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A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care
Minerva Anestesiologica 2013 June;79(6):617-25
Improved ventilation-perfusion matching by abdominal insufflation (pneumoperitoneum) with CO2 but not with air
Strang C. M. 1, 2, Ebmeyer U. 2, Maripuu E. 3, Hachenberg T. 2, Hedenstierna G. 1 ✉
1 Department of Medical Sciences, Clinical Physiology, Uppsala University, Sweden;
2 Department of Anesthesiology and Intensive Care Medicine, Otto-von-Guericke-University Magdeburg, Germany;
3 Department of Medical Physics, University hospital, Uppsala, Sweden
Background: Pneumoperitoneum (PP) by CO2-insufflation causes atelectasis however with maintained or even improved oxygenation. We studied the effect of abdominal insufflation by carbon dioxide (CO2) and air on gas exchange during PP.
Methods: Twenty-seven anesthetized pigs were studied during PP with insufflations to 12 mmHg by either 1/CO2, 2/ air or 3/CO2 during intravenous nitroprusside infusion (SNP) (N.=9 in each group). In 3 pigs in each group, gamma camera technique (SPECT) was used to study ventilation and perfusion distributions, in another 6 pigs an inert-gas technique (MIGET) was used for assessing ventilation-perfusion matching (VA/Q). Measurements were made during anesthesia before and after 60 minutes of PP.
Results: CO2-PP caused a shift of blood flow away from dependent, non-ventilated (atelectatic) to ventilated regions. Air-PP caused smaller, and SNP-PP even less shift of lung blood flow. Shunt decreased during CO2-PP (6±1% compared to baseline 9±2%, P<0.05), did not change during Air-PP (10±2%) and increased during SNP-PP (16±2%, P<0.05). PaO2 increased from baseline 35±2 to 41±3 kPa during CO2-PP and decreased to 32±3 kPa during Air-PP and to 27±3 kPa during SNP-PP (P<0.05 for all three comparisons). PaCO2 increased during CO2- and SNP-PP.
Conclusion: CO2-PP enhanced the shift of blood flow towards better ventilated areas of the lung compared to Air-PP and SNP blunted the effects seen with CO2-PP. SNP may thus have blunted and CO2 potentiated vasoconstriction, by hypoxic pulmonary vasoconstriction or another mechanism.