Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass
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Updated: Aug 8, 2026

Assessment of Pulmonary Capillary Blood Volume, Membrane Diffusing Capacity, and Intrapulmonary Arteriovenous Anastomoses During Exercise
Published on: February 20, 2017
P D Macnaughton1, S Braude, D N Hunter
1Department of Clinical Physiology, Anaesthesia, and Intensive Care, Royal Brompton National Heart and Lung Hospital, London, UK.
Objective:
To assess the possibility that changes in lung function following cardiopulmonary bypass are associated with increased pulmonary capillary permeability.
Design:
A prospective, descriptive study.
Setting:
Adult cardiothoracic ICU in a post-graduate teaching hospital.
Patients:
Ten sequential patients undergoing cardiac surgery requiring cardiopulmonary bypass.
Measurements:
Arterial blood gas tensions, helium dilution end-expiratory lung volume, and carbon monoxide transfer were measured by a rebreathing technique preoperatively and 2 hrs postoperatively. Lung extravascular protein accumulation index was measured by a double-isotope technique 2 hrs postoperatively and in a group of normal controls.
Results:
Mean +/- SEM alveolar-arterial PO2 gradient increased from 77 +/- 14 torr (10.3 +/- 1.8 kPa) to 138 +/- 24 torr (18.5 +/- 3.2 kPa) (p less than .01). Functional residual capacity decreased by 20.2 +/- 5.6% (p less than .01). Carbon monoxide transfer decreased by 26.7 +/- 5.3% (p less than .01) for the lung as a whole and by 17.9 +/- 3.2% (p less than .01) per liter of accessible gas volume. Protein accumulation index ranged from 0.03 to 3.2 x 10(-3) (median 0.6) postoperatively (median for normal subjects 0.4; p less than .05), although only one patient had a value indicative of clinically important endothelial injury.
Conclusions:
Cardiac surgery involving cardiopulmonary bypass results in a deterioration in lung function characterized by a loss of lung volume, a reduction in carbon monoxide transfer, and an increase in the alveolar-arterial PO2 gradient. These changes do not appear to be mediated by an increase in pulmonary endothelial permeability.
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