OPTIMAL VALUES FOR OXYGEN-TRANSPORT DURING HYPOTHERMIA IN SEPSIS AND ARDS

Mild hypothermia (33 degrees C to 35.5 degrees C) is reported to impro ve oxygenation and survival in patients with lung failure (1). Althoug h hypermetabolism may account for about 50% of the ventilatory demand in ARDS patients, the concept of reducing oxygen consumption (Voverdto O(2)) by lowering metabolic rate, has only recently gained attention ( 2). Our study was aimed to test whether mild hypothermia established b y continuous veno-venous haemofiltration (CVVHF), could optimize value s for oxygen kinetics in ARDS patients. Overall, we recruited 27 patie nts with ARDS and sepsis. Prior initiation of CVVHF patients had to me et the following criteria: a) Murray score >2.5, and hypoxaemia with P aO2/FIO2 <200, b) hyperthermia of >38 degrees C, c) cardiovascular ins tability requiring inotropic support. Evaluation bf cardio-respiratory data was performed within four different phases (I = before, II + III during and IV = after CVVHF) every 6 hours. Core temperature as deriv ed from the thermistor of pulmonary artery catherer was aimed to be be tween 35.0 degrees C anti 36.5 degrees C. Optimal values for oxygen de livery (DoverdotO(2)) (>550 mL/min/m(2)) and VoverdotO(2) (>160 mL/min /m(2)) were defined according to Shoemaker and achieved by fluid loadi ng, transfusion and inotropic support(3). Septic shock occurred in 10 of 14 nonsurvivors (nons) and 2 of 13 survivors (surv). Mean values fo r DoverdotO(2) and VoverdotO(2) were calculated at different body temp erature ranges. While at 37 degrees C DoverdotO(2) was identical betwe en surv and nons, (663+/-128 versus 666+/-127 mean+/-SD) moderate hypo thermia led to a small decrease of DoverdotO(2) in surv and a signific ant decrease in nons (632+/-134 versus 605+/-128 mL/min/m(2)) at 35 de grees C. Concerning VoverdotO(2) during hypothermia, there was a signi ficant drop in nonsurvivors while in survivors the decrease was less p ronounced. We could demonstrate a decrease in DoverdotO(2) and Voverdo tO(2) during mild hypothermia during CVVHF. However, decreases in nons urvivors were more pronounced than in survivors. These results suggest that the inability to achieve optimal values for DoverdotO(2) and Vov erdotO(2) during mild hypothermia induced by CVVHF could serve as a pr ognostic sign for fatal outcome. Although oxygen consumption is decrea sed during hypothermia, hypoxaemia may result due to alterations of th e oxygen transport on a cellular basis. The relationship between oxyge n transport and temperature during CVVHF therefore deserves further st udies.