The dangers of recreational inhalation of nitrous oxide

Nitrous oxide, also known as ‘laughing gas’, is one of the most widely used recreational drugs among teenagers in the UK. Copious inhalation of nitrous oxide may increase intra-alveolar pressure, resulting in barotrauma secondary to alveolar rupture. Pneumomediastinum and subcutaneous emphysema are common clinical findings in nitrous oxide-associated barotrauma. Prolonged nitrous oxide misuse may inactivate vitamin B12 through the alteration of its metabolism, causing demyelination of the central and peripheral nervous system. A spectrum of neurological manifestations has been reported, including peripheral neuropathy, myelopathy and subacute combined degeneration of the spinal cord. Medical therapies and psychosocial interventions aiming at nitrous oxide cessation are important treatment steps to achieve partial or complete recovery from the adverse effects associated with inhalation of nitrous oxide.

Diagnostic Insights from Plethysmographic Alveolar Pressure Assessed during Spontaneous Breathing in COPD Patients

Since its introduction in the clinical practice, body plethysmography has assisted pneumologists in the diagnosis of respiratory diseases and patients’ follow-up, by providing easy assessment of absolute lung volumes and airway resistance. In the last decade, emerging evidence suggested that estimation of alveolar pressure by electronically-compensated plethysmographs may contain information concerning the mechanics of the respiratory system which goes beyond those provided by the simple value of airway resistance or conductance. Indeed, the systematic study of expiratory alveolar pressure-flow loops produced during spontaneous breathing at rest has shown that the marked expansion of expiratory loops in chronic obstructive pulmonary disease patients mainly reflects the presence of tidal expiratory flow-limitation. The presence of this phenomenon can be accurately predicted on the basis of loop-derived parameters. Finally, we present results suggesting that plethysmographic alveolar pressure may be used to estimate non-invasively intrinsic positive end-expiratory pressure (PEEPi) in spontaneously breathing patients, a task which previously could be only accomplished by introducing a balloon-tipped catheter in the esophagus.

Spontaneous Pneumomediastinum in an Adolescent Soccer Player

Spontaneous pneumomediastinum (SPM) is an uncommon and usually benign self-limiting clinical disorder found in young people, often without apparent precipitating factors or diseases. A pressure gradient exists between the peripheral pulmonary alveoli and the hilum, and increased intra-alveolar pressure causes rupture of the terminal alveoli. We present the case of a 15-year-old male soccer player who presented with a complaint of anterior chest pain and dysphagia after stopping the strong ball with his chest. His symptom gradually progressed over hours. We can make the diagnosis of SPM using by chest X-ray and computed tomography (CT) scanning. His symptoms were gradually resolved over the course of approximately one week with no exercise and careful observation. We believe that our case provides very useful information to alert clinicians and coaches regarding this rare disease that may occur in anyone including adolescent soccer players.

Spontaneous pneumothorax and subpleural bullae in a patient with COVID-19: a 92-day observation

This report describes a patient with COVID-19 who developed spontaneous pneumothorax and subpleural bullae during the course of the infection. Consecutive chest computed tomography images indicated that COVID-19-associated pneumonia had damaged the subpleural alveoli and distal bronchus. Coughing might have induced a sudden increase in intra-alveolar pressure, leading to the rupture of the subpleural alveoli and distal bronchus and resulting in spontaneous pneumothorax and subpleural bullae. At the 92-day follow-up, the pneumothorax and subpleural bullae had completely resolved, which indicated that these complications had self-limiting features.

Tidal expiratory flow limitation induces expiratory looping of the alveolar pressure-flow relation in COPD patients

In stable chronic obstructive pulmonary disease (COPD) patients spontaneously breathing at rest, tidal expiratory flow limitation is the major determinant of the occurrence of expiratory looping in the plethysmographic flow-alveolar pressure diagram. In these patients the magnitude and the characteristics of the loop can be used as predictors of the presence of tidal expiratory flow limitation.

Venous return and pulmonary hemodynamics under the positive end-expiratory pressure mechanical ventilation

In the review we have discussed the mechanisms of the changes of the venous return and pulmonary hemodynamics which take place in clinical cases of the mechanical lung ventilation with positive end-expiratory pressure. In these conditions the elevating of right atrial pressure does not cause the decreasing of the venous return, because the mean circulatory filling pressure also increases. Thus, the gradient for venous return remains relatively constant. In case of the mechanical lung ventilation with positive end-expiratory pressure the decreasing of the venous return is the result of the elevation of the venous resistance as consequence of the direct increasing of the intrathoracic and transdiaphragmatic pressures and activation of the reflectory neurogenic mechanisms. In the conditions, indicated above, the increased alveolar pressure leads to the improvement of the diffused lung capacity for oxygen, which decreases the manifestations of the hypoxic pulmonary vasoconstriction and thus diminishes pulmonary vascular resistance. The character of changes of the last one is determined by the reactions of the two types (alveolar and extraalveolar) intraparenchimal pulmonary vessels. This leads to the changes of the resistive and capacitive functions of the pulmonary vessels. In case of the high levels of the positive end-expiratory pressure (more than 30 cm of water column) the value of alveolar pressure is comparable or even more excessive than pulmonary artery pressure (1216 mm Hg), which can be the reason of the decreasing of the right ventricular contractility and the venous return. The increasing of the capillary filtration coefficient of pulmonary vessels in the conditions of the mechanical lung ventilation with positive end-expiratory pressure can be the result of the activation of the mechanosensitive transient receptor potential vanilloid-4 (TRPV4) channels and the increasing endothelial calcium entry.

Airway Closure during Surgical Pneumoperitoneum in Obese Patients

Editor’s PerspectiveWhat We Already Know about This TopicWhat This Article Tells Us That Is NewBackgroundAirway closure causes lack of communication between proximal airways and alveoli, making tidal inflation start only after a critical airway opening pressure is overcome. The authors conducted a matched cohort study to report the existence of this phenomenon among obese patients undergoing general anesthesia.MethodsWithin the procedures of a clinical trial during gynecological surgery, obese patients underwent respiratory/lung mechanics and lung volume assessment both before and after pneumoperitoneum, in the supine and Trendelenburg positions, respectively. Among patients included in this study, those exhibiting airway closure were compared to a control group of subjects enrolled in the same trial and matched in 1:1 ratio according to body mass index.ResultsEleven of 50 patients (22%) showed airway closure after intubation, with a median (interquartile range) airway opening pressure of 9 cm H2O (6 to 12). With pneumoperitoneum, airway opening pressure increased up to 21 cm H2O (19 to 28) and end-expiratory lung volume remained unchanged (1,294 ml [1,154 to 1,363] vs. 1,160 ml [1,118 to 1,256], P = 0.155), because end-expiratory alveolar pressure increased consistently with airway opening pressure and counterbalanced pneumoperitoneum-induced increases in end-expiratory esophageal pressure (16 cm H2O [15 to 19] vs. 27 cm H2O [23 to 30], P = 0.005). Conversely, matched control subjects experienced a statistically significant greater reduction in end-expiratory lung volume due to pneumoperitoneum (1,113 ml [1,040 to 1,577] vs. 1,000 ml [821 to 1,061], P = 0.006). With airway closure, static/dynamic mechanics failed to measure actual lung/respiratory mechanics. When patients with airway closure underwent pressure-controlled ventilation, no tidal volume was inflated until inspiratory pressure overcame airway opening pressure.ConclusionsIn obese patients, complete airway closure is frequent during anesthesia and is worsened by Trendelenburg pneumoperitoneum, which increases airway opening pressure and alveolar pressure: besides preventing alveolar derecruitment, this yields misinterpretation of respiratory mechanics and generates a pressure threshold to inflate the lung that can reach high values, spreading concerns on the safety of pressure-controlled modes in this setting.