Raising end-expiratory volume relieves air hunger in mechanically ventilated healthy adults

Vovk, Andrea; Binks, Andrew P.

doi:10.1152/japplphysiol.01185.2006

Cited by 22 publications

(6 citation statements)

References 49 publications

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“…For example, retention of volume would cause greater lung stretch receptor activity, which is known to reduce air hunger. An increase in end-expiratory volume has been shown to relieve dyspnea in a similar model [17]. …”

Section: Discussionmentioning

confidence: 99%

“…The time traces of physiological variables and ratings were examined, and individual data points were excluded if any of the following a priori exceptions occurred during data point collection periods: 1) retention of air by the subject that raised end-expiratory volume by more than 50% of tidal volume, and consequently raised the subsequent end-inspiratory volumes (such volume increases reduce breathing discomfort [17]). 2) failure of the limiting bag to collapse on inspiration (at very low levels of stimulus drive), thus not fulfilling the criterion of limited ventilation.…”

Section: Methodsmentioning

confidence: 99%

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The Effect of Aerosol Saline on Laboratory-Induced Dyspnea

O’Donnell

Lansing

Schwartzstein

et al. 2016

Lung

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Purpose In the ‘placebo arm’ of a recent study we found that aerosol saline (sham treatment) produced substantial relief of laboratory-induced dyspnea (Breathing Discomfort – BD) in nearly half the subjects. The sham intervention included a physiological change, and instructions to subjects could have produced expectation of dyspnea relief. In the present study we attempted to discover whether the response to sham aerosol was driven by behavioral or physiological aspects of the intervention. Methods Dyspnea (air hunger) was evoked by constraining tidal volume during graded hypercapnia. We measured Petco2 vs BD relationship before and after aerosol saline. To minimize subjects’ expectations of dyspnea relief, participants in were clearly instructed that we would only deliver saline aerosol. In Protocol 1, we delivered aerosol saline with a ventilator (mimicking our prior study); in Protocol 2, we delivered aerosol without a ventilator. Results Administration of aerosol saline had little effect on BD in this group of subjects with one exception: one subject experienced appreciable reduction in BD in Protocol 1. This treatment effect was less in Protocol 2. The two most likely explanations are a) that procedures surrounding ventilator administration of aerosol produced a psychological placebo treatment effect even though the subject knew a drug was not given, b) there were behavioral changes in breathing undetected by our measurements of respiratory flow and volume that altered the subjects comfort. Conclusion When the expectation of treatment effect is minimized, a significant reduction in dyspnea in response to saline placebo is uncommon but not impossible.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

The Effect of Aerosol Saline on Laboratory-Induced Dyspnea

O’Donnell

Lansing

Schwartzstein

et al. 2016

Lung

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“…Because high flow demands, and air hunger are the worst form of dyspnea it is important to understand which ventilator settings may relieve or worsen distress. Air hunger is reduced with increased levels of PEEP by increasing EELV ( Vovk and Binks, 2007 ) For example, spontaneous breathing at low levels of PEEP is associated with greater lung and diaphragm injury whereas spontaneous breathing at higher levels of PEEP is protective ( Yoshida et al, 2016 ; Morias et al, 2018 ). Physiologically, as lung volume increases mechanical receptors provide feedback to the brainstem, which depresses inspiratory effort and signals expiratory muscles for active exhalation if needed ( Road and Leevers, 1988 ; Road and Leevers, 1990 ; Torres et al, 1993 ).…”

Section: Myth #10—patients Must Be Spontaneously Breathing For Aprv T...mentioning

confidence: 99%

Myths and Misconceptions of Airway Pressure Release Ventilation: Getting Past the Noise and on to the Signal

et al. 2022

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In the pursuit of science, competitive ideas and debate are necessary means to attain knowledge and expose our ignorance. To quote Murray Gell-Mann (1969 Nobel Prize laureate in Physics): “Scientific orthodoxy kills truth”. In mechanical ventilation, the goal is to provide the best approach to support patients with respiratory failure until the underlying disease resolves, while minimizing iatrogenic damage. This compromise characterizes the philosophy behind the concept of “lung protective” ventilation. Unfortunately, inadequacies of the current conceptual model–that focuses exclusively on a nominal value of low tidal volume and promotes shrinking of the “baby lung” - is reflected in the high mortality rate of patients with moderate and severe acute respiratory distress syndrome. These data call for exploration and investigation of competitive models evaluated thoroughly through a scientific process. Airway Pressure Release Ventilation (APRV) is one of the most studied yet controversial modes of mechanical ventilation that shows promise in experimental and clinical data. Over the last 3 decades APRV has evolved from a rescue strategy to a preemptive lung injury prevention approach with potential to stabilize the lung and restore alveolar homogeneity. However, several obstacles have so far impeded the evaluation of APRV’s clinical efficacy in large, randomized trials. For instance, there is no universally accepted standardized method of setting APRV and thus, it is not established whether its effects on clinical outcomes are due to the ventilator mode per se or the method applied. In addition, one distinctive issue that hinders proper scientific evaluation of APRV is the ubiquitous presence of myths and misconceptions repeatedly presented in the literature. In this review we discuss some of these misleading notions and present data to advance scientific discourse around the uses and misuses of APRV in the current literature.

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“…Sakurai et al ( 1998 ) similarly reported that lung expansion inhibited respiratory distress induced by airway occlusion in a dose-related manner and that bilateral vagotomy totally abolished this effect, presumably via loss of sensory feedback from PSRs. On the basis of these observations and the purported role of PSRs in the neuromodulation of breathlessness in humans (Manning et al, 1992 ; Flume et al, 1996 ; Vovk and Binks, 2007 ), it has been proposed that nebulized furosemide alleviates breathlessness by altering pulmonary vagal afferent activity from PSRs, presumably mimicking greater tidal volume (V T ) expansion (Nishino et al, 2000 ; Sudo et al, 2000 ; Nehashi et al, 2001 ; Moosavi et al, 2007 ; Nishino, 2009 ).…”

Section: Introductionmentioning

confidence: 97%

Effect of Inhaled Nebulized Furosemide (40 and 120 mg) on Breathlessness during Exercise in the Presence of External Thoracic Restriction in Healthy Men

Waskiw-Ford

Mainra

et al. 2018

Front. Physiol.

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Inhalation of nebulized furosemide has been shown to alleviate breathlessness provoked experimentally in health and disease; however, it remains unclear whether the efficacy of nebulized furosemide on breathlessness is dose-dependent. We tested the hypothesis that inhaled nebulized furosemide would be associated with a dose-dependent relief of breathlessness during exercise testing in the setting of abnormal restrictive constraints on tidal volume (VT) expansion. In a randomized, double-blind, crossover study, 24 healthy men aged 25.3 ± 1.2 years (mean ± SE) completed a symptom-limited constant-load cycle endurance exercise test in the setting of external thoracic restriction via chest wall strapping to reduce vital capacity by ~20% following single-dose inhalation nebulized furosemide (40 and 120 mg) and 0.9% saline. Compared with 0.9% saline, neither 40 nor 120 mg of inhaled nebulized furosemide had an effect on ratings of perceived breathlessness during exercise or an effect on cardiometabolic, ventilatory, breathing pattern, or dynamic operating lung volume responses during exercise. Urine production rate, the percentage of participants reporting an “urge to urinate” and the intensity of perceived “urge to urinate” were all significantly greater after inhaling the 120 mg furosemide solution compared with both 0.9% saline and 40 mg furosemide solutions. We concluded that, under the experimental conditions of this study, inhalation of nebulized furosemide at doses of 40 and 120 mg did not alleviate breathlessness during exercise in healthy men.

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Raising end-expiratory volume relieves air hunger in mechanically ventilated healthy adults

Cited by 22 publications

References 49 publications

The Effect of Aerosol Saline on Laboratory-Induced Dyspnea

The Effect of Aerosol Saline on Laboratory-Induced Dyspnea

Myths and Misconceptions of Airway Pressure Release Ventilation: Getting Past the Noise and on to the Signal

Effect of Inhaled Nebulized Furosemide (40 and 120 mg) on Breathlessness during Exercise in the Presence of External Thoracic Restriction in Healthy Men

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