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Mechanism of Snoring and Polysomnography

PART I: MECHANISM OF SNORING

Definition

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Anatomical Basis

• Luminal (intraluminal) pressure — negative inspiratory pressure tends to collapse the airway
• Neuromuscular tone — dilator muscles (genioglossus, tensor palatini, geniohyoid) act to keep the airway open
• Structural anatomy — bony framework (mandible, hyoid), soft tissue volume (tongue, tonsils, lateral pharyngeal walls, uvula, soft palate)

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Pathophysiology of Snoring — The Starling Resistor Model

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Step-by-Step Mechanism

1. During sleep, neuromuscular tone to upper airway dilator muscles decreases, especially during NREM stage 2 and most profoundly during REM sleep.
2. Reduced muscle tone → the soft palate, uvula, tonsillar pillars, and tongue base lose their active stiffness.
3. Bernoulli effect: as the airway narrows, airflow velocity increases and intraluminal pressure falls (Bernoulli's principle), drawing the soft tissue walls inward.
4. Turbulent airflow through the partially narrowed oropharynx sets the flaccid soft palate and uvula into vibration — this is the primary generator of snoring sound.
5. The tongue base, lateral pharyngeal walls, and epiglottis can contribute secondary vibrations.
6. Inspiratory airflow creates more negative intraluminal pressure than expiration → snoring louder on inspiration.

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Predisposing Factors (Why Snoring Occurs)

• Retrognathic or micrognathic mandible — reduces the anteroposterior airway dimension
• Macroglossia, tonsillar hypertrophy, elongated uvula, low soft palate
• Obesity — increased volume of lateral pharyngeal fat pads and tongue fat compresses the airway lumen
• Increased airway length predisposes to collapse
• Reduced lung volume in recumbency → less caudal tracheal traction → reduced upper airway patency

• Sleep-related decrement in dilator muscle activity (genioglossus activity is highest at wakefulness and falls with sleep onset)
• Impaired negative pressure reflexes — normally, negative intraluminal pressure triggers a reflex increase in dilator muscle activity; this reflex is blunted in snorers and OSA patients
• Upper airway sensory neuropathy (from trauma due to repeated vibration) → impairs afferent limb of the protective reflex
• Muscle fatigue and fiber-type shifts due to chronic loading

• Alcohol and sedatives → suppress upper airway muscle tone and central ventilatory drive
• Supine posture → gravity displaces tongue and soft palate posteriorly
• Nasal obstruction (deviated septum, rhinitis, polyps) → mouth breathing, increased pharyngeal resistance
• Smoking → upper airway mucosal inflammation and edema
• Hypothyroidism, acromegaly → macroglossia and soft tissue hypertrophy

• Tissue trauma from vibration → inflammation → edema → further airway narrowing
• Oxidative stress, acid-pepsin reflux, smoking → mucosal edema and collagen deposition alter airway mechanics

• Overnight rostral fluid shift from lower limbs to the neck increases soft tissue volume in the pharyngeal walls, worsening collapsibility; correlates with AHI severity

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Spectrum of Sleep-Disordered Breathing (Classification)

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PART II: POLYSOMNOGRAPHY (PSG)

Definition

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Parameters Monitored (Channels)

Mandatory (Level 1 PSG):

Optional:

• End-tidal / transcutaneous CO₂ — detect hypoventilation (ETCO₂ ≥ 50 mmHg for > 8–10% sleep time = obstructive hypoventilation)
• Esophageal pressure (Pes) — most sensitive for detecting UARS; shows progressively increasing negative Pes culminating in arousal
• Infrared video — identify parasomnias, complex behaviors
• CPAP/BiPAP (split-night study) — pressure titration

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Sleep Staging on PSG

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Respiratory Event Definitions (AASM Scoring)

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Derived Indices

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Levels of Sleep Studies

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Indications for PSG

1. Diagnosis of sleep-related breathing disorders (OSA, central sleep apnea, hypoventilation)
2. PAP titration and assessment of treatment efficacy (split-night study)
3. Pre- and post-operative assessment for sleep surgery
4. Evaluation of sleep-related violent behaviors / parasomnias (to rule out nocturnal seizures)
5. Differentiating narcolepsy from other hypersomnolence disorders (followed by MSLT the next day)
6. Periodic limb movement disorder (PLMD)
7. Patients with EDS, waking with gasping/choking, witnessed apneas

Note: PSG is not required for restless legs syndrome (RLS) diagnosis. It is not indicated in asymptomatic patients as a screening tool.

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Diagnostic Criteria for OSA on PSG (AASM)

• ≥ 5 obstructive events/hour (apneas + hypopneas + RERAs) WITH symptoms or comorbidities (EDS, witnessed apneas, hypertension, etc.), OR
• ≥ 15 obstructive events/hour regardless of symptoms

• Mild: AHI 5–14
• Moderate: AHI 15–29
• Severe: AHI ≥ 30

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Limitations of PSG

• Expensive and resource-intensive
• First-night effect: patients sleep differently in the laboratory (reduced REM, poorer sleep efficiency)
• Requires trained technologist and sleep physician for scoring/interpretation
• Limited availability — long waiting times
• Level 3/4 devices: no sleep staging, calculates respiratory events per recording time (not per sleep time) → may underestimate severity
• HSAT has high false-negative rate; if negative/inconclusive → must proceed to Level 1 PSG

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PSG Findings in Snoring and OSA (Summary)

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Summary Diagram: Mechanism of Snoring

Sleep onset
    ↓
↓ Neuromuscular tone (genioglossus, tensor palatini)
    ↓
Soft palate, uvula, tongue base lose stiffness
    ↓
Airway narrows (Bernoulli effect: ↑ velocity → ↓ intraluminal pressure)
    ↓
Negative pressure reflex fails to compensate
    ↓
Pharyngeal soft tissues vibrate in turbulent airflow
    ↓
SNORING SOUND
    ↓ (if Pcrit > 0 or neuromuscular failure worsens)
Upper airway collapse → APNEA (OSA)

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• Snoring = soft tissue vibration; loudest on inspiration; Pcrit −10 to −5 cm H₂O
• PSG is the gold standard — Level 1, in-lab, attended, overnight
• PSG records EEG + EOG + chin EMG (sleep staging) + airflow + RIP bands + SpO₂ + ECG + tibialis EMG
• AHI = gold standard severity measure; < 5 normal; ≥ 5 mild; ≥ 15 moderate; ≥ 30 severe
• RDI = AHI + RERAs/hour (broader, captures UARS)
• Paradoxical thoracoabdominal motion on PSG = obstructive event (effort without flow)
• UARS: raised RDI, negative Pes swings, EDS — diagnosed with esophageal pressure monitoring

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