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Pulmonary capillary pressures during the acute respiratory distress syndrome

Nunes, Silvia ; Ruokonen, Esko ; Takala, Jukka

In: Intensive Care Medicine, 2003, vol. 29, no. 12, p. 2174-2179

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    Titre
    • Pulmonary capillary pressures during the acute respiratory distress syndrome
    Auteur
    • Nunes, Silvia. Critical Care Research Program, Division of Intensive Care, Department of Anesthesiology and Intensive Care, Kuopio University Hospital, Kuopio, Finland
    • Ruokonen, Esko. Critical Care Research Program, Division of Intensive Care, Department of Anesthesiology and Intensive Care, Kuopio University Hospital, Kuopio, Finland
    • Takala, Jukka. Department of Intensive Care, Bern University Hospital—Inselspital, 3010, Bern, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Intensive Care Medicine, 2003, vol. 29, no. 12, p. 2174-2179. Springer-Verlag
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:322104
    Summary
    Objectives: (1)To describe the evolution of pulmonary capillary pressure (Pcap) and of the pressure drop across the pulmonary venous bed from early to established acute respiratory distress syndrome (ARDS), (2) to assess Pcap under different levels of positive end-expiratory pressure (PEEP) and (3) to compare the visual method and a mathematical model to determine Pcap. Design: Prospective, intervention study. Setting: Intensive care unit in a teaching institution. Patients: Nine ARDS patients, according to the ARDS Consensus Conference criteria. Interventions: Pulmonary arterial pressures were measured during routine respiratory mechanics measurements throughout ARDS. Four PEEP levels (6, 9, 12 and 15cmH2O) were studied. Measurements and results: Pulmonary artery occlusions were made in triplicate at each PEEP level. Pcap was determined for every occlusion trace by three observers (visual method) and a mathematical model. Diastolic pulmonary artery pressure (PAPd) and pulmonary artery occlusion pressure (PAOP) were measured. The visually determined Pcap showed a bias of 2.5±2.1mmHg as compared to the mathematical estimation. PAPd, Pcap and PAOP tended to decrease from early to late ARDS (p=0.128, 0.265, 0.121). Pcap−PAOP (6.3±2.7mmHg) did not change throughout ARDS. Higher PEEP levels were associated with increased PAPd, Pcap and PAOP, as well as with larger Pcap−PAOP throughout ARDS. Conclusions: Pulmonary capillary pressure cannot be predicted from PAOP during early and established ARDS. The high variability in Pcap−PAOP increases the risk for underestimation of filtration pressures and consequently the risk for lung edema. Pcap can be estimated at the bedside by either the visual or mathematical methods