UNDERSTANDING HEMODYNAMIC INCOHERENCE: MECHANISMS, PHENOTYPES, AND IMPLICATIONS FOR TREATMENT

Abstract

The reversal of microcirculation dysfunction is crucial for assessing the success of shock resuscitation and significantly influences patient prognosis. However, hemodynamic incoherence is observed when microcirculatory dysfunction persists despite the restoration of macrocirculatory function after resuscitation. Recent advancements in technology have enabled bedside assessment of microcirculation in shock patients, allowing for direct visualization of microcirculatory morphology and quantitative evaluation of its functional status. This article reviews the pathophysiological mechanisms that lead to hemodynamic incoherence. It also introduces the current understanding and classification framework for the different phenotypes of hemodynamic incoherence. Existing evidence indicates that the diverse mechanisms leading to microcirculatory disorders result in varied manifestations among patients experiencing hemodynamic incoherence, highlighting the heterogeneity of this population. Some classification frameworks have been proposed to enhance our understanding of these phenotypes. By integrating pathophysiological mechanisms, clinical symptoms, indicators of macrocirculation, microcirculation, tissue metabolism, and biomarkers, we can summarize certain clinical features of phenotypes in hemodynamic incoherence to form a conceptual framework. Additionally, strategies for creating targeted treatments based on different phenotypes require further validation.

Fig. 1

Multimodal monitoring to identify the specific phenotype of microcirculatory disorders in shock patients with hemodynamic incoherence. Patients’ clinical features, systemic hemodynamic parameters, ultrasonography, biochemical markers, and microcirculation need to be integrated into a comprehensive judgment. ABP, arterial blood pressure; CO, cardiac output; CVP, central venous pressure; EVLW, extravascular lung water; GEVD, global end-diastolic volume; Hb, hemoglobin; HR, heart rate; MFI, microcirculatory flow index; PAOP, pulmonary artery obstruction pressure; PBR, perfused boundary region; PEEP, positive end-expiratory pressure; PPV, proportion of perfused vessels; PVD, perfused vessel density; PVPI, pulmonary vascular permeability index; RBC, red blood cell; SBRI, snuffbox resistive index; SVRI, systemic vascular resistance index; SVV, stroke volume variation; TVD, total vessel density; VexUS, venous excess ultrasound.

Fig. 2

Proposal for an algorithm for the treatment of shock patients. First, according to the monitoring parameters of the macrocirculation, the systemic hemodynamics were optimized to ensure that the patients had sufficient cardiac output and blood volume. Attention is needed to correct anemia and hypoxemia so that the macrocirculation provides adequate blood flow and oxygen to the microcirculation. If the patient’s shock does not improve, there is hemodynamic incoherence. At this time, the phenotype of hemodynamic incoherence can be determined by multimodal monitoring, and then personalized treatment means can be adopted to restore the coherence of macrocirculation and microcirculation. With the advancement of technology, monitoring and treatment methods for oxygen utilization impairment induced by subcellular structural injury may be popularized in the future. CO, cardiac output; FFP, fresh frozen plasma; PAOP, pulmonary artery obstruction pressure; PDE-4, phosphodiesterase-4; PE, plasma exchange; PEEP, positive end-expiratory pressure; PLR, passive leg raising; SV, stroke volume; SVV, stroke volume variation.