In OHS, sleepiness may be worsened by elevated blood levels of carbon dioxide, which causes drowsiness ("CO2 narcosis").
[6] The low oxygen level leads to physiologic constriction of the pulmonary arteries to correct ventilation-perfusion mismatching, which puts excessive strain on the right side of the heart.
On physical examination, characteristic findings are the presence of a raised jugular venous pressure, a palpable parasternal heave, a heart murmur due to blood leaking through the tricuspid valve, hepatomegaly (an enlarged liver), ascites and leg edema.
Firstly, work of breathing is increased as adipose tissue restricts the normal movement of the chest muscles and makes the chest wall less compliant, the diaphragm moves less effectively, respiratory muscles are fatigued more easily, and airflow in and out of the lung is impaired by excessive tissue in the head and neck area.
Under normal circumstances, central chemoreceptors in the brain stem detect the acidity, and respond by increasing the respiratory rate; in OHS, this "ventilatory response" is blunted.
Obese people tend to have raised levels of the hormone leptin, which is secreted by adipose tissue and under normal circumstances increases ventilation.
[5][10] Furthermore, episodes of nighttime acidosis (e.g. due to sleep apnea) lead to compensation by the kidneys with retention of the alkali bicarbonate.
However, bicarbonate stays around in the bloodstream for longer, and further episodes of hypercapnia lead to relatively mild acidosis and reduced ventilatory response in a vicious circle.
This results in polycythemia, abnormally increased numbers of circulating red blood cells and an elevated hematocrit.
This usually requires brief admission to a hospital with a specialized sleep medicine department where a number of different measurements are conducted while the subject is asleep; this includes electroencephalography (electronic registration of electrical activity in the brain), electrocardiography (same for electrical activity in the heart), pulse oximetry (measurement of oxygen levels) and often other modalities.
[4] If the symptoms are significant, nighttime positive airway pressure (PAP) treatment is tried; this involves the use of a machine to assist with breathing.
This relieves the features of obstructive sleep apnea and is often sufficient to remove the resultant accumulation of carbon dioxide.
As a last resort, tracheostomy may be necessary; this involves making a surgical opening in the trachea to bypass obesity-related airway obstruction in the neck.
[4][5] Obesity hypoventilation syndrome is associated with a reduced quality of life, and people with the condition incur increased healthcare costs, largely due to hospital admissions including observation and treatment on intensive care units.
[5] The exact prevalence of obesity hypoventilation syndrome is unknown, and it is thought that many people with symptoms of OHS have not been diagnosed.
[4] About a third of all people with morbid obesity (a body mass index exceeding 40 kg/m2) have elevated carbon dioxide levels in the blood.
[5] The discovery of obesity hypoventilation syndrome is generally attributed to the authors of a 1956 report of a professional poker player who, after gaining weight, became somnolent and fatigued and prone to fall asleep during the day, as well as developing edema of the legs suggesting heart failure.
The authors coined the condition "Pickwickian syndrome" after the character Joe from Dickens' The Posthumous Papers of the Pickwick Club (1837), who was markedly obese and tended to fall asleep uncontrollably during the day.