2025 ACC专家共识声明：心源性休克的评估和管理

Authors

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PREFACE

PREFACE

The American College of Cardiology (ACC) has a long history of developing documents (eg, decision pathways, health policy statements, appropriate use criteria) to provide members with guidance on both clinical and nonclinical topics relevant to cardiovascular care. In most circumstances, these documents have been created to complement clinical practice guidelines and to inform clinicians about areas where evidence is new and evolving or where sufficient data is more limited. Despite this, numerous gaps persist, highlighting the need for more streamlined and efficient processes to implement best practices in patient care.

Central to the ACC's strategic plan is the generation of actionable knowledge-a concept that places emphasis on making clinical information easier to consume, share, integrate, and update. To this end, the ACC has shifted from developing isolated documents to creating integrated "solution sets." These are groups of closely related activities, policy, mobile applications, decision-support tools, and other resources necessary to transform care and/or improve heart health. Solution sets address key questions facing care teams and attempt to provide practical guidance to be applied at the point of care. They use both established and emerging methods to disseminate information for cardiovascular conditions and their related management. The success of solution sets rests firmly on their ability to have a measurable impact on the delivery of care. Because solution sets reflect current evidence and ongoing gaps in care, the associated tools will be refined over time to match changing evidence and member needs.

Concise Clinical Guidance represents a key component of solution sets. They are meant to be transitional providing guidance and application to practice prior to the evidence required for expert consensus decision pathways or clinical practice guidelines. Concise Clinical Guidance are intended to illustrate clinical decisionmaking processes using tools (ie, figures, tables, checklists) and are limited in scope focusing on patient populations who share certain characteristics, such as conditions, subtypes, or lines of therapy. In some cases, covered topics will be addressed in subsequent expert consensus decision pathways, appropriate use criteria, clinical practice guidelines, and other related ACC clinical policy as the evidence base evolves. In other cases, these will serve as stand-alone policy.

Nicole M. Bhave, MD, FACC Chair, ACC Solution Set Oversight Committee

1. INTRODUCTION

3] [4] [5] Whereas CS due to acute myocardial infarction (AMI-CS) has been the most extensively studied form of CS in randomized controlled trials (RCTs), the incidence and prevalence of CS due to

Sinha et al

Sinha et al

J A C C V O L . -, NO. -, 2025

6] [7] [8] Despite advances in revascularization and increasing use of temporary mechanical circulatory support (tMCS) during the past 2 decades, RCTs have largely failed to identify treatment strategies that reliably improve mortality other than early revascularization for AMI-CS. 9 The first trial to demonstrate any benefit with tMCS was the Danish-German Cardiogenic Shock (DanGer Shock) trial, which showed that early use of a microaxial flow pump in select patients with ST-segment elevation myocardial infarction (STEMI)related shock improved 180-day survival as compared with standard of care.

3. SUMMARY GRAPHIC

3. SUMMARY GRAPHIC

The summary graphic (Figure 1 ) represents key considerations and a proposed road map for the first 24 hours of CS evaluation and management. organ hypoperfusion along with evidence of congestion or decreased cardiac output, (eg, measured using a pulmonary artery catheter) 3 ; however, these criteria dichotomize a dynamic clinical entity across a spectrum of illness severity and they also fail to acknowledge the deleterious consequences of normotensive CS (ie, endorgan hypoperfusion without hypotension), which has been associated with increased mortality. 16, 17 The diagnosis of CS, however, begins with a suspicion of an underlying state of inadequate cardiac output in patients at risk. 16 This suspicion can then be confirmed using readily obtainable clinical, laboratory, and/or imaging data.

Regardless of the location of the hospitalized patient advanced HF cardiologist, as appropriate. 22 To aid clinicians in confirming a suspicion of CS, the writing committee proposes the mnemonic "SUSPECT CS" (Table 1 ), the components of which include the minimum necessary criteria needed to make an early diagnosis of CS.

It is important to highlight that the initial suspicion and diagnosis of CS does not require invasive hemodynamics 1 ; however, invasive hemodynamics are often useful in elucidating the ventricular involvement and congestive profile of the CS patient and may inform therapeutic decision making. Once a diagnosis is made, the severity of CS should be classified using the SCAI stage of CS. 19, 20, 22, [27] [28] [29] but these frameworks are largely based on expert consensus (Figure 3 ). Data pertaining to the outcomes of transferred patients are scarce, pointing to an evidence gap in CS care. 30, 31 servational studies of patients transferred to dedicated CS centers have shown mixed results with respect to associated mortality for the transferred cohort.

A multicenter, retrospective observational analysis showed higher associated mortality among transferred patients that was driven by HF-related CS. 31 In a separate study comparing AMI-CS and HF-CS patients presenting initially to Level 2 or 3 CS hospital centers or a Level 1 CS hospital center in a dedicated, regionalized network across multiple hospital systems encompassing 3 states, the authors found comparable short-term outcomes (including in-hospital and 30-day mortality) and similar rates of bleeding, vascular, and stroke complications. 30 e predictors of outcomes among patients transferred for management of CS vary based on etiology of CS.

Among HF-CS patients, older age, mechanical ventilation, renal replacement therapy, and multiple vasoactive drugs were associated with worse outcomes while use of a pulmonary artery catheter was associated with favorable outcomes. On the other hand, among AMI-CS patients, overweight size (body mass index > 28 kg/m 2 ), worsening renal failure, lactate > 3 mg/dL, and increasing number of vasoactive agents were associated with higher mortality rates, while use of any tMCS device was associated with beneficial outcomes. 31 It is important to recognize the limitations inherent with these observational data and the merits and challenges of rigorously studying regionalized networks and systems of care in CS as an area of fertile investigation. 32 e writing committee recommends that Level 2 and 3 CS hospital centers identify: 1) locally available resources;

and 2) a dedicated CS regional center that would accept appropriately selected CS patients for further evaluation and treatment as well as might provide remote consultation for patients who may not be appropriate for transfer and/or need further stabilization before a transfer can be initiated. Conversely, Level 1 CS hospital centers should welcome consultations from their regional referring hos- vasoactive medication, or those in whom a tMCS device is being considered, should also prompt communication with the CS regional center to determine whether, and when, transfer should be pursued. Once the initial suspicion of CS has been confirmed, the writing committee believes it is never too early to contact the CS regional center to discuss potential transfer vs continued management at the initial institution. or palliative care specialists may be included in some centers. 33 For Level 2 and 3 CS hospital centers that may not have on-site expertise or an established CS team, the writing committee strongly recommends early contact with the regional Level 1 CS hospital center after con- 4 ). 21, 26 pending on the institutional resources and personnel, all elements of the shock team model may not be readily available. 37 Additional expertise may be needed in certain clinical scenarios, such as cardiac electrophysiology for patients with electrical storm, maternal fetal medicine for critically ill pregnant patients, and adult congenital heart disease consultation for patients with complex adult congenital heart disease physiology. The writing committee affirms the importance and value of building and growing shock teams across time and frequently reviewing CS cases as patient safety and quality improvement initiatives to assess opportunities to refine protocols and strengthen relationships.

firming

Evaluation and Management of Cardiogenic Shock -, 2025:---

4.4. Invasive Hemodynamics

1] [42] [43] In fact, complete hemodynamic profiling as compared with incomplete or no hemodynamic assessment has been associated with lower in-hospital mortality and early hemodynamic assessment within the first 12 hours has been associated with improved clinical outcomes. 24, 25 8] [49] The writing committee suggests integrating invasive hemodynamic assessment with noninvasive cardiac imaging (ie, echocardiography or point-of-care ultrasound whenever available) to more precisely characterize the phenotype of CS patients (Figure 5 ). 27,50

4.5. Pharmacological Management of CS

In CS, the goal of pharmacological therapies is to mitigate congestion (whenever present), optimize cardiac output, Hypoperfusion can be addressed by starting intravenous vasoactive medications, including inotropes, chronotropes, inopressors, inodilators, vasodilators, and vasopressors (Table 2 ).

These drugs are commonly used in clinical practice for the management of CS but some have been associated

with increased adverse effects, including arrhythmias, and increased myocardial oxygen consumption. 51 Therefore, the writing committee advises that vasoactive medications be used in CS at the lowest possible dose to support adequate perfusion and for the shortest possible duration. 2 ).

A Cochrane analysis found insufficient evidence to support the superiority of a particular inotrope or vasodilating agent in CS, especially with respect to a mortality benefit. 53

(þ) ¼ weak binding; a1 ¼ a-1 receptor; b1 ¼ b-1 receptor; b2 ¼ b-2 receptor; BP ¼ blood pressure; CO ¼ cardiac output; CS ¼ cardiogenic shock; D1 ¼ D1 receptor; FDA ¼ U.S.

4.6. tMCS

RCTs examining tMCS in CS have primarily been focused on STEMI-CS and have been limited by sample size, study design, patient selection, timing, and other key limitations. Few head-to-head randomized comparisons exist between various tMCS devices, and the potential therapeutic benefits must be weighed against bleeding, vascular, neurological, infectious, other complications (Figure 6 ). 21 though tMCS is being increasingly utilized in the treatment of both AMI-CS and HF-CS, 55, 56

Sinha et al

Evaluation and Management of Cardiogenic Shock -, 2025:--trial of 600 patients with AMI-CS who were undergoing early revascularization with intra-aortic balloon pump vs control, and demonstrated no effect on 30-day all-cause mortality and at 6-year long-term follow-up. 57, 58 The Extracorporeal Life Support in Infarct-Related Cardiogenic Shock (ECLS-SHOCK) trial was a multicenter, randomized, open-label trial of 420 patients with AMI-CS for whom early revascularization was planned, which showed that the 30-day all-cause mortality was not lower among patients who received early extracorporeal life support (ECLS group) with medical treatment vs usual medical treatment alone (control group). 59 Indeed, the DanGer Shock trial was the first trial that demonstrated that early use of a microaxial flow pump in select patients with STEMI-related shock, randomized within 24 hours of CS at experienced centers, improved 180-day survival as compared with standard of care, noting an absolute mortality reduction of 12.7%. 9a The rigorous entry criteria for the DanGer Shock trial limit the evidence-base from the trial to a narrow cohort of patients with STEMI-CS. 60 individual patient data meta-analysis of RCTs in CS with 6-month follow-up suggested that patients with STEMI-CS without risk of hypoxic brain injury had a reduction in mortality after tMCS use, inclusive of venoarterial extracorporeal membrane oxygenation (VA-ECMO). 61 The writing group believes escalation to tMCS with a microaxial flow-pump may be considered for management. 26 The writing committee notes that From a mechanistic standpoint, the goal of tMCS is to promote ventricular unloading as well as restore systemic perfusion and is designed to bridge the CS patient to advanced therapies or facilitating myocardial recovery. In addition, the use of tMCS may allow de-escalation and weaning from pharmacological therapies that may exacerbate myocardial damage or ischemia if continued at high doses for prolonged duration. 3 The principles un- Delays in initiation of tMCS in appropriate candidates may lead to worsening end-organ perfusion and hemometabolic derangements that ultimately culminate in multiorgan failure and death. 3, 63 Thus, early CS recognition, prompt initiation of tailored and selective tMCS, and serial reassessment may improve outcomes. 27 Evidence of comprise the key elements of this structured reassessment (Table 3 ). Some components are routinely measured continuously, whereas laboratory testing is periodically obtained (Table 3 ). Early after intensive care unit admission or when the severity is high, laboratory metrics of perfusion may be useful as frequently as every 2 to 4 hours and may be spaced to every 6 to 8 hours if the patient's condition stabilizes. These data enable reassessment of CS severity and determination of the need for escalation or de-escalation of hemodynamic support.

derlying

Complications of large-bore vascular access for mechanical circulatory support devices, including bleeding and limb ischemia, warrant vigilant monitoring and preventive interventions. In AMI-CS, the incidence of major bleeding may be as high as 60% and the risk of limb ischemia is 4-fold higher in patients requiring tMCS. 71, 72 mb ischemia is associated with a 2-fold higher risk of in-hospital death among CS patients, 72 yet diagnosis and management of acute limb ischemia in CS remains poorly understood. In addition to minimizing the duration of vascular access, helpful practices for reducing complications related to large-bore arterial devices are listed in Table 4 .

If uncontrollable bleeding or limb ischemia occurs, prompt removal of the tMCS device is usually necessary.

Removal of large-bore vascular access devices ($12

Removal of large-bore vascular access devices ($12

French) in the catheterization laboratory or operating room should be considered whenever possible. 71 sitive pressure ventilation is often necessary in the management of patients with CS and carries important cardiopulmonary interactions that may impact hemodynamic status of the patient. 73 Positive end-expiratory The morbidity of CS is strongly associated with both cardiovascular and noncardiovascular complications of critical care (Figure 9 ). pressure increases pulmonary vascular resistance, decreases RV and LV preload, decreases LV afterload, and reduces LV compliance through interventricular dependence. Therefore, the hemodynamic effects of positive end-expiratory pressure will vary depending upon how much preload dependence and LV contractility is present and whether RV failure is present (Figure 10 ). 73 Both positive pressure ventilation and positive end-expiratory pressure decrease LV diameter and increase transmural LV pressure. LV afterload decreases due to baroreceptor reflex response to aortic compression. These mechanisms augment LV stroke volume, thereby benefiting patients with LV failure with or without severe mitral regurgitation. 73 cision-making regarding the weaning of tMCS is a central element of the interdisciplinary critical care management of patients with CS. Rigorous evidence to guide weaning of mechanical circulatory support is lacking. A daily assessment of readiness to wean should include evaluation of hemodynamic stability, consideration of the current total need for pharmacological vasoactive support, volume status, and whether the underlying cause of CS has been corrected or improved. 27, 74 A rational approach to weaning includes a stepwise decrease in flow from the device, the pace of which will be dictated by the nature of the initial cardiovascular insult and its reversibility. Before weaning, it is reasonable to consult an advanced HF/ transplant cardiologist to determine whether the patient is a suitable candidate for myocardial recovery versus durable LVAD, or heart transplant. The success of weaning is evaluated at each step by an integrated assessment of clinical exam, metrics of end-organ perfusion, imaging, and invasive hemodynamic data, when available, with a standard weaning interval aiming for 0.5-1L/min decrease in support (eg, 2 performance levels with Impella) every 2 to 4 hours (Figure 11 ). 27, 74 CS patients, especially those due to acute-on-chronic HF-CS, may require a bridge from tMCS with inotropes, and the latter may require a prolonged wean in certain instances.

The optimal treatment of CS represents a multiphase, team-based approach tailored to the patient's hemodynamic and metabolic profile. In this manner, the Recognize/Rescue -Optimize -Stabilize -De-Escalation/Exit framework may serve as a useful heuristic. 75 e first phase of therapy is to recognize CS and restore adequate tissue perfusion ("recognize/rescue" [Figure 12 ]). 75 Following this phase, the goal is to tailor the pharmacological support to achieve hemodynamic stability with MAP > 60 to 65 mm Hg considered a reasonable hemodynamic target ("optimization"). 75 The "stabilization" phase is characterized by recovery of end-organ function and mitigation of extra-cardiac derangements.

The "de-escalation/exit" phase enables assessment of myocardial recovery, and if not, transition to advanced therapies, such as durable LVAD or orthotopic heart transplant for appropriate candidates. Evaluation and Management of Cardiogenic Shock -, 2025:---

|CS hospital centers include early interdisciplinary| |---|

|engagement and consultation to deliver necessary|

|multifaceted care, a coordinating physician (eg, a cardiac|

|intensive care unit cardiologist, advanced HF and|

|transplant cardiologist, or interventional cardiologist,|

|depending on clinical setting) for efficient patient triage,|

|a rapid system for concurrent team activation, efficient|

|virtual and/or bedside communication, and use of inva-|

|sive hemodynamics to guide therapy selection|

|(Figure|

|inadequate. If the CS patient is undersupported with| |---|

|respect to cardiac index on the present device, escalation|

|of tMCS may be warranted. If the CS patient is not|

|adequately unloaded on present support, the range of|

|therapeutic options include increasing flow on current|

|device, escalating support device (eg, Impella CPÒ to 5.5),|

|addressing afterload (eg, LV venting for VA-ECMO), and|

|mitigating congestion. Early palliative care consultation|

|should be considered if not concurrently pursued at the|

|time of tMCS placement, as some patients may not be|

|candidates for durable LVAD, heart transplant, or|

|myocardial recovery. 62|

|data if available, tMCS selection (including device|

|capacity and risk of device-related complications) should|

|be based on attaining the desired cardiac index to|

|improve perfusion when pharmacological support alone is|

|Structured Reassessment of Patients With CS in||| |---|---|---|

|the Intensive Care Unit|||

|Category|Measure|Frequency|

|Clinical examination Mental status|Clinical examination Mental status|Q6-8 h (Q1-2 h pulse exam|

||Perfusion of extremities|with large-bore arterial|

||Vascular access sites|vascular access in place)|

||Peripheral pulses (with||

||arterial access in place)||

|Vital signs|Heart rate (and rhythm)|Continuous|

||Mean arterial pressure||

||Arterial oxygen saturation||

|Physiological|Urine output|Urine output|

|Laboratory|Serum creatinine|Serum creatinine|

||Serum bicarbonate|Serum bicarbonate|

||Arterial or venous pH||

||Central or mixed venous||

||oxygen saturation||

||Lactate||

||Liver chemistries|Liver chemistries|

|Imaging|Echocardiographic|Echocardiographic|

||assessment of|assessment of|

||biventricular|biventricular|

||performance,|performance,|

||intravascular volume,|performed as needed|

||and MCS positioning||

||(when applicable)||

||Chest radiography to aid||

||in assessment of||

||MCS/PAC/TVP/ETT||

||positioning|positioning|

|Invasive|Central venous pressure|CVP and PA pressure are|

|hemodynamics|Pulmonary artery|Pulmonary artery|

|(if invasive|pressures|pressures|

|monitoring|Pulmonary capillary|may be continuous or|

|in place)|wedge pressure|wedge pressure|

||Estimated cardiac output||

|Interdisciplinary|Shock team assessment|Daily (or more frequent|

|shock team|of clinical status|when metrics indicate|

|||clinical worsening)|

the initial diagnosis of CS. The following key considerations may be helpful for triage, potential transfer, appropriate risk stratification, and treatment of CS

addition or escalation of tMCS are as follows:

[70][71] [72]CS ¼ cardiogenic shock; CVP ¼ central venous pressure; ETT ¼ endotracheal tube; h ¼ hour; MCS ¼ mechanical circulatory support; PA ¼ pulmonary artery; PAC ¼ pulmonary artery catheter; pH ¼ potential of hydrogen; Q ¼ every; TVP ¼ transvenous pacing lead.

This table represents all relationships of reviewers with industry and other entities that were reported by authors, including those not deemed to be relevant to this document, at the time this document was under development. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of $5% of the voting stock or share of the business entity, or ownership of $$5,000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person's gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted. Please refer to https://www.acc.org/Guidelines/About-Guidelines-and-Clinical-Documents/Relationships-with-Industry-Policy for definitions of disclosure categories or additional information about the ACC Disclosure Policy for Writing Committees. *Significant relationship. †No financial benefit. ‡Relationship with this company is limited to enrolling patients in clinical trials. This disclosure was entered under the Clinical Trial Enroller category in the ACC's disclosure system. To appear in this category, the author acknowledges that there is no direct or institutional relationship with the trial sponsor as defined in the ACC/AHA Disclosure Policy for Writing Committees. Evaluation and Management of Cardiogenic Shock -, 2025:---

References

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EN_PAPER

2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock A Report of the American College of Cardiology Solution Set Oversight Committee Writing Committee members

2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock A Report of the American College of Cardiology Solution Set Oversight Committee Writing Committee members