From the Guidelines
In a 50-year-old morbidly obese man with obstructive sleep apnea (OSA), it is expected that serum bicarbonate levels will be elevated, hemoglobin concentration will be increased, and total lung capacity will be reduced due to the physiological consequences of chronic sleep apnea and morbid obesity. These expectations are based on the understanding that chronic carbon dioxide retention leads to compensatory metabolic alkalosis, resulting in elevated serum bicarbonate levels [ 1 ]. The body's response to chronic intermittent hypoxemia during apneic episodes is to increase hemoglobin concentration (polycythemia) to improve oxygen-carrying capacity [ 1 ]. Additionally, excess adipose tissue around the chest wall and abdomen limits full lung expansion, leading to restrictive ventilatory impairment and reduced total lung capacity [ 1 ]. Key findings to expect include:
- Elevated serum bicarbonate levels (above 26 mEq/L) due to chronic carbon dioxide retention
- Increased hemoglobin concentration (polycythemia, potentially above 17 g/dL) as a response to chronic intermittent hypoxemia
- Reduced total lung capacity compared to predicted values due to restrictive ventilatory impairment These findings are indicative of the physiological adaptations and consequences of chronic sleep apnea combined with morbid obesity, which together cause chronic hypoventilation, intermittent hypoxemia, and increased work of breathing [ 1 ]. The combination of these abnormalities may indicate obesity hypoventilation syndrome if the patient also has daytime hypercapnia, which frequently coexists with obstructive sleep apnea in morbidly obese individuals [ 1 ].
From the Research
Expected Findings
- Serum bicarbonate levels: The study 2 found that after one month's treatment with autoCPAP, the patient's arterial blood gases, including PaCO(2), returned to normal. This suggests that serum bicarbonate levels may also normalize with effective treatment of OSA.
- Hemoglobin (Hb) concentration: The same study 2 reported normalization of blood morphology parameters, including hemoglobin concentration, after one month's treatment with autoCPAP. This implies that Hb concentration may decrease with treatment, as polycythemia is often associated with OSA.
- Total lung capacity: The study 2 found that spirometric measurements returned to normal after the patient lost 22 kg during therapy. This suggests that total lung capacity may increase with weight loss and effective treatment of OSA. Another study 3 reported intrapulmonary restrictive changes and reduced compliance in morbidly obese men with OSA, which may improve with treatment and weight loss.
Relationship between OSA and Obesity
- The prevalence of OSA is high in morbidly obese patients, with one study 4 reporting a prevalence of 93.6% in a group of morbidly obese patients.
- Obesity is a major risk factor for OSA, and weight loss is an important aspect of treatment 5, 6.
- The mechanism of the relationship between obesity and OSA may be mechanical obstruction or hypoxemia 5, and chronic intermittent hypoxia, sleep fragmentation, and inflammatory activation are the main pathophysiological mechanisms of OSA 6.