Impairments in microvascular reactivity are related to organ failure in human sepsis
Kevin C Doerschug1, Angela S Delsing, Gregory A Schmidt
1Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA. kevin-doerschug@uiowa.edu
Abstract:
Severe sepsis is a systemic inflammatory response to infection resulting in acute organ dysfunction. Vascular perfusion abnormalities are implicated in the pathology of organ failure, but studies of microvascular function in human sepsis are limited. We hypothesized that impaired microvascular responses to reactive hyperemia lead to impaired oxygen delivery relative to the needs of tissue and that these impairments would be associated with organ failure in sepsis. We studied 24 severe sepsis subjects 24 h after recognition of organ dysfunction; 15 healthy subjects served as controls. Near-infrared spectroscopy (NIRS) was used to measure tissue 1) microvascular hemoglobin signal strength and 2) oxygen saturation of microvascular hemoglobin (StO2). Both values were measured in thenar skeletal muscle before and after 5 min of forearm stagnant ischemia. At baseline, skeletal muscle microvascular hemoglobin was lower in septic than control subjects. Microvascular hemoglobin increased during reactive hyperemia in both groups, but less so in sepsis. StO2 at baseline and throughout ischemia was similar between the two groups; however, the rate of tissue oxygen consumption was significantly slower in septic subjects than in controls. The rate of increase in StO2 during reactive hyperemia was significantly slower in septic subjects than in controls; this impairment was accentuated in those with more organ failure. We conclude that organ dysfunction in severe sepsis is associated with dysregulation of microvascular oxygen balance. NIRS measurements of skeletal muscle microvascular perfusion and reactivity may provide important information about sepsis and serve as endpoints in future therapeutic interventions aimed at improving the microcirculation.
Insights
Severe sepsis impairs microvascular function, leading to reduced oxygen delivery and organ dysfunction. Near-infrared spectroscopy revealed slower microvascular responses in sepsis patients, highlighting a critical issue in sepsis management.
Area of Science:
- Critical Care Medicine
- Vascular Physiology
- Biomedical Engineering
Background:
- Severe sepsis causes systemic inflammation and organ dysfunction.
- Microvascular perfusion abnormalities are key in sepsis-related organ failure.
- Limited studies exist on human sepsis microvascular function.
Purpose of the Study:
- Hypothesize impaired microvascular responses to reactive hyperemia in sepsis.
- Investigate if these impairments reduce oxygen delivery and correlate with organ failure.
- Assess microvascular hemoglobin and oxygen saturation (StO2) in sepsis.
Main Methods:
- Studied 24 severe sepsis patients and 15 healthy controls.
- Utilized near-infrared spectroscopy (NIRS) on thenar skeletal muscle.
- Measured microvascular hemoglobin and StO2 before and after forearm ischemia.
Main Results:
- Septic subjects had lower baseline microvascular hemoglobin.
- Reactive hyperemia response was blunted in sepsis patients.
- Septic subjects showed slower oxygen consumption and impaired StO2 increase during hyperemia, worsening with organ failure.
Conclusions:
- Organ dysfunction in severe sepsis is linked to microvascular oxygen balance dysregulation.
- NIRS measurements of skeletal muscle microcirculation offer insights into sepsis.
- NIRS may serve as an endpoint for future sepsis therapies targeting microcirculation.
