Mechanical circulatory support in cardiogenic shock

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nehal Eid, M.D.[2]

Overview

Cardiogenic shock (CS) is a clinical syndrome of inadequate tissue perfusion due to the inability of the heart to pump sufficient blood to meet metabolic demands. Despite advances in reperfusion therapy and critical care, CS remains the leading cause of in-hospital death among patients with acute myocardial infarction (AMI), with 30-day mortality approaching 40% and 1-year mortality approximately 50%.

Temporary mechanical circulatory support (tMCS) devices augment end-organ perfusion in patients with de novo or refractory CS. 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 such as a left ventricular assist device (LVAD) or heart transplantation.

The 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes provides the most current recommendations for MCS in the setting of AMI-CS, including a Class 2a recommendation for microaxial flow pumps in selected patients with ST-elevation myocardial infarction (STEMI) and severe or refractory CS, and a Class 3 (No Benefit) recommendation against the routine use of intra-aortic balloon pump (IABP) or venoarterial extracorporeal membrane oxygenation (VA-ECMO) in AMI-CS.

Definition and Pathophysiology

Definition

Cardiogenic shock is defined by systemic hypoperfusion and tissue hypoxia due to cardiac dysfunction. The hemodynamic hallmarks include:

• Systolic blood pressure *

Pathophysiology

The fundamental hemodynamic trigger of CS is an inability to maintain adequate stroke volume despite sufficient preload, leading to reduced cardiac output and tissue hypoperfusion. Peripheral vasoconstriction and fluid retention are early compensatory mechanisms that attempt to preserve organ perfusion but ultimately worsen the hemodynamic state by aggravating preload and afterload mismatch. Sympathetic and neurohormonal activation (endogenous catecholamine release, increased systemic vascular resistance, and activation of the renin-angiotensin-aldosterone system) constitute the pathophysiological foundation of the classic "cold and wet" CS phenotype.

If therapeutic interventions do not restore cardiac output and organ perfusion in a timely manner, coronary and systemic hypoperfusion and multi-organ failure become progressively worse. Metabolic derangements from acute kidney injury and congestive hepatopathy can dominate the clinical picture, referred to as hemometabolic shock.

Epidemiology

Between 40,000 and 50,000 patients in the United States develop CS associated with AMI each year, corresponding to an incidence of approximately 5% to 10% of all patients with AMI. The epidemiology of CS has undergone significant changes: while the incidence of AMI-CS is declining, there is a concurrent rise in CS attributed to heart failure (HF-CS) and structural heart disease. In a report from the Critical Care Cardiology Trials Network, 46% of CS cases were attributed to HF-CS, 30% to AMI-CS, and 17% to other identified cardiac causes.

Regardless of CS cause, the associated short-term mortality rate remains high (30%–50%), and this increases incrementally with advancing age across all SCAI stages.

Classification

SCAI Shock Classification

The Society for Cardiovascular Angiography and Interventions (SCAI) Shock Classification provides a standardized framework for risk stratification and guides clinical decision-making. The classification has been endorsed by the ACC, AHA, ESC, SCCM, ISHLT, and STS.

Stage	Name	Description	Key Features
A	At Risk	Patients with acute cardiac diagnoses at risk for CS but not yet meeting criteria for preshock or shock	Hemodynamically stable; no hypoperfusion or hypotension
B	Beginning	Intact systemic perfusion with evidence of hemodynamic instability	Hypotension (SBP 60–90 mm Hg or MAP 50–65 mm Hg) or isolated hypoperfusion (lactate 2–5 mmol/L) without need for drug or device therapy
C	Classic	Hypoperfusion requiring intervention	Hypoperfusion and hypotension, or treated with 1 drug or 1 circulatory support device
D	Deteriorating	Failure of initial supportive intervention	Hypotension and hypoperfusion (lactate 5–10 mmol/L or ALT >500 U/L) or need for 2–5 drugs or devices
E	Extremis	Refractory shock with actual or impending cardiovascular collapse	SBP 10 mmol/L, pH ≤7.2, or need for >3 drugs or 3 devices; includes cardiac arrest

Etiologic Classification

CS can be classified by etiology:

• AMI-CS: Acute myocardial infarction-related CS, including LV failure, RV failure, and mechanical complications (ventricular septal defect, papillary muscle rupture, free wall rupture)*
• HF-CS: Heart failure-related CS, including acute decompensation of chronic HF, de novo cardiomyopathy, and fulminant myocarditis*
• Non-myocardial CS: Pulmonary embolism, cardiac tamponade, severe valvular heart disease, arrhythmia-related CS*
• Post-cardiotomy CS: CS following cardiac surgery*

Hemodynamic Phenotyping

Hemodynamic assessment enables classification of CS by ventricular phenotype:

• LV-dominant CS: Elevated pulmonary capillary wedge pressure (>15 mm Hg) with relatively normal right atrial pressure*
• RV-dominant CS: Elevated right atrial or central venous pressure (>15 mm Hg) with relatively normal pulmonary capillary wedge pressure*
• Biventricular CS: Elevation in both right atrial and pulmonary capillary wedge pressures

Diagnosis

Clinical Assessment

The diagnosis of CS requires the identification of both hemodynamic compromise and end-organ hypoperfusion. Clinical signs include:

• Hypotension (SBP *

Invasive Hemodynamic Assessment

The 2022 AHA/ACC/HFSA Heart Failure Guideline provides a Class 2b recommendation that placement of a pulmonary artery catheter (PAC) may be considered in patients presenting with CS to define hemodynamic subsets and appropriate management strategies.

The 2025 ACC Expert Consensus Statement on CS emphasizes that observational data suggest utility in applying invasive hemodynamics to characterize the phenotype of CS, assess shock severity, and guide tMCS-related escalation and weaning decisions. Complete hemodynamic profiling has been associated with lower in-hospital mortality, and early hemodynamic assessment within the first 12 hours has been associated with improved clinical outcomes.

Key hemodynamic parameters include:

• Cardiac output and cardiac index*
• Cardiac power output (CPO)*
• Right atrial pressure*
• Pulmonary artery pressures*
• Pulmonary capillary wedge pressure*
• Mixed venous oxygen saturation*
• Pulmonary artery pulsatility index (PAPi)*
• Systemic vascular resistance*

Echocardiography

Echocardiography is essential for rapid assessment of ventricular function, identification of mechanical complications (e.g., ventricular septal defect, mitral regurgitation, cardiac tamponade), and guiding device selection and positioning.

Devices

Overview of Temporary MCS Devices

Options for tMCS include fully percutaneous configurations, surgical configurations with centrally implanted cannulas, and hybrid platforms. tMCS devices can provide either partial or full circulatory support and have differential effects on myocardial oxygen consumption, LV unloading, LV wall stress, and coronary artery perfusion.

Device	Mechanism	Maximum Flow (L/min)	Ventricle Supported	Cannula Size (Fr)	Key Advantages	Key Disadvantages
IABP	Counterpulsation (balloon inflation in diastole, deflation in systole)	0.5–1.0 (augmentation only; does not directly increase cardiac output)	LV	7–8	Easy to place; good safety profile; lower vascular complication rate	Limited hemodynamic support; requires cardiac rhythm synchrony
Impella 2.5	Microaxial flow pump; pumps blood from LV to ascending aorta	2.5	LV	12	Percutaneous; LV unloading	Hemolysis; vascular complications; requires adequate RV function
Impella CP	Microaxial flow pump; pumps blood from LV to ascending aorta	~4.3	LV	14	Percutaneous; greater flow than Impella 2.5; LV unloading	Hemolysis; vascular complications; limb ischemia
Impella 5.5	Microaxial flow pump; surgically placed via axillary artery	5.5	LV	21	Higher flow; allows ambulation	Requires surgical cutdown; vascular complications
Impella RP	Microaxial flow pump; pumps blood from IVC to pulmonary artery	4.0	RV	22	Percutaneous RV support	Large bore; vascular complications
TandemHeart	Centrifugal pump; drains blood from LA (via transseptal puncture) to femoral artery	4.0–5.0	LV (or RV with ProtekDuo configuration)	Inflow 21, Outflow 15–17	High cardiac output; LV unloading	Requires transseptal puncture; vascular complications
VA-ECMO	Centrifugal pump with membrane oxygenator; drains from RA, returns to aorta	4.0–6.0	LV and RV (with oxygenation)	Inflow 18–21, Outflow 15–22	Full cardiopulmonary support; rapidly deployable	Increases LV afterload; may cause LV distension; vascular complications; thrombocytopenia
CentriMag	Surgically implanted centrifugal pump	Up to 10	LV, RV, or BiV	Surgically placed	Very high flow; versatile	Requires surgical implantation; resource-intensive

Combined Device Configurations

Combining tMCS platforms is possible and may be necessary in patients with biventricular failure or inadequate support from a single device. Common configurations include:

• ECPella: VA-ECMO with an Impella for LV decompression*
• VA-ECMO + IABP: VA-ECMO with an IABP for LV unloading*
• BiPella: Left-sided support with an Impella 2.5/CP/5.5 and right-sided support with an Impella RP*
• Right-sided TandemHeart + LV Impella: For biventricular support*

Guideline Recommendations

2025 ACC/AHA/ACEP/NAEMSP/SCAI ACS Guideline

COR	LOE	Recommendation
2a	B-R	In selected patients with STEMI and severe or refractory cardiogenic shock, insertion of a microaxial intravascular flow pump is reasonable to reduce death.
2a	B-NR	In patients with mechanical complication of ACS, short-term MCS devices are reasonable for hemodynamic stabilization as a bridge to surgery.
3: No Benefit	B-R	In patients with AMI and cardiogenic shock, the routine use of IABP or VA-ECMO is not recommended due to a lack of survival benefit.

2022 AHA/ACC/HFSA Heart Failure Guideline

COR	LOE	Recommendation
1	B-NR	In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ performance.
2a	B-NR	In patients with cardiogenic shock, temporary MCS is reasonable when end-organ function cannot be maintained by pharmacologic means to support cardiac function.
2a	B-NR	In patients with cardiogenic shock, management by a multidisciplinary team experienced in shock is reasonable.
2b	B-NR	In patients presenting with cardiogenic shock, placement of a PA catheter may be considered to define hemodynamic subsets and appropriate management strategies.
2b	C-LD	For patients who are not rapidly responding to initial shock measures, triage to centers that can provide temporary MCS may be considered to optimize management.

2022 AHA Scientific Statement on Escalating and De-Escalating tMCS

This scientific statement provides a framework for tMCS escalation and de-escalation in CS. Key principles include:

• Escalation to tMCS can be considered in appropriately selected patients with evidence of clinical hypoperfusion or hemodynamic deterioration de novo, while on inotropes, or during initial tMCS support*
• Early recognition and timely initiation of tMCS in appropriate candidates may lead to improved survival*
• Device selection should be tailored to the underlying pathogenesis (AMI-CS vs. HF-CS) and the hemodynamic phenotype (LV-dominant, RV-dominant, or biventricular)*

Treatment

Initial Management

The initial approach to CS should include early recognition, hemodynamic stabilization, and identification and treatment of the underlying cause.

Pharmacologic support:

• Norepinephrine is generally preferred as the initial vasopressor in CS with significant hypotension.*
• Inotropes, including dobutamine and milrinone, are selected according to the physiologic profile to augment cardiac output. Despite ubiquitous use, there are few prospective data and a paucity of randomized trials to guide their use in CS.*
• High-dose and/or multiple vasopressors in CS have been linked to increased mortality in observational data.

Revascularization:

• In patients with ACS and CS, emergency revascularization of the culprit vessel by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) is indicated to improve survival (Class 1, LOE B-R).*
• Routine PCI of a noninfarct-related artery at the time of primary PCI should not be performed in patients with AMI-CS because of the higher risk of death or renal failure (Class 3: Harm, LOE B-R), based on the CULPRIT-SHOCK trial.*

Medical Therapy

Medical therapy in CS is primarily supportive and includes:

• Vasopressors: Norepinephrine to maintain adequate mean arterial pressure (target generally ≥65 mm Hg)*
• Inotropes: Dobutamine or milrinone to augment cardiac contractility and reduce afterload*
• Diuretics: Loop diuretics to relieve congestion when volume overload is present*
• Afterload reduction: In patients with HF-CS with a cardiac index 65 mm Hg, afterload reduction with a vasodilator such as sodium nitroprusside or inotropic support with intravenous milrinone or dobutamine may initially be considered instead of tMCS*

Procedural / Surgical Therapy

Indications for tMCS

Escalation to tMCS can be considered in appropriately selected patients with evidence of clinical hypoperfusion or hemodynamic deterioration. Possible indicators include:

• Persistently low cardiac index (2 mmol/L*
• Evidence of RV failure (RA/PCWP ratio >0.86 or PAPi ≤0.9)*
• Profound hypoxemia*
• Recurrent ventricular tachycardia or ventricular fibrillation*

Device Selection in AMI-CS

Based on the 2025 ACC/AHA ACS Guideline and the 2022 AHA Scientific Statement:

• Microaxial flow pump (Impella CP): Reasonable in selected patients with STEMI and severe or refractory CS who have clinical features consistent with the DanGer Shock trial inclusion criteria (SCAI stages C, D, or E; noncomatose; adequate peripheral vasculature for large-bore access) (Class 2a, LOE B-R).*
• IABP: Routine use in AMI-CS is not recommended due to lack of survival benefit (Class 3: No Benefit). May still have a role in patients with severe mitral regurgitation, LV thrombus, ventricular septal defect, or unrevascularized coronary artery disease.*
• VA-ECMO: Routine use in AMI-CS is not recommended due to lack of survival benefit (Class 3: No Benefit).*
• 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.*

Device Selection in HF-CS

No tMCS devices have been studied in large randomized controlled trials in HF-CS. Device selection is guided by the hemodynamic phenotype:

• LV-predominant CS: Initial support with an IABP, LV Impella, or TandemHeart may be appropriate. Severity of shock can guide device selection (e.g., Impella 5.5 rather than Impella CP for more severe CS).*
• RV-predominant CS: Impella RP, right-sided TandemHeart with or without ProtekDuo, or surgical temporary RVAD (e.g., CentriMag).*
• Biventricular CS or significant concomitant RV dysfunction, hypoxemia, or more severe shock: VA-ECMO may be considered.*

Device Selection in RV Failure

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 RVAD are potential tMCS platforms. When these are unavailable, VA-ECMO could also be considered. Given the paucity of data to support one device over another, institutional availability, individual expertise, and operator experience should factor into device selection.

LV Unloading During VA-ECMO

VA-ECMO can increase LV afterload and worsen pulmonary edema due to retrograde blood flow toward the aortic valve. Early active unloading with Impella microaxial flow pumps or IABP aims to mitigate these adverse effects and has been associated with better outcomes in observational studies. However, routine transseptal left atrial cannulation did not result in higher VA-ECMO weaning (EVOLVE-ECMO) or 30-day survival rate (EARLY-UNLOAD) in randomized trials.

Mechanical Complications of AMI

In patients with mechanical complications of ACS (e.g., ventricular septal rupture, papillary muscle rupture), short-term MCS devices are reasonable for hemodynamic stabilization as a bridge to surgery (Class 2a, LOE B-NR).

Long-Term Management

Transition to Durable Support or Transplantation

For patients who cannot be weaned from tMCS, evaluation for advanced therapies should include interdisciplinary assessment for:

• Durable left ventricular assist device (LVAD) implantation*
• Heart transplantation*
• Palliative care consultation when advanced therapies are not appropriate*

Weaning and De-Escalation of tMCS

The 2022 AHA Scientific Statement recommends daily evaluation to determine readiness to wean. It is reasonable to begin tMCS weaning in patients who are hemodynamically stable, require minimal intravenous hemodynamic support, are intravascularly euvolemic, and have had improvement or correction of the underlying cause of CS.

Hemodynamic targets during weaning:

• RA pressure *

Device-specific weaning approaches:

• 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. Concomitant systemic anticoagulation is necessary during weaning to reduce the risk of thromboembolic events.* ### Mechanical Circulatory Support in Cardiogenic Shock (Continued)

• Impella: Support is typically reduced by 2 performance levels (P-levels) every 2 to 4 hours. Echocardiographic assessment of ventricular function should be performed at each step.*
• IABP: Weaning typically involves a methodical 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. Systematically decreasing the balloon volume can also be used.*
• Combined VA-ECMO + Impella (ECPella): VA-ECMO is generally weaned first, and the Impella support (P-level) may be increased to allow ECMO decannulation.*

If hemodynamic perturbations are sustained or if the patient clinically decompensates during weaning, the process should be halted and tMCS support returned to a previously stable setting. No single validated score or metric can be reliably used to determine successful tMCS weaning or readiness for decannulation; medical teams should integrate temporal trends in multimodal cardiac monitoring and markers of noncardiac organ hypoperfusion during the weaning process.

Special Populations

Older Adults

The 2024 AHA Scientific Statement on Cardiogenic Shock in Older Adults highlights that age is an independent predictor of mortality in CS across all SCAI stages. Older adults are more likely to present with HF-CS, have more comorbidities, and are at higher risk for device-related complications including vascular injury, bleeding, and limb ischemia. Shared decision-making and goals-of-care discussions are particularly important in this population. Durable LVAD therapy may be a reasonable consideration for carefully selected older adults, given the high short-term mortality of CS with medical management alone.

Right Ventricular Failure

RV failure complicates CS management and is associated with worse outcomes. Hemodynamic indicators of RV failure include an elevated RA/PCWP ratio (>0.86 in AMI-CS, >0.63 after LVAD) and a reduced PAPi (≤0.9 in AMI-CS, 10 mm Hg and in the absence of moderate or severe pulmonary hypertension (pulmonary artery systolic pressure >50 mm Hg).

For patients with isolated RV failure refractory to medical therapy, tMCS options include the Impella RP, right-sided TandemHeart with or without ProtekDuo, and surgical temporary RVAD (e.g., CentriMag). When these are unavailable, VA-ECMO could also be considered.

Post-Cardiac Arrest

Patients with CS following cardiac arrest represent a particularly challenging population. Accurate neuroprognostication may not be feasible at the time of tMCS consideration. The DanGer Shock trial excluded patients at high risk for hypoxic brain injury, and the 2025 ACC/AHA ACS Guideline recommendation for microaxial flow pumps applies to noncomatose patients. In the post-cardiac arrest setting, the shock team clinicians may have to base risk-benefit decisions on the best information available.

Biventricular Failure

Biventricular dysfunction is increasingly recognized to be common, with more than half of patients with CS presenting with elevated biventricular filling pressures. The need for RV support may be minimized or eliminated with the rapid diagnosis and successful resolution of common, reversible causes of RV failure, including mechanical complications of LV support (e.g., tamponade, device malposition), metabolic decompensation (acidosis, hypoxemia, hypercapnia, sepsis), and pulmonary complications (pneumothorax, pulmonary embolism, pleural effusion). In patients with biventricular failure without readily reversible RV dysfunction and with inadequate circulatory support, escalation to percutaneous biventricular support (e.g., BiPella or right-sided TandemHeart with a left-sided percutaneous ventricular assist device) or VA-ECMO should be considered.

Complications

Overview

Complications in patients supported with tMCS can be broadly categorized as vascular, neurologic, hematologic, mechanical, and infectious. The occurrence of complications is influenced by device type, insertion technique, duration of support, and patient characteristics. In general, devices that provide more robust circulatory support use larger cannulas and are associated with more complications.

Vascular Complications

Vascular complications, including limb ischemia and limb loss, are most common with VA-ECMO and least common with IABP. 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 ischemia. In the case of VA-ECMO, routine placement of a distal perfusion catheter may significantly attenuate distal limb ischemia.

Bleeding

Bleeding is one of the most frequent complications of tMCS and is related to vascular cannulation, anticoagulation, or device-induced alterations in the coagulation pathway. In the DanGer Shock trial, moderate or severe bleeding occurred in 21.8% of the Impella group versus 11.9% in the standard-care group (relative risk 2.06; 95% CI 1.15–3.66). In the ECLS-SHOCK trial, moderate or severe bleeding occurred in 23.4% of the ECLS group versus 9.6% in the control group (relative risk 2.44; 95% CI 1.50–3.95).

Hemolysis

Hemolysis appears to be most common with the Impella family of devices. Serial monitoring of urine color, lactate dehydrogenase, plasma free hemoglobin, haptoglobin, and serum hemoglobin is suggested. Depending on the device, decreasing revolutions per minute may reduce hemolysis at the expense of augmented cardiac output. In the case of Impella devices, repositioning of the device may also significantly lower the rates of hemolysis when present.

Infection

Infection risk increases with duration of tMCS support. In the DanGer Shock trial, sepsis with positive blood culture occurred in 11.7% of the Impella group versus 4.5% in the standard-care group (relative risk 2.79; 95% CI 1.20–6.48).

Neurologic Complications

Stroke and intracranial hemorrhage are serious complications of tMCS. Stroke rates in the DanGer Shock trial were 3.9% in the Impella group versus 2.3% in the standard-care group (relative risk 1.75; 95% CI 0.50–6.01), a difference that was not statistically significant.

LV Distension During VA-ECMO

VA-ECMO can increase LV afterload due to retrograde blood flow toward the aortic valve, potentially leading to progressive LV distension, impairment of function, and pulmonary edema. Early active unloading with Impella microaxial flow pumps or IABP aims to mitigate these adverse effects. However, routine transseptal left atrial cannulation did not result in higher VA-ECMO weaning (EVOLVE-ECMO) or 30-day survival rate (EARLY-UNLOAD) in randomized trials.

Contraindications

Absolute Contraindications

• Irreversible cardiac failure without an exit strategy (i.e., patient is not a candidate for heart transplantation or durable LVAD)*
• Irreversible noncardiac organ failure limiting survival (e.g., severe anoxic brain injury, intracranial hemorrhage, moribund state, incurable metastatic malignancy, or other terminal illnesses)*

Relative Contraindications

• Aortic dissection*
• Severe coagulopathy*
• Contraindication to anticoagulation*
• Severe aortic valve disease (aortic stenosis for Impella; aortic regurgitation for VA-ECMO)*
• Difficult vascular access*
• Severe peripheral arterial disease*

Device-Specific Contraindications

Specific contraindications for each device should be evaluated on an individual basis and discussed by the shock team before device insertion. 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 possible at the time of concomitant shock onset.

Key Clinical Trials

DanGer Shock (2024)

The DanGer Shock trial was an international, multicenter, randomized trial that assigned 360 patients with ST-elevation myocardial infarction (STEMI) and cardiogenic shock to receive a microaxial flow pump (Impella CP) plus standard care or standard care alone. The primary endpoint was death from any cause at 180 days. Death occurred in 82 of 179 patients (45.8%) in the microaxial-flow-pump group and in 103 of 176 patients (58.5%) in the standard-care group (hazard ratio 0.74; 95% CI 0.55–0.99; P=0.04). The composite safety endpoint (severe bleeding, limb ischemia, hemolysis, device failure, or worsening aortic regurgitation) occurred in 24.0% of the Impella group versus 6.2% in the standard-care group (relative risk 4.74; 95% CI 2.36–9.55). Renal-replacement therapy was administered to 41.9% in the Impella group versus 26.7% in the standard-care group (relative risk 1.98; 95% CI 1.27–3.09).

IABP-SHOCK II (2012; 6-Year Follow-Up 2019)

The IABP-SHOCK II trial randomized 600 patients with cardiogenic shock complicating AMI undergoing early revascularization to IABP versus control. IABP did not reduce 30-day mortality (relative risk 0.96; 95% CI 0.79–1.17; P=0.69). There were no significant differences in dose and duration of catecholamine therapy, time to hemodynamic stabilization, serum lactate levels, renal function, or length of ICU stay. Safety endpoints including rates of major bleeding, peripheral ischemic complications, sepsis, and stroke did not differ between groups. At 6-year follow-up, mortality remained not different between the IABP and control groups (66.3% versus 67.0%; relative risk 0.99; 95% CI 0.88–1.11; P=0.98).Thiele H, Zeymer U, Thelemann N, Neumann FJ, Hausleiter J, Abdel-Wahab M, Meyer-Saraei R, Fuernau G, Eitel I, Hambrecht R, Böhm M, Werdan K, Felix SB, Hennersdorf M, Schneider S, Ouarrak T, Desch S, de Waha-Thiele S (2019-01-15). "Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-Term 6-Year Outcome of the Randomized IABP-SHOCK II Trial". Circulation. 139 (3): 395–403. doi:10.1161/CIRCULATIONAHA.118.038201. PMID 30586721.

ECLS-SHOCK (2023)

The ECLS-SHOCK trial randomized 417 patients with AMI complicated by cardiogenic shock with planned early revascularization to early ECLS or control. Death from any cause at 30 days occurred in 47.8% of the ECLS group versus 49.0% in the control group (relative risk 0.98; 95% CI 0.80–1.19; P=0.81). Moderate or severe bleeding occurred in 23.4% of the ECLS group versus 9.6% of the control group (relative risk 2.44; 95% CI 1.50–3.95). Peripheral vascular complications requiring intervention occurred in 11.0% versus 3.8%, respectively (relative risk 2.86; 95% CI 1.31–6.25).

Individual Patient Data Meta-Analysis (2024)

An individual patient data meta-analysis of nine randomized controlled trials comparing active MCS versus usual care in patients with AMI-CS found that unselected routine MCS use does not reduce 6-month mortality when all types of MCS are pooled together. However, patient selection restricted to STEMI-CS without high risk of hypoxic brain injury was associated with a mortality benefit of MCS. A consistent increase in major bleeding and vascular complications was noted with MCS use, independent of MCS type.

Systems of Care

Shock Teams

The 2022 AHA/ACC/HFSA Heart Failure Guideline provides a Class 2a recommendation that management of CS by a multidisciplinary team experienced in shock is reasonable. The 2025 ACC Expert Consensus Statement on CS emphasizes the importance of a multidisciplinary shock team approach, including representation from critical care cardiology, advanced heart failure and transplant cardiology, interventional cardiology, cardiac surgery, and palliative care.

Observational data from the Critical Care Cardiology Trials Network suggest that cardiac ICUs with shock teams have higher rates of PAC use, tMCS use, and advanced HF therapies, with a trend toward improved outcomes.

Hub-and-Spoke Model

A regionalized hub-and-spoke model for CS care has been proposed, analogous to STEMI systems of care. Hub centers would create mobile multidisciplinary CS teams available 24/7 for onsite or offsite consultation, referral, and ECMO/MCS insertion. Spoke hospitals would develop CS treatment algorithms according to onsite capabilities and expertise. Regional protocols should standardize management practices, provide futility parameters, and determine the timing of transfer once the diagnosis of refractory CS is established.

The 2022 AHA/ACC/HFSA Heart Failure Guideline provides a Class 2b recommendation that for patients who are not rapidly responding to initial shock measures, triage to centers that can provide temporary MCS may be considered to optimize management.

Palliative Care

Palliative care consultation should be integrated early in the management of CS, particularly for patients with refractory shock, those who are not candidates for advanced therapies, and those with a high burden of comorbidities. The 2022 AHA Scientific Statement on tMCS emphasizes that simultaneous consideration of long-term strategies, including the likelihood of recovery and eligibility for advanced therapies, should occur at the time of tMCS escalation. If weaning proves unsuccessful and the patient is not a candidate for durable LVAD or heart transplantation, a palliative care approach should be discussed with the patient and family.

Prognosis

Despite advances in reperfusion therapy and tMCS, the prognosis of CS remains poor. In-hospital mortality ranges from 30% to 50%, and 1-year mortality approaches 50%. Mortality increases incrementally with advancing SCAI stage, with SCAI stage E (extremis) carrying the highest mortality.

Prognostic factors associated with worse outcomes include:

• Advanced age*
• Higher SCAI shock stage at presentation*
• Biventricular or RV-dominant hemodynamic profiles*
• Elevated lactate and failure of lactate clearance*
• Multi-organ failure*
• Cardiac arrest before or during CS*
• Late or failed coronary artery revascularization*
• Need for multiple vasoactive medications or multiple tMCS devices*

Ongoing and Future Directions

Several randomized controlled trials are ongoing or recently completed that may further inform the use of tMCS in CS:

• UNLOAD ECMO (NCT05577195): Investigating combined tMCS approaches with VA-ECMO and LV unloading*
• ANCHOR (NCT04184635): Investigating combined tMCS approaches with VA-ECMO and LV unloading*
• IABP in HF-CS (NCT04369573): Investigating IABP versus pharmacological support in heart failure-related cardiogenic shock*

Future research priorities include better phenotyping of CS to guide device selection, identification of patients most likely to benefit from tMCS, optimal timing of tMCS initiation, and the role of tMCS in non-AMI CS populations.