Pulmonary oxygen consumption: a hypothesis to explain the increase in oxygen consumption of low birth weight infants with lung disease

Abstract.

Objective: We determined pulmonary oxygen consumption (VO_2lung) in low-birthweight infants with acute lung disease to help explain the greater whole-body oxygen consumption (VO_2wb) in these infants with than in those without lung disease. Methods and materials: Eleven infants (birth weight 1,076±364 g; gestational age 28±3 weeks) undergoing mechanical ventilation for respiratory distress syndrome were studied in their first week of life. We measured VO_2wb by indirect calorimetry and simultaneously determined systemic oxygen uptake (VO_2Fick) as the product of cardiac output (echocardiography) and the arterial–mixed venous oxygen content difference (cooximetry) assuming that VO_2wb-VO_2Fick accounts for VO_2lung. Right atrial blood samples were used to determine mixed venous oxygenation, and infants were excluded if samples returned saturations greater than 89%. Results: VO_2lung was 1.92±1.74 ml kg^–1 min^–1, representing 25% of their VO_2wb (7.58±1.48 ml kg^–1 min^–1). VO_2lung was not correlated with clinical measures of acute disease severity. However, infants with the most severe changes on follow-up radiography (Edwards score 5 as assessed by radiologist blinded for VO₂ data) all had a VO_2lung level greater than 2.0 ml kg^–1 min^–1. Conclusion: VO_2lung can account for the elevated metabolic rate in low-birthweight infants with lung injury. We speculate that this reflects in part inflammatory pulmonary processes and may herald chronic lung disease.