Assessment of lung water content by roentgen videodensitometry.

In 17 anesthetized and mechanically ventilated pigs, different degrees of lung injury were induced by iv infusion of oleic acid (mean dose 0.1 ml/kg). The change in radiologic density of the chest was measured by a videodensitometer before and 4 h after oleic acid infusion. The lungs were then removed for determination of the wet/dry weight ratio (WW/DW). The change in radiologic density was significantly correlated to WW/DW (r = .87) and to the changes in end-inspiratory pressure (r = .80), mean pulmonary arterial pressure (r = .77) and venous admixture (r = .79), but not to changes in the oncotic-hydrostatic pressure gradient of the lungs (r = .46). Roentgen videodensitometry appears to be a useful method for assessing changes in extravascular lung water content.

Effects of positive end-expiratory pressure on cardiac output distribution in the pig.

Cardiac output (CO) and the blood flow to the heart, cerebellum, kidney, pancreas, spleen and skeletal muscle were studied in 20 pigs during spontaneous breathing (SB) and intermittent positive pressure ventilation (IPPV) with a positive end-expiratory pressure (PEEP) of 0, 8, 16 or 24 cmH2O. Microspheres (15 micrometers) labelled with either 85-sr or 141-Ce were used. Injection of microspheres labelled with one of the isotopes was given during SB (all pigs) and with the other isotope during IPPV with PEEP of 0, 8, 16 or 24 cmH2O (five pigs at each level). CO decreased by 11% during IPPV with PEEP of 0 and 31%, 53% and 66% during PEEP of 8, 16 or 24 cmH2O, respectively. Mean arterial blood pressure was fairly well maintained in all groups except the group with PEEP of 24 cmH2O. The perfusion of the six organs deteriorated, but when taken as fractions of CO measured at the same time, the blood flow to the heart, cerebellum and kidney increased with increasing airway pressure, while that to the pancreas, spleen and skeletal muscle decreased. The vascular resistance of the three former organs did not change, while in the latter it increased markedly. It is concluded that when CO decreases as a result of positive pressure ventilation, a redistribution takes place, mainly due to vascular constriction in skeletal muscle, which acts to preserve the blood flow to vital organs.

The effect of positive end-expiratory pressure on central haemodynamics in the pig.

The effect on central haemodynamics of a stepwise increase in airways pressure from spontaneous breathing (SB) to intermittent positive pressure ventilation with a positive end-expiratory pressure (PEEP) of 0, 8, 16 and 24 cmH2O was studied in eight pigs under ketamine anaesthesia. Compared with SB, cardiac output (CO) was reduced by 12, 36, 50 and 64% at the respective ventilator settings. The transmural pressures of the right and left atrium, measured as the difference between atrial and pleural pressure, both decreased with increments in airway pressure. At a PEEP level of 24, there was a threefold increase in pulmonary vascular resistance. This increase was secondary to the decrease in CO and no signs of CO deterioration due to the increased right ventricular afterload were found. When 250 ml of dextran 70 was administered at a PEEP level of 24 and the airway pressure was then released stepwise, the left ventricular function curve improved, disclosing a relative myocardial failure at the highest PEEP levels. It is concluded that the principal causative mechanisms in CO reduction due to increased intrathoracic pressure is a decrease in preload to the right ventricle. At high PEEP levels there are also signs of myocardial depression.

Influence of plasma oncotic pressure on lung water accumulation and gas exchange after experimental lung injury in the pig.

In 18 anaesthetized and artificially ventilated pigs, oleic acid was infused intravenously in order to induce a lung injury characterized by increased lung water content, decreased compliance and a ventilation/perfusion disturbance. After a stabilizing period, half of the animals (group P) underwent repeated plasmapheresis, which halved their plasma oncotic pressure (POP). The rest of the animals were bled and re-transfused with the shed blood, thus serving as a control group. In both groups, care was taken to keep the mean left atrial pressure as constant as possible. During plasmapheresis and "shamapheresis", there was no significant increase in venous admixture (F102 0.21 and 0.6) in either of the groups. At the end of the study, end-inspiratory pressure, dead space/tidal volume ratio and wet/dry lung weight ratio (WW/DW) were significantly higher in group P. Venous admixture and WW/DW correlated significantly with pulmonary arterial pressure and calculated pulmonary capillary pressure, but not with POP or POP minus pulmonary arterial occlusion pressure. It is concluded that reduction of plasma oncotic pressure may increase the lung water content in previously injured lungs, but this extra water accumulation does not necessarily impair oxygenation in the lungs.