alexa

GET THE APP

Dersleri yüzünden oldukça stresli bir ruh haline sikiş hikayeleri bürünüp özel matematik dersinden önce rahatlayabilmek için amatör pornolar kendisini yatak odasına kapatan genç adam telefonundan porno resimleri açtığı porno filmini keyifle seyir ederek yatağını mobil porno okşar ruh dinlendirici olduğunu iddia ettikleri özel sex resim bir masaj salonunda çalışan genç masör hem sağlık hem de huzur sikiş için gelip masaj yaptıracak olan kadını gördüğünde porn nutku tutulur tüm gün boyu seksi lezbiyenleri sikiş dikizleyerek onları en savunmasız anlarında fotoğraflayan azılı erkek lavaboya geçerek fotoğraflara bakıp koca yarağını keyifle okşamaya başlar
Obstructive Sleep Apnea Syndrome and its Comorbid Medical Conditions
ISSN: 2161-119X
Otolaryngology: Open Access

Like us on:

Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on Medical, Pharma, Engineering, Science, Technology and Business
  • Editorial   
  • Otolaryngol 2012, Vol 2(1): e103
  • DOI: 10.4172/2161-119X.1000e103

Obstructive Sleep Apnea Syndrome and its Comorbid Medical Conditions

Baharudin Abdullah*
Department of Otorhinolaryngology - Head and Neck Surgery, School of Medical Sciences, Universiti Sains Malaysia, Kelantan, Malaysia
*Corresponding Author: Dr. Baharudin Abdullah, Associate Professor, Consultant ORL-Head and Neck Surgeon, Department of Otorhinolaryngology - Head and Neck Surgery, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia, Tel: +6097676416, Fax: +6097676424, Email: [email protected]

Received: 14-Mar-2012 / Accepted Date: 16-Mar-2012 / Published Date: 21-Mar-2012 DOI: 10.4172/2161-119X.1000e103 /

Obstructive sleep apnea syndrome (OSAS) is a common global health disorder which carries multiple medical and social impacts. OSAS is characterized by periodic complete or partial upper airway obstruction during sleep, causing intermittent cessations of breathing (apnea) or reductions in airflow (hypopnea) despite ongoing respiratory effort. It is associated with sleep disorder symptoms including loud snoring, disturbed and frequent wake-up during sleep and excessive daytime sleepiness. Apnea is a Greek word means “without breath”.

The disorder is associated with hypertension [1], cardiovascular diseases [2], decreased libido [3] and emotional problems [4]. Unsurprisingly, this disorder has been linked to heart failure [5], myocardial infarction [6], chronic obstructive pulmonary disease (COPD) [7], stroke [8] and motor vehicle crashes [9,10].

Systemic hypertension is very common among the OSAS patients. It constitutes about 56% of OSAS patient having hypertension [11]. Cyclic intermittent hypoxia as experienced at night by OSAS patient leads to sympathetic activation [12]. This sustained sympathoexcitation through augmentation of peripheral chemoreflex sensitivity and stimulation on central sympathetic regulator causing increases of heart rate, cardiac output, peripheral vascular resistance and systemic arterial pressure thus increases the blood pressure [13,14].

Lavie et al. [15] monitored 24 hour blood pressure (BP) on 38 OSAS patients and their results revealed that diastolic, systolic and mean BP were significantly related to the severity of sleep apnea syndrome. Few hemodynamic studies on OSAS patients showed the systemic arterial pressure increases and remains at higher level during apnea episode compared to wakefulness [16-18]. The blood pressure can rise by 25% of the baseline during apnea episode and systolic and diastolic pressure can exceed 200 mmHg and 120 mmHg respectively [17]. Studies by Lies et al. [19], Sanner et al. [20] and Tun et al. [21] showed significant improvement in blood pressure in OSAS patient treated by CPAP which proves the causal relationship between systemic hypertension and OSAS.

The clinical spectrum of OSAS related cardiovascular disease comprises of systemic arterial hypertension with prevalence of 40- 60%, pulmonary hypertension, 20-30%; coronary artery disease, 20- 30%; congestive heart failure, 5-10%; and arrhythmia, 50-60% [22]. Sajkov et al. [23] in a pulmonary hemodynamic study on 32 patients with OSA found that pulmonary hypertension is associated with small airways closure during tidal breathing and increased pulmonary press or responses to hypoxia and during increased pulmonary blood flow. These changes are consistent with remodeling of the pulmonary vascular bed in OSAS patients with pulmonary hypertension and unrelated to severity of sleep-disordered breathing.

OSAS is commonly found in patients with coronary heart disease and these patients must be classified as a high risk group because of apnea-associated silent myocardial ischemia and electric instability of the myocardium [24]. The risk of myocardial infarction is increased 20-fold in untreated OSA [25].

The occurrence of arrhythmia in patients with OSAS is closely related to the apnea and hyperventilation events and depends on the sympathovagal balance [24]. Sinus arrhythmia occurs with decreased heart rate during apnea and increased heart rate when breathing resumes. Marked sinus bradycardia is due to hypoxic induced vagal activity. Severe oxygen desaturation can lead to conduction defect such as premature ventricular contraction, second degree heart block and ventricular tachyarrhythmia [26].

The association between OSAS and stroke are much debated, but increasing evidence demonstrates that the OSAS is an independent risk factor for ischemic stroke especially in young patient [27]. Many studies have showed 70 to 95% of acute stroke patients were found to have OSAS [28,29].

Multiple medical conditions are linked to the mechanisms of stroke in OSAS such as arterial hypertension, cardiac arrhythmia, increased atherogenesis, coagulation disorders, and cerebral haemodynamic changes [28]. Presence of OSAS in stroke patients could lead to a poor outcome and increased long-term stroke mortality. Therefore, OSAS should be systematically screened at the moment it is clinically suspected in patients with acute stroke.

Studies worldwide revealed the presence of OSA has been found in 5 to 63% of patients with epilepsy. Patients with neurological disorders seem to have a greater prevalence for sleep disturbance than normal subjects and epilepsy also seemed to have similar preponderance. Miller et al. [30] showed that more than two thirds of patients with epilepsy seen at a university center had complaints regarding sleep. Polysomnographic investigation by Malow et al. [31] showed that nearly one third of patients with medically refractory epilepsy had a respiratory disturbance index of more than 5. Vaughn et al. [32] studied a cohort of 25 patients with intractable epilepsy and found 36% had a respiratory disturbance index of more than 10. Frequency rates were higher in patients with refractory epilepsy or epilepsy patients referred to a sleep center [33,34] and lower [35,36] in unselected populations.

References

  1. Feng J, Chen BY (2009) Prevalence and incidence of hypertension in obstructive sleep apnea patients and the relationship between obstructive sleep apnea and its confounders. Chin Med J (Engl) 122: 1464-1468.
  2. Jennum P, Hein HO, Suadicani P, Gyntelberg F (1992) Cardiovascular risk factors in snorers. A cross-sectional study of 3,323 men aged 54 to 74 years: the Copenhagen Male Study. Chest 102: 1371-1376.
  3. Koseoglu N, Koseoglu H, Itil O, Oztura I, Baklan B, et al. (2007) Sexual function status in women with obstructive sleep apnea syndrome. J Sex Med 4: 1352-1357.
  4. Kawahara S, Akashiba T, Akahoshi T, Horie T (2005) Nasal CPAP improves the quality of life and lessens the depressive symptoms in patients with obstructive sleep apnea syndrome. Intern Med 44: 422-427.
  5. Hung J, Whitford EG, Parsons RW, Hillman DR (1990) Association of sleep apnoea with myocardial infarction in men. Lancet 336: 261-264.
  6. Collop N (2010) Sleep and sleep disorders in chronic obstructive pulmonary disease. Respiration 80: 78-86.
  7. Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, et al. (2005) Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med 353: 2034-2041.
  8. Mulgrew AT, Nasvadi G, Butt A, Cheema R, Fox N, et al. (2008) Risk and severity of motor vehicle crashes in patients with obstructive sleep apnoea/hypopnoea. Thorax63: 536-541.
  9. de Pinho RS, da Silva-Junior FP, Bastos JP, Maia WS, de Mello MT, et al. (2006) Hypersomnolence and accidents in truck drivers: A cross-sectional study. Chronobiol Int 23: 963-971.
  10. Benaim P, Foucher A, Leroy M, Hagenmuller MP, Benasouli R, et al. (1992) Obstructive sleep apnea syndrome in adults and cardiovascular risk. Ann Cardiol Angeiol (Paris) 41: 531-539.
  11. Weiss JW, Liu MD, Huang J (2007) Physiological basis for a causal relationship of obstructive sleep apnoea to hypertension. Exp Physiol92: 21-26.
  12. Fletcher EC (2003) Sympathetic over activity in the etiology of hypertension of obstructive sleep apnea. Sleep 26: 15-19.
  13. Smith ML, Pacchia CF (2007) Sleep apnoea and hypertension: role of chemoreflexes in humans. Exp Physiol 92: 45-50.
  14. Lavie P, Yoffe N, Berger I, Peled R (1993) The relationship between the severity of sleep apnea syndrome and 24-h blood pressure values in patients with obstructive sleep apnea. Chest 103: 717-721.
  15. Coccagna G, di Donato G, Verucchi P, Cirignotta F, Mantovani M, et al. (1976) Hypersomnia with periodic apneas in acquired micrognathia. A bird-like face syndrome. Arch Neurol 33: 769-776.
  16. Tilkian AG, Guilleminault C, Schroeder JS, Lehrman KL, Simmons FB, et al. (1976) Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep. Ann Intern Med 85: 714-719.
  17. Guilleminault C, Kurland G, Winkle R, Miles LE (1981) Severe kyphoscoliosis, breathing, and sleep: the "Quasimodo" syndrome during sleep. Chest 79: 626-630.
  18. Lies A, Nabe B, Pankow W, Kohl FV, Lohmann FW (1996) Hypertension and obstructive sleep apnea. Ambulatory blood pressure monitoring before and with nCPAP-therapy. Z Kardiol 85: 140-142.
  19. Sanner BM, Tepel M, Markmann A, Zidek W (2002) Effect of continuous positive airway pressure therapy on 24-hour blood pressure in patients with obstructive sleep apnea syndrome. Am J Hypertens15: 251-257.
  20. Tun Y, Hida W, Okabe S, Ogawa H, Kikuchi Y, et al. (2003) Can nasal continuous positive airway pressure decrease clinic blood pressure in patients with obstructive sleep apnea? Tohoku J Exp Med 201: 181-190.
  21. Schulz R, Grebe M, Eisele HJ, Mayer K, Weissmann N, et al. (2006) Obstructive sleep apnea-related cardiovascular disease. Med Klin (Munich) 101: 321-327.
  22. Sajkov D, Wang T, Saunders NA, Bune AJ, Neill AM, et al. (1999) Daytime pulmonary hemodynamics in patients with obstructive sleep apnea without lung disease. Am J Respir Crit Care Med 159: 1518-1526.
  23. Schafer H, Koehler U, Hasper E, Ewig S, Luderitz B (1995) Sleep apnea and cardiovascular risk. Z Kardiol 84: 871-884.
  24. Grigg-Damberger M (2006) Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack. J Clin Neurophysiol 23: 21-38.
  25. Shepard JW Jr (1985) Gas exchange and hemodynamics during sleep. Med Clin North Am 69: 1243-1264.
  26. Poza JJ, Martinez A, Emparanza JI, Lopez de Munain A, Marti Masso JF (2000) Sleep apnea syndrome and cerebral infarction. Neurologia 15: 3-7.
  27. Neau JP, Paquereau J, Meurice JC, Chavagnat JJ, Gil R (2002) Stroke and sleep apnoea: cause or consequence? Sleep Med Rev 6: 457-469.
  28. Casado-Naranjo I, Ramírez-Moreno JM (2005) Prevalence of breathing disorders during sleep in patients with cerebrovascular disease. Rev Neurol 41: S7-S12.
  29. Miller MT, Vaughn BV, Messenheimer JA, Finkel AG, D’Cruz OF (1996) Subjective sleep quality in patients with epilepsy. Epilepsia 36: S43.
  30. Malow BA, Levy K, Maturen K, Bowes R (2000) Obstructive sleep apnea is common in medically refractory epilepsy patients. Neurology 55: 1002-1007.
  31. Vaughn BV, D'Cruz OF, Beach R, Messenheimer JA (1996) Improvement of epileptic seizure control with treatment of obstructive sleep apnoea. Seizure 5: 73-78.
  32. Beran RG, Plunkett MJ, Holland GJ (1999) Interface of epilepsy and sleep disorders. Seizure 8: 97-102.
  33. Weatherwax KJ, Lin X, Marzec ML, Malow BA (2003) Obstructive sleep apnea in epilepsy patients: the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ) is a useful screening instrument for obstructive sleep apnea in a disease-specific population. Sleep Med 4: 517-521.
  34. Manni R, Terzaghi M, Arbasino C, Sartori I, Galimberti CA, et al. (2003) Obstructive sleep apnea in a clinical series of adult epilepsy patients: frequency and features of the comorbidity. Epilepsia 44: 836-840.
  35. Malow BA, Weatherwax KJ, Chervin RD, Hoban TF, Marzec ML, et al. (2003) Identification and treatment of obstructive sleep apnea in adults and children with epilepsy: a prospective pilot study. Sleep Med 4: 509-515.

Citation: Abdullah B (2012) Obstructive Sleep Apnea Syndrome and its Comorbid Medical Conditions. Otolaryngol 2:e103. Doi: 10.4172/2161-119X.1000e103

Copyright: © 2012 Abdullah B. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Select your language of interest to view the total content in your interested language

Post Your Comment Citation
Share This Article
Article Usage
  • Total views: 13085
  • [From(publication date): 3-2012 - Dec 09, 2022]
  • Breakdown by view type
  • HTML page views: 8869
  • PDF downloads: 4216
Share This Article
Top