In Reply

We sincerely thank Dr. Roth for his interest and positive comments on our recent article¹  on prophylactic perioperative positive pressure ventilation (“P.O.P. ventilation” bundle) to prevent postoperative pulmonary complications, and we are happy to propose the following responses to his letter.

As for patients experiencing acute respiratory distress syndrome (ARDS), evidence is accumulating that lung-protective ventilation, including but not limited to the use of lower tidal volume (VT),²  should be considered in patients receiving mechanical ventilation for shorter duration in the operating room. The rationale behind the use of low VT is that surgery and anesthesia do place even normal lungs at risk of injury by cyclic recruitment and derecruitment of unstable units and that the lung parenchyma should not be strained up to an unphysiologic level. There is a widespread opinion that hypercapnia is the almost inevitable consequence of the decrease in the required minute ventilation induced by lower VT ventilation. The mechanical and physical constraints associated with mechanical ventilation that can lead to a tolerant approach to moderate elevations in arterial carbon dioxide (“permissive hypercapnia”) in the context of ARDS should however be distinguished from the perioperative setting in patients with healthy lungs for whom normocapnia is achieved without the need for sophisticated ventilator settings. In most clinical situations, arterial carbon dioxide is maintained within physiological ranges during lower VT ventilation through a moderate increase in respiratory rate (in the absence of intrinsic positive end-expiratory pressure) combined, where appropriate, with a longer expiratory time. For example, a recent randomized trial highlighted that, compared with standard ventilation, a lung-protective ventilation composed of lower VT ventilation, positive end-expiratory pressure, and recruitment maneuver was associated with a statistically, although clinically not relevant, difference in the respiratory rate (11.0 ± 1.0 vs. 12.8 ± 2.2 breath/min, respectively, P < 0.0001) to maintain the end-tidal carbon dioxide below 40 mmHg. It must be emphasized that, in the two recent IMPROVE and PROVHILO randomized trials,^3,4  the study protocol stressed that arterial carbon dioxide had to be maintained within normal ranges throughout the surgical procedure.

We fully concur with the author that both preclinical and clinical studies have documented beneficial effects of hypercapnia beyond the scope of ARDS. The benefits of hypercapnia are often related to the decrease in airway pressure and VT leading to less baro-volutrauma and atelectrauma. Hypercapnia was also found to improve arterial and tissue oxygenation,⁵  to increase local alveolar ventilation,⁶  and to induce microvascular vasodilation, thus promoting oxygen delivery and tissue perfusion.⁷  However, as mentioned by the author, hypercapnic acidosis is not without risks and whether there is or not added benefit to provide hypercapnia in lung-protective ventilation in the perioperative setting needs to be elucidated before being implemented in routine clinical practice. It is our opinion that a physiological approach to mechanical ventilation must remain the objective, which certainly involves to keep a close eye on the respiratory rate.