multidisciplinary approach to

T A B L E 2 CS Definitions Used in Clinical Trials

SHOCK Trial (1999) (2) IABP-SHOCK II Trial (2012) (22) IMPRESS Trial (2017) (23) CULPRIT-SHOCK Trial (2017) (20)

Study design RCT RCT RCT RCT

Study arms Emergent revascularization IABP vs. optimal medical therapy in Impella CP vs. IABP in Culprit lesion PCI (with option of
vs. initial medical AMI-CS treated with early mechanically ventilated staged revascularization) vs. ad
stabilization in AMI-CS revascularization (PCI or CABG) patients with AMI complicated hoc multivessel PCI in AMI-CS
by severe CS with multivessel CAD
Sample size 302 600 48 786*
Clinical criteria
SBP <90 mm Hg
Sustained SBP <90 mm Hg
Sustained SBP #90 mm Hg
Sustained SBP #90 mm Hg for
for $30 mins OR vaso- for $30 min or catecholamines to for >30 min or need for va- >30 min or need for vasopres-
pressors to maintain maintain SBP >90 mm Hg AND sopressors/inotropes to sors/inotropes to maintain SBP
SBP $90 mm Hg AND
Clinical pulmonary congestion maintain SBP >90 mm Hg >90 mm Hg

End-organ hypoperfusion AND
Clinical pulmonary congestion
(urine output <30 ml/h
Impaired end-organ perfusion
Impaired end-organ perfusion
or cool extremities) with $1 of the following criteria: with $1 of the following
a) Altered mental status criteria:
b) Cold/clammy skin and a) Altered mental status
extremities b) Cold/clammy skin and
c) Urine output <30 ml/h extremities
d) Lactate >2.0 mmol/l c) Urine output <30 ml/h
d) Lactate >2.0
Hemodynamic
CI #2.2 l/min/m2 and — — —
criteria PCWP >15 mm Hg

*Data was evaluated for 686 patients.

AMI ¼ acute myocardial infarction; CABG ¼ coronary artery bypass grafting; CAD ¼ coronary artery disease; CI ¼ cardiac index; CS ¼ cardiogenic shock; CULPRIT-SHOCK ¼ Culprit Lesion Only PCI versus
Multi-vessel PCI in Cardiogenic Shock; IABP ¼ intra-aortic balloon pump; IABP-SHOCK II ¼ Intraaoartic Balloon Pump in Cardiogenic Shock II; IMPRESS in Severe Shock ¼ IMPella versus IABP Reduces
mortality in STEMI patients treated with primary PCI in Severe cardiogenic SHOCK; PCI ¼ percutaneous coronary intervention; NA ¼ not applicable; PCWP ¼ pulmonary capillary wedge pressure;
RCT ¼ randomized controlled trial; SBP ¼ systolic blood pressure; SHOCK ¼ Should We Emergently Revascularize Occluded Arteries in Cardiogenic Shock.
884 Tehrani et al. JACC: HEART FAILURE VOL. 8, NO. 11, 2020

Standardized Management of Cardiogenic Shock NOVEMBER 2020:879–91

F I G U R E 2 Current Mechanical Circulatory Support Devices Used for the Treatment of Cardiogenic Shock

The hemodynamic profiles of the various circulatory support devices available for treatment of cardiogenic shock. ADHF ¼ acute decompensated heart failure;
AMI ¼ acute myocardial infarction; AO ¼ aorta; Bi-V ¼ biventricular; CS ¼ cardiogenic shock; FA ¼ femoral artery; FDA ¼ Food and Drug Administration; HR-PCI ¼ high
risk percutaneous coronary intervention; IABP ¼ intra-aortic balloon pump; IJ ¼ internal jugular; LA ¼ left atrium; LV ¼ left ventricular; LVAD ¼ left ventricular assist
device; PA ¼ pulmonary artery; RA ¼ right atrium; RPM ¼ revolutions per minute; RV ¼ right ventricular; RVF ¼ right ventricular failure; VA-ECMO ¼ venoarterial
extracorporeal membrane oxygenation. Adapted with permission from Thiele et al. (15).

management is recommended with emphasis on
evaluation of the patient’s overall prognosis, likeli-
hood of a meaningful neurological recovery and
candidacy for revascularization and device-based
therapies. The potential role for extracorporeal life
support in the treatment of AMI-CS patients with re-
fractory CA is of a particular interest, following a
single-center study suggesting improved outcomes
when employed early in select patients and using a
systematic approach (41).
MECHANICAL CIRCULATORY SUPPORT. Mechanical
circulatory support (MCS) devices are increasingly
used in CS to stabilize hemodynamics (7) although
exactly when, whether, and how to incorporate them
in shock care remain controversial (3,15). Potential
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NOVEMBER 2020:879–91 Standardized Management of Cardiogenic Shock

F I G U R E 3 CICU Management of CS

This schematic illustrates the longitudinal and multidisciplinary care pathways for cardiogenic shock (CS) care in a contemporary level 1 cardiac intensive care unit
(CICU). CI ¼ cardiac index; CO ¼ cardiac output; CPO ¼ cardiac power output; DNR ¼ Do Not Resuscitate order; dPAP ¼ diastolic pulmonary arterial pressure; L ¼ left;
MAP ¼ mean arterial pressure; MCS ¼ mechanical circulatory support; PAPi ¼ pulmonary arterial pulsatility index; PCWP ¼ pulmonary capillary wedge pressure;
pVAD ¼ percutaneous ventricular assist device; R ¼ right; sPAP ¼ systolic pulmonary arterial pressure; other abbreviations as in Figure 2.

benefits of MCS include reduction of LV stroke work
and intracardiac filling pressures, and enhancement
of coronary and end-organ perfusion (42). Device se-
lection should be guided by acuity of illness, CS
phenotype, degree of circulatory and ventricular
support required, vascular access or anatomy and
operator- or center-specific procedural volume and
expertise (Figure 2). Understanding
platform alters ventricular pressure-volume re-
lationships is critical to implementing the optimal
strategy (Supplemental Figure) (42). Although axial-
and centrifugal-flow devices may improve hemody-
namic compared with the intra-aortic balloon pump,
no survival benefit has yet been demonstrated
(Supplemental Table) (43). In addition, recent obser-
how each vational data from the CathPCI and Chest Pain-MI
886 Tehrani et al. JACC: HEART FAILURE VOL. 8, NO. 11, 2020

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T A B L E 3 Opportunities for Future Research in CS Care

Clinical Realms in CS Care Clinical Gaps in Knowledge Study Design

1. Diagnosis
a) Pulmonary arterial catheters
b) Classification of CS
2. Tailored therapeutics
a) MCS
b) Revascularization in AMI-CS
c) Vasopressors and inotropes in CS
d) Antithrombotics in AMI-CS
3. Care delivery models
a) Regionalized systems of CS with:
i) Hub-and-spoke networks
ii) Multidisciplinary shock teams
b) Multidisciplinary CICUs with 24/7
staffing
4. Palliative care
a) Early implementation of palliative
services in multidisciplinary CS care
1) Shared decision making
2) Goals of care and health
values discussions

Clinical utility of invasive hemodynamics in
Prospective multicenter registries
CS treatment algorithms
RCT

Prospective validation of risk stratification tools
Prospective multicenter registries
Management
Prospective multicenter registries

Patient selection
RCT

Vascular access strategies

MCS tailored to individual CS phenotypes

Optimal strategies for anticoagulation and
monitoring (TEG, aPTT, ACT)

Weaning and escalation strategies
Impella in AMI-CS
Prospective multicenter registries (NCSI, cVAD)

Clinical benefit of LV unloading pre-PCI
RCT (DanGer Shock [NCT01633502])
VA-ECMO in AMI-CS
ECLS-SHOCK (NCT02544594)

ECMO-CS (NCT02301819)

EURO SHOCK (NCT03813134)

ANCHOR (NCT04184635)
LV venting strategies with VA-ECMO
Prospective multicenter registries
1) Pharmacologic
RCT
2) IABP
3) Impella
4) Atrial septostomy
5) Pulmonary artery cannulation
6) Surgical LV venting
Decongestion in cardiorenal syndrome
Prospective multicenter registries
i. Aortix (Procyrion)
RCT
ii. Reitan Catheter Pump
iii. Second Heart Assist

Culprit-vessel vs. multivessel PCI
RCT

PCI vs. CABG
Safety and efficacy
RCT

Milrinone versus dobutamine in critically ill patients
(NCT03207165)

Norepinephrine vs. Norepinephrine and Dobutamine in
Cardiogenic Shock (SHOCK-NORDOB [NCT03340779])

Efficacy and Safety on Heart Rate Control with Ivabradine in
Cardiogenic Shock (ES-FISH [NCT03437369])
Intravenous P2Y12 inhibition to achieve timely platelet
RCT (DAPT-AMI-SHOCK [NCT03551964])
inhibition and to mitigate bleeding risk

Improved clinical outcomes
Prospective multicenter registries

Improved clinical outcomes
Prospective multicenter registries

Reduced complications

Reduced hospital length of stay

Reduced costs

Improved patient QOL, well-being
Prospective multicenter registries

Reduced Complications
RCT

Reduced costs

ACT ¼ activated clotting time; aPTT ¼ activated partial thromboplastin time; cVAD ¼ catheter-based ventricular assist device; DanGer Shock ¼ Danish-German Cardiogenic Shock Trial; DAPT-AMI-
SHOCK ¼ Dual Antiplatelet Therapy for Shock Patients with Acute Myocardial Infarction; ECLS-SHOCK ¼ extracorporeal life support in cardiogenic shock; ECMO-CS ¼


; LV ¼ left ventricular;
MCS ¼ mechanical circulatory support; NCSI ¼ National Cardiogenic Shock Initiative; QOL ¼ quality of life; RCT ¼ randomized controlled trial; SHOCK-NORDOB ¼ Norepinephrine vs Norepinephrine and
Dobutamine in Cardiogenic Shock; TEG ¼ thromboelastography; other abbreviations as in Table 2.

registries as well as the Premier Healthcare database
show wide variations in axial flow device use across
the United States and raise safety concerns, in
particular major bleeding, stroke, and mortality
(44,45). Emerging data from dedicated shock center
registries, however, suggest that when MCS devices
are deployed selectively using
hemodynamics and standardized multidisciplinary
treatment algorithms, improvements in survival may
be achieved (4–6). In patients with prohibitive ilio-
femoral vasculature, expertise in alternative access is
key. The axillary artery, in particular, has been
demonstrated to be a suitable conduit for intra-aortic
early invasive balloon pump and Impella (Abiomed, Danvers,
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NOVEMBER 2020:879–91
Massachusetts) in patients with CS, as it may also
facilitate earlier ambulation and improved nutritional
status for patients requiring prolonged circulatory
support while awaiting cardiac replacement therapy
(46,47). Current guidelines provide a Class IIb (Level
of Evidence: C) recommendation for utilizing MCS in
AMI-CS patients who do not stabilize with pharma-
cological therapy (48).
Our current practice is to deploy MCS selectively in
suitable patients with acute severe or refractory CS
after expedited consultation with the multidisci-
plinary shock team, which consists of an interven-
tional cardiologist, cardiothoracic surgeon, cardiac
intensivist, and advanced heart failure specialist.
Lactate levels, cardiac power output, and pulmonary
arterial pulsatility index help facilitate both MCS se-
lection and weaning strategies. MCS may be utilized
as a bridge to myocardial recovery, cardiac replace-
ment therapy, or as a temporizing measure to assess a
patient's candidacy for a durable ventricular assist
device or cardiac transplantation. Strict adherence to
best vascular access and closure practices, familiarity
with device troubleshooting, and multidisciplinary
care in a level 1 CICU are critical components of
optimal care (49).
CICU MANAGEMENT. CS is one of the leading in-
dications for CICU admission (50). The care of these
patients is inherently resource intensive and com-
plex. Although optimal organizational structure and
staffing models continue to be defined, emerging data
suggest that “high-intensity” staffing with a dedi-
cated cardiac intensivist or co-management among
cardiologists and intensivists may provide more
comprehensive, collaborative, and effective critical
care delivery (51). As proposed in the 2017 American
Heart Association consensus recommendations, CS
management in the CICU requires 24/7 care in a level 1
shock center with invasive hemodynamic monitoring
and capability to provide comprehensive multiorgan
system care (3). Ongoing multidisciplinary shock
team consultation may facilitate escalation and
weaning strategies in (Figure 3).
REGIONALIZED SYSTEMS OF CARE. Comprehensive
CS care should ideally be provided at a level 1 center
(49). The majority of patients with CS, however,
initially present to less well-resourced level 2 centers,
which may only offer primary PCI and intra-aortic
balloon pump support, or to level 3 centers without
PCI capability. Given the demonstrated volume-
outcome relationships in CS care, there is a need for
regionalized systems of care with shock networks
similar to those validated for ST-segment elevation
myocardial infarction and trauma (49,52). In this
Tehrani et al. 887
Standardized Management of Cardiogenic Shock
model, emergency medical services and level 2 to 3
centers collaborate in the triage, identification, and
stabilization of patients with CS, followed by expe-
dited transfer to a level 1 center using efficient “one-
call” communication systems. We direct these
referral calls to a single call center that activates the
multidisciplinary shock team to render initial treat-
ment recommendations and expedite transfer.
LV ASSIST DEVICES AND HEART TRANSPLANTATION.
Early and ongoing assessment of the potential need
for cardiac replacement therapy, either with durable
MCS or heart transplantation, is necessary for pa-
tients with refractory CS. Therapeutic considerations
include conventional risk factors such as age, renal
and hepatic function, coagulopathy, aortic valve
regurgitation, RV function and medication compli-
ance (54). Thorough clinical and psychosocial evalu-
ation is required. With the updated United Network
for Organ Sharing heart allocation protocol priori-
tizing patients with temporary MCS for expedited
heart transplantation, an increasing number of pa-
tients with CS have used this pathway (55). Given the
high risk of post-transplant mortality in this critically
ill patient population, further research is needed to
guide patient selection for such advanced thera-
pies (56).
SHOCK RESEARCH. Ongoing data collection and
feedback between physician and administrative
champions at hub-and-spoke shock care centers is
key to ensuring adherence to best practices, appro-
priate use of resources, and refinement of system-
wide strategies to sustain enhanced outcomes. Such
local collaboration may then spur the development of
larger multicenter registries and clinical trials on a
national level to address clinical gaps in knowledge
and assess innovative therapies and care models to
inform clinical practice (53).
SPECIAL CONSIDERATIONS FOR AMI-CS
VASCULAR ACCESS. Transradial access is recom-
mended as the default approach for coronary angi-
ography and PCI in AMI, following clinical trial
evidence of reduced major bleeding, vascular com-
plications, and major adverse cardiovascular events
compared with transfemoral access (57). It has also
been shown to be a viable access site across the
severity spectrum of AMI-CS (58). If radial access is
not feasible or if MCS is required, safe femoral access
techniques should be employed, incorporating com-
bined ultrasound and fluoroscopic guidance, use of
micropuncture needles, initial and final runoff angi-
ography, and dedicated hemostasis protocols to avoid
vascular complications and bleeding (58).
888 Tehrani et al.
Standardized Management of Cardiogenic Shock
ANTITHROMBOTIC THERAPIES. Prompt and potent
antithrombotic therapy is paramount in AMI-CS.
Several factors, however, pose challenges to
achieving prompt and safe antithrombotic effects: 1)
delayed absorption of oral P2Y 12 inhibitors due to
opioid induced enteral dysmotility; 2) impaired cy-
tochrome P450–dependent activation of clopidogrel
due to splanchnic and hepatic malperfusion; 3)
platelet dysfunction stemming from targeted tem-
perature management and microvascular thrombosis;
and 4) bleeding risks associated with large bore access
(59). Given limited safety and efficacy data for
antithrombotic therapy in AMI-CS, treatment recom-
mendations have been derived from stable AMI pop-
ulations. These include the preferential use of
intravenous unfractionated heparin due to impaired
subcutaneous absorption of low-molecular-weight
heparin, administration of crushed ticagrelor or pra-
sugrel to effect more rapid and predictable platelet
inhibition, and selective administration of the rapid-
acting parenteral antiplatelet agent cangrelor to
limit the gap in platelet inhibition at the time of
PCI (59).
REVASCULARIZATION STRATEGIES. Although over
70% of patients with AMI-CS present with multivessel
coronary artery disease, <4% undergo emergent cor-
onary artery bypass grafting (22). Observational data
suggest that PCI and coronary artery bypass grafting
share similar mortality rates in AMI-CS (60).
Notwithstanding the established benefits of complete
revascularization in AMI, the optimal management of
non–infarct-related artery lesions in AMI-CS remains
unclear (61). To date, the CULPRIT-SHOCK (Culprit
Lesion Only PCI versus Multi-vessel PCI in Cardio-
genic Shock) trial is the only study to address this
question, and demonstrated lower rates of 30-day
death or renal replacement therapy with culprit-
vessel PCI versus multivessel intervention (20). A
recent substudy of the National Cardiogenic Shock
Initiative showed comparable mortality, acute kidney
injury, and hospital length of stay between the 2
strategies when axial-flow MCS was implanted prior
to reperfusion (62), suggesting that revascularization
of nonculprit lesions may be feasible when supported
by MCS. Ad hoc multivessel PCI in AMI-CS currently
receives a Class IIb guideline recommendation (48).
SPECIAL CONSIDERATIONS FOR ADHF-CS
AND RV FAILURE
Early elucidation of the primary cause of ADHF-CS,
which can account for at least 30% of all CS clinical
presentations, is necessary because distinct etiologies
respond differently to medical and device-based
JACC: HEART FAILURE VOL. 8, NO. 11, 2020
NOVEMBER 2020:879–91
therapies. In addition to electrocardiography and
echocardiography, PAC use facilitates identification
of CS phenotype (25). For invasive hemodynamic
assessment, the direct Fick method of measuring CO
has served as the historic gold standard. However,
despite potential limitations (low-output state or se-
vere tricuspid regurgitation), a recent comparison
showed thermodilution CO to be superior to estimate
Fick measurements (63).
The optimal management of ADHF-CS is predi-
cated on accurate assessment of volume status. The
traditional mantra that the RV is preload dependent
often leads to inappropriate and detrimental volume
loading in the setting of RV dysfunction, which may
worsen RV dilation and tricuspid regurgitation. The
RV prefers euvolemia with a central venous pressure
of 8 to 12 mm Hg (64). RV distention causes leftward
interventricular septal shift, compromising LV filling
and reducing CO. Diuresis reduces ventricular dila-
tion and improves biventricular coupling (18). In
contrast, the RV has less contractile reserve than the
more muscular LV, and accordingly, the use of calci-
tropic agents has been associated with a progressive
decline in RV function (65). This may be due, in part,
to systemic vasodilation and decreased right-sided
perfusion pressures in the setting of elevated RV
pressures that accompany pulmonary hypertension.
Concomitant use of agents that increase systemic
afterload without increasing pulmonary vascular
resistance, such as vasopressin or norepinephrine,
may be needed to maintain RV perfusion during
inodilator therapy, particularly with milrinone (66).
In select patients with persistent isolated RV failure
refractory to medical therapy, RV MCS may be indi-
cated. Although the Impella RP and Protek Duo
(TandemLife, Pittsburgh, Pennsylvania) platforms
both bypass the failing RV, the centrifugal pump with
Protek Duo allows for splicing of an oxygenator
should there also be concomitant respiratory insuffi-
ciency (67). RV failure from progressive pulmonary
hypertension, however, is poorly treated with devices
that only provide RV support, given that the primary
lesion is the pulmonary vasculature and forced
perfusion may precipitate pulmonary hemorrhage. In
these cases, venoarterial extracorporeal membrane
oxygenation may be preferred (68).
In select patients with LV-dominant CS and
normotensive hypoperfusion, pure vasodilators such
as nitroprusside may improve CO by reducing after-
load, while the vasodilatory effects of milrinone and
dobutamine can also be effective for high-afterload
LV failure (3,69). Intravenous or inhaled pulmonary
vasodilators reduce RV afterload for pulmonary
arterial hypertension and RV failure (70). Minimizing
JACC: HEART FAILURE VOL. 8, NO. 11, 2020
NOVEMBER 2020:879–91
intrathoracic positive pressure ventilation, correcting
acidosis, and improving hypoxic pulmonary vaso-
constriction may also improve LV filling in the setting
of RV failure (18).
CONCLUSIONS
Only recently has the dismal prognosis of CS been
significantly altered. However, persistent gaps in
knowledge and wide treatment variations continue to
hamper progress (Table 3). We propose a standardized
approach to CS emphasizing early diagnosis, multi-
disciplinary care, selective MCS use, and invasive
hemodynamics to tailor therapies for CS phenotype.
This approach supplemented by dedicated CS shock
teams and networks holds promise in improving
outcomes. An urgent need for pragmatic randomized
clinical trials remains, so that existing and emerging
therapies can be adequately evaluated to further
inform clinical practice.
ACKNOWLEDGMENTS The authors thank the Dudley
family for their continued contributions and support
of the Inova Dudley Family Center for Cardiovascular
Innovation. The authors also acknowledge Dr. Daniel
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AUTHOR RELATIONSHIP WITH INDUSTRY
Dr. Tehrani has received consulting and speaker honoraria from
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KEY WORDS acute decompensated heart
failure, acute myocardial infarction,
cardiogenic shock, mechanical circulatory
support, multidisciplinary care
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