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

We read with interest the study of Lakhal and colleagues [1] suggesting that respiratory pulse pressure variation (PPV) is not an accurate predictor of fl uid responsiveness in patients with acute respiratory distress syndrome (ARDS) ventilated with low tidal volume (Vt). Th ey 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. Th ese fi ndings are not surprising since in this study [1] the mean static compliance was not very low (40 cmH 2 O); therefore, the percentage of transmission of alveolar pressure to the pleural space was not really altered. Th us, 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 cmH 2 O) is now recommended [2]. Consequently, respira tory 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 fl uid responsiveness [3]. Th e fi ndings of Lakhal and colleagues [1] perhaps provide insuffi cient 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 cmH 2 O) are necessary to investigate whether or not PPV could be used in such cases.

We read with interest the study of Lakhal and colleagues [1] suggesting that respiratory pulse pressure variation (PPV) is not an accurate predictor of fl uid responsiveness in patients with acute respiratory distress syndrome (ARDS) ventilated with low tidal volume (Vt). Th ey 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. Th ese fi ndings are not surprising since in this study [1] the mean static compliance was not very low (40 cmH 2 O); therefore, the percentage of transmission of alveolar pressure to the pleural space was not really altered. Th us, 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 cmH 2 O) is now recommended [2]. Consequently, respira tory 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 fl uid responsiveness [3].
Th e fi ndings of Lakhal and colleagues [1] perhaps provide insuffi cient 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 cmH 2 O) are necessary to investigate whether or not PPV could be used in such cases.

L E T T E R 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]. Th eir 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 fi ndings [4] and their recalculated data [5]: the lower the lung compliance, the lower the alveolarto-pleural space transmission of pressure. By contrast, in the case of lower respiratory system compli ance [Crs], the alveolar-to-pleural pressure transmission may be altered in quite diff erent ways, depending on the causal mechanism: stiff er chest wall with no change in lung compliance leads to an increase in respiratory pleural pressure changes [ΔP pleural ] [6]; and stiff er lungs lead to lower ΔP pleural (and lower respiratory variations in pulse pressure (Δ RESP PP)) for similar changes in alveolar pressure (ΔP alveolar ). 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 P alveolar swings increase ΔP pleural but (ii) high lung stiff ness prevents P alveolar from being transmitted to the pleural space, therefore lowering ΔP pleural . Confusion may arise when one takes the 'pressure transmission-reasoning shortcut' and thinks, as Dr Mallat and colleagues do, that the fi rst phenomenon outweighs the second. Actually, basic physiological equations (ΔP pleural = Vt/Chest wall compliance) remind us that ΔP pleural depends only on the Vt [5] and chest wall compliance [6] and not on lung compliance: the increase in P alveolar (induced by decreased lung compliance) does not outweigh, but exactly compensates, the decrease in *Correspondence: jihad_mallat@msn.com Service de Réanimation Polyvalente, Centre hospitalier Dr Schaff ner de Lens, 62307 Lens Cedex, France alveolar-to-pleural space transmission of pressure, as previously observed [4,5]. Further, other limitations for Δ RESP PP (heart-to-respiratory rate ratio or acute cor pulmonale [1]) would become even more prominent in a severe ARDS population, and further studies are likely to yield the same conclusion: Δ RESP PP fails to predict fl uid responsiveness in ARDS.