Regional physiology of ARDS

Abstract

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.

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Figures

Fig. 1

Strain (tidal volume divided by the functional residual capacity) and total lung capacity (y axis) are represented as a function of the applied transpulmonary pressure (x axis) [22]. In the resting position, the collagen fibers are folded within the elastic spring [23]. Increasing the transpulmonary pressure, the excessive strain may lead firstly to an inflammatory reaction and, when the collagen is completely unfolded, to stress at rupture. At ~ 12 cmH2O transpulmonary pressure (i.e., the specific elastance), the initial lung volume is doubled [7]

Fig. 2

Visceral pleura from which an alveolar wall departs. The interface between these two structures of different elasticity acts as a stress raiser with a possible local multiplication of stress and strain. Photograph courtesy of Dr. Edward C. Klatt, M.D., © WebPath

Fig. 3

a The first button-like densities (arrows) appear at the interface with the visceral pleura and, after 20 h of 2.5 strain ventilation (b), are extended to the whole parenchyma. Note that these VILI lesions are almost fully recruitable, suggesting that they develop primarily as interstitial edema

Fig. 4

Relationship between the power computed through the power equation and that measured through the graphic analysis of the pressure-volume loops. As shown, the relationship (p < 0.001) is close to the identity line