Snoring and Upper Airway Resistance

Physics of Airway Resistance and Snoring

Airway resistance varies inversely with the fourth power of the radius, so even modest narrowing has a disproportionate effect: halving the airway diameter multiplies resistance sixteen-fold. [1]
As the airway narrows, airflow velocity rises and, by Bernoulli's principle, generates negative pressure against the soft walls that pulls them inward to collapse and vibrate, producing the snoring sound. [1]

Snoring is technically stertor, a low-pitched noise arising from obstruction at the nasopharyngeal and oropharyngeal level, distinguishing it from sounds generated lower in the airway. [1]
Stridor, by contrast, is a high-pitched sound originating in the larynx or trachea, while obstruction of the small airways instead produces a wheeze. [1]
The level of obstruction can be inferred from the accompanying voice and cough: nasopharyngeal or oropharyngeal obstruction gives stertor with a muffled voice and typically no cough, whereas supraglottic or glottic obstruction gives inspiratory stridor with a hoarse voice and barking cough. [1]

A primary snorer is someone who snores without any significant apnoeas or hypopnoeas, placing them at the benign end of the obstruction-disorder spectrum. [2]
Upper airway resistance syndrome describes daytime somnolence caused by repeated arousals known as respiratory-effort-related arousals (RERAs) that arise from increased upper airway resistance, yet still without frank apnoeas or hypopnoeas. [2]
In children, sleep-disordered breathing forms a graded spectrum running from snoring, through upper airway resistance syndrome and obstructive hypoventilation, to obstructive sleep apnoea. [3]
Approximately 10% of children snore while obstructive sleep apnoea affects only 1-3%, showing that most snoring children sit at the milder end of the spectrum. [3]

Paediatric sleep-disordered breathing is defined as an abnormal respiratory pattern during sleep encompassing snoring, mouth breathing, and pauses in breathing. [3]
Any degree of daytime sleepiness in a child is abnormal and warrants investigation rather than reassurance. [3]

Overlap syndrome is the coexistence of obstructive sleep apnoea with COPD, where the reduced baseline PaO2 and ventilation-perfusion mismatch produce exaggerated desaturations during apnoeas, more pulmonary hypertension, and higher mortality than COPD alone. [2]
Obesity-hypoventilation syndrome is daytime hypoventilation with hypercapnia (PaCO2 above 45 mmHg) arising from severe obesity (BMI over 40 kg/m2) rather than any respiratory or neuromuscular disorder, and it requires BiPAP to improve ventilation. [2]
Complex sleep apnoea is a combination of obstructive and central sleep apnoea that is typically unmasked after over-titrating CPAP for OSAS or in the context of opiate use. [2]

Obstructive sleep apnoea raises sympathetic tone, shortens the R-R interval to produce tachycardia, and increases blood pressure variability with raised afterload and endothelin. [2]
A range of arrhythmias occurs in OSAS, with sinus arrhythmias being most common, alongside sinus pauses, bradycardia, premature ventricular complexes, ventricular tachycardia, and AV block. [2]
The repeated negative intrathoracic pressure of obstructed breathing raises transmural pressure and wall stress, enlarging the atria and predisposing to aortic aneurysm and aortic dissection. [2]
A raised monocyte adhesion index in OSAS contributes to endothelial injury, and increased cardiac risk is driven by reoxygenation of hypoxic tissues generating free radicals, altered gene expression, raised proinflammatory cells and adhesion molecules, and ultimately endothelial dysfunction. [2]

OSAS produces a characteristic endocrine profile of raised C-reactive protein, serum amyloid and cortisol, with reduced growth hormone and prolactin. [2]
The condition drives a proinflammatory immune state with elevated IL-6, CRP and TNF and reduced IL-10, and the raised proinflammatory cytokines improve with CPAP treatment. [2]