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Additional file 1. Additional figures and tables.

Administration of bolus intravenous fluid is associated with respiratory dysfunction and increased mortality, findings with no clear mechanistic explanation. The objective of this study was to examine whether bolus intravenous (i.v.) fluid administration results in acute lung injury in a rat model and further, to examine whether this injury is associated with transient receptor potential vallinoid (TRPV)4 channel function and endothelial inflammatory response. Healthy male Sprague-Dawley rats were administered 60 ml/kg 0.9% saline i.v. over 30 min. Manifestation of acute lung injury was assessed by lung physiology, morphology, and markers of inflammation. The role of TRPV4 channels in fluid-induced lung injury was subsequently examined by the administration of ruthenium red (RR) in this established rat model and again in TRPV4 KO mice. In endothelial cell culture, permeability and P-selectin expression were measured following TRPV4 agonist with and without antagonist; 0.9% saline resulted in an increase in lung water, lavage protein and phospholipase A2, and plasma angiopoietin-2, with worsening in arterial blood oxygen (PaO2), lung elastance, surfactant activity, and lung histological injury score. These effects were ameliorated following i.v. fluid in rats receiving RR. TRPV4 KO mice did not develop lung edema. Expression of P-selectin increased in endothelial cells following administration of a TRPV4 agonist, which was ameliorated by simultaneous addition of RR. Bolus i.v. 0.9% saline resulted in permeability pulmonary edema. Data from ruthenium red, TRPV4 KO mice, and endothelial cell culture suggest activation of TRPV4 and release of angiopoietin 2 and P-selectin as the central mechanism. Refereed/Peer-reviewed

BACKGROUND: Advancements in tracheostomy tube design now provide clinicians with a range of options to facilitate communication for individuals receiving ventilator assistance through a cuffed tube. Little is known about the impact of these modern design features on resistance to air flow. METHODS: We undertook a bench model test to measure pressure-flow characteristics and resistance of a range of tubes of similar outer diameter, including those enabling subglottic suction and speech. A constant inspiratory +/- expiratory air flow was generated at increasing flows up to 150 L/min through each tube (with or without optional, mandatory, or interchangeable inner cannula). Driving pressures were measured, and resistance was calculated (cm H2O/L/s). RESULTS: Pressures changed with increasing flow (P < .001) and tube type (P < .001), with differing patterns of pressure change according to the type of tube (P < .001) and direction of air flow. The single lumen reference tube encountered the lowest inspiratory and expiratory pressures compared with all double-lumen tubes (P < .001); placement of an optional inner cannula increased bidirectional tube resistance by a factor of 3. For a tube with interchangeable inner cannulas, the type of cannula altered pressure and resistance differently (P < .001); the speech cannula in particular amplified pressure-flow changes and increased tube resistance by more than a factor of 4. CONCLUSIONS: Tracheostomy tube type and inner cannula selection imposed differing pressures and resistance to air flow during inspiration and expiration. These differences may be important when selecting airway equipment or when setting parameters for monitoring, particularly for patients receiving supported ventilation or during the weaning process. Refereed/Peer-reviewed

Purpose: Dynamometry is an objective tool for volitional strength evaluation that may overcome the limited sensitivity of the Medical Research Council scale for manual muscle tests, particularly at grades 4 and 5. The primary aims of this study were to investigate the reliability, minimal detectable change, and time to peak muscle force, measured with portable dynamometry, in critically ill patients. Materials and methods: Isometric hand grip, elbow flexion, and knee extension were measured with portable dynamometry. Results: Interrater consistency (intraclass correlation coefficient [95% confidence interval]) (0.782 [0.321-0.930] to 0.946 [0.840-0.982]) and test-retest agreement (0.819 [0.390-0.943] to 0.918 [0.779- 0.970]) were acceptable for all dynamometry forces, with the exception of left elbow flexion. Despite generally good reliability, a mean change (upper 95% confidence interval) of 2.8 (7.8) kg, 1.9 (5.2) kg, and 2.6(7.1) kg may be required from a patient's baseline force measurement of right grip, elbow flexion, and knee extension to reflect real force changes. There was also a delay in the time for critically ill patients to generate peak muscle forces, compared with healthy controls (P ≤ .001). Conclusions: Dynamometry can provide reliable measurements in alert critically ill patients, but moderate changes in strength may be required to overcome measurement error, during the acute recovery period. Deficits in force timing may reflect impaired neuromuscular control. Refereed/Peer-reviewed

Rationale: Chronic elevation of pulmonary microvascular pressure in chronic heart failure results in compensatory changes in the lung that reduce alveolar fluid filtration and protect against pulmonary microvascular rupture. Objectives: To determine whether these compensatory responses may have maladaptive effects on lung function. Methods: Six weeks after myocardial infarction (chronic heart failure model) rat lung composition, both gross and histologic; air and saline mechanics; surfactant production; and immunological mediators were examined. Measurements and Main Results: An increase in dry lung weight, due to increased insoluble protein, lipid and cellular infiltrate, without pulmonary edema was found. Despite this, both forced impedance and air pressure–volume mechanics were normal. However, there was increased tissue stiffness in the absence of surface tension (saline pressure–volume curve) with a concurrent increase in both surfactant content and alveolar type II cell numbers, suggesting a novel homeostatic phenomenon. Conclusions: These studies suggest a compensatory reduction in pulmonary surface tension that attenuates the effect of lung parenchymal remodeling on lung mechanics, hence work of breathing. Refereed/Peer-reviewed