Dependence of shunt on cardiac output in unilobar oleic acid edema : distribution of ventilation and perfusion

In acute respiratory failure, increased cardiac output (Qt) increases shunt (Qs/Qt). We have tested if this is caused by: 1) a redistribution of blood flow towards edematous regions, or 2) a decrease of regional ventilation in the edematous region. Oleic acid edema was induced in the left lower lobe...

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Bibliographic Details
Published in:Intensive care medicine 1993-04, Vol.19 (4), p.185-190
Main Authors: FREDEN, F, CIGARINI, I, MANNTING, F, HAGBERG, Å, LEMAIRE, F, HEDENSTIERNA, G
Format: Article
Language:English
Subjects:
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Biological and medical sciences
Cardiac Output - drug effects
Cardiac Output - physiology
Emergency and intensive respiratory care
Intensive care medicine
Lung - blood supply
Medical sciences
Oleic Acid
Oleic Acids
Pulmonary Edema - chemically induced
Pulmonary Edema - physiopathology
Pulmonary Gas Exchange - drug effects
Pulmonary Gas Exchange - physiology
Regional Blood Flow - drug effects
Regional Blood Flow - physiology
Swine
Ventilation-Perfusion Ratio - drug effects
Ventilation-Perfusion Ratio - physiology
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Summary:In acute respiratory failure, increased cardiac output (Qt) increases shunt (Qs/Qt). We have tested if this is caused by: 1) a redistribution of blood flow towards edematous regions, or 2) a decrease of regional ventilation in the edematous region. Oleic acid edema was induced in the left lower lobe (LLL) of 11 pigs. Qt was varied with bleeding and infusion of blood and dextran. Blood flow to the LLL was measured at low and high Qt with electromagnetic low probes in 6 animals and with a gamma camera in 5. In the gamma camera pigs regional ventilation was also measured. Qt was increased by 45% (electromagnetic flow probes) and 73% (gamma camera). Qs/Qt increased from 24.9-31.3% (p < 0.05) and from 17.6-28.8% (p < 0.001) respectively. No change in fractional perfusion of LLL could be seen, neither with flow probes nor with gamma camera. A decrease in ventilation of LLL, 2.6%, was observed when Qt was increased (p < 0.05). Theoretically a small decrease in ventilation can explain the increase in shunt, if regions with low ventilation/perfusion (VA/Q) ratio are transformed to shunt. This is, however, unlikely since earlier studies have shown that blood flow is distributed either to regions with normal VA/Q ratio or to shunt regions. We conclude that the cardiac output dependent shunt is not caused by redistribution of blood flow between lobes or by decreased ventilation in the edematous region. We cannot exclude that blood flow is redistributed within the edematous lobe.
ISSN:0342-4642
1432-1238
DOI:10.1007/BF01694768