Beyond Blood Pressure: The Role of Flow Parameters and Biomarkers of Hypoperfusion in Cardiogenic Shock

Cardiogenic shock (CS) remains a heterogeneous syndrome with persistently high mortality across acute myocardial infarction, decompensated heart failure, and post-cardiotomy states. Blood pressure, the most commonly used marker of hemodynamic status, is the product of cardiac output and systemic vascular resistance and can be preserved by compensatory vasoconstriction even as flow and tissue perfusion deteriorate. This review examines the evidence for measuring flow-derived hemodynamic parameters and biomarkers of hypoperfusion, rather than relying on pressure alone, to risk-stratify and inform therapy in CS. We propose a practical framework that distinguishes blood pressure targets, measured native flow, device-generated flow, and perfusion biomarkers, and that separates prognostic association from demonstrated treatment-guiding utility, since these are frequently conflated in the existing literature. We summarize data on pulmonary artery catheter-derived cardiac output and cardiac index, cardiac power output and index, the pulmonary artery pulsatility index, transpulmonary thermodilution and other advanced hemodynamic monitoring methods, echocardiographic flow assessment, and perfusion biomarkers including lactate, lactate clearance, and multimarker scores. We review how these parameters are incorporated into the Society for Cardiovascular Angiography and Interventions (SCAI) SHOCK staging and protocols for initiating, titrating, and weaning mechanical circulatory support (Impella, veno-arterial extracorporeal membrane oxygenation), including combined ECPELLA strategies, and we discuss the contemporary randomized trials most relevant to this field, DanGer Shock, ECLS-SHOCK, and ECMO-CS. We also examine how cardiogenic shock etiology and hemodynamic phenotype (e.g., right ventricle-predominant, cardiorenal, cardiometabolic) modify the interpretation and likely generalizability of these parameters. We conclude that integrating flow and perfusion markers with pressure provides a more complete, if not yet fully validated as treatment-guiding, picture of shock severity, while highlighting the continued scarcity of trials that test monitoring strategies themselves rather than the devices they inform.