Cardiogenic shock describes a syndrome of systemic hypoperfusion due to insufficient cardiac output. Therapeutic interventions aim to restore systemic perfusion and oxygen delivery, relieve congestion, and reverse the primary culprit pathologies that precipitate shock. Cardiogenic shock care often emphasizes acute rescue and survival; however, survival does not always equal meaningful recovery. In this review, we propose a recovery-focused framework in which myocardial and end-organ recovery are treated as explicit, measurable targets. Building upon prior frameworks proposed for the management of shock, we organize cardiogenic shock management into four overlapping phases: salvage, optimization, stabilization, and de-escalation. Each phase addresses a distinct clinical question: can the patient be rescued, is perfusion and unloading sufficient to prevent further injury, is meaningful myocardial and end-organ recovery occurring, and is recovery durable enough to withdraw support? We synthesize current strategies and highlight emerging targets and research priorities spanning early identification and triage, integrated macro- and microcirculatory monitoring, phenotype-guided management, targeted metabolic and immunologic therapies, use of mechanical circulatory support as a recovery platform, and structured de-escalation of care.

Cardiogenic shock remains the leading cause of death in patients with acute myocardial infarction and severe acute heart failure. Temporary mechanical circulatory support devices have emerged as important adjuncts for restoring systemic perfusion, unloading the failing ventricle, and stabilizing patients for cardiogenic shock and during high-risk percutaneous coronary interventions. However, currently available devices are associated with important limitations, including vascular complications, hemolysis, and uncertain survival benefit. Technological innovation has led to the development of new percutaneous mechanical support systems designed to deliver higher cardiac output with more limited vascular access and improved hemocompatibility. This review summarizes the current evidence regarding current and emerging temporary mechanical circulatory support devices used in cardiogenic shock and high-risk percutaneous coronary interventions. Literature from major clinical trials, observational registries, and device development studies was reviewed to evaluate device mechanisms, hemodynamic performance, and emerging technologies.

Acute kidney injury (AKI) is a frequent and prognostically decisive complication of cardiogenic shock (CS), conferring substantially increased short- and long-term mortality. As understanding of CS has evolved beyond an isolated low-output model, AKI is increasingly recognized as a consequence of multifactorial pathophysiology encompassing venous congestion, neurohormonal dysregulation, microcirculatory dysfunction, inflammation, and iatrogenic injury from shock therapies. Despite this expanded mechanistic framework, approaches to the diagnosis and management of AKI in CS remain highly variable, and no single strategy has consistently improved renal or survival outcomes. Emerging data suggest multiple biologically distinct phenotypes of AKI in CS that may enable future targeted therapeutics. This review synthesizes contemporary evidence on the classification, epidemiology, and mechanisms of AKI in CS across distinct phenotypes, including early- versus late-onset, acute versus acute-on-chronic, and cardiorenal versus cardiometabolic presentations. We further discuss the renal effects of contemporary shock therapies, including vasoactive agents, temporary mechanical circulatory support, and renal replacement strategies. Finally, we highlight emerging diagnostic tools, including noninvasive vascular imaging and renal biomarkers, alongside novel device-based approaches to improve renal perfusion and congestion. Advancing care in CS will depend on redefining AKI not only as a binary marker of renal dysfunction but also as a mechanistically heterogeneous component of shock biology amenable to targeted intervention.

Cardiogenic shock (CS) is a cardiovascular emergency with short-term mortality ranging from 30% to 40% despite an expanding therapeutic armamentarium. Structured systems of care have transformed outcomes in ST-segment-elevation myocardial infarction, stroke, and out-of-hospital cardiac arrest through tiered hospital designations, standardized protocols, and regionalized networks, yet no analogous framework exists for CS. CS differs from these conditions in ways that complicate direct application of existing models: the appropriate intervention varies by cause, hemodynamic phenotype, and shock severity; the therapeutic trajectory is iterative and uncertain rather than binary and time-fixed; prehospital identification is rarely feasible; and the exit strategy, encompassing myocardial recovery, durable mechanical support, transplantation, or palliation, has no parallel in other cardiovascular emergencies. Observational data suggest an association between structured multidisciplinary care, regionalized networks, and more consistent care delivery though causal relationships remain unestablished, and no standardized national framework for CS center designation yet exists. We propose that CS systems of care should be organized around a node-based model in which each hospital tier has a defined role, transfer is guided by physiological trajectory and exit strategy candidacy rather than geography, and system performance is evaluated by metrics of timing, outcomes, and equity. The American Heart Association Cardiogenic Shock Registry, designed to enroll consecutive patients across all etiologies and severity levels, represents the natural infrastructure around which this framework can be constructed. Realizing this vision will require dedicated registries, implementation research, and a definition of success that extends beyond in-hospital survival to encompass recovery, function, and equitable access to care.

Cardiogenic shock (CS) is a highly heterogeneous syndrome with persistently high mortality despite advances in therapies, including temporary mechanical circulatory support. The disparate results of trials on temporary mechanical circulatory support in CS suggest that improved strategies, including better patient selection, are needed in the context of CS heterogeneity. Notably, a microaxial flow pump device has recently shown a survival benefit in ST-segment-elevation myocardial infarction-associated CS in the DanGer Shock trial (Danish-German Cardiogenic Shock), marking a positive outcome amid many negative or neutral trials. As CS phenotyping becomes increasingly important for developing tailored therapeutic strategies, it is essential to identify factors contributing to variable phenotypes, including shock severity, cause, hemodynamic profile, ventricular function, shock pattern, and patient-centered factors that may influence microaxial flow pump candidacy. Successful CS management with a microaxial flow pump may be best guided by an individualized and proactive approach, tailored to each patient's risk profile and clinical course. It is rational to implement this strategy at centers capable of providing and managing advanced temporary mechanical circulatory support options while determining candidacy for advanced heart failure therapies. Our review underscores the importance of CS phenotyping and tailoring temporary mechanical circulatory support-particularly microaxial flow pump support-to patient-specific factors that are central to optimizing outcomes in CS management.

Acute decompensated heart failure is a clinical syndrome characterized by upregulation of neurohormonal compensatory mechanisms that, while intended to preserve organ perfusion as a response to reduced cardiac output, progressively exacerbate systemic congestion. Perfusion, defined by adequate oxygen delivery to the tissues, is more complex than simple cardiac output and arterial inflow, and is also significantly influenced by venous backpressure, as well as microcirculatory autoregulation. Therefore, as venous pressures continue to rise, these may ultimately contribute to hypoperfusion and, therefore, cardiogenic shock (CS). Other mechanisms, such as inflammation and increased organ capsular pressure, can contribute to further impairments in tissue oxygenation. This gradual and often clinically unrecognized deterioration from acute decompensated heart failure to heart failure-related CS (HF-CS) contrasts with acute myocardial infarction-related CS, where underlying compensatory mechanisms are more limited. Furthermore, prolonged and unrecognized hypoperfusion may further worsen HF-CS through progressive microcirculatory dysfunction with subsequent uncoupling of macrocirculation and microcirculation. At this point, normalization of macrocirculatory parameters may no longer restore tissue oxygenation. Early identification of hypoperfusion is, therefore, critical so that interventions targeting systemic hemodynamics may still improve tissue perfusion and reverse circulatory collapse. This review (1) outlines the pathophysiology of hypoperfusion in HF-CS; (2) summarizes invasive, biochemical, and imaging parameters to detect hypoperfusion; (3) phenotypes HF-CS profiles; and (4) proposes a monitoring framework for hypoperfusion in HF-CS.