ATELECTASIS IS A MAJOR CAUSE OF HYPOXEMIA AND SHUNT AFTER CARDIOPULMONARY BYPASS - AN EXPERIMENTAL-STUDY

Citation
L. Magnusson et al., ATELECTASIS IS A MAJOR CAUSE OF HYPOXEMIA AND SHUNT AFTER CARDIOPULMONARY BYPASS - AN EXPERIMENTAL-STUDY, Anesthesiology, 87(5), 1997, pp. 1153-1163
Citations number
42
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
87
Issue
5
Year of publication
1997
Pages
1153 - 1163
Database
ISI
SICI code
0003-3022(1997)87:5<1153:AIAMCO>2.0.ZU;2-9
Abstract
Background: Respiratory failure after cardiopulmonary bypass (CPB) rem ains a major complication after cardiac surgery. The authors tested th e hypothesis that atelectasis is an important factor responsible for t he increase in intrapulmonary shunt after CPB. Methods: Six pigs recei ved standard CPB (bypass group). Six other pigs had the same surgery b ut without CPB (sternotomy group). Another six pigs were anesthetized for the same duration but without any surgery (control group). The ven tilation-perfusion distribution was measured with the inert gases tech nique, extravascular lung water was quantified by the double-indicator distribution technique, and atelectasis was analyzed by computed tomo graphy, 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 l ower 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 (R-2 = 0.67; P < 0.0001). C onclusions: 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 c ontributes to a lesser extent to postoperative atelectasis and gas exc hange impairment.