Driving pressure decoded: Precision strategies in adult respiratory distress syndrome management

Abstract

Mechanical ventilation (MV) is an important strategy for improving the survival of patients with respiratory failure. However, MV is associated with aggravation of lung injury, with ventilator-induced lung injury (VILI) becoming a major concern. Thus, ventilation protection strategies have been developed to minimize complications from MV, with the goal of relieving excessive breathing workload, improving gas exchange, and minimizing VILI. By opting for lower tidal volumes, clinicians seek to strike a balance between providing adequate ventilation to support gas exchange and preventing overdistension of the alveoli, which can contribute to lung injury. Additionally, other factors play a role in optimizing lung protection during MV, including adequate positive end-expiratory pressure levels, to maintain alveolar recruitment and prevent atelectasis as well as careful consideration of plateau pressures to avoid excessive stress on the lung parenchyma.

Key Words: Driving pressure, Mechanical ventilation, Lung-protective ventilation strategies, Ventilator-induced lung injury

Core Tip: Mechanical ventilation (MV) is an important strategy that both prolong survival of patients and improve their prognosis. However, as MV is associated with ventilator-induced lung injury, strategies to prevent and minimize lung injury in patients are needed. Currently, an increasing number of studies have shown that lowering tidal pressure and increasing positive end-expiratory pressure are beneficial for preventing lung injury. Additionally, there is growing evidence that lowering driving pressure not only preserves gas exchange but also prevents lung injury. Regardless of the technique, there is consensus that strategies to prevent lung injury are needed, and that the ultimate goal of MV should be to provide adequate gas exchange while preventing lung injury.

INTRODUCTION

Mechanical ventilation (MV) is a life-saving intervention that is employed in several situations, including single-organ failure to surgical procedures or multiple-organ failure. Ventilatory support was indispensable during the 1952 polio epidemic in Copenhagen, reducing mortality among patients with paralytic polio from over 80% to approximately 40%[1]. The importance of MV was further highlighted during the coronavirus disease pandemic when scientific societies issued guidelines on how to connect multiple patients to a single machine[2]. Therefore, understanding the mechanics of MV and safely applying them is essential for healthcare providers, especially when providing MV to those at high risk of cardiac or lung compromise. These complications may be related to the mechanical effects of the intrathoracic pressures generated by the ventilator, systemic and alveolar inflammation, or neural feedback[3].

Ventilator-induced lung injury (VILI) has currently become a major concern. MV can induce or worsen lung injury that affects patients especially those with or at risk of acute respiratory distress syndrome (ARDS). VILI occurs because of ventilation at high lung volumes, leading to alveolar rupture, air leaks, and gross barotrauma. Insidious lung injury can result in pulmonary edema due to lung overdistension. Conversely, when ventilation occurs at low lung volumes, lung injury can occur because of the opening and closing of lung units, referred to as atelectrauma. Webb and Tierney ventilated rats with high peak airway pressures, causing overdistension and zero positive end-expiratory pressures (PEEP)[4]. They showed that hypoxemia developed in these rats compared with those with the same peak airway pressures but received an additional 10 cm of water of positive end-expiratory pressure. They described an interaction between overdistention and low end-expiratory lung volume concerning lung injury. Another study by Dreyfuss et al[5] showed that pulmonary edema developed in animals undergoing ventilation with high tidal volumes compared with those undergoing ventilation with similar airway pressures but with straps around their abdomens and chests that reduced the tidal volumes. The experiments showed that lung stretching from high volumes, not airway pressure, was the most important factor for inducing lung injury; this is now referred to as volutrauma. Hence, the goal of MV is to maintain gas exchange that sustains life while minimizing VILI, and this recognition has led to a change in the philosophy of MV.

AIRWAY DRIVING PRESSURE

There is growing evidence for the benefits of lung-protective ventilation strategies in patients with and without ARDS[6,7], including the use of low tidal volumes to limit overdistension, higher PEEP to prevent atelectrauma, and recruitment maneuvers to minimize ventilation heterogeneity. Results of multiple randomized clinical trials involving patients with ARDS showed survival benefits when applying low end-inspiratory pressure with lower tidal volumes and high PEEP[8-10]. Airway driving pressure (∆P) gained attention after Amato et al[11] showed that driving pressures, as opposed to tidal volume and PEEP, were the variables that best correlated with survival in patients with ARDS.

In the landmark observational study by Amato et al[11] that analyzed over 3000 patients with ARDS, driving pressure was examined as an independent variable for predicting outcomes in ARDS. Using a statistical approach, they concluded that driving pressure was the variable most strongly associated with survival, and reductions in tidal volume or increases in positive end-expiratory pressure were beneficial only if associated with a decrease in ∆P. Therefore, ∆P is determined by variables already known to affect mortality in ARDS. Results from a meta-analysis of observational data suggests that a reduction in driving pressure is associated with a 20% reduction in the relative risk of death[11]. Compliance (the inverse of elastance) reflects the severity and extent of lung injury. Interestingly, they observed that the aerated lungs in patients with ARDS were “small” rather than “stiff,” with nearly normal compliance in the preserved areas. Driving pressures were the surrogate for cyclic lung strain imposed on ventilated and preserved lung units. Amato et al[11] hypothesized that the functional lung size of a diseased lung is better quantified by its compliance than the predicted ideal body weight. However, this study was interpreted only in patients without spontaneous respiration and did not account for patients with low chest wall compliance.

Zaidi et al[12] studied the use of driving pressures in MV as a protective strategy in improving the survival of patients with ARDS. Driving pressure is the difference between the end-inspiratory airway pressure, also known as plateau pressure, and the PEEP in the absence of spontaneous respirations. ∆P is effectively the pressure required to keep the alveoli open. Numerous trials and articles have shown that limiting tidal volume and plateau pressures while providing high PEEP can improve survival in patients with ARDS, demonstrating the importance of respiratory mechanics[13]. Because driving pressure is the tidal increase in static transpulmonary pressure, it is essentially proportional to tidal volume and inversely proportional to compliance. The authors compared various trials that demonstrated increased mortality from increased driving pressures. In their review, Zaidi et al[12] included important studies conducted by Blondonnet et al[14], which showed that delta pressure as a predictor of ARDS development, and Haudebourg et al[15], which demonstrated that delta pressure-targeted ventilation significantly reduced mechanical power, representing the energy applied to the respiratory system by the ventilator and considered a surrogate for the risk of VILI[16-18].

The authors also brought up the concept of the “baby lung,” which was also hypothesized by Amato et al[11], wherein a portion of the lung in patients with ARDS collapses or floods and does not participate in gas exchange, leaving the rest of the lung (i.e., the “baby lung”) as the only portion that participates in gas exchange. Therefore, limiting driving pressures may be a method to scale the delivered breath to the size of the lung available to participate in gas exchange rather than scaling to body size, which may be less biologically relevant. Although the concept of limiting ΔP is appealing, the question of whether manipulating ΔP rather than tidal volume is more beneficial remains controversial.

A major limitation of the use of driving pressure is its dependence on the properties of the whole respiratory system rather than just the lungs. External to the lungs, the chest wall and abdomen influence driving pressure parameters; this influence could be misleading because chest wall properties do not reflect an increased risk of lung injury. This is commonly observed in cases of increased intraabdominal pressure due to obesity, ascites, and abdominal insufflation. When external properties are abnormal, a direct measurement of transpulmonary pressure is required to appropriately quantify the damaging stress applied to the lungs from MV.

CONCLUSION

In conclusion, the goal of MV is to relieve the excessive workload of breathing and improve gas exchange without inducing iatrogenic lung injury.