Pulmonary gas exchange capacity is reduced during normovolaemic haemodilution in healthy human subjects

• Published in: Canadian journal of anesthesia Vol. 43; no. 7; pp. 672 - 677
• Main Authors: LE MERRE, C, DAUZAT, M, POUPARD, P, TARGHETTA, R, FABRE, C, BOUGES, S, ELEDJAM, J.-J, BALMES, P
• Format: Journal Article
• Language: English
• Published: Toronto, ON Canadian Anesthesiologists' Society 01.07.1996
• Subjects: Adult; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis; Female; Hemodilution; Humans; Male; Medical sciences; Middle Aged; Pulmonary Gas Exchange; Transfusions. Complications. Transfusion reactions. Cell and gene therapy; Human; Induced hemodilution; Lung function; Compensation; Gas exchange; Normal; Normovolemia
• ISSN: 0832-610X; 1496-8975
• DOI: 10.1007/BF03017949

To test the hypothesis that a physiological compensatory mechanism maintains respiratory gas exchange during normovolaemic haemodilution. Pulmonary gas exchange capacity was evaluated in seven healthy subjects by measuring the lung diffusion of carbon monoxide (DLCO). During the measurement, various breath-holding times, inspiratory volumes, and sitting or supine positions, were randomly selected in an attempt to alter pulmonary capillary perfusion. KCO was calculated as the percentage of theoretical values of the ratio of DLCO by alveolar volume and normalized by sex, age, and height. Normovolaemic haemodilution (NH) was performed by bleeding an average blood volume of 1 L with simultaneous Dextran 60 replacement to obtain an haematocrit below 35%. After NH, haemoblogin concentration [Hb] decreased from 14.94 +/- 0.96 to 12.5 +/- 0.98 g.dl-1 (P < 0.001). KCO decreased (P < 0.02) but remained closely correlated to [Hb] at every lung volume (P < 0.02). Breathholding time and body position had no effect. Moderate NH impairs pulmonary gas exchange capacity in awake, resting healthy subjects. There is no evidence of any compensatory mechanism since the KCO vs [Hb] relationship is unchanged.