Is a raised bicarbonate, without hypercapnia, part of the physiological spectrum of obesity-related hypoventilation?

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Is a raised bicarbonate, without hypercapnia, part of the physiological spectrum of obesity-related hypoventilation?

Chest. 2014 Jul 31;

Authors: Manuel AR, Hart N, Stradling JR

Abstract
ABSTRACT: IntroductionObesity hypoventilation syndrome (OHS) conventionally includes awake hypercapnia, but an isolated raised bicarbonate, even in the absence of awake hypercapnia, may represent evidence of 'early' OHS. We have investigated whether such individuals exhibit certain features characteristic of established obesity hypoventilation syndrome. MethodsObese subjects (BMI >30 kgs/m2) were identified from a variety of sources, and divided into those with: 1) normal blood gases and normal acid-base balance, 2) an isolated raised base excess (≥2mmol/l), and 3) awake hypercapnia (>6kPa, i.e. established OHS). Two-point ventilatory responses to hypoxia and hypercapnia were performed. Polygraphic sleep studies were done to identify intermittent and prolonged hypoxia. Results71 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 PaCO2 and base excess values were: 5.15, 5.42, 6.62 kPa, and +0.12, +3.01, +4.78 mmol/l respectively. For nearly all the ventilatory response and sleep study measures, group 2 (with only an isolated raised base excess) represented an intermediate group, and for some of the measures they were more similar to the third group with established OHS. ConclusionThese data suggest that obese individuals with a raised base excess, despite normocapnia whilst awake, should probably be regarded as having early obesity-related hypoventilation. This has important implications for clinical management as well as randomized controlled treatment trials, as they may represent a group with a more reversible disease process.
Introduction: Obesity hypoventilation syndrome (OHS) conventionally includes awake hypercapnia, but an isolated raised bicarbonate, even in the absence of awake hypercapnia, may represent evidence of 'early' OHS. We have investigated whether such individuals exhibit certain features characteristic of established obesity hypoventilation syndrome.
Methods: Obese subjects (BMI >30 kgs/m2) were identified from a variety of sources, and divided into those with: 1) normal blood gases and normal acid-base balance, 2) an isolated raised base excess (≥2mmol/l), and 3) awake hypercapnia (>6kPa, i.e. established OHS). Two-point ventilatory responses to hypoxia and hypercapnia were performed. Polygraphic sleep studies were done to identify intermittent and prolonged hypoxia.
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 PaCO2 and base excess values were: 5.15, 5.42, 6.62 kPa, and +0.12, +3.01, +4.78 mmol/l respectively. For nearly all the ventilatory response and sleep study measures, group 2 (with only an isolated raised base excess) represented an intermediate group, and for some of the measures they were more similar to the third group with established OHS.
Conclusion: These data suggest that obese individuals with a raised base excess, despite normocapnia whilst awake, should probably be regarded as having early obesity-related hypoventilation. This has important implications for clinical management as well as randomized controlled treatment trials, as they may represent a group with a more reversible disease process.

PMID: 25080050 [PubMed - as supplied by publisher]

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