Medically reviewed by
Dacelin St Martin, MD
Triple board-certified in Sleep Medicine,
Internal Medicine, and Pediatrics.

What is Obstructive Sleep Apnea? | Epidemiology | Risk Factors | Signs and Symptoms | OSA & Heart Health | The Role of Obesity | The Effect of Forced Inspiration | Diagnosis | Treatment

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Introduction

Obstructive sleep apnea (OSA) is a significant health concern for millions of Americans. Recent studies reveal a strong link between OSA and a higher risk of cardiovascular disorders, like systemic hypertension, cardiac arrhythmias, stroke, and heart failure.

There’s a need to educate people about this insidious condition and its effect on cardiovascular health. Read on to learn about the various mechanisms involved in the development of these conditions as they pertain to OSA.

What is Obstructive Sleep Apnea?

Obstructive Sleep Apnea (OSA) is a sleep disorder that can affect your physical and mental well-being. This condition is characterized by disturbed sleep caused by frequent interruptions in breathing.

OSA can prevent you from getting a sound and refreshing sleep, which may lead to severe complications, some of which are linked to cardiovascular health. 

Let us first have a glimpse of the epidemiology, risk factors, and symptoms of OSA. Then we will look at how OSA can affect your heart’s health and functions and contribute to the development of high blood pressure and atrial fibrillation.

Epidemiology 

OSA is more common in men above 60 years of age.^[1] Approximately 15 to 30% of men and 10 to 15% of women in North America have OSA characterized by the apnea-hypopnea index higher than five events during each hour of sleep.^[2,3]

Risk Factors

• Gender: OSA is more common in men than in women. The incidence of OSA rises in women after menopause.^[4,5]
• Obesity: Excessive deposition of fats around the air passages may obstruct breathing, causing OSA
• Genetics: The risk of OSA is higher in the first-degree relatives
• Larger Neck Size: More than 16″ in women and 17″ in men 
• Narrowing of the airways due to the enlargement of the tonsils or adenoids
• Unhealthy lifestyle habits, like smoking
  
  

Signs and Symptoms

• Episodic choking and gasping during sleep
• Daytime drowsiness
• Lack of focus or alertness in the morning
• Frequent headaches
• Irritability due to the lack of sleep
• Forgetfulness
• Poor job and academic performance
• Hyperactivity, especially in children
• Increased risk of accidents and injuries due to reduced alertness
  
  

OSA and Heart Heath

1) Heart Functions

Research studies have shown that patients with OSA tend to have compromised cardiac output and functionality due to disturbed sleep and frequent awakening. OSA might increase your risk for systemic hypertension, cardiac arrhythmias, stroke, and heart failure when left untreated. 

The episodic obstruction of the upper airways may cause hypoxemia, which leads to reduced oxygen to your organs. As a result, your brain sends signals to wake you up so that you can resume breathing. 

The reduced oxygen supply at frequent intervals can affect your body’s hemodynamic stability, which affects the heart’s functionality. 

Research studies have shown that the reduced oxygen supply to the heart muscles can depress the force of the myocardium’s contractile activity. This physiological response can reduce the flow or output of blood from your heart during each beat. As a result, your heart has to pump harder to ensure an efficient supply of oxygen to all the organs, leading to hypertension.^[6]

2) Strains on Heart Muscles 

The prevalence of OSA in patients with atrial fibrillation is estimated to be nearly 32 to 49%.^[7]

A sudden drop in your blood’s oxygen levels due to the obstruction in the airways can create more strain on your heart. As a result, the SA and AV nodes’ rhythm and rate activities, which initiate and control the impulses traveling through the heart muscles to induce pumping, become irregular.

As a result, your heart is forced to pump faster to ensure your body’s organs receive an adequate supply of oxygen and blood.  This action leads to SA and AV nodes being stimulated, sending faster signals per minute, resulting in atrial fibrillation.^[8]

3) Increased Mean Blood Pressure

Recurring episodes of OSA while sleeping may produce a surge in your systolic and diastolic pressure, causing a rise in the mean blood pressure at night. 

Your blood pressure may remain higher during the daytime, even after the breathing has returned to normal. This hypertension pattern, which is present even during the day, can be attributed to the sympathetic nervous system’s overactivity. 

Vascular structure and functionality change because of inflammation and oxidative stress, which may further increase blood pressure, making you more prone to developing hypertension.^[9]

4) Hemodynamic Effects of OSA

OSA’s short-lasting hemodynamic effects due to the occlusion of the upper airways and subsequent reduction in your blood oxygen levels can lead to the constriction of the blood vessels.^[10]

The hemodynamic effect refers to the changes that occur in the blood parameters, such as the levels of oxygen and carbon dioxide. The oxygen level in the blood reduces while the carbon dioxide level increases when the breathing stops intermittently due to OSA.

So, to cope with the reduced oxygen supply, the blood vessels constrict so that the available oxygen can last longer. This constriction of the blood vessels may increase your blood pressure. This physiological response is one of the possible mechanisms by which OSA can increase your blood pressure. 

The Role of Obesity 

Obesity is both a cause and effect of OSA. Obesity linked to OSA can increase your risk of hypertension and atrial fibrillation independently by contributing to inflammation and free radical damage to the heart’s muscles and endocardial lining.^[11]

The Effect of Forced Inspiration

Forced inspiration against obstructed airways can also result in negative pressure in your intrathoracic cage. This occurrence would increase your cardiac afterload and create unfavorable changes in the atrium structure, thus predisposing you to develop atrial fibrillation.^[12] 

Diagnosis 

OSA’s most notable symptoms include frequent awakenings at night, daytime drowsiness, and snoring; however, further physical examination and tests can help confirm a diagnosis. 

During the physical check-up, the doctor will examine the mouth, back of the throat, and nose for swelling, enlargement of tissues, or other abnormalities. The doctor might measure the waist and neck circumference and check blood pressure to ascertain OSA’s possible causes.

Diagnostic Tools

1. Polysomnography (sleep study at a sleep center)
2. Home sleep studies through MHSleepTesting.com

An AHI: Apnea hypopnea index of at least 5 in either polysomnography or home sleep study is required to be classified as OSA.

The Severity of Sleep Apnea Based on AHI:
1. AHI of 0-5: No Sleep Apnea
2. AHI: 5-15: Mild OSA
3. AHI: 15-30: Moderate OSA
4. AHI: >30 Severe OSA

Treatment

OSA can be managed in one of these 3 ways:

1) CPAP
Short for continuous positive airway pressure, this is considered the gold standard for all levels of severity. The CPAP machine consists of a mask that patients wear over the nose or mouth while sleeping. The machine then pumps oxygen into the airways through the mask, thus improving oxygen flow. It allows the airways to remain open while sleeping and reduces the incidences of awakening.

2) Oral Appliances
Oral Appliances or mandibular advancement devices, shaped like a mouth guard, can also be used to treat OSA. This device keeps the airways open while you are sleeping.

3) Surgery
Surgery is necessary for severe OSA cases that cannot be treated with CPAP or oral appliances, like:

• Upper pharyngeal procedures like UPP (uvulopalatopharyngoplasty), adenoidectomy, or tonsillectomy
• Nasal procedures like septoplasty, nasal valve surgery, or rhinoplasty
• Tracheostomy Maxillomandibular advancement surgery
• Lower pharyngeal procedures, like hyoid and tongue suspension, mandibular advancement, or genioglossus advancement
• Upper airway stimulation through the placement of a medical device from a company called Inspire. You simply turn on the device with the click of a button, and it helps your airways remain open, thereby preventing obstruction in the airflow. 

Conclusion

The pathophysiological changes occurring in your body due to OSA cannot just cause a rise in your nocturnal blood pressure but also lead to sustained daytime hypertension. OSA may also increase your risk of atrial fibrillation if not managed properly by affecting the pathways that regulate inflammation, endothelial dysfunctions, and oxidative stress. 

Being aware of OSA’s implications will help you adopt healthier and more efficient ways to manage this sleep disorder and prevent its adverse impact on your cardiovascular health. If you feel that you or a loved one are exhibiting symptoms of OSA, talk to your doctor. It could be the first step towards wellness.

References:

1. Young, T., Palta, M., Dempsey, J., Skatrud, J., Weber, S., & Badr, S. (1993). The occurrence of sleep-disordered breathing among middle-aged adults. The New England journal of medicine, 328(17), 1230–1235. https://doi.org/10.1056/NEJM199304293281704
2. Young, T., Palta, M., Dempsey, J., Peppard, P. E., Nieto, F. J., & Hla, K. M. (2009). Burden of sleep apnea: rationale, design, and major findings of the Wisconsin Sleep Cohort study. WMJ : official publication of the State Medical Society of Wisconsin, 108(5),246–249. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858234/
3. Peppard, P. E., Young, T., Barnet, J. H., Palta, M., Hagen, E. W., & Hla, K. M. (2013). Increased prevalence of sleep-disordered breathing in adults. American journal of epidemiology, 177(9), 1006–1014. https://doi.org/10.1093/aje/kws342
4. Bixler, E. O., Vgontzas, A. N., Lin, H. M., Ten Have, T., Rein, J., Vela-Bueno, A., & Kales, A. (2001). Prevalence of sleep-disordered breathing in women: effects of gender. American journal of respiratory and critical care medicine, 163(3 Pt 1), 608–613. https://doi.org/10.1164/ajrccm.163.3.9911064
5. Bixler, E. O., Vgontzas, A. N., Ten Have, T., Tyson, K., & Kales, A. (1998). Effects of age on sleep apnea in men: I. Prevalence and severity. American journal of respiratory and critical care medicine, 157(1), 144–148. https://doi.org/10.1164/ajrccm.157.1.9706079
6. Bradley, T. D., & Floras, J. S. (2009). Obstructive sleep apnoea and its cardiovascular consequences. Lancet (London, England), 373(9657), 82–93. https://doi.org/10.1016/S0140-6736(08)61622-0
7. Gami, A. S., Friedman, P. A., Chung, M. K., Caples, S. M., & Somers, V. K. (2005). Therapy Insight: interactions between atrial fibrillation and obstructive sleep apnea. Nature clinical practice. Cardiovascular medicine, 2(3), 145–149. https://doi.org/10.1038/ncpcardio0130
8. Digby, G. C., & Baranchuk, A. (2012). Sleep apnea and atrial fibrillation; 2012 update. Current cardiology reviews, 8(4), 265–272. https://doi.org/10.2174/157340312803760811
9. Dopp, J. M., Reichmuth, K. J., & Morgan, B. J. (2007). Obstructive sleep apnea and hypertension: mechanisms, evaluation, and management. Current hypertension reports, 9(6), 529–534. https://doi.org/10.1007/s11906-007-0095-2
10. Phillips, C. L., & O’Driscoll, D. M. (2013). Hypertension and obstructive sleep apnea. Nature and science of sleep, 5, 43–52. https://doi.org/10.2147/NSS.S34841
11. Lubbers, E. R., Price, M. V., & Mohler, P. J. (2018). Arrhythmogenic Substrates for Atrial Fibrillation in Obesity. Frontiers in physiology, 9, 1482. https://doi.org/10.3389/fphys.2018.01482
12. Marulanda-Londoño, E., & Chaturvedi, S. (2017). The Interplay between Obstructive Sleep Apnea and Atrial Fibrillation. Frontiers in neurology, 8, 668. https://doi.org/10.3389/fneur.2017.00668