Mechanical ventilation in acute respiratory distress syndrome (ARDS) aims to maintain gas exchange and support respiratory muscles during the critical phase of illness. It is important to prevent possible harm from ventilation-induced lung injury (VILI) during this period. Limiting tidal volumes to 6 ml/kg of predicted body weight and plateau pressures to 30 cm of H2O are considered to be crucial in preventing VILI (1). However, ARDS is characterized by non-homogenous involvement of the lung; the extent of relatively normal lung available for ventilation is highly variable and has been conceptualized as the “baby lung”(2). Hence, a ventilation strategy targeting tidal volume based on the predicted body weight may result in hyperinflation of relatively normal lungs and lead to VILI (3).
Cyclic strain leads to mechanical stress and triggers VILI. The difference between the plateau pressure (Pplat) and PEEP, known as the driving pressure (ΔP) may be a surrogate for the degree of cyclic strain.
Driving pressure (ΔP) = Pplat – PEEP
Lung compliance (CRS) = ΔV/ ΔP
Hence, ΔP = ΔV/ CRS
As evident from this equation, to maintain a constant driving pressure, the tidal volume (ΔV) must decrease as the compliance decreases. Hence, the tidal volume will need to be adjusted based on compliance to control the driving pressure. Targeting tidal volume based on predicted body weight, on the contrary, may lead to excessive driving pressures and cause VILI.
Amato et al. re-analyzed data involving 3562 patients with ARDS from nine randomized controlled trials (4). A statistical methodology called multilevel mediation analysis was used to evaluate the impact of the driving pressure as an independent predictor of survival. Four parameters, including tidal volume, Pplat, PEEP, and driving pressure were tested for possible association with survival. Three important findings were observed. 1. For a constant level of PEEP, mortality increased as the driving pressure increased (Fig. 1); 2. A higher Pplat did not increase mortality if the driving pressure was maintained constant (Fig. 2); 3. Even with similar Pplat, the mortality decreased as the driving pressure decreased (Fig. 3) (for the same Pplat, the driving pressure becomes lower with an increase of PEEP). In simple terms, even if the Pplat rose, the mortality was higher only if driving pressure increased. Another interesting finding was that the tidal volume predicted survival only if it was adjusted for compliance. The tidal volume did not predict survival when adjusted for the predicted body weight.
Fig. 1 For a constant level of PEEP (red bracket) the mortality increased with an increase of driving pressure (green bracket)
Fig. 2 A higher Pplat did not increase mortality if the driving pressure (green bracket) remained constant
Fig 3. At constant Pplat, the mortality decreased with lower driving pressures (green bracket) (Figures adapted from Amato MBP, Meade MO, Slutsky AS, Brochard L, Costa ELV, Schoenfeld DA, et al. Driving Pressure and Survival in the Acute Respiratory Distress Syndrome. N Engl J Med. 2015 Feb 19;372(8):747–55)
Aoyoma et al. performed a meta-analysis including secondary analyses of five randomized controlled and two observational studies to assess the mortality risk associated with high driving pressures (5). They found a significant association of higher driving pressures with increased mortality among patients with ARDS (RR, 1.44; 95% CI, 1.11–1.88). From a sensitivity analysis of three studies with similar driving pressure thresholds, the authors suggested a target driving pressure of 13–15 cm of H2O.
Lung stress (calculated from esophageal and airway pressures), driving pressure, and lung and chest wall elastance were studied in 150 patients with ARDS at PEEP levels of 5 and 15 cm H2O (6). At both PEEP levels, increasing driving pressures were significantly associated with lung stress. The optimal cutoff value of driving pressure was 15 cm of H2O to prevent significant lung stress.
The driving pressure may also be useful as a tool to titrate PEEP for optimizing lung recruitment. Lower driving pressures for a constant tidal volume with increasing levels of PEEP suggests improved compliance and potential for recruitment (7).
VILI may be conceptualized to occur from excessive mechanical power applied to the lung (8). The mechanical power may be directly related to the driving pressure; high tidal volumes probably contribute to the damage indirectly through an increase in driving pressures. The mechanical power applied to the lung may also be a function of the respiratory rate. The lack of benefit with high-frequency oscillation ventilation, despite minimal tidal excursions, may be related to the rate-related increase in mechanical power.
There are several caveats to the application of the concept of driving pressure to clinical practice. First, the driving pressure may be significant only within the range of airway pressures commonly employed in clinical practice (Pplat less than 40 and PEEP more than 5 cm of H2O). Second, measurement of Pplat and driving pressure in spontaneously breathing patients is unreliable; hence driving pressure-guided ventilation is applicable only in patients who do not have spontaneous breathing efforts. Third, most of the available data are based on secondary analysis from previous randomized controlled studies. Controlled studies comparing driving pressure-guided with tidal volume and Pplat-guided ventilatory management are required to validate the applicability of driving pressure in clinical practice; besides, optimal cutoff levels for driving pressure need to be defined.
The bottom line
- A ventilatory strategy targeting tidal volume and plateau pressure may not prevent VILI.
- Conventionally accepted limits for “low” tidal volume may lead to hyperinflation and injury to relatively normal lung regions in ARDS.
- The driving pressure (Pplat – PEEP) may be a more significant determinant of the mechanical power applied to the lungs.
- Secondary analysis of previous randomized controlled studies of ARDS suggests that a higher Pplat does not increase mortality at constant driving pressures.
- Similarly, a lower driving pressure may reduce mortality for the same level of Pplat.
- Based on the limited evidence available, a target driving pressure of 13-15 cm of H2O may be appropriate to prevent VILI.
- Controlled studies are required to validate the superiority of driving pressure targeted ventilator management with a tidal volume and Pplat-guided approach.
- Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. N Engl J Med. 2000 May 4;342(18):1301–8.
- Gattinoni L, Pesenti A. The concept of “baby lung.” Intensive Care Med. 2005 Jun;31(6):776–84.
- Terragni PP, Rosboch G, Tealdi A, Corno E, Menaldo E, Davini O, et al. Tidal hyperinflation during low tidal volume ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2007 Jan 15;175(2):160–6.
- Amato MBP, Meade MO, Slutsky AS, Brochard L, Costa ELV, Schoenfeld DA, et al. Driving Pressure and Survival in the Acute Respiratory Distress Syndrome. N Engl J Med. 2015 Feb 19;372(8):747–55.
- Aoyama H, Pettenuzzo T, Aoyama K, Pinto R, Englesakis M, Fan E. Association of Driving Pressure With Mortality Among Ventilated Patients With Acute Respiratory Distress Syndrome: A Systematic Review and Meta-Analysis*. Crit Care Med. 2018 Feb;46(2):300–6.
- Chiumello D, Carlesso E, Brioni M, Cressoni M. Airway driving pressure and lung stress in ARDS patients. Crit Care [Internet]. 2016 Aug 22 [cited 2019 Mar 4];20. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4993008/
- Aoyama H, Yamada Y, Fan E. The future of driving pressure: a primary goal for mechanical ventilation? J Intensive Care [Internet]. 2018 Dec [cited 2019 Mar 4];6(1). Available from: https://jintensivecare.biomedcentral.com/articles/10.1186/s40560-018-0334-4
- Gattinoni L, Quintel M. How ARDS should be treated. Crit Care [Internet]. 2016 Dec [cited 2019 Mar 4];20(1). Available from: http://ccforum.biomedcentral.com/articles/10.1186/s13054-016-1268-7