Targeting transpulmonary pressure to prevent ventilator-induced lung injury

Gattinoni, Luciano; Giosa, Lorenzo; Bonifazi, Matteo; Pasticci, Iacopo; Busana, Mattia; Macrí, Matteo Maria; Romitti, Federica; Vassalli, Francesco; Quintel, Michael

doi:10.1080/17476348.2019.1638767

Cited by 46 publications

(86 citation statements)

References 61 publications

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“…* BMI: body mass index; SOFA: sequential organ failure assessment; CAD: coronary artery disease; DM: diabetic mellitus; SAP: severe acute pancreatitis; RM: recruitment maneuver; PPV: prone position ventilation; ECMO: extracorporeal membrane oxygenation; PEEP: positive end-expiratory pressure; ICU: intensive care unit. BioMed Research International spontaneous breathing efforts, the Ptp may increase significantly due to the significant decrease in intrathoracic pressure, which may aggravate lung injury [26]. Therefore, the inhibition of the spontaneous breathing efforts in ARDS patients by deep sedation significantly reduced the MP, at the same time significantly reducing the inspiratory Ptp.…”

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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“…In Type L patients with dyspnea, several noninvasive options are available: high-flow nasal cannula (HFNC), continuous positive airway pressure (CPAP) or noninvasive ventilation (NIV). At this stage, the measurement (or the estimation) of the inspiratory esophageal pressure swings is crucial [13]. In the absence of the esophageal manometry, surrogate measures of work of breathing, such as the swings of central venous pressure [14] or clinical detection of excessive inspiratory effort, should be assessed.…”

Section: Respiratory Treatmentmentioning

confidence: 99%

COVID-19 pneumonia: different respiratory treatments for different phenotypes?

et al. 2020

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Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has spread to almost 100 countries, infected over 10M patients and resulted in 505K deaths worldwide as of 30 th June 2020. The major clinical feature of severe COVID-19 requiring ventilation is acute Respiratory Distress Syndrome (ARDS) with multi-functional failure as a result of a cytokine storm with increased serum levels of cytokines. The pathogenesis of the respiratory failure in COVID-19 is yet unknown, but diffuse alveolar damage with interstitial thickening leading to compromised gas exchange is a plausible mechanism. Hypoxia has been seen in the COVID-19 patients however, patients present with a distinct phenotype. Intracellular levels of NO playing important role in the vasodilation of small vessels. Objectives: To elucidate the intracellular levels of NO inside of RBCs in COVID-19 patients compared with that of healthy control subjects. Methods: We recruited 14 COVID-19 infected cases who had pulmonary involvement of their disease, 4 non-COVID-19 healthy controls (without pulmonary involvement and were not hypoxic) and 2 hypoxic non-COVID-19 patients subjects who presented at the Masih Daneshvari Hospital of Tehran, Iran between March-May 2020. Whole blood samples were harvested from patients and intracellular levels of NO in 1 million red blood cells (RBC) was measured by DAF staining using ow cytometry (FACS Calibour, BD, CA, USA). Results: The Mean orescent of intensity for NO was signi cantly enhanced in COVID-19 patients compared with healthy control subjects (P≤0.05). As a further control for whether hypoxia induced this higher intracellular NO, we evaluated the levels of NO inside RBC of hypoxic patients. No signi cant differences in NO levels were seen between the hypoxic and non-hypoxic control group. Conclusions: This pilot study demonstrates increased levels of intracellular NO in RBCs from COVID-19 patients. Future studies should examine whether intracellular NO would be increased in large number of COVID-19 patients for usage of possible NO therapy in severe patients.

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“…Both were able to improve oxygenation compared to baseline settings with the latter slightly increasing possible over-distension. In accordance with an also recently published expert review by Gattinoni et al, they recognized diverse limitations and assumptions while using esophageal pressure (P es ) as a surrogate for pleural pressure (P pl ) [2]. Nonetheless, another animal and human cadaver study revealed that P es accurately reflects P pl in the mid to dependent lung [3].…”

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confidence: 54%