Dynamic modulation of upper airway function during sleep: a novel single-breath method

1 Johns Hopkins Sleep Disorders Center, Baltimore, Maryland; and 2 School of Anatomy and Human Biology, University of Western Australia, Perth, Western Australia, Australia Submitted 9 February 2006 ; accepted in final form 17 June 2006 To examine the dynamic modulation of upper airway (UA) function...

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Published inJournal of applied physiology (1985) Vol. 101; no. 5; pp. 1489 - 1494
Main Authors Kirkness, Jason P, Schwartz, Alan R, Patil, Susheel P, Pichard, Luis E, Marx, Jason J, Smith, Philip L, Schneider, Harmut
Format Journal Article
LanguageEnglish
Published Bethesda, MD Am Physiological Soc 01.11.2006
American Physiological Society
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Online AccessGet full text
ISSN8750-7587
1522-1601
DOI10.1152/japplphysiol.00173.2006

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Abstract 1 Johns Hopkins Sleep Disorders Center, Baltimore, Maryland; and 2 School of Anatomy and Human Biology, University of Western Australia, Perth, Western Australia, Australia Submitted 9 February 2006 ; accepted in final form 17 June 2006 To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18–50 yr; 20–35 kg/m 2 ; apnea-hypopnea index >20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 ± 2.0 cmH 2 O) was significantly lower than the opening pressure (10.8 ± 2.4 cmH 2 O). Rus was higher for deflation (18.1 ± 2.4 cmH 2 O·l –1 ·s) than during inflation (7.5 ± 1.9 cmH 2 O·l –1 ·s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by 4 cmH 2 O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep. sleep apnea; critical pressure; upper airway occlusion; pathophysiology Address for reprint requests and other correspondence: J Kirkness, Div. of Pulmonary and Critical Care Medicine, The Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224 (e-mail: jason_kirkness{at}jhmi.edu )
AbstractList To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18–50 yr; 20–35 kg/m 2 ; apnea-hypopnea index >20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 ± 2.0 cmH 2 O) was significantly lower than the opening pressure (10.8 ± 2.4 cmH 2 O). Rus was higher for deflation (18.1 ± 2.4 cmH 2 O·l −1 ·s) than during inflation (7.5 ± 1.9 cmH 2 O·l −1 ·s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by ∼4 cmH 2 O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep.
To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18-50 yr; 20-35 kg/m^sup 2^ apnea-hypopnea index > 20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 ± 2.0 cmH2O) was significantly lower than the opening pressure (10.8 ± 2.4 cmH2O). Rus was higher for deflation (18.1 ± 2.4 cmH2O*1^sup -1^*s) than during inflation (7.5 ± 1.9 cmH2O*1^sup -1^*s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by ~4 cmH2O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep. [PUBLICATION ABSTRACT]
To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18-50 yr; 20-35 kg/m2; apnea-hypopnea index >20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 +/- 2.0 cm H2O) was significantly lower than the opening pressure (10.8 +/- 2.4 cm H2O). Rus was higher for deflation (18.1 +/- 2.4 cm H2O x l(-1) x s) than during inflation (7.5 +/- 1.9 cm H2O x l(-1) x s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by approximately 4 cm H2O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep.
To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18-50 yr; 20-35 kg/m2; apnea-hypopnea index >20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 +/- 2.0 cm H2O) was significantly lower than the opening pressure (10.8 +/- 2.4 cm H2O). Rus was higher for deflation (18.1 +/- 2.4 cm H2O x l(-1) x s) than during inflation (7.5 +/- 1.9 cm H2O x l(-1) x s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by approximately 4 cm H2O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep.To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18-50 yr; 20-35 kg/m2; apnea-hypopnea index >20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 +/- 2.0 cm H2O) was significantly lower than the opening pressure (10.8 +/- 2.4 cm H2O). Rus was higher for deflation (18.1 +/- 2.4 cm H2O x l(-1) x s) than during inflation (7.5 +/- 1.9 cm H2O x l(-1) x s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by approximately 4 cm H2O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep.
1 Johns Hopkins Sleep Disorders Center, Baltimore, Maryland; and 2 School of Anatomy and Human Biology, University of Western Australia, Perth, Western Australia, Australia Submitted 9 February 2006 ; accepted in final form 17 June 2006 To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18–50 yr; 20–35 kg/m 2 ; apnea-hypopnea index >20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 ± 2.0 cmH 2 O) was significantly lower than the opening pressure (10.8 ± 2.4 cmH 2 O). Rus was higher for deflation (18.1 ± 2.4 cmH 2 O·l –1 ·s) than during inflation (7.5 ± 1.9 cmH 2 O·l –1 ·s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by 4 cmH 2 O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep. sleep apnea; critical pressure; upper airway occlusion; pathophysiology Address for reprint requests and other correspondence: J Kirkness, Div. of Pulmonary and Critical Care Medicine, The Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224 (e-mail: jason_kirkness{at}jhmi.edu )
Author Pichard, Luis E
Marx, Jason J
Schneider, Harmut
Patil, Susheel P
Kirkness, Jason P
Schwartz, Alan R
Smith, Philip L
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IsPeerReviewed true
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Issue 5
Keywords Occlusion
Nervous system diseases
Sleep apnea syndrome
Pathophysiology
Respiratory disease
Respiratory system
Respiratory tract
Critical pressure
Vertebrata
Mammalia
Sleep
upper airway occlusion
Sleep wake cycle
sleep apnea
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Snippet 1 Johns Hopkins Sleep Disorders Center, Baltimore, Maryland; and 2 School of Anatomy and Human Biology, University of Western Australia, Perth, Western...
To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a...
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StartPage 1489
SubjectTerms Adolescent
Adult
Airway Resistance - physiology
Biological and medical sciences
Catheters
Eye movements
Female
Fundamental and applied biological sciences. Psychology
Humans
Insufflation - methods
Male
Medical instruments
Middle Aged
Neuromuscular diseases
Pharynx - physiopathology
Polysomnography
Positive-Pressure Respiration
Pressure
Pressure distribution
Protective equipment
Respiratory Mechanics - physiology
Respiratory system
Sleep
Sleep apnea
Sleep Apnea, Obstructive - physiopathology
Trachea - physiopathology
Tracheostomy
Work of Breathing - physiology
Title Dynamic modulation of upper airway function during sleep: a novel single-breath method
URI http://jap.physiology.org/cgi/content/abstract/101/5/1489
https://www.ncbi.nlm.nih.gov/pubmed/16825526
https://www.proquest.com/docview/222211927
https://www.proquest.com/docview/68958799
Volume 101
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