Continuous ultrafiltration attenuates the pulmonary injury that follows open heart surgery with cardiopulmonary bypass

Abstract

Background Pulmonary injury after cardiac surgery is one of the complications of cardiopulmonary bypass. We evaluated the ultrafiltration technique in preventing and relieving the pulmonary injury that can follow open heart surgery with cardiopulmonary bypass (CPB). Methods Thirty patients with congenital heart defects were divided into two groups. In the control group conventional cardiopulmonary bypass was used without ultrafiltration. In the treated group, in addition to the same cardiopulmonary bypass procedure, balanced ultrafiltration plus modified ultrafiltration was used throughout cardiopulmonary bypass. Pulmonary function, hematocrit, serum albumin, and some inflammatory mediators were measured. Results Compared with measurements before anesthesia the pulmonary static compliance at 15 minutes and 6 hours post bypass had decreased by 27.8% and 34.0% in the control group versus 12.6% and 15.4% in the treated group, the airway resistance had increased by 38.0% and 45.2% in the control group versus 9.5% and 4.7% in the treated group, and the alveolar-arterial oxygen difference increased by 73.4% and 62.0% in the control group versus 52.1% and 35.9% in the treated group. Hemodilution from cardiopulmonary bypass caused the hematocrit and serum albumin to decrease by 35.8% and 32.8% in the control group versus 36.1% and 34.5% in the treated group at the termination of CPB. After 10 to 15 minutes modified ultrafiltration the hematocrit and serum albumin increased by 40.0% and 47.6%. At the termination of CPB the serum concentrations of interleukin-6, thromboxane B2, and endothelin-1 were increased by 160%, 265%, and 890% in the control group versus 103%, 208%, and 838% in the treated group compared with those before anesthesia. Conclusions The combined use of balanced ultrafiltration and modified ultrafiltration can effectively concentrate the blood, modify the increase of some harmful inflammatory mediators, attenuate the lung edema and inflammatory pulmonary injury, and mitigate the impairment of pulmonary function.