Pathophysiology of Sleep-Disordered Breathing

SDB Basics - Night Noises 101

• Sleep Disordered Breathing (SDB): Spectrum of breathing abnormalities during sleep.
• Obstructive Sleep Apnea (OSA): Airway obstruction despite respiratory effort.
• Central Sleep Apnea (CSA): Absent respiratory effort.
• Mixed Apnea: Central onset, then obstructive component.

- Mild: **5-15/hr**
- Moderate: **15-30/hr**
- Severe: **>30/hr**

⭐ AHI is the number of apneas and hypopneas per hour of sleep.

OSA Mechanics - Airway Antics

• Anatomical Factors (Narrowing the Stage):
  • Bony: Retrognathia.
  • Soft Tissue: Macroglossia, tonsillar/adenoidal hypertrophy, elongated/floppy soft palate/uvula, lateral pharyngeal wall thickening (fat deposition).
• Neuromuscular Dysfunction (Guard Duty Failure):
  • ↓ Activity of upper airway dilator muscles (e.g., genioglossus, tensor palatini) crucial for patency, especially during REM sleep.
• Airway Collapse Dynamics:
  • Inspiratory Suction: Negative intrathoracic pressure during inspiration exacerbates collapse.
  • Venturi Effect: Airflow accelerates at narrow points, ↓ lateral pressure, promoting closure.
  • Starling Resistor: Airway behaves like a collapsible tube; upstream/downstream pressures and wall compliance dictate patency.

⭐ The oropharynx, particularly the velopharynx, is the most common site of collapse in OSA.

CSA Central - Control Chaos

• Definition: Airflow cessation from absent/reduced respiratory effort.
• Primary CSA:
  • Idiopathic.
  • Cheyne-Stokes Respiration (CSR): cyclic crescendo-decrescendo breathing, central apneas.
• Secondary CSA:
  • Medical conditions: heart failure, stroke, renal failure.
  • High altitude.
  • Drugs: opioids, sedatives.
• CSR Pathophysiology: Ventilatory instability from:
  • ↑ Circulatory delay (e.g., heart failure).
  • ↑ Chemosensitivity (high loop gain).
  • Unstable chemoreceptor-respiratory center feedback.

⭐ Cheyne-Stokes respiration is commonly associated with advanced congestive heart failure.

SDB Fallout - System Shockers

Recurrent apneas/hypopneas unleash widespread systemic damage:

• Immediate Insults:
  • Intermittent hypoxemia & hypercapnia.
  • Marked intrathoracic pressure swings.
  • Recurrent arousals disrupting sleep architecture.
• Hypoxemia/Reoxygenation Damage:
  • Leads to oxidative stress.
  • Promotes systemic inflammation (evidenced by ↑CRP, TNF-α, IL-6).
• Sleep Fragmentation Effects:
  • Excessive Daytime Sleepiness (EDS).
  • Cognitive impairments (e.g., attention, executive function).
  • Mood disturbances (e.g., depression, anxiety).
• Cardiovascular Storm:
  • Chronic sympathetic activation & endothelial dysfunction.
  • Results in: systemic hypertension, arrhythmias (notably Atrial Fibrillation), Ischemic Heart Disease (IHD), stroke, and pulmonary hypertension.

• Metabolic Meltdown:
  • Insulin resistance, predisposing to Type 2 Diabetes Mellitus.
  • Dyslipidemia.
  • Key contributor to Metabolic Syndrome.

⭐ Obstructive Sleep Apnea (OSA) is an independent risk factor for systemic hypertension.

High‑Yield Points - ⚡ Biggest Takeaways

• Upper airway collapse during sleep is central to OSA pathophysiology.
• Key consequences include intermittent hypoxia, hypercapnia, and sleep fragmentation.
• Increased negative intrathoracic pressure during obstructed breathing efforts.
• Obesity is a major risk factor, causing ↑ pharyngeal soft tissue.
• Craniofacial abnormalities (e.g., retrognathia) can predispose to collapse.
• Impaired neuromuscular control of upper airway dilator muscles is crucial.
• Leads to sympathetic activation, oxidative stress, and systemic inflammation.