The future of mechanical ventilation: lessons from the present and the past

Gattinoni, Luciano; Marini, John J.; Collino, Francesca; Maiolo, Giorgia; Rapetti, Francesca; Tonetti, Tommaso; Vasques, Francesco; Quintel, Michael

doi:10.1186/s13054-017-1750-x

Cited by 224 publications

(216 citation statements)

References 75 publications

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“…Mechanical ventilation is still the most important supportive treatment in patients with ARDS. Lung ventilation is the dynamic process of breathing to drive gases in and out the lungs [18]. During the mechanical ventilation treatment in ARDS, improper ventilator settings or excessive spontaneous breathing can cause ventilator-related damage, aggravate disease progression, and increase mortality [19].…”

Section: Discussionmentioning

confidence: 99%

Effect of Deep Sedation on Mechanical Power in Moderate to Severe Acute Respiratory Distress Syndrome: A Prospective Self-Control Study

Xie

Cao

Qian

et al. 2020

BioMed Research International

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Mechanical power (MP) is a parameter for assessing ventilator-induced lung injury (VILI) in patients with acute respiratory distress syndrome (ARDS). Deep sedation inhibits the respiratory center and reduces the excessive spontaneous breathing in ARDS patients, thereby reducing transpulmonary pressure (Ptp) and lung injury. However, the effect of sedation on MP in ARDS patients is not yet clear. Therefore, the purpose of this study was to investigate the effect of deep sedation on MP in ARDS patients. Patients with moderate to severe ARDS who required mechanical ventilation were considered. Different degrees of sedation were performed on patients in three stages after 24 hours of mechanical ventilation. The three stages are as follows: stage 1 (H+3): 0 to 3 hours of sedation; patients’ Ramsay score was 2-3 to obtain mild sedation; stage 2 (H+6): 4 to 6 hours of sedation; the sedation depth was adjusted to 5-6 points; and stage 3 (H+9): 7 to 9 hours of sedation; the sedation depth was adjusted to 2-3 points. Under deep sedation (H+6), MP, respiratory rate (RR), and Ptp were significantly lower than the ones in the patients under mild sedation (H+3) (all P<0.01) although PaO2/FiO2 (P/F) and static lung compliance (Cst) were significantly higher (both P<0.01). However, no significant difference in the above parameters was observed between H+3 and H+9. Correlation analysis showed that ΔMP was significantly and positively correlated with ΔRR and ΔPtp (both P<0.001), while no correlation was observed neither between ΔMP and ΔCst nor between ΔMP and ΔP/F. The 28-day Kaplan-Meier survival curve showed the occurrence of 19 deaths, and the overall survival rate was 63.46%. The survival rate was 53.12% in the high-MP (HMP) group and 80.95 in the low-MP (LMP) group (P<0.05). In conclusion, deep sedation significantly reduced MP in patients with moderate to severe ARDS, thereby reducing the occurrence of VILI. In addition, MP monitoring in deep sedation predicted the 28-day survival of patients with moderate to severe ARDS.

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Section: Discussionmentioning

confidence: 99%

Effect of Deep Sedation on Mechanical Power in Moderate to Severe Acute Respiratory Distress Syndrome: A Prospective Self-Control Study

Xie

Cao

Qian

et al. 2020

BioMed Research International

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“…Recently, the development of MP was shown to be related to mortality in patients on mechanical ventilation, which included all aspects of ventilator parameters [14]; however, in our study, the discrimination of MP was also lower than that of LHPI. This result might be related to the MP itself still having some problems [22], such as the power not normalizing [31], the lack of ascertainment of the impact of MP throughout the lung, and the effect of expiratory phase on MP [32]. In our study, we observed that LHPI played a relatively important role in the random forest model.…”

Section: Discussionmentioning

confidence: 69%

“…Patients with elevated LHPI usually have high DP and low MAP. DP is the surrogate for cyclic lung strain [20], and high DP indicates excessive tidal volume and lung strain relative to "baby lungs," resulting in VILI [21,22].…”

Section: Discussionmentioning

confidence: 99%

Lung-heart pressure index is a risk factor for acute respiratory distress syndrome (ARDS): A machine learning and propensity score-matching study.

X¹,

Chen²,

Hu³

et al. 2019

Preprint

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Background Ventilator-induced lung injury (VILI) and haemodynamic instability play vital roles in acute respiratory distress syndrome (ARDS). The principle of driving pressure (DP) is the response to “volutrauma”, and the mean arterial pressure (MAP) is a haemodynamic systemic manifestation. In this study, we explored a novel lung-heart pressure index (LHPI) based on DP and MAP and explored its prognostic value in patients with ARDS.Methods This is a retrospective study based on the MIMIC-III database. ARDS patients who had undergone mechanical ventilation for more than 48 hours were selected through structured query language. The focus of the study was whether a high LHPI was associated with 30-day mortality and whether its predictive power was better than that of DP and mechanical power (MP). We used random forest, propensity-score matching, and logistic regression to test our hypothesis.Results A total of 448 ICU ARDS patients were enrolled. The mortality rate of ARDS patients was 29.02%. The LHPI was more important than DP and MP in the random forest. A significant adverse effect of high LHPI on 30-day mortality was observed in the high-LHPI group compared to the effect observed in the low-LHPI group (OR=1.86, 95% CI 1.08–3.26, p =0.027). More importantly, LHPI was significantly better than DP (NRI=0.054, 95% CI (0.014-0.094), P=0.008; IDI=0.011, 95% CI (0.002-0.019), P=0.014) and MP (NRI=0.061, 95% CI (0.001-0.122), P=0.049; IDI=0.047, 95% CI (0.022-0.071), P<0.001) in predicting mortality.Conclusions The study showed that the LHPI was a powerful prognostic indicator of 30-day mortality in ARDS patients, and its predictive discrimination was better than that of DP and MP. Further experimental trials are needed to investigate whether adjusting treatment decisions according to the LHPI will significantly improve clinical outcomes.

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“…An increase in intra-abdominal pressure (IAP) affects lungs [4,5] producing atelectasis [6], impaired function [7] and, indirectly, inflammation and edema [8]. On the other side, an increase in thoracic pressure due to MV [9] may have an effect on inflammation and edema in the abdominal compartment. In fact, the decrease in venous return related to high positive end-expiratory pressure (PEEP) ventilation [10] has been well described.…”

Section: Introductionmentioning

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 future of mechanical ventilation: lessons from the present and the past

Cited by 224 publications

References 75 publications

Effect of Deep Sedation on Mechanical Power in Moderate to Severe Acute Respiratory Distress Syndrome: A Prospective Self-Control Study

Effect of Deep Sedation on Mechanical Power in Moderate to Severe Acute Respiratory Distress Syndrome: A Prospective Self-Control Study

Lung-heart pressure index is a risk factor for acute respiratory distress syndrome (ARDS): A machine learning and propensity score-matching study.

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

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