The objective of this document was to standardise published cardiopulmonary exercise testing (CPET) protocols for improved interpretation in clinical settings and multicentre research projects. This document: 1) summarises the protocols and procedures used in published studies focusing on incremental CPET in chronic lung conditions; 2) presents standard incremental protocols for CPET on a stationary cycle ergometer and a treadmill; and 3) provides patients' perspectives on CPET obtained through an online survey supported by the European Lung Foundation. We systematically reviewed published studies obtained from EMBASE, Medline, Scopus, Web of Science and the Cochrane Library from inception to January 2017. Of 7914 identified studies, 595 studies with 26 523 subjects were included. The literature supports a test protocol with a resting phase lasting at least 3 min, a 3-min unloaded phase, and an 8- to 12-min incremental phase with work rate increased linearly at least every minute, followed by a recovery phase of at least 2–3 min. Patients responding to the survey (n=295) perceived CPET as highly beneficial for their diagnostic assessment and informed the Task Force consensus. Future research should focus on the individualised estimation of optimal work rate increments across different lung diseases, and the collection of robust normative data.

Nicotine, the primary addictive substance in tobacco, is widely abused. Relapse to cues associated with nicotine results in increased glutamate release within nucleus accumbens core (NAcore), modifying synaptic plasticity of medium spiny neurons (MSNs) which contributes to reinstatement of nicotine seeking. However, the role of cholinergic interneurons (ChIs) within the NAcore in mediating these neurobehavioral processes in unknown. ChIs represent less than 1% of the accumbens neuronal population yet are activated during drug seeking and reward-predicting events. Thus, we hypothesized that ChIs may play a significant role in mediating glutamatergic plasticity that underlies nicotine seeking behavior. Using chemogenetics transgenic rats that express Cre under the control of the choline acetyltransferase (ChAT) promoter, ChIs were bi-directionally manipulated prior to cue-induced reinstatement. Following nicotine self-administration and extinction training, ChIs were activated or inhibited prior to a cue reinstatement session. Following reinstatement, whole-cell electrophysiology from NAcore MSNs was used to assess changes in plasticity, measured via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) / N-Methyl-D-Aspartate (NMDA) (A/N) ratios. Chemogenetic inhibition of ChIs inhibited cued nicotine seeking and resulted in decreased A/N, whereas activation of ChIs had no effect, demonstrating that ChI inhibition prevents transient synaptic potentiation (t-SP) associated with cue-induced nicotine seeking. To assess potential underlying mechanisms, accumbens α₄β₂- and α₇-containing nicotinic ACh receptors (nAChRs) were pharmacologically inhibited and MSN synaptic morphology was assessed following reinstatement. Inhibition of both nAChR subtypes prevented cue-induced nicotine seeking and t-SP (measured via changes in spine head diameter). Together, these results demonstrate that these neurons mediate cue-induced nicotine reinstatement and underlying synaptic plasticity within the NAcore.

Humidified high-flow therapy (HFT) is a noninvasive respiratory therapy, typically delivered through a nasal cannula interface, which delivers a stable fraction of inspired oxygen (FIO₂) at flow rates of up to 60 L·min⁻¹. It is well-tolerated, simple to set up and ideally applied at 37°C to permit optimal humidification of inspired gas. Flow rate andFIO₂should be selected based on patients' inspiratory effort and severity of hypoxaemia. HFT yields beneficial physiological effects, including improved mucociliary clearance, enhanced dead space washout and optimisation of pulmonary mechanics. Robust evidence supports its application in the critical care setting (treatment of acute hypoxaemic respiratory failure and prevention of post-extubation respiratory failure) and emerging data supports HFT use during bronchoscopy, intubation and breaks from noninvasive ventilation or continuous positive airway pressure. There are limited data on HFT use in patients with hypercapnic respiratory failure, as an adjunct to pulmonary rehabilitation and in the palliative care setting, and further research is needed to validate the findings of small studies. The COVID-19 pandemic raises questions regarding HFT efficacy in COVID-19-related hypoxaemic respiratory failure and concerns regarding aerosolisation of respiratory droplets. Clinical trials are ongoing and healthcare professionals should implement strict precautions to mitigate the risk of nosocomial transmission.Educational aims: Provide a practical guide to HFT setup and delivery. Outline the physiological effects of HFT on the respiratory system. Describe clinical applications of HFT in adult respiratory and critical care medicine and evaluate the supporting evidence. Discuss application of HFT in COVID-19 and aerosolisation of respiratory droplets.

Introduction: Although the use of e-cigarettes is increasing worldwide, their short and long-term effects remain undefined. We aimed to study the acute effect of short-term use of e-cigarettes containing nicotine on lung function and respiratory symptoms in smokers with airways obstructive...

Chronic obstructive pulmonary disease (COPD) causes load-capacity-drive imbalance in both wakefulness and sleep, principally driven by expiratory flow limitation and hyperinflation. Sleep imposes additional burdens to the respiratory muscle pump, driven by changes in respiratory muscle tone, neural respiratory drive and consequences of the supine position. COPD patients are therefore at higher risk of decompensation during sleep, which may manifest as altered sleep architecture, isolated nocturnal desaturation, sleep hypoventilation and restless legs. Each form of sleep disordered breathing in COPD is associated with adverse clinical and patient-reported outcomes, including increased risk of exacerbations, hospitalisation, cardiovascular events, reduced survival and poorer quality of life. COPD-obstructive sleep apnoea (OSA) overlap syndrome represents a distinct clinical diagnosis, in which clinical outcomes are significantly worse than in either disease alone, including increased mortality, risk of cardiovascular events, hospitalisation and exacerbation frequency. Sleep disordered breathing is under-recognised by COPD patients and their clinicians, however early diagnosis and management is crucial to reduce the risk of adverse clinical outcomes. In this narrative review, we describe the pathophysiology of COPD and physiological changes that occur during sleep, manifestations and diagnosis of sleep disordered breathing in COPD and associated clinical outcomes.

Background. Respiratory symptoms are usually underestimated in patients with chronic kidney disease undergoing maintenance hemodialysis. Therefore, we set out to investigate the prevalence of patients chronic dyspnea and the relationship of the symptom to lung function indices.Methods. Twenty-five clinically stable hemodialysis patients were included. The mMRC dyspnea scale was applied before and after hemodialysis. Spirometry, single breath nitrogen test, arterial blood gases, static maximum inspiratory (Pimax⁡) and expiratory (Pemax⁡) muscle pressures, and mouth occlusion pressure (P0.1) were also measured.Results. Despite normal spirometry, all patients (100%) reported mild to moderate degree of chronic dyspnea pre which was reduced after hemodialysis. The sole predictor of (Δ) mMRC was the (Δ)P0.1(r=0.71, P<0.001). ThePimax⁡was reduced before and correlated with the duration of hemodialysis (r=0.614, P<0.001), whilst after the session it was significantly increased (P<0.001). Finally (Δ) weight was correlated with the (Δ)Pimax⁡ %pred(r=0.533, P=0,006) and with the (Δ) CV(%pred)(r=0.65, P<0.001).Conclusion. We conclude that dyspnea is the major symptom among the CKD patients that improves after hemodialysis. The neuromechanical dissociation observed probably is one of the major pathophysiologic mechanisms of dyspnea.