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BJA Advance Access published online on May 4, 2006
British Journal of Anaesthesia, doi:10.1093/bja/ael093
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Accepted March 15, 2006

Clinical Investigation

Tissue oxygenation response to mild hypercapnia during cardiopulmonary bypass with constant pump output

O. Akça 1 *, D. I. Sessler 2, D. Delong 3, R. Keijner 4, B. Ganzel 5, and A. G. Doufas 1

1 Outcomes Research Institute, University of Louisville, Louisville, KY, USA; Department of Anesthesiology and Perioperative Medicine, Neuroscience Intensive Care Unit, University of Louisville, Louisville, KY, USA
2 Outcomes Research Institute, University of Louisville, Louisville, KY, USA; Department of Outcomes Research, Cleveland Clinic Foundation, Cleveland, OH, USA
3 Outcomes Research Institute, University of Louisville, Louisville, KY, USA
4 Cardiothoracic and Vascular Surgery Team, Jewish Hospital, Louisville, KY, USA
5 Department of Surgery, Division of Cardiothoracic and Vascular Surgery, University of Louisville, Louisville, KY, USA

* To whom correspondence should be addressed.
O. Akça, E-mail: ozan.akca{at}louisville.edu


  Abstract

Background. Tissue oxygenation is the primary determinant of wound infection risk. Mild hypercapnia markedly improves cutaneous, subcutaneous (s.c.), and muscular tissue oxygenation in volunteers and patients. However, relative contributions of increased cardiac output and peripheral vasodilation to this response remains unknown. We thus tested the hypothesis that increased cardiac output is the dominant mechanism.

Methods. We recruited 10 ASA III patients, aged 40-65 yr, undergoing cardiopulmonary bypass for this crossover trial. After induction of anaesthesia, a Silastic tonometer was inserted s.c. in the upper arm. S.C. tissue oxygen tension was measured with both polarographic electrode and fluorescence-based systems. Oximeter probes were placed bilaterally on the forehead to monitor cerebral oxygenation. After initiation of cardiopulmonary bypass, in random order patients were exposed to two arterial CO2 partial pressures for 30 min each: 35 (normocapnia) or 50 mm Hg (hypercapnia). Bypass pump flow was kept constant throughout the measurement periods.

Results. Hypercapnia during bypass had essentially no effect on PaO2, mean arterial pressure, or tissue temperature. PaCO2 and pH differed significantly. S.C. tissue oxygenation was virtually identical during the two PaCO2 periods [139 (50-163) vs 145 (38-158), P=0.335] [median (range)]. In contrast, cerebral oxygen saturation (our positive control measurement) was significantly less during normocapnia [57 (28-67)%] than hypercapnia [64 (37-89)%, P=0.025].

Conclusions. Mild hypercapnia, which normally markedly increases tissue oxygenation, did not do so during cardiopulmonary bypass with fixed pump output. This suggests that hypercapnia normally increases tissue oxygenation by increasing cardiac output rather than direct dilation of peripheral vessels.

Keywords: carbon dioxide, hypercapnia; carbon dioxide, hypercarbia; complications, acidosis, respiratory; heart, cardiac output; oxygenation, tissue, cutaneous; oxygenation, tissue, subcutaneous.
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