Significant oxygen desaturation occurs as a consequence of the apnoea. This is detected by the absence of flow. This pattern of oxygen desaturation is often referred to as intermittent hypoxia.
Secondly, during the apnoea there is increasing negative intra-thoracic pressure - down to -80 mmHG. It is extremely difficult for the heart to pump effectively against such a negative pressure and cardiac output decreases.
|Physiological Consequences of OSA|
In response to this potentially life-threatening situation there is an arousal, which terminates the apnoea. The arousal is accompanied by a huge increases in sympathetic output, which causes a significant increase in blood pressure (at a max about 200/140), heart rate and cardiac output.
The huge swings in all these parameters occur against a background of hypoxia and during the time when the cells are rapidly trying to reoxygenate. It is thought that it is this intermittent reoxygenation (occurring sometimes hundreds of times a night), that plays a significant role in the development of cardio-metabolic disease due to the up-regulation of free radicals and inflammatory cytokines.
This increase in inflammatory cytokines and free radicals is not a localised response but results in systemic inflammation which is positively correlated with incident cardiovascular disease and incident type 2 diabetes.