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An increasing number of patients admitted to the intensive care unit are obese [1]. Many of them require mechanical ventilation, which may promote ventilator-induced lung injury (VILI) when applied to both injured and healthy lungs. Obesity induces functional changes in the respiratory system, resulting in a reduction of the end-expiratory lung volume, increased incidence of airway closure and formation of atelectasis, and alterations in lung and chest wall mechanics [2]. These alterations explain the high occurrence of gas exchange impairment, respiratory mechanics alterations, and hemodynamic compromise. To approach to the obese patient requiring mechanical ventilation, we propose a schematic algorithm (i-STAR, Fig. 1) as follows: (1) induction and intubation, (2) setting up initial mechanical ventilation, (3) titrating mechanical ventilation parameters, (4) assessing harmfulness of mechanical ventilation, and (5) rescue strategies.

Keywords: ARDS, Obesity, ICU

Prof Pelosi served as President of the European Society of Anaesthesiology (ESA) from 2010 to 2011, and had important roles in the World Federation of Societies of Intensive Care and Critical Care Medicine (WFSCCM) and European Respiratory Society (ERS). Professor Pelosi made the difference in the field of mechanical ventilation and acute respiratory distress syndrome (ARDS), in particular through the work of the PROVEnet group, which allowed to create large-scale observational studies and randomized clinical trials, providing high quality evidence which revolutionised the field of anaesthesiology and intensive care medicine. Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative Obituary Open Access Published:27 June 2023 A tribute to Paolo Pelosi Chiara Robba ORCID: orcid.org/0000-0003-1628-38451,2, Denise Battaglini1,2 & Lorenzo Ball1,2 Critical Care volume 27, Article number: 253 (2023) Cite this article 1040 Accesses 4 Altmetric Metrics details figure a On the 30th of May, Professor Paolo Pelosi passed away. Prof Pelosi served as President of the European Society of Anaesthesiology (ESA) from 2010 to 2011, and had important roles in the World Federation of Societies of Intensive Care and Critical Care Medicine (WFSCCM) and European Respiratory Society (ERS).

A personalized mechanical ventilation approach for patients with adult respiratory distress syndrome (ARDS) based on lung physiology and morphology, ARDS etiology, lung imaging, and biological phenotypes may improve ventilation practice and outcome. However, additional research is warranted before personalized mechanical ventilation strategies can be applied at the bedside. Ventilatory parameters should be titrated based on close monitoring of targeted physiologic variables and individualized goals. Although low tidal volume ( V T ) is a standard of care, further individualization of V T may necessitate the evaluation of lung volume reserve (e.g., inspiratory capacity). Low driving pressures provide a target for clinicians to adjust V T and possibly to optimize positive end-expiratory pressure (PEEP), while maintaining plateau pressures below safety thresholds. Esophageal pressure monitoring allows estimation of transpulmonary pressure, but its use requires technical skill and correct physiologic interpretation for clinical application at the bedside. Mechanical power considers ventilatory parameters as a whole in the optimization of ventilation setting, but further studies are necessary to assess its clinical relevance. The identification of recruitability in patients with ARDS is essential to titrate and individualize PEEP. To define gas-exchange targets for individual patients, clinicians should consider issues related to oxygen transport and dead space. In this review, we discuss the rationale for personalized approaches to mechanical ventilation for patients with ARDS, the role of lung imaging, phenotype identification, physiologically based individualized approaches to ventilation, and a future research agenda.

Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease characterized by progressive loss of lung function and poor prognosis. The so-called acute exacerbation of IPF (AE-IPF) may lead to severe hypoxemia requiring mechanical ventilation in the intensive care unit (ICU). AE-IPF shares several pathophysiological features with acute respiratory distress syndrome (ARDS), a very severe condition commonly treated in this setting. A review of the literature has been conducted to underline similarities and differences in the management of patients with AE-IPF and ARDS. During AE-IPF, diffuse alveolar damage and massive loss of aeration occurs, similar to what is observed in patients with ARDS. Differently from ARDS, no studies have yet concluded on the optimal ventilatory strategy and management in AE-IPF patients admitted to the ICU. Notwithstanding, a protective ventilation strategy with low tidal volume and low driving pressure could be recommended similarly to ARDS. The beneficial effect of high levels of positive end-expiratory pressure and prone positioning has still to be elucidated in AE-IPF patients, as well as the precise role of other types of respiratory assistance (e.g., extracorporeal membrane oxygenation) or innovative therapies (e.g., polymyxin-B direct hemoperfusion). The use of systemic drugs such as steroids or immunosuppressive agents in AE-IPF is controversial and potentially associated with an increased risk of serious adverse reactions. Common pathophysiological abnormalities and similar clinical needs suggest translating to AE-IPF the lessons learned from the management of ARDS patients. Studies focused on specific therapeutic strategies during AE-IPF are warranted.

Data on the pathology of COVID-19 are scarce; available studies show diffuse alveolar damage; however, there is scarce information on the chronologic evolution of COVID-19 lung lesions. The primary aim of the study is to describe the chronology of lung pathologic changes in COVID-19 by using a post-mortem transbronchial lung cryobiopsy approach. Our secondary aim is to correlate the histologic findings with computed tomography patterns. SARS-CoV-2-positive patients, who died while intubated and mechanically ventilated, were enrolled. The procedure was performed 30 min after death, and all lung lobes sampled. Histopathologic analysis was performed on thirty-nine adequate samples from eight patients: two patients (illness duration < 14 days) showed early/exudative phase diffuse alveolar damage, while the remaining 6 patients (median illness duration—32 days) showed progressive histologic patterns (3 with mid/proliferative phase; 3 with late/fibrotic phase diffuse alveolar damage, one of which with honeycombing). Immunohistochemistry for SARS-CoV-2 nucleocapsid protein was positive predominantly in early-phase lesions. Histologic patterns and tomography categories were correlated: early/exudative phase was associated with ground-glass opacity, mid/proliferative lesions with crazy paving, while late/fibrous phase correlated with the consolidation pattern, more frequently seen in the lower/middle lobes. This study uses an innovative cryobiopsy approach for the post-mortem sampling of lung tissues from COVID-19 patients demonstrating the progression of fibrosis in time and correlation with computed tomography features. These findings may prove to be useful in the correct staging of disease, and this could have implications for treatment and patient follow-up.

Background The effects of positive end-expiratory pressure (PEEP) on lung ultrasound (LUS) patterns, and their relationship with intracranial pressure (ICP) in brain injured patients have not been completely clarified. The primary aim of this study was to assess the effect of two levels of PEEP (5 and 15 cmH 2 O) on global (LUStot) and regional (anterior, lateral, and posterior areas) LUS scores and their correlation with changes of invasive ICP. Secondary aims included: the evaluation of the effect of PEEP on respiratory mechanics, arterial partial pressure of carbon dioxide (PaCO 2 ) and hemodynamics; the correlation between changes in ICP and LUS as well as respiratory parameters; the identification of factors at baseline as potential predictors of ICP response to higher PEEP. Methods Prospective, observational study including adult mechanically ventilated patients with acute brain injury requiring invasive ICP. Total and regional LUS scores, ICP, respiratory mechanics, and arterial blood gases values were analyzed at PEEP 5 and 15 cmH 2 O. Results Thirty patients were included; 19 of them (63.3%) were male, with median age of 65 years [interquartile range (IQR) = 66.7–76.0]. PEEP from 5 to 15 cmH 2 O reduced LUS score in the posterior regions (LUSp, median value from 7 [5–8] to 4.5 [3.7–6], p  = 0.002). Changes in ICP were significantly correlated with changes in LUStot (rho = 0.631, p  = 0.0002), LUSp (rho = 0.663, p  < 0.0001), respiratory system compliance (rho = − 0.599, p  < 0.0001), mean arterial pressure (rho = − 0.833, p  < 0.0001) and PaCO 2 (rho = 0.819, p  < 0.0001). Baseline LUStot score predicted the increase of ICP with PEEP. Conclusions LUS-together with the evaluation of respiratory and clinical variables-can assist the clinicians in the bedside assessment and prediction of the effect of PEEP on ICP in patients with acute brain injury.

See PDF.] Professor Paolo Pelosi As active member of national and international societies, as past president of the European Society of Anesthesia and Intensive Care (ESAIC) and as president elect of the Italian Society of Anesthesia, Intensive Care and Pain Medicine (SIAARTI), he has promoted and supported the unity of our discipline in its different branches, he contributed enormously to the understanding of the pathophysiology of respiratory failure and was a pioneer in translating to the operating theatre the concepts of protective ventilation. In this context, he did not only contribute to the scientific research in the field, but he passionately shared his thoughts, intuitions and clinical experience with colleagues around the globe through countless online conferences, and with the general audience with several interviews in topnotch international broadcast networks, in a phase when the whole world was looking at Italy to understand how this disease was impacting our society. Professor Pelosi was a demanding and stimulating research chief, but always open to discussion and unceasingly keen to motivate his team in carrying on both physiological and clinical studies with the final aim of improving the quality of care of our patients.

Background In COVID-19 patients with acute respiratory distress syndrome (ARDS), the effectiveness of ventilatory rescue strategies remains uncertain, with controversial efficacy on systemic oxygenation and no data available regarding cerebral oxygenation and hemodynamics. Methods This is a prospective observational study conducted at San Martino Policlinico Hospital, Genoa, Italy. We included adult COVID-19 patients who underwent at least one of the following rescue therapies: recruitment maneuvers (RMs), prone positioning (PP), inhaled nitric oxide (iNO), and extracorporeal carbon dioxide (CO 2 ) removal (ECCO 2 R). Arterial blood gas values (oxygen saturation [SpO 2 ], partial pressure of oxygen [PaO 2 ] and of carbon dioxide [PaCO 2 ]) and cerebral oxygenation (rSO 2 ) were analyzed before (T0) and after (T1) the use of any of the aforementioned rescue therapies. The primary aim was to assess the early effects of different ventilatory rescue therapies on systemic and cerebral oxygenation. The secondary aim was to evaluate the correlation between systemic and cerebral oxygenation in COVID-19 patients. Results Forty-five rescue therapies were performed in 22 patients. The median [interquartile range] age of the population was 62 [57–69] years, and 18/22 [82%] were male. After RMs, no significant changes were observed in systemic PaO 2 and PaCO 2 values, but cerebral oxygenation decreased significantly (52 [51–54]% vs. 49 [47–50]%, p  < 0.001). After PP, a significant increase was observed in PaO 2 (from 62 [56–71] to 82 [76–87] mmHg, p  = 0.005) and rSO 2 (from 53 [52–54]% to 60 [59–64]%, p  = 0.005). The use of iNO increased PaO 2 (from 65 [67–73] to 72 [67–73] mmHg, p  = 0.015) and rSO 2 (from 53 [51–56]% to 57 [55–59]%, p  = 0.007). The use of ECCO 2 R decreased PaO 2 (from 75 [75–79] to 64 [60–70] mmHg, p  = 0.009), with reduction of rSO 2 values (59 [56–65]% vs. 56 [53–62]%, p  = 0.002). In the whole population, a significant relationship was found between SpO 2 and rSO 2 ( R  = 0.62, p  < 0.001) and between PaO 2 and rSO 2 (R0 0.54, p  < 0.001). Conclusions Rescue therapies exert specific pathophysiological mechanisms, resulting in different effects on systemic and cerebral oxygenation in critically ill COVID-19 patients with ARDS. Cerebral and systemic oxygenation are correlated. The choice of rescue strategy to be adopted should take into account both lung and brain needs. Registration The study protocol was approved by the ethics review board (Comitato Etico Regione Liguria, protocol n. CER Liguria: 23/2020).

Mechanical ventilation is a life-supportive therapy, but can also promote damage to pulmonary structures, such as epithelial and endothelial cells and the extracellular matrix, in a process referred to as ventilator-induced lung injury (VILI). Recently, the degree of VILI has been related to the amount of energy transferred from the mechanical ventilator to the respiratory system within a given timeframe, the so-called mechanical power. During controlled mechanical ventilation, mechanical power is composed of parameters set by the clinician at the bedside—such as tidal volume ( V T ), airway pressure (Paw), inspiratory airflow ( V ′), respiratory rate (RR), and positive end-expiratory pressure (PEEP) level—plus several patient-dependent variables, such as peak, plateau, and driving pressures. Different mathematical equations are available to calculate mechanical power, from pressure-volume (PV) curves to more complex formulas which consider both dynamic (kinetic) and static (potential) components; simpler methods mainly consider the dynamic component. Experimental studies have reported that, even at low levels of mechanical power, increasing V T causes lung damage. Mechanical power should be normalized to the amount of ventilated pulmonary surface; the ratio of mechanical power to the alveolar area exposed to energy delivery is called “intensity.” Recognizing that mechanical power may reflect a conjunction of parameters which may predispose to VILI is an important step toward optimizing mechanical ventilation in critically ill patients. However, further studies are needed to clarify how mechanical power should be taken into account when choosing ventilator settings.