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Pulmonary pressure-flow curves can be easily generated in the intact animal by using a combination of systemic arteriovenous (a-v) fistulas and inferior vena cava (IVC) occlusion. By combining this technique with pulmonary artery occlusion, pulmonary pressure-flow curves may be studied over a broader range of pressures than has been previously been done in the intact, resting animal using pulsatile flow. Pressure-flow curves were generated by varying flow through opening and closing of the a-v fistulas in conjunction with inflating and deflating a balloon in the inferior vena cava. The pressure-flow curves were done under two conditions; (1) with both lungs perfused; (2) with the right lung excluded from the circulation (PA occlusion). PA occlusion resulted in no change in alveolar arterial oxygen tension gradient. The pressure-flow relationships for one lung and two lungs were well described by linear equations (r2 = 0.83 +/- 0.03 and 0.82 +/- 0.04 respectively). The slope of the equations increased with PA occlusion (3.6 +/- 0.4 mmHg.L-1 to 5.9 +/- 0.9 mmHg.L-1). There was no change in the pressure axis intercept with PA occlusion (8.34 +/- 0.8 mmHg pre-occlusion and 8.9 +/- 1.3 mmHg post-occlusion). It is concluded that the pulmonary pressure-flow relationship is well described by a linear function above a mean pulmonary artery pressure (PAP) of 10-12 mmHg.

Mecanismes de transport des gaz. Ventilateurs et circuits. Monitorage. Clearance mucociliaire au cours de l'oscillation a haute frequence. Fonction du surfactant et stabilite pulmonaire

We ventilated seven mongrel dogs with high frequency oscillatory ventilation (HFO) at frequencies from 3 to 30 Hz. At each frequency, the tidal volume required to achieve isocapnia (VTiso) was measured by plethysmography. In an individual dog, VTiso could be related to frequency by an equation of the form VTiso = KfA. A was similar for the seven dogs, A = -0.54 +/- 0.03. K varied from 179 to 325 cc- Hz-A, reflecting differences between the dogs in dead space, CO2 production and gradient for gas transport. This relation is consistent with that predicted from the data of previous investigators who used different ventilators, circuits and methodology. From 3 to 30 Hz, VTiso decreased from 1.2 to 0.4 times anatomic plus equipment dead space, but minute volumes required to maintain isocapnia increased from 6 to 18 times those required during conventional ventilation. We conclude that low tidal volume ventilation is also high minute volume ventilation.

Oxygenation and mean lung volume were investigated during high frequency oscillation (HFO) and conventional mechanical ventilation (CMV) in two models of lung disease and related to the lung mechanics of the lesions. Oleic acid (n = 10) or lung lavage (n = 12) pulmonary injury was induced in a series of rabbits. Each animal was alternately ventilated with HFO (15 Hz sinusoidal wave form) and CMV (flow generator I:E, 1:2; f, 30 breaths/min; VT, 10 to 15 ml/kg) at matched mean airway pressure. Pao2 was measured 5 minutes after onset of ventilation. In the lung lavage model Pao2 was significantly greater during HFO than CMV (Pao2 228 +/- 116 torr vs 71 +/- 42 torr) provided that mean airway pressure was greater than the distinct opening pressure characteristic of this lesion. In the oleic acid model oxygenation was again superior during HFO (Pao2 269 +/- 116 torr vs 110 +/- 83 torr), but only if HFO was preceded by a sustained inflation. Plethysmography in a subset of six rabbits from each group revealed that the improvements in oxygenation were associated with significantly higher mean lung volumes during HFO than CMV (58 +/- 30 ml vs 29 +/- 14 ml lung lavage model, 45 +/- 15 ml vs 30.9 +/- 13 ml on the oleic acid model). The importance of a sustained inflation in rapidly optimizing gas exchange during HFO but not CMV was demonstrated. A sustained inflation resulted in immediate and sustained increases in Pao2 (from 134 +/- 102 torr to 274 +/0 124 torr in the oleic acid model; from 115 +/- 105 torr to 291 +/- 143 torr in the lung lavage model) and mean lung volume (41.8 +/- 11 to 53.8 +/- 9.7 ml in the oleic acid model, 30.9 +/- 7.7 ml to 42.8 +/- 5 ml in the lung lavage model). It is suggested that in these two particular models of lung disease, HFO, when combined with a sustained inflation (to provide opening forces), can more fully exploit the pressure volume hysteresis of unstable lung units than CMV, thereby resulting in the larger mean lung volumes and better oxygenation observed during HFO.