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The current gold-standard treatment for COVID-19-related hypoxemic respiratory failure is invasive mechanical ventilation. However, do not intubate orders (DNI), prevent the use of this treatment in some cases. The aim of this study was to evaluate if non-invasive ventilatory supports can provide a good therapeutic alternative to invasive ventilation in patients with severe COVID-19 infection and a DNI. Data were collected from four centres in three European countries. Patients with severe COVID-19 infection were included. We emulated a hypothetical target trial in which outcomes were compared in patients with a DNI order treated exclusively by non-invasive respiratory support with patients who could be intubated if necessary. We set up a propensity score and an inverse probability of treatment weighting to remove confounding by indication. Four-hundred patients were included: 270 were eligible for intubation and 130 had a DNI order. The adjusted risk ratio for death among patients eligible for intubation was 0.81 (95% CI 0.46 to 1.42). The median length of stay in acute care for survivors was similar between groups (18 (10–31) vs. (19 (13–23.5); p = 0.76). The use of non-invasive respiratory support is a good compromise for patients with severe COVID-19 and a do not intubate order.

The patient's brother had died at the same age, from pulmonary veno-occlusive disease associated with hypertrophic cardiomyopathy. 1 year previously he had been diagnosed with end-stage kidney disease of unknown origin; he had had no history of cognitive impairment. The most frequent and severe presentation occurs in neonates.1,2 Pulmonary artery hypertension (PAH) and renal TMA have been described in early-onset cblC deficiency, whereas isolated neuropsychiatric symptoms prevail in adult-onset forms.1,2 A case of adult-onset renal TMA had similar renal outcomes to our patient.3 The family history and coexistence of a specific glomerulopathy in our patient suggest that PAH, renal TMA, and the glomerular lesions are consequences of the variants in MMACHC.

Acute exacerbation of interstitial lung disease (AE-ILD) may lead to acute respiratory failure with poor prognosis. Little is known about the optimal oxygenation strategy in this indication, in particular since the development of high-flow nasal oxygen therapy (HFNO). Therefore, we conducted a nationwide survey among respiratory and intensive care unit (ICU) physicians to assess their real-life practices. Between January and June 2024, physicians were questioned, using an online survey (11 questions), regarding the non-invasive oxygenation strategy they used in the management of patients with AE-ILD: face mask (FM), HFNO, continuous positive airway pressure (CPAP) or non-invasive ventilation (NIV). The response rate was 119/270 (44.1%), including 59.5% of ICU and 40.5% of respiratory physicians.=

Pulmonary arterial hypertension (PAH) is a chronic and progressive disease leading to right heart failure and ultimately death if untreated. The first classification of PH was proposed in 1973. In 2008, the fourth World Symposium on PH held in Dana Point (California, USA) revised previous classifications. Currently, PH is devided into five subgroups. Group 1 includes patients suffering from idiopathic or familial PAH with or without germline mutations. Patients with a diagnosis of PAH should systematically been screened regarding to underlying mutations of BMPR2 gene (bone morphogenetic protein receptor type 2) or more rarely of ACVRL1 (activine receptor-like kinase type 1), ENG (endogline) or Smad8 genes. Pulmonary veno occusive disease and pulmonary capillary hemagiomatosis are individualized and designated as clinical group 1'. Group 2 'Pulmonary hypertension due to left heart diseases' is divided into three sub-groups: systolic dysfonction, diastolic dysfonction and valvular dysfonction. Group 3 'Pulmonary hypertension due to respiratory diseases' includes a heterogenous subgroup of respiratory diseases like PH due to pulmonary fibrosis, COPD, lung emphysema or interstitial lung disease for exemple. Group 4 includes chronic thromboembolic pulmonary hypertension without any distinction of proximal or distal forms. Group 5 regroup PH patients with unclear multifactorial mechanisms. Invasive hemodynamic assessment with right heart catheterization is requested to confirm the definite diagnosis of PH showing a resting mean pulmonary artery pressure (mPAP) of ≥ 25 mmHg and a normal pulmonary capillary wedge pressure (PCWP) of ≤ 15 mmHg. The assessment of PCWP may allow the distinction between pre-capillary and post-capillary PH (PCWP > 15 mmHg). Echocardiography is an important tool in the management of patients with underlying suspicion of PH. The European Society of Cardiology and the European Respiratory Society (ESC-ERS) guidelines specify its role, essentially in the screening proposing criteria for estimating the presence of PH mainly based on tricuspid regurgitation peak velocity and systolic artery pressure (sPAP). The therapy of PAH consists of non-specific drugs including oral anticoagulation and diuretics as well as PAH specific therapy. Diuretics are one of the most important treatment in the setting of PH because right heart failure leads to fluid retention, hepatic congestion, ascites and peripheral edema. Current recommendations propose oral anticoagulation aiming for targeting an International Normalized Ratio (INR) between 1.5-2.5. Target INR for patients displaying chronic thromboembolic PH is between 2–3. Better understanding in pathophysiological mechanisms of PH over the past quarter of a century has led to the development of medical therapeutics, even though no cure for PAH exists. Several specific therapeutic agents were developed for the medical management of PAH including prostanoids (epoprostenol, trepoprostenil, iloprost), endothelin receptor antagonists (bosentan, ambrisentan) and phosphodiesterase type 5 inhibitors (sildenafil, tadalafil). This review discusses the current state of art regarding to epidemiologic aspects of PH, diagnostic approaches and the current classification of PH. In addition, currently available specific PAH therapy is discussed as well as future treatments.

Background The ventilatory physiopathology of patients with interstitial lung disease (ILD) remains poorly understood. We aimed to personalize a mechanical simulator to model healthy and ILD profiles ventilation, and to evaluate the effect of spontaneous breathing on respiratory mechanics at rest and during exercise. Methods In a 2-compartment lung simulator (ASL 5000 ® ), we modeled 1 healthy and 3 ILD profiles, at rest and during exercise, based on physiological data from literature and patients. Measurements were: tidal volume, end-expiratory lung volume, driving pressure, transpulmonary driving pressure, dynamic alveolar strain, mechanical power, and time lag of inspiratory flow between compartments 1 and 2. Results Healthy and ILD models were validated: maximum differences between real and simulated tidal volume were 5% (96 ml) and 6% (54 ml) at rest and during exercise respectively, considered clinically negligible. When we simulated lung inhomogeneity (compliance in compartment 1 > compartment 2), tidal volume, end-expiratory lung volume, driving pressure and mechanical power increased in compartment 1 and decreased in compartment 2. Driving transpulmonary pressure and dynamic alveolar strain increased in compartment 2 and decreased in compartment 1. Time lag of inspiratory flow between compartments 1 and 2 was positively correlated with a difference of compliance between compartments ( r  = 0.98, CI95% (0.9106; 0.9962), p  < 0.0001). Conclusion In this bench study, we personalized a mechanical simulator thatmodels the lung inhomogeneity and spontaneous breathing of healthy subjects and ILD patients at rest and during exercise. Our results suggest that lung inhomogeneity could increase lung vulnerability to volo-atelec-trauma mechanisms in ILD. Further physiological studies are needed to evaluate the impact of this vulnerability on acute or chronic ILD worsening.

IntroductionA wide range of recent ventilators, dedicated or not, is available for non-invasive ventilation (NIV) in respiratory or intensive care units (ICU). We conducted a bench study to compare their technical performances.MethodsVentilators, including five ICU ventilators with NIV mode on, two dedicated NIV ventilators and one transport ventilator, were evaluated on a test bench for NIV, consisting of a 3D manikin head connected to an ASL 5000 lung model via a non-vented mask. Ventilators were tested according to three simulated lung profiles (normal, obstructive, restrictive), three levels of simulated air leakage (0, 15, 30 L/min), two levels of pressure support (8, 14 cmH2O) and two respiratory rates (15, 25 cycles/min).ResultsThe global median Asynchrony Index (AI) was higher with ICU ventilators than with dedicated NIV ventilators (4% (0; 76) vs 0% (0; 15), respectively; p<0.05) and different between all ventilators (p<0.001). The AI was higher with ICU ventilators for the normal and restrictive profiles (p<0.01) and not different between ventilators for the obstructive profile. Auto-triggering represented 43% of all patient-ventilator asynchrony. Triggering delay, cycling delay, inspiratory pressure-time product, pressure rise time and pressure at mask were different between all ventilators (p<0.01). Dedicated NIV ventilators induced a lower pressure-time product than ICU and transport ventilators (p<0.01). There was no difference between ventilators for minute ventilation and peak flow.ConclusionDespite the integration of NIV algorithms, most recent ICU ventilators appear to be less efficient than dedicated NIV ventilators. Technical performances could change, however, according to the underlying respiratory disease and the level of air leakage.

PurposeTracheostomized patients often present with muscle weakness, altered consciousness, or swallowing difficulties. Hence, the literature is scarce regarding the challenging management of tracheostomy weaning. There is a need to strengthen the understanding of respiratory mechanisms with the different tracheostomy tube modalities that compose this weaning pathway. We aimed to evaluate the impact of these modalities on the work of breathing (WOB), total positive end-expiratory pressure (PEEPtot), and tidal volume (VT).MethodsWith a three-dimensional (3D) printed head mimicking human upper airways, we added a tracheal extension, and pierced to allow insertion of a size 7.0 tracheostomy cannula. The whole was connected to an artificial lung. Three lung mechanics were simulated (normal, obstructive and restrictive). We compared five different tracheostomy tube modalities to a control scenario in which the tube was capped and the cuff was deflated.ResultsA marginal difference was observed on the WOB within conditions with a slight increase + 0.004 [95% CI (0.003–0.004); p < 0.001] when the cuff was inflated in the normal and restrictive models and a slight decrease in the obstructive model. The highest PEEPtot that was reached was + 1 cmH2O [95% CI (1–1.1); p < 0.001] with high-flow therapy (HFT) with the cuff inflated in the obstructive model. We observed a statistically significant reduction in VT [up to − 57 mL 95% CI (− 60 to − 54); p < 0.001] when the cuff was inflated, in both the normal and obstructive models.ConclusionsOur results support the use of conditions that involve cuff deflation. Intermediate modalities with the cuff deflated produced similar results than cannula capping.

Case Presentation. This clinical case presents the history of a woman hospitalized for acute respiratory distress syndrome (ARDS). A 62-year-old woman, with regular physical activity and no history of respiratory disease or smoking, was hospitalized for moderate ARDS with bilateral pneumonitis. Fourteen days later, she was discharged from the intensive care unit and received respiratory physical therapy. One month later, she experienced exertional dyspnea. A regression of alveolar condensation with persistent sequelae at the pulmonary bases was noted. Three months later, the patient continued daily physical activity with satisfactory tolerance. A reduction in alveolar-capillary transfer, inappropriate hyperventilation upon exercise, and impairment of gas exchanges at maximal effort, suggestive of pulmonary shunt, were demonstrated. At the 6-month evaluation, the patient displayed exertional dyspnea with residual bilateral basal consolidations. Six months later, the dyspnea had ceased. The persistence of bilateral basal interstitial syndrome associated with bronchial dilatation and pleural-based consolidations was noted, as well as a stable impaired alveolar-capillary diffusing capacity. Discussion. Upon discharge from intensive care, pulmonary follow-up should be proposed to ARDS survivors. Moreover, pulmonary function testing at rest and exercise is advised as soon as possible to evaluate the respiratory sequelae. This will help to limit the severity of complications through adapted exercise rehabilitation and then regular physical activity.

In this narrative review, we discuss the relevant issues of therapeutic plasma exchange (TPE) in critically ill patients. For many conditions, the optimal indication, device type, frequency, duration, type of replacement fluid and criteria for stopping TPE are uncertain. TPE is a potentially lifesaving but also invasive procedure with risk of adverse events and complications and requires close monitoring by experienced teams. In the intensive care unit (ICU), the indications for TPE can be divided into (1) absolute, well-established, and evidence-based, for which TPE is recognized as first-line therapy, (2) relative, for which TPE is a recognized second-line treatment (alone or combined) and (3) rescue therapy, where TPE is used with a limited or theoretical evidence base. New indications are emerging and ongoing knowledge gaps, notably regarding the use of TPE during critical illness, support the establishment of a TPE registry dedicated to intensive care medicine.

IntroductionAlthough home non-invasive ventilation (NIV) is increasingly used to manage patients with chronic ventilatory failure, there are limited data on the long-term outcome of these patients. Our aim was to report on home NIV populations and the long-term outcome from two European centres.MethodsCohort analysis including all patients established on home NIV from two European centres between 2008 and 2014.ResultsHome NIV was initiated in 1746 patients to treat chronic ventilatory failure caused by (1) obesity hypoventilation syndrome±obstructive sleep apnoea (OHS±OSA) (29.5%); (2) neuromuscular disease (NMD) (22.7%); and (3) obstructive airway diseases (OAD) (19.1%). Overall cohort median survival following NIV initiation was 6.6 years. Median survival varied by underlying aetiology of respiratory failure: rapidly progressive NMD 1.1 years, OAD 2.7 years, OHS±OSA >7 years and slowly progressive NMD >7 years. Multivariate analysis demonstrated higher mortality in patients with rapidly progressive NMD (HR 4.78, 95% CI 3.38 to 6.75), COPD (HR 2.25, 95% CI 1.64 to 3.10), age >60 years at initiation of home NIV (HR 2.41, 95% CI 1.92 to 3.02) and NIV initiation following an acute admission (HR 1.38, 95% CI 1.13 to 1.68). Factors associated with lower mortality were NIV adherence >4 hours per day (HR 0.64, 95% CI 0.51 to 0.79), OSA (HR 0.51, 95% CI 0.31 to 0.84) and female gender (HR 0.79, 95% CI 0.65 to 0.96).ConclusionThe mortality rate following initiation of home NIV is high but varies significantly according to underlying aetiology of respiratory failure. In patients with chronic respiratory failure, initiation of home NIV following an acute admission and low levels of NIV adherence are poor prognostic features and may be amenable to intervention.