STUDY OF SLEEP RELATED RESPIRATORY DISORDERS IN VARIABLE DEGREES OF OBESITY

Abstract

Morbid obesity is associated with excessive daytime sleepiness and fatigue even without OSAHS.

Sleep fragmentation, hyperarousal, daytime sleepiness and night time disturbance are manifestations of a circadian and/or metabolic abnormalities due to several mediators, particularly cytokines; tumor necrosis factor a (1NFa) and interleukin 6 (IL-6) which play a role in mediating sleepiness in obese subjects.

Increased neck circumference and fat deposition in the pharyngeal area lead to the development ofOSAHS and not the crude value of the body mass index (BMI).

All obese subjects become more hypoxemic during sleep than during resting wakefulness, the main causes of this nocturnal hypoxemia are: the hypoventilation occurring during sleep, decrease in functional residual capacity (FRC), and V/Q mismatch.

This nocturnal hypoxia could be a cause of pulmonary hypertension, increased red cell mass, nocturnal dysrrhythmias, and increased incidence of death during sleep.

Several studies have studied the phenomenon of nocturnal desaturation but did not reach an agreement of what constitutes "the clinically significant" nocturnal desaturation.

All obese subjects become also more hypoxemic in supine than sitting position due to V/Q mismatch as a result of airway closure and alveolar collapse which become obvious in obese subjects with small lung volumes and in supine position.