Influence of ventilatory settings on static and functional haemodynamic parameters during experimental hypovolaemia

Abstract

The influence of ventilatory settings on static and functional haemodynamic parameters during mechanical ventilation is not completely known. The purpose of this study was to evaluate the effect of positive end-expiratory pressure, tidal volume and inspiratory to expiratory time ratio variations on haemodynamic parameters during haemorrhage and after transfusion of shed blood. Ten anaesthetized pigs were instrumented and mechanically ventilated with a tidal volume of 8 mlkg(-1), a positive end-expiratory pressure of 5 cmH(2)O and an inspiratory to expiratory ratio of 1:2. Then, they were submitted in a random order to different ventilatory settings (tidal volume 16 mlkg(-1), positive end-expiratory pressure 15 cmH(2)O or inspiratory to expiratory time ratio 2:1). Functional and static haemodynamic parameters (central venous pressure, pulmonary artery occlusion pressure, right ventricular end-diastolic volume and pulse pressure variation) were evaluated at baseline, during hypovolaemia (withdrawal of 20% of estimated blood volume) and after an infusion of withdrawn blood (posttransfusion). During baseline, a positive end-expiratory pressure of 15 cmH(2)O significantly increased pulmonary artery occlusion pressure from 14.6 +/- 1.6 mmHg to 17.4 +/- 1.7 mmHg (P < 0.001) and pulse pressure variation from 15.8 +/- 8.5% to 25.3 +/- 9.5% (P < 0.001). High tidal volume increased pulse pressure variation from 15.8 +/- 8.5% to 31.6 +/- 10.4% (P < 0.001), and an inspiratory to expiratory time ratio of 2: 1 significantly increased only central venous pressure. During hypovolaemia, high positive end-expiratory pressure influenced all studied variables, and high tidal volume strongly increased pulse pressure variation (40.5 +/- 12.4% pre vs. 84.2 +/- 19.1% post, P < 0.001). The inversion of the inspiratory to expiratory time ratio only slightly increased filling pressures during hypovolaemia, without affecting pulse pressure variation or right ventricle end-diastolic volume. We concluded that pulse pressure variation measurement is influenced by cyclic variations in intrathoracic pressure, such as those caused by augmentations in tidal volume. The increase in mean airway pressure caused by positive end-expiratory pressure affects cardiac filling pressures and also pulse pressure variation, although to a lesser extent. Inversion of the inspiratory to expiratory time ratio does not induce significant changes in static and functional haemodynamic parameters.