How does obesity trigger sleep apnea? Scientific weight loss is key.

Mechanism of Obesity-Induced Sleep Apnea Syndrome: Obstructive sleep apnea syndrome is closely related to obesity. Two-thirds of individuals who are more than 20% overweight have this syndrome, and most patients with obstructive sleep apnea syndrome are obese, with an average weight of 114.7 ± 30 kg and an average BMI of 31.1. Obese patients have fat accumulation, a relatively short and thick neck, a small upper airway diameter, and a soft airway, making it prone to collapse. Narrowing of the upper airway during sleep can lead to this syndrome.

In extremely obese individuals, excessive fat in the chest wall and abdomen restricts movement, which can cause shallow breathing, reduced inspiratory reserve, and consequently, reduced functional residual capacity, placing the lungs in a near-expiratory position. According to the Bohr equation, alveolar ventilation = tidal volume - dead space ventilation. When breathing is shallow, tidal volume decreases, thus reducing alveolar ventilation. When tidal volume decreases to the clinical threshold, even increasing the respiratory rate cannot maintain alveolar ventilation.

Haekney et al. argued that in significantly obese individuals, increased intra-abdominal pressure and elevated diaphragm lead to increased intrathoracic pressure, resulting in decreased expiratory volume reserve (EVR) and vital capacity. In a control group of 10 individuals, they artificially tightened the chest and abdomen to increase intra-abdominal pressure, replicating functional abnormalities similar to those observed in obese patients with hypoventilation; both vital capacity responsiveness and maximum voluntary ventilation were reduced. They concluded that these functional abnormalities inevitably lead to decreased pulmonary ventilation, causing carbon dioxide retention and hypoxia, which in turn inhibits the respiratory center, exacerbating hypoventilation. Hypoxia can cause polycythemia and increased blood volume, even pulmonary hypertension, cor pulmonale, and right heart failure.

Some researchers have pointed out that in extremely obese individuals, respiratory oxygen consumption is significantly increased. This is due to increased mechanical function required for movement of the thoracic cavity, diaphragm, abdominal wall, and internal organs, increased elastic resistance of the thoracic cavity, and increased oxygen consumption during respiration, which is inevitably accompanied by decreased arterial oxygen tension and increased carbon dioxide tension.

A study of 20 cases suggests that in extremely obese individuals, reduced vital capacity can lead to small airway obstruction and localized atelectasis, resulting in impaired pulmonary capillary circulation, uneven alveolar blood perfusion, and increased ventilation-airflow ratio.

Vital capacity, expiratory capacity reserve, functional residual capacity, and lung volume are all reduced, but residual capacity is often normal, thus increasing residual rate.

Due to continuous weight gain, the degree of uneven gas exchange also increases. This leads to an increase in arterial carbon dioxide partial pressure (PaCO₂) at rest, while oxygen partial pressure (PaO₂) decreases slightly, and the venous mixing ratio increases. Hypoxemia is also related to impaired blood distribution in gas exchange. If the patient also has chronic bronchitis or pneumonia, i.e., obstructive or restrictive ventilatory dysfunction, hypercapnia and hypoxemia are more severe.

Due to prolonged hypoxia, patients are prone to secondary polycythemia, which increases blood viscosity, thereby increasing circulatory resistance, increasing the load on the right heart, and making them more susceptible to right ventricular hypertrophy and even right ventricular failure.