Pulmonary Effects of Positive-pressure Ventilation

Abstract Summary Mechanical ventilation represents a life-support system to ensure blood gas exchange and to assist respiratory muscles to ventilate the non-compliant lung during the acute phase of lung disease or following surgery. Positive-pressure mechanical ventilation considerably differs from normal physiologic negative-pressure breathing. If applied incorrectly, mechanical ventilation can cause a secondary lung injury known as ventilator-induced lung injury (VILI). Multiple parameters that comprise the mechanical breath, including tidal volume (VT), positive end-expiratory pressure (PEEP), plateau (Pplat) and driving (ΔP) pressures, respiratory rate (RR), and airflow (Vʹ), must all be adjusted appropriately in order to minimize VILI. Numerous mechanisms have been hypothesized for VILI including (1) inspiratory stress (i.e. the respiratory system Pplat), (2) dynamic strain (i.e. the ratio between VT and the end-expiratory lung volume), (3) static strain (i.e. the end-expiratory lung volume determined by PEEP), (4) driving pressure (i.e. the difference between Pplat and PEEP), (5) energy (i.e. the changes in airway pressure as a function of VT), and (6) and power (the amount of energy as a function of RR). Two of these mechanisms are predominantly associated with VILI: (1) volutrauma, inappropriate tidal volumes leading to alveolar overdistension, and (2) atelectrauma, cyclic closing and opening of small airways and alveoli due to low PEEP levels. Understanding VILI mechanisms and identifying the optimal combination of mechanical ventilator parameters to block these mechanisms can be personalized to the pathology of each patient’s lung.