Cristina Lalmolda

Background/Objectives: Thoraco-abdominal asynchrony (TAA) is a key mechanical consequence of severe chronic obstructive pulmonary disease (COPD), particularly during acute exacerbations (AECOPD), when dynamic hyperinflation and diaphragmatic dysfunction impair the coordination between rib cage and abdominal motion. Continuous, non-invasive monitoring of respiratory mechanics may provide valuable information on clinical evolution during hospitalization. This study aimed to evaluate Global Phase Delay (GPD) as a longitudinal marker of TAA in hospitalized AECOPD patients and to explore its ability to reflect disease severity and short-term clinical evolution using repeated measurements obtained with thoracic and abdominal respiratory belts using respiratory inductance plethysmography (RIP). Methods: We conducted an observational longitudinal study in hospitalized adults with AECOPD. Respiratory inductance plethysmography signals were recorded daily over four consecutive days using thoracic and abdominal RIP belts. Five-breath sequences were analyzed to derive GPD, phase angle, and loop rotation direction through automated MATLAB processing. Clinical data included demographics, lung function, blood gases, dyspnea severity, and need for intermediate respiratory care unit (IRCU) admission. Temporal changes in TAA indices and subgroup differences (FEV₁ < 35%, IRCU admission) were assessed using repeated-measures ANOVA. Results: Twenty-one patients were included. On admission, mean absolute GPD was 49 ± 58°, with larger delays observed in patients with more severe airflow limitation and in those requiring IRCU support. During hospitalization, GPD showed a significant reduction over time (p < 0.05), particularly in these subgroups, indicating progressive improvement in thoraco-abdominal synchrony. Directional analysis of GPD revealed heterogeneous patterns consistent with different underlying mechanical behaviors. Conclusions: Serial assessment of TAA using respiratory bands and GPD provides clinically meaningful information on the evolution of respiratory mechanics during AECOPD hospitalization. This approach may support bedside monitoring and help track patient response to treatment, offering potential value for individualized respiratory management.

Background/Objectives: Amyotrophic lateral sclerosis is a progressive neurodegenerative disease in which respiratory failure is the leading cause of death. Mechanical ventilation improves both survival and quality of life; however, the prognostic implications of built-in ventilator software monitoring remain insufficiently characterized. The aim of the study was to determine whether built-in ventilator software-based monitoring is associated with enhanced survival in amyotrophic lateral sclerosis subjects. Methods: Cohort study of amyotrophic lateral sclerosis subjects, stratified into two groups: those monitored through detailed built-in ventilator software and those not monitored. Clinical and ventilatory data were systematically evaluated during a 24-month follow-up. Results: Among 120 ALS subjects (57 detailed built-in ventilator software, 63 non-detailed ventilator software), median survival from diagnosis was significantly longer in the detailed built-in ventilator software group (3.42 vs. 2.12 years; p < 0.001). Survival from mechanical ventilation initiation was also significantly longer in the built-in ventilator software group (2.79 years vs. 0.78 years). Greater daily mechanical ventilation usage was associated with shorter survival (p < 0.003). Paradoxically, subjects with the lowest proportion of spontaneous inspirations exhibited superior survival outcomes (p = 0.04). Neither persistent leaks nor asynchronies were independently predictive of survival. Conclusions: BVS-monitoring was associated with improved survival in amyotrophic lateral sclerosis subjects receiving home mechanical ventilation. Its integration into clinical practice may enable timely, data-driven ventilatory adjustments, ultimately contributing to more individualized and optimized patient management.

Objectives: This study aimed to evaluate how non-invasive ventilation (NIV) and high-flow nasal cannula therapy (HFT) versus conventional oxygen therapy (COT) affect neural ventilatory drive during exercise in patients with severe chronic obstructive pulmonary disease (COPD). Methods: We conducted an experimental, controlled study with one arm and three different conditions for the same cohort. After initial testing on conventional oxygen therapy (COT), patients exercised under NIV and HFT in sequential days and a random order. Participants: Twenty patients (mean age 60 years old (SD 3.9), 6 female) with severe COPD (30% women) on home NIV as a bridge to lung transplantation were enrolled in this study, with a mean FEV₁ of 19.78% predicted and marked hyperinflation. Protocol: Participants performed constant-load cycling exercises at 75% maximum tolerated workload under three conditions: COT, NIV, and HFT. Neuro-respiratory drive (NRD) was measured using surface parasternal and sternocleidomastoid electromyography, and mixed ANOVA was performed to analyze repeated measures across conditions. Results: In total, 20 patients were included in this study. NIV demonstrated superior performance, with 60% lower NRD compared to COT (488.81 µV vs. 1180.63 µV, p < 0.05). HFT showed intermediate effects (807.8 µV). NIV also achieved greater reduction in respiratory rate (4.2 breaths/min), lower perceived exertion (Borg score decrease: 1.8 points), and more pronounced CO₂ reduction (5.3 mmHg) compared to both COT and HFT. Conclusions: NIV significantly reduces NRD during exercise in severe COPD patients compared to HFT and COT. This supports its use as a valuable adjunct to pulmonary rehabilitation in severe COPD.

Objectives: To evaluate how non-invasive ventilation (NIV) and high-flow nasal can-nula therapy (HFT) versus conventional oxygen therapy (COT) affect neural ventilatory drive during exercise in patients with severe chronic obstructive pulmonary disease (COPD). Methods Design: Experimental, controlled study with one arm and three dif-ferent conditions for the same cohort. After initial testing on conventional oxygen threapy (COT) patients performed in sequential days, in a random order, exercise under NIV and HFT. Participants: Twenty patients with severe COPD (30% women) on home NIV as a bridge to lung transplantation, with mean FEV₁ 19.78% predicted and marked hyperinflation. Protocol: Participants performed constant-load cycling exercises at 75% maximum tol-erated workload under three conditions: COT, NIV, and HFT. Neuro-respiratory drive (NRD) was measured using surface parasternal and sternocleidomastoid electromyog-raphy. Mixed ANOVA analyzed repeated measures across conditions. Results: 20 patients (age 60+- 3.9 years, 6 female) were included. NIV demonstrated superior performance with 60% lower NRD compared to COT (488.81 µV vs. 1180.63 µV, p< 0.05). HFT showed intermediate effects (807.8 µV). NIV also achieved greater reduc-tion in respiratory rate (4.2 breaths/min), lower perceived exertion (Borg score decrease: 1.8 points), and more pronounced CO₂ reduction (5.3 mmHg) compared to both COT and HFT. Conclusions: NIV significantly reduces NRD during exercise in severe COPD patients compared to HFT and COT. This supports its use as a valuable adjunct to pulmonary rehabilitation in severe COPD.

Background: Non-invasive ventilation (NIV) improves outcomes in acute life-threatening hypercapnic respiratory failure due to exacerbations of COPD (ECOPD), but the benefits of long-term home NIV (LTH-NIV) for managing hypercapnic chronic respiratory failure (CRF) in COPD remain unclear. Purpose: 1) To assess the long-term survival of severe COPD patients with hypercapnic CRF started on LTH-NIV and mortality related factors; 2) To evaluate the impact of LTH-NIV on ECOPD and hospital admissions at follow-up. Patients and Methods: COPD patients who started LTH-NIV between January 2009 and December 2018 were included. Medical records and clinical outcomes were retrospectively reviewed. Results: Forty-four COPD patients (mean [SD] age 66.5 [10.4] years, 81.8% men) with severe airflow obstruction (mean [SD] FEV₁ 36 [16] % of predicted), hypercapnic CRF (mean [SD] PaCO₂ 60.8 [9.2] mmHg) and exacerbator phenotype (mean [IQR] moderate-severe ECOPD 3 [3] in previous year) were included. Median survival from LTH-NIV was 100.3 months. Survival at one, three and five years was 86.4%, 72.7% and 68.2%, respectively. In a multivariate Cox regression model, patients with a significantly increased risk of death were those with older age, lower absolute FVC, more hospitalisations and especially those adapted to LTH-NIV in the acute phase (HR 3.67 (IC 1.04– 13), p< 0.05). LTH-NIV allowed an estimated mean reduction in ECOPD of 39.7% (65.2% in hospitalisations) at 12 months and 57.4% (81% in hospitalisations) at 24 months. Conclusion: The survival rate of COPD patients with hypercapnic CRF on LTH-NIV is currently high (> 50% at 5 years). Adaptation to LTH-NIV in the stable phase is the most important prognostic determinant and should be considered especially in patients with more hospitalisations and lower FVC values. Initiation of LTH-NIV reduces moderate to severe ECOPD at follow-up.

The choice of a ventilator model for a single patient is usually based on parameters such as size (portability), presence or absence of battery and ventilatory modes. However, there are many details within each ventilator model about triggering, pressurisation or autotitration algorithms that may go unnoticed, but may be important or may justify some drawbacks that may occur during their use in individual patients. This review is intended to emphasize these differences. Guidance is also provided on the operation of autotitration algorithms, in which the ventilator is able to take decisions based on a measured or estimated parameter. It is important to know how they work and their potential sources of error. Current evidence on their use is also provided.

Purpose: The European Task Force for chronic non-invasive ventilation in stable COPD recommends the use of high pressure-support (PS) level to maximize the decrease in PaCO2. It is possible that the ventilator model can influence the need for higher or lower pressure levels. Research Question: To determine the differences between ventilators in a bench model with an increased inspiratory demand; and to compare the degree of muscular unloading measured by parasternal electromyogram (EMGpara) provided by the different ventilators in real patients with stable COPD. Patients and Methods: Bench: four levels of increasing progressive effort were programmed. The response of nine ventilators to four levels of PS and EPAP of 5 cm H2O was studied. The pressure-time product was determined at 300 and 500 msec (PTP 300/500). Clinical Study: The ventilators were divided into two groups, based on the result of the bench test. Severe COPD patients with non-invasive ventilation (NIV) were studied, randomly comparing the performance of one ventilator from each group. Muscle unloading was measured by the decrease in EMGpara from its baseline value. Results: There were significant differences in PTP 300 and PTP 500 in the bench study. Based on these results, home ventilators were classified into two groups; group 1 included four models with higher PTP 300. Ten COPD patients were recruited for the clinical study. Group 1 ventilators showed greater muscle unloading at the same PS than group 2. Conclusion: The scale of pressure support in NIV for high intensity ventilation may be influenced by the ventilator model. Clinical Trials.gov: NCT03373175.

Treatments that require the introduction of external gas into the non-invasive ventilation (NIV) circuit, such as aerosol and oxygen therapy, may influence the performance of the ventilator trigger system. The aim of the study was to determine the presence and type of asynchronies induced by external gas in the NIV circuit in a bench model and in a group of patients undergoing chronic NIV. Bench study: Four ventilators (one with two different trigger design types) and three gas sources (continuous flow at 4 and 9 l/min and pulsatile flow at 9 l/min) were selected in an active simulator model. The sensitivity of the trigger, the gas introduction position, the ventilatory pattern and the level of effort were also modified. The same ventilators and gas conditions were used in patients undergoing chronic NIV. Bench: the introduction of external gas caused asynchronies in 35.9% of cases (autotriggering 73%, ineffective effort 27%). Significant differences (p < 0.01) were detected according to the ventilator model and the gas source. In seven patients, the introduction of external gas induced asynchrony in 20.4% of situations (77% autotriggering). As in the bench study, there were differences in the occurrence of asynchronies depending on the ventilator model and gas source used. The introduction of external gas produces alterations in the ventilator trigger. These alterations are variable, and depend on the ventilator design and gas source. This phenomenon makes it advisable to monitor the patient at the start of treatment.

Background and objective: Treatments that require the introduction of external gas into the non-invasive ventilation (NIV) circuit, such as aerosol and oxygen therapy, may influence the performance of the ventilator trigger system. The aim of the study was to determine the presence and type of asynchronies induced by external gas in the NIV circuit in a bench model and in a group of patients undergoing chronic NIV.Methods: Bench study: Four ventilators (one with two different trigger design types) and three gas sources (continuous flow at 4 and 9 l/min and pulsatile flow at 9 l/min) were selected in an active simulator model. The sensitivity of the trigger, the gas introduction position, the ventilatory pattern and the level of effort were also modified.Clinical study: The same ventilators and gas conditions were used in patients undergoing chronic NIV.Results: Bench: The introduction of external gas caused asynchronies in 35.9% of cases (autotriggering 73%, ineffective effort 27%). Significant differences (p<0.01) were detected according to the ventilator model and the gas source.Clinical study: In seven patients, the introduction of external gas induced asynchrony in 20.4% of situations (77% autotriggering). As in the bench study, there were differences in the occurrence of asynchronies depending on the ventilator model and gas source used.Conclusion: The introduction of external gas produces alterations in the ventilator trigger. These alterations are variable, and depend on the ventilator design and gas source. This phenomenon makes it advisable to monitor the patient at the start of treatment.

Humidification and non-invasive ventilation are frequently used together, despite the lack of precise recommendations regarding this practice. We aimed to analyse the impact of active external and built-in humidifiers on the performance of home ventilators, focusing on their pressurization efficacy and their behaviour under different inspiratory efforts. We designed a bench study of a lung simulator programmed to emulate mechanical conditions similar to those experienced by real respiratory patients and to simulate three different levels of inspiratory effort: five different commonly used home NIV devices and active humidifiers attached to the latter (internal or "built-in") or to the circuit (external). To test ventilator pressurization under different humidification and effort settings, pressure-time products in the first 300ms and 500ms of the respiratory cycle were calculated in the 45 situations simulated. Inferential statistical analysis was performed. A significant reduction of PTP 300 and PTP 500 was observed with the external humidifier in three of the devices. The same pattern was noted for another device with an internal humidifier, and only one device showed no significant changes. This impact on pressurization was commonly higher under high inspiratory effort. These results indicate the need to monitor pressure changes in the use of external humidification devices in some home NIV ventilators.