Airway & Sleep Blog

Display by Category

Study on oral flow and its findings related to mild versus severe sleep disordered breathing

Symptoms of Sleep Apnea
Middle-aged man snoring
This excerpt was taken from a study by the Journal of Clinical Sleep Medicine: Relationship between Oral Flow Patterns, Nasal Obstruction, and Respiratory Events during Sleep by Masaaki Suzuki, MD, PhD; Taiji Furukawa, MD, PhD; Akira Sugimoto, MD, PhD; Koji Katada, MD, PhD; Ryosuke Kotani, MD; Takayuki Yoshizawa, MD, PhD
Department of Otorhinolaryngology, Teikyo University Chiba Medical Center, Tokyo, Japan; Department of Laboratory Medicine, Teikyo University School of Medicine, Chiba, Japan; Division of Respiratory Medicine, Kaname Sleep Clinic, Tokyo, Japan

Nasal breathing is physiologic during sleep. Respiratory physiology and the nature of the upper and lower airways encourage nasal breathing during sleep. However, in nasal diseases such as nasal deviation or inferior turbinate hypertrophy, nasal obstruction can be bypassed by opening the mouth and allowing a greater volume of air to be inspired and expired. McLean et al.1 showed that oral breathing during sleep is induced by increased nasal resistance. Mouth opening increased upper airway collapsibility during sleep, which is different from that seen when awake. Fitzpatrick et al.3 confirmed that during sleep, upper airway resistance during oral breathing was 2.5 times higher than that during nasal breathing. Mouth opening may be associated with narrowing of the pharyngeal lumen and decreases in the retroglossal diameter. Mouth opening and oral breathing may, but not necessarily, lead to hypopnea or apnea. However, Lavie et al.4 showed that nasal obstruction caused a significant increase in the number of arousals during sleep in patients with nonapneic breathing disorders. In another recent study, Hsia et al.5 described a snoring pattern during nasal breathing in patients with nasal obstruction that was alleviated with oral breathing.

Against this background, we hypothesized that different kinds of oral flow (OF) patterns exist during sleep and are associated with distinct sleep related respiratory events. The aim of this study was to clarify the relationship between OF patterns, nasal airway obstruction, and obstructive respiratory events such as flow limitation, respiratory effort-related arousal (RERA), hypopnea, and apnea.

Oral flow could be divided into three main patterns: OF after a respiratory event (postevent OF), OF during a respiratory event (during-event OF), and spontaneous arousal-related OF (SpAr-related OF). Respiratory patterns not conforming to the definitions of these three patterns were collectively categorized as “Other.” The postevent OF pattern refers to OF events starting at the end of obstructive respiratory events, often preceded by respiratory arousal, and accompanied by hyperventilation. This type of OF event is well known to clinicians.

The Three Patterns of OF

This is the first study to describe the relationships among specific patterns of oral flow (postevent OF, during-event OF, and SpAr-related OF), nasal airway obstruction, and respiratory events during sleep. Both the postevent and during-event OF patterns were associated with respiratory events, possibly because mouth opening during sleep can increase the collapsibility of the pharyngeal airway, increasing the risk of airway obstruction. Indeed, both patterns were typically seen in patients with moderate or severe SDB. They are “apnea or hypopnea inductors” and are closely related. These two OF patterns periodically repeat in the presence of many obstructive respiratory events.

SpAr-related OF, however, is a “nasal obstruction bypasser” rather than an “apnea/ hypopnea inductor” and functions as a bypasser to prevent apnea and hypopnea. Oral breathing with increased nasal resistance leads to mouth opening and oral breathing, but it does not induce apnea or hypopnea. SpAr-related OFs in patients with nasal obstruction may disturb sleep. We usually do not focus much attention on patients with mild SDB with nasal obstruction, but their abnormal breathing and sleep quality might be improved by nasal treatment. Thus, physicians should be concerned about nasal obstruction not only in continuous positive airway pressure-intolerant users but also in patients with mild SDB.

OF Hidden in Respiratory Events

Physicians should be aware that OF can be hidden in obstructive respiratory events. It is difficult, however, to distinguish during-event OFs due to nasal flow reduction from obstructive respiratory events. First, during–event OFs may cause an arousal through oronasal transition5 that meets the definition of a RERA or hypopnea. Second, during–event OFs could be accompanied by desaturation. Oral and nasal breathing may occur simultaneously, and during–event OFs accompanied by desaturation could be scored as hypopnea events. The fraction of time spent in NREM sleep significantly predicted during event OF incidence. One possible explanation for this finding is that there were episodes of flow reduction associated with OF that did not meet the criteria for obstructive respiratory events during NREM sleep, whereas apnea or hypopnea did occur

during REM sleep. An obstructive respiratory event could be a manifestation of OF. We can recognize these respiratory events by introducing OF scoring. Clinicians and sleep laboratory technologists should be aware of OF events hidden in obstructive respiratory events. Oral breathing during sleep is abnormal, and measuring OF may supplement AHI assessment.

OF Patterns, the Nasal Airway, and SDB

Upper airway collapse during sleep may occur because of negative intraluminal pressure due to occlusion in the upper airway. The Starling resistor model, which works in accordance with the Bernoulli principle, explains this mechanism. The model predicts that an upstream obstruction in the nasal cavity generates a suction force and negative intraluminal pressure downstream at the pharynx under a closed-mouth condition. However, this model fails to take oral breathing into account. Mouth opening is associated with increased upper airway collapsibility during sleep.1 It has been reported that upper airway collapsibility and resistance during sleep were significantly higher in subjects who were breathing through the mouth than in those who were breathing through the nose, which is different from that seen during the conscious state.2,3 Other reasons for nasal breathing over mouth breathing during normal sleep are based on the physiological effects of decreased nasal airflow. First, bypassing the nasal airway can lead to reduced nasal receptor activation, deactivation of the nasal ventilatory reflex, and reduced spontaneous ventilation.

Douglas et al.12 found that nasal breathing activates nasal receptors, which have a direct positive effect on spontaneous ventilation, resulting in higher minute ventilation and resting breathing frequency. Furthermore, ventilation is significantly greater during obligate nasal breathing than during predominant oral breathing in normal subjects.13 Second, decreased nasal ventilation may result in reduced nitric oxide delivery to the lungs and reduced oxygen exchange capability.14,15 Nitric oxide is produced in significant amounts in the nose and sinuses, and has been shown to be a potent lung vasodilator that improves overall blood oxygenation.

Taken together, the balance of evidence suggests that the nasal route of breathing during sleep is physiologic. The physiology of the upper and lower airways and respiratory control encourage nasal breathing during sleep rather than bypassing nasal obstruction. If nasal airway obstruction is severe with high inspiratory resistive loads, nasal resistance exceeds a certain threshold and nose breathing is switched to oral breathing to bypass the nasal airway obstruction. This case of OF may be SpAr-related OF.

However, in patients with airways susceptible to collapse or habitual oral breathing, postevent or during-event OFs would occur and induce respiratory events. Nasal resistance is an important factor if it exceeds a certain threshold and triggers the switch to oronasal or oral breathing. Pressure receptors in the nose and other parts of the upper airway are responsible for sensing increased resistance to nasal airflow, and activation of these receptors alters the movement of palatopharyngeal, palatoglossal, and palatal elevator muscles, thereby changing the breathing route, but at a high physiological cost. Mild SDB may be attributed to an adaptive response to reversible nasal airway obstruction with a change in the breathing route.

However, the pathological role of the pressure receptors and their pathways in the nose and other parts of the upper airway is not fully understood, especially during sleep. Further exploration in this area is needed.

A limitation of this study is that we were not able to use the ideal methods to measure the parameters under investigation, namely, nasal resistance measurement during sleep by PSG and nasal and oral flow measurement with a sealed mask and two pneumotachometers. Nevertheless, our methodology clearly revealed distinct OF patterns and their relationships with nasal airway obstruction and obstructive respiratory events.

In conclusion, OF events during sleep could be divided into three main patterns: postevent OF, during-event OF, and SpAr-related OF. SpAr-related OF events were significantly more common in patients with nasal obstruction than in those without nasal obstruction. SpAr-related OF events were not associated with obstructive respiratory events but functioned as a “nasal obstruction bypass” predominantly in normal subjects and patients with mild SDB. By contrast, postevent and during-event OF events were related to obstructive respiratory events and were more frequently observed in patients with moderate to severe SDB.

Read the full report here: relationship between oral flow, nasal obstruction, and respiratory events -mouthbreathing

, ,

Airway & Sleep Group

11800 Sunrise Valley Dr.
Suite 200
Reston, VA 20191

Office Hours

Monday
7am – 4pm
Tuesday
7am – 4pm
Wednesday
7am – 4pm
Thursday
7am – 4pm
Friday
7am – 4pm
Menu