Complications of Sleep Apnea

Sleep apnea refers to intermittent, cyclical cessations or reductions of airflow, with or without obstruction of the upper airway. This is manifested to the patient and the observers as snoring. On a long-term basis, Obstructive sleep apnea (extreme snoring) can cause several major and minor complications to an individual’s health and well-being, which will be the primary focus of this article.

Why complications?

Major complications that occur in a patient with apnea are due to the compromised airway and reduced or inefficient oxygenation of blood. This leads to significant arterial hypoxemia and hypercapnia which in the long run can give rise to severe medical conditions.

What are the main complications & how they occur?

Endothelial (Cells lining blood vessel lumen) dysfunction & Atherosclerosis (Fat plaques in vessel walls), Hypertension, Coronary artery disease, Stroke, Congestive heart failure, Cardiac arrhythmias, metabolic conditions and Cognitive impairment are the most detrimental and dreaded long term effects of sleep apnea.

Repetitive episodes of oxygen desaturation and reoxygenation, which is a hallmark feature of OSA (Obstructive Sleep Apnea), imparts a risk for increased oxidative stress which increases free radical production.¹ Increase in oxygen free radical production results in lipid peroxidation, protein oxidation, DNA damage, and alteration in cellular homeostasis, leading to up regulation of certain proinflammatory genes. This proinflammatory state coupled with elevated sympathetic nerve activation leads to endothelial dysfunction. Endothelial dysfunction is a major accelerating factor for Atherosclerosis which makes the individual vulnerable for other illnesses.

Sympathetic over activity caused by OSA is considered as the cause for Hypertension. Intermittent hypoxia and negative intra-thoracic pressure leads to chemoreceptor activation and increased sympathetic outflow, and subsequently endothelial dysfunction that predisposes to increased arterial stiffness which leads to development of hypertension.²

It has also been shown that OSA is associated with activation of thrombotic pathways and leads to cardiovascular diseases, especially coronary artery disease. Furthermore, repetitive episodes of hypoxia, intra thoracic pressure swings, and increased afterload create a state of demand-supply mismatch causing cardiac ischemia as demonstrated electrocardiographically by ST depression, accompanying episodes of hypoxia and apnea.³

OSA is another known factor for strokes. As described above, OSA causes hypertension, atherosclerosis, and thrombosis which are major causes for the development of strokes. Several case–control studies have demonstrated an increased prevalence of OSA in individuals with cerebrovascular disease.⁴

OSA and cardiac failure has a bidirectional relationship. OSA affects cardiac function through adverse effects of hypertension, atherosclerosis and ischemic injury. Conversely, heart failure may contribute to the development of OSA by accumulation of fluid (pulmonary edema) of the upper airway.

Several mechanisms have been investigated linking OSA and insulin resistance/ diabetes mellitus. Intermittent hypoxia associated with increased sympathetic activity directly can alter glucose metabolism or indirectly increase other counter-regulatory hormones like cortisol and, possibly, growth hormone that increases insulin resistance.⁵

OSA related hypoxia, fluctuating intra thoracic pressure and imbalanced autonomic nervous function predisposes the patient to cardiac arrhythmias (irregular heart rhythm). Untreated sleep apnea has been identified as a risk factor for recurrent atrial fibrillation after treatment by cardioversion. Furthermore, the future development of atrial fibrillation in individuals with sleep apnea was retrospectively investigated; nocturnal hypoxia was identified as a future predictor of arrhythmia development.⁶

Since it impairs the oxygenation of blood, OSA is known to cause cognitive impairment on a long term basis. Patients with sleep apnea are mostly unaware of their nocturnal symptoms. Patients with OSA commonly experience difficulties in working, memory problems, and concentration, and these symptoms have been best correlated with a degree of hypoxia at night.⁷

Treatment of OSA has shown to significantly improve the symptoms and quality of life of many patients.

OSA and day to day life

OSA patients are often subject to excessive daytime sleepiness, insomnia, social/sexual dysfunction, impaired work performance and higher prevalence of psychological problems such as depression. As a result, usually these individuals have poor quality of life and poor general health.

Preventing Complications

So, it is of utmost importance to identify sleep apnea early and direct these individuals to get the correct treatment in order to prevent complications. Getting yourself educated about complications of sleep apnea, things you can do at home (proper sleeping position) and when and where to get proper treatment are some important measures. Significant reduction in morbidity and mortality can be achieved by early intervention.

References

1. Christou K, Markoulis N, Moulas AN, Pastaka C, Gourgoulianis KI. Reactive oxygen metabolites (ROMs) as an index of oxidative stress in obstructive sleep apnea patients. Sleep Breath. 2003 Sep; 7(3):105-10.
2. Brooks D, Horner RL, Kozar LF, Render-Teixeira CL, Phillipson EA. Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model. J Clin Invest. 1997 Jan 1; 99(1):106-9.
3. Hanly P, Sasson Z, Zuberi N, Lunn K. ST-segment depression during sleep in obstructive sleep apnea. Am J Cardiol. 1993 Jun 1; 71(15):1341-5.
4. Bassetti C, Aldrich MS. Sleep apnea in acute cerebrovascular diseases: final report on 128 patients. Sleep. 1999 Mar 15; 22(2):217-23.
5. Bratel T, Wennlund A, Carlström K. Pituitary reactivity, androgens and catecholamines in obstructive sleep apnoea. Effects of continuous positive airway pressure treatment (CPAP). Respir Med. 1999 Jan; 93(1):1-7.
6. Gami AS, Hodge DO, Herges RM, Olson EJ, Nykodym J, Kara T, Somers VK. Obstructive sleep apnea, obesity, and the risk of incident atrial fibrillation. J Am Coll Cardiol. 2007 Feb 6; 49(5):565-71.
7. Quan SF, Wright R, Baldwin CM, Kaemingk KL, Goodwin JL, Kuo TF, Kaszniak A, Boland LL, Caccappolo E, Bootzin RR. Obstructive sleep apnea-hypopnea and neurocognitive functioning in the Sleep Heart Health Study. Sleep Med. 2006 Sep; 7(6):498-507.

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