Only a few studies have systematically investigated temperature changes during CRRT and evaluated their relationship to hemodynamics in ICU patients [14
]. In one of these studies, marked hypothermia induced by CRRT led in some patients to shivering, profound peripheral vasoconstriction, and immune system dysfunction [14
]. Yagi et al. reported that patients experienced temperature <35.5°C in 31 of the 67 of the CVVH sessions without deleterious effect of hypothermia [16
]. In this latter study, there was no heating device within the circuit. In our study, the tympanic temperature rapidly decreased in both groups after the start of hemofiltration. Only two patients had temperature <35.5°C and were excluded from the study before randomization, as specified in the protocol, and no patient had temperature <35.5°C during the study period of the protocol. There were no tympanic differences for either temperature setting in the heating device (36°C or 38°C). However, because the heating device was placed on the infusate line, persisting energy transfer on the remaining part of the tubing may have attenuated the effect of the warming. We did not measure energy transfer in the circuit directly, but our in vitro
experiment demonstrated a potential difference of 0.7°C to 0.8°C close to the venous return site of the circuit. This decrease was probably too low to induce significant differences in tympanic temperature of the patients. In the study byRokyta et al. despite induced high variations in temperature setting, only moderate change in cutaneous temp (0.9°C) and limited CT (1.3°C) were observed [17
In chronic renal failure patients, several studies reported a significant reduction in the frequency of hypotensive episodes during hemofiltration [11
], but in ICU patients the impact of temperature variation induced by CVVH on hemodynamic parameters is not established. Matamis et al. reported an increase of MAP and SVR only in patients who became hypothermic during hemofiltration [15
]. Conversely, in one retrospective study, MAP was similar in hypothermic and nonhypothermic patients [16
]. Finally, in a study involving nine patients submitted to a dramatic cooling of the circuit from 39°C to 20°C, there was a significant increase of vascular resistance and mean arterial pressure, whereas heart rate, cardiac output, systemic oxygen delivery, and consumption decreased [17
]. However, in this study, hypothermia lasted only 2 hours, and potential deleterious effect could be observed.
Our study is the first prospective, controlled study to show a significant increase of SAP and MAP in a group of patients treated with CVVH set at a low temperature (36°C) for 6 h after a baseline period of 2 h at 38°C. This increase was associated with a significant decrease in catecholamine infusion dosage, indicating improvement of hemodynamic status. The suspected mechanisms for cardiovascular tolerance during cold HD are a greater catecholamine release, an increase in vascular peripheral resistances, and in venous tone [18
]. In our practice, noninvasive investigation are privileged to manage hemodynamic instability and invasive monitoring was not systematically performed in our patients, thus the increase of vascular resistances during the 36°C period could not be demonstrated. Interestingly and contrasting with other studies, improvement of hemodynamic condition was not associated with differences in core temperature. This is in accordance with a study performed in chronic patients, showing that postdilution hemodiafiltration with a 2.5 l.h-1
volume exchange was associated with a better blood pressure stability compared with hemodiafiltration with low-volume exchange of dialysis without cooling, whereas CT was not decreased [4
]. This was explained by the increased loss of extracorporeal energy, which may prevent cutaneous vasodilation [11
There was no significant hemodynamic difference during the second period of the crossover experiment. On the one hand, maintenance of elevated SAP and MAP as well as reduced catecholamine infusion dosage suggest that this short period of hypothermia induces long-term benefits for the patient without the need for prolonged hypothermia and associated risks. On the other hand, the absence of hemodynamic difference during the second period of the crossover experiment in group A (lowered to 36°C at H6) suggests that the beneficial hemodynamic effects of the 36°C compared with the 38°C temperature setting is not straightforward. Timing the hypothermic period early in the treatment seems to be beneficial compared with a later hypothermic period. However, specific effect of temperature variation during a prolonged observation period may be blunted by many factors that may interfere with the hemodynamic status of a critically ill patient. Additionally, the reduced number of patients of the second period due to hemofilter dysfunction has probably limited the statistical power of the study.
Furthermore, the beneficial effect of cooling on the life span of the extracorporeal circuit has been suggested [19
]. In our series, the relatively short duration of the temperature variation period and the limited number of patients did not allow evaluation of the impact of modest hypothermic temperature on the potential reduction in extracorporeal clotting and we did not evaluate the consequences of the two regimen of temperature on blood coagulation tests.
Our study has several limitations: 1) tympanic temperature measure may not precisely indicate CT, and the absence of body temperature difference might be related to the lack of accuracy of the technique [20
]. However, there was no intraindividual variation of temperature for the duration of the study; 2) the duration of the study periods may have been too short for the evaluation of the hemodynamic consequences of these two setting regimens; 3) better temperature setting for the heating device (e.g., 39°C vs. 36°C) might have been more efficient to evidence hemodynamic differences. However, we chose these levels to be comparable with the studies performed during IHD, even though the thermal energy involved mechanisms are different, as we indicated; 4)finally, only a limited number of patients were enrolled in this study. However, this number was similar or higher than in most of the studies performed on the effect of temperature variation in ICU patients undergoing CRRT.
In conclusion, our study suggests that warming the infusate over 36°C has no impact on body temperature and may not be indicated in critically ill patients undergoing CVVH to limit heat loss. We show that setting the fluid temperature at 36°C in CVVH for a short period of time at the beginning of the treatment increased mean arterial pressure while allowing for a decrease in catecholamine infusion dosage. We believe this pilot study warrants an investigation involving a larger number of patients to confirm these findings.