Driving Pressure & Transpulmonary Pressure

Elizabeth C. Williams, M. D., Gabriel C. Motta-Ribeiro, D. Sc., Marcos F. Vidal Melo, M. D., Ph. D. C

To prevent lung injury during mechanical ventilation, the factors causing most injury to the lungs must be identified. In the centuries-old engineering field of materials science, limits of maximal stress and strain are listed as key possible causes for materials to fail and rupture under the action of external loads. Recently, these concepts of stress and strain have been applied to increase understanding of mechanisms of injury during mechanical ventilation8–10 and better explain the positive clinical outcomes associated with lung-protective ventilation. 5–8,10–12 Stress is defined as a force divided by the area over which it is applied.

Intuitively, if a fixed force is distributed throughout a large cross-sectional area of lung tissue, the force per unit area (i. e. , stress) will be smaller than if that same force were distributed over a smaller area of lung tissue. More stress is expected to increase the risk of injury. Strain is a measure of a change in the dimension of a structure from its original dimension. For instance, linear strain is defined as change in length divided by the original length (fig. 1). The most pertinent strain in ventilation is the volumetric strain created by inspiration and expiration. Volumetric strain is defined as change in volume divided by initial volume. In elastic materials, strain is directly proportional to stress.

Volumetric strain during ventilation has both static and dynamic components and is heterogeneous throughout the lungs. 8 Downloaded from http://pubs. asahq. org/anesthesiology/article-pdf/131/1/155/454902/20190700_0-00034. pdf by guest on 24 June 2023

• ncern over the potential for lung injury due to mechanical ventilation has fueled investigations on lung protection in the operating room.1–3 Based on the intensive care literature,4 tidal volume (VT) and positive end-expiratory pressure (PEEP) settings have been the focus of intraoperative clinical trials.1–3 Recent results in acute respiratory distress syndrome (ARDS)5 and surgical patients6,7 have suggested that the benefits associated with

VT and PEEP settings are mediated by driving pressures. As our understanding of the physical and biologic effects

• f mechanical ventilation evolves, the concepts of driving pressure and transpulmonary pressure have been increasingly used to quantify the mechanical forces acting over the lungs during mechanical ventilation and to guide clinical care. In this perspective, we discuss the definition of those concepts, their measurement in the clinical setting, their interpretation, and their use in typical scenarios.

During tidal breathing, the change in lung volume is represented by VT, and the initial lung volume corresponds to the functional residual capacity (FRC). Global volumetric lung strain can, thus, be estimated as VT/FRC. This relationship shows that reduction of VT lowers lung strain, and also that FRC can have an effect on strain. The markedly low FRC of ARDS patients emphasizes the relevance of this concept. For instance, with a VT of 500 ml, a healthy lung during anesthesia (FRC, 2,000 ml) would have a strain of 25% (500/2,000). That same VT in an ARDS patient (FRC, 500 ml) would produce a strain of 100% (500/500), a fourfold increase in strain and augmented risk of injury.

These considerations also suggest that, while reducing VT is important in surgical and ARDS patients,4,12 VT is not the final determinant of lung injury. This is because it does not take the size of lung parenchyma to which that VT applies (FRC) into account. Consequently, simply controlling VT is not enough to minimize injurious lung strain. These arguments are consistent with recent clinical outcome results in ARDS and surgical patients showing that the effect of VT on clinical outcomes is mediated by a variable associated with lung strain. 5–7 The heterogeneity of lung expansion, e. g. , as lung derecruitment develops, also increases the risk for lung injury.

This is because this heterogeneity can produce regional strains larger than whole-lung strains in healthy and inflamed lungs of anesthetized ventilated large animals even if those whole-lung strains are acceptable. 8,13 Theoretical computations indicated that in heterogeneously inflated lungs, regional pressures could be substantially larger than whole-lung pressures, by as much as three to four times when an atelectatic area is surrounded by expanded lung. 14 Systemic inflammation, a common clinical finding, amplifies the injurious effect of strain. 10,15 This article is featured in “This Month in Anesthesiology,” page 1A. Submitted for publication September 5, 2018. Accepted for publication March 12, 2019.

From the Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts. Current Affiliation: Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland (E. C. W.)

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Driving pressure is composed of two pressures: that distributed to the lung itself, the transpulmonary pressure (∆PL), and that applied to the chest wall (∆Pcw). Rearrangement of the standard respiratory system compliance (CRS) equation leads to driving pressure as equal to the tidal volume (VT) divided by CRS. Strain is a measure of material deformation relative to its original state. For example, the linear displacement of a spring (∆L) relative to its rest length (Lo), or equivalently the ratio of VT to functional residual capacity (FRC). As CRS changes in proportion to FCR, i. e., FRC = k × CRS, VT/CRS is an approximation of tidal volume normalized to FRC, and ∆P is proportional to lung strain. TLC, total lung capacity; VL, lung volume.

Driving pressure is defined as plateau pressure minus PEEP (fig. 1). 16 Plateau pressure is measured at the end of an inspiratory pause during volume-controlled constant flow ventilation and at the end of inspiration during pressure-controlled ventilation. Accordingly, in the absence of respiratory muscle effort by the patient, driving pressure is the pressure above PEEP applied to the entire respiratory system to achieve tidal ventilation. A caveat on the computation of plateau pressures is that they cannot be presumed to represent end-inspiratory alveolar pressures when end-inspiratory flows are not zero, indicating lack of equilibration between airway and alveolar pressures.

During volume-controlled ventilation, an inspiratory pause greater than or equal to 3 s provides best accuracy for plateau pressure measurements in normal and diseased lungs. 17,18 Short inspiratory pauses of 0. 5 s overestimate plateau pressure by 11% in ARDS patients and 17% in chronic obstrictive pulmonary disease patients. 17 Examination of the airway pressure tracing available in current anesthesia machines for the presence of a plateau at the end of the inspiratory pause allows for better decision on reliability of plateau pressure measurement.

Auto-PEEP is another potential source of error by leading to driving pressure overestimation as the end-expiratory pressure in alveolar units would be higher than the PEEP set in the ventilator and used to compute the driving pressure. It is important to recognize that driving pressure and total airway pressure measured during mechanical ventilation have two components: one related to the expansion of the lungs, the other to the expansion of the chest wall. Each

• f these two components can change substantially during disease and surgical conditions and affect the interpretation
• f the driving pressure measurements.

Downloaded from http://pubs. asahq. org/anesthesiology/article-pdf/131/1/155/454902/20190700_0-00034. pdf by guest on 24 June 2023 Fig. 1. Driving pressure (∆P) is calculated as the difference between plateau pressure (Pplat) and positive end-expiratory pressure (PEEP).

Transpulmonary pressure is defined as the pressure difference between the airway opening and the pleural surface (fig. 2). 19,20 Accordingly, transpulmonary pressure comprises the pressure to move air through the airways (airway opening – alveolar pressure) and the pressure to overcome the lung tissue elastic recoil (alveolar – pleural pressure), the latter most frequently associated with lung injury. 19 Although continuous estimation of transpulmonary pressure is feasible, it is usually assessed at two critical points during the breathing cycle: the end of inspiration, relevant to prevent hyperinflation, and the end of expiration, relevant to avoid lung derecruitment.

If respiratory flows are zero at these points, the airway pressures (plateau pressure at end-inspiration and PEEP at end-expiration) are presumed to represent alveolar pressures, a reasonable assumption in the absence of gas trapping. 21 This approach to measure transpulmonary pressure may have led to the misconception that it exclusively expresses pressures at the alveolar level. 19,22,23 The essential concept is that in static, i. e. , zero flow, conditions (end-inspiration and end-expiration), the transpulmonary pressure approximates the lung tissue elastic recoil component, which is the relevant pressure to quantify stress applied Downloaded from http://pubs. asahq. org/anesthesiology/article-pdf/131/1/155/454902/20190700_0-00034.

pdf by guest on 24 June 2023 Fig. 2. Airway opening, esophageal (Peso), and transpulmonary pressures (PL) measurements. PL is defined as the difference between airway

• pening pressure (blue lines) and pleural pressure. Pleural pressure is frequently estimated from esophageal balloon pressure measurements (Peso). Using a specific protocol, the esophageal balloon is placed in the lower third of the esophagus (A). Cardiac oscillations in Peso (B, green lines) indicate accurate placement of the balloon, which can be confirmed by observation of similar airway pressure and Peso measurements as gentle chest compressions are performed during expiratory pause or with occluded airway opening (A). PL can be estimated as the difference between airway and esophageal pressures (red and orange lines). Interventions such as pneumoperitoneum (B, mid panel) produce a marked change in driving pressures (∆P = plateau pressure, PPlat, minus positive end-expiratory pressure, PEEP). In this example, ∆P increased by 7 cm H2O. Yet ∆PL (end-inspiratory PL, PL EI, minus end-expiratory PL, PL EE) does not increase to the same degree as ∆P and

PPlat. The change in ∆PL in this example was 4 cm H2O. This demonstrates that part of the increases in ∆P and PPlat are due to the chest wall component and not to pressures applied to the lung parenchyma. This contribution of the chest wall is evidenced by the increased EI to EE

• scillation in Peso after as compared to before pneumoperitoneum.

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