Ability of respiratory pulse pressure variation to predict fluid responsiveness in ARDS: still an unanswered question?

  • Jihad Mallat1Email author,

    Affiliated with

    • Malcolm Lemyze1 and

      Affiliated with

      • Didier Thevenin1

        Affiliated with

        Critical Care201115:432

        DOI: 10.1186/cc10222

        Published: 10 June 2011

        We read with interest the study of Lakhal and colleagues [1] suggesting that respiratory pulse pressure variation (PPV) is not an accurate predictor of fluid responsiveness in patients with acute respiratory distress syndrome (ARDS) ventilated with low tidal volume (Vt). They stated that the poor performance of PPV is attributed to small changes in respiratory pleural pressure related to low Vt, such that PPV is low even in the case of marked cardiac preload dependency. These findings are not surprising since in this study [1] the mean static compliance was not very low (40 cmH2O); therefore, the percentage of transmission of alveolar pressure to the pleural space was not really altered. Thus, the ventilation with low Vt induced small variations in pleural and transpulmonary pressures.

        It must be stressed, however, that patients with ARDS usually exhibit a severe decrease in lung compliance and high plateau pressure. Moreover, in ARDS patients ventilated with low Vt, application of relatively high levels of positive end expiratory pressure (between 10 and 15 cmH2O) is now recommended [2]. Consequently, respiratory changes in transpulmonary pressure should remain greater than normal, and in spite of reduced lung compliance, cyclic changes in intrathoracic pressure may still be high enough for PPV to predict fluid responsiveness [3].

        The findings of Lakhal and colleagues [1] perhaps provide insufficient support for the assertion that PPV is unable to predict volume responsiveness in ARDS patients ventilated with low Vt. Additional studies in severe ARDS patients (compliance <30 cmH2O) are necessary to investigate whether or not PPV could be used in such cases.

        Authors' response: In ARDS, stiff lungs keep the pressure inside

        Stephan Ehrmann, Karim Lakhal and Thierry Boulain

        We thank Dr Mallat and colleagues for giving us the opportunity to clarify some physiological points tackled in our study [1]. Their assertion that 'the mean static compliance was not very low(...); therefore, the percentage of transmission of alveolar pressure to the pleural space was not really altered' is in accordance with Jardin and colleagues findings [4] and their recalculated data [5]: the lower the lung compliance, the lower the alveolar-to-pleural space transmission of pressure. By contrast, in the case of lower respiratory system compliance [Crs], the alveolar-to-pleural pressure transmission may be altered in quite different ways, depending on the causal mechanism: stiffer chest wall with no change in lung compliance leads to an increase in respiratory pleural pressure changes [ΔPpleural] [6]; and stiffer lungs lead to lower ΔPpleural (and lower respiratory variations in pulse pressure (ΔRESPPP)) for similar changes in alveolar pressure (ΔPalveolar). Importantly, the latter is the predominant mechanism of low Crs in ARDS [7].

        In ARDS, two phenomena work in opposite directions for a given Vt [4, 5]: (i) high Palveolar swings increase ΔPpleural but (ii) high lung stiffness prevents Palveolar from being transmitted to the pleural space, therefore lowering ΔPpleural. Confusion may arise when one takes the 'pressure transmission-reasoning shortcut' and thinks, as Dr Mallat and colleagues do, that the first phenomenon outweighs the second. Actually, basic physiological equations (ΔPpleural = Vt/Chest wall compliance) remind us that ΔPpleural depends only on the Vt [5] and chest wall compliance [6] and not on lung compliance: the increase in Palveolar (induced by decreased lung compliance) does not outweigh, but exactly compensates, the decrease in alveolar-to-pleural space transmission of pressure, as previously observed [4, 5]. Further, other limitations for ΔRESPPP (heart-to-respiratory rate ratio or acute corpulmonale [1]) would become even more prominent in a severe ARDS population, and further studies are likely to yield the same conclusion: ΔRESPPP fails to predict fluid responsiveness in ARDS.

        Abbreviations

        ARDS: 

        acute respiratory distress syndrome

        Crs: 

        respiratory system compliance

        Palveolar

        alveolar pressure

        Ppleural

        pleural pressure

        PPV: 

        respiratory pulse pressure variation

        Vt: 

        tidal volume

        Declarations

        Authors’ Affiliations

        (1)
        Service de Réanimation Polyvalente, Centre hospitalier

        References

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        Copyright

        © BioMed Central Ltd 2011

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