Body position does not influence the location of ventilator-induced lung injury

Nishimura, Masaji; Honda, Osamu; Tomiyama, Noriyuki; Johkoh, Takeshi; Kagawa, Kazufumi; Nishida, Teruo

doi:10.1007/s001340000664

Cited by 32 publications

(24 citation statements)

References 12 publications

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“…CT allows an opportunity to address mechanisms underlying VILI in future studies, both in the presence or absence of sepsis. Similar to what has been reported in nonseptic animals (27), VILI occurred predominantly in dependent regions first in both sham and CLP rats (Figs. 5 and 7).…”

Section: Discussionsupporting

confidence: 88%

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Cecal ligation and puncture accelerates development of ventilator-induced lung injury

Yehya

Xin

Oquendo

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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-Sepsis is a leading cause of respiratory failure requiring mechanical ventilation, but the interaction between sepsis and ventilation is unclear. While prior studies demonstrated a priming role with endotoxin, actual septic animal models have yielded conflicting results regarding the role of preceding sepsis on development of subsequent ventilator-induced lung injury (VILI). Using a rat cecal ligation and puncture (CLP) model of sepsis and subsequent injurious ventilation, we sought to determine if sepsis affects development of VILI. Adult male Sprague-Dawley rats were subject to CLP or sham operation and, after 12 h, underwent injurious mechanical ventilation (tidal volume 30 ml/kg, positive end-expiratory pressure 0 cmH 2O) for either 0, 60, or 120 min. Biochemical and physiological measurements, as well as computed tomography, were used to assess injury at 0, 60, and 120 min of ventilation. Before ventilation, CLP rats had higher levels of alveolar neutrophils and interleukin-1␤. After 60 min of ventilation, CLP rats had worse injury as evidenced by increased alveolar inflammation, permeability, respiratory static compliance, edema, oxygenation, and computed tomography. By 120 min, CLP and sham rats had comparable levels of lung injury as assessed by many, but not all, of these metrics. CLP rats had an accelerated and worse loss of end-expiratory lung volume relative to sham, and consistently higher levels of alveolar interleukin-1␤. Loss of aeration and progression of edema was more pronounced in dependent lung regions. We conclude that CLP initiated pulmonary inflammation in rats, and accelerated the development of subsequent VILI.sepsis; acute lung injury NONPULMONARY SEPSIS IS A leading cause of acute respiratory distress syndrome (15); however, the etiology of the lung injury from sepsis is unclear. This is confounded by the fact that many septic patients with respiratory failure require mechanical ventilation, which itself causes injury from regional overdistension and cyclic reopening of atelectatic lung (22). This ventilator-induced lung injury (VILI) is characterized by epithelial (7, 9) and endothelial (12, 37) dysfunction, with barrier failure leading to alveolar flooding. Because sepsis and VILI share similar proinflammatory cytokine profiles (34), it is possible that an initial septic insult predisposes lungs for secondary injury from VILI.Characterization of potential interaction between sepsis and VILI requires appropriate animal models that both recapitulate the proinflammatory cascade seen in humans and allow for the testing of a priming septic insult on development of subsequent VILI. The cecal ligation and puncture (CLP) model and its variants (8) induce a systemic inflammatory response from a polymicrobial abdominal infection. CLP, unlike surrogates like endotoxin injection (31), recreates sepsis progression most similarly to humans, with comparable hemodynamic and inflammatory profiles (8).Exogenous endotoxin administration is well established to predispose lung to further injury (5, 39)...

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Section: Discussionsupporting

confidence: 88%

“…We provide for the first time imaging analysis of septic rats subjected to injurious ventilation. This is one of the few studies to radiographically characterize VILI in sham animals (27). CT allows an opportunity to address mechanisms underlying VILI in future studies, both in the presence or absence of sepsis.…”

Section: Discussionmentioning

confidence: 99%

Cecal ligation and puncture accelerates development of ventilator-induced lung injury

Yehya

Xin

Oquendo

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…In the prone position, in both humans [72] and experimental settings [73], regional inflation is more uniformly distributed along the vertical axis, indicating a significant reduction in the PL gradient. This suggests that the stress and strain are more homogeneously distributed within the lung parenchyma, and this is the rational basis for the possible effectiveness of prone positioning in attenuating VILI, as shown experimentally in dogs [59] and rabbits [60]. Unfortunately proof is still lacking in patients that prone positioning affects outcome.…”

Section: Prone Positioningmentioning

confidence: 99%

“…In some experiments, VILI was induced by using different VT normalised to body weight (in kilograms) (table 2) [43,48,49,59,60]. Unfortunately, lung volume, alveolar size and body weight are not linearly related across the various species.…”

Section: Ventilator-induced Lung Injury and Speciesmentioning

confidence: 99%

Physical and biological triggers of ventilator-induced lung injury and its prevention

Gattinoni¹,

Carlesso²,

Cadringher³

et al. 2003

European Respiratory Journal

272

185

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Ventilator-induced lung injury is a side-effect of mechanical ventilation. Its prevention or attenuation implies knowledge of the sequence of events that lead from mechanical stress to lung inflammation and stress at rupture.A literature review was undertaken which focused on the link between the mechanical forces in the diseased lung and the resulting inflammation/rupture.The distending force of the lung is the transpulmonary pressure. This applied force, in a homogeneous lung, is shared equally by each fibre of the lung9s fibrous skeleton. In a nonhomogeneous lung, the collapsed or consolidated regions do not strain, whereas the neighbouring fibres experience excessive strain. Indeed, if the global applied force is excessive, or the fibres near the diseased regions experience excessive stress/strain, biological activation and/or mechanical rupture are observed. Excessive strain activates macrophages and epithelial cells to produce interleukin-8. This cytokine recruits neutrophils, with consequent full-blown inflammation.In order to prevent initiation of ventilator-induced lung injury, transpulmonary pressure must be kept within the physiological range. The prone position may attenuate ventilator-induced lung injury by increasing the homogeneity of transpulmonary pressure distribution. Positive end-expiratory pressure may prevent ventilator-induced lung injury by keeping open the lung, thus reducing the regional stress/strain maldistribution. If the transpulmonary pressure rather than the tidal volume per kilogram of body weight is taken into account, the contradictory results of the randomised trials dealing with different strategies of mechanical ventilation may be better understood. Eur Respir J 2003; 22: Suppl. 47, 15s-25s.

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“…However, lung overdistension (excessive pressure applied to acutely-injured parenchyma) can occur without concomitant overinflation [14]; consequently, the rationale for optimal PEEP level selection (PEEP optimising arterial oxygenation and minimising oxygen toxicity/VILI risks) still holds. Prone positioning may attenuate VILI [15][16][17]. Prone position causes more homogenous lung inflation and eliminates lung compression by the heart and abdominal contents, thus limiting atelectasis [14,18,19].…”

mentioning

confidence: 99%

Prone position reduces lung stress and strain in severe acute respiratory distress syndrome

Mentzelopoulos

Roussos²,

Zakynthinos³

2005

European Respiratory Journal

130

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The present authors hypothesised that in severe acute respiratory distress syndrome (ARDS), pronation may reduce ventilator-induced overall stress (i.e. transpulmonary pressure (PL)) and strain of lung parenchyma (i.e. tidal volume (VT)/end-expiratory lung volume (EELV) ratio), which constitute major ventilator-induced lung injury determinants. The authors sought to determine whether potential pronation benefits are maintained in post-prone semirecumbent (SRPP) posture under pressure-volume curve-dependent optimisation of positive end-expiratory pressure (PEEP).A total of 10 anesthetised/paralysed, mechanically ventilated (VT59.0¡0.9 mL?kg -1 predicted body weight; flow50.91¡0.04 L?s -1 ; PEEP59.4¡1.3 cmH 2 O) patients with early/severe ARDS were studied in pre-prone semirecumbent (SRBAS), prone, and SRPP positions. Partitioned respiratory mechanics were determined during iso-flow (0.91 L?s -1 ) experiments (VT varied within 0.2-1.0 L), along with haemodynamics, gas exchange, and EELV. Compared with SRBAS, pronation/SRPP resulted in reduced peak/plateau PL at VTso0.6 L; static lung elastance and additional lung resistance decreased and chest wall elastance (in prone position) increased; EELV increased (23-33%); VT/EELV decreased (27-33%); arterial oxygen tension/inspiratory oxygen fraction and arterial carbon dioxide tension improved (21-43/10-14%, respectively), and shunt fraction/physiological dead space decreased (21-50/20-47%, respectively).In early/severe acute respiratory distress syndrome, pronation under positive end-expiratory pressure optimisation may reduce ventilator-induced lung injury risk. Pronation benefits may be maintained in post-prone semirecumbent position.

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Body position does not influence the location of ventilator-induced lung injury

Abstract: Body position affected the time course of the development of VILI, but it did not affect the location.

Cited by 32 publications

References 12 publications

Cecal ligation and puncture accelerates development of ventilator-induced lung injury

Cecal ligation and puncture accelerates development of ventilator-induced lung injury

Physical and biological triggers of ventilator-induced lung injury and its prevention

Prone position reduces lung stress and strain in severe acute respiratory distress syndrome

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