2025 ACC Concise Clinical Guidance: Evaluation and Management of Cardiogenic Shock

Authors, Journal, Affiliations, Type, DOI

• Authors: Shashank S. Sinha (Chair), David A. Morrow (Vice Chair), Navin K. Kapur, Rachna Kataria, Robert O. Roswell, Martha Gulati, Dharam J. Kumbhani, Gurusher S. Panjrath, Barbara Wiggins, and others
• Journal: Journal of the American College of Cardiology, Vol. 85, No. 16, April 29, 2025 (pp. 1618–1641)
• Affiliations: ACC Solution Set Oversight Committee; multidisciplinary international expert panel
• Type: Expert Consensus — Concise Clinical Guidance (ACC Solution Set)
• DOI: https://doi.org/10.1016/j.jacc.2025.02.018

Overview

Cardiogenic shock (CS) is a complex, heterogeneous syndrome in which cardiac dysfunction causes end-organ hypoperfusion, carrying 30–40% short-term and ~50% 1-year mortality. This ACC 2025 Concise Clinical Guidance addresses early diagnosis (SUSPECT CS mnemonic), SCAI severity staging, regionalized systems of care (Level 1/2/3 CS centers), pharmacological management, and temporary mechanical circulatory support (tMCS). The document introduces the Recognize/Rescue → Optimize → Stabilize → De-Escalate/Exit framework and highlights that the DanGer Shock trial was the first positive tMCS RCT — demonstrating an absolute 12.7% 180-day mortality reduction with microaxial flow pump in select STEMI-CS patients. Two principal CS phenotypes are emphasized: AMI-CS (historically predominant in RCTs) and HF-CS (rising in prevalence, underrepresented in trials).

Keywords

Cardiogenic shock, SCAI staging, temporary mechanical circulatory support, AMI-CS, HF-CS, SUSPECT CS, DanGer Shock, pulmonary artery catheter, shock team, vasoactive agents, hemodynamic monitoring, tMCS weaning

Key Takeaways

Epidemiology and Definition

• CS is defined as a cardiac disorder causing both clinical and biochemical evidence of sustained tissue hypoperfusion irrespective of blood pressure
• Short-term mortality 30–40%; 1-year mortality approaching or exceeding 50%
• HF-CS has increased in prevalence over the past decade in the United States, with notable differences in baseline characteristics and outcomes compared to AMI-CS
• CS is one of the most common causes of admission to contemporary cardiac intensive care units

Initial Evaluation — SUSPECT CS Mnemonic

The writing committee proposes the SUSPECT CS mnemonic to aid early diagnosis (minimum criteria required):

• Symptoms/Signs: altered mental status, confusion, cold/clammy extremities, rapid pulse, low pulse pressure (<25% of SBP), elevated JVP, crackles, orthopnea, PND, edema
• Urine output: oliguria/anuria <30 mL/h (<0.5 mL/kg·h)
• Sustained hypotension: SBP <90 mmHg, MAP <65 mmHg for >30 min or >30 mmHg decrease from baseline, or pharmacological/mechanical support needed
• Perfusion: lactate >2 mmol/L; ALT >200 U/L or >3× ULN; creatinine ≥2× ULN; pH <7.2; metabolic acidosis
• ECG/Echocardiogram: acute ischemia, STEMI, wall motion abnormality, LV/RV dilation/dysfunction, valvular pathology
• Congestion: presence/absence based on physical signs and hemodynamics; LV vs RV vs BiV involvement
• Triage: shock team activation or transfer to higher level of care
• Initial CS diagnosis does NOT require invasive hemodynamics; it begins with clinical suspicion
• Normotensive CS (end-organ hypoperfusion without hypotension) carries increased mortality — do not rely solely on blood pressure

SCAI Staging and CS Classification

• Severity classified using SCAI stages (A–E) per the CS Working Group–SCAI Shock Criteria
• Etiologies further classified per Shock Academic Research Consortium: AMI-CS, HF-CS, postcardiotomy CS, secondary CS (arrhythmias, valvular, pericardial)
• AMI-CS subcategories: STEMI vs non-STEMI; with/without mechanical complications
• HF-CS subcategories: de novo HF-CS vs acute-on-chronic HF-CS; by specific etiology (myocarditis, takotsubo, peripartum, tachycardia-related, HCM, infiltrative)
• SCAI Stage B patients are at highest risk of worsening shock severity within 24 hours from diagnosis
• Most CS patients change SCAI stages within the first 24 hours from diagnosis — the first 24 hours is critical

Systems of Care — CS Center Tiers

• Level 1 CS hospital center: full on-site 24/7 medical and surgical expertise; full tMCS device portfolio; high procedural volumes; may offer durable LVAD and heart transplant
• Level 2 CS hospital center: intermediate capabilities; some tMCS devices; limited advanced HF therapies
• Level 3 CS hospital center: community hospitals; basic acute CV care; no advanced tMCS/LVAD/transplant
• No universal consensus classification system (unlike trauma centers) exists currently — mainly expert consensus
• AMI-CS patients remaining in refractory CS post-revascularization should almost always be transferred to Level 1 center
• Patients with cardiac arrest, those on ≥1 vasoactive agent, or those in whom tMCS is considered → prompt communication with regional Level 1 CS center
• Observational data on transfer outcomes are mixed; HF-CS transfers have higher associated mortality; use of PAC at transfer associated with favorable outcomes

Shock Team Activation

• Standardized interdisciplinary shock team associated with lower risk-adjusted cardiac ICU mortality (multicenter data)
• Key team members: critical care cardiology, advanced HF/transplant cardiology, interventional cardiology, cardiac surgery ± ECMO/perfusion ± palliative care
• Common elements: interdisciplinary engagement, coordinating physician, concurrent team activation system, virtual/bedside communication, invasive hemodynamics for therapy selection
• For Level 2/3 centers: recommend early contact with regional Level 1 CS center after confirming diagnosis

Invasive Hemodynamic Monitoring

• Pulmonary artery catheter (PAC) use associated with improved outcomes in retrospective and registry data; no RCT evidence in CS (ESCAPE trial excluded CS patients)
• Complete hemodynamic profiling vs incomplete/none → lower in-hospital mortality
• Early hemodynamic assessment within first 12 hours → improved outcomes
• PACCS trial (ongoing) testing early PAC within 6 hours of randomization in HF-CS
• Congestion profiles (critical for treatment selection):
  • LV dominant: PCWP or LVEDP >15 mmHg
  • RV dominant: RA pressure (CVP) >15 mmHg with relatively normal PCWP
  • Biventricular: elevation of both RA and PCWP
• Biventricular and RV congestion profiles → associated with adverse outcomes, need for durable LVAD and heart transplant
• Adverse hemodynamic markers: low MAP; elevated RA pressure; RA/PCWP ratio >0.6; reduced pulmonary artery pulsatility index (PAPi)
• PAPi (PA systolic − PA diastolic / CVP): reflects RV contractility, RV pulsatile load, RV congestion; most useful when RA >10 mmHg and no moderate/severe PH (PA systolic <50 mmHg)
• Low PAPi thresholds differ: AMI-CS <0.9; HF patients pre-LVAD implantation <1.85
• Integrate PAC data with echo/POCUS for full CS phenotyping

Pharmacological Management

Key principles: use lowest possible dose; shortest possible duration; address congestion first.

Congestion management: IV loop diuretics → thiazide diuretic augmentation → renal replacement therapy/ultrafiltration if refractory. Transrenal perfusion pressure = MAP − CVP (conceptual model).

Vasoactive agents (Table 2 summary):

• Norepinephrine is a reasonable first choice for most hypotensive CS patients
• Pure vasopressors (phenylephrine) as sole first-line agent strongly discouraged — reflex bradycardia reduces CO
• Inodilators/vasodilators may be considered in normotensive CS with high SVR
• Milrinone: judiciously used in worsening renal function (renal excretion; long half-life)
• DOREMI trial (n=192; SCAI B–E): dobutamine vs milrinone — no difference in primary composite endpoint
• No superior inotrope/vasodilator established for mortality benefit (Cochrane analysis)

Temporary Mechanical Circulatory Support (tMCS)

• Routine tMCS in all CS patients strongly discouraged
• Goal of tMCS: ventricular unloading + restore systemic perfusion; bridge to recovery, advanced therapies, or palliation

Key trials:

• IABP-SHOCK II (n=600; AMI-CS): intra-aortic balloon pump vs control — no mortality benefit at 30 days or 6-year follow-up
• ECLS-SHOCK (n=420; AMI-CS): early VA-ECMO + medical treatment vs medical treatment alone — no reduction in 30-day mortality
• DanGer Shock (STEMI-CS): early microaxial flow pump (Impella CP) vs standard of care — 12.7% absolute reduction in 180-day mortality (first positive tMCS RCT); rigorous entry criteria limit to narrow STEMI-CS cohort at experienced centers; randomized within 24 hours of CS
• Individual patient data meta-analysis (6-month follow-up): STEMI-CS without risk of hypoxic brain injury → mortality reduction after tMCS including VA-ECMO

tMCS selection principles:

• Based on desired cardiac index to improve perfusion when pharmacological support inadequate
• If undersupported (CI): escalate tMCS
• If inadequately unloaded: increase current device flow, escalate device (e.g., Impella CP→5.5), address afterload (LV venting for VA-ECMO), mitigate congestion
• LV-dominant STEMI-CS with clinical hypoperfusion or hemodynamic deterioration: microaxial flow pump may be considered
• Early palliative care consultation if patient is not a candidate for durable LVAD/transplant/recovery
• Delays in appropriate tMCS → multiorgan failure; pulmonary edema + persistent congestion + worsening perfusion/multiorgan dysfunction → prompt escalation discussion

Critical Care Management — Reassessment Framework (Table 3)

Continuous monitoring: HR, MAP, SpO2, urine output (hourly), CVP/PA pressures.
Q2–8h (depending on phase): lactate, creatinine, bicarbonate, pH, ScvO2, liver chemistries.
Daily echo (POCUS minimum), chest X-ray as needed, daily shock team assessment.

Complications of large-bore vascular access:

• Major bleeding in AMI-CS: up to 60%
• Limb ischemia: 4× higher with tMCS; associated with 2× higher in-hospital death
• Prevention: serial exam of access sites/limbs, avoid excessive anticoagulation, proper catheter angulation/securement
• If uncontrollable bleeding or limb ischemia: prompt tMCS removal; prefer cath lab/OR for removal of ≥12Fr devices

Mechanical ventilation in CS:

• Positive pressure ventilation: increases PVR; decreases RV and LV preload; decreases LV afterload (reduces LV compliance via interventricular dependence)
• LV failure ± mitral regurgitation → benefit from PPV (reduced LV diameter + transmural pressure + LV afterload via baroreceptor reflex)
• Hemodynamic effects of PEEP vary based on preload dependence, LV contractility, and presence of RV failure

tMCS Weaning

• Daily assessment: hemodynamic stability, current vasoactive drug burden, volume status, correction of underlying CS cause
• Stepwise flow reduction: 0.5–1 L/min (e.g., 2 performance levels with Impella) every 2–4 hours
• Success evaluated by: clinical exam, perfusion metrics, imaging, hemodynamic data
• Before weaning: advanced HF/transplant consult for myocardial recovery vs durable LVAD vs heart transplant assessment
• Acute-on-chronic HF-CS may need bridge from tMCS with prolonged inotrope wean

Recognize/Rescue → Optimize → Stabilize → De-Escalate/Exit Framework

1. Recognize/Rescue: Identify CS, restore adequate tissue perfusion (golden hour)
2. Optimize: Pharmacological support → hemodynamic stability (MAP >60–65 mmHg target)
3. Stabilize: Recovery of end-organ function, mitigate extra-cardiac derangements
4. De-Escalate/Exit: Assess myocardial recovery → durable LVAD / heart transplant (if appropriate) / palliative care/hospice

Limitations of the document

• Predominantly expert consensus with limited high-quality RCT evidence, especially in HF-CS
• Most RCT evidence derived from AMI-CS (specifically STEMI-CS); HF-CS markedly underrepresented
• DanGer Shock trial benefits limited to a narrow STEMI-CS cohort at experienced centers
• No head-to-head randomized data for most tMCS device comparisons
• Regional CS center tiering framework based largely on expert consensus without validated outcomes data
• Observational data on PAC use (not RCT level); PACCS trial results pending
• ESCAPE trial (negative for PAC in HF) is not directly applicable to CS population but is often cited
• HF-CS subtypes (myocarditis, takotsubo, amyloid, HOCM) largely excluded from RCTs; guidance extrapolated

Key Concepts Mentioned

• concepts/Cardiogenic-Shock — central subject; SUSPECT CS mnemonic; SCAI staging; Recognize/Rescue framework
• concepts/SCAI-Shock-Classification — A–E staging for severity; prognostic implications; Stage B highest risk of escalation
• concepts/Temporary-Mechanical-Circulatory-Support — device selection principles; DanGer Shock; IABP-SHOCK II; ECLS-SHOCK; weaning
• concepts/Invasive-Hemodynamic-Monitoring-CS — PAC; congestion profiles; PAPi; PACCS trial
• concepts/Vasoactive-Agents-in-CS — norepinephrine; dobutamine vs milrinone (DOREMI); pharmacology table
• concepts/Pulmonary-Artery-Pulsatility-Index — PAPi definition; RV failure marker; thresholds for AMI-CS and pre-LVAD

Key Entities Mentioned

• entities/DanGer-Shock-Trial — microaxial flow pump in STEMI-CS; first positive tMCS RCT; 12.7% absolute mortality reduction at 180 days
• entities/IABP-SHOCK-II-Trial — IABP in AMI-CS; no mortality benefit at 30 days or 6 years
• entities/ECLS-SHOCK-Trial — VA-ECMO in AMI-CS; no 30-day mortality reduction
• entities/DOREMI-Trial — dobutamine vs milrinone in CS; no difference in primary composite endpoint
• entities/PACCS-Trial — ongoing RCT of early PAC in HF-CS

Wiki Pages Updated

• Created wiki/sources/cardiogenic-shock-acc-2025.md (this file)
• Created wiki/concepts/Cardiogenic-Shock.md
• Created wiki/concepts/SCAI-Shock-Classification.md
• Created wiki/concepts/Temporary-Mechanical-Circulatory-Support.md
• Updated wiki/wikiindex.md
• Updated wiki/sourceindex.md