Introduction: Lung dysfunction following cardiac surgery is currently viewed as the consequence of atelectasis and lung injury. While the mechanism of atelectasis has been largely detailed, the pathogenesis of lung injury after cardiopulmonary bypass is still unclear. Based upon clinical and experimental studies, we hypothesized that lungs could be injured through a mechanical phenomenon. Methods: We recorded pulmonary compliance at six key moments of a heart operation in 62 adult patients undergoing elective cardiac surgery. We focused on the period lasting from anesthetic induction to aorta unclamping. We calculated the variation of static and dynamic pulmonary compliance caused by thorax opening; ΔCstat1 and ΔCdyn1 and that caused by cardiopulmonary bypass, ΔCstat2 and ΔCdyn2. Blood gases were performed under standardized ventilation after anesthetic induction and after surgical closure. The PaO2/FiO2 ratio was calculated. ∆PaO2/FiO2 was the criterion for lung dysfunction. We compared ΔCstat1 and ΔCdyn1 with both ∆PaO2/FiO2 and, respectively, ΔCstat2 and ΔCdyn2. Results: Static and dynamic compliance increased with the opening of the thorax and decreased with the start of cardiopulmonary bypass. The PaO2/FiO2 ratio diminished after surgery. ΔCstat1 and ΔCdyn1 were negatively correlated with both ∆PaO2/FiO2 (r=-0.42; p<0.001 and r=-0.44; p<0.001) and, respectively, with ΔCstat2 and ΔCdyn2 (r=-0.59; p<0.001 and r=-0.53; p<0.001). Conclusions: Increased pulmonary compliance induced by the opening of the thorax is correlated with worsened intrapulmonary shunt after cardiopulmonary bypass. A mechanical phenomenon could be partly responsible for post-operative hypoxemia.
