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  • Obstructive Sleepapenia and its Systemic impact: From Disease Mechanism to Clinical Management

  • Photo Harsh Vardhan*

  • Minerva College of Pharmacy, Indora Kangra, Himachal Pradesh

Abstract

Sleep apnea is a sleep disorder where people stop breathing or breathe very shallowly over and over again during the night. Usually, this happens because their airway gets blocked, or their brain doesn’t keep their breathing steady. The result? Rest that’s constantly interrupted, and their body doesn’t get enough oxygen. It’s more common than most folks realize, but it often slips under the radar—especially in places with fewer medical resources. What’s worrying is that sleep apnea doesn’t just mean you wake up tired. It’s linked to heart problems, metabolic issues, and just feeling lousy overall. There are a few types: obstructive sleep apnea (OSA), where the airway actually gets blocked; central sleep apnea (CSA), where the brain doesn’t send the right signals to keep you breathing; and mixed sleep apnea, which is, well, a bit of both. OSA is by far the most common, especially in middle-aged and older adults. Even though people are talking about it more these days, way too many cases still go undiagnosed.

Keywords

Epidemiology, Sleep-apenia, Etiology, Obstructive, Pharmacotherapy.

Introduction

People with obstructive sleep apnea (OSA) stop breathing or breathe too shallowly during sleep because their upper airway gets blocked, either partly (that’s hypopnea) or completely (apnea).[1] This messes with their oxygen levels and often wakes them up, even if they don’t remember it.[2] The result? Sleep that feels anything but refreshing.[3] OSA doesn’t just make you tired—it hits your heart health, messes with mood and behavior, affects how you feel day-to-day, and can even make driving dangerous.[4] There are also other sleep breathing problems, like central sleep apnea, upper airway resistance, and obesity hypoventilation, but those are topics for another time.Other symptoms include loud and disruptive snoring, observed apneas during sleep, and excessive daytime sleepiness. See "Central Sleep Apnea" and "Upper Airway Resistance Syndrome," two StatPearls companion sites, for additional details. [5] Obstructive sleep apnea (OSA) is a disorder caused by upper airway obstruction (which can be partial or complete) during sleep.[6] The change in airway muscle tone during sleep leads to collapse of the upper airways (predominantly during the inspiratory phase of breathing), which leads to intermittent episodes of hypopnea and/or apnea. During these episodes the arterial oxygen saturation falls, which can lead to autonomic dysregulation.[7] These acute changes result over time in chronic conditions that affect the cardiovascular, pulmonary, and neurocognitive systems.[8] However, the most widely used metric for defining daytime sleepiness is the Epworth Sleepiness Scale (ESS) (9,10). Sleep recordings were only made in subsamples with a high risk of OSA in a first-stage screening procedure, and the estimated prevalence in the entire population was predicated on the supposition that there was no OSA at all among the remaining participants in the early prevalence surveys when sleep apnea was still regarded as a rare disorder. In these studies, the estimated frequency of OSA syndrome varied from 0.7% to 3.3% (11-15).

2. ETIOLOGY AND RISK FACTORS

Based on these and other sources, here are major etiologic (causal) factors for Obstructive Sleep Apnea (OSA) you can include: Pharyngeal constriction can be caused by anatomical reasons such as blood vessels, bony structures, extra soft tissue, or a large neck circumference.[16] Numerous of these structures have the potential to raise the pressure surrounding the upper airway, which can result in pharyngeal collapsibility and a lack of room for airflow in a portion of the upper airway as you sleep.[17] Furthermore, a repeated complete or partial airway collapse results from a reduction in upper airway muscular tone. Adult OSA is most frequently linked to male sex, obesity, and aging.[18] Anatomical/structural predisposition: narrow or collapsible upper airway, pharyngeal narrowing, enlarged tonsils, fatty deposits in neck area. [19] Obesity, excess weight: increased soft?tissue around airway, increased collapsibility.[20] Aging / male gender: older age and male sex increase risk via changes in muscle tone, airway structure. [21] Muscle dysfunction / neuromuscular control: reduced tone of dilator muscles of the upper airway (e.g., genioglossus), altered neuromuscular responsiveness. [22] Fluid shifts / positional factors: during sleep fluid redistribution to neck region causing airway narrowing. [23] Low arousal threshold / high loop gain: individuals whose ventilatory control system is more unstable may be prone to apneas. [24] Cranio?facial morphology: small jaw, retrognathia, large tongue relative to mandible, nasal obstruction. [25] Lifestyle and external risk factors: alcohol, sedatives (muscle relaxation), smoking (airway inflammation), nasal congestion. [26]

3. EPIDEMIOLOGY

According to reports, 9% to 17% of women and 25% to 30% of males in the US fit the criteria for OSA.[27] Asian, Black, and Hispanic groups have higher prevalences. The condition affects as many women as males, and its prevalence rises with age, reaching 50 years of age or more. The rising rates of obesity, which range from 14% to 55%, are linked to the rising prevalence of OSA.[28] Obesity and the soft tissue anatomy of the upper airways are two risk factors that are inherited genetically.[29] Sleep apnea is a highly prevalent sleep disorder affecting people across all age groups, though it is most common in middle-aged and older adults. [30] The global prevalence of obstructive sleep apnea (OSA) in adults is estimated to range between 9% and 38%, with higher rates observed in men compared to women. [31] Studies indicate that about 1 in 4 men and 1 in 10 women experience clinically significant OSA. A lot of cases slip through the cracks because symptoms creep in slowly and quietly. In places like the US, Canada, and much of Europe, moderate-to-severe OSA keeps climbing. Blame it on more obesity, aging populations, people moving less—it all adds up.[32-34] Meanwhile, developing countries are catching up. As lifestyles shift to look more “Western,” with different diets and more city stress, the same risk factors start popping up. Sleep apnea doesn’t care about ethnicity—it hits everyone. Still, some groups, like people of Asian descent, seem more at risk because of differences in craniofacial structure, even if they’re not overweight. Kids aren’t immune either.[35] For them, it often comes down to enlarged tonsils or adenoids. This isn’t just a personal health issue. Sleep apnea ties in with high blood pressure, heart disease, type 2 diabetes, and stroke, so it’s a big deal for public health.[36-39] Millions of people around the world have it and don’t even know, which weighs heavily on healthcare systems and economies.[40-41] To tackle this, we need better screening and more awareness—otherwise, the costs just keep stacking up.

4. PATHOPHYSIOLOGY OF OBSTRUCTIVE SLEEP APNEA (OSA) AND DISEASE MECHANISMS

Sleep apnea messes with your breathing while you sleep. Sometimes your airflow drops; sometimes it stops completely.[42] When that happens, your blood oxygen dips and you wake up—usually for just a moment, sometimes without even realizing it.[43] In obstructive sleep apnea, the primary problem is relaxation and collapse of the upper airway usually at the level of the soft palate, tongue, or pharyngeal walls combined with inadequate neuromuscular tone that fails to keep the airway open.[44] In central sleep apnea, the brain’s respiratory centers momentarily stop sending signals to the breathing muscles, causing a pause in ventilation.[45-46] Both forms of sleep apnea create cycles of hypoxia, carbon dioxide buildup, and sympathetic nervous system activation.[47-48] Over time, these cycles contribute to cardiovascular strain, inflammation, metabolic dysregulation, and excessive daytime sleepiness due to fragmented sleep.[49]

5. SIGNS AND SYMPTOMS OF SLEEP APNEA

Sleep apnea often presents with a combination of nighttime and daytime manifestations, which can vary depending on the type and severity of the disorder. [50]

5.1. Nocturnal (Nighttime) Symptoms

Loud, chronic snoring, often interrupted by pauses in breathing. [51] Gasping, choking, or abrupt awakenings during sleep. [52] Restless sleep or frequent tossing and turning. [53] Night sweats. [54] Dry mouth or sore throat upon waking. [55]

5.2. Daytime Symptoms:

People often feel really tired during the day, sometimes even nodding off when they shouldn’t. Morning headaches aren’t unusual, either.[56] It gets tough to focus, and memory can slip, making you less alert than normal. Some folks get irritable or moody, and it’s easy to feel down or just not yourself. Motivation drops, and daytime performance takes a hit.[57-58]

5.3. Associated Signs (Clinical Observations):

Doctors notice a few things, too. Obesity stands out, especially when fat collects around the belly or upper body. Kids might have big tonsils or adenoids. Some people have a narrow airway or facial features that make breathing tougher. Blood pressure often runs high—sometimes stubbornly so. There are also signs linked to metabolic syndrome or insulin resistance.[59-60]

5.4. Red Flags There are some warning signs you really shouldn’t ignore.

Bed partners sometimes see you stop breathing or even choke during sleep.[61-63] Getting up a lot at night to pee happens more than you’d think. And if your heart skips beats or you’re exhausted during the day even though you got enough sleep, that’s a big clue something’s up.[64]

5.5. Treatment of Sleep Apnea

Treatment of sleep apnea aims to restore normal breathing during sleep, improve oxygenation, reduce daytime sleepiness, and prevent long-term complications.[65] Management can be classified into non-pharmacological and pharmacological approaches, depending on the severity, type, and underlying cause.[66]

6. NON-PHARMACOLOGICAL TREATMENTS

6.1 Lifestyle Modifications

  • Weight loss: Reduces fat deposition around the upper airway, particularly effective in obese patients. [67-70]
  • Exercise: Improves cardiovascular health and may reduce apnea severity. [71]
  • Sleep hygiene: Establishing consistent sleep schedules and avoiding sleep deprivation.
  • Alcohol and sedative avoidance: Reduces airway relaxation and prevents worsening of apneas. [72-75]

6.2 Positional Therapy:

  • Encourages sleeping on the side rather than the back to reduce airway collapse.

6.3 Continuous Positive Airway Pressure (CPAP):

  • Gold standard for moderate-to-severe OSA.
  • Delivers pressurized air through a mask to keep the airway open. [76- 79]
  • Used nightly during sleep, duration usually 6–8 hours. [80]

6.4 Oral Appliances:

  • Mandibular advancement devices reposition the jaw and tongue to maintain airway patency. [81-83]
  • Usually worn every night during sleep.

6.5 Surgical Interventions:

  • Uvulopalatopharyngoplasty (UPPP), tonsillectomy, or maxillomandibular advancement may be indicated in anatomical obstruction. [84]
  • Reserved for patients who fail CPAP or oral appliance therapy. [85]

7. PHARMACOLOGICAL TREATMENTS

Currently, no drugs cure obstructive sleep apnea, but medications can be used adjunctively in certain cases or for specific symptoms:

Table no.01 Drug Dose

Drug

Indication / Effect

Typical Dose & Route

Notes / Frequency

Modafinil / Armodafinil

Daytime sleepiness in OSA patients on CPAP

Modafinil: 200 mg orally once daily in the morning; Armodafinil: 150–250 mg orally once daily

Adjunct only; does not treat underlying airway obstruction

Solriamfetol

Excessive daytime sleepiness

75–150 mg orally once daily in the morning

Used in CPAP-adherent patients; monitor BP and heart rate

Acetazolamide

Central sleep apnea, high- altitude sleep apnea

125–250 mg orally twice daily

Adjust based on renal function; diuretic effect

Oxygen therapy

Central sleepapnea or hypoxemia

Supplemental oxygen via nasal cannula

Typically nocturnal; dose titrated to maintain SpO? > 90%

Note: Pharmacologic treatments are adjunctive; the primary management for OSA remains CPAP, lifestyle modifications, and/or surgery.

  • First-line: CPAP and lifestyle changes.
  • Adjunctive: Oral appliances, positional therapy, or select pharmacologic agents for daytime sleepiness or central apnea.
  • Surgery: Reserved for anatomical obstruction or CPAP intolerance.

8. EVALUATION

    1. Clinical Assessment:
  • Improvement in daytime alertness, reduction of fatigue, and resolution of snoring are key subjective measures. [86-89]
  • Standardized tools such as the Epworth Sleepiness Scale (ESS) or the Functional Outcomes of Sleep Questionnaire (FOSQ) can quantify changes in daytime function.
  • Regular follow-up visits help evaluate tolerance, compliance, and side effects, particularly with continuous positive airway pressure (CPAP) and pharmacological agents. [90-93]

8.2 Objective Monitoring:

  • Polysomnography (PSG) or home sleep apnea testing (HSAT) is performed to reassess the apnea–hypopnea index (AHI), oxygen saturation, and sleep architecture after initiating therapy. [94]
  • Reduction of AHI to <5 events/hour or by ≥50% from baseline is generally considered a marker of adequate control. [95]
  • For CPAP users, machine-recorded data such as usage hours, leak rates, and residual AHI are valuable for monitoring adherence and therapeutic effectiveness. [96]

9. SLEEPAPENIA AND CARDIOVASCULAR DISORDERS

Why Sleep Apnea Affects the Heart

When breathing stops during sleep, oxygen levels drop. The body responds by activating stress systems, increasing heart rate and blood pressure. Repeated night after night, these reactions strain the cardiovascular system and can contribute to several heart conditions.

Cardiovascular Diseases Linked to Sleep Apnea

9.1 Hypertension (High Blood Pressure)

Sleep apnea triggers repeated surges of adrenaline-like hormones, which tighten blood vessels.[97] This causes:

  • Persistent high blood pressure
  • Reduced effectiveness of blood pressure medications
  • Treating sleep apnea (especially with CPAP) often improves blood pressure levels.

9.2. Coronary Artery Disease

Low oxygen levels and increased inflammation can damage the lining of blood vessels, encouraging plaque buildup.[102] This raises the risk of:

  • Heart attacks
  • Chest pain (angina)
  • Reduced blood flow to the heart muscle

9.3. Heart Failure

Sleep apnea forces the heart to work harder because oxygen levels fluctuate. Over time, this strain can contribute to:

  • Left-sided heart failure (difficulty pumping blood to the body)
  • Right-sided heart failure (caused by increased pressure in the lungs due to breathing problems)

9.4 Arrhythmias (Irregular Heartbeats)

Sleep apnea can disrupt the heart’s electrical system. Common rhythm issues include:

  • Atrial fibrillation
  • Premature heartbeats
  • Pauses in heart rhythm
  • Improving sleep apnea often reduces the frequency of these irregular rhythms.[98]

9.5 Stroke

Interrupted breathing reduces blood flow to the brain and increases clotting tendencies. People with untreated sleep apnea have a higher risk of:

  • Ischemic stroke (blocked blood vessels)
  • Worse recovery after a stroke

9.6 Diagnosis

To evaluate sleep apnea and its effects on the heart, healthcare providers may use:

  • Polysomnography (sleep study)
  • Heart monitoring (ECG, Holter monitor)

9.7 Blood pressure tracking

  • Echocardiogram if heart damage is suspected[99]

10. TREATMENT AND PREVENTION

10.1 Sleep Apnea Treatment

  • CPAP or BiPAP devices to keep the airway open Weight management
  • Position therapy (sleeping on the side) Avoiding alcohol and sedatives
  • Oral devices or surgery in selected cases

10.2. Cardiovascular Management

  • Blood pressure control
  • Medications for heart rhythm, cholesterol, or heart failure Exercise and a heart-healthy diet
  • Avoiding smoking and limiting caffeine

10.3 Combined Benefits

  • Treating sleep apnea often leads to:
  • Better blood pressure control Reduced arrhythmia episodes Improved heart function
  • Lower long-term cardiovascular risk [100]

10. CONCLUSION

Sleep apnea isn’t just about snoring or feeling groggy in the morning. It sneaks into daily life, messing with focus, draining your energy, and throwing your emotions off balance. If you ignore it, things can get serious— think high blood pressure, heart problems, messed-up metabolism, and a constant wave of exhaustion. That’s why catching it early and doing something about it really matters. When you understand what sleep apnea does, you’re more likely to step up and deal with it. These days, doctors have all sorts of ways to figure out what’s going on and how to help. There’s the classic CPAP machine, mouthpieces, ways to adjust how you sleep, and sometimes even surgery. Making a few lifestyle changes can help a lot too. All of this isn’t just about getting better sleep (though that’s huge); it’s about protecting your heart, your brain, and your immune system from the stress of never getting enough oxygen at night. But here’s the thing—support matters just as much as treatment. Whether it’s your doctor, a sleep specialist, or a partner nudging you to get checked out, having people in your corner makes a big difference. With the right help and a bit of persistence, people with sleep apnea can feel a real shift—more energy, a better mood, and just feeling like themselves again. In the end, tackling sleep apnea is about taking back control of your health. Good sleep isn’t some extra perk; it’s something everyone needs. Spot the signs, reach out for help, and stick with your treatment. That way, you can leave the fog of bad sleep behind and wake up to a life that actually feels good.

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  88. Jordan AS, McEvoy RD, Edwards BA. Pathogenesis of obstructive sleep apnea: focus on muscle responsiveness. J Appl Physiol. 2014;116(1):9–17.
  89. Carberry JC, Amatoury J, Eckert DJ. Personalized OSA therapy: new horizons. Sleep Med Rev. 2018;41:139–52.
  90. Kishore J, Anand S, Singh S. Obstructive sleep apnea: primary care approach. J Family Med Prim Care. 2020;9(10):5150–6.
  91. Lam B, Bradley TD. Pro–con debate: CPAP versus oral appliance therapy. J Clin Sleep Med. 2020;16(9):1647–8.
  92. Frohapture CR, Hopps I, Hwang D. Updates in OSA diagnosis and management. Med Clin North Am. 2022;106(1):143–59.
  93. White DP. The pathogenesis of obstructive sleep apnea—advances in the last 100 years. Am J Respir Cell Mol Biol. 2006;34(1):1–6.
  94. Randerath WJ, Bassetti CL, Bonsignore MR, et al. ERS statement: OSA management in adults. Eur Respir J. 2021;57:2003091.
  95. Sateia MJ. International classification of sleep disorders—overview. Chest. 2014;146(5):1387–94.
  96. Shamsuzzaman ASM, Gersh BJ, Somers VK. Cardiovascular consequences of OSA. J Am Coll Cardiol. 2003;41:1429–37.
  97. Redline S, Yenokyan G, Gottlieb DJ, et al. Obstructive sleep apnea and cardiovascular disease biomarkers. Sleep. 2014;37(4):725–34.
  98. Iber C, Ancoli-Israel S, Chesson AL Jr, Quan SF. The AASM manual for scoring sleep. Westchester (IL): American Academy of Sleep Medicine; 2007.
  99. Patil SP, Ayappa IA, Caples SM, et al. Treatment of adult obstructive sleep apnea: AASM guideline. J Clin Sleep Med. 2019;15(3):335–43.
  100. Zamarrón C, García Paz V, Riveiro A. Obstructive sleep apnea syndrome and systemic hypertension. Chest. 1999;115:1491–8.

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Harsh Vardhan
Corresponding author

Minerva College of Pharmacy, Indora Kangra, Himachal Pradesh

Harsh Vardhan, Obstructive Sleepapenia and its Systemic impact: From Disease Mechanism to Clinical Management, Int. J. of Pharm. Sci., 2025, Vol 3, Issue 12, 1433-1443. https://doi.org/10.5281/zenodo.17855189

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