LAUSR

The obesity-hypoventilation syndrome (OHS) is defined by the presence of obesity (BMI greater than 30 kg/m2) and daytime hypercapnia, in the absence of other situations that could explain the alveolar hypoventilation. Treatment consists of applying positive airway pressure (PAP), either in the form of CPAP or non-invasive ventilation (NIV) [1]. In addition to hypercapnia, OHS presents with hypoxemia, mainly nocturnal, and sometimes also diurnal [2, 3]. This has been attributed to alterations in the ventilation/perfusion ratio (V/Q) [3, 4]; however, this phenomenon is rarely measured and quantified. Our objective was to quantify this degree of V/Q alteration by measuring the Qs/Qt ratio and to explore other possible causes of sustained daytime hypoxemia in a group of patients with OHS. The Qs/Qt ratio is a measure of the portion of the right ventricular cardiac output that reaches the systemic circulation without participating in gas exchange. A value up to 5% is accepted as normal, and higher than that reflects an imbalance in the V/Q ratio and, therefore, a factor that will cause hypoxemia [5]. From January 2017 to June 2020, among the patients diagnosed with OHS undergoing PAP treatment, we selected 11 cases who had corrected diurnal hypercapnia but who maintained diurnal pO2 < 60 mmHg on a regular basis. The assessment was carried out in a stable clinical situation (without exacerbation in the last 4 weeks), and the variables that were considered were age, sex, pO2, and pCO2 (baseline and after treatment with PAP), apnea–hypopnea index (AHI), time during the night with SpO2 < 90% (T90), and pulmonary function studies. To explore anatomical causes of hypoxemia, a chest radiograph, chest CT scan, and transthoracic echocardiography (TTE) were performed. The Qs/ Qt ratio was measured with the 100% O2 breathing technique, assuming a difference in arteriovenous O2 content (CaO2–CvO2) of 5% when dealing with subjects in a stable situation [6]. The results are presented in Table 1. In our study, the Qs/Qt value was higher than the physiological value with a mean of 12% [5]. Chest CT showed abnormalities in 3 cases: basal laminar atelectasis, isolated signs of emphysema, and bronchiectasis of segmental distribution. TTE did not detect any changes in contractility with a mean left ventricular ejection fraction (LVEF) greater than 50%. In one case, patent foramen ovale (PFO) was diagnosed by performing TTE with infusion of stirred serum. In our group of patients with OHS and residual diurnal hypoxemia, we have detected high Qs/Qt values, and only in the PFO case we could attribute that circumstance to a structural abnormality that caused a right-left shunt [7]. We think that the alterations in V/Q could have been caused by obesity itself in the 10 patients without other underlying pathological conditions. Previous studies reflect the existence of hypoxemia in OHS and its persistence despite treatment with PAP [2, 3]. Thus, in the study by Masa et al. [3], out of 43 patients treated with PAP, 3 cases were reported with diurnal PaO2 less than 55 mmHg. In our study, we found that 9% of patients with OHS may present pO2 values lower than 60 mmHg during the day. On the other hand, we established that in 10 of the 11 cases, this respiratory failure could be attributed to obesity itself, since we reasonably excluded other possible causes. In this sense, Rivas et al. [4] studied 19 patients with morbid obesity before undergoing bariatric surgery, detecting the presence of a mean D (A-a) O2 of * Ramón Fernández Álvarez [email protected]