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Nocturnal Ventilation Defects (VDefs) in Asthma May Be Caused by Effects of Sleep and Obesity on Lung Volume and Tidal Volume
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A4679 - Nocturnal Ventilation Defects (VDefs) in Asthma May Be Caused by Effects of Sleep and Obesity on Lung Volume and Tidal Volume
Author Block: T. Winkler; Dept of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States.
INTRODUCTION: 75% of asthma patients report having nighttime symptoms causing them to wake up. However, it is unclear if this nocturnal asthma is a separate phenotype or a sign of more advanced asthma. The aim of this study was to investigate if effects of supine position, sleep, and obesity on lung volume and tidal volume can explain the emergence of VDefs in an airway tree with airway inflammation or remodeling.
METHODS: An integrative computational model of bronchoconstriction (Nature 2005;434:777) was used to compare the effects of upright position awake (normal functional residual capacity (FRC) = 2400 ml, normal VT = 650 ml), supine asleep (FRC - 750 ml, VT - 15%), and obese supine asleep (FRC - 1125 ml, VT - 15%) on the emergence of VDefs. Airway smooth muscle had a constant baseline tone (Tr = 0.6), and different degrees of increased airway wall thickness (AWT) (0...25%) mimicking airway inflammation and remodeling were assigned to 1/8th of the bronchial tree of the model, which is based on evidence showing that airway inflammation and remodeling in asthma may be a regional rather than global process. For comparison between regional and randomly scattered changes in AWT, regional changes applied to the individual airways were randomly reassigned within each airway generation.
RESULTS: No VDefs emerged for upright awake conditions. In contrast, conditions of supine sleep led to VDefs for regional AWT increases above 15%. In obesity, this threshold was dramatically lowered resulting in consistent VDefs for AWT increases above 2%. Also, the fraction of VDefs (FVDefs) relative to total volume was higher for obese supine asleep compared to supine asleep, e.g. FVDefs = 12.5% vs. 8.9% respectively at an AWT increase of 18%. For randomly scattered changes, VDefs emerged above 9% AWT increase for obese supine asleep, which suggest a substantial effect of regional clustering in AWT compared to scattered changes.
CONCLUSIONS: The decrease in lung volume and tidal volume during sleep may explain the emergence of nocturnal VDefs in patients with increased AWT. Particularly obese patients may be highly susceptible since a relative small increases in AWT may lead to VDefs, even without any additional stimulus of airway smooth muscle above baseline tone. Such nocturnal VDefs may explain the high frequency of nighttime symptoms in patients with asthma.
FUNDED BY: Internal Funds of the Department of Anesthesia, Critical Care, and Pain Medicine at Massachusetts General Hospital.
Author Block: T. Winkler; Dept of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States.
INTRODUCTION: 75% of asthma patients report having nighttime symptoms causing them to wake up. However, it is unclear if this nocturnal asthma is a separate phenotype or a sign of more advanced asthma. The aim of this study was to investigate if effects of supine position, sleep, and obesity on lung volume and tidal volume can explain the emergence of VDefs in an airway tree with airway inflammation or remodeling.
METHODS: An integrative computational model of bronchoconstriction (Nature 2005;434:777) was used to compare the effects of upright position awake (normal functional residual capacity (FRC) = 2400 ml, normal VT = 650 ml), supine asleep (FRC - 750 ml, VT - 15%), and obese supine asleep (FRC - 1125 ml, VT - 15%) on the emergence of VDefs. Airway smooth muscle had a constant baseline tone (Tr = 0.6), and different degrees of increased airway wall thickness (AWT) (0...25%) mimicking airway inflammation and remodeling were assigned to 1/8th of the bronchial tree of the model, which is based on evidence showing that airway inflammation and remodeling in asthma may be a regional rather than global process. For comparison between regional and randomly scattered changes in AWT, regional changes applied to the individual airways were randomly reassigned within each airway generation.
RESULTS: No VDefs emerged for upright awake conditions. In contrast, conditions of supine sleep led to VDefs for regional AWT increases above 15%. In obesity, this threshold was dramatically lowered resulting in consistent VDefs for AWT increases above 2%. Also, the fraction of VDefs (FVDefs) relative to total volume was higher for obese supine asleep compared to supine asleep, e.g. FVDefs = 12.5% vs. 8.9% respectively at an AWT increase of 18%. For randomly scattered changes, VDefs emerged above 9% AWT increase for obese supine asleep, which suggest a substantial effect of regional clustering in AWT compared to scattered changes.
CONCLUSIONS: The decrease in lung volume and tidal volume during sleep may explain the emergence of nocturnal VDefs in patients with increased AWT. Particularly obese patients may be highly susceptible since a relative small increases in AWT may lead to VDefs, even without any additional stimulus of airway smooth muscle above baseline tone. Such nocturnal VDefs may explain the high frequency of nighttime symptoms in patients with asthma.
FUNDED BY: Internal Funds of the Department of Anesthesia, Critical Care, and Pain Medicine at Massachusetts General Hospital.
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