High Positive End-Expiratory Pressure Renders Spontaneous Effort Non-Injurious.

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Abstract

RATIONALE

In ARDS, atelectatic 'solid-like' lung tissue impairs transmission of negative 'swings' in pleural pressure (Ppl) resulting from diaphragmatic contraction. The localization of more negative Ppl proportionally increases dependent lung stretch by drawing gas either from other lung regions, e.g., non-dependent lung (Pendelluft) or from the ventilator. Lowering of the level of spontaneous effort and/or converting solid-like to fluid-like lung might render spontaneous effort non-injurious.

HYPOTHESIS

That spontaneous effort increases dependent lung injury; and, that such injury would be reduced by recruiting atelectatic 'solid-like' lung with PEEP.

METHODS

Established models of severe ARDS (rabbit, pig) were used. Regional histology (rabbit), inflammation (positron emission tomography, PET; pig), regional inspiratory Ppl (intrabronchial balloon manometry) and stretch (electrical impedance tomography, EIT; pig) were measured. Respiratory drive was evaluated in eleven patients with ARDS.

MEASUREMENTS AND MAIN RESULTS

While injury during muscle paralysis was predominantly in non-dependent and middle lung at low (vs. high) PEEP, strong effort increased injury (indicated by PET and histology) in dependent lung. Stronger effort (vs. muscle paralysis) caused local overstretch and greater tidal recruitment in dependent lung, where more negative Ppl was localized and greater stretch was generated. In contrast, high PEEP minimized lung injury by the uniform distribution of negative Ppl; and lowering spontaneous effort (i.e. deflection in esophageal pressure, observed in rabbits, pigs, patients).

CONCLUSIONS

Strong effort increased dependent lung injury, where higher local lung stress and stretch was generated; effort-dependent lung injury was minimized by high PEEP in severe ARDS which could offset need for paralysis.

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