Institute for Continuing Education

The Cardiovascular Consequences of OSA

Course Objectives

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

• Define obstructive sleep apnea (OSA) as a clinical syndrome and describe contemporary diagnostic criteria and physiologic metrics, emphasizing those most relevant to cardiovascular risk.
• Identify major risk factors for OSA, including demographic, anatomic, metabolic, and pharmacologic contributors, and recognize distinct OSA phenotypes that influence cardiovascular consequences and treatment response.
• Explain the interconnectivity between OSA, systemic hypertension, atherosclerotic vascular disease, heart failure, and cardiac arrhythmias, highlighting shared mechanisms and bidirectional relationships.
• Describe in detail the pathophysiologic mechanisms linking OSA to adverse cardiovascular outcomes, including intermittent hypoxia, sympathetic activation, intrathoracic pressure swings, endothelial dysfunction, inflammation, and metabolic dysregulation.
• Critically evaluate current and emerging treatment modalities for OSA—such as PAP therapy, oral appliances, weight-loss strategies, positional therapy, upper-airway surgery, hypoglossal nerve stimulation, and experimental pharmacologic approaches—with specific attention to their cardiovascular impact.
• Interpret and communicate polysomnographic and home sleep testing data in a way that captures cardiovascular risk, including metrics like AHI subtypes, hypoxic burden, oxygen desaturation index (ODI), time below 90% SpO? (T90), arousal index, event duration, and autonomic/cardiac responses.
• Apply practical strategies to optimize adherence to PAP and other therapies, identify barriers to effective treatment, and appropriately triage cardiovascular concerns discovered during diagnostic testing to multidisciplinary teams.

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.