Circulation

AHA SCIENTIFIC STATEMENT

Escalating and De-escalating Temporary

Mechanical Circulatory Support in Cardiogenic
Shock: A Scientific Statement From the American
Heart Association
Bram J. Geller, MD, Chair; Shashank S. Sinha, MD, MSc, FAHA, Vice Chair; Navin K. Kapur, MD, FAHA; Marie Bakitas, DNSc, CRNP;
Leora B. Balsam, MD; Joanna Chikwe, MD; Deborah G. Klein, MSN, ACNS-BC, FAHA; Ajar Kochar, MD, MHS;
Sofia C. Masri, MD; Daniel B. Sims, MD, FAHA; Graham C. Wong, MD, MPH, FAHA; Jason N. Katz, MD, MHS, FAHA;
Sean van Diepen, MD, MSc, FAHA; on behalf of the American Heart Association Acute Cardiac Care and General Cardiology
Committee of the Council on Clinical Cardiology; Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation;
Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular and Stroke Nursing; Council on Peripheral
Vascular Disease; and Council on Cardiovascular Surgery and Anesthesia

ABSTRACT: The use of temporary mechanical circulatory support in cardiogenic shock has increased dramatically despite
a lack of randomized controlled trials or evidence guiding clinical decision-making. Recommendations from professional
societies on temporary mechanical circulatory support escalation and de-escalation are limited. This scientific statement
provides pragmatic suggestions on temporary mechanical circulatory support device selection, escalation, and weaning
strategies in patients with common cardiogenic shock causes such as acute decompensated heart failure and acute
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myocardial infarction. The goal of this scientific statement is to serve as a resource for clinicians making temporary
mechanical circulatory support management decisions and to propose standardized approaches for their use until more
robust randomized clinical data are available.

Key Words: AHA Scientific Statements ◼ clinical decision-making ◼ extracorporeal membrane oxygenation ◼ heart failure
◼ heart-assist devices ◼ intra-aortic balloon pumping ◼ shock, cardiogenic

C
ardiogenic shock (CS) remains an acute, highly
morbid, multifactorial syndrome, with short-term
mortality ranging from 40% to 50%.1–4 The use of
temporary mechanical circulatory support (tMCS) in CS
has increased dramatically despite a lack of robust ran-
domized controlled trials or evidence suggesting a signifi-
cant improvement in mortality.5 Although ample literature
describes and compares various tMCS options, tMCS
escalation and de-escalation recommendations from pro-
fessional societies are limited in nature. As a result, time-
sensitive and life-sustaining decisions are often based on
anecdotal clinical experience or institutional practices.
The goal of this scientific statement is to provide prac-
tical suggestions for the escalation and de-escalation of
tMCS for CS in contemporary clinical practice. For the
purposes of this document, escalation of tMCS refers
to initiating tMCS for patients not on mechanical sup-
port, transitioning from 1 form of tMCS to another plat-
form with more circulatory support, or transitioning from
1 device to multiple tMCS devices. De-escalation refers
to the weaning or subsequent explantation of 1 or mul-
tiple tMCS devices. Within this framework, this scientific
statement provides (1) an overview of tMCS devices
used in CS attributable to common CS causes such as
acute decompensated heart failure (HF) and acute myo-
cardial infarction (AMI); (2) principles underlying appro-
priate device selection, including the use of invasive
hemodynamic monitoring; (3) escalation strategies for

The devices listed here serve only to illustrate examples of these types of devices. This is not intended to be an endorsement of any commercial product, process,
service, or enterprise by the American Heart Association.
© 2022 American Heart Association, Inc.
Circulation is available at www.ahajournals.org/journal/circ

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 Geller et al Escalating and De-escalating tMCS in Cardiogenic Shock

tMCS in severe or refractory shock in patients who do

CLINICAL STATEMENTS
not respond to initial medical management; (4) manage-

AND GUIDELINES
ment strategies for patients with tMCS in the intensive
care unit (ICU); and (5) review options for de-escalating
tMCS as a bridge to recovery, transitioning from tMCS
to more durable support (eg, left ventricular [LV] assist
devices [LVAD] or cardiac transplantation), or referring to
palliative care and hospice when appropriate.

DEFINITION AND MEDICAL MANAGEMENT

OF CS
CS is a life-threatening physiological condition in which
cardiac dysfunction leads to sustained inadequate tissue
perfusion at both the tissue and cellular levels.6 CS is
most commonly caused by AMI (AMI-CS) or acute de-
compensated HF (HF-CS).
The definition of CS used in clinical trials is variable
and includes systolic blood pressure <90 mm Hg for
≥30 minutes (or support in order to maintain blood pres-
sure), a cardiac index ≤2.2 L∙min−1∙m−2, pulmonary capil-
lary wedge pressure (PCWP) ≥15 mm Hg, and markers
of end-organ hypoperfusion (urine output <30 mL/h,
altered mental status, cool extremities, lactate >2.0
mmol/L).6,7 Several approaches have been used to char-
acterize the severity of CS, but in current practice, the
Society for Cardiovascular Angiography and Interven-
tions shock classification and the Interagency Registry
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for Mechanically Assisted Circulatory Support profile are

most frequently used.3,8–10 Both of these methods have
proved useful in risk-stratifying CS severity and predict-
ing mortality.3,10–14
Most patients with CS are initially supported with
inotropes or vasopressors.1,15,16 However, inotropic sup-
port is often insufficient to improve tissue hypoperfusion
and to adequately resolve the metabolic derangements
associated with CS. In addition, although these medi-
cations can increase cardiac output and restore blood
pressure to more normal ranges, they do so at the cost
of increased myocardial oxygen consumption. Further-
more, vasopressor use can increase LV afterload and
worsen microvascular congestion, which may reduce
cardiac output and worsen the hemodynamic and meta-
bolic sequelae of CS.17
OVERVIEW OF tMCS DEVICES USED IN CS
tMCS can augment end-organ perfusion in patients with
de novo or refractory CS.6,18–21 tMCS offers short-term
hemodynamic support, from hours to weeks, and may be
used as a bridge to decision, a bridge to recovery, or a
bridge to a more durable platform (LVAD or transplanta-
tion). Options for tMCS (right, left, and biventricular tMCS)
include fully percutaneous configurations with catheter
or cannula entry in peripheral vessels, surgical configura-
Figure 1. Standard configurations of tMCS devices.
Alternative configurations such as the axillary artery also can be
used and have certain advantages such as ease of ambulation.
IABP indicates intra-aortic balloon pump; LV, left ventricular;
RVAD, right ventricular assist device; tMCS, temporary mechanical
circulatory support; and VA-ECMO, venoarterial extracorporeal
membrane oxygenation.
tions with centrally implanted cannulas or grafts connect-
ed to extracorporeal tMCS devices, or hybrid platforms
(Figure 1). tMCS devices can provide either partial or full
circulatory support and can provide differential effects on
myocardial oxygen consumption, LV unloading, LV wall
stress, or coronary artery perfusion (Table 1).19,20,22,23 Com-
bining tMCS platforms is also possible, and numerous
configurations exist. Examples include but are not limited
to ECPella (venoarterial extracorporeal membrane oxy-
genation [VA-ECMO] with an Impella for LV decompres-
sion), VA-ECMO with an intra-aortic balloon pump (IABP),
BiPella (left-sided support with an Impella 2.5/CP/5.5 and
right-sided support with an Impella RP), and right-sided

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 Geller et al Escalating and De-escalating tMCS in Cardiogenic Shock

Table 1. Comparison of tMCS Devices for CS

CLINICAL STATEMENTS

Biventricular
AND GUIDELINES

RV support LV support support

Impella RP TandemHeart RVAD IABP Impella TandemHeart LVAD VA-ECMO*
(Abiomed) (±Protek Duo) (Abiomed) (LivaNova)
(LivaNova)
Mechanism Axial-flow con- Centrifugal-flow Balloon inflation-deflation Axial-flow continuous Centrifugal-flow con- Centrifugal-flow
tinuous pump continuous pump (aortic counterpulsation) pump tinuous pump continuous pump
(RA to PA) (RA to PA) (LV to AO) (LA to FA through (RA to AO)
transeptal cannula)
Support RV RV LV LV LV RV and LV
Oxygenator may be Includes oxygen-
added to the circuit ator
Insertion/placement Femoral vein IJ vein Femoral artery Femoral artery or axil- Femoral vein to LA Femoral vein
Axillary artery lary artery (2.5, CP) Femoral artery Femoral artery
Axillary artery (5.5)
Cannula size 22F venous 29F/31F venous 7F–8F arterial 2.5–12F arterial 21F venous 17F–28F venous
CP–14F arterial 12F–19F arterial 14F–22F arterial
5.5–21F arterial
Flow, L/min 2–4 Maximum 4.5 0–1 2.5–5.5 Maximum 5–8 2–7
Maximum pump 33 000 7500 NA 2.5/CP 51 000/46 000 7500 5000
speed, rpm 5.0/5.5 33 000/33 000
LV unloading … … ↑ ↑–↑↑↑ ↑↑ ↓↓
RV unloading ↑ ↑ … … … ↑↑
Cardiac power ↑ ↑ ↑ ↑↑ ↑↑ ↑↑
Coronary perfusion … … ↑ ↑ … …

CVP ↓ ↓ ↔ or ↓ ↔ or ↓ ↔ or ↓ ↓
MAP - - ↑ ↑↑ ↑↑ ↑↑
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LVEDP ↑ ↑ ↓ ↓↓ ↓↓ ↔

PCWP ↑ ↑ ↓ ↓↓ ↓↓ ↔ or ↑
Myocardial oxygen ↓ ↓ ↓ ↓↓ ↔↓ ↔ or ↑
demand
Surgical tMCS con- Pump options include Centrimag (Abbott), Cardiohelp (Getinge), and Rotaflow (Getinge). These can be used with or without an oxygen-
siderations ator in multiple configurations, including the following: (1) A temporary RVAD can have a drainage cannula in the femoral vein or RA with
a return cannula from the IJ into the PA; (2) a temporary central RVAD can have a drainage cannula in the RA or RV with a return cannula
into the PA; (3) a temporary central LVAD can have a drainage cannula in the LA or LV with a return cannula into the aorta; or (4) multiple
central and percutaneous BiVAD configurations are possible.

AO indicates aorta; BiVAD, biventricular assist device; CS, cardiogenic shock; CVP, central venous pressure; FA, femoral artery; IABP, intra-aortic balloon pump;
IJ, internal jugular; LA, left atrium; LV, left ventricle; LVAD, left ventricular assist device; LVEDP, left ventricular end-diastolic pressure; MAP, mean arterial pressure; NA,
not applicable; PA, pulmonary artery; PCWP, pulmonary capillary wedge pressure; RA, right atrium; RV, right ventricle; RVAD, right ventricular assist device; tMCS,
temporary mechanical circulatory support; and VA-ECMO, venoarterial extracorporeal membrane oxygenation.
*Other percutaneous cannulation sites and multiple cannulation sites can be used: arterial access (axillary, subclavian or carotid) or venous access (IJ). Central
configurations are also possible.

TandemHeart with an LV Impella. If pulmonary support is
needed, an oxygenator can be added to an extracorporeal
right ventricular (RV) assist device (TandemHeart or surgi-
cal RV assist device) or a TandemHeart LVAD. VA-ECMO
can also be considered, as discussed in detail later.
Common causes of CS that may require tMCS ini-
tiation and contraindications for tMCS are listed in
Tables 2 and 3‚ respectively.6,18 Absolute contraindica-
tions to tMCS include irreversible cardiac failure with
a lack of an exit strategy (ie, heart transplantation or
durable mechanical circulatory support) and concomi-
tant irreversible noncardiac organ failure (eg, severe
anoxic brain injury, intracranial hemorrhage, moribund
state, incurable metastatic malignancy, or other termi-
nal illnesses). Often absolute contraindications to tMCS
initiation may, in certain circumstances, become relative
contraindications. For example, definitively diagnosing
noncardiac organ failure may not be feasible at the time
of tMCS consideration such as in the post–cardiac arrest
setting when accurate neuroprognostication is not pos-
sible at the time of concomitant shock onset. In these
instances, the shock team clinicians may have to base
risk-benefit decisions on the best information available.
All relative contraindications should be discussed by the
interdisciplinary team before consideration of device
implantation.6,24

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 Geller et al
Table 2. Causes of CS That May Warrant tMCS Escalation in
the Appropriate Clinical Context
AMI complications
CS
Acute ischemic mitral regurgitation
Ventricular septal defect
Advanced right-sided or left-sided heart failure
Acute cardiomyopathy
Fulminant myocarditis
Stress cardiomyopathy
Peripartum cardiomyopathy
Acute cardiac allograft failure
Posttransplantation RV failure
Postcardiotomy shock
Refractory arrhythmias
Drug overdose with profound cardiac depression
Massive pulmonary embolism
Cardiac arrest
AMI indicates acute myocardial infraction; CS, cardiogenic shock; RV, right
ventricular; and tMCS, temporary mechanical circulatory support.
ESCALATION OF tMCS
The decision to initiate and escalate tMCS for patients
with CS is based on a comprehensive assessment of
clinical, laboratory, imaging, and hemodynamic param-
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eters. Figure 2 gives clinical practice suggestions.25–34
These parameters should be assessed at a frequency
dictated by shock severity and clinical trajectory; some
unstable patients may require reassessment on the order
of minutes to hours, whereas patients with more stable
shock can be re-evaluated every 4 to 6 hours. Although
several risk prediction models have been developed for
AMI-CS, including the CardShock Score, IABP-Shock II
Score, and IHVI Risk Score, no single model has been
externally validated in all populations of CS, especially
the HF-CS population.35–38 Furthermore, these models
have not been validated to inform tMCS decisions.
Utility of Invasive Hemodynamic Profiling in CS
Emerging data suggest that invasive hemodynamic
profiling is important to characterize the hemodynamic
phenotype of CS, its severity, and to guide tMCS-re-
lated escalation and weaning decisions. Although it is
acknowledged that no definitive prospective or random-
ized data support the use of pulmonary artery catheters
(PACs) in the setting of CS, observational retrospective
data suggest that their use is associated with improved
outcomes.39,40 In fact, complete hemodynamic profiling
compared with incomplete or no hemodynamic assess-
ment has been associated with a reduction in mortality.41
We suggest a complete hemodynamic assessment of
patients with significant CS as early as possible when
Circulation. 2022;146:e50–e68. DOI: 10.1161/CIR.0000000000001076
Escalating and De-escalating tMCS in Cardiogenic Shock
Table 3. Absolute and Relative Contraindications for all
tMCS Platforms and Additional Device-Specific Relative
CLINICAL STATEMENTS
Contraindications
AND GUIDELINES
Device Contraindications
All devices Absolute
 Severe irreversible noncardiac organ failure limiting
survival (eg, severe anoxic brain injury or metastatic
cancer)
 Irreversible cardiac failure if transplantation or long-
term VAD is not an option
Relative
Moderate to severe aortic regurgitation
 Severe coagulopathy or contraindication to antico-
agulation, including advanced liver disease
Limited vascular access
 Aortic dissection, aneurysm, or severe atherosclerosis
Advanced age
Prolonged CPR >45 min
IABP Aortic dissection
Abdominal aortic aneurysm
Tachyarrhythmias
Impella LV thrombus
Severe aortic stenosis is a consideration, but if the valve
can be crossed with a wire is not an absolute contra-
indication
Mechanical aortic valve
Aortic dissection
TandemHeart Intra-atrial thrombus
VA-ECMO Aortic dissection (if peripheral cannulation)
CPR indicates cardiopulmonary resuscitation; IABP, intra-aortic balloon
pump; LV, left ventricular; tMCS, temporary mechanical circulatory support; VA-
ECMO, venoarterial extracorporeal membrane oxygenation; and VAD, ventricu-
lar assist device.
CS is identified and at an appropriate frequency relative
to shock severity and stability. Pressure tracings can be
monitored continuously, and cardiac output measure-
ments can be performed every 1 to 2 hours, depending
on shock severity. When PACs are not available, clinically
appropriate, or specific invasive hemodynamic measure-
ments are not required (ie, PCWP or RV metrics), non-
invasive cardiac output monitoring can be considered,
although the diagnostic accuracy of these data is lim-
ited.42,43
Defining the CS phenotype (LV-dominant, RV-domi-
nant, or biventricular shock) with respect to the conges-
tion profile may be associated with improved short-term
outcomes.22 LV-dominant congestion in CS is often char-
acterized by an elevated PCWP or LV end-diastolic pres-
sure >15 mm Hg. When LV congestion is present with
decreased cardiac output, this is consistent with an LV
shock profile, although it is important to note that some
patients may also have an LV shock profile without con-
gestion. Furthermore, in an LV shock profile, the RA pres-
sure may be normal, but it may also be elevated because
of biventricular congestion.
RV-dominant congestion in CS is accompanied by
a relatively normal PCWP in the setting of an elevated
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CLINICAL STATEMENTS
AND GUIDELINES
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Figure 2. Clinical, hemodynamic, imaging, and laboratory data that guide decisions of escalation and de-escalation of tMCS.
CO indicates cardiac output; CVP, central venous pressure; CXR, chest x-ray; ECMO, extracorporeal membrane oxygenation; LV, left ventricular;
MAP, mean arterial pressure; mPAP, mean pulmonary artery pulsatility; PADP, pulmonary arterial diastolic pressure; PAP, pulmonary artery
pulsatility; PASP, pulmonary arterial systolic pressure; PEEP, positive end-expiratory pressure; RV, right ventricular; SVi, stroke volume index; and
tMCS, temporary mechanical circulatory support.

right atrial (RA) pressure (>15 mm Hg) and an elevated
ratio of RA pressure to PCWP (>0.63 or 0.86), which
should trigger further evaluation for RV failure. The cut-
off for an abnormal RA/PCWP has been described as
>0.86 in AMI and >0.63 after LVAD, but the RA/PCWP
ratio exists on a spectrum with higher levels predictive
at higher sensitivity and specificity of RV failure.20,25,32 In
clinical practice, we suggest considering the RA/PCWP
along with other hemodynamic, clinical, biochemical, and
imaging parameters on a spectrum of severity to inform
escalation and de-escalation decisions.
The pulmonary artery pulsatility index (PAPi; [sys-
tolic pulmonary artery pressure−diastolic pulmonary
artery pressure]/RA) is a hemodynamic variable used to
identify RV failure.25–27,33,34 The PAPi is a derived value
that reflects RV contractility, RV pulsatile load, and RV

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 Geller et al
congestion and has been associated with adverse
outcomes in both AMI-CS and HF-CS after LVAD
implantation.20,33,34 The PAPi in CS is most useful in the
setting of an elevated RA pressure >10 mm Hg and in
the absence of moderate or severe pulmonary hyperten-
sion (pulmonary artery systolic pressure <50 mm Hg).
The prognostic cutoffs for concerning PAPi values dif-
fer between AMI-CS (≤0.9) and patients with HF under-
going LVAD implantation (<1.85).20,33,34,44 However, it is
important to note that there is no hemodynamic gold
standard for defining RV failure because the aforemen-
tioned hemodynamic values can be confounded by vol-
ume resuscitation, passive congestion, or concurrent
valvular disease (ie, tricuspid stenosis, tricuspid regurgi-
tation, pulmonic stenosis, and pulmonic regurgitation).45
As a result, to diagnose RV or biventricular failure, we
suggest integrating the invasive hemodynamic assess-
ment of RV failure with noninvasive cardiac imaging (ie,
echocardiography).
Suggestion for Clinical Practice
Unless there are absolute contraindications, PAC place-
ment is suggested to guide tMCS device selection and
use. Continuous PAC assessments combined with nonin-
vasive imaging may also facilitate the appropriate escala-
tion of tMCS if clinical improvement is not seen with an
initial tMCS platform.
Principles of tMCS Escalation
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In patients with AMI-CS or HF-CS, tMCS escalation
should involve an interdisciplinary team that may include
but is not limited to a cardiac intensivist, advanced HF
and transplantation cardiologist, interventional cardiolo-
gist, clinical cardiologist, cardiac surgeon, ECMO spe-
cialist, palliative care specialist, nursing specialist, and
relevant consultants. Escalation to tMCS can be consid-
ered in appropriately selected patients with evidence of
clinical hypoperfusion or hemodynamic deterioration de
novo, while on inotropes, or during initial tMCS support.
Possible indicators of ongoing severe CS may include
(1) persistently low cardiac index (<2.2 L∙min−1∙m−2); (2)
cardiac power output <0.6 W; (3) hypotension (systolic
blood pressure <90 mm Hg or mean arterial pressure
[MAP] <65 mm Hg); (4) inadequate lactate clearance
and lactate >2 mmol/L; (5) evidence of RV failure, in-
cluding a ratio of RA to PCWP >0.86 or PAPi ≤0.9; (6)
profound hypoxemia; or (7) recurrent ventricular tachy-
cardia or ventricular fibrillation.20,26,28,34,46–48
Early recognition of appropriate patients who can be
considered for escalation to tMCS may lead to improved
survival.7 tMCS in appropriately selected candidates
should be initiated as soon as possible with sufficient
support to fully reverse the potential hemometabolic
consequences of shock. If there is a delay to sufficient
early support with tMCS, worsening end-organ perfusion
and metabolic derangements can make future attempts
Circulation. 2022;146:e50–e68. DOI: 10.1161/CIR.0000000000001076
Escalating and De-escalating tMCS in Cardiogenic Shock
at escalating tMCS ineffective.49 Selection of tMCS
CLINICAL STATEMENTS
in CS requires an approach tailored to the underlying
AND GUIDELINES
pathogenesis, namely AMI-CS and HF-CS (Figures 3
and 4, respectively).
Escalation of tMCS in Patients With AMI-CS
Patients presenting with AMI at risk for CS, or in CS,
should undergo emergency revascularization. For pa-
tients at risk for shock, it may be reasonable to pursue
culprit vessel percutaneous coronary intervention (PCI)
via the radial approach because randomized data suggest
that radial access decreases bleeding complications and
may reduce mortality in the ST-segment–elevation myo-
cardial infarction setting.53–56 However, patients with ob-
jective evidence of CS within the AMI-CS context should
be considered for an initial femoral access strategy that
provides a rapid route for escalation to tMCS if required.
In patients with AMI at risk for shock, an LV end-diastolic
pressure should be obtained to provide rapid evaluation
of left-sided filling pressures.
We do not support routine tMCS for all patients with
AMI-CS given the lack of randomized data; however,
depending on shock severity, tMCS may be appropriate
even before PCI. In select patients before PCI, deploy-
ment of a tMCS device may provide hemodynamic sta-
bilization that enables culprit lesion or complex coronary
revascularization.57–59 If not performed before PCI, post-
PCI PAC placement should be considered because it
may be integrated with imaging data (either echocar-
diographic or left ventriculography) to provide valuable
prognostic data and to inform the type of shock (pre-
dominantly RV, LV, or biventricular).60 With these data,
a decision on the need for tMCS may be feasible (Fig-
ure 3). We suggest that tMCS initiation or escalation be
considered by an interdisciplinary shock team as soon as
significant CS is identified so that timely tMCS can be
deployed if clinically indicated. This may occur in a variety
of different clinical settings, including but not limited to
the emergency room, cardiac catheterization laboratory,
or cardiac ICU. However, randomized controlled trials
are needed to better define the most appropriate role of
tMCS in AMI-CS.61–63
In the presence of hypotension, elevated serum lac-
tate, or other signs and symptoms of hypoperfusion, with
evidence of LV failure, initial left-sided tMCS device sup-
port may include an IABP or Impella CP. Both provide
variable ventricular unloading and circulatory support.
Other potential options include a TandemHeart; however,
the transseptal cannulation is time-consuming and may
be particularly challenging in the setting of an ST-seg-
ment–elevation myocardial infarction.
Although IABP remains the most common tMCS plat-
form for AMI-CS, from currently available data, we sus-
pect that patterns may change moving forward. The IABP
SHOCK II trial (Intraaortic Balloon Pump in Cardiogenic
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CLINICAL STATEMENTS
AND GUIDELINES
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Figure 3. An algorithm for escalation of tMCS in AMI-CS.

Acute myocardial infarction with cardiogenic shock (AMI-CS) represents a complex and heterogeneous group of disorders that include ST-segment–
elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) in patients with or without diabetes, multivessel coronary artery disease, chronic
total occlusions, or preexisting heart failure with reduced ejection fraction. This figure highlights differences in timing of patient management with
STEMI vs NSTEMI, but other differences in management exist. CABG indicates coronary artery bypass graft; CI, cardiac index; CPR, cardiopulmonary
resuscitation; HR, heart rate; IABP, intra-aortic balloon pump; ICU, intensive care unit; LM, left main; LV, left ventricular; LVEDP, left ventricular end-
diastolic pressure; MI, myocardial infarction; PA, pulmonary artery; PAPi, pulmonary artery pulsatility index; PCI, percutaneous coronary intervention;
PCWP, pulmonary capillary wedge pressure; RA, right atrial; RV, right ventricular; SBP, systolic blood pressure; tMCS, temporary mechanical circulatory
support; TTE, transthoracic echocardiography; VA-ECMO, venoarterial extracorporeal membrane oxygenation; and VT/VF, ventricular tachycardia/
ventricular fibrillation. *These are some of the factors included in the multivariable ORBI (Observatoire Régional Breton sur l’Infarctus) score that
predicts the onset of CS among patients with AMI.50 †Although femoral access is associated with higher bleeding complications in STEMI and
potentially higher mortality, femoral access would provide the opportunity to rapidly escalate mechanical circulatory support in the setting of rapid
hemodynamic collapse. ‡In patients with NSTEMI, it is reasonable to place a PA catheter before revascularization. However, most patients with STEMI
should undergo emergency revascularization before PA catheter placement. §Extracorporeal CPR should be part of a previously established cardiac
arrest system of care in collaboration with a shock team to facilitate assessment of survival. Factors associated with low risk of survival attributable
to cardiac arrest include unwitnessed arrest, initial rhythm not ventricular fibrillation, no bystander CPR, >30 minutes to return of spontaneous
circulation, age >85 years, lactate >7, pH <7.2, and end-stage renal disease.51,52

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 Geller et al Escalating and De-escalating tMCS in Cardiogenic Shock

CLINICAL STATEMENTS
AND GUIDELINES
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Figure 4. A proposed algorithm for escalation of tMCS and device selection in patients with HF-CS.
HF-CS indicates heart failure caused by cardiogenic shock; IABP, intra-aortic balloon pump; LVAD, left ventricular assist device; MAP, mean
arterial pressure; PA, pulmonary artery; PAPi, pulmonary artery pulsatility index; PCWP, pulmonary capillary wedge pressure; RA, right atrial; RVAD,
right ventricular assist device; tMCS, temporary mechanical circulatory support; and VA-ECMO, venoarterial extracorporeal membrane oxygenation.
*Shock profile should include an assessment of congestion, hypoperfusion, and ventricular function (with hemodynamic and echocardiographic
assessments if available).

Shock II) did not show a net clinical benefit with IABP
use in patients with CS with ST-segment–elevation myo-
cardial infarction or non–ST-segment–elevation myocar-
dial infarction.1,7,64 Small trials have suggested that IABP
use before, but not after, PCI may improve survival in
AMI-CS.65 Data suggest that when an IABP successfully
reverses hypoperfusion in AMI-CS, survival is improved.66
However, in patients with significant CS, there is concern
that an IABP may not provide enough support to alleviate
hypoperfusion; notably, a single-center report suggested
a high rate of escalation, nearly 50%, for patients with
AMI-CS initially managed with an IABP.37
The National Cardiogenic Shock Initiative prospective
registry reported survival rates of at least 70% among
patients receiving an Impella CP either immediately
before or after reperfusion for AMI-CS.46 However, other
data (including data from AMI-CS and high-risk PCI
populations) have suggested adverse outcomes and
potential harm with an initial Impella support strategy.67,68
Overall, for patients with significant AMI-CS, Impella
devices may be a better first-line approach than IABP
unless the patient has severe mitral regurgitation, an LV
thrombus, a ventricular septal defect, or unrevascularized
coronary artery disease, in which case IABP may still
have a role. Appropriate patient selection remains critical,
and patients with more severe CS may derive a greater
benefit with Impella support according to the high rates
of tMCS escalation observed with IABP use.69 Similarly,
for patients with severely low cardiac indices or patients
on multiple vasoactive medications, an Impella 5.5 or
VA-ECMO should be considered because an Impella CP
may not provide adequate hemodynamic support.
For patients with isolated, primary RV failure in the setting
of AMI-CS that is refractory to medical therapy, the Impella
RP, right-sided TandemHeart with or without ProtekDuo,
and surgical temporary RV assist device (eg, CentriMag)

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 Geller et al
are potential first-line tMCS platforms.70–72 When these are
CLINICAL STATEMENTS
unavailable, VA-ECMO could also be considered. Given the
AND GUIDELINES
paucity of data to support one device over another, institu-
tional availability, individual expertise, and operator experi-
ence, should also factor into device selection.
Patients with AMI-CS with univentricular LV or RV
tMCS should be serially assessed for the need for biven-
tricular support. Biventricular dysfunction is increas-
ingly recognized to be common, with more than half of
patients with CS presenting with elevated biventricular
filling pressures, which may indicate biventricular fail-
ure or passive right-sided congestion in the setting of
LV shock.27 The optimal therapy for biventricular failure
depends on the cause and sequelae of RV failure and
prognosis. The need for RV support may be minimized
or even eliminated with the rapid diagnosis and suc-
cessful resolution of common, reversible causes of
RV failure, including mechanical complications of LV
support (eg, tamponade, LV device malposition and
obstruction); metabolic decompensation attributable
to acidosis, hypoxemia, hypercapnia, and sepsis; and
pulmonary complications such as pneumothorax, pul-
monary embolism, and pleural effusion.73 In patients
with biventricular failure without readily reversibly RV
dysfunction and with inadequate circulatory support,
escalation to percutaneous biventricular support (eg,
either an Impella RP or a right-sided TandemHeart with
a left-sided percutaneous ventricular assist device) or
VA-ECMO should be considered.74,75
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Escalation of tMCS in Patients With HF-CS
In contrast to AMI-CS, HF-CS device escalation initially
depends on congestive status and evidence of hypoper-
fusion because relative hypotension may be common and
well tolerated in the chronic HF population.76 In patients
with HF-CS with a cardiac index <2.2 L∙min−1∙m−2, evi-
dence of hypoperfusion, and a stable MAP >65 mm Hg,
afterload reduction with a vasodilator such as sodium
nitroprusside or inotropic support with intravenous milri-
none or dobutamine may initially be considered instead
of tMCS.16 However, if a patient is hypotensive with a low
cardiac index and worsening hypoperfusion (ie, rising lac-
tate level or worsening renal function), then initial therapy
with inotropes and vasopressors can be attempted with
an option to escalate to tMCS if medical management is
insufficient (Figure 4). Data from a large multicenter reg-
istry demonstrated that in-hospital mortality in patients
with HF-CS was associated with a high prevalence of
biventricular congestion and markers of end-organ hypo-
perfusion, including serum lactate, serum creatinine, and
elevated liver function tests. Although significant hetero-
geneity was noted with respect to tMCS device use in
HF-CS, IABP was the most common device used in the
overall cohort and in patients receiving durable LVAD and
heart transplantation.77
e58 August 9, 2022
Escalating and De-escalating tMCS in Cardiogenic Shock
In HF-CS, relative LV or RV failure will help guide
device selection. In LV-predominant CS, initial support
with an IABP, LV Impella, or TandemHeart may be appro-
priate. The severity of shock can be used to aid in device
selection.76 For example, a patient with more severe CS
may be better supported with an Impella 5.5 rather than
an Impella CP. For patients with HF-CS with significant
concomitant RV dysfunction, hypoxemia, or more severe
shock, VA-ECMO may be considered.44 Many of the
other principles described in regard to AMI-CS remain
relevant in the HF-CS population.78
Suggestion for Clinical Practice
Incorporating an invasive hemodynamic assessment
with laboratory and imaging data as part of a patient’s
clinical management strategy may help ascertain CS
severity and guide appropriate device selection. Pa-
tients with more severe or refractory shock may be
more likely to benefit from tMCS devices that generate
more systemic perfusion such as Impella 5.5, Tandem-
Heart, or VA-ECMO.6,7
MANAGEMENT OF tMCS IN THE ICU
Providing High-Quality Care for Patients With
CS
We suggest that patients with refractory CS be trans-
ferred to centers with appropriate interdisciplinary ex-
pertise and adequate patient volumes to ensure optimal
outcomes; community hospitals are encouraged to de-
velop collaborative care models when local resources
and expertise are not available.6 Within individual hospi-
tal systems, adoption of an interdisciplinary shock team
may further improve clinical outcomes.37,79,80 The goals of
the shock team and collaboration with a centralized CS
hub are to streamline care, minimize treatment delays,
and centralize advanced HF services.6,37 The shock team
and centralized CS hub also ensure equitable access to
high-quality care and opportunities to escalate to tMCS
when appropriate.
Suggestion for Clinical Practice
We suggest the adoption of interdisciplinary CS teams
and a centralized hub-and-spoke model of critical care
delivery for regional CS care. In this model, patients who
require tMCS care beyond what the local hospital is able
to offer can be transferred to a centralized hub hospital
as early as possible once the patient has been stabilized.
Clinical and Laboratory Goals
Management of tMCS in the intensive care setting re-
quires continuous monitoring to ensure that adequate
hemodynamic support is being achieved and that the
metabolic derangements of CS are resolving. Hemody-
namically, we suggest a goal MAP of at least 65 mm Hg
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 Geller et al
for most patients, although we acknowledge that the lit-
erature to support this goal in CS is weak. A post hoc
analysis of a randomized trial comparing intravenous
dobutamine with milrinone in patients with CS demon-
strated that a low MAP (defined as an average MAP <70
mm Hg) was associated with worse clinical outcomes.81
Other studies have similarly suggested that MAPs <65
mm Hg are associated with worse outcomes.82
We also suggest that the MAP goal may need to
be individualized for patients with worsening metabolic
derangements such as worsening acute kidney injury
despite MAPs ≥65 mm Hg.83 Clinical parameters such as
urine output should be closely monitored, with a general
goal of 0.5 mL/h per 1 kg body weight, although this
may vary, depending on the specific patient. In addition,
we suggest trending neurologic status along with tem-
poral monitoring of lactate, serum creatinine, and liver
function tests to determine whether adequate hemomet-
abolic support is achieved.84 Finally, regular examinations
of peripheral perfusion, often done in conjunction with
the bedside nurse, should be performed frequently (ie,
hourly or every 2 hours), especially until the shock state
has resolved (these concepts are outlined in Figure 2).
Basic laboratory markers should be checked every 4
to 6 hours, but lactate may be checked every 1 to 4 hours
until stable support is achieved. Acidosis may interfere
with appropriate blood pressure response to vasoactive
medications; we therefore suggest avoiding significant
acidosis (pH <7.3). Other markers such as urine color,
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lactate dehydrogenase, and plasma free hemoglobin may
be important to trend if a complication such as hemolysis
is suspected.
Suggestion for Clinical Practice
We suggest a goal MAP of at least 65 mm Hg for most
patients with CS.
Invasive Cardiac Monitoring
As is the case for escalation, PACs may provide impor-
tant hemodynamic information to guide the care of pa-
tients in CS. Therefore, we suggest the use of PACs in
most patients supported with tMCS, as discussed previ-
ously.39,64,85
For most patients in the ICU setting, it is reasonable
to target an RA pressure <10 to 15 mm Hg and a PCWP
<18 mm Hg. In general, we suggest targeting a cardiac
index of at least 2.2 L∙min−1∙m−2, although this may be
individualized in cases of mixed shock or for patients with
continued end-organ hypoperfusion. With some forms of
tMCS such as VA-ECMO, the cardiac indices calculated
with the Fick equation or thermodilution are not valid. In
these cases, the flow from the ECMO circuit suggests
the tMCS contribution to net cardiac output but gener-
ally slightly underestimates any cardiac index calculation
because it would fail to include the contribution of native
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Escalating and De-escalating tMCS in Cardiogenic Shock
cardiac output. In these settings, the clinical, laboratory,
CLINICAL STATEMENTS
and imaging parameters become increasingly important
AND GUIDELINES
during ICU management. Other hemodynamic param-
eters such as pulse pressure, which can be variably
affected by the tMCS platform being used, are similarly
less useful in tMCS monitoring. Furthermore, many of
the invasive quantifications of LV/RV function that have
been discussed previously are either not accurate or not
validated in the setting of tMCS support.
Echocardiography
The indications for echocardiography in the ICU depend
on the tMCS platform being used. In VA-ECMO manage-
ment, echocardiography can, with either M-mode or 2-di-
mensional imaging, determine when the LV has reached
a state of maximal LV unloading and frequency of aortic
valve opening.86 Contrast echocardiography may also be
useful in identifying the watershed area, defined as the
intersection between the antegrade pulsatile flow from
the LV and the retrograde nonpulsatile flow from the
ECMO arterial output.87
Although Impella devices are usually placed under
direct fluoroscopy, echocardiography is the main imaging
modality used for LV Impella adjustments. Impella posi-
tioning can be tenuous, and in the case of the Impella
CP, the inlet should ideally be located 3.5 cm below the
aortic annulus. We suggest monitoring Impella position-
ing with the use of limited echocardiography in the set-
ting of various clinical changes (eg, suction alarms on the
controller, worsening patient hemodynamics, hemolysis,
and ventricular arrhythmias). Impella implanting centers
should therefore have 24-hour access to echocardiogra-
phy to assist with Impella placement and to evaluate for
potential device migration.88
Complications
Complications in patients supported with tMCS can be
broadly categorized as vascular, neurologic, hematologic,
mechanical, and infectious.89,90 The occurrence of com-
plications is influenced by device type, insertion tech-
nique, duration of support, and patient characteristics.
Accurately determining complication rates in the litera-
ture is challenging; individual studies have widely variable
incidence rates, and larger studies report wide ranges
that belie a true assessment of complication rates.89
In general, devices that provide more robust circula-
tory support often use larger cannulas and therefore are
associated with more complications. For example, vas-
cular complications, including limb ischemia and limb
loss, are most common with VA-ECMO and least com-
mon with IABP.90–93 Most vascular events are attributable
to arterial thrombosis or occlusion of blood flow to the
distal extremity by the tMCS cannula. Larger sheaths
and smaller access vessels increase the risk of limb
August 9, 2022 e59
 Geller et al
ischemia.90–93 In the case of VA-ECMO, routine place-
CLINICAL STATEMENTS
ment of a distal perfusion catheter may significantly
AND GUIDELINES
attenuate distal limb ischemia.94 The same trend of more
complications being associated with devices that provide
more support is also found in regard to other complica-
tions such as bleeding, stroke, and infection.67,89,95 Hemo-
lysis, however, appears to be most common with the
Impella family of devices.88,96
Serial monitoring of urine color, lactate dehydroge-
nase, plasma free hemoglobin, haptoglobin, and serum
hemoglobin is suggested to monitor for hemolysis. We
suggest a hemolysis evaluation using many of the tests
described at least daily or more often if clinical concerns
for hemolysis exist. Depending on the device, decreas-
ing revolutions per minute, as with Impella or VA-ECMO,
may reduce hemolysis at the expense of augmented car-
diac output. In the case of Impella devices, repositioning
of the device may also significantly lower the rates of
hemolysis when present.97,98 Mechanical complications
include device-related cardiac perforation, aortic valve
or mitral chordal/leaflet injury (LV Impella), and pump
thrombosis. Malpositioning is an issue with all devices
but may be most deleterious in the case of a left-sided
TandemHeart; malpositioning of the inflow cannula can
lead to catheter migration, culminating in systemic cir-
culation of deoxygenated blood. Device malfunction can
include pump failure (all platforms) and oxygenator fail-
ure (VA-ECMO).89
A complication with VA-ECMO is LV distention due
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to increased afterload caused by retrograde perfusion
from the circuit, which can result in pulmonary edema
and potential intracardiac thrombus formation. Peripheral
VA-ECMO can also result in different cerebral and lower-
extremity oxygen saturations attributable to underoxy-
genated blood ejected from the LV preferential going to
the brain and relatively hyperoxic blood from the ECMO
circuit going to the lower extremities. Therefore, patients
on peripheral VA-ECMO need to be monitored for differ-
ential hypoxia (also known as north-south syndrome or
Harlequin syndrome) with blood gases from a right radial
arterial line and often with noninvasive cerebral satura-
tions.99 A surgically placed LV vent into the LV apex or
pulmonary vein addresses differential hypoxia by mini-
mizing blood ejected from the LV. Alternatively, the addi-
tion of a venous return cannula (veno-arterial-venous
ECMO) can improve differential hypoxia. In this configu-
ration, there are 2 return cannulas: 1 is arterial and the
other is venous. The additional venous return cannula
brings oxygenated blood from the ECMO circuit back
toward the RA, thereby improving the oxygen content of
blood returned to the heart and minimizing differential
hypoxia. Other LV unloading or venting strategies may
address pulmonary edema caused by increased LV after-
load but may not improve north-south syndrome. These
include an IABP and LV Impella used in conjunction with
VA-ECMO.100,101 A more detailed discussion of LV vent-
e60 August 9, 2022
Escalating and De-escalating tMCS in Cardiogenic Shock
ing strategies is beyond the scope of this scientific state-
ment.102–104
Although infections can develop with any tMCS
device, we suggest against the routine use of prophy-
lactic antibiotics.105 Prophylactic antibiotics may be con-
sidered in patients with central VA-ECMO with an open
chest. Infection is a complication that is not necessarily
specific to the device pump but more likely is related to
the duration of support and location of access (ie, femo-
ral versus axillary or peripheral versus central). We sug-
gest a clinically driven infectious workup for patients with
a fever, leukocytosis, or other clinical manifestations of
local or systemic infections. It is important to note that
fevers may be less pronounced in patients on VA-ECMO;
therefore, the threshold for an infectious workup needs
to be adjusted accordingly.
DE-ESCALATING tMCS
Weaning in the ICU
The timing to initiate tMCS weaning has not been well
studied, but it is reasonable to begin weaning on resolu-
tion of cardiac dysfunction or evidence of at least partial
myocardial recovery, improvement in end-organ hypo-
perfusion, intravascular euvolemia, minimal intravenous
inotropic support, and improved contractility on echo-
cardiography. In some circumstances such as when sig-
nificant complications arise from ongoing tMCS support,
weaning may need to be initiated before the patient has
been fully optimized. In these situations, the benefits of
tMCS support need to be balanced against the risks of
continued complications related to the tMCS device.
We suggest weaning tMCS with an intention of
explanting the device as soon as it is safe because longer
duration of support is associated with worse outcomes.
To this end, we suggest daily assessments to determine
readiness to wean. During tMCS weaning, we advocate
for a stepwise decrease in tMCS support that is device
specific (Table 4).106 tMCS can be weaned rapidly or in
a more prolonged manner. Rapid weaning may be more
appropriate for patients with AMI-CS who have been fully
revascularized and had a recovery in ejection fraction or
for patients with CS attributable to a valvular lesion that
has subsequently resolved. Alternatively, a slower wean
may be appropriate for patients with HF-CS. If weaning
is successful, defined by stable clinical, hemodynamic,
and laboratory findings on low levels of support, the
patient may be ready for device explantation and libera-
tion from tMCS.
For patients on VA-ECMO, flows are typically
reduced in increments of 0.5 to 1 L/min until a level
of 1.5 to 2.0 L/min is reached (although some centers
may transiently reduce flows to 1 L/min often under
echocardiographic guidance to assess ventricular
function).107,108 Concomitant systemic anticoagulation
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 Geller et al Escalating and De-escalating tMCS in Cardiogenic Shock

Table 4. Weaning Strategies for tMCS

CLINICAL STATEMENTS
Rapid weaning Standard weaning Lowest level before

AND GUIDELINES
Device Weaning increment frequency frequency decannulation
LV support* IABP From 1:1 to 1:2 to 1:3 (or Direct from full support Every 2–4 h 1:3 (or 1:4/1:8)
1:4/1:8, depending on the manu- to 1:3 (or 1:4) 75% reduction of volume
facturer) 75% reduction of vol-
Alternatively, may decrease vol- ume
ume serially by 10%–25%
Impella 2.5, CP, or 5.5 P1–P2 Every 5 min Every 2–4 h P2
TandemHeart LVAD 0.5 L/min Every 5 min Every 2–4 h 2 L/min
RV support* Impella RP P1–P2 Every 5 min Every 2–4 h P2 (though maintain flows
>1.5 L/min)
TandemHeart RVAD 0.5 L/min Every 5 min Every 2–4 h 2 L/min
±ProtekDuo
Biventricular VA-ECMO 0.5–1 L/min Every 5–15 min Every 2–4 h 1–2 L/min (generally not
support* maintained at 1 L/min)

IABP indicates intra-aortic balloon pump; LV, left ventricular; RV, right ventricular; RVAD, right ventricular assist device; tMCS, temporary mechanical circulatory
support; and VA-ECMO, venoarterial extracorporeal membrane oxygenation.
*Surgical tMCS devices (Centrimag, Cardiohelp, or Rotaflow) can be used in a variety of configurations. Weaning of these platforms needs to be individualized to
the tMCS configuration and underlying patient physiology. For surgical tMCS, typically flow is decreased by 0.5 L/min every 2 to 4 hours.

is necessary to reduce the risk of thromboembolic
events. If hemodynamic stability is maintained despite
the reduction in support, decannulation can be con-
sidered. For patients supported with VA-ECMO and
another platform, VA-ECMO is generally weaned first,
and in the case of an Impella, the support (in terms
of P-level) may be increased to allow ECMO decan-
nulation. When an IABP is used alone to support the
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success be determined and decisions for decannula-
tion be made by interdisciplinary teams using available
clinical, hemodynamic, laboratory, and imaging data.
Successful Weaning and Decannulation
Strategies
It is reasonable to use low-dose inotropic or vasopressor
support to facilitate weaning of tMCS, with support tai-

patient in CS, weaning typically involves a methodi-

cal reduction in counterpulsation frequency from 1:1
to 1:2 and then to 1:3 (or 1:4/1:8, depending on the
IABP manufacturer) before removal. Although less
frequent, systematically decreasing the balloon vol-
ume can also be used for IABP weaning.109 For the
Impella and TandemHeart devices, systematic weaning
approaches to low levels of support before removal
should also be performed.
Although weaning algorithms have been proposed,
there is no single validated score or metric that can be
reliably used to determine successful tMCS weaning
or readiness for decannulation.23,73,107,108,110–112 Medical
teams caring for patients receiving tMCS should inte-
grate temporal trends in multimodal cardiac monitoring
and markers of noncardiac organ hypoperfusion during
the weaning process. Additional metrics to monitor dur-
ing weaning include invasive cardiovascular hemody-
namics, echocardiographic imaging, laboratory tests, and
clinical examination (outlined in Figure 2).
Suggestion for Clinical Practice
We suggest a daily evaluation to determine readiness
to wean. It is reasonable to begin tMCS weaning in pa-
tients who are hemodynamically stable, require minimal
intravenous hemodynamic support, are intravascularly
euvolemic, and have had improvement or correction of
the underlying cause of CS. We suggest that weaning
lored to a patient’s unique pathophysiology. In many cas-
es, an inotropic agent such as intravenous dobutamine
or milrinone may be used to enhance cardiac contractility
and to reduce ventricular afterload. In other cases, par-
ticularly among patients with mixed shock, a vasoactive
medication with inotropic and vasopressor properties
may be more ideal.
Invasive hemodynamic monitoring with a PAC can
help guide the weaning process by identifying ade-
quate decongestion and ventricular unloading, includ-
ing an RA pressure <10 to 15 mm Hg and a PCWP
<18 mm Hg. MAPs should remain ≥65 mm Hg on mini-
mal vasoactive support. Hemodynamic targets should,
however, be highly individualized; in some patients with
chronic HF, optimization may occur at slightly higher
filling pressures or with lower MAPs, assuming that
end-organ dysfunction has resolved. Laboratory mark-
ers such as lactate should remain ≤2 mmol/L. Last,
echocardiographic parameters may be helpful, depend-
ing on whether the patient requires LV, RV, or biven-
tricular support. Weaning algorithms are scarce in the
literature, but a tMCS weaning algorithm has recently
been proposed.106 Here, we propose a novel weaning
algorithm in Figure 5.23,73,107,108,110–112
In addition to imaging, invasive hemodynamic, and lab-
oratory markers that may suggest successful weaning,
clinical parameters must be reassessed continuously and

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 Geller et al Escalating and De-escalating tMCS in Cardiogenic Shock
CLINICAL STATEMENTS
AND GUIDELINES
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Figure 5. tMCS de-escalation algorithm.

ECMO indicates extracorporeal membrane oxygenation; LV, left ventricular; LVEF, left ventricular ejection fraction; LVOT, left ventricular outflow
tract; MAP, mean arterial pressure; MCS, mechanical circulatory support; PAPi, pulmonary artery pulsatility index; PCWP, pulmonary capillary
wedge pressure; RA, right atrial; RV, right ventricular; RVEF, right ventricular ejection fraction; tMCS, temporary mechanical circulatory support; and
VTI, velocity-time integral. *No single metric should be used in isolation to determine weaning suitability.

evaluated systematically throughout the weaning process
both to confirm hemodynamic stability and to inform the
need for adjunctive pharmacotherapies. If hemodynamic
perturbations are sustained or if the patient clinically
decompensates, the weaning process should be halted,
and the tMCS support should be returned to a previously
stable setting.
Unsuccessful Weaning
Unsuccessful weaning is a frequent outcome of tMCS
de-escalation. As a result, we suggest simultaneous
consideration of long-term strategies, including the likeli-
hood of recovery and explantation of tMCS, as well as
the need and eligibility for advanced therapies (durable
LVAD or orthotopic heart transplantation), at the time of
tMCS escalation. Ultimately, if weaning proves unsuc-
cessful and decannulation is not possible and the patient
or family wishes to pursue invasive management, transfer
of patients to an LVAD- or transplant-capable hospital
should be pursued as soon as possible. At this point, pa-
tients undergo an extensive medical and psychosocial
evaluation to exclude contraindications that would pre-
clude candidacy for advanced therapies.
With the change in the United Network for Organ Shar-
ing heart allocation system in the United States in 2018,
patients treated with tMCS receive the highest-priority
consideration; thus, an increased number of patients
have been transplanted with this pathway.113–115 However,
given acuity of illness and frequent multiorgan impairment,
adverse outcomes have been reported in patients bridged
from tMCS such as VA-ECMO to heart transplantation

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 Geller et al
or durable mechanical circulatory support.116–118 Further
research is needed to identify which patients are best
suited for advanced therapies as a bridge from tMCS.
Suggestion for Clinical Practice
We suggest early simultaneous evaluation for long-term
strategies (transplantation or durable mechanical circula-
tory support) in patients with CS managed with tMCS in
case myocardial recovery or the tMCS weaning process
is unsuccessful.
Role of Palliative Care in Shared Decision-
Making
In accordance with recommendations from multiple pro-
fessional organizations, we advocate for palliative care
engagement early in CS management, including dur-
ing decisions of tMCS escalation and de-escalation.6,119
When tMCS weaning is unsuccessful, palliative care is
crucial in discussions about durable LVAD candidacy (as
short-term or long-term mechanical circulatory support),
cardiac transplantation candidacy, or transitioning of goals
to focus on comfort care.6,120 Palliative care engagement
involves advanced care planning/preparedness planning;
skillful communication; eliciting patient and family cultural
values, goals, and preferences; identification and docu-
mentation of surrogate decision makers; symptom man-
agement; and patient/family support.120–123 Palliative care
engagement is best accomplished by a combined work-
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force of an interdisciplinary team that has been trained
in palliative care communication skills about prognostic
awareness and goals of care and palliative care special-
ists who can consult in cases of complex psychosocial
care needs and decision-making, refractory symptoms, or
existential distress.124,125
Suggestion for Clinical Practice
We suggest routine collaboration with palliative care ex-
perts in the process of tMCS escalation and de-escala-
tion with the goals of supporting the patient, family, and
interdisciplinary team, enhancing preparedness planning,
and assisting with symptom relief, especially in cases of
withdrawal of life-sustaining therapy.
CONCLUSIONS
tMCS may be a lifesaving intervention in patients with
CS refractory to medical therapy. However, patients
with CS represent a heterogeneous population; there-
fore, the use of tMCS devices needs to be tailored to
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Escalating and De-escalating tMCS in Cardiogenic Shock
the patient’s cause of CS (ie, AMI-CS versus HF-CS),
CLINICAL STATEMENTS
shock profile (ie, LV, RV, or biventricular), and severity of
AND GUIDELINES
hemodynamic compromise. The evidenced-based use
of this technology is limited by a paucity of randomized
controlled trials; therefore, this scientific statement en-
deavors to provide a standardized framework for tMCS
escalation and de-escalation that is based on contem-
porary best practices. Integrating invasive hemodynam-
ic, imaging, laboratory, and clinical parameters is vital to
both the escalation and de-escalation of tMCS. Future
maturation of escalation and de-escalation strategies,
with the goal of improving patient outcomes, hinges on
more accurately, precisely, and consistently profiling pa-
tients with CS and understanding how to develop treat-
ment algorithms to match the right tMCS device to the
right patient at the right time. To this aim, we support
ongoing efforts to conduct randomized clinical trials
and to create large, multicenter, population-based reg-
istries to better inform real-world evidence and to guide
clinical practices regarding tMCS in CS.
ARTICLE INFORMATION
The American Heart Association makes every effort to avoid any actual or poten-
tial conflicts of interest that may arise as a result of an outside relationship or a
personal, professional, or business interest of a member of the writing panel. Spe-
cifically, all members of the writing group are required to complete and submit a
Disclosure Questionnaire showing all such relationships that might be perceived
as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science
Advisory and Coordinating Committee on March 24, 2022, and the American
Heart Association Executive Committee on April 11, 2022. A copy of the docu-
ment is available at https://professional.heart.org/statements by using either
“Search for Guidelines & Statements” or the “Browse by Topic” area. To pur-
chase additional reprints, call 215-356-2721 or email Meredith.Edelman@
wolterskluwer.com.
The American Heart Association requests that this document be cited as
follows: Geller BJ, Sinha SS, Kapur NK, Bakitas M, Balsam LB, Chikwe J, Klein
DG, Kochar A, Masri SC, Sims DB, Wong GC, Katz JN, van Diepen S; on behalf
of the American Heart Association Acute Cardiac Care and General Cardiology
Committee of the Council on Clinical Cardiology; Council on Cardiopulmonary,
Critical Care, Perioperative and Resuscitation; Council on Cardiovascular Radiol-
ogy and Intervention; Council on Cardiovascular and Stroke Nursing; Council on
Peripheral Vascular Disease; and Council on Cardiovascular Surgery and Anes-
thesia. Escalating and de-escalating temporary mechanical circulatory support in
cardiogenic shock: a scientific statement from the American Heart Association.
Circulation. 2022;146:e50–e68. doi: 10.1161/CIR.0000000000001076
The expert peer review of AHA-commissioned documents (eg, scientific
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August 9, 2022 e63
 Geller et al Escalating and De-escalating tMCS in Cardiogenic Shock

Disclosures
CLINICAL STATEMENTS
AND GUIDELINES

Writing Group Disclosures

Other Speakers’
Writing group research bureau/ Expert Ownership Consultant/
member Employment Research grant support honoraria witness interest advisory board Other
Bram J. Geller Maine Medical Center None None None None None None None
Shashank S. Sinha Inova Fairfax Medical Center Ino- None None None None None None None
va Heart and Vascular Institute
Marie Bakitas University of Alabama at Birming- None None None None None None None
ham School of Nursing
Leora B. Balsam University of Massachusetts None None None None None None None
Joanna Chikwe Heart Institute, Cedars Sinai None None None None None None None
Medical Center
Navin K. Kapur Tufts Medical Center Abbott†; Abiomed†; None Abiomed†; None None Abbott†; None
Boston Scientific†; Getinge†; Abiomed†; Bos-
Getinge†; LivaNova† LivaNova† ton Scientific†;
(all PI for institutional Edwards*; Liva-
grant) Nova†; Getinge†
Jason N. Katz Duke University Abbott Corp (re- None None None None None None
search support)*
Deborah G. Klein Cleveland Clinic (retired) None None None None None None None
Ajar Kochar Brigham and Women’s Hospital/ None None None None None None None
Harvard Medical School
Sofia C. Masri University of Washington None None None None None LivaNova* None
Daniel B. Sims Albert Einstein College of Medicine None None None None None None None
Sean van Diepen University of Alberta, Edmonton None None None None None None None
(Canada)
Graham C. Wong University of British Columbia None None Novartis* None None Kye Pharmaceu- None
and Vancouver Coastal Health ticals*; Pendo-
Downloaded from http://ahajournals.org by on June 26, 2024

Authority (Canada) pharm*

This table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure
Questionnaire, which all members of the writing group are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $10 000
or more during any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns
$10 000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.
*Modest.
†Significant.

Reviewer Disclosures

Speakers’ Consultant/
Research bureau/ Expert Ownership advisory
Reviewer Employment grant Other research support honoraria witness interest board Other
Jacob Abraham Providence Heart None None Abiomed*; None None Abiomed* None
Institute Abbott*
David M. Massachusetts Gen- None None None None None None None
Dudzinski eral Hospital
Arthur R. Beth Israel Deacon- Abbott (I am on a research consortium Abiomed*;
Garan ess Medical Center, supported by Abbott. I do not receive NuPulseCV*
Harvard Medical direct payment for this, but Abbott sup-
School ports these research efforts by bringing
the members together on a yearly basis
for in person, 1- to 2-d meetings.)*
Manreet K. Cardiovascular In- None None Abiomed* None None Abiomed* None
Kanwar stitute at Allegheny
Health Network
Joyce Wald University of Penn- None None None None None None None
sylvania

This table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure
Questionnaire, which all reviewers are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $10 000 or more dur-
ing any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $10 000
or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.
*Modest.

e64 August 9, 2022 Circulation. 2022;146:e50–e68. DOI: 10.1161/CIR.0000000000001076

 Geller et al
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