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Department of Anesthesiology and Intensive Care Medicine, The Gilead University Teaching Hospital at Bethel, Bielefeld, Germany Institute of Physiology and Pathophysiology, Applied Clinical Physiology, Johannes Gutenberg University, Mainz, Germany
To the Editor:
Standl et al. (1) contribute new values for muscle oxygen tension (ptO2; mm Hg), which challenge their published scope of baseline ranges, i.e., 21–50 mm Hg (1–12). Inevitably, hyperoxia either increased (from 25 to 99 mm Hg (3,12) or decreased ptO2(from 43 to 26 mm Hg (11). Hemodilution by administration of crystalloids (hematocrit 25 %) either did not influence ptO2 (10,11) or caused an increase from 32 to 38 mm Hg (8,9). Using HES resulted in ptO2 increases [6% HES 40, hematocrit 32%: from 16 to 23 mm Hg (4); HES 200/0.5, hematocrit 20%: from 35 to 45 mm Hg (5)]. A ptO2decrease (hematocrit 10%) was related to the diluent [HES 200/0.5: from 29/34 to 14/18 mm Hg (6); crystalloid or crystalloid/HES 70/0.5: from 32 to 18 mm Hg (8,9)]. Presently (1), hemodilution (6% HES 130/0.4, 70/0.5, and 200/0.5) caused increases in the 50th percentile of ptO2 (from 44/49 to 56/60 mm Hg). Notably, the relative changes in the 10th percentile of ptO2 (6 % HES 130/0.4) are advocated for a "larger and faster ptO2 increase" (1), although clearly caused by the varying ptO2 baseline values [18 mm Hg with HES 130/0.4 vs 21.5 or 27 mm Hg (1)]. In addition, ptO2proved clinically irrelevant due to the lack of normal values.
References
Department of Anesthesiology, University Hospital Hamburg-Eppendorf, Hamburg, Germany
In Response:
In reaction to our recently published study where we could show a larger and faster increase in skeletal muscle tissue oxygen tension (tpO2) using HES 130/0.4 for normovolemic hemodilution in comparison with other HES solutions (1), Mertzlufft at al. criticize the variety of baseline muscular tpO2values in our studies. However, the examples that Mertzlufft et al. are citing are not comparable, since they are based on completely different studies, i.e., animal experiments (2–4), clinical trials in patients receiving anesthesia with different concentrations of inspired oxygen and different anesthetics (5,6) or mechanically ventilated patients in the ICU (7), and, finally, the present study in healthy spontaneously breathing volunteers (1).
It is indisputable that the median muscular tpO2shows a wide range between 25 and 45 mm Hg and that it is difficult to assess "normal" tpO2 values. We also agree that there are many influences on the muscular tpO2 (as well as on the tpO2in other organs), such as arterial oxygen partial pressure, hemoglobin concentration, blood rheology, perfusion pressure, blood flow, temperature of the tissue, and activity of the muscle.
However, it does not make any sense to compare muscular tpO2 values that were taken from different studies performed in different populations and under conditions of completely different clinical or experimental settings. While baseline tpO2 values from animal experiments (34 mm Hg) (2–4,8,9) were in accordance with clinical data (33 mm Hg) (10) under the condition of identical FiO2 of 0.3, it is not surprising that muscular median baseline tpO2 values were different in patients ventilated with higher FiO2 of 0.4 (60 mm Hg) (5), and in critically ill patients with sepsis (16 mm Hg) (7).
Moreover, different reactions of the muscular tpO2 on different treatment protocols, such as isovolemic hemodilution with different crystalloids, colloids (2,4,8), or even hemoglobin-based oxygen carriers (3,9), compared with changes in FiO2 (5) during artificial ventilation can be expected.
In contrast to the remarks of Mertzlufft et al., the hemodilution experiments are all highly reproducible and show increased tpO2 values during hemodilution until hematocrit 20% irrespective of the applied solution (Ringer or HES) but anemia-related decreasing tpO2 during profound hemodilution at Hct 5–15% (2,4,8,11).
Finally, as we pointed out in all our articles dealing with tissue oxygenation, it is not the single measurement that allows statements about the quality of tissue oxygenation, but the repetitive measurement at different sites of the muscle (as provided by the applied Eppendorf polarographic needle), which at different time points indicates a trend towards higher or lower tpO2 values. Thus, the trend of the muscular tpO2 reflects the impact of a specific treatment (fluids or inspiratory oxygen fraction) on the quality of tissue oxygenation.
We agree that the muscular tpO2 does not allow conclusions on the oxygenation of other organs. However, although less important than vital organs, the skeletal muscle mass represents a major part of mammal and human tissues, is easily accessible, and can be used for tpO2 measurements, even in patients, as shown by different authors (5–7,10–13). Moreover, we have shown in another animal experiment that muscular and hepatic tpO2 increased in parallel during isovolemic hemodilution (14).
Although Mertzlufft et al. might have the impression that the tpO2 values were different at baseline of our recently published study with HES (1), this is not based on any statistical significance. As we clearly pointed out in the article, there was no statistical difference among groups at any time point (including baseline) with regard to the muscular tpO2. The larger and faster increase in tpO2 was seen with HES 130 in comparison to baseline, and this was highly significant for all percentiles using the Friedman test, which is appropriate for the testing of multiple paired data within groups. In contrast, there was no significant increase in the HES 70 or HES 200 groups (except for the 90th percentile in group HES 200).
In conclusion we do not believe that—in the absence of a more specific parameter for the monitoring of changes in tissue oxygenation—repetitive or continuous measurement of muscular tpO2 is clinically irrelevant. In contrast, the technique of tissue oxygen tension measurement is used not only in experimental settings but also routinely in patients undergoing maxillofacial plastic surgery to supervise the quality of perfusion and oxygenation of muscular flaps (15).
References
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