Show Summary Details
Page of

Acute and Emergent Pulmonary Events During Sleep 

Acute and Emergent Pulmonary Events During Sleep
Chapter:
Acute and Emergent Pulmonary Events During Sleep
Author(s):

Chadi Bou Serhal

, Roobal Sekhon

, and Reena Mehra

DOI:
10.1093/med/9780195377835.003.0010
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2016. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

Subscriber: null; date: 15 November 2019

Introduction

Adverse events and life-threatening emergencies during polysomnography (PSG) are rare, and the prevalence has been reported to be approximately 0.35%.1 PSG, however, is often performed in patients with substantial comorbidities, often cardiopulmonary in nature, which include but are not limited to hypertension, coronary artery disease, congestive heart failure, obstructive lung disease, neuromuscular disease, and stroke.2 One study has reported a 6-fold increase in the absolute number of patients referred to regional sleep centers for evaluation, and a greater than 20-fold increase for the diagnosis of obstructive sleep apnea.3 Attendant with the dramatic increase in the number of PSGs performed over the past 20 years, there is the need to ensure proper vigilance, training, and background for sleep physicians and particularly sleep technicians to monitor for potential pulmonary-related urgent or emergent events or issues during sleep monitoring. The sleep center-referred patient population likely has a higher risk in general for respiratory-related problems. Emergencies that involve the respiratory system are often the most debilitating and likely result in higher mortality, usually requiring the urgent attention of medical personnel.

All patients should undergo a thorough evaluation process prior to the PSG. Depending on the practice model, this may mean a comprehensive sleep specialist evaluation versus an intensive review by the sleep laboratory medical director or manager assessing pertinent sleep history and examination obtained from the referring physician prior to the sleep study. In the latter situation, in particular, this may also help determine if the patient should be evaluated for consultation by a sleep specialist prior to the sleep study in order to optimize care. This detailed pre-PSG evaluation is essential to prepare satisfactorily, to allow for preventive measures to be taken if needed, and to communicate relevant information to the sleep technicians so that they are adequately prepared before and during the procedure in case an urgent or emergent situation arises during the monitoring. Collecting this information also helps with decisions regarding the type of PSG monitoring to perform (e.g., addition of CO2 monitoring in those with morbid obesity at risk for obesity hypoventilation syndrome). In addition, it can help identify the need to remind the patient to bring along his or her rescue bronchodilator to the scheduled sleep study, and allow for preparedness regarding the need for supplemental oxygen. This information may also help determine whether a sleep study is scheduled in a free-standing facility versus in a more monitored setting such as in hospital-based facility (for sleep centers that have both venues available). The level of care required should also be assessed, as certain patients may require more intensive monitoring and a lower staff-to-patient ratio, particularly for patients with a complex medical history requiring long-term nocturnal mechanical ventilation or other measures.

Dealing with special cases such as those with existing comorbid pulmonary diseases can present a challenge. It is important in these cases for the staff to be well prepared in advance and to have a plan. Educating the patients in detail prior to the study, including what to expect, can minimize study night complications. This should be extended to the patient’s caregivers as well if indicated. Proper triage and collection of information relevant to sleep and pulmonary issues may prevent emergent and urgent situations. Emergency protocols, including information regarding how to handle pulmonary emergencies, should be in place and readily available in the technician monitoring room as a resource, and regular quality control should be performed to keep errors to a minimum. A well-trained staff that knows what to do in urgent or emergent situations is more likely to react in the correct manner and minimize adverse outcomes.

Evaluation of Acute and Emergent Aspects of Pulmonary Events in Sleep

Evaluation of urgent and emergent aspects of pulmonary-related issues that arise during sleep requires a basis of understanding the respiratory physiologic data that are collected during sleep monitoring. There are several sensors used in the identification of the disease process during the PSG. For respiratory evaluation, the primary signals that are monitored include airflow, respiratory effort, and oxygen saturation. These signals, when taken together, provide information that allows for the accurate determination of apneas and hypopneas as well as pulmonary-related physiologic derangements that occur independently from apneas and hypopneas. Carbon dioxide levels can also be monitored to allow greater insight into the patient’s effectiveness of ventilation as well as central control of breathing. In addition to understanding the respiratory physiologic sensors used and pertinent patterns suggesting underlying pulmonary disease, the recognition of symptoms indicative of a pulmonary problem is also imperative.

Practical Aspects and Recognition of Salient Respiratory Characteristics Using Sensors

Airflow Monitoring

Most airflow sensors detect apneas reliably, but the detection and quantification of decreased flow needed to diagnose hypopneas depend on the type of sensor used. Hypopneas make up the majority of obstructive respiratory events,4 and therefore measurement needs to be reliable. Use of the pneumotachometer is a method of airflow monitoring that provides a direct quantitative measurement of airflow or tidal volume; however, it requires connection to a sealed mask placed over the nose or mouth, which may be obtrusive and disrupt sleep. It is considered the reference standard for obstructive apnea and hypopnea detection. Although this provides a beneficial and accurate research tool, in the clinical setting this technique is somewhat cumbersome.

The use of the intranasal pressure transducer provides an indirect measurement of airflow by detecting pressure changes with an excellent response to airflow profile, and is capable of detecting airflow limitation. Nasal pressure transducers provide a significantly more sensitive measure of airflow than temperature-based transducers, and many believe that the pressure transducers may provide a measure of upper airway resistance, as inspiration and expiration provide transducer signal fluctuations similar to airflow.5 Nasal pressure sensors connected to the nose via nasal prongs are more accurate than thermoelements in detecting hypopneas.6 However, nasal pressure is falsely increased in the presence of nasal obstruction, and there is a non-linear relation between nasal pressure and nasal flow. Square root linearization of nasal pressure greatly increases the accuracy for quantifying hypopneas and detecting flow limitation.7,8 Mouth breathing can affect the measurement, but pure mouth breathing is uncommon.9,10

Nasal and/or oral thermocouple is an inexpensive way to assess airflow via indirect semi-quantitative assessment detecting increased temperature of expired air with only directional changes providing reliable results. Given the limitations of thermal sensors in accurately detecting quantitative measures of airflow, with measures correlating poorly with pneumotachography,9,11 these sensors have been determined not to provide quantitative measures of airflow for detection of hypopneas; however, they may be a fairly reliable method to detect complete airflow cessation (i.e., apneas). The American Academy of Sleep Medicine (AASM) Respiratory Task Force has recently recognized the oronasal thermal sensor as the sensor to detect absence of airflow for apnea identification.12

Respiratory airflow monitoring sensors are useful when scoring apneas and hypopneas during a PSG, and they may also provide other clues to underlying pathophysiology. It is important during the triage process to note if the patient has underlying medical problems that may be relevant to breathing. These include pulmonary, neuromuscular, or structural nasal anatomic abnormality as well as nasal congestion that causes the patient to be a “mouth-breather,” which may adversely affect the quality of nasal flow or pressure monitoring. Effectively addressing nasal congestion with use of nasal saline, nasal corticosteroids, and/or antihistamines prior to the sleep study visit will optimize the signal quality during the PSG recording and also optimize ability to tolerate nasal positive airway pressure.

Reduction or absence of nasal breathing due to nasal congestion or anatomical obstruction may present a significant challenge to scoring hypopneas in particular. Often during these times the nasal pressure transducer will be noted to have a poor signal throughout the study, and the scorer may have to rely solely on other signals. A loss or decrease in signal in more than one sensor, such as loss of thermistor signal in a mouth-breather, can often lead to underscoring of respiratory events, but this may be identified by using other sensors such as oxygen desaturation or arousals. The use of oronasal thermistor and nasal pressure transducers may be helpful in these situations.

Respiratory Effort

The literature supports that respiratory inductance plethysmography is acceptable for the semi-quantitative measurement of ventilation assessed by thoracic and abdominal pressure changes.13 With this technique, transducers are placed at the level of the nipples and at the umbilicus to monitor cross-sectional changes reflected by changes in inductance or resistance to change in flow of the transducers.14 The sum of the signals may provide an estimate of tidal volume and respiratory pattern during sleep. Respiratory inductance plethysmography allows an acceptable semi-quantitative measurement of ventilation and therefore hypopneas. The AASM Task Force recommends the use of respiratory inductance plethysmography or measurement of nasal pressure using nasal cannulas to detect airflow and ventilation.15

The measurement of esophageal pressure with continuous overnight monitoring is the reference standard for measuring respiratory effort during PSG. Respiratory efforts are associated with changes in pleural pressure, which can be accurately measured using esophageal manometry. This method is useful when distinguishing central versus obstructive apneas, and is useful for detecting respiratory effort–related arousals in the setting of upper airway resistance syndrome, during which there is increasingly more negative esophageal pressures immediately preceding an arousal, subsequent to which the esophageal pressure fairly rapidly returns to normal levels.16,17

The identification and respiratory pattern recognition based on airflow and effort on the part of the recording technician are very important in order to ensure adherence to laboratory-specific protocols, which may stipulate contacting the on-call physician. For example, for a certain frequency of respiratory events, there may be a protocol in place to perform a split-night study. In addition, if the respiratory events are associated with a severe degree of hypoxia or arrhythmia during a routine PSG, then the threshold to perform a titration the same night may be lowered.

While scoring the PSG, increased respiratory effort secondary to respiratory muscle fatigue or obstructive respiratory events can sometimes be identified by abdominal paradox, in which, during inspiration, the abdomen moves inward as the chest wall expands. In this situation, the waveforms for the chest wall and abdomen are dyssynchronous. Classically, the patient has an apnea or hypopnea during this time and the snore sensor is often noted to detect snoring as the patient overcomes the obstruction. The presence of snoring and thoracoabdominal paradox may be helpful when attempting to distinguish between an obstructive versus central hypopnea (Fig. 10–1).

Figure 10–1. A representative hypnogram showing paradoxical movement of the chest wall and abdomen during obstruction. Note that prior to the respiratory events the chest and abdomen are in synchrony.

Figure 10–1.
A representative hypnogram showing paradoxical movement of the chest wall and abdomen during obstruction. Note that prior to the respiratory events the chest and abdomen are in synchrony.

Pulse Oximetry Monitoring

The fundamental physical property that allows the measurement of arterial oxygen saturation is that blood changes color with saturation. Oximeters may be prone to artifact such as during states of poor perfusion, excessive patient motion (particularly at the probe site), and electrical noise, and may also be affected by changes in heart rate and circulation time.18 Overall, pulse oximetry is easy to use, inexpensive, readily available, and noninvasive and permits continuous monitoring of oxygen saturation. The utility of pulse oximetry solely in clinical decision making in the realm of sleep/pulmonary medicine has been assessed by a recent study, and determined to be an area in need of further standardization and refinement of physician interpretation.19

Certain conditions are noted to result in specific characteristics on PSG. For example, often sleep apnea is observed solely or predominantly in REM sleep accompanied by severe oxygen desaturation. In general, it is anticipated that sleep apnea will be more pronounced during REM sleep due to the associated reduction in muscle tone as well as a reduction in hypoxic and hypercapnic ventilatory drive; however, a significant degree of oxygen desaturation relative to the degree of sleep apnea may suggest underlying cardiopulmonary disease (Fig. 10–2). Patients with diseases such as chronic obstructive pulmonary disease (COPD) or neuromuscular disease where accessory muscles are heavily recruited often have significant worsening of hypoxia during REM sleep. On the other hand, Cheyne-Stokes respiration central sleep apnea, a disorder characterized by hyperventilation during wakefulness and sleep, generally arises due to respiratory system instability that occurs during transitions of wakefulness to NREM sleep or during stable REM sleep.

Figure 10–2. A representative hypnogram of a patient with chronic obstructive pulmonary disease (COPD). Note the mild hypoxemia at baseline, and respiratory events occurring during REM sleep consisting of primarily hypopneas. The severe degree of hypoxia noted during REM periods is out of proportion to the degree of apnea, and this observation is typical in patients with COPD and is related to REM-associated reduction in muscle tone.

Figure 10–2.
A representative hypnogram of a patient with chronic obstructive pulmonary disease (COPD). Note the mild hypoxemia at baseline, and respiratory events occurring during REM sleep consisting of primarily hypopneas. The severe degree of hypoxia noted during REM periods is out of proportion to the degree of apnea, and this observation is typical in patients with COPD and is related to REM-associated reduction in muscle tone.

Sleep laboratories should have protocols in place to outline the procedure for addressing hypoxia noted on baseline oximetry testing, and also during PSG. For example, an abbreviated version of our laboratory protocol is as follows. The approach to the hypoxic patient who is not on home supplemental oxygen is to verify oximetry signal quality, and if the baseline awake oxygen saturation on room air at rest is less than 90%, then the technician should contact the physician on call. The technician is also instructed to take note if the patient is short of breath, coughing, or wheezing. Our approach to the patient on home nocturnal supplemental oxygen is to perform the sleep study without supplemental oxygen if the patient’s room air awake oxygen saturation at rest is 90% or more. On the other hand, if the patient’s room air oxygen saturation at rest is less than 90%, then the sleep study should be performed with the addition of 2 liters/minute supplemental oxygen (or home setting) via nasal cannula for PSG or 2 L oxygen supplementation bleed-in for titration studies. If 2 L oxygen supplementation (or home setting) is administered but the patient remains hypoxic (oxygen saturation <90%), then the technician is instructed to contact the on-call physician. The approach to significant hypoxia (saturations <88% unassociated with respiratory events) noted during the positive airway pressure titration study should involve eliminating respiratory events on room air with positive airway pressure therapy. If pressures effectively address apneas and hypopneas and oxygen saturation is persistently less than 88% in the absence of hypoventilation, then the technician is instructed to contact the physician on call to initiate oxygen at 2L/min to maintain saturations of at least 90%. If hypoxia persists despite use of 2L oxygen supplementation, then the technician is instructed to notify the physician on call for further instruction.

Carbon dioxide Monitoring

Studies have assessed end-tidal and transcutaneous monitoring of CO2 and concluded that none of these measurements were an accurate reflection of CO2 levels and therefore should not be used during routine PSG.20 The transcutaneous values tended to have a smaller bias compared to arterial values than the end-tidal CO2 measurements, with a tendency for overestimating CO2 values.21,22

Expired end-tidal CO2 monitoring works by drawing a stream of air from the nose or the mouth to a chamber in which a light is shined through the air. Values for CO2 are near or at zero on inspiration and show an abrupt rise until the end of expiration, when there is a plateau in the CO2 level. The end-expiratory value is correlated with arterial PCO2 provided that there is complete gas emptying to functional residual capacity, and little effect of ventilation–perfusion mismatch. End-tidal CO2 monitoring may help in identifying hypoventilation in obesity hypoventilation syndrome, as well as COPD, congestive heart failure, and neurologic diseases that produce neuromuscular weakness. In addition, end-tidal CO2 values can be helpful in assessing disorders of chronic hyperventilation, distinguishing pathophysiologic from psychogenic causes by the persistence or resolution of hypocapnia during sleep. A limitation of end-tidal CO2 monitoring includes the inability to measure levels in the setting of continuous positive airway pressure (CPAP) or bi-level pressure therapy in order to assess response to treatment. In general, studies appear to indicate that end-tidal CO2 values tend to underestimate arterial CO2, with the largest discrepancies occurring in hypercapnic subjects or in subjects with respiratory disease.2224

Acute Aspects of Non-Apnea-Related Pulmonary Disorders in Sleep

Acute and emergent aspects of pulmonary issues during sleep can be broadly divided into emergencies involving the following categories: upper airway obstruction, sleep-related hypoventilation/hypoxemia due to lower airway obstruction, sleep-related hypoventilation/hypoxemia due to pulmonary vasular pathology, sleep-related hypoventilation/hypoxemia due to pulmonary parenchyma pathology, and sleep-related hypoventilation/hypoxemia due to neuromuscular and chest wall disorders.25

Upper Airway Emergencies

The maintenance of a patent airway is the first step in resuscitative efforts, and the absence of a patent airway can result in serious events, which include death. Occasionally airway abnormalities are evident before the start of PSG, which may be anticipated and even prevented.

A large number of conditions located in a variety of anatomic airway locations can produce airway obstruction, and present with expiratory or inspiratory wheezing. These conditions are generally classified by the location of obstruction: intrathoracic versus extrathoracic obstruction. Extrathoracic obstruction can be suspected based upon the flow volume loop on simple spirometry in which the inspiratory limb of the loop shows flattening and flow rates decreased relative to the expiratory limb.26 This can be observed in patients with enlarged goiter resulting in tracheal compression, and also in vocal cord dysfunction. Vocal cord dysfunction is a functional disorder of vocal cord adduction. On the other hand, in intrathoracic obstruction the transmural pressure gradient during expiration results in compression of the intrathoracic trachea, as it does in the lower airways in asthma and COPD. This narrowing in the trachea results in a flow ceiling (plateau) during expiration.26 During inspiration, the gradient across the tracheal wall distends the airway and flow limitation at this site does not occur (Figs. 10–3 and 10–4). Asthma should be considered when patients present symptomatically with episodic wheezing; however, upper airway obstruction and disease should also always be considered in the differential diagnosis. While asthmatics with wheeze typically will present with reversible expiratory airflow obstruction demonstrated by spirometry, a restrictive ventilatory pattern also may be seen occasionally. The diagnosis of wheezing conditions other than asthma should be considered when the initial evaluation suggests its presence (i.e., wheezing noted upon auscultation at the sternal notch) or when wheeze does not respond to conventional asthma medications. Patients with wheezing and dyspnea in whom the sleep technician suspects upper airway involvement should be handled as an emergency, and the physician on call should be notified immediately. Patients studied in the sleep laboratory could also experience upper airway compromise when in the supine position due to an enlarged thyroid resulting in tracheal compression; aspiration due to abnormal swallowing mechanisms, which is further compromised in the supine position; or worsening of their breathing due to vocal cord dysfunction. These patients may develop stridor and upper airway wheezes, and a decision as to whether the study should be terminated and whether these patients should undergo medical evaluation prior to further studying is appropriate.

Figure 10–3. Transmural pressure changes during a respiratory cycle can have different effects on the severity of obstruction at different airway sites. Panel A shows extrathoracic upper airway obstruction. During expiration, intrapleural pressure (Ppl) and intratracheal pressure (Ptr) are greater than atmospheric pressure (Patm), causing the site of the obstruction to widen. During inspiration, because Ppl and Ptr are less than Patm, the site narrows. Panel B shows intrathoracic upper airway obstruction. During expiration Ppl is greater than Ptr, so the site narrows. During inspiration Ptr is greater than Ppl, so the site widens.

Figure 10–3.
Transmural pressure changes during a respiratory cycle can have different effects on the severity of obstruction at different airway sites. Panel A shows extrathoracic upper airway obstruction. During expiration, intrapleural pressure (Ppl) and intratracheal pressure (Ptr) are greater than atmospheric pressure (Patm), causing the site of the obstruction to widen. During inspiration, because Ppl and Ptr are less than Patm, the site narrows. Panel B shows intrathoracic upper airway obstruction. During expiration Ppl is greater than Ptr, so the site narrows. During inspiration Ptr is greater than Ppl, so the site widens.

Figure 10–4. Schematic flow–volume loops in a spectrum of airway obstruction. A is normal; B is variable extrathoracic upper airway obstruction; C is variable intrathoracic upper airway obstruction; D is fixed upper airway obstruction; and E is small airways obstruction.

Figure 10–4.
Schematic flow–volume loops in a spectrum of airway obstruction. A is normal; B is variable extrathoracic upper airway obstruction; C is variable intrathoracic upper airway obstruction; D is fixed upper airway obstruction; and E is small airways obstruction.

Sleep-Related Hypoventilation/Hypoxemia due to Lower Airway Obstruction

Asthma

The most recent estimate of asthma prevalence is from 2002 and shows that 72 people per 1,000, or 20 million people, currently have asthma. In 2002, 43 people per 1,000 (12 million people) had experienced an asthma attack in the previous year—in other words, about 60% of the people who had asthma at the time of the survey had experienced an asthma attack in the previous year.27 It is therefore inevitable that a sleep laboratory will eventually encounter the need to manage a patient with asthma or asthma exacerbation.

Patients known to have asthma should be instructed to bring their bronchodilator medications with them. It could also prove beneficial to ask the patient to check a peak flow value and compare it to his or her baseline to determine if the patient’s asthma is controlled and to rule out early-stage asthma exacerbation. Airway reactivity typically worsens nocturnally, and this is a salient aspect of physiology with which the recording technician conducting a PSG should be familiar. The vast majority of asthmatic patients have symptoms mainly at night, and a dramatic peak in subjective dyspnea is seen at 4 a.m.28 Objective measures of airflow in asthmatic subjects demonstrate diurnal variation in disease activity, with marked declines in peak expiratory flow rates between midnight and 8 a.m., reaching a nadir at 4 a.m.29 This nocturnal worsening in symptoms is likely due to increased vagal tone during sleep promoting bronchoconstriction, and decrements in cortisol that may lead to down-regulation of the beta 2-adrenergic receptors.30 Patients who are experiencing daytime and nocturnal symptoms of asthma should be evaluated by a physician before the sleep study for possible addition of an inhaled corticosteroid to the regimen. If postnasal drip and gastroesophageal reflux symptoms are effectively addressed and nocturnal asthma symptoms persist, then the addition of a long-acting beta-agonist may be considered. It is also important to be cognizant of potential allergens and triggers in the PSG room; therefore, it is also useful to recognize individual-based potential asthma triggers such as cold air and so forth. Allergen exposure, which includes the detergents used, linen material, and floor detergents in the PSG room, can also worsen reactive airway disease. A patient who develops wheezing and dyspnea should use his or her prescribed bronchodilators immediately to attempt to abort early attacks of bronchospasm. If the patient comes unprepared or if the bronchospasm persists, the patient should be evaluated by medical personnel as per laboratory or institution protocol.

Chronic Obstructive Pulmonary Disease

COPD is defined as a disease state characterized by chronic airflow limitation due to chronic bronchitis and emphysema. As with asthma, COPD is a widely prevalent disorder and the sleep laboratory should be prepared to deal with emergencies related to this disease. In the United States at present, estimates from national interviews obtained by the National Center for Health Statistics have shown that more than 16 million people are afflicted with COPD; about 14 million are thought to have chronic bronchitis, while 2 million people have emphysema. In the National Health and Nutrition Examination Survey (NHANES) III, using surveys, physical examinations, and pulmonary function testing, prevalence estimates using World Health Organization definitions showed that 23.6 million adults (13.9% of the adult population) have COPD.31

Patients with COPD should be instructed in a similar fashion to asthmatic patients to bring their bronchodilator on the night of the sleep study. These patients also suffer a certain degree of hyperreactivity of the airways that is secondary to the inflammation involved in COPD. An important caveat when studying COPD patients is the fact that patients with advanced obstructive lung disease may have hypercapnia. The use of carbon dioxide monitoring with end-tidal CO2 or transcutaneous CO2 may be considered. Patients with advanced COPD often experience enhanced hypoxia and hypercapnia during sleep due to sleep-related reduction in functional residual capacity (in normal subjects, there is an approximately 10% decrease32 in tidal volume), resulting in impairment in gas exchange, hypoventilation due to alterations in respiratory center sensitivity, and also changes in the ventilation–perfusion relationship. These physiologic changes are more pronounced during REM sleep due to further blunting of hypoxic and hypercapnic ventilatory responses as well as loss of contribution of intercostal respiratory muscles and diminution in diaphragmatic contribution to ventilation in a hyperinflated lung with increased dead space. If the technician encounters a patient with COPD experiencing significant hypoxia in the context of apneas and hypopneas, then this should be addressed with positive airway pressure therapy. If hypoxia occurs in the absence of respiratory events, then initiation of supplemental oxygen is recommended with the goal of maintaining oxygen saturation around 88% to 92%. It would be reasonable to contact the sleep physician on call for guidance in order to avoid excess CO2 retention and hypercapnic respiratory failure, which can occur due to worsened ventilation–perfusion mismatching with increasing oxygen administration in the setting of significant obstructive lung disease.

Another consideration in the patient with known COPD is the presence of concomitant sleep apnea. This has been referred to as the overlap syndrome.33 In this group of patients, there are typically oscillations in the oxygen saturation throughout the sleep period, with marked worsening in REM sleep. The consequences of hypoxemia during sleep in COPD include cardiac arrhythmias (which may be an indication for a lower threshold for institution of positive airway pressure therapy) and the development of pulmonary arterial hypertension and polycythemia.33,34

Sleep-Related Hypoventilation/Hypoxemia due to Pulmonary Vascular Pathology

Pulmonary Vasculopathies

Features noted during the sleep study in the setting of pulmonary vasculopathy/pulmonary hypertension include the sustained oxyhemoglobin desaturation in the absence of apneas, hypopneas, inspiratory flow limitation, or snoring. There are data to suggest that pulmonary arterial hypertension may occur in the setting of sleep apnea, although the prevalence is low. Sleep apnea may result in transient and possibly permanent elevations in pulmonary pressures secondary to hypoxic vasoconstriction. Prevalence estimates of pulmonary hypertension in sleep apnea range anywhere from 17% to 53%, and most studies indicate that the degree of pulmonary hypertension is mild.35

Pulmonary arterial hypertension in sleep apnea appears to be most strongly associated with other risk factors, such as left-sided heart disease, parenchymal lung disease, nocturnal desaturation, and obesity. Clinical practice guidelines from the American College of Chest Physicians recommend assessment for sleep apnea in patients with pulmonary arterial hypertension, but they do not endorse the evaluation of pulmonary hypertension in those with sleep apnea.35 It also recognized that in patients with sleep apnea and pulmonary hypertension, treatment of sleep apnea with positive airway pressure therapy should be provided with the expectation that pulmonary pressures will decrease but may not normalize, particularly when pulmonary hypertension is very severe.35 It is prudent to be aware that many patients with pulmonary hypertension who present to the sleep laboratory for evaluation of sleep apnea may be receiving continuous prostacyclin infusions. If access to these infusions becomes compromised, then this constitutes a medical emergency to obtain access for resumption of infusion, as abrupt discontinuation of such treatment may result in hemodynamic compromise. In addition, in sickle cell disease and related pulmonary vasculopathy, data support that the degree of oxyhemoglobin desaturation is related to painful sickle cell crises, which may be observed in the setting of sleep apnea during sleep study monitoring.36

Sleep-Related Hypoventilation/Hypoxemia due to Pulmonary Parenchymal Pathology

Patients with interstitial lung disease suffer from severe dyspnea initially on exertion and later even at rest as their parenchymal disease progresses. This severe shortness of breath frequently leads to hyperventilation, which is driven by cardiopulmonary reflexes persisting into sleep, and is occasionally related to the development of abnormal breathing patterns.37 Pulmonary parenchymal diseases are characterized by reduction in lung volumes and abnormal ventilation–perfusion relationships, often translating into daytime in addition to nocturnal hypoxia. Examples of interstitial lung diseases include usual interstitial pneumonitis, desquamative interstitial pneumonitis, and hypersensitivity pneumonitis. Similar to patients with COPD, patients with pulmonary parenchymal disease may experience accentuated sleep hypoventilation and desaturation due to abnormal ventilation–perfusion relationships, lower baseline hypoxia (starting at a steeper portion of the oxyhemoglobin curve), and altered ventilatory muscle action during sleep.25 Of note, sleep quality has been found to be worse in interstitial lung disease (increased stage 1, reduced REM sleep and increased sleep fragmentation), and individuals who have baseline hypoxia are more likely to have this abnormal sleep architecture. Compared to controls, those with interstitial lung disease are also noted to have a shorter expiratory time and inspiratory time.37

Sleep-Related Hypoventilation/Hypoxemia due to Neuromuscular and Chest Wall Disorders

Neuromuscular Disease

Neuromuscular disorders can have a significant impact on a patient’s sleep and can also present a challenge due to the pulmonary sequelae. Although many factors such as pain and limited mobility may contribute to poor sleep, the pulmonary emergency arises from impaired ventilation. The pulmonary pathophysiology of these diseases is based upon respiratory compromise secondary to muscle weakness or increased fatigue leading to hypoventilation and sleep apnea along with oxygen desaturation in diseases such as amyotrophic lateral sclerosis, myotonic dystrophy, Charcot-Marie-Tooth disease, post-polio syndrome, and myasthenia gravis. A common complaint seen in patients with neuromuscular disorders is daytime sleepiness, which may be a sign of underlying sleep apnea.

These diseases often worsen during certain portions of the patient’s sleep or during certain positions. The recording technician should be aware of the presence of neuromuscular disease in a patient in order to be vigilant with respect to noting hypoxia and hypercapnia. REM sleep can often lead to increased hypoventilation due to inhibition of respiratory muscles except the diaphragm and also can cause an increase in sleep-disordered breathing severity due to collapse of the airway. Oxygen desaturation may occur, particularly in the presence of diaphragmatic dysfunction. The patient’s position must also be considered, as certain patients may experience worsening of respiratory symptoms in the supine position (particularly if diaphragmatic dysfunction is present) along with the possibility of aspiration of secretions, especially if there is bulbar disease. Either end-tidal or transcutaneous CO2 monitoring may be considered during PSG in those with underlying neuromuscular disease to obtain a sense of the severity of hypoventilation, and potential benefit from positive airway pressure therapy.

Sleep apnea may be observed in a large percentage of the population with neuromuscular disorders—up to 42% in one study.38 During sleep, the changes that occur with respiration, both centrally and peripherally, may lead to worsening of the patient’s sleep-related complaints. Patients with underlying neuromuscular disease may require nocturnal ventilatory assistance. Standard modes of continuous or bi-level positive airway pressure therapy may be useful; however, advanced ventilatory modes such as average volume assured pressure support may theoretically be beneficial.

Obesity Hypoventilation Syndrome

Obesity hypoventilation syndrome (OHS) is defined by obesity (body mass index −>30 kg/m2) and chronic waking hypercapnia (PaCO2 greater than 45 mmHg), often occurring concomitantly with sleep apnea.39 When it is associated with sleep apnea (90%), it is often referred to as hypercapnic sleep apnea. In 10% of patients there is an increase in PaCO2 of 10 mmHg above wakefulness or significant oxygen desaturation without evidence of significant sleep apnea.39 As it is a diagnosis of exclusion, obstructive airway disease, interstitial lung disease, chest wall disorders, severe hypothyroidism, neuromuscular disease, and congenital central hypoventilation syndrome must be considered. The true prevalence of OHS is uncertain, but given the increase in morbid obesity, up to 20% of patients with sleep apnea may have obesity hypoventilation.40

Patients with OHS are typically middle-aged; the male-to-female ratio is 2:1, and they tend to be obese, with severe sleep apnea. Signs and symptoms consistent with classic sleep apnea are usually present, such as snoring, witnessed apneas, excessive daytime sleepiness, morning headaches, and fatigue. Additional symptoms of dyspnea, lower extremity edema, and decreased waking oxygen saturation are typically seen. Pulmonary function testing often demonstrates a restrictive mechanical defect due to obesity. If left untreated, these patients can proceed to develop pulmonary hypertension and cor pulmonale.41 In the absence of arterial blood gas results, serum bicarbonate levels combined with the severity of sleep apnea may be used to clinically predict obesity hypoventilation in patients with severe sleep apnea, morbid obesity, and significant oxygen desaturation. It is reasonable to obtain arterial blood gas measurements to confirm daytime hypercapnia. Patients with obesity hypoventilation have a reduced quality of life, increased healthcare expenses, and an increased risk of pulmonary hypertension. They are also more likely to be hospitalized, requiring intensive care treatment, than those with eucapnic obesity.

If there is clinical suspicion for OHS, then sleep study monitoring should include CO2 monitoring. Transcutaneous CO2 monitoring would be of most benefit if a split-night study or titration study is planned. The sleep technician should be aware of the higher acuity level of this subgroup of patients with OHS, particularly the potential to experience hypercapnic respiratory failure. If a patient with suspected OHS is particularly somnolent and difficult to arouse from sleep upon presentation to the sleep laboratory, then the notion of significant hypercapnia should be considered and the sleep physician on call should be contacted for instructions as to how to proceed.

OHS is an underdiagnosed condition that may have significant impact on the long-term morbidity and mortality of these patients if left untreated. Treatment in OHS patients has not been systematically studied, but the first line is positive airway pressure therapy to eliminate obstructive events, hypopneas, and flow limitation. Treatment of OHS is associated with improved long-term morbidity and mortality. The long-term mortality rate for patients with OHS treated with positive airway pressure is less than 10%.42 A, 50-month study, however, showed that there was a 46% mortality associated in 15 patients with OHS who refused positive airway pressure therapy.42 Another long-term study showed 23% mortality in an 18-month study in 47 patients where OHS was untreated.43 Oxygen therapy is needed in up to 50% of the patients with OHS at the initiation of therapy in the clinical setting, particularly if hypoxia persists despite use of bi-level positive airway pressure therapy.42 In extremely severe cases, surgical intervention for weight loss or tracheostomy with or without mechanical ventilation may be needed.

Conclusion

In summary, although adverse events during PSG, including those related to respiratory events, are uncommon, it is important to be prepared for respiratory issues that may arise during PSG. Specifically, it is important to obtain information about underlying respiratory comorbidity before the patient arrives at the sleep laboratory, preferably with a sleep physician assessment in an outpatient setting prior to the scheduled sleep study, to ensure adequate control of respiratory symptoms. In addition, it would be reasonable to instruct patients with underlying obstructive lung disease who use rescue bronchodilators to bring these inhalers when they present for their sleep study, particularly given the known diurnal variability of reactive airways disease such that there are worsening symptoms during the early morning hours. Obtaining detailed information regarding the type of underlying pulmonary disease can be very helpful to the recording technician and on-call sleep physician to ensure vigilance for disease-specific issues that may arise. Furthermore, this information is beneficial to inform the type of sleep study to be performed—for instance, carbon dioxide monitoring in the setting of neuromuscular disease and OHS.

References

1. Mehra R, Strohl KP. Incidence of serious adverse events during nocturnal polysomnography. Sleep. 2004;27(7):1379–1383.Find this resource:

    2. Kostoglou-Athanassiou I, Athanassiou P. Metabolic syndrome and sleep apnea. Hippokratia. 2008;12(2):81–86.Find this resource:

      3. Punjabi NM, Welch D, Strohl K. Sleep disorders in regional sleep centers: a national cooperative study. Coleman II Study Investigators. Sleep. 2000;23(4):471–480.Find this resource:

        4. Shahar E, Whitney CW, Redline S, Lee ET, Newman AB, Javier Nieto F, O'Connor GT, Boland LL, Schwartz JE, Samet JM. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;163(1):19–25.Find this resource:

          5. Hosselet JJ, Norman RG, Ayappa I, Rapoport DM. Detection of flow limitation with a nasal cannula/pressure transducer system. Am J Respir Crit Care Med. 1998;157(5 Pt 1):1461–1467.Find this resource:

            6. Series F, Marc I. Nasal pressure recording in the diagnosis of sleep apnoea/hypopnoea syndrome. Thorax. 1999;54(6):506–510.Find this resource:

              7. Montserrat JM, Farré R, Ballester E, Felez MA, Pastó M, Navajas D. Evaluation of nasal prongs for estimating nasal flow. Am J Respir Crit Care Med. 1997;155(1):211–215.Find this resource:

                8. Thurnheer R, Xie X, Bloch KE. Accuracy of nasal cannula pressure recordings for assessment of ventilation during sleep. Am J Respir Crit Care Med. 2001;164(10 Pt 1):1914–1919.Find this resource:

                  9. Farre R, Montserrat JM, Rotger M, Ballester E, Navajas D. Accuracy of thermistors and thermocouples as flow-measuring devices for detecting hypopnoeas. Eur Respir J. 1998;11(1):179–182.Find this resource:

                    10. Ballester E, Badia JR, Hernández L, Farré R, Navajas D, Montserrat JM. Nasal prongs in the detection of sleep-related disordered breathing in the sleep apnoea/hypopnoea syndrome. Eur Respir J. 1998;11(4):880–883.Find this resource:

                      11. Akre H, Skatvedt O, Borgersen AK. Diagnosing respiratory events and tracing air flow by internal thermistors. Acta Otolaryngol. 2000;120(3):414–419.Find this resource:

                        12. Iber C, Ancoli-Israel S, Chesson A, et al, for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications, 1st ed. Westchester, IL: American Academy of Sleep Medicine, 2007.Find this resource:

                          13. Cantineau JP, Escourrou P, Sartene R, Gaultier C, Goldman M. Accuracy of respiratory inductive plethysmography during wakefulness and sleep in patients with obstructive sleep apnea. Chest. 1992;102(4):1145–1151.Find this resource:

                            14. Kryger MH, Roth T, Dement WC. Principles and Practice of Sleep Medicine. Philadelphia: WB Saunders, 2000:1217–1230.Find this resource:

                              15. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep. 1999;22(5):667–689.Find this resource:

                                16. Guilleminault C, Stoohs R, Duncan S. Snoring (I). Daytime sleepiness in regular heavy snorers. Chest. 1991;99(1):40–48.Find this resource:

                                  17. Guilleminault C, Stoohs R, Clerk A, Cetel M, Maistros P. A cause of excessive daytime sleepiness. The upper airway resistance syndrome. Chest. 1993;104(3):781–787.Find this resource:

                                    18. West P, George CF, Kryger MH. Dynamic in vivo response characteristics of three oximeters: Hewlett-Packard 47201A, Biox III, and Nellcor N-100. Sleep. 1987;10(3):263–271.Find this resource:

                                      19. Ramsey R, Mehra R, Strohl KP. Variations in physician interpretation of overnight pulse oximetry monitoring. Chest. 2007;132(3):852–859.Find this resource:

                                        20. Sanders MH, Kern NB, Costantino JP, Stiller RA, Strollo PJ Jr, Studnicki KA, Coates JA, Richards TJ. Accuracy of end-tidal and transcutaneous PCO2 monitoring during sleep. Chest. 1994;106(2):472–483.Find this resource:

                                          21. McLellan PA, Goldstein RS, Ramcharan V, Rebuck AS. Transcutaneous carbon dioxide monitoring. Am Rev Respir Dis. 1981;124(2):199–201.Find this resource:

                                            22. Oshibuchi M, Cho S, Hara T, Tomiyasu S, Makita T, Sumikawa K. A comparative evaluation of transcutaneous and end-tidal measurements of CO2 in thoracic anesthesia. Anesth Analg. 2003;97(3):776–779.Find this resource:

                                              23. Phan CQ, Tremper KK, Lee SE, Barker SJ. Noninvasive monitoring of carbon dioxide: a comparison of the partial pressure of transcutaneous and end-tidal carbon dioxide with the partial pressure of arterial carbon dioxide. J Clin Monit. 1987;3(3):149–154.Find this resource:

                                                24. Reid CW, Martineau RJ, Miller DR, Hull KA, Baines J, Sullivan PJ. A comparison of transcutaneous end-tidal and arterial measurements of carbon dioxide during general anaesthesia. Can J Anaesth. 1992;39(1):31–36.Find this resource:

                                                  25. American Academy of Sleep Medicine. International Classification of Sleep Disorders. Westchester, IL: American Academy of Sleep Medicine. 2005.Find this resource:

                                                    26. Quanjer PH, Tammeling GJ, Cotes JE, Pedersen OF, Peslin R, Yernault JC. Lung volumes and forced ventilatory flows. Report Working Party Standardization of Lung Function Tests, European Community for Steel and Coal. Official Statement of the European Respiratory Society. Eur Respir J Suppl. 1993;16:5–40.Find this resource:

                                                      27. Mannino DM, Homa DM, Akinbami LJ, Moorman JE, Gwynn C, Redd SC. Surveillance for asthma—United States 1980-1999. MMWR Surveill Summ. 2002;51(1):1–13.Find this resource:

                                                        28. Turner-Warwick M. Epidemiology of nocturnal asthma. Am J Med. 1988;85(1B):6–8.Find this resource:

                                                          29. Barnes P, FitzGerald G, Brown M, Dollery C. Nocturnal asthma and changes in circulating epinephrine, histamine, and cortisol. N Engl J Med. 1980;303(5):263–267.Find this resource:

                                                            30. Szefler SJ, Ando R, Cicutto LC, Surs W, Hill MR, Martin RJ. Plasma histamine, epinephrine, cortisol, and leukocyte beta-adrenergic receptors in nocturnal asthma. Clin Pharmacol Ther. 1991;49(1):59–68.Find this resource:

                                                              31. Viegi G, Scognamiglio A, Baldacci S, Pistelli F, Carrozzi L. Epidemiology of chronic obstructive pulmonary disease (COPD). Respiration. 2001;68(1):4–19.Find this resource:

                                                                32. Hudgel DW, Devadatta P. Decrease in functional residual capacity during sleep in normal humans. J Appl Physiol. 1984;57(5):1319–1322.Find this resource:

                                                                  33. Shepard JW Jr., Garrison MW, Grither DA, Dolan GF. Relationship of ventricular ectopy to nocturnal oxygen desaturation in patients with chronic obstructive pulmonary disease. Am J Med. 1985;78(1):28–34.Find this resource:

                                                                    34. Douglas NJ, White DP, Weil JV, Pickett CK, Martin RJ, Hudgel DW, Zwillich CW. Hypoxic ventilatory response decreases during sleep in normal men. Am Rev Respir Dis. 1982;125(3):286–289.Find this resource:

                                                                      35. Atwood CW Jr., McCrory D, Garcia JG, Abman SH, Ahearn GS. Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines. Chest. 2004;126(1 Suppl):72S–77S.Find this resource:

                                                                        36. Hargrave DR, Wade A, Evans JP, Hewes DK, Kirkham FJ. Nocturnal oxygen saturation and painful sickle cell crises in children. Blood. 2003;101(3):846–848.Find this resource:

                                                                          37. Perez-Padilla R, West P, Lertzman M, Kryger MH. Breathing during sleep in patients with interstitial lung disease. Am Rev Respir Dis. 1985;132(2):224–229.Find this resource:

                                                                            38. Labanowski M, Schmidt-Nowara W, Guilleminault C. Sleep and neuromuscular disease: frequency of sleep-disordered breathing in a neuromuscular disease clinic population. Neurology. 1996;47(5):1173–1180.Find this resource:

                                                                              39. Olson AL, Zwillich C. The obesity hypoventilation syndrome. Am J Med. 2005;118(9):948–956.Find this resource:

                                                                                40. Mokhlesi B, Tulaimat A, Faibussowitsch I, Wang Y, Evans AT. Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea. Sleep Breath. 2007;11(2):117–124.Find this resource:

                                                                                  41. Mokhlesi B, Tulaimat A. Recent advances in obesity hypoventilation syndrome. Chest. 2007;132(4):1322–1336.Find this resource:

                                                                                    42. Perez de Llano LA, Golpe R, Ortiz Piquer M, Veres Racamonde A, Vázquez Caruncho M, Caballero Muinelos O, Alvarez Carro C. Short-term and long-term effects of nasal intermittent positive pressure ventilation in patients with obesity-hypoventilation syndrome. Chest. 2005;128(2):587–594.Find this resource:

                                                                                      43. Nowbar S, Burkart KM, Gonzales R, Fedorowicz A, Gozansky WS, Gaudio JC, Taylor MR, Zwillich CW. Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome. Am J Med. 2004;116(1):1–7.Find this resource: