Obesity and Hypoventilation Syndrome (OHS) – A Biomechanical Prospective
Praveen, JS and Nair, SC and Nagarajan, M and Kannan, AK, Obesity and Hypoventilation Syndrome (OHS) - A Biomechanical Prospective, MASO 2009 Scientific Conference on Obesity Obesity & Our Environment' Abstracts, 12-13 August, Kuala Lumpur, pp. 23. (2009) [Conference Extract]
An extensive literature review was carried out using Ovid, Science direct,
Pubmed and Proquest to find the baseline biomechanical alterations
leading to Hypoventilation Syndrome in obesity. The World Health
Organization (WHO) estimates that, by 2015, nearly 2.3 billion adults
will be overweight and more than 700 million will be obese. Obesity
impairs health-related quality of life and is a major cause of morbidity
and premature mortality because of an increased risk of developing
cardiovascular as well as metabolic complications and now recognized
as an important risk factor for developing several respiratory diseases.
This alteration in respiratory mechanics causes major respiratory
compromises and increasing susceptibility for respiratory disorders.
Obesity–hypoventilation syndrome (OHS) is characterized by a triad of
obesity, daytime hypoxemia, and diurnal hypoventilation, as defined by
PaCO2 > 45 mmHg in the absence of other causes of hypoventilation.
Total respiratory system resistance is elevated in OHS 100% during
inspiration when compared to simple obesity which is only 30%. This
further reduces the lung volumes, but FEV1 /FVC ratio remains normal.
There is increased pulmonary loading and further reduction in FRC.
Studies show reduced lung, chest wall, and total respiratory system
compliance due to increased pulmonary blood volume and closure of
dependent airways, excess elastic load posed by excess weight on the
thorax and abdomen, as well as by an enhanced threshold load,
wherein a greater (more negative) pleural pressure must be generated
by the respiratory muscles to initiate airflow. In people OHS have 25%
greater respiratory rate and 25% lower VT causing impaired alveolar
ventilation leading to abnormal ventilatory control/drive. Studies showed
blunted mouth occlusion pressure responses to CO2 and by the ability to
correct PaCO2 during a voluntary hyperventilation maneuver.