Lung Inhomogeneities and Time Course of Ventilator-induced Mechanical Injuries

Cressoni, Massimo; Chiurazzi, Chiara; Gotti, Miriam; Amini, Martina; Brioni, Matteo; Algieri, Ilaria; Cammaroto, A; Rovati, C; Massari, Dario; Castiglione, Caterina B acile di; Nikolla, K; Montaruli, C; Lazzerini, M.; Dondossola, Daniele; Colombo, Angelo; Gatti, Stefano; Valerio, Vincenza; Gagliano, Nicoletta; Carlesso, Eleonora; Gattinoni, Luciano

doi:10.1097/aln.0000000000000727

Cited by 87 publications

(83 citation statements)

References 26 publications

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“…An attractive possibility to tie the existence of a pressure range to an injury threshold is that local stress risers amplify the actual effect of applied pressure on local tissue tension-and locally inflicted power-that results from a given transpulmonary driving pressure. Damage would then propagate from those zones [10].…”

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confidence: 99%

Dynamic predictors of VILI risk: beyond the driving pressure

Marini

Jaber

2016

Intensive Care Med

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confidence: 99%

Dynamic predictors of VILI risk: beyond the driving pressure

Marini

Jaber

2016

Intensive Care Med

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confidence: 99%

“…However, convincing investigations have uncovered at least three ways in which adverse tidal cycling pressures may injure the lung: (1) over distension of already inflated alveoli, with cellular distortion, epithelial wounding, and capillary stress fracture [1]; (2) tidal opening and closure with attendant (or causal) surfactant dysfunction, liquid bridge disruption, and high interfacial surface forces [2]; and (3) stress focusing/shear at points of micromechanical heterogeneity [3]. Over the years each has had a spokesperson for its primacy, backed by an impressive body of supportive scientific literature.…”

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confidence: 99%

“…Sustained high alveolar pressure distorts but does not dramatically injure epithelium until it cycles sufficiently often to lower pressure [9]. Moreover, VILI tends to propagate from points of mechanical heterogeneity, wherever they occur [3]. Thus, experimental VILI concentrates in gravitationally dependent zones, which are subject to less transpulmonary pressure but greater stress focusing and wider swings of transpulmonary DP [10].…”

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confidence: 99%

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Does high-pressure, high-frequency oscillation shake the foundations of lung protection?

Marini

2015

Intensive Care Med

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There is a strong temptation to take a reductionist approach that would permit us to assign a single mechanistic cause for ventilation-induced lung injury (VILI) and thereby identify a simple bedside intervention to avoid its consequences. However, convincing investigations have uncovered at least three ways in which adverse tidal cycling pressures may injure the lung: (1) over distension of already inflated alveoli, with cellular distortion, epithelial wounding, and capillary stress fracture [1]; (2) tidal opening and closure with attendant (or causal) surfactant dysfunction, liquid bridge disruption, and high interfacial surface forces [2]; and (3) stress focusing/shear at points of micromechanical heterogeneity [3]. Over the years each has had a spokesperson for its primacy, backed by an impressive body of supportive scientific literature.Whatever the emphasized viewpoint, however, consensus exists that attaining high peak transpulmonary cycling pressures is an essential precondition for VILI. Excessive transpulmonary forces reflect the reduced capacity of the 'baby lung' to accept its distending and tidal volumes [4]. But with such critical elements respected and most unstable units held open, it seems reasonable that high-frequency oscillation (HFO), a strategy that targets reduced tidal volume and open lung, should be nearly ideal as a lungprotective methodology. It was therefore upsetting that a rigorously designed and executed clinical trial demonstrated that HFO could increase mortality risk [5].In this issue of Intensive Care Medicine, pioneering contributors to VILI research (Didier Dreyfuss and colleagues) present a cogent, detailed, and deliberately provocative argument that the cause of this unexpected result might be violation of the basic directive to avoid high airway pressures, with the likely mechanism being sustained and excessive tissue stretch [6]. The implication is that opening/closure and stress focusing, though acknowledged contributors to VILI at conventional ventilation frequencies, have received disproportionate attention. To evaluate the plausibility and vulnerability of this argument, the challenging complexity of VILI must be appreciated.VILI is a multifaceted process influenced by mechanical and non-mechanical factors. From the mechanical side, two factors are keys: maximal alveolar pressure and excursion of alveolar pressure. This duo is estimated clinically as the plateau and driving pressures (DP = VT/C or plateau minus PEEP), and both are important. There appears to be a fuzzy threshold of maximal applied transpulmonary pressure below which generation of extensive tissue damage is unlikely and above which the risks for cellular distortion and wounding, increased vascular permeability, and inflammation rise in nonlinear fashion [1,7]. Once above threshold, frequency of breath delivery becomes increasingly important, in part because native repair processes have inadequate time to mend cell membranes between cycles [8]. A persuasive case has been made for the primacy of surfacta...

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“…Some authors have shown that the inflamed lung releases cytokines into the blood stream, possibly leading to multi-organ failure [7,34]. There is extensive experimental evidence that mechanical ventilation itself can damage healthy lungs [15,19,26]. Several theories to explain the possible mechanisms of lung damage in healthy and diseased lungs have been proposed over the years [17,19].…”

Section: Introductionmentioning

confidence: 99%