- Poster presentation
- Open Access
The static pressure–volume curve does not predict the mechanical properties of the respiratory system during mechanical ventilation in acute respiratory distress syndrome (ARDS) and acute lung injury (ALI)
© BioMed Central Ltd. 2004
- Published: 15 March 2004
- Mechanical Ventilation
- Acute Lung Injury
- Respiratory System
- Acute Respiratory Distress Syndrome
- Versus Curve
The pathophysiology of ALI and ARDS induces distinct changes in respiratory mechanics. For more than 30 years respiratory mechanics have been assessed by analysis of the static pressure–volume (P–V) curve. Ventilation, however, is a dynamic process and the mechanical properties of the respiratory system can be assessed under dynamic conditions . If the respiratory system shows a specific dynamic behaviour that is not present during static conditions, differing results are to be expected if mechanics are analysed during dynamic conditions. The aim of the present study was to test whether such differences can be observed in ARDS and ALI.
Twenty-eight patients with ARDS and ALI were included in the study. Patients were ventilated with the Evita4Lab measurement system (Dräger, Germany). Static respiratory mechanics were obtained using a low-flow inflation. Dynamic P–V curves covering the whole vital capacity range were obtained by increasing the positive end expiratory pressure (PEEP) by 2 mbar every eight breaths during ongoing mechanical ventilation until a plateau pressure of 45 mbar was attained. For statistical analysis, the Wilcoxon test was used.
In patients with ARDS/ALI, the static P–V curve does not predict the mechanical behaviour of the respiratory system during mechanical ventilation. Under the dynamic conditions of mechanical ventilation, the end expiratory pulmonary volume is higher and respiratory compliance lower than expected from the static measurement. This effect cannot be assigned to dynamic hyperinflation. It represents an actual shift in functional residual capacity because the differences increase with PEEP and are similar in patients with and without intrinsic PEEP. The differences can be explained by a slow time-dependent and pressure-dependent phenomenon such as alveolar recruitment.