Introduction Obesity Hypoventilation Syndrome (OHS) is conventionally defined by the combination of obesity (BMI >30 kg/m2) and daytime hypercapnia (PaCO2 >6 kPa, with no other explanation) and sleep-disordered breathing may or may not be included. OHS patients have a higher morbidity, mortality, and health care utilisation compared with non-hypercapnic obese subjects. We hypothesised that in obese patients, even in the absence of a raised daytime PaCO2, the presence of a raised plasma standard bicarbonate, or base excess (BE, as a biomarker of whole body acid-base balance) would be associated with some well-recognised features of OHS (reduced ventilatory drives to hypoxia and hypercapnia, and nocturnal hypoventilation), thus suggesting they represent ‘early’ OHS.
Methods Obese subjects (BMI >30 kgs/m2) were identified from a variety of sources, and divided into those with: 1) normal arterial blood gases and normal acid-base balance, 2) an isolated raised arterial BE (≥2 mmol/L), and 3) awake arterial hypercapnia (>6 kPa, i.e. established OHS). Two-point ventilatory responses to hypoxia (15 min poikilocapnic response to 15% O2) and hypercapnia (15 min response to 5%CO2 in O2) were performed. Derivatives included the fall in SaO2 and rise in end-tidal CO2 when stable, and conventional ventilatory drive calculations. Polygraphic sleep studies were done with the derivatives of intermittent (oxygen desaturation index) and prolonged hypoxia (time below 90% SaO2) reported here.
Results 71 subjects (BMI 47.2, SD 9.8; age 52.1, SD 8.8) were recruited into the above three groups (33, 22, and 16 respectively). The table shows the BMI, PaCO2 and BE for the three groups, along with the selected derivatives of the ventilatory drive measurements and sleep studies. For nearly all the ventilatory response and sleep study derivatives, group 2 (with only an isolated raised BE) represented a middling group, and for some of the measures this middle group was more similar to group 3, with established OHS, rather than group 1.