Publications

Cardiogenic shock is classically defined by systemic hypotension with evidence of hypoperfusion and end organ dysfunction. In modern practice, however, these metrics often incompletely describe cardiogenic shock because patients present with more advanced cardiovascular disease and greater degrees of multiorgan dysfunction. Understanding how perfusion, congestion, and end organ dysfunction contribute to hypoxia at the cellular level are central to the diagnosis and management of cardiogenic shock. Although, in clinical practice, increased lactate level is often equated with hypoxia, several other factors might contribute to an elevated lactate level including mitochondrial dysfunction, impaired hepatic and renal clearance, as well as epinephrine use. To this end, we present the evidence underlying the value of lactate to pyruvate ratio as a potential discriminator of cellular hypoxia. We will then discuss the physiological implications of hypoxia and congestion on hepatic, intestinal, and renal physiology. Organ-specific susceptibility to hypoxia is presented in the context of their functional architecture. We discuss how the concepts of contractile reserve, fluid responsiveness, tissue oxygenation, and cardiopulmonary interactions can help personalize the management of cardiogenic shock. Finally, we highlight the limitations of using lactate for tailoring therapy in cardiogenic shock.