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Summary
Obstructive Sleep Apnea (OSA)
Pathogenesis and Clinical Findings
- Pathogenesis:
- Multiple factors contribute to reduced airflow (hypopnoea) or complete cessation (apnoea), resulting in episodes of hypoxia and hypercapnia, leading to surges in sympathetic activation.
- Without abnormal anatomy, OSA involves repeated collapse of the pharyngeal airway due to decreased oropharyngeal muscle tone (relaxation of genioglossus and pharyngeal constrictor muscles), increasing inspiratory pressures and altering the arousal threshold.
- Hypoxia/reperfusion injury occurs due to fluctuations in oxygenation during the sleep cycle, leading to the release of oxygen radicals, activation of the inflammatory system, endothelial dysfunction, and increased platelet aggregation.
- Cellular and endothelial damage leads to vascular smooth muscle proliferation and increased sympathetic vasoconstrictor activity, resulting in hypertension and atherosclerosis.
- Perioperative Considerations:
- Surgical stress, postoperative pain, and endocrine changes can increase sympathetic activation, potentially leading to cardiovascular insults such as myocardial ischemia/infarction and arrhythmias.
- Physiological changes include polycythemia, systemic hypertension, cardiac rhythm disturbances, pulmonary hypertension, and right ventricular failure.
Pathophysiology
Neuromuscular Factors
- Sleep onset reduces the drive of respiratory muscles, leading to decreased upper airway neuromuscular activity, increased upper airway resistance, and increased upper airway collapsibility during sleep.
Structural Factors
- Factors include obesity, tonsillar or adenoid hypertrophy, macroglossia, increased neck circumference, and craniofacial abnormalities.
- Excess pressure or deformity in the upper airway increases the risk of airway collapse.
Vascular Factors
- Recumbent sleep leads to increased bodily fluids in the head and neck area, increasing the volume of tissue surrounding the upper airway, which may cause obstruction.
Clinical Findings
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Clinical Signs and Complications
- Morning headaches
- Hypoxia during day and night
- Pulmonary hypertension
- Systemic hypertension
- Cor Pulmonale: Right heart failure due to pulmonary hypertension
- Ischemic stroke
Diagnosis
Definitions
- OSA: Absence of breathing >10s during sleep despite continuing respiratory effort due to transient closure of the upper airway.
- Apnoea: Cessation of airflow or a decrease in flow >90% for >10s (2 breaths or more).
- Hypopnoea: Decrease in flow >50% or >30% for >10s with a 3-4% decrease in saturations or EEG evidence of arousal.
- Central Apnoea: Absence of airway flow and respiratory effort.
- Obstructive Apnoea: Absence of airway flow with the presence of respiratory effort.
Polysomnography
- Criterion 1: ≥ 5 events of apnoea lasting ≥ 10 seconds per hour PLUS one of:
- Sleep interruption
- Daytime symptoms
- OSA-related morbidity (mood disorders, cognitive dysfunction, cardiovascular disease)
- Criterion 2: ≥ 15 events of apnoea or other obstructed breathing events per hour.
- Monitors chest movement, airflow dynamics, HR, BP, and arterial oxygen saturation.
- Apnoeic episode: complete or near-complete disruption to airflow lasting at least 10 seconds.
- Hypopnoeic episode: ≥ 30% reduction in airflow for at least 10 seconds with 4% oxygen desaturation.
- Apnoea-Hypopnoea Index (AHI):
- 5-14: mild OSA
- 15-30: moderate OSA
- More than 30: severe OSA
Alternative Diagnostic Strategies
- Home sleep apnoea testing
- Peripheral artery tonometry-based ambulatory devices
- Overnight SaO₂; oxygen desaturation index
Oxygen Desaturation Index (ODI)
- Average number of oxygen desaturations ≥ 4% below baseline per hour in polysomnography.
- Overnight pulse oximetry provides satisfactory diagnostic performance in detecting severe OSA.
Screening: STOP-BANG Questionnaire
- S: Snoring loud enough to be heard through closed doors.
- T: Tiredness causing daytime sleepiness.
- O: Observed apnoea events lasting ≥ 10 seconds.
- P: Pressure (hypertension).
- B: BMI ≥ 35.
- A: Age ≥ 50 years.
- N: Neck circumference ≥ 40 cm.
- G: Gender (male).
- Risk Stratification:
- 0-2: Low risk
- 3-4: Intermediate risk
- 5-8: High risk
Serum HCO₃
- Serum bicarbonate level > 28 mmol/L combined with a STOP-Bang score ≥ 3 improves specificity.
- Elevated due to renal retention as a consequence of frequent respiratory acidosis during obstructive episodes.
Electroencephalography (EEG)
- Less commonly used.
Treatment of OSA
- Gold Standard: Nasal Continuous Positive Airway Pressure (CPAP).
- Set between 5 and 20 cm H₂O, worn during sleep.
- Acts as a pneumatic splint, reducing pharyngeal collapse.
- Decreases platelet aggregation, improves endothelial function, reduces cardiac arrhythmias, improves cardiac function, blood pressure, and atherosclerosis.
- Other Treatments:
- Weight loss
- Mandibular advancement device for mild OSA
- Surgical procedures like somnoplasty or uvulopalatopharyngoplasty (UPPP) with demonstrated success via polysomnography.
Conduct of Anaesthesia in OSA
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Obesity Hypoventilation Syndrome
Diagnosis of OHS
- Formal criteria:
- BMI > 30 kg/m².
- Arterial CO₂ level > 45 mmHg or 6.0 kPa on ABG.
- No alternative explanation for hypoventilation (e.g., narcotics, severe obstructive/interstitial lung disease, severe chest wall disorders, severe hypothyroidism, neuromuscular disease, congenital central hypoventilation syndrome).
- Daytime hypoxia.
- Chest wall mechanics associated with obesity.
Prevalence and Pathophysiology
- Prevalence: 9-20% of OSA patients have OHS, 90% of OHS patients have OSA.
- Pathophysiology:
- Obesity:
- Leptin resistance and increased mechanical load.
- Blunted ventilatory response.
- Chronic hypercapnia.
- OSA:
- Acute hypercapnia during sleep.
- Decreased compensatory hyperventilation and HCO₃ excretion rate.
- Increased serum HCO₃.
- Obesity:
Perioperative Management of Suspected OHS
- Screening:
- STOP-Bang questionnaire.
- SpO₂ and serum HCO₃ levels.
- High Risk for OHS:
- STOP-Bang ≥ 3.
- SpO₂ < 90%.
- Elevated HCO₃.
- Major Elective Surgery:
- Refer to sleep medicine for polysomnography and PAP therapy titration.
- Consider echocardiogram to assess RV dysfunction and pulmonary hypertension.
- Emergency Surgery:
- Potential difficult airway.
- Rapid emergence.
- Opioid-induced ventilatory impairment.
- Postextubation PAP therapy.
- Low Risk for OHS:
- STOP-Bang < 3.
- SpO₂ ≥ 90%.
- Normal HCO₃.
- Routine Management.
Differences between Obesity Hypoventilation Syndrome and Overlap Syndrome
| Condition | Obesity Hypoventilation Syndrome | Overlap Syndrome |
|---|---|---|
| Definition | Obesity (BMI > 30 kg/m²) + Daytime hypercapnia (PaCO₂ ≥ 45 mmHg) ± OSA | COPD + OSA |
| Prevalence | 0.15-0.6% | 0.5-1% |
| Relationship with OSA | Pathophysiological link in 90% of cases | Coexistent, no pathophysiological link |
| Hypercapnic Ventilatory Response | Decreased | Normal, enhanced, or decreased |
| Pulmonary Hypertension | + to +++ | ++ to +++ |
Links
References:
- OSA Wits refresher 2013. Dr B Gardner
- Barajas van Langen, M. E., Meesters, M. I., Hiensch, R. J., Bouwman, R. A., & Buise, M. P. (2023). Perioperative management of obstructive sleep apnoea: limitations of current guidelines. British Journal of Anaesthesia, 131(4), e133-e134. https://doi.org/10.1016/j.bja.2023.07.011
- Practice Guidelines for the Perioperative Management of Patients with Obstructive Sleep Apnea: An Updated Report by the American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Obstructive Sleep Apnea. Anesthesiology 2014; 120:268–286 doi: https://doi.org/10.1097/ALN.0000000000000053
- FRCA Mind Maps. (2024). Retrieved June 5, 2024, from https://www.frcamindmaps.org/
- Anesthesia Considerations. (2024). Retrieved June 5, 2024, from https://www.anesthesiaconsiderations.com/
- The Calgary Guide to Understanding Disease. (2024). Retrieved June 5, 2024, from https://calgaryguide.ucalg
Summaries:
OSAS
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