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A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care
ORIGINAL ARTICLES ANESTHESIOLOGY
Minerva Anestesiologica 2001 September;67(9):629-36
Alterations in carbon dioxide release during abdominal aortic clamping for aneurysmal or occlusive repair
Vretzakis G., Papadopoulos G. *, Koutsias S. **, Papaziogas B. **, Antoniadou E. ***, Pitoulias G. **, Papadimitriou D. **
From the Department of Anaesthesiology “G. Gennimatas” Hospital, Thessaloniki, Greece
*Anesthesiology Clinic University Hospital of Ioannina, Greece
**Department of Vascular Surgery 2nd Surgical Clinic of the Aristoteles University of Thessaloniki, Greece
***Intensive Care Unit “G. Gennimatas” Hospital, Thessaloniki, Greece
Background. Application and removal of an infrarenal aortic clamp is associated with changes in oxygen consumption, especially when collateral perfusion is limited. Carbon dioxide production during abdominal aortic clamping is expected also to change. The aim of this study was to evaluate the alterations of CO2 release during abdominal aortic surgery.
Methods. Design: prospective study. Setting: University Hospital, Greece. Patients: 17 patients undergoing abdominal aortic aneurismal (AAA) repair and 8 patients undergoing repair of aortoiliac occlusive disease. Interven-tion: intraoperative record or calculation of PaCO2, PetCO2, PECO2, VD, VDalv, and VCO2. Patients with aneurysms were randomly divided to have constant ventilation (group AA) or modified ventilation to preserve normocapnia (group AB) during clamping. Ventilation was kept constant in the occlusive patients group (group OD).
Results. Patients with AAA showed a significant decrease of VCO2 during clamping and an elevation after unclamping in both groups (AA and AB), with no difference of statistical importance between them. During clamping, PetCO2/ PaCO2 ratio was decreased and VDalv was increased especially in group AA, while unclamping produced the opposite effect. Occlusive patients showed insignificant alterations.
Conclusions. Our results suggest that, the calculated alveolar dead space is only an indicator of the true V/Q in patients with AAA, because it is strongly dependent on the CO2 load to the lungs, which is markedly altered in the same period. The modification of ventilation during clamping based only on PetCO2 and not on arterial sampling, could possibly lead to hypercarbia in these patients.