Institute for Continuing Education

The Cardiovascular Consequences of OSA

Course Objectives

Upon successful completion of this module, you will be able to:

• Define the OSA syndrome and list the ways it can impact the cardiovascular system.
• Identify the risk factors for OSA.
• Explain the interconnectivity of Hypertension, Vascular Disease, and Sleep-Disordered Breathing.
• Identify treatment modalities available for OSA.

Course Information

It has become abundantly clear that disorders of breathing during sleep can have profound effects, only some of which are apparent during wakefulness. There is significant interaction between sleep and breathing in both directions: sleep changes the way we breath, and problems with breathing can profoundly fragment sleep.

Sleep is not homogeneous and is conventionally divided into two states - non rapid eye movement (NREM) sleep and rapid eye movement sleep (REM) - which can be distinguished on behavioural and electrophysiological criteria. NREM sleep is further divided into stages 1 - 4; stages 3 and 4 represent the deeper levels of sleep (that are thought to be required to refresh the brain) and together are known as slow wave sleep (SWS). Periods of NREM and REM sleep alternate cyclically through the night at intervals of 90 - 120 minutes. The minimum amount of sleep that can be tolerated without adverse side effects varies between individuals, but the mean is approximately 6 - 7 hours.

There are two clinically important changes in ventilatory control and mechanics that normally accompany sleep:

The ventilatory activity of all respiratory muscles (including the upper airway) is reduced. Consequently, ventilation falls by approximately 10% and upper airway resistance increases, both of which lead to a rise in PaCO2 of 3 - 7 mm Hg. This reduction in ventilatory drive is largely due to the removal of the awake (or behavioral) drive, leaving just the chemical drive from hypercapnia and hypoxia. This behavioral drive is important in preventing ventilation dropping below about 5 litres/min during wakefulness.

During REM sleep, there is generalized inhibition of skeletal muscles, including the intercostal, accessory and pharyngeal dilators. Thus, ventilation during REM is virtually dependant on diaphragmatic function, and upper airways function is yet more precarious than during SWS.