Respiratory gases of synovial fluids

Synovial fluids from thirty patients were analyzed for partial pressure of oxygen (Po2) and carbon dioxide (Pco2), pH, lactate concentration and cell counts. Synovial biopsy specimens from twenty-four of these patients were evaluated for cellular proliferation, microvascular changes and ischemic necrosis. Po2 values ranged from 53 to 9 mm Hg with corresponding ranges for pH of 7.43 to 6.84, for Pco2 of 35 to 98 mm Hg and for lactate of 0.65 to 6.4 mM/L. Decrements in Po2 from 53 to 27 were associated with small decreases in pH, and minimal elevation in Pco2 and lactate. Decrements in Po2 from 27 to 9 were accompanied by large decreases in pH and large increases in Pco2 and lactate. Severe joint disease led to a fall in Po2 and pH and a rise in Pco2 and lactate concentration. These changes correlated with proliferation of synovial cells, focal necrosis and focal obliterative microangiopathy. The relationship between in vivo synovial fluid pH and Pco2 or lactate concentration was also determined. By utilizing the Henderson-Hasselbalch equation we were able to calculate the bicarbonate concentration of each fluid and correlate the changes in bicarbonate with the increases in lactate. A ratio of regional blood flow to joint oxygen consumption was derived from the Fick equation. By using published in vitro oxygen consumption values for synovial membrane, it was possible to calculate the relative effective blood flows in rheumatoid and nonrheumatoid joints. Regional flow is increased in rheumatoid arthritis but is relatively insufficient to meet the marked increase in metabolic demands imposed by disease. This relative insufficiency is believed to cause the fall in Po2 and pH in diseased synovial fluids. Synovial fluids from thirty patients were analyzed for partial pressure of oxygen (Po2) and carbon dioxide (Pco2), pH, lactate concentration and cell counts. Synovial biopsy specimens from twenty-four of these patients were evaluated for cellular proliferation, microvascular changes and ischemic necrosis. Po2 values ranged from 53 to 9 mm Hg with corresponding ranges for pH of 7.43 to 6.84, for Pco2 of 35 to 98 mm Hg and for lactate of 0.65 to 6.4 mM/L. Decrements in Po2 from 53 to 27 were associated with small decreases in pH, and minimal elevation in Pco2 and lactate. Decrements in Po2 from 27 to 9 were accompanied by large decreases in pH and large increases in Pco2 and lactate. Severe joint disease led to a fall in Po2 and pH and a rise in Pco2 and lactate concentration. These changes correlated with proliferation of synovial cells, focal necrosis and focal obliterative microangiopathy. The relationship between in vivo synovial fluid pH and Pco2 or lactate concentration was also determined. By utilizing the Henderson-Hasselbalch equation we were able to calculate the bicarbonate concentration of each fluid and correlate the changes in bicarbonate with the increases in lactate. A ratio of regional blood flow to joint oxygen consumption was derived from the Fick equation. By using published in vitro oxygen consumption values for synovial membrane, it was possible to calculate the relative effective blood flows in rheumatoid and nonrheumatoid joints. Regional flow is increased in rheumatoid arthritis but is relatively insufficient to meet the marked increase in metabolic demands imposed by disease. This relative insufficiency is believed to cause the fall in Po2 and pH in diseased synovial fluids.