Please see Bibliography of References for a list of abstracts, manuscripts and posters.
Thooft A, Favory R, Salgado DR, De Backer D, Vincent JL, Creteur J. Int Care Med. 2009;35(Suppl 1):S80.
Background: Conflicting data exist concerning the effects on the microcirculation of increasing mean arterial pressure (MAP) with norepinephrine (NE) in septic shock. Near infrared spectroscopy (NIRS) has been proposed as a tool to quantify microvascular dysfunction in patients with sepsis. By inducing a vaso-occlusive test (VOT), a variety of NIRS derived variables can be measured to assess local metabolic demand and microvascular dysfunction. This trial was conducted to test the effects of increasing MAP by NE on microvascular reactivity in patients with septic shock.
Materials and Methods: After Local Ethical Committee approval and informed consent, we enrolled 10 patients in septic shock with an arterial pressure stabilized by NE. In addition to hemodynamic measurements, SvO2 and blood lactate level, we measured thenar muscle oxygen saturation (StO2) and muscle tissue hemoglobin index (THI) by a tissue spectrometer (InSpectraTM Model 650, Hutchinson Technology Inc, MN). Serial VOT (upper limb ischemia induced by a rapid pneumatic cuff inflation around the upper arm) were performed. We also recorded during the VOT: basal StO2, THI, the slope of the decrease in StO2 during the occlusion (desc slope; %/min) and the slope of the increase in StO2 following the ischemic period (asc slope; %/s). Muscle oxygen consumption (nirVO2I) was calculated as the product of the inverse of the slope value by the mean of THI over the first minute of arterial occlusion and is expressed in arbitrary units (U) (Skarda Shock 2007). All these data were obtained at 5 different times: baseline 1 and 2 with MAP of 65 mmHg, then at 75 mmHg and 85 mmHg of MAP by increasing the NE doses and finally to baseline 3. We report here data corresponding to the mean and SD of baseline 1 and 2 versus MAP 85 mmHg analyzed by repeated measures analysis of variance (at 5% level) with Bonferroni adjustment to account for multiple comparisons.
Results: Increasing NE dose induced an increase in cardiac output (from 6.08 ± 1.20 to 6.81 ± 1.62 L/min, p<0.05) without any changes in heart rate and an increase of SvO2 (from 70.9 ± 3.2 to 77.7 ± 5.8%, p<0.05). Lactate level decreased from 2.6 ± 1.5 to 2.3 ± 1.4 mEq/l (p<0.05). Neither basal StO2 nor THI changed, whereas the asc slope increased from 108 ± 50 to 172 ± 61%/min (p<0.05). This improvement in vascular reactivity did not significantly influence nirVO2I (from 138.3 ± 39.8 to 166.8 ± 70.7 U, p = 0.25).
Conclusion: Increasing mean arterial pressure by norepinephrine in patients with septic shock can improve microvascular reactivity; this observation was associated with a decrease in blood lactate concentration.