DOCSLIB.ORG

Syncope in Hypoxemic Respiratory Arrest

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Syncope in Hypoxemic Respiratory Arrest Central Journal of Sleep Medicine & Disorders Case Report *Corresponding author Daniel A. Barone, Assistant Professor of Neurology, Weill Cornell Medical College, Center for Sleep Medicine, Syncope in Hypoxemic 425 East 61st 5thFloor, New York, NY, 10065, USA, Tel: 646-962-7378; Fax: 646-962-0455; Email: Respiratory Arrest Submitted: 06 January 2015 Daniel Barone1*, Lina Fine2, Nipun Bhandari3 and Ana C. Accepted: 02 March 2015 Krieger1 Published: 03 March 2015 Copyright 1Department of Neurology, Weill Cornell Medical College of Cornell University, USA 2Department of Neurology, Swedish Neuroscience Institute, USA © 2015 Barone et al. 3Keck School of Medicine, University of South California, USA OPEN ACCESS Abstract Keywords • Obstructive sleep apnea This is a case report of an 81 year-old female with severe obstructive sleep apnea • Hypoxemia and hypoxemia presenting with recurrent episodes of unexplained syncope. Treatment • Syncope with continuous positive airway pressure eliminated the syncopal episodes. ABBREVIATIONS on previous arterial blood gases. An overnight sleep study was performed. OSA: Obstructive Sleep Apnea; CPAP: Continuous Positive Airway Pressure; SDB: Sleep Disordered Breathing; EEG: Electroencephalography (Figure 1). Loud snoring with frequent obstructive apneas The detailed sleep study findings are demonstrated in CASE PRESENTATION (apnea-hypopnea index was 60 events/hour) and severe oxygen An 81 year-old female with a history of paroxysmal atrial desaturation to below 60% were documented shortly after sleep onset due to prolonged obstructive apneas, which lasted an for sleep evaluation due to recurrent episodes of apparent syncope fibrillation, hypertension, and hypercholesterolemia presented average of 30 seconds. Oxygen levels failed to recover to normal Positivelevels in-between Airway Pressure events as (CPAP) a result was of recurrent implemented. apneas. After After CPAP 23 over the preceding 18 months, unresolved despite an extensive minutes of sleep recording, emergent treatment with Continuous workup. The patient had no recall of these episodes, which most The titration was continued to 14 cmH episodes were described as a sudden loss of consciousness while initiation, oxygen saturation levels progressively increased. occurred at home, and were witnessed by family members. The respiratory events and snoring were2 mostly eliminated. No arrhythmias were detected. O. At this pressure level, sitting quietly or lying down, becoming unarousable for up to 3 The dramatic oxygen desaturation seen in this patient in minutes, often triggering a call to EMS. There were no specific association with severe obstructive sleep apnea (OSA) was triggers, no seizure activity or incontinence present. The patient the most likely etiology of her recurrent episodes of loss of would resume consciousness after the events, and described no consciousness. Impending respiratory arrest was witnessed whilepain, nausea,watching or television.other associated During symptoms.multiple hospital The last emergency episode was preceded by a loud snort after she apparently dozed off by the technicians during the night, associated with the severe and sustained oxygen desaturation shortly after sleep onset, andadmissions Holter duemonitoring to loss ofwere consciousness, non-revealing. extensive A pacemaker neurological was patient was mostly asleep based on electroencephalographic shown by the arrows in (Figure 1). During CPAP application, the implantedand cardiac due evaluations, to concerns includingregarding severalpotential electrocardiograms bradyarrhythmias despite the negative cardiac evaluation. A sleep evaluation was (EEG) monitoring. No abnormal EEG activity, including slowing requested in order to complete her work-up. Her sleep history or spikes suggestive of seizure activity were seen. This patient revealed long-term snoring. There were no reports of other sleep was sent home on CPAP. She is currently 86 years-old and has related problems. The history was limited by the fact that she was One recurrent episode of loss of consciousness occurred while been followed for 5 years with excellent CPAP compliance. widowed and slept alone despite sharing a home with her son. On temporarily off CPAP due to an upper airway infection, and in the pastDISCUSSION 2 years, no further episodes have occurred. physical exam, she presented as a thin and fragile elderly2 lady, with normal vital signs, body mass index of 25 kg/m , normal There has been a suggestion that hypoxemia in OSA may elicit andoro-pharyngeal no lower extremity exam, clearedema. chest Resting to auscultation, oxygen saturation regular during rate and rhythm, 2/6 systolic murmur at the left upper sternal border mpatible with a PaO cardiac vagal reflex and sympathetic activation in the peripheral wakefulness was 93%, co 2 of 75 mm Hg seen vasculature, and one report in the literature describes severe Cite this article: Barone D, Fine L, Bhandari N, Krieger AC (2015) Syncope in Hypoxemic Respiratory Arrest. J Sleep Med Disord 2(2): 1019. Barone et al. (2015) Email: Central Figure 1 and respiratory Compressed events sleepimprove study as apneashypnogram. turn into Shortly hypopneas after sleep which onset start (A), to resolve marked as dropsCPAP levelsin oxygen are increased. saturation (B) are seen, associated with multiple obstructive apneas (C). Increased heart rate variability is seen during these episodes (D). After CPAP initiation (E), oxygen saturation levels hypoxemia leading to cardiopulmonary arrest during a sleep with OSA. The parasympathetic hyper reactivity in these patients episodes in our patient were related to similar mechanisms. In study in a non-obese patient [1,2]. We believe that the syncopal may also be present during the daytime, detected by Valsalva or airwayMueller obstruction maneuvers [9,10].may lead Finally, to the atrial release stretch of atrial during natriuretic repeated predisposed individuals, the triggering of a vagal reflex leads to respiratory efforts equivalent to Mueller maneuvers during bradycardia, a drop in blood pressure, and loss of consciousness, and results in vasovagal syncope [3,4].In a report of 11 patients peptide, which can result in reductions in blood volume and a with sleep disordered breathing (SDB), including both OSA and reductionTreatment of blood of SDBpressure with [11]. CPAP has been demonstrated to upper airway resistance syndrome, and vasovagal syncope, resultingthe authors from hypothesized respiratory that efforts the inintermittent these patients hypoxia, may sleeplead of this treatment for improving daytime syncopal episodes fragmentation, and large variations of intra thoracic pressures improve the sympathovagal balance [12-14]. The effectiveness Situations of strong stimulation of the sympathetic system to chronic adaptations in the autonomic nervous system [5]. thisin our improvement patient, as wellpersists as ininto the the11 patientsday. Longer with followvasovagal up syncope described earlier [11] bolsters the hypothesis that may trigger a secondary vagal hyper reactivity, potentially elucidate the use of CPAP as a means of treating syncope in the longleading sinus to pauses recurrent and secondvasovagal degree episodes atrio-ventricular [5]. Furthermore, blocks in faceand randomizedof SDB. The casecontrolled here reported studies inhighlights the future the maynecessity further of parasympathetic/vagal hyperactivity during apneas may induce broadening the differential diagnosis of unexplained syncopal episodes and respiratory arrests to include life-threatening sleep some patients [6,7]. Apnea-related sympathetic hyperactivity increased incidence of high blood pressure in some patients related respiratory abnormalities. may persist into the daytime [8], partly accounting for the J Sleep Med Disord 2(2): 1019 (2015) 2/3 Barone et al. (2015) Email: Central REFERENCES 8. 1. Som Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural hyperresponsiveness and bradyarrhythmias during apnoea in mechanisms in obstructive sleep apnea. J Clin Invest. 1995; 96: 1897- ers VK, Dyken ME, Mark AL, Abboud FM. Parasympathetic 9. 1904. hypertension. Clin Auton Res. 1992; 2: 171-176. Hanly PJ, George CF, Millar TW, Kryger MH.Heart rate response to breath-hold, valsalva and Mueller maneuvers in obstructive sleep 2. Khoo SM, Mukherjee JJ, Phua J, Shi DX. Obstructive sleep apnea apnea. Chest. 1989; 95: 735-739. presenting as recurrent cardiopulmonary arrest. Sleep Breath. 2009; 13: 89-92. 10. Andreas S, Hajak G, von Breska B, Rüther E, Kreuzer H. Changes in heart rate during obstructive sleep apnoea. Eur Respir J. 1992; 5: 853- 3. Alboni P, Alboni M, Bertorelle G. The origin of vasovagal syncope: to 11. 857. protect the heart or to escape predation? Clin Auton Res. 2008; 18: Guilleminault C1, Faul JL, Stoohs R.Sleep-disordered breathing and 4. 170-178. human fear-circuitry and fear-induced fainting in healthy individuals- hypotension. Am J Respir Crit Care Med. 2001; 164: 1242-1247. Bracha HS, Bracha AS, Williams AE, Ralston TC, Matsukawa JM. The 12. lowersChrysostomakis vagal tone SI, Simantirakisin patients EN, with Schiza obstructive SE, Karalis sleep IK, Klapsinos apnoea- NC, Siafakas NM, et al. Continuous positive airway pressure therapy -the paleolithic-threat hypothesis. Clin Auton Res. 2005; 15: 238-241. 5. Puel V, Pepin JL, Gosse P. Sleep related breathing disorders and hypopnoea syndrome. Hellenic J Cardiol. 2006; 47:13-20. vasovagal syncope, a possible causal link? Int J Cardiol. 2013; 168: airway pressure
Load more

Recommended publications
  • Expiratory Positive Airway Pressure (EPAP) for Obstructive Sleep Apnea
    Subject: Expiratory Positive Airway Pressure (EPAP) for Obstructive Sleep Original Effective Date: Apnea 10/30/13 Policy Number: MCP-145 Revision Date(s): 11/8/2016, 12/10/19 Review Date: 12/16/15, 9/19/17, 7/10/18, 12/10/19, 12 9/20 MCPC Approval Date: 7/10/18, 12/10/19, 12/9/20 Contents DISCLAIMER ............................................................................................................................................................................. 1 Description of Procedure/Service/Pharmaceutical .................................................................................................................. 1 Position Statement ................................................................................................................................................................... 2 Limitations ............................................................................................................................................................................... 3 Summary of Medical Evidence................................................................................................................................................ 3 Coding Information: ................................................................................................................................................................ 7 Resource References ................................................................................................................................................................ 7 REVIEW/REVISION
    [Show full text]
  • Apnea and Control of Breathing Christa Matrone, M.D., M.Ed
    APNEA AND CONTROL OF BREATHING CHRISTA MATRONE, M.D., M.ED. DIOMEL DE LA CRUZ, M.D. OBJECTIVES ¢ Define Apnea ¢ Review Causes and Appropriate Evaluation of Apnea in Neonates ¢ Review the Pathophysiology of Breathing Control and Apnea of Prematurity ¢ Review Management Options for Apnea of Prematurity ¢ The Clinical Evidence for Caffeine ¢ The Role of Gastroesophageal Reflux DEFINITION OF APNEA ¢ Cessation of breathing for greater than 15 (or 20) seconds ¢ Or if accompanied by desaturations or bradycardia ¢ Differentiate from periodic breathing ¢ Regular cycles of respirations with intermittent pauses of >3 S ¢ Not associated with other physiologic derangements ¢ Benign and self-limiting TYPES OF APNEA CENTRAL ¢ Total cessation of inspiratory effort ¢ Absence of central respiratory drive OBSTRUCTIVE ¢ Breathing against an obstructed airway ¢ Chest wall motion without nasal airflow MIXED ¢ Obstructed respiratory effort after a central pause ¢ Accounts for majority of apnea in premature infants APNEA IS A SYMPTOM, NOT A DIAGNOSIS Martin RJ et al. Pathogenesis of apnea in preterm infants. J Pediatr. 1986; 109:733. APNEA IN THE NEONATE: DIFFERENTIAL Central Nervous System Respiratory • Intraventricular Hemorrhage • Airway Obstruction • Seizure • Inadequate Ventilation / Fatigue • Cerebral Infarct • Hypoxia Infection Gastrointestinal • Sepsis • Necrotizing Enterocolitis • Meningitis • Gastroesophageal Reflux Hematologic Drug Exposure • Anemia • Perinatal (Ex: Magnesium, Opioids) • Polycythemia • Postnatal (Ex: Sedatives, PGE) Cardiovascular Other • Patent Ductus Arteriosus • Temperature instability • Metabolic derangements APNEA IN THE NEONATE: EVALUATION ¢ Detailed History and Physical Examination ¢ Gestational age, post-natal age, and birth history ¢ Other new signs or symptoms ¢ Careful attention to neurologic, cardiorespiratory, and abdominal exam APNEA IN THE NEONATE: EVALUATION ¢ Laboratory Studies ¢ CBC/diff and CRP ¢ Cultures, consideration of LP ¢ Electrolytes including magnesium ¢ Blood gas and lactate ¢ Radiologic Studies ¢ Head ultrasound vs.
    [Show full text]
  • Asphyxia Neonatorum
    CLINICAL REVIEW Asphyxia Neonatorum Raul C. Banagale, MD, and Steven M. Donn, MD Ann Arbor, Michigan Various biochemical and structural changes affecting the newborn’s well­ being develop as a result of perinatal asphyxia. Central nervous system ab­ normalities are frequent complications with high mortality and morbidity. Cardiac compromise may lead to dysrhythmias and cardiogenic shock. Coagulopathy in the form of disseminated intravascular coagulation or mas­ sive pulmonary hemorrhage are potentially lethal complications. Necrotizing enterocolitis, acute renal failure, and endocrine problems affecting fluid elec­ trolyte balance are likely to occur. Even the adrenal glands and pancreas are vulnerable to perinatal oxygen deprivation. The best form of management appears to be anticipation, early identification, and prevention of potential obstetrical-neonatal problems. Every effort should be made to carry out ef­ fective resuscitation measures on the depressed infant at the time of delivery. erinatal asphyxia produces a wide diversity of in­ molecules brought into the alveoli inadequately com­ Pjury in the newborn. Severe birth asphyxia, evi­ pensate for the uptake by the blood, causing decreases denced by Apgar scores of three or less at one minute, in alveolar oxygen pressure (P02), arterial P02 (Pa02) develops not only in the preterm but also in the term and arterial oxygen saturation. Correspondingly, arte­ and post-term infant. The knowledge encompassing rial carbon dioxide pressure (PaC02) rises because the the causes, detection, diagnosis, and management of insufficient ventilation cannot expel the volume of the clinical entities resulting from perinatal oxygen carbon dioxide that is added to the alveoli by the pul­ deprivation has been further enriched by investigators monary capillary blood.
    [Show full text]
  • Sleep-Apnea-Protocol.Pdf
    Evidence-based Practice Center Systematic Review Protocol Project Title: Continuous Positive Airway Pressure Treatment for Obstructive Sleep Apnea in Medicare Eligible Patients I. Background Sleep apnea is a common disorder that affects people of all ages. It is characterized by periods of airflow cessation (apnea) or reduced airflow (hypopnea) during sleep. Sleep apnea may be caused by mechanical obstruction of the airways resulting in disturbed airflow patterns, by a central loss of respiratory drive, or a combination of the two (mixed). Obstructive sleep apnea- hypopnea syndrome, more commonly called obstructive sleep apnea (OSA), is the most common type of sleep apnea.1 Definition and severity of obstructive sleep apnea Sleep apnea is primarily diagnosed with sleep tests that measure sleep time (and often other sleep measures) and respiratory events. OSA is distinguished from central sleep apnea by the presence of respiratory effort during episodes of apnea and hypopnea (in contrast with central sleep apnea where respiratory effort is lacking). The severity of OSA is typically quantified by the sum of the number of apneas and hypopneas per hour of sleep, a quantity that has been termed the apnea-hypopnea index (AHI). AHI is often used as part of both diagnosis (and, thus, study inclusion criteria) and as a surrogate measure for health outcomes (also called an intermediate outcome) in studies. The American Academy of Sleep Medicine (AASM) publishes scoring manuals for AHI and other physiological events to characterize OSA. In the United States, AASM is the predominant accrediting institution for sleep laboratories. AASM first published its scoring manual in 1999 (known as the “Chicago” Criteria).2 They have amended their definitions of breathing events, sleep time, and how these are measured multiple times since their first set of criteria, with major revisions in 2007,3 and in 2012.4 Minor revisions have been made almost annually since (the current version is v2.6,5 released in 2020).
    [Show full text]
  • Sleep Apnea Sleep Apnea
    Health and Safety Guidelines 1 Sleep Apnea Sleep Apnea Normally while sleeping, air is moved at a regular rhythm through the throat and in and out the lungs. When someone has sleep apnea, air movement becomes decreased or stops altogether. Sleep apnea can affect long term health. Types of sleep apnea: 1. Obstructive sleep apnea (narrowing or closure of the throat during sleep) which is seen most commonly, and, 2. Central sleep apnea (the brain is causing a change in breathing control and rhythm) Obstructive sleep apnea (OSA) About 25% of all adults are at risk for sleep apnea of some degree. Men are more commonly affected than women. Other risk factors include: 1. Middle and older age 2. Being overweight 3. Having a small mouth and throat Down syndrome Because of soft tissue and skeletal alterations that lead to upper airway obstruction, people with Down syndrome have an increased risk of obstructive sleep apnea. Statistics show that obstructive sleep apnea occurs in at least 30 to 75% of people with Down syndrome, including those who are not obese. In over half of person’s with Down syndrome whose parents reported no sleep problems, sleep studies showed abnormal results. Sleep apnea causing lowered oxygen levels often contributes to mental impairment. How does obstructive sleep apnea occur? The throat is surrounded by muscles that are active controlling the airway during talking, swallowing and breathing. During sleep, these muscles are much less active. They can fall back into the throat, causing narrowing. In most people this doesn’t affect breathing. However in some the narrowing can cause snoring.
    [Show full text]
  • Potential Protective Mechanism of Arousal in Obstructive Sleep Apnea
    Editorial Potential protective mechanism of arousal in obstructive sleep apnea Naomi Deacon, Atul Malhotra Department of Medicine, Pulmonary, Critical Care and Sleep Medicine, University of California San Diego, La Jolla, California, USA Correspondence to: Naomi Deacon, PhD. 9300 Campus Point Drive #7381, La Jolla, CA 92037-7381, USA. Email: [email protected]. Submitted Jul 01, 2016. Accepted for publication Jul 02, 2016. doi: 10.21037/jtd.2016.07.43 View this article at: http://dx.doi.org/10.21037/jtd.2016.07.43 Obstructive sleep apnea (OSA) pathophysiology is thought increase the magnitude of post-occlusion hyperventilation to be due to the interaction of traits including airway (and consequently hypocapnia) due both to arousal associated anatomy and neuromuscular control which vary between sympathetic activation and the state dependent differences individuals. These traits include a low arousal threshold in eupneic CO2 and sensitivity. This theory is based on (wake easily from sleep), upper airway gain (how effectively the founding work by Iber and colleagues in 1986 (7) activation of upper airway dilator muscles improves who studied tracheostomized OSA patients following ventilation), loop gain (stability of the negative feedback experimental tracheal occlusion during stable NREM sleep. chemoreflex control system) and upper airway collapsibility They found that tracheal occlusion yielded arousal and (anatomical predisposition to passive airway collapse) (1). pharyngeal opening which resulted in hyperventilation and While deficits in these traits and how they interact varies hypocapnia, followed by a reduction in minute ventilation between individuals, generally mechanisms that increase and prolongation of expiratory time. The magnitude of activation of upper airway dilator muscles are considered to hypocapnia correlated with expiratory prolongation and help protect the airway from collapse.
    [Show full text]
  • Acute Respiratory Failure As the First Sign of Arnold-Chiari Malformation Associated with Syringomyelia
    Eur Respir J, 1995, 8, 661–663 Copyright ERS Journals Ltd 1995 DOI: 10.1183/09031936.95.08040661 European Respiratory Journal Printed in UK - all rights reserved ISSN 0903 - 1936 CASE REPORT Acute respiratory failure as the first sign of Arnold-Chiari malformation associated with syringomyelia D. Alvarez*, I. Requena**, M. Arias**, L. Valdés*, I. Pereiro+, R. De la Torre++ Acute respiratory failure as the first sign of Arnold-Chiari malformation associated with Services of *Pneumology, **Neurology, syringomyelia. D. Alvarez, I. Requena, M. Arias, L. Valdés, I. Pereiro, R. De la Torre. +Neuroimaging and ++Intensive Care, Hos- ERS Journals Ltd 1995. pital Provincial and Dept of Medicine of ABSTRACT: We report a rare case of acute respiratory failure in a previously the University of Santiago de Compostela, Santiago de Compostela, Spain. asymptomatic patient showing clinical signs of inferior cranial nerve palsy together with weakness and muscular atrophy of the upper limbs. Correspondence: D. Alvarez García, c) Magnetic resonance imaging revealed Arnold-Chiari malformation associated with Rosalía de Castro 57, 4º I., 15706 Santiago platybasia, basilar impression, syringomyelia and Klippel-Feil syndrome. Episodes de Compostela, Spain of apnoea required tracheostomy and recurred upon tentative closure of the tracheostome, but remitted upon decompression of the posterior fossa. Keywords: Adult respiratory distress, This case involved both obstructive mechanisms and dysfunction of the respiratory Arnold-Chiari malformation, sleep apnoea, centre. Patients with respiratory failure not explained by pulmonary pathology syringomyelia should be checked for underlying neurological disease. Received: October 29 1993 Eur Respir J., 1995, 8, 661–663. Accepted after revision September 13 1994 Arnold-Chiari malformation is a dysraphic congenital attempts at extubation were each followed by respiratory disorder, frequently associated with other malformations failure.
    [Show full text]
  • Obstructive Sleep Apnea in Adults? NORMAL AIRWAY OBSTRUCTED AIRWAY
    American Thoracic Society PATIENT EDUCATION | INFORMATION SERIES What Is Obstructive Sleep Apnea in Adults? NORMAL AIRWAY OBSTRUCTED AIRWAY Obstructive sleep apnea (OSA) is a common problem that affects a person’s breathing during sleep. A person with OSA has times during sleep in which air cannot flow normally into the lungs. The block in CPAP DEVICE airflow (obstruction) is usually caused by the collapse of the soft tissues in the back of the throat (upper airway) and tongue during sleep. Apnea means not breathing. In OSA, you may stop ■■ Gasping breathing for short periods of time. Even when you are or choking trying to breathe, there may be little or no airflow into sounds. the lungs. These pauses in airflow (obstructive apneas) ■■ Breathing pauses observed by someone watching can occur off and on during sleep, and cause you to you sleep. wake up from a sound sleep. Frequent apneas can cause ■■ Sudden or jerky body movements. many problems. With time, if not treated, serious health ■■ Restless tossing and turning. problems may develop. ■■ Frequent awakenings from sleep. OSA is more common in men, women after menopause CLIP AND COPY AND CLIP Common symptoms you may have while awake: and people who are over the age of 65. OSA can also ■■ Wake up feeling like you have not had enough sleep, occur in children. Also see ATS Patient Information Series even after sleeping many hours. fact sheet on OSA in Children. People who are at higher ■■ Morning headache. risk of developing sleep apnea include those with: ■■ Dry or sore throat in the morning from breathing ■■ enlarged tonsils and/or adenoids through your mouth during sleep.
    [Show full text]
  • Obstructive Sleep Apnea Causing Chest Pain and Cardiac Arrhythmias
    Journal of Cardiology & Cardiovascular Therapy ISSN 2474-7580 Case Report J Cardiol & Cardiovasc Ther Volume 1 Issue 3 - September 2016 Copyright © All rights are reserved by Irtaqa Ali Hasnain DOI: 10.19080/JOCCT.2016.01.555565 Obstructive Sleep Apnea Causing Chest Pain and Cardiac Arrhythmias Irtaqa Ali Hasnain1 and Mujtaba Ali Hasnain2 1Department of Emergency Medicine, Bahria Town Hospital, Lahore, Pakistan 2Department of Medicine, Saint Barnabas Medical Center, USA Submission: September 16, 2016; Published: September 28, 2016 *Corresponding author: Irtaqa Ali Hasnain, Bahria Town Hospital, 670 Gul Mohar Block, Sector C, Bahria Town, Lahore, Pakistan Introduction Discussion Chest pain is one of the most common complaints for patients Although most patients with obstructive sleep apnea (OSA) presenting to the hospital. It can be a manifestation of coronary present with typical features like snoring, day-time sleepiness, artery disease, acid peptic disease, pleuritis, or musculoskeletal fatigue, and restlessness but they can present with chest pain problems. Patients with obstructive sleep apnea may present or cardiac arrhythmias only. The prevalence of obstructive sleep with chest pain and heart block but lack typical features such as day-time sleepiness, poor concentration, fatigue, and apnea in the general population is 20 percent if defined as an restlessness. Obstructive sleep apnea can cause these problems apnea hypopnea index is the number of apneas and hypopneas apnea hypopnea index greater than five events per hour (the due to episodes of transient nocturnal hypoxia. per hour of sleep). The most important risk factors for obstructive sleep apnea are obesity, craniofacial abnormalities, and upper Patient report airway abnormalities.
    [Show full text]
  • Sleep Apnea Facts and Figures
    Sleep Apnea Facts and Figures What is sleep-disordered breathing (SDB)? Classification of sleep apnea SDB describes a number of breathing disorders Apnea–hypopnea index (AHI) that occur during sleep ■■ Number of apneas and/or hypopneas per hour of sleep (or study time) ■■ Obstructive sleep apnea (OSA) ■■ Reflects the severity of sleep apnea ■■ Central sleep apnea (CSA) AHI = 0–5 Normal range ■■ Nocturnal hypoventilation AHI = 5–15 Mild sleep apnea ■■ Cheyne–Stokes respiration (CSR) AHI = 15–30 Moderate sleep apnea AHI > 30 Severe sleep apnea What is obstructive sleep apnea (OSA)? ■■ A partial or complete collapse of the upper airway caused by Prevalence of sleep apnea relaxation of the muscles controlling the soft palate and tongue ■■ Approximately 42 million American adults have SDB1 ■■ Person experiences apneas, hypopneas and flow limitation ■■ 1 in 5 adults has mild OSA2 —■ Apnea: a cessation of airflow for ≥10 seconds ■■ 1 in 15 has moderate to severe OSA2 —■ Hypopnea: a decrease in airflow lasting ≥10 seconds ■■ 9% of middle-aged women and 25% of middle-aged men with a 30% oxygen reduction in airflow and with at least suffer from OSA3 a 4% oxygen desaturation from baseline ■■ Prevalence similar to asthma (20 million) and diabetes —■ Flow limitation: narrowing of the upper airway and an (23.6 million) of US population4 indication of an impending upper airway closure ■■ 75% of severe SDB cases remain undiagnosed5 Prevalence of Sleep Apnea in Comorbidities Drug-Resistant Hypertension 83% 6 Obesity 77% 7 Congestive Heart Failure 76% 8
    [Show full text]
  • Women & Sleep Apnea
    WOMEN & SLEEP APNEA Nearly 1 in 5 women have sleep apnea, a disorder that affects daytime functioning. But about 9 in 10 women with sleep apnea don't know they have it. Here's what you need to know: The signs of sleep apnea in women may not be the same Sleep apnea is treatable. It is important to start a conver- Treatment can improve your life. From your overall as those in men. For women, signs may be mistaken for sation with your healthcare provider to discuss whether well-being to cognition, mental, and physical health, depression or menopause. Or they may have no obvious you are at risk for sleep apnea or another sleep disorder. the benefits of treatment can be life-changing. symptoms at all. Why does it matter? Untreated sleep apnea can lead to: High blood pressure, diabetes, heart disease, and stroke Depression and other mood problems Missing out on the joys of life: fun, laughter, relationships, intimacy * Fatigue, daytime sleepiness, and accidents NIGHTTIME CLUES DAYTIME CLUES Problems with alertness, memory and learning Increased sensitivity to pain Frequent or loud snoring, gasping, or snorting sounds Feeling depressed, anxious, irritable, or impatient Overtreatment or mistreatment for Difficulty falling asleep, frequent awakenings Feeling tired, drained, or lacking energy other disorders Restless sleep, changes in dreaming Feeling sleepy or falling asleep at the wrong time or place Frequent bathroom visits at night Forgetfulness, foggy or fuzzy thinking, trouble with Nighttime heartburn focus and concentration *some of which could be observed by a bed partner or roommate Accident proneness even without these symptoms, you may still be at risk.
    [Show full text]
  • Study of Survivors of Acute Respiratory Distress Syndrome and Systematic Review of Literature
    323 Research Article Sleep after critical illness: Study of survivors of acute respiratory distress syndrome and systematic review of literature Sahajal Dhooria, Inderpaul Singh Sehgal, Anshu Kumar Agrawal1, Ritesh Agarwal, Ashutosh Nath Aggarwal, Digambar Behera Background and Aims: This study aims to evaluate the sleep quality, architecture, Access this article online sleep‑related quality of life, and sleep‑disordered breathing (SDB) in acute respiratory Website: www.ijccm.org distress syndrome (ARDS) survivors early after discharge. Materials and Methods: In DOI: 10.4103/0972-5229.183908 this prospective, observational study, consecutive patients with ARDS discharged from Quick Response Code: Abstract the Intensive Care Unit (ICU) underwent evaluation with Epworth sleepiness scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Functional Outcomes of Sleep Questionnaire (FOSQ), and overnight polysomnography. Patients having one or more of the following characteristics were classified as having abnormal sleep: ESS >10, PSQI >5, FOSQ <17.9, apnea–hypopnea index (AHI) ≥5, or AHI during rapid eye movement (REM) sleep ≥5. Results: Twenty patients (median interquartile range [IQR] age of 24 [22–28] years, 11 [55%] females) were included in the study. Acute febrile illness of unknown etiology with multi‑organ dysfunction syndrome was the most common underlying etiology for ARDS. The median (IQR) PaO2/FiO2 ratio and APACHE II scores on admission were 176 (151–191.5) and 14 (14–16), respectively. The median (IQR) duration of stay in the ICU was 10 days (7.3–19.5). The overall sleep efficiency (median [IQR], 54% [32.3–65.4%]) was poor. None of the patients had ESS >10, seven (35%) had global PSQI >5 and one had FOSQ <17.9.
    [Show full text]