Obesity hypoventilation syndrome

Abstract

Obesity hypoventilation syndrome (OHS) is defined as a combination of obesity (body mass index ≥30 kg·m^-2), daytime hypercapnia (arterial carbon dioxide tension ≥45 mmHg) and sleep disordered breathing, after ruling out other disorders that may cause alveolar hypoventilation. OHS prevalence has been estimated to be ∼0.4% of the adult population. OHS is typically diagnosed during an episode of acute-on-chronic hypercapnic respiratory failure or when symptoms lead to pulmonary or sleep consultation in stable conditions. The diagnosis is firmly established after arterial blood gases and a sleep study. The presence of daytime hypercapnia is explained by several co-existing mechanisms such as obesity-related changes in the respiratory system, alterations in respiratory drive and breathing abnormalities during sleep. The most frequent comorbidities are metabolic and cardiovascular, mainly heart failure, coronary disease and pulmonary hypertension. Both continuous positive airway pressure (CPAP) and noninvasive ventilation (NIV) improve clinical symptoms, quality of life, gas exchange, and sleep disordered breathing. CPAP is considered the first-line treatment modality for OHS phenotype with concomitant severe obstructive sleep apnoea, whereas NIV is preferred in the minority of OHS patients with hypoventilation during sleep with no or milder forms of obstructive sleep apnoea (approximately <30% of OHS patients). Acute-on-chronic hypercapnic respiratory failure is habitually treated with NIV. Appropriate management of comorbidities including medications and rehabilitation programmes are key issues for improving prognosis.

FIGURE 1

Management of patients with obesity hypoventilation syndrome (OHS) from diagnosis to integrated care to modify health trajectories. After being diagnosed with OHS, these patients are typically initiated on positive airway pressure (PAP) therapy (continuous positive airway pressure or noninvasive ventilation). Although respiratory insufficiency improves quite consistently in patients adherent to PAP therapy, pulmonary hypertension may also improve in some patients with OHS. There is no evidence that other cardiovascular and metabolic comorbidities improve with PAP treatment alone. Therefore, a multimodality therapeutic approach is necessary to combine PAP therapy with strategies aimed at weight reduction and increased physical activity. P_aCO2: arterial carbon dioxide tension.

FIGURE 2

Pathophysiology of obesity hypoventilation syndrome (OHS). The implicated mechanisms leading to daytime hypercapnia are, potentially, the obesity-related changes in the respiratory system, central hypoventilation, obstructive sleep apnoeas and hypoventilation during sleep, mainly during rapid eye movement (REM). PEEP_i: intrinsic positive end-expiratory pressure; P_aO2: arterial oxygen tension; FRC: functional residual capacity; ERV: expiratory reserve volume; RV: residual volume; TLC: total lung capacity.

FIGURE 3

Obesity hypoventilation syndrome (OHS) management strategy. Continuous positive airway pressure (CPAP) could be first-line treatment for OHS patients with concomitant severe obstructive sleep apnoea (OSA). Noninvasive ventilation (NIV) should be considered as first-line therapy for OHS patients with no OSA or milder forms of OSA. If patients initially treated with CPAP have no favourable response to therapy despite objectively documented high levels of adherence to CPAP, they should be changed to NIV therapy. AHI: apnoea–hypopnoea index.

FIGURE 4

Positive airway pressure adjustment in acute decompensated obesity-related respiratory failure. The adjustment of continuous positive airway pressure/expiratory positive airway pressure (EPAP) has the objective of eliminating obstructive events, snoring and intermittent oxygen desaturations. Adjustments in inspiratory positive airway pressure (IPAP) are aimed at eliminating hypoventilation and sustained hypoxaemia. For both EPAP and IPAP, the pressure should increase progressively until attaining the objectives (resolution of upper airway obstructive events and sleep hypoventilation) or until the maximal tolerated pressure is reached. Alternatively, EPAP/continuous positive airway pressure can be adjusted to eliminate obstructive apnoeas and IPAP can be further increased to eliminate obstructive hyponoeas, snoring and hypoventilation. With this strategy, the patient may require lower EPAP and therefore achieve higher levels of pressure support in order to improve hypoventilation [96]. Supplemental oxygen is habitually added to positive airway pressure therapy when an adequate oxygenation level is not achieved despite adequate titration of positive airway pressure therapy. NIV: noninvasive ventilation; P_aO2: arterial oxygen tension; S_aO2: arterial oxygen saturation.