Ventilator Management Guided by Driving Pressure: A Better Way to Protect the Lungs?*

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One of the major mechanisms causing ventilator-induced lung injury (VILI) is excessive stretching of alveolar structures from positive pressure mechanical ventilation (1). This overstretching is thought to occur from both an excessive maximal stretch at end inspiration as well as an excessive repetitive tidal stretch during breath delivery. Indeed, a number of well-designed randomized clinical trials have clearly shown that a cornerstone of safe ventilator management of the acutely injured lung involves limiting maximal applied pressure to less than the normal maximal stretching pressure of the lungs (i.e., roughly < 30 cm H2O transpulmonary pressure) and limiting tidal volume (VT) to the normal range (i.e., roughly 5–7 mL/kg ideal body weight [IBW]) (2).
Unfortunately, the acutely injured lung consists of a markedly heterogeneous distribution of mechanically deranged alveolar units—grossly inflamed and edematous units coexisting with near normal units in the same lung (3). Under these circumstances, while an applied positive pressure is distributed uniformly, the distribution of volume is clearly not uniform. Indeed, minimal regional volume may be delivered to stiff, collapsed alveolar units, whereas excessive regional volume may be delivered to healthier units. Regional development of VILI would thus be more likely in the healthier, more compliant units.
Because of these considerations, a reevaluation of the recommended strategy of delivering a normal sized VT based on IBW has been occurring. When setting VT referenced to IBW, the lung is assumed to be normal in size with normal mechanics—a situation as noted above that clearly does NOT exist in acutely injured lungs. As a consequence, a VT of 6 mL/kg IBW in a lung that has half of its gas volume replaced by inflammatory edema would be equivalent to a 12 mL/kg IBW VT in the remaining ventilated half of the lung.
This phenomenon was initially described as the “baby lung” effect—an adult lung with much of its gas volume replaced by inflammation is functionally a small pediatric lung (3). Adjusting the VT target to reflect these changes would seem logical, and several approaches have been described in recent years. One approach uses imaging techniques (e.g., CT scans or electrical impedance tomography scans) to determine functional lung size and adjust VT targets accordingly (4). Another approach uses gas dilution measurements of functional residual capacity to again guide VT settings (5). Unfortunately, neither of these techniques are routinely available to clinicians.
The latest approach is the simplest—target the VT to system compliance (VT/C). Mathematically, VT/C is the driving pressure (DP)—the applied pressure above positive end-expiratory pressure (PEEP) to deliver the VT. With this approach, system compliance is taken as a surrogate of the severity of lung injury and, by extension, a surrogate of the degree of alveolar volume loss (6). Practically, DP can be estimated by subtracting total PEEP from the measured airway plateau pressure at end inspiration. Importantly, the transpulmonary DP would probably be a better way to express DP as extrapulmonary effects on system compliance would be eliminated. Unfortunately, this requires an esophageal balloon.
In this issue of Critical Care Medicine, Aoyama et al (7) have examined the role of DP through a systematic review of seven studies that evaluated VT size based on IBW and plateau pressure effects on mortality. Although none of these studies used DP as a set independent variable, DP could be calculated, and it was clearly shown that a high value was a strong predictor of mortality. Furthermore, the results suggested that a “safe” DP was less than 13–15 cm H2O. However, answering the question of whether setting the VT using a DP target is a better approach to lung protection than VT/kg IBW awaits a randomized trial (RCT).
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