Increase In Inspiratory Flow Research Articles

Performance of Different Low-Flow Oxygen Delivery Systems.

The delivery of a high and consistent [Formula: see text] is imperative to treat acute hypoxemia. The objective of this study was to analyze the effective inspired oxygen concentration delivered by different low-flow oxygen therapy systems challenged with different oxygen flows and respiratory patterns in an experimental lung model. An adult lung model ventilated in volume control mode simulated different respiratory patterns to obtain mean inspiratory flow of 22.5, 30.0, 37.5, or 45.0 L/min. The oxygen concentration sampled inside the lung model by nasal cannula, simple face mask, non-rebreather mask, and double-trunk mask above nasal cannula tested at oxygen flows of 10, 12.5, and 15 L/min was quantified. The 3 masks were sealed tight onto the model's airway opening. They were also tested with standardized leaks to determine their clinical performance. All oxygen delivery systems delivered higher oxygen concentration with increasing oxygen flows, regardless of the respiratory pattern. Within each device, the increase in inspiratory flow decreased oxygen concentration when using nasal cannula (P = .03), the simple face mask (P = .03), but not the non-rebreather mask (P = .051) nor the double-trunk mask (P = .13). In sealed condition, the double-trunk mask outperformed the non-rebreather mask and simple face mask (P < .001); mean oxygen concentration was 84.2%, 68.5%, and 60.8%, respectively. Leaks amplified oxygen concentration differences between the double-trunk mask and the other masks as the oxygen delivery decreased by 4.6% with simple face mask (95% CI 3.1-6.1%, P < .001), 7.8% with non-rebreather mask (95% CI 6.3-9.3%, P < .001), and 2.5% with double-trunk mask (95% CI 1-4%, P = .002). With leaks, the oxygen concentration provided by the simple face mask and the non-rebreather mask was similar (P = .15). Lung oxygen concentration values delivered by the double-trunk mask were higher than those obtained with other oxygen delivery systems, especially when leaks were present.

Sleep increases leaks and asynchronies during home noninvasive ventilation: a polysomnographic study.

In patients treated with noninvasive ventilation, sleep-related breathing changes can modify patient-ventilator interactions, which could reduce its effectiveness. The aim of this prospective observational study was to determine the impact of sleep/wake state on leaks, upper airway obstructive events, and asynchronies in patients treated by long-term noninvasive ventilation. Stable patients adapted to noninvasive ventilation were considered for nocturnal polysomnography. Unintentional leaks, upper airway obstructive events, and asynchronies were compared between sleep and awake periods. Twenty-eight patients were enrolled. Underlying diagnoses were neuromuscular disease (n = 11), chest wall disease (n = 8), and obesity-hypoventilation (n = 9). Leaks were more frequent in sleep than in awake periods, with a median of 10% (interquartile range [IQR], 0%-75%) vs 1% (IQR, 0%-9%) of time (P < .001), respectively. During sleep, asynchronies with and without associated leak affected 27% of breaths (IQR, 16%-39%) compared with non-leak-related asynchronies that were recorded in 8% (IQR, 3%-25%) of breaths (P < .001). Asynchronies affecting more than 10% of total breaths were more frequent in sleep (25 patients, 89%) than in awake time (8 patients, 29%; P = .25). Eleven patients (39%) presented with 5 or more upper airway obstructive events without reduction in ventilatory drive per hour of sleep. In patients adapted to home noninvasive ventilation, leaks, asynchronies, and upper airway obstructive events are frequent during the night and are concentrated in sleep periods. Asynchronies are often associated with leaks. These findings may have clinical implications considering that in patients with low sleep efficiency respiratory events could be underestimated if sleep is not evaluated. Martí S, Ferré A, Sampol G, etal. Sleep increases leaks and asynchronies during home noninvasive ventilation: a polysomnographic study. J Clin Sleep Med. 2022;18(1):225-233.

Innovative sprayable in situ gelling fluticasone suspension: Development and optimization of nasal deposition

The aim of this study was to develop an innovative in situ gelling suspension for effective nasal delivery of fluticasone. Pectin, gellan gum and sodium hyaluronate were used as gelling/thickening agents, and Tween 80 as a suspending agent. The influence of the formulation and/or administration parameters on formulation sprayability and nasal deposition was explored with an appropriate experimental design with the range for parameters in the design obtained from previous research and domain knowledge. All formulations exhibited appropriate sprayability and instant gelation upon mixing with simulated nasal fluid exhibiting weak gel properties convenient for nasal delivery. Targeted turbinate deposition depended on administration and formulation parameters, including their interactions. Decrease in the administration angle from horizontal plane, increase in inspiratory flow and presence of sodium hyaluronate significantly increased deposition in turbinate region. Parameters in interactions included concentration of polymers, surfactant and fluticasone, as well as administration angle. Selected formulations with high turbinate deposition exhibited significant increase in viscosity upon gelation, showing potential to prolong the drug retention at the nasal mucosa. The highest effect on the gel viscosity, strength and fluticasone release profile was observed for gellan gum, thus recognised as crucial parameter for the optimisation of overall therapeutic effect.

Effect of inspiratory time and flow settings during assist-control ventilation.

The effect of the settings of inspiratory time and inspiratory flow during assist-control ventilation on the response of a patient's respiratory controller has been the subject of intense research during the last few years. An increase in inspiratory flow or a decrease in tidal volume delivered by the ventilator is associated with prompt increases in respiratory frequency. The changes occur before any change in arterial blood gases can take place. These responses occur both during wakefulness and sleep and in health and disease states. Whether the responses are the result of Hering-Breuer reflex activity or they arise in flow-sensitive receptors remains to be defined. Important clinical implications of the respiratory rate response to changes in ventilatory settings include effects on carbon dioxide, intrinsic positive end-expiratory pressure, and, possibly, on the instability of the respiratory rate in the transition between wakefulness and sleep.

Termination of inspiration by phase-dependent respiratory vagal feedback in awake normal humans.

Imperceptible levels of proportional assist ventilation applied throughout inspiration reduced inspiratory time (TI) in awake humans. More recently, the reduction in TI was associated with flow assist, but flow assist also reaches a maximum value early during inspiration. To test the separate effects of flow assist and timing of assist, we applied a pseudorandom binary sequence of flow-assisted breaths during early, late, or throughout inspiration in eight normal subjects. We hypothesized that imperceptible flow assist would shorten TI most effectively when applied during early inspiration. Tidal volume, integrated respiratory muscle pressure per breath, TI, and TE were recorded. All stimuli (early, late, or flow assist applied throughout inspiration) resulted in a significant increase in inspiratory flow; however, only when the flow assist was applied during early inspiration was there a significant reduction in TI and the integrated respiratory muscle pressure per breath. These results provide further evidence that vagal feedback modulates breathing on a breath-by-breath basis in conscious humans within a physiological range of breath sizes.

Measurements of Occlusion Pressure during Anesthesia with Volatile Anesthetics in Humans

Department of Anaesthetics University of Edinburgh, Royal Infirmary, Edinburgh EH3 9YW Scotland.To the Editor:—Recently, Canet et al., [1] reporting on changes in occlusion pressure and ventilation with different depths of anesthesia using either halothane or isoflurane, suggested that only one study previously analyzed occlusion pressure in humans, at increasing concentrations of a halogenated anesthetic agent and that studies of the occlusion pressure wave are scarce.In an analysis of the occlusion pressure wave and inspiratory flow patterns of patients anesthetized with enflurane and nitrous oxide, [2] I found that ventilatory depression caused by an increase in inspired enflurane concentration was related solely to a reduction in central drive and not to the peripheral factors more favored by Canet et al. in their discussion. The same study also reported changes in the occlusion pressure and inspiratory flow pattern caused by opioid administration. There was no marked change in estimates of active elastance and impedance, again suggesting that the depression was central. Occlusion pressure also was used in a further study, investigating the findings of Wahba and Sadkova, [3] who found that atropine increased ventilation during anesthesia with enflurane. The effects of atropine administration were studied in patients anesthetized with enflurane and halothane, using occlusion pressure to distinguish central effects from peripheral, mechanical effects. The findings suggested a minor effect after premedication with meperidine, consistent with the possibility of bronchodilation: Atropine caused an increase in inspiratory flow, although occlusion pressure was unlatered. [4].These observations support the suggestion of Canet et al that further analysis of occlusion pressure waveform in spontaneously breathing anesthetized patients can be helpful to investigate the neural mechanisms of respiratory depression.G. B. Drummond, M.B.Ch.B., Department of Anaesthetics University of Edinburgh, Royal Infirmary, Edinburgh EH3 9YW Scotland.(Accepted for publication December 9, 1994.)

Contribution of central and reflex nervous activity to the rapid increase in pulmonary ventilation at the start of muscular exercise in man.

To investigate the relative contributions of the central and peripheral neural drive to hyperventilation at the onset of muscular exercise, five volunteers were tested during the first ten breaths while performing both voluntary (VM) and passive (PM) ankle rotations with a frequency of 1 Hz and through an angle of 10 degrees. Resulting breathing patterns for the two movements were compared. Hypocapnic hyperventilation, found in both PM and VM, indicated its neural origin. Respiratory changes were higher in VM than in PM. In both experimental conditions, increases in ventilation (VE) depended more on respiratory frequency (f) than on tidal volume (VT). Moreover, increases in VT adapted, breath-by-breath, to values lower than the initial ones, while increases in f rose progressively. Expiratory time was reduced more than inspiratory time (TI); increases in inspiratory flow (VT/TI) depended to the same extent on changes in both TI and VT. Increases in expiratory tidal volume were initially higher than in inspiratory tidal volume, thereby producing a reduction in functional residual capacity. Because PM respiratory changes could be considered to be of nervous reflex origin only, the identical breathing patterns in PM and VM indicated that the hyperventilation found also in VM was mainly of reflex origin. The increase in VE was considered to be dependent on a greater stimulus from muscle proprioreceptors.

Inspiratory muscles during exercise: a problem of supply and demand.

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Within-breath PCO2 levels in the airways and at the pulmonary stretch receptor sites.

The discharge frequency of pulmonary stretch receptors (PSRs) shows an inverse responsiveness to the CO2 partial pressure (PCO2), which is limited to an extremely hypocapnic range. During inspiration extremely hypocapnic PCO2 levels are obtained in a large part of the respiratory tract due to the diffusion limited gas mixing. The question remains whether PSRs in combination with these low levels of PCO2 are involved in the regulation of breathing. As a necessary first step to be able to answer this question, this paper is devoted to the calculation of the within-breath PCO2 transients in the respiratory tract and the corresponding PCO2 oscillations in the superficial airway tissue. For PSRs located in the smooth muscles of large bronchi, the calculations predict a time delay of a few seconds to adapt their discharge frequency to a change in PCO2 in the airway lumen. The result is in good agreement with the observed time delay reported in the literature. For the PSRs located in the acini the calculated time constant of their discharge response to PCO2 variations in the lumen is much smaller than 250 ms. This implies a within-breath response to the oscillating luminal PCO2. Further, the calculations show that a CO2 diffusion front is established within the acini during early inspiration. This diffusion front penetrates further and further into the acini with increasing work load due to the concomitant increase in inspiratory flow. As a consequence, the discharge frequency vs. volume response curve of PSRs, especially those located in distal airways, may be modified by a flow-induced PCO2-related contribution.(ABSTRACT TRUNCATED AT 250 WORDS)