Key learning points

  • Obesity impairs pulmonary physiology and functions
  • Obesity is an important cause of breathlessness and adds to morbidity from asthma and COPD
  • Obstructive sleep apnoea due to neck obesity increases the cardiometabolic risks of obesity
  • Obesity hypoventilation syndrome is emerging as a common cause of acute and chronic ventilatory failure 


Obesity adversely affects pulmonary physiology and function through both mechanical and systemic inflammatory effects.1,2 Obesity is an important cause of unexplained breathlessness, obstructive sleep apnoea (OSA) and obesity hypoventilation syndrome (OHS), and adds to the morbidity from asthma and chronic obstructive pulmonary disease (COPD).2 Obesity management can eliminate breathlessness, OSA and OHS, and improve asthma and COPD control.2

The effect of obesity on the lungs

Obesity is an important and often overlooked cause of breathlessness on exertion.3 It is directly related to the severity of obesity – most (80%) morbidly obese patients report exertional breathlessness (demonstrated by climbing two flights of stairs).2 This may be caused by an increase in the work of breathing required to overcome reduced chest wall compliance, as well as increased airway resistance and weakness of respiratory muscles.2,3

Chest wall obesity can cause extrapulmonary restrictive impairment on spirometry as a result of a reduction in expiratory reserve volume and vital capacity. Spirometry may demonstrate a reduction in forced expiratory volume in 1 second (FEV1) because of an increase in airway resistance. Abdominal obesity restricts diaphragmatic movement and reduces basal air entry, causing atelectasis and ventilation/perfusion (V/Q) mismatch which leads to hypoxemia.4


Neck obesity (collar size >17 inches) is the main cause of OSA.5 It causes narrowing and increased floppiness of the upper airways. During sleep, upper airway obstruction, resulting from a supine position and muscle hypotonia/atonia, leads to recurrent apnoeas and hypopnoeas associated with recurrent oxygen desaturation and sleep disruption.2 Patients with OSA are excessively sleepy and tired during the daytime, impacting on their driving, work and quality of life. Chronic intermittent hypoxia caused by OSA adds to the systemic inflammatory state induced by adipocytokines and increases the risk of cardiometabolic diseases.5

Obese patients who have disturbed sleep and excessive daytime sleepiness should be screened for OSA using the Berlin or STOP-Bang questionnaires. Continuous positive airways pressure is the most effective treatment for controlling OSA but weight loss can cure OSA. A 10% reduction in body weight can reduce the severity of OSA by one third.6 Massively obese patients not only have a high prevalence of OSA but are at risk of reduced central respiratory drive. Their breathing becomes shallow during sleep (hypoventilation), causing prolonged hypoxia.2,3


Patients with oxygen saturation levels below 90% for one third of sleep duration are more likely to have OHS. They have daytime hypercapnia (chronic ventilatory failure) on arterial blood gas measurement.2 Patients with OHS are at higher risk of developing pulmonary hypertension and cor pulmonale, and decompensate leading to right-sided heart failure and acute on chronic ventilatory failure.2 OHS is one of the commonest but often overlooked causes of acute hypercapnic respiratory failure requiring admission to hospital.7

Obese patients, particularly those who are morbidly obese, should be suspected to have OHS if they demonstrate features of right-sided heart failure (swollen ankles) and have low oxy-haemoglobin saturation.2


Obesity is associated with a higher prevalence of asthma.8 This may be partly due to over-diagnosis of asthma in breathless obese patients as there is no direct effect of obesity on bronchial inflammation and hyperreactivity.8,9

Nevertheless, the mechanical effects of obesity add to the effect of airflow obstruction in asthma. Systemic inflammatory effects of obesity may account for the reduced effectiveness of inhaled steroids.8 Obese patients with asthma experience more acute attacks and require more hospital admission than non-obese patients.8


Similarly, obesity adds to the effect of impaired respiratory function and gas exchange in patients with COPD.10 Obesity is common among patients with COPD and worsens breathlessness, quality of life and acute exacerbations.11 Obese patients with COPD who have OSA are at higher risk of developing chronic ventilatory failure (overlap syndrome) despite mild to moderate COPD.2 Weight loss can reduce breathlessness in obese patients with COPD.

Dr Himender Makker is a consultant respiratory physician, University College London and North Middlesex University Hospital, London

This project was initiated and funded by Teva Respiratory. Teva have had no influence over content. Topics and content have been selected and written by independent experts.