The Open Lung Approach Improves Pulmonary Vascular Mechanics in an Experimental Model of Acute Respiratory Distress Syndrome

Santos, Arnoldo; Lucchetta, Luca; Monge-Garcia, M Ignacio; Borges, João Batista; Tusman, Gerardo; Hedenstierna, Göran; Larsson, Anders; Suárez-Sipmann, Fernando

doi:10.1097/ccm.0000000000002082

Cited by 11 publications

(16 citation statements)

References 26 publications

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Section: Pulmonary Vascular Mechanics (Pvm) In Ards and Ventilator-inmentioning

confidence: 99%

“…In a recent experimental ARDS model, Santos and colleagues tested whether PEEP consistent with an open lung approach (OLA) improves PVM compared to higher or lower PEEP (28). In that study, the PEEP level associated with the highest compliance during a decremental PEEP trial after lung recruitment resulted in best PVM (as measured by effective arterial elastance and vascular compliance) compared to higher or lower PEEP settings (28,29). In concept, the Acute Respiratory Distress Syndrome Network (ARDSnet) approach (30), which aims at limiting VT (adapted to the reduced size of the functional lung) and entails more heterogeneity in the distribution of ventilation due to the persistence of dependent lung collapse, differs from the OLA.…”

Section: Pulmonary Vascular Mechanics (Pvm) In Ards and Ventilator-inmentioning

confidence: 99%

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Physiology-guided management of hemodynamics in acute respiratory distress syndrome

Cortes-Puentes¹,

Oeckler²,

Marini³

2018

Ann. Transl. Med.

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Skillfully implemented mechanical ventilation (MV) may prove of immense benefit in restoring physiologic homeostasis. However, since hemodynamic instability is a primary factor influencing mortality in acute respiratory distress syndrome (ARDS), clinicians should be vigilant regarding the potentially deleterious effects of MV on right ventricular (RV) function and pulmonary vascular mechanics (PVM). During both spontaneous and positive pressure MV (PPMV), tidal changes in pleural pressure (P PL), transpulmonary pressure (P TP , the difference between alveolar pressure and P PL), and lung volume influence key components of hemodynamics: preload, afterload, heart rate, and myocardial contractility. Acute cor pulmonale (ACP), which occurs in 20-25% of ARDS cases, emerges from negative effects of lung pathology and inappropriate changes in P PL and P TP on the pulmonary microcirculation during PPMV. Functional, minimally invasive hemodynamic monitoring for tracking cardiac performance and output adequacy is integral to effective care. In this review we describe a physiology-based approach to the management of hemodynamics in the setting of ARDS: avoiding excessive cardiac demand, regulating fluid balance, optimizing heart rate, and keeping focus on the pulmonary circuit as cornerstones of effective hemodynamic management for patients in all forms of respiratory failure.

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Section: Pulmonary Vascular Mechanics (Pvm) In Ards and Ventilator-inmentioning

confidence: 99%

Section: Pulmonary Vascular Mechanics (Pvm) In Ards and Ventilator-inmentioning

confidence: 99%

Physiology-guided management of hemodynamics in acute respiratory distress syndrome

Cortes-Puentes¹,

Oeckler²,

Marini³

2018

Ann. Transl. Med.

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“…Whether to try to recruit collapsed lungthe so-called "open lung approach"-or leave it derecruited is thus a key question that continues to vex the clinical community (31). Promising results with the open-lung approach in animal models have been obtained [e.g., (32)], but recent studies in patients have been inconclusive (33,34). It thus remains a puzzle as to why a strategy that appears to be based on such sound physiological principles should not be resoundingly successful in the clinic.…”

mentioning

confidence: 99%

Ventilator-induced lung injury and lung mechanics

Bates

Smith

2018

Ann. Transl. Med

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Mechanical ventilation applies physical stresses to the tissues of the lung and thus may give rise to ventilator-induced lung injury (VILI), particular in patients with acute respiratory distress syndrome (ARDS). The most dire consequences of VILI result from injury to the blood-gas barrier. This allows plasma-derived fluid and proteins to leak into the airspaces where they flood some alveolar regions, while interfering with the functioning of pulmonary surfactant in those regions that remain open. These effects are reflected in commensurately increased values of dynamic lung elastance (E L), a quantity that in principle is readily measured at the bedside. Recent mathematical/computational modeling studies have shown that the way in which E L varies as a function of both time and positive end-expiratory pressure (PEEP) reflects the nature and degree of lung injury, and can even be used to infer the separate contributions of volutrauma and atelectrauma to VILI. Interrogating such models for minimally injurious regimens of mechanical ventilation that apply to a particular lung may thus lead to personalized approaches to the ventilatory management of ARDS.

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“…A double-hit ARDS model consisting of lung lavage followed by injurious ventilation was used. Such a model, which has been used extensively, mirrors many of the characteristics found in early human ARDS [20,21]. The severity of the lung injury was restricted to mild to moderate to prevent the animals from failed SB.…”

Section: Discussionmentioning

confidence: 99%

Effect of mechanical ventilation versus spontaneous breathing on abdominal edema and inflammation in ARDS: an experimental porcine model

et al. 2020

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Background: Mechanical ventilation (MV), compared to spontaneous breathing (SB), has been found to increase abdominal edema and inflammation in experimental sepsis. Our hypothesis was that in primary acute respiratory distress syndrome (ARDS) MV would enhance inflammation and edema in the abdomen. Methods: Thirteen piglets were randomized into two groups (SB and MV) after the induction of ARDS by lung lavage and 1 h of injurious ventilation. 1. SB: continuous positive airway pressure 15 cmH 2 O, fraction of inspired oxygen (FIO 2 ) 0.5 and respiratory rate (RR) maintained at about 40 cycles min − 1 by titrating remifentanil infusion. 2. MV: volume control, tidal volume 6 ml kg − 1 , positive end-expiratory pressure 15 cmH 2 O, RR 40 cycles min − 1 , FIO 2 0.5. Main outcomes: abdominal edema, assessed by tissues histopathology and wet-dry weight; abdominal inflammation, assessed by cytokine concentration in tissues, blood and ascites, and tissue histopathology. Results: The groups did not show significant differences in hemodynamic or respiratory parameters. Moreover, edema and inflammation in the abdominal organs were similar. However, blood IL6 increased in the MV group in all vascular beds (p < 0.001). In addition, TNFα ratio in blood increased through the lungs in MV group (+ 26% ± 3) but decreased in the SB group (− 17% ± 3). Conclusions: There were no differences between the MV and SB group for abdominal edema or inflammation. However, the systemic increase in IL6 and the TNFα increase through the lungs suggest that MV, in this model, was harmful to the lungs.

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The Open Lung Approach Improves Pulmonary Vascular Mechanics in an Experimental Model of Acute Respiratory Distress Syndrome

Abstract: In this experimental setting, positive end-expiratory pressure consistent with the open lung approach resulted in the best pulmonary vascular mechanics compared with higher or lower positive end-expiratory pressure settings.

Cited by 11 publications

References 26 publications

Physiology-guided management of hemodynamics in acute respiratory distress syndrome

Physiology-guided management of hemodynamics in acute respiratory distress syndrome

Ventilator-induced lung injury and lung mechanics

Effect of mechanical ventilation versus spontaneous breathing on abdominal edema and inflammation in ARDS: an experimental porcine model

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