Microvascular dysfunction and skeletal muscle oxygenation assessed by phase-modulation near-infrared spectroscopy in patients with septic shock

Objective: Sepsis is now considered a disease of the microcirculation. Little is known about the various sepsis-induced changes responsible for microvascular dysfunction. We investigated human microvascular function, regulation, oxygenation, and cellular metabolism during subacute septic shock. Design and setting: Prospective case-control study in a nine-bed polyvalent surgical ICU of a university hospital. Patients and participants: A prospectively enrolled group of 26 patients (13 with septic shock, 13 nonseptic postsurgical patients) and 15 healthy volunteer controls. Measurements and results: The absolute tissue hemoglobin concentrations (oxygenated hemoglobin and deoxyhemoglobin) were measured noninvasively in arterioles, capillaries, and venules by phase-modulation near-infrared spectroscopy in the human brachioradial muscle during a series of venous occlusions and an arterial occlusion (ischemia) induced by applying a pneumatic cuff. These measurements were used to calculate tissue blood volume, postischemic hemoglobin resaturation time, microvascular compliance, and O-2 consumption. Patients with sepsis had significantly higher tissue blood volume values and lower compliance than healthy controls. They also had longer postischemic hemoglobin resaturation times than the other two groups and blunted resaturation curves. O-2 consumption was lower in patients with sepsis than in healthy controls. In patients with septic shock cuff-induced ischemia left O-2 consumption unchanged, whereas in healthy volunteers it reduced O-2 consumption to values almost matching those of patients with septic shock. Conclusions: These findings show that septic shock alters microvascular muscle function and regulation. Diminished local VO2 presumably reflects maldistribution and faulty autoregulation of local blood flow.