The PCS population is unique due to patients’ exposure to cardiopulmonary bypass (CPB) and temporary cardiac arrest, which are associated with cytokine release, vasoplegia syndrome (VPS), coagulopathy, myocardial dysfunction and pulmonary hypertension (PHTN). CPB causes cytokine release from the interaction with the CPB circuit, the removal of blood into a reservoir and reintroduction into the body, and the shear stress from blood passing through the centrifugal impeller.¹ The release of

Conventional cardiogenic shock (CS) definition does not apply to the postcardiotomy (PC) population due to the high incidence of vasopressor and inotrope requirements that is expected after exposure to CPB and sedation. Although relatively infrequent (occurring in ∼0.5% to 1.5% of adult cardiac surgery cases), PCS carries an extremely high mortality approaching 2 in 3 patients.² This condition was historically referred to as low cardiac output syndrome (LCOS), a term that carries significant

Postoperative patients can exhibit multiple shock phenotypes which are often a combination of multiple pathologies rather than an isolated mechanism. Hemodynamic profiling entails a systematic assessment of cardiac function, perfusion, and vascular tone in these high-risk patients using standard and advanced monitoring techniques to delineate the predominant shock mechanism and severity (Fig. 1).

The main goal of fluid management is to maximize CO and tissue perfusion while minimizing complications and volume overload. Guidelines support goal-directed fluid protocols in cardiac surgery that integrate both dynamic fluid volume indices with flow-directed goals as they outperform single-target protocols.²⁹

Ongoing fluid resuscitation requires frequent reassessment of static filling pressure and perfusion indices after dynamic interventions to avoid exceeding fluid tolerance. Fluid tolerance 

Lactate metabolism is a sensitive marker of tissue hypoperfusion and anaerobic metabolism in PCS. Serial lactate measurements and lactate clearance serve as diagnostic and prognostic indicators. Serial trends and clearance are more clinically useful than absolute values in guiding resuscitation decisions. However, lactate interpretation requires careful clinical contextualization in this population: (1) epinephrine administration causes type B lactic acidosis through beta-mediated accelerated