International Journal of Respiratory Medicine

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (629)348-3199

Perspective - International Journal of Respiratory Medicine (2023) Volume 8, Issue 3

Sleep apnea-induced respiratory disturbances: Pathophysiology and effects

Laura Javaheri*

Department of Medicine and Public Health, Flinders University, Bedford Park, Australia

*Corresponding Author:
Laura Javaheri
Department of Medicine and Public Health
Flinders University, Bedford Park, Australia
E-mail: javaura@gmail.com

Received: 30-May-2023, Manuscript No. AAIJRM-23-103911; Editor assigned: 03-Jun-2023, PreQC No. AAIJRM-23-103911(PQ); Reviewed: 17-Jun-2023, QC No. AAIJRM-23-103911; Revised: 20-Jun-2023, Manuscript No. AAIJRM-23-103911(R); Published: 27-Jun-2023, DOI: 10.35841/aaijrm-8.3.153

Citation: Javaheri L. Sleep apnea-induced respiratory disturbances: Pathophysiology and effects. Int J Respir Med. 2023; 8(3):153

Visit for more related articles at International Journal of Respiratory Medicine

Introduction

Sleep apnea is a common sleep disorder characterized by repeated pauses in breathing during sleep. These pauses, known as apnea, can occur due to either a complete blockage of the airway (obstructive sleep apnea) or a failure of the brain to signal the muscles to breathe (central sleep apnea). Regardless of the type, sleep apnea leads to respiratory disturbances that have significant pathophysiological effects on the body. The pathophysiology of sleep apnea-induced respiratory disturbances begins with the partial or complete collapse of the upper airway during sleep, leading to airway obstruction. This obstruction can be caused by various factors, including anatomical abnormalities, such as a narrow airway or enlarged tonsils, or by the relaxation of the muscles responsible for maintaining the patency of the airway. When the airway becomes obstructed, the individual's efforts to breathe against the resistance result in increased negative pressure in the airway. This negative pressure leads to the collapse of the soft tissues in the throat, further exacerbating the obstruction. As a result, airflow is significantly reduced or completely blocked, leading to apnea [1].

During an apnea event, the brain detects the lack of oxygen and the increase in carbon dioxide levels, triggering an arousal response. The individual partially or fully wakes up, which restores muscle tone and reopens the airway, allowing normal breathing to resume. These arousals often accompanied by loud snoring or gasping for air, disrupt the normal sleep architecture and prevent the individual from reaching restorative sleep stages. The repeated occurrence of apnea and arousals throughout the night leads to a cascade of physiological effects on the respiratory system and other body systems. One of the primary consequences is intermittent hypoxia, which refers to the cyclic periods of decreased oxygen saturation during apnea. The decreased oxygen levels not only impair the oxygen supply to vital organs but also trigger a series of systemic responses to compensate for the hypoxic state [2].

Intermittent hypoxia activates the sympathetic nervous system, leading to increased heart rate, elevated blood pressure and vasoconstriction. These responses contribute to the development of systemic hypertension and cardiovascular diseases, such as coronary artery disease, heart failure and stroke. Additionally, the repeated oxygen deprivation and oxygenation cycles promote oxidative stress and inflammation, further contributing to vascular dysfunction. The respiratory disturbances caused by sleep apnea also impact the respiratory system itself. The recurrent collapse of the upper airway results in increased work of breathing, as the individual must exert more effort to overcome the airway obstruction and maintain adequate ventilation. This increased effort can lead to daytime fatigue, excessive daytime sleepiness and impaired cognitive function [3].

Furthermore, sleep apnea-induced respiratory disturbances can disrupt the normal gas exchange process in the lungs. The reduced airflow during apnea decreases the elimination of carbon dioxide and impairs the oxygenation of the blood [4]. Consequently, individuals with sleep apnea may experience nocturnal hypoxemia and hypercapnia, which can have detrimental effects on organ systems and overall health. In addition to the respiratory and cardiovascular consequences, sleep apnea-induced respiratory disturbances have been associated with metabolic and endocrine deregulation. Sleep apnea is linked to insulin resistance, glucose intolerance and an increased risk of developing type II diabetes. Moreover, hormonal imbalances, such as elevated levels of cortisol and decreased levels of growth hormone, have been observed in individuals with sleep apnea, which can contribute to weight gain, metabolic dysfunction and impaired overall well-being [5].

Conclusion

In conclusion, sleep apnea-induced respiratory disturbances are a significant medical condition characterized by repeated episodes of partial or complete obstruction of the upper airway during sleep. These disturbances can lead to fragmented sleep patterns, oxygen desaturation and various physiological and neurobehavioral consequences. The pathophysiology of sleep apnea involves the collapse or narrowing of the upper airway, leading to obstructive events during sleep. Factors such as obesity, anatomical abnormalities and decreased muscle tone in the upper airway contribute to the development of sleep apnea. Central sleep apnea, on the other hand, is caused by the brain's failure to send appropriate signals to the muscles involved in breathing.

References

  1. Eckert DJ, Younes MK. Arousal from sleep: implications for obstructive sleep apnea pathogenesis and treatment. J Appl Physiolo. 2014;116(3):302-13.
  2. Indexed at, Google Scholar, Cross Ref

  3. Goldbart AD, Goldman JL, Veling MC, et al. Leukotriene modifier therapy for mild sleep-disordered breathing in children. Am J Respir Crit Care Med. 2005;172(3):364-70.
  4. Indexed at, Google Scholar, Cross Ref

  5. Lozic B, Johansson S, Lovric Kojundzic S, et al. Novel NALCN variant: altered respiratory and circadian rhythm, anesthetic sensitivity. Ann Clin Transl Neurol. 2016;3(11):876-83.
  6. Indexed at, Google Scholar, Cross Ref

  7. Rochemaure J, Laaban JP, Orvoen-Frija E, et al. Cardio-respiratory complications of sleep apnea in obese patients. Bull Acad Natl Med. 1993;177(5):649-70.
  8. Indexed at, Google Scholar

  9. Yun CH. Central Sleep Apnea in Heart Failure: Clinical Implications, Recognition and Management. J. Korean Neurosurg. Soc.2008;5(1):17-25.
  10. Indexed at, Google Scholar, Cross Ref

Get the App