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

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...

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Published inCanadian 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
LanguageEnglish
Published Toronto, ON Canadian Anesthesiologists' Society 01.07.1996
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Abstract 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.
AbstractList 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.
PURPOSETo test the hypothesis that a physiological compensatory mechanism maintains respiratory gas exchange during normovolaemic haemodilution.METHODSPulmonary 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%.RESULTSAfter 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.CONCLUSIONModerate 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.
Author POUPARD, P
ELEDJAM, J.-J
TARGHETTA, R
BALMES, P
LE MERRE, C
DAUZAT, M
FABRE, C
BOUGES, S
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Induced hemodilution
Lung function
Compensation
Gas exchange
Normal
Normovolemia
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Snippet To test the hypothesis that a physiological compensatory mechanism maintains respiratory gas exchange during normovolaemic haemodilution. Pulmonary gas...
PURPOSETo test the hypothesis that a physiological compensatory mechanism maintains respiratory gas exchange during normovolaemic...
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StartPage 672
SubjectTerms 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
Title Pulmonary gas exchange capacity is reduced during normovolaemic haemodilution in healthy human subjects
URI https://www.ncbi.nlm.nih.gov/pubmed/8807171
https://search.proquest.com/docview/78325817
Volume 43
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