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March 1998

Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: an experimental study.


Magnusson L, Zemgulis V, Tenling A, Wernlund J, Tyden H, Thelin S, Hedenstierna G; Anesthesiology 1998; 88:134-42


[ see abstract below ]


Cardiopulmonary bypass (CPB) may have adverse effects on postoperative pulmonary function via two mechanisms: inflammatory lung injury, caused by contact activation of mediators by perfusion of blood through the extracorporeal circuit, and atelectasis, caused by allowing the lungs to collapse during CPB. It is not uncommon to observe an increase in intrapulmonary shunt (Qs/Qt) to 20-25% in the postoperative period. This may contribute to prolongation of postoperative ventilation time and length of ICU stay.

In a pig model, Magnusson et al1 demonstrated by means of computer tomography scans that atelectasis induced by lung collapse during CPB may occupy up to 35% of the total lung area, and that its extent correlates well with hypoxemia and intrapulmonary shunting.

Over the years, various maneuvers have been designed in an attempt to prevent or reverse atelectasis that occurs during CPB. These have included continuous positive airway pressure and maintenance of standard mechanical ventilation during CPB. Results have been conflicting: some studies have indicated improved lung function, some have indicated no change and some have even demonstrated a worsening of lung function with these maneuvers. Even when a benefit is seen, it may not be sustained for more than 5 hours into the postoperative period.

Rothen at al2,3 demonstrated that inflation of the lungs to vital capacity and a peak airway pressure of 40 cmH2O reversed practically all atelectasis in patients with healthy lungs. If the patient were subsequently oxygenated with 100% oxygen, however, atelectasis recurred within 5 min, presumably through rapid absorption of oxygen from alveoli, which would then collapse. However, breathing 40% oxygen prevented the reappearance of atelectasis by providing nitrogen as a supportive "strut" for the alveoli.

In the January 1998 issue of Anesthesiology, Magnusson et al present the results of a pig model study developed to test the hypothesis that a vital capacity maneuver (VCM), a single breath with a peak airway pressure of 40 cmH2O, sustained for 15 seconds at the end of cardiopulmonary bypass, would reverse atelectasis and that it would be sustained better by breathing 40% oxygen than 100% oxygen. Pigs were subjected to CPB for 90 minutes, with a 45 minute aortic cross-clamp time, and then randomized to three groups at the end of CPB. In the control group, no VCM was given. The other two groups received either a VCM followed by ventilation with 40% oxygen or 100% oxygen. One hour after CPB measurements of intrapulmonary shunt and a computed tomographic (CT) scan of the thorax were performed.

In the control group, intrapulmonary shunt increased from 4.9% at baseline to 20.8% after CPB. In the VCM with 40% oxygen group the shunt increased from 3.3 to 5.0% (no significant change) and in the VCM with 100% oxygen group the shunt increased from 2.2 to 6.9% (a significant increase from baseline, but significantly smaller than in the control group). The proportional area of atelectasis revealed by CT scan in the control pigs was 21.3%, one fifth of the entire cross-sectional lung area. In contrast, the proportional area of atelectasis in the VCM-40% oxygen pigs was only 2.3%, and in the VCM-100% oxygen pigs 5.7%.

Although these data must be confirmed in human subjects undergoing cardiac surgery, they suggest strongly that (a) atelectasis that occurs during CPB may be reversed on weaning from bypass by a sustained vital capacity insufflation and (b) expansion is best maintained by ventilating with an oxygen:air mixture. Use of 100% oxygen promotes absorption atelectasis and somewhat mitigates the benefit of the VCM. These findings may have useful application to our clinical practice.

1 Atelectasis is a major cause of hypoxemia and shunt after extra-corporeal circulation. An experimental study. Magnusson L, Zemgulis V, Wicky S et al.Anesthesiology 1997; 87:1153-63.

2 Re-expansion of atelectasis during general anesthesia: a computed tomography study. Rothen HU, Sporre B, Engberg , Wegenius G, Hedenstierna G; Br J Anaesth 1993;71:788-95.

3. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia: a computed tomography study. Rothen HU, Sporre B, Engberg G, Wegenius G, Hogman M, Hedenstierna G; Anesthesiology 1995; 82:832-42.


Return to the Current Literature Review Front Page , or read the abstract:

 


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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