Pathophysiological response of bovine pulmonary function to gastric distension

The purpose was to determine whether gastric overdistension leads to life-threatening perturbations of pulmonary gas exchange in healthy calves. Six animals were studied with normal (0 kPa) and increased (1, 2, 3, 4 and 5 kPa) intragastric pressure (IGP). Changes in pleural pressures and peak expiratory flow paralleled those of IGP. Inspiratory pressure-time index remained stable throughout the insufflation process. Pulmonary function values were characterized by abrupt changes with increasing IGP. Tidal volume declined as IGP increased and, along with inspiratory flow, decreased abruptly with the highest pressure (5 kPa). Respiratory rate progressively increased up to an IGP of 4 kPa, then decreased by 30%, due to breath-holding at the end of inspiration. Minute volume increased with IGP up to 4 kPa, but dramatically declined at 5 kPa. Total pulmonary resistance remained stable throughout the insufflation process, whereas lung dynamic compliance fell abruptly to one-half of its baseline value at IGPs of 1 kPa and above. Arterial oxygen tension was maintained at an IGP of 1 kPa, slightly diminished at 2-3 kPa, and markedly decreased at 4-5 kPa. Hypercapnia and respiratory acidosis developed progressively with increasing IGP. Changes in arterial gases were probably due to a combination of (1) alveolar hypoventilation, caused by altered tidal to dead space volume ratio, inadequate central nervous system "drive", altered effectiveness of inspiratory muscle action, or end-inspiratory breath-holding, and (2) ventilation to perfusion mismatch, caused by perfusion of collapsed lung units. In the range of IGPs used, standardized arterial pH did not decline below the control value, which suggests that perfusion of peripheral tissues remained sufficient, and that respiratory failure rather than cardiovascular failure may be the principal physiopathological effect of increased gastric pressure.