Dysautonomia and sleep apnoea

Obstructive sleep apnoea produces major acute haemodynamic changes and causal relationships with arterial hypertension and cardiovascular morbidity have been proposed.(1) Autonomic dysfunction has been independently associated with obstructive sleep apnoea (OSA), and while autonomic abnormalities are generally considered to be secondary to OSA, it is also felt that autonomic dysfunction may also contribute to OSA.

Sleep apnoea is characterized by sleep fragmentation and/or intermittent hypoxia. Both impose a physiologic stress which may be involved in the pathogenesis of insulin resistance via one of several biological mechanisms.(2)

Proposed Mechanisms linking Sleep Apnoea to Diabetes

Source: International Diabetes Federation. Sleep Apnoea and Type 2 Diabetes. The IDF Consensus Statement. 2008. (2)

Sleep apnoea, cardiovascular disease and cardiac arrhythmias

OSA has an important impact on the ANS and therefore plays a major role in the development of cardiac arrhythmias.(3) The ANS is an important regulator of the cardiovascular system and contributes to the development of cardiovascular diseases including hypertension and coronary artery disease.

Several studies in OSA patients have shown ANS alterations, in particular sympathetic overactivity, both acutely during apnoea events and chronically during the daytime, being both also involved in cardiovascular consequences of sleep disordered breathing. The association between OSA and sympathetic dysregulation suggests a dose response relationship between OSA severity and the degree of sympathetic overactivity and this association seems to be reversible as the treatment of OSA is implemented.

OSA severity was related to sympathetic but not parasympathetic abnormalities. (4) The acute haemodynamic changes in OSA are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory manoeuvres.(1)

These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. Normalising respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity.(1)

The sympathetic activation is considered to be the main mechanism involved in the development of cardiovascular diseases in obstructive sleep apnoea (OSA). The heart rate variability (HRV) analysis, as best measured by the mean RR interval represents a non-invasive tool allowing the study of the autonomic nervous system, as the impairment of HRV parameters in OSA has been documented. This impact has been correlated to the severity of the disease.

References:

  1. Smith,R.,Veale,D., Pepin,J., Levy,P.: Autonomic Nervous System and Sleep Apnea Syndromes. https://pubmed.ncbi.nlm.nih.gov/10939104/
  • International Diabetes Federation. Sleep Apnoea and Type 2 Diabetes. The IDF Consensus Statement. 2008.
  • Woodson. B.,Brusky,L.,Saurajen,A.,Jaradeh,S.: Association of Autonomic Dysfunction and Mild Obstructive Sleep Apnea. 2004. Otolaryngol Head Neck Surg.130(6): 643-8

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