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- Magnusson, Lennart, et al.
(författare)
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Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass : An experimental study
- 1997
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Ingår i: Anesthesiology. - 0003-3022 .- 1528-1175. ; 87:5, s. 1153-1163
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Respiratory failure after cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors tested the hypothesis that atelectasis is an important factor responsible for the increase in intrapulmonary shunt after CPB. METHODS: Six pigs received standard CPB (bypass group). Six other pigs had the same surgery but without CPB (sternotomy group). Another six pigs were anesthetized for the same duration but without any surgery (control group). The ventilation-perfusion distribution was measured with the inert gases technique, extravascular lung water was quantified by the double-indicator distribution technique, and atelectasis was analyzed by computed tomography. RESULTS: Intrapulmonary shunt increased markedly after bypass but was unchanged over time in the control group (17.9 +/- 6.2% vs. 3.5 +/- 1.2%; P < 0.0001). Shunt also increased in the sternotomy group (10 +/- 2.6%; P < 0.01 compared with baseline) but was significantly lower than in the bypass group (P < 0.01). Extravascular lung water was not significantly altered in any group. The pigs in the bypass group showed extensive atelectasis (32.3 +/- 28.7%), which was significantly larger than in the two other groups. The pigs in the sternotomy group showed less atelectasis (4.1 +/- 1.9%) but still more (P < 0.05) than the controls (1.1 +/- 1.6%). There was good correlation between shunt and atelectasis when all data were pooled (R2 = 0.67; P < 0.0001). CONCLUSIONS: Atelectasis is produced to a much larger extent after CPB than after anesthesia alone or with sternotomy and it explains most of the marked post-CPB increase in shunt and hypoxemia. Surgery per se contributes to a lesser extent to postoperative atelectasis and gas exchange impairment.
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- Magnusson, Lennart, et al.
(författare)
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Effect of CPAP during cardiopulmonary bypass on postoperative lung function : An experimental study
- 1998
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Ingår i: Acta Anaesthesiologica Scandinavica. - 0001-5172 .- 1399-6576. ; 42:10, s. 1133-1138
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Respiratory failure secondary to cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. We tested the hypothesis that post-CPB lung function impairment can be prevented by continuous positive airway pressure (CPAP) applied during the CPB. METHODS: In 6 pigs, CPAP with 5 cmH2O pressure was applied during CPB. Six other pigs served as control, i.e. the lungs were open to the atmosphere during CPB. After median sternotomy, the right atrial appendage as well as the ascending aorta were cannulated. The total CPB duration was 90 min with 45 min cardioplegic arrest. Ventilation-perfusion distribution was measured with the multiple inert gas elimination technique and atelectasis by CT-scanning. RESULTS: Large atelectasis appeared after CPB, corresponding to 14.5% +/- 5.5 (percent of the total lung area) in the CPAP group and 18.7% +/- 5.2 in the controls (P = 0.20). Intrapulmonary shunt increased and PaO2 decreased after the CPB in both groups. CONCLUSIONS: We conclude that in this pig model post-CPB atelectasis is not effectively prevented by CPAP applied during CPB.
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- Magnusson, Lennart, et al.
(författare)
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Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass : an experimental study
- 1998
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Ingår i: Anesthesiology. - 0003-3022 .- 1528-1175. ; 88:1, s. 134-142
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Respiratory failure secondary to cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors previously found that the increase in intrapulmonary shunt was well correlated with the amount of atelectasis. They tested the hypothesis that post-CPB atelectasis can be prevented by a vital capacity maneuver (VCM) performed before termination of the bypass. METHODS: Eighteen pigs received standard hypothermic CPB (no ventilation during bypass). The VCM was performed in two groups and consisted of inflating the lungs during 15 s to 40 cmH2O at the end of the bypass. In one group, the inspired oxygen fraction (FIO2) was then increased to 1.0. In the second group, the FIO2 was left at 0.4. In the third group, no VCM was performed (control group). Ventilation-perfusion distribution was measured with the inert gas technique and atelectasis by computed tomographic scanning. RESULTS: Intrapulmonary shunt increased after bypass in the control group (from 4.9 +/- 4% to 20.8 +/- 11.7%; P < 0.05) and was also increased in the vital capacity group ventilated with 100% oxygen (from 2.2 +/- 1.3% to 6.9 +/- 2.9%; P < 0.01) but was unaffected in the vital capacity group ventilated with 40% oxygen. The control pigs showed extensive atelectasis (21.3 +/- 15.8% of total lung area), which was significantly larger (P < 0.01) than the proportion of atelectasis found in the two vital capacity groups (5.7 +/- 5.7% for the vital capacity group ventilated with 100% oxygen and 2.3 +/- 2.1% for the vital capacity group ventilated with 40% oxygen. CONCLUSION: In this pig model, postcardiopulmonary bypass atelectasis was effectively prevented by a VCM.
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