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Partitioning of Inhaled Ventilation Between the Nasal and Oral Routes During Sleep in Normal Subjects

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Partitioning of Inhaled Ventilation Between the Nasal and Oral Routes During Sleep in Normal Subjects J Appl Physiol 94: 883–890, 2003. First published November 1, 2002; 10.1152/japplphysiol.00658.2002. Partitioning of inhaled ventilation between the nasal and oral routes during sleep in normal subjects MICHAEL F. FITZPATRICK, HELEN S. DRIVER, NEELA CHATHA, NHA VODUC, AND ALISON M. GIRARD Department of Medicine, Queen’s University, Kingston, Ontario, Canada K7L 3N6 Submitted 18 July 2002; accepted in final form 28 October 2002 Fitzpatrick, Michael F., Helen S. Driver, Neela the snore vibration, which can originate from the soft Chatha, Nha Voduc, and Alison M. Girard. Partitioning palate or from the tongue base (30), may vary during of inhaled ventilation between the nasal and oral routes the night (10). In patients with obstructive sleep apnea during sleep in normal subjects. J Appl Physiol 94: 883–890, (OSA), one study demonstrated a change in the pri- 2003. First published November 1, 2002; 10.1152/jappl- mary site of upper airway obstruction with sleep stage, physiol.00658.2002.—The oral and nasal contributions to from the velopharyngeal level in non-REM sleep to the inhaled ventilation were simultaneously quantified during sleep in 10 healthy subjects (5 men, 5 women) aged 43 Ϯ 5 yr, hypopharyngeal level during REM sleep (4). Ϫ1 Ϫ1 The advent of the nasal cannula pressure transducer with normal nasal resistance (mean 2.0 Ϯ 0.3 cmH2O⅐l ⅐s ) by use of a divided oral and nasal mask. Minute ventilation as the preferred device for airflow measurement during awake (5.9 Ϯ 0.3 l/min) was higher than that during sleep sleep, because of its higher sensitivity for detection of (5.2 Ϯ 0.3 l/min; P Ͻ 0.0001), but there was no significant airflow limitation (27), is also predicated on the as- difference in minute ventilation between different sleep sumption that airflow during sleep is primarily via the stages (P ϭ 0.44): stage 2 5.3 Ϯ 0.3, slow-wave 5.2 Ϯ 0.2, and nasal route, regardless of sleep stage. Indeed, not all rapid-eye-movement sleep 5.2 Ϯ 0.2 l/min. The oral fraction commercial nasal cannula pressure transducer devices of inhaled ventilation during wakefulness (7.6 Ϯ 4%) was not include a sensor for oral airflow. significantly different from that during sleep (4.3 Ϯ 2%; Ϫ Limited available evidence suggests that more of the mean difference 3.3%, 95% confidence interval 2.1–8.8%, exhaled minute ventilation occurs through the oral P ϭ 0.19), and no significant difference (P ϭ 0.14) in oral fraction was observed between different sleep stages: stage route in snorers and patients with OSA than is the case two 5.1 Ϯ 2.8, slow-wave 4.2 Ϯ 1.8, rapid-eye-movement in normal subjects (9). Jaw opening was observed to 3.1 Ϯ 1.7%. Thus the inhaled oral fraction in normal subjects increase at end inspiration, compared with end expira- is small and does not change significantly with sleep stage. tion, in both normal subjects and patients with OSA, but, at both points in the breathing cycle, jaw opening upper airway; control of breathing; sleep apnea; oronasal was greater in patients with OSA than in normal subjects (12). Oral-nasal partitioning of inhaled venti- lation is an important aspect of respiratory physiology ALTHOUGH MUCH IS KNOWN ABOUT respiration during sleep, during sleep to understand, because there is quite it is remarkable that the partitioning of inhaled venti- consistent literature demonstrating an increased ten- lation between the oral and nasal routes during sleep dency to OSA with nasal obstruction (and presumably in healthy humans with normal nasal resistance has increased mouth breathing). In particular, because na- not been described. In particular, although it is widely sal resistance varies considerably from time to time in assumed that inhalation takes place via the nasal normal subjects but is a major determinant of mouth route throughout all sleep stages, there have been no breathing (18, 33) and is higher among snorers and objective measurements of inhaled oral ventilation patients with OSA (26, 19), it is important to document during sleep to support this assumption. A description the nasal resistance when describing the breathing of the inhaled breathing route during sleep is an im- route during sleep in normal subjects. portant step in understanding normal upper airway We hypothesized that, once subjects were asleep, the physiology during sleep and may provide an important oral fraction of inhaled ventilation would vary with reference point for assessment of patients with disease. sleep stage; this hypothesis was based on the rather It is conceivable that oral-nasal partitioning of in- preliminary evidence mentioned above, that snoring haled ventilation could change with different stages of volume and the site of upper airway obstruction may sleep or with position. For example, snoring was re- change with sleep stage. This study was undertaken to ported to be louder during slow wave and rapid-eye- test that hypothesis and to describe nasal and oral movement (REM) sleep than other sleep stages (11). In addition, the primary site responsible for generating The costs of publication of this article were defrayed in part by the Address for reprint requests and other correspondence: M. F. payment of page charges. The article must therefore be hereby Fitzpatrick, Division of Respiratory and Critical Care Medicine, marked ‘‘advertisement’’ in accordance with 18 U.S.C. Section 1734 Queen’s Univ., 102 Stuart St., Kingston, Ontario, Canada K7L 3N6. solely to indicate this fact. http://www.jap.org 8750-7587/03 $5.00 Copyright © 2003 the American Physiological Society 883 Downloaded from www.physiology.org/journal/jappl (081.243.030.141) on November 11, 2019. 884 BREATHING ROUTE DURING SLEEP IN NORMAL SUBJECTS partitioning of inhaled ventilation during sleep in a anterior nares (this provided the reference pressure for cal- group of healthy subjects with normal nasal resistance. culation of the differential pressure across the nasal airway). This tube was passed through a port in the CPAP mask, the MATERIALS AND METHODS port was then made airtight by using adhesive, and the proximal end of the catheter was attached to the differential Ten subjects (5 men, 5 women) were studied (Table 1). pressure transducer. Each pneumotach was calibrated with a Subjects were recruited by newspaper advertisement and 3-liter syringe to an accuracy of Ϯ0.5% before each study. screened by questionnaire, spirometry, and acoustic rhinom- Nasal resistance was measured as the change in pressure etry to exclude those with 1) upper or lower respiratory tract (cmH2O) across the nose for a standardized inspiratory flow disease, including any history of nasal allergy; 2) current rate of 0.3 l/s (9). respiratory tract infection; 3) known sleep disorders (sleep Sleep recordings. Each subject underwent overnight poly- apnea, insomnia, irregular sleep-wake cycle); 4) a history of somnography at the Sleep Laboratory, Kingston General regular loud snoring; 5) moderate or severe obesity (body Hospital. Sleep recordings were similar to the routine clinical mass index Ͼ 30); 6) claustrophobia; 7) current or recent polysomnogram [4 EEG channels (C4–A1, C3–A2, O2–A1, (within 2 yr) cigarette smoking; and 8) those currently taking O1–A2); 2 electrooculogram channels (ROC-A1, LOC-A2); medication. All patients had normal spirometry and flow submental electromyogram (EMG); intercostal (diaphrag- volume contours: mean forced expiratory volume in1s(% predicted) 112 Ϯ 19, range 82 Ϫ140%; mean forced vital matic surface) EMG; ECG; chest and abdominal movement; capacity (%predicted) 104 Ϯ 15, range 85–131%. Within 2 wk piezo bands; finger pulse oximetry; bilateral anterior tibialis of the screening measurements being performed, subjects EMG, vibration snore sensor] except for the measurements of were scheduled to return for measurement of nasal resis- oral and nasal ventilation (see Simutaneous measurement of tance and for overnight polysomnography, including simul- oral and nasal ventilation during sleep studies). The sleep taneous measurement of oral and nasal inhaled ventilation. data were collected and scored by use of “Sandman” software Subjects were asked to refrain from caffeine for 12 h before [Mallinckrodt, Nellcor Puritan Bennett (Melville), Ottawa, the overnight study and to avoid any naps during the 12 h Ontario, Canada]. The overnight sleep recordings were con- before study. ducted from 11 PM until 7 AM, continuously or until the Nasal resistance was measured in the erect seated posi- subject requested that the study be terminated. Data for one tion, by posterior active rhinomanometry, 2 h before the start full epoch (30 s) of continuous sleep, or until tidal volume of the overnight sleep study. An infant nasogastric feeding stabilized for three consecutive breaths during sleep, before catheter (6-Fr diameter-MED-Rx Benlan, Oakville, Ontario, and after spontaneous arousals, were excluded from analysis. Canada) was lubricated and inserted through the right nos- Because physiological central hypopneas and apneas are tril until it was visible at the pharynx on mouth opening. The known to occur during phasic REM sleep, data surrounding distal catheter tip was then retracted 1.5 cm above the free (30 s of continuous sleep before and after) respiratory events margin of the soft palate. The proximal end of the cannula associated with cortical arousals were excluded from REM was attached to a differential pressure transducer (Ultima sleep analysis. dual-pressure sensor, model 0585; Braebon Medical, Kanata, Simultaneous measurement of oral and nasal ventilation Ontario, Canada), which was calibrated to Ϯ4VϭϮ20 during sleep studies. Subjects wore a molded single-piece cmH2O. A continuous positive airway pressure (CPAP) mask translucent silicone rubber mask (7900 series mask, Hans was placed over the patient’s nose, taking care to ensure that Rudolph), with a built-in partition separating the oral and there was no compression of the nasal airway by the mask nasal ports.
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