Metabolic and endocrine disorders

Abstract

The findings in patients with the obesity-hypoventilation (Pickwickian) and obstructive sleep apnoea syndromes were considered in section 13.1. Here we are concerned with the effects of simple obesity on conventional tests of respiratory function in patients with a normal arterial PCO₂. Gross obesity may result in a mild restrictive ventilatory defect but the reductions in vital capacity and total lung capacity are usually only minor, even when body weight is double the ideal value.¹ There are corresponding reductions in the compliance of both the lungs and chest wall² and the decreased distensibility of the respiratory system is proportional to both the reduction in VC and to the increase in weight.³ The altered elastic properties probably account for the typical ‘restrictive’ pattern of breathing with small tidal volume and rapid frequency. Although other volumes are little affected, obesity consistently results in falls in FRC and, more particularly, in the expiratory reserve volume (ERV) which is often close to zero (i.e. FRC is close to RV). Although there is no evidence of airflow obstruction,⁴ the mechanical abnormalities lead to some increase in the mechanical work of breathing; the oxygen cost of breathing is relatively higher still,⁴ apparently because of inefficiency of the respiratory muscles owing to the adiposity of the chest wall.⁵–⁶ It has been suggested that the respiratory muscles might hypertrophy in obese subjects,⁴ but there is no anatomical evidence on this; neither are there any data on respiratory pressures during maximum static efforts which might support this hypothesis.