Driving Pressure and Transpulmonary Pressure: How Do We Guide Safe Mechanical Ventilation?

Abstract

The physiological concept, pathophysiological implications and clinical relevance and application of driving pressure and transpulmonary pressure to prevent ventilator-induced lung injury are discussed.

Fig. 1.

Driving pressure (ΔP) is calculated as the difference between plateau pressure (P_plat) and positive end-expiratory pressure (PEEP). Driving pressure is composed of two pressures: that distributed to the lung itself, the transpulmonary pressure (ΔP_L), and that applied to the chest wall (ΔP_cw). Rearrangement of the standard respiratory system compliance (C_RS) equation leads to driving pressure as equal to the tidal volume (V_T) divided by C_RS. Strain is a measure of material deformation relative to its original state. For example, the linear displacement of a spring (ΔL) relative to its rest length (L_o), or equivalently the ratio of V_T to residual functional capacity (FRC). As C_RS changes in proportion to FCR, i.e FRC=k × C_RS, V_T/C_RS is an approximation of tidal volume normalized to FRC, and ΔP is proportional to lung strain. TLC=Total lung capacity. V_L = lung volume.

Fig.2.

Airway opening, esophageal (P_eso) and transpulmonary pressures (P_L) measurements. P_L is defined as the difference between airway opening pressure (blue lines) and pleural pressure. Pleural pressure is frequently estimated from esophageal balloon pressure measurements (P_eso). Using a specific protocol, the esophageal balloon is placed in the lower third of the esophagus (2A). Cardiac oscillations in P_eso (2B, green lines) indicate accurate placement of the balloon, which can be confirmed by observation of similar airway pressure and P_eso measurements as gentle chest compressions are performed during expiratory pause or with occluded airway opening (2A). P_L can be estimated as the difference between airway and esophageal pressures (red and orange lines). Interventions such as pneumoperitoneum (2B, mid panel) produce a marked change in driving pressures (ΔP = plateau pressure, P_Plat, minus positive end-expiratory pressure, PEEP). In this example, ΔP increased by 7 cmH₂O. Yet, delta P_L (end-inspiratory P_L, P_L EI, minus end-expiratory P_L, P_L EE) does not increase to the same degree as ΔP and P_Plat. The change in delta P_L in this example was 4 cm H₂O. This demonstrates that part of the increase in ΔP and P_Plat 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 end-inspiratory (EI) to end-expiratory (EE) oscillation in P_eso after as compared to before pneumoperitoneum. In addition, the esophageal pressure at end-expiration (P_eso EE, at ~4 seconds on time scale) is positive before pneumoperitoneum while it is negative after pneumoperitoneum. This implies mechanical conditions consistent with lung collapse after pneumoperitoneum. Indeed, while P_L did not increase by the same magnitude as ΔP, it also increased, indicating loss of lung compliance. Such conditions could prompt use of higher PEEP to prevent lung derecruitment.

Fig. 3.

Approach for use of driving and transpulmonary pressures to guide mechanical ventilation during anesthesia. Limits presented are based on current experimental and clinical literature. Safety limits have not yet been defined in clinical trials.