Applied Physiologic Analysis of Clinically Tested Protective Ventilation Strategies
摘要
The pathophysiology of acute respiratory distress syndrome (ARDS), involves changes in alveolar and alveolar duct microanatomy and dynamic inflation mechanics. These alterations predispose the lung to a secondary ventilator-induced lung injury (VILI), a topic extensively discussed in Chaps. 2 and 4 . This chapter will analyze protective ventilation strategies tested in randomized controlled trials (RCTs). Our analysis will be guided by the unifying hypothesis concerning how ARDS pathophysiology sets the stage for VILI). Specifically, we will evaluate whether these ventilation strategies effectively address the pathophysiologic mechanisms of VILI. Moreover, we’ll explore potential adjustments to enhance their lung-protective nature. The studies under scrutiny include: (1) the ARDSNetwork Acute Respiratory Management Approach (ARMA) method aims to avoid overdistension of the remaining normal lung (referred to as the “baby lung”) by employing low tidal volume (VT) and low plateau pressure (Pplat). Positive end-expiratory pressure (PEEP) is set based on oxygenation to prevent further collapse of lung tissue and mitigate the risk of slipping into the VILI vortex, (Acute Respiratory Distress Syndrome Network et al., N Engl J Med 342:1301-1308, 2000) (2) the Open Lung Approach (OLA) is a variation of the ARMA study and attempts to forcibly open collapsed lung tissue using higher PEEP, with or without recruitment maneuvers (RM) over a short period (seconds or minutes), and (3) High-Frequency Oscillation Ventilation (HFOV) is another OLA method that utilizes a higher mean airway pressure held constant with very small oscillations to facilitate gas exchange. Unfortunately, none of these methods has significantly reduced ARDS-related mortality. Recent studies have introduced physiological principles and suggested modifications in the ARMA and OLA methods. It is now recognized that the size of the VT alone is not the sole determinant of lung protection or injury. Instead, the relationship between VT, end-expiratory lung volume (EELV), and respiratory system compliance (CRS) is crucial. Applied physiology strongly supports a personalized approach involving the titration of the mechanical breath profile (MBP—all airway pressures, volumes, flows, rates, and the time during inspiration and expiration that they are applied) to minimize driving pressure (ΔP). This approach must incorporate an assessment of lung size (EELV) and pathophysiology, which ΔP does by incorporating CRS into the calculation (ΔP = VT/CRS). An effective protective ventilation strategy would use an MBP that is personalized and guided by changes in lung pathophysiology. It would have to leverage inspiratory and expiratory time to effectively counter the altered viscoelastic behavior of the lungs caused by ARDS. The objective is to gradually (hours or days) and gently reopen the lung and prevent re-collapse, facilitating its healing in its normal inflated state.