From this article:
This has been my policy for a long time, albeit not for the reasons cited in this article.
I keep a higher etCO2 to maintain the drive to breath during the operation. That is my twitch monitor. If the etCO2 is high enough for the patient to breath there will be a “curare cleft” in the etCO2 waveform, which indications that the relaxant is waning. The administration of more relaxant may be warranted at this time depending on the remaining duration of the operation.
I now have a published article to indirectly support my beliefs, even though my practice is still NOT evidence proven:
Intraoperative end-tidal CO2: When asked about the relationship between end-tidal CO2 and arterial CO2, most anesthesia providers would reply that arterial
values are approximately 3 to 5 mm Hg higher than end-tidal values. This relationship between end-tidal and arterial carbon dioxide, although highly variable and dependent on multiple physiologic factors, is the basis for the common tradition of keeping the endtidal CO2 in the range of 32 to 37 mm Hg intraoperatively, corresponding to an approximate arterial level of 37 to 42 mm Hg. What is not realized, and what Hill and Joshi, among others, have emphasized, is that when the level of arterial CO2 is within the control of the anesthesia provider, there are often significant advantages to maintaining this level above the usual physiologic limits. Yet, many clinicians do not avail themselves of these numerous advantages. Although far from an exhaustive list, elevated arterial CO2 levels improve tissue oxygenation, increase cerebral, coronary and tissue bloodflow, and help to maintain arterial blood pressure by both sympathetic stimulation and less reduction in venous return. The work of Akca et al. summarizes many of these benefits and Hill and Joshi suggest an end-tidal CO2 of 40 to 45 or higher should come to be the standard of care intraoperatively. Thus, the best practice of anesthesia in 2011 might very well include maintaining higher end-tidal CO2 levels. The resulting modest level of respiratory acidosis shifts the oxygen hemoglobin dissociation curve to the right, thus unloading more oxygen to tissues and increasing the effectiveness of oxidative killing by neutrophils; acidosis improves hemodynamics as a result of the mild sympathetic stimulation and reduced interference with venous return; and improves arteriolar bloodflow. The detrimental effects of mild hypercarbia are significantly outweighed by the numerous positive benefits. Distressing clinical reports of cerebral ischemia during surgery in the sitting position, due to hypotension and a reduced effective cerebral perfusion pressure below that measured by a traditional arm blood pressure cuff, are often accompanied by end-tidal CO2 values in the low 30s. In Pohl and Cullen’s report, the end-tidal CO2 varied from the high 20s to the low 30s mm Hg. New Advanced Cardiac Life Support guidelines also stress the detrimental influence of hypocarbia on global cerebral perfusion. In conclusion, from a pathophysiological standpoint, it would appear prudent when possible to maintain a mildly elevated end-tidal CO2 in any case involving controlled hypotension.
Caveat: There are clearly acute and chronic medical conditions where elevated end-tidal CO2 values are inappropriate, such as elevated intracerebral pressure, hyperkalemia, and cor pulmonale. We recommend higher CO2 levels in routine clinical practice.