Background: The time course of impairment of respiratory mechanics and gas exchange in the acute respiratory distress syndrome (ARDS) remains poorly ...
Acta Anaesthesiol Scand 2006; 50: 80—91 Printed in UK. All rights reserved
Copyright # Acta Anaesthesiol Scand 2005 ACTA ANAESTHESIOLOGICA SCANDINAVICA
doi: 10.1111/j.1399-6576.2005.00767.x
Changes in respiratory mechanics and gas exchange during the acute respiratory distress syndrome S. NUNES1, P. VALTA2 and J. TAKALA3 1
Division of Intensive Care, Department of Anesthesiology and Intensive Care, Kuopio University Hospital, Kuopio, Finland, 2Department of Anesthesiology and Intensive Care, Helsinki University Hospital, Jorvi Hospital, Espoo, Finland, and 3Department of Intensive Care Medicine, Bern University Hospital — Inselspital, Bern, Switzerland
Background: The time course of impairment of respiratory mechanics and gas exchange in the acute respiratory distress syndrome (ARDS) remains poorly defined. We assessed the changes in respiratory mechanics and gas exchange during ARDS. We hypothesized that due to the changes in respiratory mechanics over time, ventilatory strategies based on rigid volume or pressure limits might fail to prevent overdistension throughout the disease process. Methods: Seventeen severe ARDS patients {PaO2/FiO2 10.1 (9.2—14.3) kPa; 76 (69—107) mmHg [median (25th75th percentiles)] and bilateral infiltrates} were studied during the acute, intermediate, and late stages of ARDS (at 1—3, 4—6 and 7 days after diagnosis). Severity of lung injury, gas exchange, and hemodynamics were assessed. Pressure-volume (PV) curves of the respiratory system were obtained, and upper and lower inflection points (UIP, LIP) and recruitment were estimated. Results: (1) UIP decreased from early to established (intermediate and late) ARDS [30 (28—30) cmH2O, 27 (25—30) cmH2O and 25 (23—28) cmH2O (P ¼ 0.014)]; (2) oxygenation improved in survivors and in patients with non-pulmonary etiology in late ARDS, whereas all patients developed hypercapnia from early to
established ARDS; and (3) dead-space ventilation and pulmonary shunt were larger in patients with pulmonary etiology during late ARDS. Conclusion: We found a decrease in UIP from acute to established ARDS. If applied to our data, the inspiratory pressure limit advocated by the ARDSnet (30 cmH2O) would produce ventilation over the UIP, with a consequent increased risk of overdistension in 12%, 43% and 65% of our patients during the acute, intermediate and late phases of ARDS, respectively. Lung protective strategies based on fixed tidal volume or pressure limits may thus not fully avoid the risk of lung overdistension throughout ARDS.
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volume relationships (PV curves) for the evaluation of respiratory mechanics (4—7), they remain the only available bedside tool to assess respiratory mechanics. Lung-protective strategies based on the use of PV curves have been shown to improve outcome (8) and decrease the cytokine response during mechanical ventilation (9). However, these strategies were determined only once during the early phase of ARDS and remained unchanged throughout the course of the disease. Possible longitudinal changes in respiratory mechanics were not taken into consideration. The evolution of respiratory mechanics, as assessed by PV curves and lung recruitment from early to established ARDS, has been scarcely studied. Few data exist on the correspondent longitudinal changes in gas exchange. This study was
CUTE respiratory distress syndrome (ARDS) is characterized by impairment of respiratory mechanics and gas exchange. The severity of this impairment changes according to the pathophysiological development of the disease. An initial inflammatory phase is usually followed by fibroproliferation, which may give place to eventual regeneration (1). The elastic properties of the lung may therefore vary markedly over time and cause changes in the respiratory mechanics which have to be taken into account in the clinical management of ARDS (2). Ventilator settings may necessitate frequent modifications in order to avoid further lung damage. Protective strategies, including fixed tidal volume or inspiratory pressure limits (3), ignore the dynamic evolution of acute lung injury. Despite all the limitations attributed to the use of pressure-
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Accepted for publication 3 March 2005
Key words: Acute respiratory distress syndrome; endexpiratory lung volume; gas exchange, lung recruitment; oxygenation, pressure-volume relationships; respiratory inductive plethysmography. #
Acta Anaesthesiologica Scandinavica 50 (2005)
Clinical pattern of ARDS
designed to assess the changes in respiratory mechanics and gas exchange during the clinical course of ARDS. We hypothesized that the mechanics of the respiratory system change from acute to established ARDS, and that a fixed protective ventilatory strategy chosen during the acute phase does not necessarily avoid further lung injury throughout the entire course of the disease. We have (1) assessed the severity of lung injury (10), (2) constructed PV curves and estimated their respective inflection points, (3) assessed changes in endexpiratory lung volume and estimated recruitment at the bedside during construction of the PV curves, and (4) assessed gas exchange and hemodynamics. All measurements were carried out during the acute phase of ARDS and repeated during the intermediate and late phases.
Methods Patients All ARDS patients admitted to the Intensive Care Unit of Kuopio University Hospital in Finland have respiratory mechanics measurements performed as required by clinical judgment. During a period of 4 years we prospectively collected clinical data from every ARDS patient admitted to our unit. No interventions were made for research purposes. From this data pool, we retrospectively chose to study those 17 patients who had PV curves performed at least once during the first 3 days after diagnosis (acute phase) and measurements repeated both during the fourth to sixth days after diagnosis (intermediate) and on the seventh day of the disease or later (late phase). Intermediate measurements were not available in three patients. Five patients were previously included in another study (11). The criteria for ARDS diagnosis were those established by the ARDS consensus conference (12) [known triggering etiology, PaO2/FiO2 26.7 kPa (200 mmHg) during mechanical ventilation, no other clinical explanation for impaired oxygenation, a PAOP
