Reliability of pulse oximetry during exercise in pulmonary patients.

To evaluate the reliability of pulse oximetry during exercise, we studied 101 patients primarily with chronic pulmonary diseases. Three devices were used on different patients. Radial arterial blood was sampled at rest and maximal exercise simultaneously to pulse oximetric determination. Measured blood oxygen saturation was significantly different from noninvasive saturation at rest and also at exercise for each device. Nevertheless, changes in pulse oximetry from rest to exercise were significantly correlated with measured saturation for all three devices. Direction of changes in saturation from rest to exercise was correctly evaluated by transcutaneous oximetry in all but six instances where changes were less than 4 percent. Although measured and transcutaneous saturations are significantly different, we conclude that pulse oximetry reliably estimates changes in arterial saturation between rest and exercise for a clinical purpose. None of the three tested devices was better compared with the others in estimating saturation changes at exercise.

Mechanism of improvement in pulmonary gas exchange during growth in awake piglets.

Previous studies have shown a lower arterial PO2 (PaO2) in infants and young animals than in adults. To investigate the mechanism of this impairment of gas exchange we studied 13 piglets from 12 to 65 days of age. Two days after instrumentation we measured the distribution of ventilation-perfusion ratios (VA/Q) by use of the multiple inert gas technique on awake animals. We showed that PaO2 is lower in young animals, increasing from 72 +/- 11.5 Torr before 2 wk to 102 Torr at 2 mo. This hypoxemia is due to an enlarged alveolar-arterial O2 pressure difference that significantly decreases with age. This impairment in gas exchange is not due to shunting (0.6 +/- 1.3%). Mean dead space (36 +/- 11%) was not related to age. Mean modes of perfusion and ventilation did not differ significantly between age groups. However, the dispersion of perfusion as expressed by its logSD decreased significantly with age, whereas dispersion of ventilation remained constant. Furthermore, in the young animals only, a significant difference was evidenced between measured alveolar-arterial PO2 gradient and the value predicted by the inert gas model. We therefore conclude that the impairment of gas exchange in piglets is due to two mechanisms: VA/Q mismatch and diffusion limitation for O2.

Improvement of gas exchange during inhibition of hypoxic pulmonary vasoconstriction by nitrendipine in piglets.

To determine how nitrendipine (N), a calcium antagonist, interferes with haemodynamics and gas exchange during hypoxia, we studied 12 piglets (4-6 weeks, 4.3-9.0 kg) anaesthetized with pentobarbital (20 mg.kg-1 i.p.). Haemodynamics, blood gases and multiple inert gas elimination were measured at the end of three consecutive 30 min periods of spontaneous breathing: room air (RA), 11-12% FIO2 (H) and 11-12% FIO2 with a randomly selected infusion of N (3 micrograms.kg-1.min-1) (HN) or the carrier solution (HP) (6 animals in each group). Pulmonary vascular resistance (Rpv) doubled from 8.7 +/- 2.8 mmHg.min-1.1-1 in RA to 19.5 +/- 10.0 (mean +/- SD) in H while PaO2 fell from 83 +/- 8.3 mmHg to 28.7 +/- 5.2. With N, Rpv fell back to room air value: 8.7 +/- 2.0 (p less than 0.02; comparison H and HN), while PaO2 rose from 29.3 +/- 6.3 mmHg in H to 46.1 +/- 6.1 HN (p less than 0.001) and PaCO2 fell from 33.8 +/- 10 to 23.9 +/- 3.7 mmHg. There was a small non-significant rise in VE. Haemodynamics and blood gases of the placebo group were not statistically different in H and HP. No extrapulmonary shunting was evidenced during any experimental period. The perfusion to lung zones with VA/Q lower than 0.005 rose from 1.1 +/- 2.1% in RA to 8.9 +/- 5.7% in H, but no further increase was obtained with N: 5.1 +/- 2.5%. Overall VA/Q matching did not deteriorate with N during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)