What is the difference between Obesity Hypoventilation Syndrome (OHS) and Obstructive Sleep Apnea (OSA)?

Difference Between Obesity Hypoventilation Syndrome (OHS) and Obstructive Sleep Apnea (OSA)

OHS is fundamentally distinguished from OSA by the presence of awake daytime hypercapnia (PaCO₂ > 45 mm Hg at sea level), whereas OSA patients maintain normal daytime carbon dioxide levels unless they also have OHS. 1

Defining Characteristics

Obesity Hypoventilation Syndrome (OHS)

• Requires three components: obesity (BMI > 30 kg/m²), sleep-disordered breathing, AND awake daytime hypercapnia (PaCO₂ > 45 mm Hg), after excluding other causes of hypoventilation 1
• Represents the most severe form of obesity-induced respiratory compromise with significantly higher morbidity and mortality than OSA alone 1
• Patients develop chronic hypercapnic respiratory failure that persists during wakefulness 1

Obstructive Sleep Apnea (OSA)

• Characterized by recurrent upper airway obstruction during sleep causing apneas and hypopneas 1
• Patients maintain normal daytime PaCO₂ levels (eucapnic) 2, 3
• Does not require obesity for diagnosis, though obesity is a major risk factor 1

The Critical Overlap

Approximately 90% of patients with OHS also have coexistent OSA (AHI > 5 events/h), with nearly 70% having severe OSA (AHI > 30 events/h). 1 This means:

• OHS is NOT simply "severe OSA" - it is a distinct disease entity requiring daytime hypercapnia 1, 2
• The remaining 10% of OHS patients have sleep hypoventilation without significant obstructive events 1
• OSA alone does not cause daytime hypercapnia - additional pathophysiologic mechanisms must be present 4, 5

Pathophysiologic Distinctions

Why OHS Develops Beyond OSA

OHS requires multiple failing mechanisms that OSA patients compensate for: 4

• Impaired central respiratory drive: Decreased ventilatory responsiveness to CO₂ prevents compensatory hyperventilation despite rising PaCO₂ 4
• Severe mechanical respiratory dysfunction: Chest wall restriction and reduced lung compliance from extreme obesity 4
• Inadequate respiratory muscle strength to meet ventilatory demands 4
• Chronic nocturnal hypoventilation even during periods without discrete apneas 4

In contrast, OSA patients maintain adequate daytime ventilatory drive and mechanics to normalize their PaCO₂ when awake 3, 6.

Clinical Consequences: Why the Distinction Matters for Outcomes

OHS Carries Substantially Worse Prognosis

• Increased mortality rates compared to eucapnic obese patients with OSA 1, 3
• Pulmonary hypertension develops in 30-88% of OHS patients versus lower rates in OSA alone 1, 4
• Chronic heart failure and cor pulmonale from chronic hypoxemia and hypercapnia 1, 4
• Higher risk of acute-on-chronic hypercapnic respiratory failure requiring hospitalization 1, 4
• Increased perioperative mortality 1

OSA Without Hypercapnia

• Lower cardiovascular morbidity than OHS 3
• Does not typically cause cor pulmonale unless severe and untreated for prolonged periods 1

Diagnostic Algorithm to Distinguish Them

Step 1: Screen for Hypercapnia

For obese patients with known or suspected sleep-disordered breathing: 1

• High pretest probability (severely obese with typical symptoms): Measure arterial PaCO₂ directly 1
• Low to moderate probability (<20%): Use serum bicarbonate as initial screen 1
  • If bicarbonate < 27 mmol/L: OHS is very unlikely, diagnosis is OSA alone 1, 7
  • If bicarbonate ≥ 27 mmol/L: Measure arterial PaCO₂ to confirm or exclude OHS 1, 7

Step 2: Confirm Diagnosis

• PaCO₂ > 45 mm Hg at sea level during wakefulness = OHS (if other causes excluded) 1, 7
• PaCO₂ ≤ 45 mm Hg = OSA without OHS 5, 8

Step 3: Polysomnography

• Required for both conditions to determine pattern of sleep-disordered breathing and guide treatment 1
• Distinguishes obstructive versus non-obstructive hypoventilation in OHS patients 1

Treatment Differences

For OHS with Severe OSA (AHI > 30)

• CPAP is first-line treatment (not BiPAP initially) 1, 9
• Similar effectiveness to BiPAP but less costly for this phenotype 9

For OHS without Severe OSA

• BiPAP (noninvasive ventilation) is first-line 9
• Approximately 30% of OHS patients fall into this category 5

For OSA Alone (Without Hypercapnia)

• CPAP is standard first-line treatment 9
• BiPAP not typically required unless CPAP fails 9

Common Pitfalls

• Do not assume severe OSA equals OHS - you must document daytime hypercapnia 1, 2
• Do not rely on SpO₂ alone to screen for OHS - it has insufficient evidence for this purpose 1, 9
• Do not confuse OHS with COPD - both cause hypercapnia, but OHS requires obesity, sleep-disordered breathing, and exclusion of significant lung disease 7, 8
• Do not miss screening obese patients with OSA - prevalence of OHS is 8-20% in this population 1