Nasal Obstruction and Sleep-Disordered Breathing


Nasal Obstruction and Sleep-Disordered Breathing

The link between nasal airway obstruction (NAO) and restless sleep has been known since antiquity: Hippocrates reported an association between poor sleep and nasal polyposis. Case reports and series as early as the 1890s showed an association between the nasal valve and sleep-disordered breathing (SDB). Modern studies report that subjective or objective NAO is a risk factor for SDB. Approximately 15% of patients with SDB also have NAO, and in a prospective population study of almost 5000 patients, self-reported nocturnal congestion was associated with a threefold increased incidence of snoring and daytime sleepiness. Lofaso et al. analyzed cephalometrics, body mass index (BMI), and posterior rhinometry and showed that daytime NAO is an independent risk factor for obstructive sleep apnea (OSA). Others have explored the relationship between NAO and SDB, showing that there is no association between SDB severity and the severity of NAO, although nasal resistance has been associated with snoring severity. McNicholas observed that SDB is more likely to be associated with reversible nasal obstructive disease than chronic obstruction, implying that acute reversible processes (e.g. allergic rhinitis) may have a more severe impact on SDB than static structural problems.

NAO often plays a major role in SDB and its treatment despite variable reports of the association between them. Normal patients have been shown to experience sleep disturbances after acute, complete bilateral NAO, including sleep stage disruption, new-onset snoring, and even mild OSA. One study demonstrated that objective NAO assessed using acoustic rhinometry is associated with optimal titrated nasal continuous positive airway pressure (CPAP) and the Respiratory Disturbance Index (RDI) in patients with a BMI <25.

Mouth breathing has been shown to destabilize the pharyngeal airway and contribute to the development of SDB. Nasal airflow is therefore desired for the treatment of OSA with positive airway pressure therapy, and NAO can interfere with treatment and decrease compliance with therapy. Lafond and Series induced increased nasal resistance in OSA patients with histamine and demonstrated increased airflow limitation using nasal CPAP. Zozula and Rosen emphasized the role of NAO in positive airway pressure therapy tolerance and adherence in their paper reviewing and classifying reasons for CPAP noncompliance.

Four different theories have been proposed to explain the relationship between NAO and SDB ( Table 21.1 ). These will be considered separately after a discussion of nasal anatomy.

Table 21.1
Pathophysiologic Mechanisms for the Contribution of Nasal Obstruction to OSA
Adapted from Reproduced from Georgalas C. The role of the nose in snoring and obstructive sleep apnoea: an update. Eur Arch Otorhinolaryngol 2011;268(9):1365–73.
Association Between Nasal Airway Obstruction and Sleep-Disordered Breathing
Theory Mechanism
Starling resistor model Upstream nasal resistance results in increased negative pressure downstream in the pharyngeal airway
Unstable oral breathing Nasal airway resistance forces an increase in oral breathing fraction, resulting in increased total airway resistance by breathing through an unstable oral airway
Nasal-ventilatory reflex Decreased activation of nasal airflow receptors due to obstruction leads to inhibitory action on muscle tone and minute ventilation
Nitric oxide (NO) Decreased nasal airflow reduces nasal NO production, causing potential perfusion ventilation mismatch, as well as multiple other poorly defined effects on oropharyngeal musculature and arousals

Functional Valvular Anatomy

Anatomic models ( Figs. 21.1 and 21.2 ) have shown that inspiratory nasal airflow follows a parabolic curve up through the nostril, across the turbinates, and then downward posteriorly through the nasopharynx. The internal nasal valve area is the narrowest part of the nasal passage and greatest nasal resistance in normal patients. The internal nasal valve is composed of the upper lateral cartilage superiorly, the nasal septum medially, the pyriform aperture inferiorly, and the head of the inferior turbinate posteriorly. Patients with internal nasal valve angles of <10 degrees are more prone to internal nasal valve collapse on inspiration.

FIG. 21.1, Sagittal view of the internal nasal valve.

FIG. 21.2, Diagram of the external nasal valve.

The external nasal valve is composed of the nares and the nasal vestibule. The nasal vestibule lies just inside the external naris and is located caudal to the internal nasal valve area. Vibrissae serve to direct the air posteriorly into the nasal cavity and to slow the inspired air. The nares are composed of the alar margin, the soft tissue triangle, the columella, and the nasal sill.

The internal and external nasal valves function together to deliver what is ideally laminar airflow to the nasal cavities for humidification. The investing nasal musculature consists of alar rim elevator muscles, depressor muscles, compressor muscles, and minor dilator muscles. The alar muscles contract and stabilize the internal nasal valve area to resist collapse. During deep inspiration, intraluminal pressure in the internal valve area decreases as airflow increases (due to the Venturi effect). The cartilaginous framework of the nose passively resists collapse, but as airflow increases, the nostrils flare and the diameter of the external nasal valve is increased to actively counter collapse. Throughout normal nasal airflow, the internal nasal valve area should remain unchanged. Collapse demonstrable only during forced inspiration generally does not require intervention. Patients with OSA may generate significant negative pressures within the upper airway during obstructive events; however, the sites of resistance and obstruction vary significantly between individuals. Studies have not been done to determine if nasal valve collapse is more common in OSA.

Subjects with certain nasal anatomic characteristics may be predisposed to NAO. However, no specific anatomic feature of NAO has been found to correlate with OSA severity. Individuals with a narrow upper cartilaginous vault have a narrower internal nasal valve and may exhibit collapse in the resting state. The impact of a relatively small decrease in cross-sectional area of the internal nasal valve can be substantial due to Poiseuille law, which indicates that the rate of airflow is proportional to the fourth power of the radius of the conduit. Subjects who possess weak upper lateral cartilages and/or lateral nasal walls may be more predisposed to collapse of the internal nasal valve during inspiration.

Patients who have preexisting or traumatic septal deviation can have significant obstructive issues. Insufficient support of the alar rim and alar lobule may lead to external valve collapse on inspiration. Short nasal bones and a long upper cartilaginous vault; narrow, projecting nose; slitlike nostrils; exaggerated supraalar creases; visible pinching of the lateral wall with inspiration; thin cartilages and skin; and cephalically positioned lateral crura, which provide minimal support to the alar margins, are all attributes that the surgeon should consider when planning surgical correction.

Mechanisms Associating Nasal Obstruction With Sleep-Disordered Breathing

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