Understanding the Nuanced Concept of Hemodynamic Incoherence and Its Underlying Physiology

Hemodynamic incoherence is commonly defined as a dissociation between normalization of macrocirculatory variables and persistent impairment of tissue perfusion. However, this phenomenon is not physiologically homogeneous. We propose a conceptual distinction between two forms of macro-microcirculatory incoherence. Type 1 incoherence represents primary microcirculatory dysfunction, in which intrinsic alterations in microvascular regulation and flow distribution lead to heterogeneous capillary perfusion despite apparently adequate upstream hemodynamics, as observed in sepsis. In contrast, Type 2 incoherence reflects secondary impairment of microcirculatory flow resulting from hemodynamic constraints elsewhere in the circulation, including excessive vasoconstriction, limited cardiac forward flow, or venous congestion. In this setting, impaired perfusion arises from ineffective transmission of flow across the system rather than primary microvascular failure. The four-interface model of the circulation provides a unifying physiological framework to interpret these mechanisms as failures of energy transfer across sequential hemodynamic domains. Recognizing these distinct forms of incoherence may improve not only physiologic interpretation of shock and help avoid conflating fundamentally different mechanisms under a single conceptual entity, but also be key in individualizing therapeutic interventions to the proper phenotypes of tissue malperfusion.