Caring for the Patient With Obstructive Sleep Apnea: Implications for Health Care Providers in Postanesthesia Care

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  • CONTINUING EDUCATIONCaring for the Patient With ObstructiveSleep Apnea: Implications for Health Care

    Providers in Postanesthesia CarePamela D. Diffee, DNP, CRNA, Michelle M. Beach, DNP, CRNA,

    Norma G. Cuellar, DSN, RN, FAAN

    Obstructive sleepapnea (OSA) is a sleep disorderaffecting18millionAmer-Pamela D. Diffe

    Capstone College o

    caloosa, AL; Miche

    dent at the Capsto

    Alabama, Tuscalo

    FAAN, is a Professo

    ing, The University

    Conflict of intere

    Address correspo

    of Alabama, Capst

    loosa, AL 35487; e

    2012 by Ame1089-9472/$36.

    Journal of PeriAnesthicans. The prevalence of OSA is increasing due to an epidemic rise in obe-

    sity, which is amajor contributing factor. The primary treatment forOSA is

    continuous positive airway pressure, designed to maintain a patent air-

    way for unobstructed breathing. OSA patients may experience postopera-

    tive hypoventilation due to residual anesthetic, analgesic requirements,

    and other comorbidities. Postoperative health care providers must be pre-

    pared to assess for hypoventilation and intervene using evidence-based in-

    terventions to improve outcomes. It is incumbent that the PACU nurse be

    aware of and implement evidence-based clinical guidelines for patients

    with OSA. Therefore, the purpose of this manuscript is to (1) describe the

    physiology, comorbidities, diagnosis, and treatment of OSA; (2) identify

    the effects ofanesthesia in personswithOSA; (3) discuss clinical guidelines;

    and (4) describe implications for care in an effort to improve health out-

    comes in persons with OSA during the perianesthesia period.

    Keywords: obstructive sleep apnea, postoperative complications, contin-uous positive airway pressure, anesthesia, continuing education.

    2012 by American Society of PeriAnesthesia NursesObjectivesOn completion of this activity, thelearner will be able to: (1) Describe the physiology,

    comorbidities, diagnosis, and treatment of OSA,

    (2) Identify the effects of anesthesia in personswith OSA, and (3) Discuss implications for care

    across the perianesthesia setting.e, DNP, CRNA, is a doctoral student at the

    f Nursing, The University of Alabama, Tus-

    lle M. Beach, DNP, CRNA, is a doctoral stu-

    ne College of Nursing, The University of

    osa, AL; and Norma G. Cuellar, DSN, RN,

    r of Nursing at Capstone College of Nurs-

    of Alabama, Tuscaloosa, AL.

    st: None to report.

    ndence to Pamela D. Diffee, The University

    one College of Nursing, Box 870358, Tusca-

    -mail address:

    rican Society of PeriAnesthesia Nurses



    esia Nursing, Vol 27, No 5 (October), 2012: pp 329-340OBSTRUCTIVE SLEEP APNEA (OSA), one of themost common sleep disorders, is characterized by

    airway obstruction with periods of apnea. It affects

    18 million Americans1 and up to 64% of adults invarying degrees. Men are twice as likely as women

    to be diagnosed with OSA,2,3 with middle-aged

    obese males being the most susceptible.3 There

    has been an eightfold increase in the occurrence

    ofOSA, likely associatedwith the increase in obesity

    in the last 10 years.4 The incidence appears to in-

    crease with age, although it is reported by some to

    plateau after the age of 65 years.3,5-8

    In the general population, studies estimate that

    nearly 80% of men and 95% of women with

    moderate-to-severe OSA are undiagnosed.1,7,9-15

    Surgical candidates have an even higher inci-

    dence of OSA when compared with the general

    population.16 This is true for all surgical specialties,329

    Delta:1_given nameDelta:1_given nameDelta:1_surnameDelta:1_given nameDelta:1_given nameDelta:1_surnamemailto:diffdawglet@cox.net

  • 330 DIFFEE, BEACH, AND CUELLARbut the occurrence varies with the specialty; for

    example, more than 70% of bariatric surgical can-

    didates present with OSA.17-19 Postmenopausal

    women have a higher probability of having OSA

    than their premenopausal contemporaries,5 and50% of nursing home residents presenting for sur-

    gery exhibit symptoms of the disorder.8 Patients

    with OSA have an increased risk of complications

    due to comorbidities associated with OSA.20

    In 2006, the American Society of Anesthesiologists

    (ASA) formed a task force with the aim of examin-

    ing the perioperative management of patients withOSA. This task force developed a practice guide-

    line .to improve the perioperative care and re-duce the risk of adverse outcomes in patients

    with OSAwho receive sedation, analgesia, or anes-

    thesia for diagnostic or therapeutic procedures un-

    der the care of an anesthesiologist.21 As the effects

    of administered anesthetics can extend well past

    the period when a patient is directly under thecare of an anesthesiologist, these guidelines have

    application in several health care settings.

    Anesthesia is increasingly beingperformedoutsideof

    traditional operative settings in departments such as

    heart catheterization and electrophysiology laborato-

    ries, radiology and endoscopy suites, emergency

    rooms, and brachytherapy sites. Procedures per-formed in these areas often require deep sedation,

    with the patient recovered in the same area by the

    procedural nursing staff. As these areas are often far

    fromthecoreof surgical activity, additional expert air-

    waymanagement personnelmay not be immediately

    available. Perianesthesia nurses must be aware of the

    treatment of postanesthesia patients with OSA. Care

    providers inpostanesthesia areasmay lack awarenessof the implications of OSA for perioperative out-

    comes. Therefore, the purpose of this manuscript is

    to (1) describe the physiology, comorbidities, diagno-

    sis, and treatment of OSA; (2) identify the effects of

    anesthesia in persons with OSA; (3) discuss clinical

    guidelines; and (4) describe implications for care in

    the perianesthesia period.

    Obstructive Sleep Apnea

    One of the first descriptions of OSA was from an

    1837 Charles Dickens novel and was referred to

    as Pickwickian syndrome, in which a characterexhibited the triad features of OSA: somnolence,

    snoring, and obesity.22 The earliest written articlefound to medically describe these characteristics

    was published in 1956 and coined the term ob-

    structive sleep apnea.23 Other than Pickwickian

    syndrome, the disorder has also been referred to

    as upper airway apnea, but should not be confusedwith central sleep apnea, which is associated with

    central nervous system dysfunction of respiratory


    Physiology of OSA

    The physiology underlying OSA typically involves

    the upper airway, or pharynx. Normal activation ofpharyngealmuscle tone inanalert individual isoften

    reduced during sleep cycles, when turbulent air-

    flow can result in snoring.1 With severe reductions

    of pharyngeal tone, the negative force of inspiration

    is not sufficient to maintain patency of the pharyn-

    geal lumen, and breathing temporarily stops, de-

    spite persistent ventilatory effort.1 This respiratory

    cessation leads tohypoxic and hypercarbic derange-ments critical enough to arouse the sleeper for

    a brief period of air exchange.1 As the sleeper then

    settles back into attempted rest patterns, the cycle

    repeats, oftenhundredsof timesper night.1 Because

    the affected individual may never achieve deep

    rhythmic sleep, thehallmark symptomofOSA isday-

    time somnolence.25Understandably, other reported

    symptoms include frequent nocturnal awakeningsand morning headaches.4

    During an OSA event, soft tissue of the nose and

    pharynx collapses.26 As the pharynx is a multipur-

    pose organ, it is modulated by neural and chemical

    controls responsible for changing the size and stiff-

    ness, depending on its purpose.26 This is accom-

    plished by a change in the degree of muscularcontractionof thepharynx and airway. For example,

    while eating, the contractions are used to propel

    food into the esophagus for eventual digestion,

    while voice tone can be affected by pharyngeal

    size and stiffness during speech.26 For adequate res-

    piration tooccur, a rigid andpatentpharynxmustbe

    maintained. With inspiration of large tidal volumes,

    such as those seenduring sleep, the trachea ispulledcaudally by pharyngeal musculature, and airway pa-

    tencydependson themechanical act of breathing.26

    With OSA, pharyngeal patency is diminished, as

    thosewith the disorder have a structurally narrower

    pharyngeal lumen and, consequently, are more

    prone to collapse when these muscles are de-

    pressed during sleep or under the influence of

  • CARING FOR PERSONS WITH OSA 331anesthesia.26When these forces areweightedby the

    addition of excess soft tissue surrounding the phar-

    ynx and then compounded by the smaller tidal vol-

    umes frequently seen in obese individuals, the

    ability of the airway to resist collapsibility de-creases.26 During an OSA episode, apnea is abated

    only when an increase in longitudinal tension of

    the pharynx overcomes its potential for collapse.26

    Comorbidities of OSA

    OSA does not exist in isolation of other systemic

    comorbidities, particularly in those who are undi-agnosed or individuals noncompliant with its

    recommended treatments. Table 1 lists major sys-

    tems that could be targets of OSA comorbidities

    with their attendant conditions and prevalence.27

    Because OSA is heavily linked with hypertension,Table 1. Comorbidities Associated WithObstructive Sleep Apnea

    Category Condition Prevalence (%)

    Cardiac Treatment-resistant



    Congestive heart



    Ischemic heart



    Atrial fibrillation 49

    Dysrhythmias 58

    Respiratory Asthma 18




    Neurologic First-ever stroke 71-90

    Metabolic Type II diabetes



    Metabolic syndrome 50

    Hypothyroidism 45

    Morbid obesity 50-90

    Surgical Bariatric surgery 71

    Intracranial tumor



    Epilepsy surgery 33

    Others Gastroesophageal

    reflux disease


    Nocturia 48

    Alcoholism 17

    Primary open-angle



    Head and neck cancer 76

    Reproduced with permission from Seet and Chung.27

    Copyright 2010 Elsevier.all related associations with cardiovascular disease

    may be present. A noncompliant left ventricle with

    congestive heart failure can occur.5,9,10,13,14,28-33

    Of significance is that 40% to 50% of patients with

    heart failure also have OSA.1 The most commonarrhythmias associated with OSA are vagal brady-

    cardia and atrial-ventricular block as well as atrial

    fibrillation.1,5,8,28,29 Higher incidences of pulmo-

    nary hypertension, right ventricular hypertrophy,

    cor pulmonale and polycythemia occur when

    compared with those without OSA. In extreme

    cases, cardiomyopathy may occur, resembling

    that seen with pheochromocytoma or chroniccocaine use.34 When coupled with arrhythmias

    and myocardial infarction, which frequently occur

    during sleep, thismayexplain the associationswith

    sudden death seen in this population.4,29

    In untreated OSA, the episodic fluctuations of hy-

    poxemia and hypercarbia produce a physiologic

    stress response in the individual, which ultimatelycascades into systemic derangements. Vascular

    inflammation and atherosclerosis have been linked

    to the stresses induced by the hypoxia-reoxy-

    genation episodes of OSA.1,5,7,10,30 The resulting

    increase in catecholamines activates the renin-

    angiotensin-aldosterone axis, leading to sodium re-

    tention and further increases in vasoconstriction

    with the possibility of renal failure.1,2,7,32,34

    Other affected organs include the cerebrovas-

    cular, endocrine, gastrointestinal, and pulmonary

    systems. Increased intracranial pressure can be

    present, and may be linked to stroke, frequent

    impaired cognition, and depression.6,8,13,14,25,31,

    33,35-37 Metabolic irregularities have been connec-

    ted to OSA, with higher rates of diabetes mellitusand hormone suppression demonstrated.1,5,15,19,

    27,32,36 These irregularities have also been

    determined to have a strong association with

    stroke.38 The increase in intrathoracic pressures

    necessary to overcome an apnea episodemaybe re-

    sponsible for the common symptoms of gastro-

    esophageal reflux.7,14,25,28 This can culminate in

    asthma and chronic obstructive pulmonarydisease (COPD) from passive aspiration of acidic

    stomach contents during sleep.27,34,35

    Diagnosis of OSA

    In undiagnosed individuals, abnormalities of the

    head, face, or mouth such as those seen in patients

  • 332 DIFFEE, BEACH, AND CUELLARwith Down syndrome, muscular dystrophy, or cra-

    niosyntosis may be used as clues for the possible

    presence of OSA.21 Also, those complaining of

    chronic nasal stuffiness or possessing tonsil hyper-

    trophymay be candidates for anOSA evaluation.9,21

    OSA severity appears to positively correlate not only

    with obesity, but also with neck circumference.21 A

    body mass index higher than 35 kg/m2 coupled

    with a neck circumference greater than 40 cm

    may serve as a marker for the existence of OSA.21

    Withmale gender and agemore than 50 years added

    to the list of variables, studies have implicated

    a greater than 90% likelihood for patients havingmoderate-to-severe OSA.16 The Mallampati classi-

    fication can be used as a visual aid to determine

    a relationship between the size of the tongue and

    pharyngeal structures, including visualization of

    soft palate, fauces, uvula, and anterior/posterior


    The diagnosis of OSA begins with a patient screen-ing. The interviewer begins with questions di-

    rected toward symptoms such as snoring and

    daytime somnolence.2 The interview should then

    progress toward physical evaluation for obesity,

    chin recession, and neck circumference, as well

    as determination for the existence of comorbid-

    ities such as hypertension.2 If the screening reveals

    positive results for the likelihood of OSA, a morecomprehensive sleep history and physical exami-

    nation should be performed, with consideration

    for a sleep study, or polysomnography (PSG).2

    OSA is clinically diagnosedbyPSG.2,4,17 Patients are

    monitored during sleep and physiologic signals are

    measured. These signals are chin electromyogram,

    electroencephalogram, electrooculogram, airflowoxygen saturation, respiratory effort, and electro-

    cardiogram.17 A PSG technologist monitors for

    technical adequacy, patient compliance in com-

    pleting the study, and relevant patient behaviors.17

    The frequency of obstructions is reported as an ap-

    nea/hypopnea index.17 Confirmation of an OSA di-

    agnosis is made if the number of obstructive events

    on PSG is greater than 15 events/hour or greaterthan 5 events/hour in a patient complaining of

    any of the following: unintentional sleep during

    wakefulness; daytime sleepiness; unrefreshing

    sleep; fatigue; insomnia,waking up breath holding,

    choking, or gasping; or if the bed partner describes

    breath holding or loud snoring during the patients

    sleep. Severity is scored as mild for events $5 and,15, moderate for events $15 and #30, and se-vere for events.30/hour.2,25

    Treatment of OSA

    OSA is a complex disorder with wide-ranging treat-

    ment recommendations. Conservative approaches

    include lifestyle modifications such as weight loss

    for those who are obese, cessation of smoking, es-

    trogen replacement for postmenopausal women,

    and a decrease in alcohol consumption.5,14,40

    Supportive treatment options incl...


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