Arterial oxygen tension (PaO2) is known to decrease with age, and this is accompanied by a number of changes in mechanical properties of the lungs, including loss of elastic recoil and increase in closing volume. The changes in respiratory mechanics with age could induce greater ventilation/perfusion (VA/Q) mismatch and thus explain the decrease in PaO2. In 64 normal subjects aged 18 to 71 yr (lifetime nonsmokers with normal spirometry), we measured VA/Q inequality and arterial respiratory blood gases (PaO2 and PaCO2) at rest in the seated position. VA/Q mismatch, represented by the second moments of the blood flow and ventilation distributions (log SDQ and log SDV) increased with age, but only slightly (mean log SDQ was 0.36 at age 20 yr and 0.47 at age 70 yr). PaO2 fell by a correspondingly small amount of 6 mm Hg. Previously established upper 95% confidence limits for log SDQ (0.60) and log SDV (0.65) in subjects at age 20 yr were confirmed. At age 70 yr, the upper limits of reference for log SDQ are 0.70 and for log SDV 0.75. The study shows that an increased alveolar-arterial O2 gradient with age is due to VA/Q inequality rather than to shunting.

Pleural effusion (PE) often causes abnormal pulmonary gas exchange. Thoracentesis is commonly used to relieve dyspnea in patients with PE, but its effect upon arterial oxygenation is varied and poorly understood. This investigation sought to: (1) characterize the distribution of ventilation-perfusion (VA/Q) ratios in patients with PE and (2) assess the effects of PE drainage by thoracentesis upon pulmonary gas exchange. We studied nine patients (two females) with a mean age of 39+/-20 (SD) yr. All of them had PE of recent clinical onset (< 2 wk of symptoms), without other apparent medical conditions. Before thoracentesis, PaO2 was 82.3+/-10.2 mm Hg and AaPO2 was 28.7+/-10.0 mm Hg. Patients had broadened unimodal VA/Q distributions with small amounts of blood flow perfusing lung units with low VA/Q ratios (< 0.1) (1.4+/-2.2%) and mild intrapulmonary shunt (6.9+/-6.7%). PaO2 was significantly related to the amount of shunt (rho = -0.82; p < 0.01) but not to the percentage of blood flow perfusing low VA/Q units. While thoracentesis drained 693+/-424 ml of fluid and caused a significant fall in mean pleural pressure (by -10.7 +/- 7.1 mm Hg; p < 0.01), PaO2, AaPO2, and shunt remained unchanged; only the amount of blood flow perfusing low VA/Q ratios increased slightly (2.4+/-2.6%; p < 0.05). This study shows that: (1) intrapulmonary shunt is the main mechanism underlying arterial hypoxemia in patients with PE and (2) effective thoracentesis has minor short-term effects upon pulmonary gas exchange. These findings are in accord with delayed (> 30 min) pulmonary volume re-expansion after thoracentesis with or without the coexistence of mild ex vacuo pulmonary edema.

In a recent study of completely sedentary normal young subjects, leg VO2max was reduced by hypoxia in proportion to mean capillary PO2 as F(I)O2 was reduced from 0.15 to 0.12. However, the increase in VO2max from F(I)O2 = 0.15 to 0.21 was less than expected for the increase in mean capillary PO2. This finding has led us to hypothesize that in sedentary subjects breathing room air, VO2max is not limited by O2 supply but rather by oxidative capacity of mitochondria. The present study sought to obtain further evidence for or against this hypothesis in sedentary subjects by assessing leg VO2max (VO2leg) breathing 100% O2, as well as in normoxia and hypoxia. Data from 18 subjects studied at F(I)O2 = 0.12, 0.15, and 0.21 and from six more studied at 0.12, 0.15, and 1.00 were analyzed. In all 24 we measured VO2leg by arterial and venous blood sampling and thermodilution leg blood flow during maximal cycle ergometry at each F(I)O2. VO2leg was not increased by room air or 100% O2 breathing relative to that observed at F(I)O2 = 0.15, but it was reduced while breathing 12% O2. The data at F(I)O2 = 0.12 and 0.15 conformed to the predictions of O2 supply limitation of maximal VO2 as previously. These results confirm and extend our prior observations that in sedentary, as opposed to trained subjects, muscle VO2max is O2 supply limited only in hypoxia.