Upper Inflection Point Research Articles

Current modes of conventional ventilation in intensive care

In practical terms, ventilation of critically ill patients should be established in the following way: • Setting a level of PEEP that is adequate to keep the alveoli open (above the lower inflection point; Fig. 3) • Ensuring that the maximum inspiratory pressure does not exceed 30 cmH 2 O (the upper inflection point), even if this results in small tidal volumes and permissive hypercapnia • Ensuring that expiratory time is adequate to prevent gas trapping and intrinsic PEEP, by checking that the end‐expiratory flow returns to zero on the waveforms • Accepting a PaO 2 of 60 mmHg (8 kPa) when setting inspired oxygen.

Reinterpreting the pressure-volume curve in patients with acute respiratory distress syndrome.

New evidence requires a reinterpretation of the inflation pressure-volume curve and suggests that neither the lower nor the upper inflection point provides reliable information to determine safe ventilator settings in the acute respiratory distress syndrome. Recruitment probably continues throughout the inflation pressure-volume curve, and studies of the deflation pressure-volume curve, reinflations after partial deflation, or decremental positive end-expiratory pressure trials after a recruitment maneuver are probably needed to determine open-lung positive end-expiratory pressure.

Significance of the changes in the respiratory system pressure-volume curve during acute lung injury in rats.

The hypothesis that the changes in the respiratory system pressure- volume (PV) curve during pulmonary edema mainly reflect distal airway obstruction was investigated in rats. Normal rats had a well-defined upper inflection point (UIP) at low airway pressure. Airway occlusion by liquid instillation decreased compliance (Crs) and the volume (Vuip) of the UIP, and increased end-inspiratory pressure. The same changes were observed during the progression of edema produced by high volume ventilation (HV). Changes in Vuip and in Crs produced by HV were correlated with edema severity in normal rats or rats with lungs preinjured with alpha-naphthylthiourea. Vuip and Crs changes were proportional, reflecting compression of the PV curve on the volume axis and suggesting reduction of the amount of ventilatable lung at low airway pressure. In keeping with this explanation, the lower Vuip and Crs were before HV, the more severe HV-induced edema was in alpha-naphthylthiourea-injected rats. When edema was profuse, PV curves displayed a marked lower inflection point (LIP), the UIP at low pressure disappeared but another was seen at high volume above the LIP, and the correlation between Vuip changes and edema severity was lost. These observations may have clinical relevance in the context of the "open lung" strategy. ventilator-induced lung injury; respiratory mechanics; acute respiratory distress syndrome

Modification of the pressure-volume curve of the respiratory system after ascites evacuation in a patient with acute respiratory distress syndrome

Objective: To report the modification of the pressure-volume curve of the respiratory system (P.Vst,rs curve) observed after ascitic drainage in a patient with ARDS. Design, methods: P.Vst,rs curves were acquired 1 hour before and after the draining of ascites, using a classic airway occlusion method. Setting: General intensive care unit (ICU). Results: The upper inflection point, the slope of the curve, the lower inflection point, measured on the P.Vsr,rs curve before ascites evacuation, were greatly modified after removal of 2500 ml of fluid. Conclusion: The modification of the P.Vst,rs curve after ascitic drainage suggests that the chest wall mechanics (and not the lung) was mainly responsible for the shape of the curve before draining. This observation emphasizes the importance of partitioning the respiratory system mechanics into its two (chest wall and lung) components.

Modification of the pressure-volume curve of the respiratory system after ascites evacuation in a patient with acute respiratory distress syndrome

Objective: To report the modification of the pressure-volume curve of the respiratory system (P.Vst,rs curve) observed after ascitic drainage in a patient with ARDS. Design, methods: P.Vst,rs curves were acquired 1 hour before and after the draining of ascites, using a classic airway occlusion method. Setting: General intensive care unit (ICU). Results: The upper inflection point, the slope of the curve, the lower inflection point, measured on the P.Vsr,rs curve before ascites evacuation, were greatly modified after removal of 2500 ml of fluid. Conclusion: The modification of the P.Vst,rs curve after ascitic drainage suggests that the chest wall mechanics (and not the lung) was mainly responsible for the shape of the curve before draining. This observation emphasizes the importance of partitioning the respiratory system mechanics into its two (chest wall and lung) components.

Effects of Positive End-Expiratory Pressure and Different Tidal Volumes on Alveolar Recruitment and Hyperinflation

DAMBROSIO, MICHELE; ROUPIE, ERIC; MOLLET, JEAN-JACQUES; ANGLADE, MARIE-CHRISTINE; VASILE, NORBERT; LEMAIRE, FRANCLOIS; BROCHARD, LAURENT

Effects of positive end-expiratory pressure and different tidal volumes on alveolar recruitment and hyperinflation.

The morphologic effect of positive end-expiratory pressure (PEEP) and of two tidal volumes were studied by computed tomography to determine whether setting the tidal volume (Vt) at the upper inflection point (UIP) of the pressure-volume (P-V) curve of the respiratory system or 10 ml/kg have different effects on hyperinflation and alveolar recruitment. Alveolar recruitment and hyperinflation were quantified by computed tomography in nine patients with the acute respiratory distress syndrome (ARDS). First, end expiration was compared without PEEP and with PEEP set at the lower inflection point of the P-V curve; second, at end inspiration above PEEP, a reduced Vt set at the UIP (rVt) and a standard 10 ml/kg Vt (Vt) ending above the UIP were compared. Three lung zones were defined from computed tomographic densities: hyperdense, normal, and hyperinflated zones. Positive end-expiratory pressure induced a significant decrease in hyperdensities (from 46.8 +/- 18% to 38 +/- 15.1% of zero end-expiratory pressure (ZEEP) area; P < 0.02) with a concomitant increase in normal zones (from 47.3 +/- 20.9% to 56.5 +/- 13.2% of the ZEEP area; P < 0.05), and a significant increase in hyperinflation (from 8.1 +/- 5.9% to 17.8 +/- 12.7% of ZEEP area; P < 0.01). At end inspiration, a significant increase in hyperinflated areas was observed with Vt compared with rVt (33.4 +/- 17.8 vs. 26.8 +/- 17.3% of ZEEP area; P < 0.05), whereas no significant difference was observed for both normal and hyperdense zones. Positive end-expiratory pressure promotes alveolar recruitment; increasing Vt above the UIP seems to predominantly increase hyperinflation.

Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome.

Mechanical ventilation may promote overdistension-induced pulmonary lesions in patients with acute respiratory distress syndrome (ARDS). The static pressure-volume (P-V) curve of the respiratory system can be used to determine the lung volume and corresponding static airway pressure at which lung compliance begins to diminish (the upper inflection point, or UIP). This fall in compliance may indicate overdistension of lung units. We prospectively studied 42 patients receiving mechanical ventilation with an FIO2 of 0.5 or more for at least 24 h. According to the Lung Injury Score (LIS), 25 patients were classified as having ARDS (LIS > 2.5), while 17 patients constituted a non-ARDS control group. The P-V curve was obtained every 2 d. Mechanical ventilation initially used standard settings (volume-control mode, a positive end-expiratory pressure [PEEP] adjusted to the lower inflection point on the P-V curve, and a tidal volume [VT] of 10 ml/kg). The end-inspiratory plateau pressure (Pplat) was compared to the UIP, and VT was lowered when the Pplat was above the UIP. In the range of lung volume studied on the P-V curves (up to 1600 ml), a UIP could be shown in only one control patient (at 23 cm H2O). By contrast, a UIP was present on the P-V curve obtained from all patients with ARDS, corresponding to a mean airway pressure of 26 +/- 6 cm H2O, a lung volume of 850 +/- 200 ml above functional residual capacity and 610 +/- 235 ml above PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)