Obesity and Hypoventilation Syndrome (OHS) – A Biomechanical Prospective

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.