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Regional physiology of ARDS
© The Author(s). 2017
- Published: 28 December 2017
The acute respiratory distress (ARDS) lung is usually characterized by a high degree of inhomogeneity. Indeed, the same lung may show a wide spectrum of aeration alterations, ranging from completely gasless regions, up to hyperinflated areas. This inhomogeneity is normally caused by the presence of lung edema and/or anatomical variations, and is deeply influenced by the gravitational forces.
For any given airway pressure generated by the ventilator, the pressure acting directly on the lung (i.e., the transpulmonary pressure or lung stress) is determined by two main factors: 1) the ratio between lung elastance and the total elastance of the respiratory system (which has been shown to vary widely in ARDS patients, between 0.2 and 0.8); and 2) the lung size. In severe ARDS, the ventilatable parenchyma is strongly reduced in size (‘baby lung’); its resting volume could be as low as 300 mL, and the total inspiratory capacity could be reached with a tidal volume of 750–900 mL, thus generating lethal stress and strain in the lung. Although this is possible in theory, it does not explain the occurrence of ventilator-induced lung injury (VILI) in lungs ventilated with much lower tidal volumes. In fact, the ARDS lung contains areas acting as local stress multipliers and they could multiply the stress by a factor ~ 2, meaning that in those regions the transpulmonary pressure could be double that present in other parts of the same lung. These ‘stress raisers’ widely correspond to the inhomogenous areas of the ARDS lung and can be present in up to 40% of the lung.
Although most of the literature on VILI concentrates on the possible dangers of tidal volume, mechanical ventilation in fact delivers mechanical power (i.e., energy per unit of time) to the lung parenchyma, which reacts to it according to its anatomical structure and pathophysiological status. The determinants of mechanical power are not only the tidal volume, but also respiratory rate, inspiratory flow, and positive end-expiratory pressure (PEEP). In the end, decreasing mechanical power, increasing lung homogeneity, and avoiding reaching the anatomical limits of the ‘baby lung’ should be the goals for safe ventilation in ARDS.
During the acute respiratory failure caused by inflammatory edema—the condition to which we will limit our discussion—the lungs present a high degree of inhomogeneity . Indeed aerated, poorly aerated, and consolidated/collapsed regions do coexist throughout the lung parenchyma.
From the sternum to the vertebrae and in the supine position, the lung with acute inflammatory edema (acute respiratory distress syndrome (ARDS)) presents as a rough simplification: 1) few regions of possible hyperinflation (difficult to define by computed tomography (CT) due to the increased lung mass); 2) regions with normal ratio between gas and tissue (usually defined as well aerated); 3) regions with gas-tissue ratios lower than normal (usually defined as the ones with a ratio between gas and tissue below 1); and 4) completely gasless areas in the most dependent lung regions (situated at different lung heights depending on the severity of the syndrome). It is important to realize that these gasless regions may be due either to a complete collapse of ‘empty’ pulmonary units (which can be possibly reopened and refilled with gas) or to a complete consolidation of the pulmonary units, in which the inner space is occupied by solid/liquid material . Obviously, the differences in lung inflation are a signal of inhomogeneity and we may infer that the difference in gas-tissue ratio (i.e., in inflation) between different lung regions may be due either to anatomical variations in a given area of interest, or to the presence of different forces acting on contiguous structures of the lung parenchyma.
The interest for the pathophysiology of the ARDS lung derives from the need (in most of these patients) for mechanical ventilation. This technique substitutes the respiratory muscles, completely or in part, in the role of providing the energy needed to inflate the lung. Therefore, the possible harm of mechanical ventilation derives from the interaction between the anatomical-physiological characteristics of the lung parenchyma and the mechanical power delivered to it. Ideally, a proper setting of mechanical ventilation should find the best compromise between mechanical power and lung structure. In extreme synthesis, we should provide the lowest mechanical power in a parenchyma made as much homogeneous as possible. In this brief paper we will give our view on the interaction between mechanical power and regional lung physiology.
Forces acting on the lung
where Pawplat is the airway plateau pressure, Pawend–exp is the airway pressure at PEEP or ZEEP, Pesplat is the esophageal pressure at plateau and Pesend–exp is the esophageal pressure at PEEP or ZEEP.
where ∆PL is the driving transpulmonary pressure, ∆Paw is the driving airway pressure, EL is the lung elastance and Ers is the total elastance of the respiratory system (i.e., Ers = EL + Ew, where Ew is the chest wall elastance).
The stress raisers
from which it has been often claimed that at 30 cmH2O the local pressure could be as high as ~ 120 cmH2O . Actually, when we estimated the inhomogeneity by comparing the inflation ratio of neighboring lung regions , we found that the multiplication factor was ~ 2. According to the ARDS severity, the stress raisers were present in up to 40% of the lung parenchyma, suggesting that a given transpulmonary pressure is doubled in ~ 40% of the lung.
The literature on VILI concentrates primarily on the possible danger of tidal volume. Recently the possible relevance of airway driving pressure (i.e., tidal volume normalized to the respiratory system compliance) has been emphasized . Other possible causes of VILI have been identified in the respiratory rate  and in the inspiratory flow . Additional factors, such as total/regional perfusion, local acidity, and temperature, may play a role in modulation of VILI but, for simplicity, will not be considered here.
This ‘mechanical hypothesis’ obviously needs further studies: 1) the mechanical power should be related to the transpulmonary pressure; and 2) it should be normalized for lung size and, likely, for specific lung elastance to allow comparison between different mammalian species. It is possible that in identifying an unsafe threshold for mechanical ventilation, based on ‘lung-directed/normalized’ mechanical power, a more rational approach to safe mechanical ventilation and indications for possible extracorporeal support may be established.
Whatever the decrease in mechanical power (due to the reduction of whichever of its components) should decrease the likelihood of ventilator-induced lung injury.
The best available maneuver to increase lung homogeneity (without causing any increase in mechanical power) is prone positioning . This is clearly indicated in patients with moderate-severe and severe ARDS, who present with the highest degree of lung inhomogeneity.
PEEP has a dual effect: on one side, it may decrease lung inhomogeneity, at least in the patients in whom lung collapse can be substantially reduced. On the other hand, for a given tidal volume, PEEP increases the mechanical power and the likelihood of reaching the anatomical threshold for VILI, i.e., the total lung capacity.
The authors declare no funding. Publication of this supplement was supported by Fresenius Kabi.
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This article has been published as part of Critical Care Volume 21 Supplement 3, 2017: Future of Critical Care Medicine (FCCM) 2016. The full contents of the supplement are available online at https://ccforum.biomedcentral.com/articles/supplements/volume-21-supplement-3.
LG designed the paper and drafted the manuscript. TT helped draft the manuscript and revised it critically for important intellectual content. MQ helped draft the manuscript and revised it critically for important intellectual content. All authors approved the final manuscript.
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