Abstract
In Response: Tatara states that the continuous determination of PiCO2 is unnecessary and takes as basis for his opinion a review article by Fiddian-Green [1]. In this review, Fiddian-Green describes the results of the important work on the physiology of intestinal ischemia by Haglund and colleagues [2] that observed: "the progression to transmural infarction occurs over a period of many hours or even days in patients who are critically ill." However, Tatara's assumption that an increase in PiCO2 occurs parallel to the development of irreversible histologic damage that develops over hours to days is inappropriate. PiCO2 changes can actually happen long before the occurrence of irreversible tissue damage. In recent experimental work (unpublished data), we saw that the reduction of mesenteric blood flow by 60% causes a sudden and rapid increase to 300%-400% of baseline of the continuously measured PiCO2. This PiCO2 increase was completely reversible when inadequate perfusion was restored in due time and did not result in permanent tissue damage. However, after three hours of reduced mesenteric perfusion, the PiCO2 remained increased, indicating a permanent tissue injury. These results are in agreement with the reports of other authors, which demonstrate in animal models that changes in PiCO2 and the calculated pHi occur immediately with the onset of mesenteric ischemia and not only after the occurrence of irreversible intestinal ischemic injury [3-5]. Therefore, it is this early increase in PiCO2 that allows the detection of inadequate tissue perfusion and, thus, the early therapy before irreversible damage. In conclusion, we cannot understand the denial of a new method for the continuous determination of PiCO2 before its clinical value has been tested and sufficient experience and data are available. Apart from the advantage of a continuous determination, there are several other reasons underlining the importance of the fiberoptic CO2 sensor. The conventional intermittent method via the nasogastric tonometer is a indirect method that has been associated with a number of methodological errors. Each blood gas analyzer has its own instrumental bias when measuring CO2 in aqueous solutions. Therefore, every user has to establish individual correction factors according to the blood gas analyzer, the tonometric solution, and the equilibration time used. Only this will allow the comparison of collected data. A phosphate-buffered solution will, indeed, attenuate the enormous errors; however, it will not totally abolish the instrumental bias [6]. Furthermore, the equilibration of CO2 in the tonometric balloon is very slow and takes at least 60 minutes. In the clinical routine, PiCO2 and pHi will not be determined every 60-90 minutes. As a result, the measured PiCO2 value can only be regarded as the average of a certain time period that does not pick up short time variations. Unintendent PiCO2 alterations, due to hypoventilation or administration of bicarbonate, for example, will not be observed and, thus, not corrected for. Finally, the conventional tonometry bears other causes for error, such as difficult handling with airfree instillation and aspiration of the tonometric fluid, the storage and processing of samples, and the calculation of PiCO2 data. As the continuous PiCO2 measurement determines the PiCO2 directly in the gastrointestinal lumen, these errors are eliminated, and the collected data can be directly compared with those of other patients in different critical care units. Only this will allow the introduction of normal PiCO2 range for the first time. The gastrointestinal tract is thought to play a major role in the development of sepsis and multiorgan failure. Multiorgan failure is the most common cause of death in critical care patients. Its therapy is considered to be the foremost challenge of intensive care of this century's last decade. The ability to detect gastrointestinal malperfusion in its early stages by continuous PiCO2 measurement will allow appropriate therapy and offer an interesting tool to eventually reduce mortality from multiorgan failure. This would clearly outweigh the costs of this new device. Gisbert Knichwitz, MD Thomas Brussel, MD Thomas Mollhoff, MD, MSc Klinik und Poliklinik fur Anasthesiologie und operative Intensivmedizin; Westfalischen Wilhelms-Universitat; Munster, Germany
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