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Clear, detailed guidance on anesthesia and pre-existing conditions Order your copy today at elsevierhealth.com/9780443286841 From Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition Exclusive preview: Sleep-Related Breathing Disorder 5 CHAPTER 1 Sleep-Related Breathing Disorder utilization, decreased productivity, and years of potential life lost. It is estimated that the yearly incidence of OSA-related motor vehicle accidents alone costs approximately $16 billion and 1400 lost lives. It is also estimated that treating all drivers with OSA with positive airway therapy (at a cost of ~$3 bil- lion/year) would save about $11 billion and 1000 lives. OSA has a significant public health impact due to its high prevalence (estimated 25 million in the United States), high proportion of undiagnosed cases (80% for males and 90% for females), and association with significant morbidity, mortality, and decreased quality of life. Treatment of Adult OSA Treatment of OSA includes the use of devices, surgery, and med- ications. All modes of treatment should include patient educa- tion and long-term follow-up. General measures that should be applied with all modes of therapy include reducing modifiable risk factors and treating comorbid conditions. Potentially modi- fiable risk factors include alcohol consumption, use of sedative medication, cigarette smoking, obesity, nasal obstruction, and tonsil grade ( ≥ 3). General measures in the treatment of OSA include weight reduction, avoiding alcohol and central nervous system (CNS) depressant drugs, improving sleep hygiene, and refraining from driving when sleepy. In extreme cases of sleepi- ness (e.g., patients reporting the maximum score of 24 on the Epworth sleepiness scale [ESS]), patients should be forbidden from driving unless they are treated and their OSA and ESS are improved. Positive Airway Pressure Therapy for OSA PAP therapy is the most commonly studied and prescribed therapy for OSA as well as for some forms of central and mixed sleep apnea. PAP therapy is considered tier 1 therapy for OSA. The most common form of PAP is continuous PAP (CPAP). Other forms of PAP therapy consist of various electronic modifications of PAP delivery patterns such as bilevel PAP (BPAP), autotitrated PAP (APAP), and adaptive servo ventila- tion (ASV). The three elements of a PAP device are the flow generator, a connecting hose, and a patient interface, which EMGgg (Volts) 5.0 2.5 0.0 –2.5 –5.0 50 0 –50 50 25 0 –25 –50 –2 100 95 90 85 80 0 –50 2 0 EMGsub ( V) EEG ( V) Pepi (cm H 2 O) Flow (L/sec) Snoring Snoring Oxygen desaturation Arousal threshold APNEA AROUSAL 20 sec Sao 2 (%) Fig. 1.4 Experimental polysomnography (PSG) in obstructive sleep apnea (OSA) showing sequence and resolution of apnea events. This experimental PSG in a patient with OSA includes recordings of electromy- ography (EMG) of upper airway muscles (genioglossus [ EMGgg ] and submental muscles [ EMGsub ]), elec- troencephalography ( EEG ), intrathoracic pressure approximated by epiglottic catheter ( Pepi ), nasal airflow ( Flow ) by thermal sensor, and oxygen saturation ( Sa O 2 ) by pulse oximetry with a minimal sampling rate of 10 Hz. The top channel ( EMGgg ) demonstrates progressively increased EMGgg activity (amplitude) until this increased activity reaches a sufficient level to open the upper airway and allow breathing (Flow) to resume. The middle channel (Pepi) demonstrates a progressive increase in respiratory muscle effort until breathing (Flow) resumes. The increase in respiratory muscle effort is considered the primary stimulus for EEG arousal, through stimulation of the mechanoreceptors in the chest muscles, which provide input both to the medullary respiratory centers and the wake/sleep neurochemical pathways. The EEG channel shows that the occur- rence of the EEG arousal occurs immediately following the peaks in EMGgg and Pepi and coincides with the resumption of breathing as demonstrated by nasal airflow (Flow). The airflow (Flow) thermal sensor channel shows the resumption of breathing at the time of EEG arousal, immediately after the peaks of upper airway (EMGgg) and respiratory (Pepi) muscle activity. The oxygen saturation channel (Sa O 2 ) demonstrates the lag time between ventilation and oxygenation, which leads to paradoxical restoration of oxygen saturation during the apnea episode, and the occurrence of oxygen desaturation during the resumption of the breathing period. The increased activity of EMG, Pepi, and EEG at the end of the apnea period results in a subsequent period of hyperpnea. The cyclic alteration of periods of apnea and hyperpnea disrupts the chemoreceptor stability of the respiratory control system and leads to a periodic breathing pattern similar to that encountered in several forms of central sleep apnea. 6 CHAPTER 1 Sleep-Related Breathing Disorder has three forms: nasal mask, nasal pillows, and full-face mask. Nasal masks are better tolerated than oronasal masks and are associated with better adherence, require lower CPAP levels, and result in lower residual AHI. Technologic advancements have allowed a reduction in the size and the noise level of flow generators as well as the options of PAP delivery patterns. The aim of these modifications is to enhance individual customiza- tion of PAP therapy and therefore improve adherence to and effectiveness of the therapy. Critical steps in the application of PAP therapy are patient education, mask fitting, and titration of Cardiac dysfunction Endothelial dysfunction syndrome RV afterload, RVH Heart rate MVO2 O 2 delivery Ppl Redux gene attraction, oxidation stress inflammation, hypercoagulability PO2 PCO2 Hypoxic and hypercapnic pulmonary vasoconstriction Sympathetic activation Parasympathetic withdrawal Arousals Sleep apnea/ hypopnea Transmural pressure of cardiac chambers, aorta, and pulmonary microvascular bed BP and LV afterload: MVO 2 , myocardial toxicity, arrythmias Aortic dilation Lung H 2 O Changes in RV and LV afterload, MVO2 arrythmias Fig. 1.5 Schematic representation of cardiovascular pathophysiologic consequences of obstructive sleep apnea. Male sex Age 40–70 y Familial aggregation Suspected Genetics Smoking Menopause Alcohol use before sleep Nighttime nasal congestion Demographic correlates of increased OSA prevalence Established Body habitus Overweight and obesity Central body fat distribution Large neck girth Craniofacial and upper airway abnormalities Risk factors Symptoms Habitual, loud snoring Nocturnal breathing pauses, choking, gasping Excessive daytime sleepiness OSA Cardiovascular and cerebrovascular disease Hypertension Coronary artery disease Myocardial infarction Congestive heart failure Stroke Diabetes and the metabolic syndrome Problems with daytime functioning Daytime sleepiness Motor vehicle crashes Psychosocial problems Decreased cognitive function Reduced quality of life Outcomes and/or comorbid conditions Fig. 1.6 Schematic representation of the overlap between risk factors, symptoms, and outcomes of obstruc- tive sleep apnea (OSA). There is significant overlap between what are considered risk factors, symptoms, and outcomes in OSA. Overlap can be seen between symptoms (e.g., excessive daytime sleepiness [EDS]) and outcomes. This overlap may be a causal association or due to shared risk factors of chronic sleep deprivation and disrupted sleep architecture. Overlap can be observed between risk factors and outcomes in the form of metabolic and cardiovascular disorders. This overlap may represent reciprocal causal association or noncausal association due to shared risk factors. 11 CHAPTER 1 Sleep-Related Breathing Disorder gravis, cerebral palsy, spinal muscle atrophy, and kyphoscolio- sis. Multiple causes of CSA can coexist as well as multiple types of SRBD. CSA due to High-Altitude Periodic Breathing CSA due to HAPB is usually encountered at altitudes of 7600 m (25,000 ft) or more (but occasionally less). It usually has a peri- odic pattern of alternating periods of apnea and hyperpnea of 35-second cycle length or less (apnea plus hyperpnea). If the periodic breathing pattern of HAPB meets the criteria of CSB, then it is called CSA with CSB due to HAPB. CSA due to a Medication or Substance CSA due to a medication or substance is caused by a medica- tion or substance that suppresses the chemical or neural control of breathing. Long-term opioid use ( ≥ 2-month use of long- acting opioid [e.g., methadone]) is the most common cause of this CSA. Opioids suppress both the chemical and neural con- trol of breathing through μ -opioid receptors in the medullary pre-Botzinger complex, the main autonomic respiratory pace- maker. Opioid-induced CSA is more prominent during NREM sleep and may resolve during REM sleep. The severity of opi- oid-induced CSA correlates with a daily morphine milligram equivalent of 200 mg or more and with low to normal body mass CHIN(1) 250 V C3-A2 125 V O2-A1 125 V ROC-A1 125 V LOC-A2 125 V ECG 2.5 mv LEG(L) LEG(R) THOR RES x1 ABD RES x1 PULSE bpm Pco 2 mm Hg AIRFLOW 62.5 V –4 30 3295 3370 3445 3520 Period Period Period 5 min/page 3447 30 sec/page Cursor: 23:35:58 Epoch: 115 - STAGE 2 3445 3442 3440 3437 3435 3432 3430 3427 3425 3422 Period Period Period Period Period Period Period Period Period 120 40 85 100 Sao 2 % Fig. 1.8 Polysomnography (PSG) features of central sleep apnea with Cheyne-Stokes breathing in a patient with congestive heart failure (CHF). This PSG display is split into upper and lower windows of different dura- tions. The upper window is a 30-s epoch that displays the channels that are used for the recording and stag- ing of sleep: electromyography, electroencephalography (EEG), electrooculography, and electrocardiography (ECG). The lower window is a 5-min epoch that displays the channels that are used to document movement disorders and breathing disorders. Starting from the bottom of the lower window, the airflow channel shows a flow pattern of periodic oscillation between periods of apnea that last more than 10 s and periods of hyper- pnea that have a crescendo-decrescendo pattern. The P cO 2 channel shows that P cO 2 recordings very slightly lag behind airflow recordings and display an identical periodic oscillation between periods of apnea and hyper- pnea. The pulse channel shows heart rate changes that are most prominent at the peak of hyperpnea periods, which usually corresponds with nadir Sp O 2 and EEG arousal. The abdominal and thoracic resistance channels show that the apnea events are central apneas since there is no respiratory effort during the apnea periods. These respiratory effort channels demonstrate the same crescendo-decrescendo pattern during the hyper- pnea periods, which reflect tidal volume. The Sp O 2 channel shows that the nadir Sp O 2 level corresponds with the peak of the hyperpnea period and the recovery of Sp O 2 occurs during the apnea period. The LEG channels record the occurrence of periodic leg movements (PLMs), which are common in CHF . In the upper window, the ECG channel shows wide complex paced beats and narrow complex irregular beats that represent an underlying atrial fibrillation. 7 CHAPTER 1 Sleep-Related Breathing Disorder PAP therapy. Effective PAP titration can result in the elimina- tion of apnea events and normalization of oxygen saturation. Long-term effects of effective PAP therapy include improved sleep efficacy and architecture, improved neurocognitive func- tion, and reversal of many of the metabolic and cardiovascular effects of OSA. Adherence to PAP therapy is the major limitation of its effectiveness. Initial acceptance rates of PAP therapy of 70% might decrease to 50% or less over time. Complications of PAP therapy are uncommon and can be managed with therapy modification. The most common complications are mechanical and include nasal obstruction or stuffiness, facial pressure ulcers, and skin rash. Other complications are social or psychological in nature and are related to self-image and intimacy. The goal of PAP titration is to select the lowest airway pres- sure that eliminates all respiratory events, including apneas, hypopneas, arousals, and snoring, so that the RDI decreases to less than 5 per hour, with acceptable oxygenation (SpO2 ≥ 90%), and an acceptable mask leak level (Fig. 1.7). 21:49 W R 1 2 3 4 B R F L 90 80 70 60 50 Des 20 AHI=108 AHI=11.7 AHI=9.5 AHI=4.0 8 7 6 5 4 CPAP 3 2 1 Hours 16 12 8 4 0 100 HYP APN 22:49 23:49 00:49 01:49 Sleep Stages Position Apneas and Hypopneas Sao2 02:49 03:49 04:49 05:37 Fig. 1.7 All-night hypnogram demonstrating optimal continuous positive airway pressure ( CPAP ) titration. This is an all-night hypnogram of about 8-h duration that represents a split-night PSG study, in which the first half of the study is used for diagnosis and the second half for therapeutic titration of CPAP . The time in hours is listed at the bottom of the graph. The first panel from the bottom shows the CPAP level. During the first half of the study, the diagnostic PSG study yielded an AHI of 108/h. Toward the middle of the study, CPAP titration started at 6 cm H2O, then increased to 8 cm H2O, which resulted in reducing the AHI to 11.7/h; progressive increases in CPAP and decreases in AHI follow. The second panel from the bottom shows the oxygen satura- tion ( Sa O 2 ) during the night and demonstrates the frequent desaturation episodes during the first half of the night to Sa O 2 levels of 75%, and resolution during CPAP titration. The third panel from the bottom shows the apnea and hypopnea events, with frequent occurrence of these events during the first half of the night (AHI 108/h) and the significant resolution of these events by CPAP (AHI 4/h). The fourth panel from the bottom shows the patient position, which demonstrates that the patient avoided the supine position ( labeled B for back ) during the first half of the night and only maintained the supine position during the last period of sleep during the CPAP titration. The top panel shows the sleep stage with the REM sleep period indicated in black. It shows that CPAP titration achieved adequate resolution of the respiratory events even during the REM sleep period. The patient was not able to achieve any deep sleep (N3) during the first half of the night, while compensatory N3 sleep was reached during CPAP titration. N3 normally occurs during the first third of the night. This CPAP titration is considered optimal because it was the lowest level of CPAP that reduced AHI to 5/h or less and achieved that reduction during all sleep positions, including supine, and during all stages of sleep, including REM. 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Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 1 O U T L I N E Obstructive Sleep Apnea (OSA), 1 Adult Obstructive Sleep Apnea, 1 Diagnosing OSA in Adults, 3 Pathogenesis of OSA, 4 Cardiovascular Consequences, 4 Neurocognitive Consequences, 4 Metabolic Consequences, 4 Mortality and Economic Consequences, 4 Treatment of Adult OSA, 5 Pediatric Obstructive Sleep Apnea, 9 Central Sleep Apnea (CSA) Syndromes, 10 CSA With Cheyne-Stokes Breathing, 10 CSA due to a Medical Disorder Without Cheyne-Stokes Breathing, 10 CSA due to High-Altitude Periodic Breathing, 11 CSA due to a Medication or Substance, 11 Primary CSA, 12 Primary CSA of Infancy, 12 Treatment-Emergent CSA, 13 Sleep-Related Hypoventilation (SRHV) Disorders, 13 Obesity Hypoventilation Syndrome, 13 Congenital Central Alveolar Hypoventilation Syndrome, 13 Late-Onset Central Hypoventilation Syndrome With Hypothalamic Dysfunction, 13 Idiopathic Central Alveolar Hypoventilation, 13 SRHV due to a Medication or Substance, 14 SRHA due to a Medical Disorder, 14 Sleep-Related Hypoxemia Disorder, 14 Isolated Symptoms and Normal Variants, 14 Snoring, 14 Catathrenia, 14 Effect of Sleep on Control of Breathing, 14 Control of Upper Airway Patency, 15 Effect of Sleep on Control of Upper Airway Patency, 15 Perioperative Considerations in Patients With Sleep-Related Breathing Disorder, 15 Practice Guidelines for Perioperative Management of Patients With OSA, 15 Key Points, 17 Resources, 17 Jean Gabriel Charchaflieh Sleep-Related Breathing Disorder 1 Among the six categories of sleep disorders classified by the International Classification of Sleep Disorders (ICSD-3), sleep- related breathing disorder (SRBD) is second only to insomnia in frequency of occurrence and is the most common sleep disorder encountered in sleep medicine labs. SRBD can refer to an exclusively sleep-related disorder or sleep-induced exacerbation of a baseline persistent disorder. SRBDs are divided into four main categories: obstructive sleep apnea (OSA) disorders, central sleep apnea (CSA) syndromes, sleep-related hypoventilation (SRHV) disorders, and sleep- related hypoxemia (SRHO) disorders. OSA accounts for about 90% of SRBDs, CSA syndromes for 9%, and SRHV/SRHO dis- orders for 1% (Box 1.1). Standardized classifications of sleep disorders serve as a tool for disease definition, establishing criteria for diagnosis and treatment, compiling epidemiologic data, and managing coding and billing. OBSTRUCTIVE SLEEP APNEA Adult Obstructive Sleep Apnea OSA refers to decreased or absent airflow in the presence of muscular inspiratory effort. On the polysomnography (PSG) recording, obstructive apnea events can take one of three forms: apnea, hypopnea, or respiratory effort–related arousals (RERAs) (Figs. 1.1 and 1.2). Defining these events depends on recordings of airflow, thoracic and abdominal respiratory muscle movement (Mvmt), oxygen saturation (SpO2), and electroencephalography (EEG). A duration of O U T L I N E Obstructive Sleep Apnea (OSA), 1 Adult Obstructive Sleep Apnea, 1 Diagnosing OSA in Adults, 3 Pathogenesis of OSA, 4 Cardiovascular Consequences, 4 Neurocognitive Consequences, 4 Metabolic Consequences, 4 Mortality and Economic Consequences, 4 Treatment of Adult OSA, 5 Pediatric Obstructive Sleep Apnea, 9 Central Sleep Apnea (CSA) Syndromes, 10 CSA With Cheyne-Stokes Breathing, 10 CSA due to a Medical Disorder Without Cheyne-Stokes Breathing, 10 CSA due to High-Altitude Periodic Breathing, 11 CSA due to a Medication or Substance, 11 Primary CSA, 12 Primary CSA of Infancy, 12 Treatment-Emergent CSA, 13 Sleep-Related Hypoventilation (SRHV) Disorders, 13 Obesity Hypoventilation Syndrome, 13 Congenital Central Alveolar Hypoventilation Syndrome, 13 Late-Onset Central Hypoventilation Syndrome With Hypothalamic Dysfunction, 13 Idiopathic Central Alveolar Hypoventilation, 13 SRHV due to a Medication or Substance, 14 SRHA due to a Medical Disorder, 14 Sleep-Related Hypoxemia Disorder, 14 Isolated Symptoms and Normal Variants, 14 Snoring, 14 Catathrenia, 14 Effect of Sleep on Control of Breathing, 14 Control of Upper Airway Patency, 15 Effect of Sleep on Control of Upper Airway Patency, 15 Perioperative Considerations in Patients With Sleep-Related Breathing Disorder, 15 Practice Guidelines for Perioperative Management of Patients With OSA, 15 Key Points, 17 Resources, 17 Jean Gabriel Charchaflieh Sleep-Related Breathing Disorder 1 Among the six categories of sleep disorders classified by the International Classification of Sleep Disorders (ICSD-3), sleep- related breathing disorder (SRBD) is second only to insomnia in frequency of occurrence and is the most common sleep disorder encountered in sleep medicine labs. SRBD can refer to an exclusively sleep-related disorder or sleep-induced exacerbation of a baseline persistent disorder. SRBDs are divided into four main categories: obstructive sleep apnea (OSA) disorders, central sleep apnea (CSA) syndromes, sleep-related hypoventilation (SRHV) disorders, and sleep- related hypoxemia (SRHO) disorders. OSA accounts for about 90% of SRBDs, CSA syndromes for 9%, and SRHV/SRHO dis- orders for 1% (Box 1.1). Standardized classifications of sleep disorders serve as a tool for disease definition, establishing criteria for diagnosis and treatment, compiling epidemiologic data, and managing coding and billing. OBSTRUCTIVE SLEEP APNEA Adult Obstructive Sleep Apnea OSA refers to decreased or absent airflow in the presence of muscular inspiratory effort. On the polysomnography (PSG) recording, obstructive apnea events can take one of three forms: apnea, hypopnea, or respiratory effort–related arousals (RERAs) (Figs. 1.1 and 1.2). Defining these events depends on recordings of airflow, thoracic and abdominal respiratory muscle movement (Mvmt), oxygen saturation (SpO2), and electroencephalography (EEG). A duration of
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 2 CHAPTER 1 Sleep-Related Breathing Disorder 10 seconds or more is required to score any of these respira- tory events. Apnea On the PSG, apnea is diagnosed using an oral/nasal thermal sen- sor that detects airflow and displays a nonlinear signal. Apnea is defined as a 90% or more reduction in the amplitude of airflow signal from the thermal airflow sensor on the PSG, independent of oxygen saturation values. Defining the type of apnea event requires examining the respiratory effort channel on the PSG montage, in addition to the airflow channel. Based on the record- ings of the coinciding respiratory effort channel and the airflow channel, the apnea event is classified into one of three types: • Obstructive apnea event: There is breathing effort during the apnea. • Central apnea event: There is no breathing effort during the apnea. • Mixed apnea event: The apnea event starts as a central apnea and ends as an obstructive apnea. Hypopnea Hypopnea is defined based on the findings of two or three PSG channels, using a nasal pressure sensor to detect airflow. The nasal pressure sensor is used for scoring hypopnea because its BOX 1.1 Sleep-Related Breathing Disorders According to ICSD-3 Obstructive sleep apnea (OSA) disorders 1. OSA, adult 2. OSA, pediatric Central sleep apnea (CSA) syndromes 1. CSA with Cheyne-Stokes breathing (CSB) 2. CSA due to a medical disorder without CSB 3. CSA due to high-altitude periodic breathing 4. CSA due to a medication or substance 5. Primary CSA 6. Primary CSA of prematurity 7. Treatment-emergent CSA Sleep-related hypoventilation (SRHV) disorders 1. Obesity hypoventilation syndrome 2. Congenital central alveolar hypoventilation syndrome 3. Late-onset central hypoventilation with hypothalamic dysfunction 4. Idiopathic central alveolar hypoventilation 5. SRHV due to a medication or substance 6. SRHV due to a medical disorder Sleep-related hypoxemia disorder Isolated symptoms and normal variants 1. Snoring 2. Catathrenia Flow RCMvmt ABMvmt A B C Fig. 1.1 Polysomnography features of the three types of apnea events. (A) Obstructive apnea event. The top Flow channel demonstrates no airflow while the bottom two channels demonstrate respiratory efforts in the chest ( RCMvmt ) and abdomen ( ABMvmt ). (B) Central apnea event. The top Flow channel demonstrates no airflow while the bottom two channels demonstrate no respiratory efforts in the chest ( RCMvmt ) and abdomen ( ABMvmt ). (C) Mixed apnea event. The apnea event starts as a central apnea event (no Flow and no effort) and ends as an obstructive apnea event (no Flow with respiratory muscle effort). Airflow 10 sec Central apnea Obstructive apnea Respiratory effort Fig. 1.2 The relation between airflow and respiratory effort in apnea events. In the central apnea event, the airflow channel shows a cessation of airflow for more than 10 s, and the respiratory effort channel shows no respiratory effort during the entire apnea period. In the obstructive apnea event, the airflow channel shows cessation of airflow, and the respiratory effort channel shows persistent and progressively increasing effort during the entire apnea period. ICSD , International Classification of Sleep Disorders
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 3 CHAPTER 1 Sleep-Related Breathing Disorder signal is linear, which allows diagnosis of less severe reduction in airflow than the 90% that is used to diagnose apnea. The nasal pressure sensor is not used for apnea scoring because it may be misleading in a mouth breather. The sensor for oxygen satura- tion (SpO2) is a pulse oximeter with signal averaging of 3 sec- onds (3 Hz) or less. Any coinciding arousal is diagnosed using an EEG recording. The duration requirement for hypopnea is 10 seconds or more. Hypopnea events have two definitions, rec- ommended and alternative. The recommended definition of hypopnea is a drop of 30% or more in the amplitude of the nasal pressure sensor that lasts for 90% or more of the event and is associated with a 4% or more drop in SpO2. This definition of hypopnea is simplified as the 30-4 rule. It is the recommended definition by the American Academy of Sleep Medicine (AASM) and the definition accepted by Medicare; there- fore it is also known as the Medicare hypopnea rule. This definition requires examining two PSG channels: the airflow as measured by the nasal pressure sensor and SpO2 (Fig. 1.3). An alternative definition of hypopnea is a drop of 50% or more in the amplitude of airflow as measured by the nasal pres- sure sensor that lasts 90% or more of the event and is associated with either a 3% or more drop in SpO2 or EEG arousal. EEG arousal refers to an abrupt shift in EEG frequency lasting more than 3 seconds and preceded by more than 10 seconds of stable EEG and has different rules for scoring based on sleep stage (rapid eye movement [REM] or non-REM [NREM] sleep). In PSG sleep studies, arousal refers to EEG arousal, whereas awak- ening refers to clinical awakening. This alternative definition of hypopnea is simplified as the 50-3a rule, with the a standing for arousal . This is considered an alternative definition by AASM and is not accepted by Medicare for the purposes of scoring respiratory events, diagnosing OSA, or coding and billing. The total number of apnea and hypopnea events during a PSG study is used to calculate an apnea-hypopnea index (AHI), defined as the number of apnea and hypopnea events per hour of sleep. The PSG-derived AHI is used in the diag- nosis of sleep apnea disorders, assessing severity, titrating positive airway pressure (PAP) therapy, evaluating the thera- peutic efficacy of various interventions, assessing the diag- nostic utility of other tools and surveys, and establishing a severity-outcome relationship when studying the association between sleep apnea, or its treatment, and a given outcome. Respiratory Effort–Related Arousals RERA is determined based on the findings of three PSG chan- nels: airflow, respiratory effort, and EEG. RERA is defined as a limitation in the airflow followed by an arousal on the EEG channel, with the limitation in airflow being defined either by flattening of the airflow in a way that does not meet the criteria for apnea or hypopnea or by increased respiratory effort. Unlike apnea and hypopnea, the definition of RERA lacks numeric cri- teria, other than a duration of 10 seconds or more. Using RERA events as part of scoring respiratory events on the PSG is an option, not a recommendation. When RERA events are added to the apnea and hypopnea events, a respiratory disturbance index (RDI) is calculated, rather than an AHI. The ICSD-3 allows the use of RDI as a substitute for AHI in the diagnosis of OSA. Medicare allows only the use of AHI and allows only one rule for the definition of hypopnea. Diagnosing OSA in Adults The diagnosis of OSA in adults can be based either on the presence of an AHI of 15 or above alone or on the combina- tion of an AHI of 5 or above plus clinical signs and symptoms (associated sleepiness, fatigue, insomnia [more common in females than males], snoring, subjective nocturnal respira- tory disturbance, or observed apnea) or associated medical and psychiatric disorders (hypertension [HTN, including during pregnancy], coronary artery disease, atrial fibrillation [AF], congestive heart failure [CHF], stroke, diabetes melli- tus, cognitive dysfunction, or mood disorder [more common in females than males]). The term obstructive sleep apnea syn- drome (OSAS) refers to the combination of an AHI of 5 or above and daytime somnolence that is present for 2 or more Press 0 128 128 90 95 95 94 94 94 93 92 90 92 92 90 86 96 9 128 128 Flow Chest Micro ABD SaO2 Fig. 1.3 Polysomnography features of obstructive hypopnea event. The top channel (Press) displays airflow as measured by a nasal pressure transducer. It demonstrates 30% or more reduction from baseline in the amplitude of the signal that lasts for 90% or more of the event, which lasts 10 or more seconds. The channel Flow displays airflow as measured by a thermal sensor. It demonstrates less reduction from baseline in the amplitude of the signal. The channel Sa O 2 demonstrates a drop in oxygen saturation by 4%, from 90% to 86%. Thus the findings on the two channels of airflow pressure and oxygen saturation meet the definition of the 30-4 rule for hypopnea. The bottom channels (Chest and ABD) display chest and abdomen movement as measured by inductance plethysmography. They demonstrate continuous respiratory effort during the hypop- nea event, which defines it as an obstructive hypopnea.
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 4 CHAPTER 1 Sleep-Related Breathing Disorder days/week. Based on this definition, the prevalence of OSAS is about 2% for females and 4% for males, while the prevalence of AHI of 5 or above alone is about 9% in females and 24% in males. After menopause, the prevalence of OSA in females equals that of males. In using AHI to assess the severity of OSA, three grades are defined: mild (AHI 5–15), moderate (AHI 15–30), and severe (AHI ≥ 30). Common comorbidities of OSA include difficult-to-control HTN, AF, coronary artery disease, myocardial infarction, CHF, stroke, type 2 diabetes mellitus (T2DM), hypothyroidism, Graves disease, acromegaly, nonalcoholic steatohepatitis (NASH), and polycystic ovarian syndrome (PCOS). Females with OSA are more likely than males to present with atypical symptoms including insomnia, thyroid disease, depression, and antidepressant use. Levels of Sleep Apnea Testing There are four levels of sleep apnea testing. Level I is attended comprehensive (7–12 channels) PSG, the gold standard. Level II is an unattended comprehensive PSG, which is rarely done. Level III is unattended four-channel portable monitoring, including airflow, respiratory effort, and Sao2, with additional electrocardiography (ECG) and/or actigraphy. Level III is commonly used to diagnose OSA in someone with high pre- test probability and no comorbidity. It cannot rule out OSA, lacks information about sleep stage and body position, and tends to underestimate AHI because it uses recording time as the denominator, which is usually longer than sleep time. Level IV is home monitoring of SaO2 with or without airflow. Level IV cannot diagnose OSA because it lacks a respiratory effort channel, but it can provide an oxygen desaturation index (ODI), the hourly rate of decreased SaO2 of 3% or more, and T-90, the total time spent with SaO2 of 90% or less. Level IV oximetry can be enhanced by adding both actigraphy, which measures wrist activity as an indication of sleep state, and peripheral arterial tonometry (PAT). PAT measures finger plethysmography as an indication of sympathetic α -adrenergic activity, which in turn is used as a marker of apnea, hypopnea, and hypoxia events. Pathogenesis of OSA Direct physiologic mechanisms involved in the pathogenesis of OSA include anatomic and functional upper airway obstruction (UAO), decreased respiratory-related EEG arousal response, and instability of the ventilatory response to chemical stimuli. The apnea episodes are resolved as a result of three events: (1) increased muscular activity at the upper airway muscles that restores airway patency; (2) increased muscular activity at the thoracoabdominal respiratory muscles that generates increased negative intrathoracic pressure; and (3) EEG arousal, which stimulates central respiratory centers. PSG recording can help elucidate the sequence of, and relationships between, events during both apnea episodes and their resolution (Fig. 1.4). Cardiovascular Consequences Cardiovascular pathophysiologic consequences of OSA are the result of hypoxia/hypercarbia, EEG arousal, and increased inspiratory efforts (Fig. 1.5). OSA-induced hypoxia and reoxygenation cycles activate redox-sensitive genes, oxidative stress, inflammatory pro- cesses, the sympathetic nervous system, and the coagulation cascade, all of which can contribute to endothelial dysfunction and ultimately to systemic HTN, pulmonary HTN, atherosclerosis, right and left ventricular systolic and diastolic dysfunction, coronary artery dis- ease, CHF, AF, stroke, and sudden cardiac death. Pathophysiologic consequences of OSA contribute to the dif- ference in timing of cardiac death between patients with OSA and the general population, in whom peak incidence of death due to cardiac arrhythmias and ischemia occurs during the daytime (06:00–12:00). In the patient with OSA, the peak inci- dence of death due to cardiac arrhythmias and ischemia occurs at night (00:00–06:00). The causal relationship between OSA and cardiovascular mor- bidity and mortality is supported by observational studies dem- onstrating a dose-response relationship between severity of OSA and observed morbidity and mortality, positive effect of OSA treatment, and dose-response relationship between efficacy of treatment and observed morbidity and mortality. Outcomes for which such relationships have been found include all-cause mor- tality; a composite outcome of stroke, transient ischemic attack, and all-cause mortality; stroke; coronary artery disease; HTN; and need for repeat revascularization after percutaneous coro- nary intervention. The causal relationship between stroke and OSA may be bidirectional, as stroke is considered both a risk fac- tor for and an outcome of OSA. The causal relationship between OSA and cardiovascular and metabolic disorders may also be bidirectional, or noncausal due to shared risk factors (Fig. 1.6). Neurocognitive Consequences Repeated EEG arousal, clinical awakening, and disrupted sleep architecture (decreased deep sleep and increased lighter sleep) induce a state of overall slowing of the EEG, chronic sleep depri- vation, excessive daytime sleepiness (EDS), increased number of lapses on psychomotor vigilance task testing, decrease in cogni- tion and performance (attention, memory, executive function- ing), decreased quality of life, mood disorders, and increased rates of motor vehicle collisions. Metabolic Consequences Pathophysiologic mechanisms for metabolic derangements in OSA include hypoxic injury, systemic inflammation, increased sympathetic activity, alterations in hypothalamic-pituitary-adre- nal function, and hormonal changes. Metabolic derangements of OSA lead to worsening of OSA and produce a vicious perpetuat- ing cycle. Metabolic derangements and disorders linked to OSA include insulin resistance, glucose intolerance, dyslipidemia, T2DM, central obesity, and metabolic syndrome. OSA is com- mon in patients with NASH (50%) and PCOS (30%–50%). Sleep deprivation has been implicated as a risk factor for common can- cers, including cancers of the breast, colon, and prostate. Mortality and Economic Consequences The mortality impact of OSA is evident in moderate-to-severe OSA. The economic impact is due to increased healthcare
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 5 CHAPTER 1 Sleep-Related Breathing Disorder utilization, decreased productivity, and years of potential life lost. It is estimated that the yearly incidence of OSA-related motor vehicle accidents alone costs approximately $16 billion and 1400 lost lives. It is also estimated that treating all drivers with OSA with positive airway therapy (at a cost of ~$3 bil- lion/year) would save about $11 billion and 1000 lives. OSA has a significant public health impact due to its high prevalence (estimated 25 million in the United States), high proportion of undiagnosed cases (80% for males and 90% for females), and association with significant morbidity, mortality, and decreased quality of life. Treatment of Adult OSA Treatment of OSA includes the use of devices, surgery, and med- ications. All modes of treatment should include patient educa- tion and long-term follow-up. General measures that should be applied with all modes of therapy include reducing modifiable risk factors and treating comorbid conditions. Potentially modi- fiable risk factors include alcohol consumption, use of sedative medication, cigarette smoking, obesity, nasal obstruction, and tonsil grade ( ≥ 3). General measures in the treatment of OSA include weight reduction, avoiding alcohol and central nervous system (CNS) depressant drugs, improving sleep hygiene, and refraining from driving when sleepy. In extreme cases of sleepi- ness (e.g., patients reporting the maximum score of 24 on the Epworth sleepiness scale [ESS]), patients should be forbidden from driving unless they are treated and their OSA and ESS are improved. Positive Airway Pressure Therapy for OSA PAP therapy is the most commonly studied and prescribed therapy for OSA as well as for some forms of central and mixed sleep apnea. PAP therapy is considered tier 1 therapy for OSA. The most common form of PAP is continuous PAP (CPAP). Other forms of PAP therapy consist of various electronic modifications of PAP delivery patterns such as bilevel PAP (BPAP), autotitrated PAP (APAP), and adaptive servo ventila- tion (ASV). The three elements of a PAP device are the flow generator, a connecting hose, and a patient interface, which EMGgg (Volts) 5.0 2.5 0.0 –2.5 –5.0 50 0 –50 50 25 0 –25 –50 –2 100 95 90 85 80 0 –50 2 0 EMGsub ( V) EEG ( V) Pepi (cm H 2 O) Flow (L/sec) Snoring Snoring Oxygen desaturation Arousal threshold APNEA AROUSAL 20 sec Sao 2 (%) Fig. 1.4 Experimental polysomnography (PSG) in obstructive sleep apnea (OSA) showing sequence and resolution of apnea events. This experimental PSG in a patient with OSA includes recordings of electromy- ography (EMG) of upper airway muscles (genioglossus [ EMGgg ] and submental muscles [ EMGsub ]), elec- troencephalography ( EEG ), intrathoracic pressure approximated by epiglottic catheter ( Pepi ), nasal airflow ( Flow ) by thermal sensor, and oxygen saturation ( Sa O 2 ) by pulse oximetry with a minimal sampling rate of 10 Hz. The top channel ( EMGgg ) demonstrates progressively increased EMGgg activity (amplitude) until this increased activity reaches a sufficient level to open the upper airway and allow breathing (Flow) to resume. The middle channel (Pepi) demonstrates a progressive increase in respiratory muscle effort until breathing (Flow) resumes. The increase in respiratory muscle effort is considered the primary stimulus for EEG arousal, through stimulation of the mechanoreceptors in the chest muscles, which provide input both to the medullary respiratory centers and the wake/sleep neurochemical pathways. The EEG channel shows that the occur- rence of the EEG arousal occurs immediately following the peaks in EMGgg and Pepi and coincides with the resumption of breathing as demonstrated by nasal airflow (Flow). The airflow (Flow) thermal sensor channel shows the resumption of breathing at the time of EEG arousal, immediately after the peaks of upper airway (EMGgg) and respiratory (Pepi) muscle activity. The oxygen saturation channel (Sa O 2 ) demonstrates the lag time between ventilation and oxygenation, which leads to paradoxical restoration of oxygen saturation during the apnea episode, and the occurrence of oxygen desaturation during the resumption of the breathing period. The increased activity of EMG, Pepi, and EEG at the end of the apnea period results in a subsequent period of hyperpnea. The cyclic alteration of periods of apnea and hyperpnea disrupts the chemoreceptor stability of the respiratory control system and leads to a periodic breathing pattern similar to that encountered in several forms of central sleep apnea.
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 6 CHAPTER 1 Sleep-Related Breathing Disorder has three forms: nasal mask, nasal pillows, and full-face mask. Nasal masks are better tolerated than oronasal masks and are associated with better adherence, require lower CPAP levels, and result in lower residual AHI. Technologic advancements have allowed a reduction in the size and the noise level of flow generators as well as the options of PAP delivery patterns. The aim of these modifications is to enhance individual customiza- tion of PAP therapy and therefore improve adherence to and effectiveness of the therapy. Critical steps in the application of PAP therapy are patient education, mask fitting, and titration of Cardiac dysfunction Endothelial dysfunction syndrome RV afterload, RVH Heart rate MVO 2 O 2 delivery Ppl Redux gene attraction, oxidation stress inflammation, hypercoagulability PO 2 PCO2 Hypoxic and hypercapnic pulmonary vasoconstriction Sympathetic activation Parasympathetic withdrawal Arousals Sleep apnea/ hypopnea Transmural pressure of cardiac chambers, aorta, and pulmonary microvascular bed BP and LV afterload: MVO 2 , myocardial toxicity, arrythmias Aortic dilation Lung H2O Changes in RV and LV afterload, MVO2 arrythmias Fig. 1.5 Schematic representation of cardiovascular pathophysiologic consequences of obstructive sleep apnea. Male sex Age 40–70 y Familial aggregation Suspected Genetics Smoking Menopause Alcohol use before sleep Nighttime nasal congestion Demographic correlates of increased OSA prevalence Established Body habitus Overweight and obesity Central body fat distribution Large neck girth Craniofacial and upper airway abnormalities Risk factors Symptoms Habitual, loud snoring Nocturnal breathing pauses, choking, gasping Excessive daytime sleepiness OSA Cardiovascular and cerebrovascular disease Hypertension Coronary artery disease Myocardial infarction Congestive heart failure Stroke Diabetes and the metabolic syndrome Problems with daytime functioning Daytime sleepiness Motor vehicle crashes Psychosocial problems Decreased cognitive function Reduced quality of life Outcomes and/or comorbid conditions Fig. 1.6 Schematic representation of the overlap between risk factors, symptoms, and outcomes of obstruc- tive sleep apnea (OSA). There is significant overlap between what are considered risk factors, symptoms, and outcomes in OSA. Overlap can be seen between symptoms (e.g., excessive daytime sleepiness [EDS]) and outcomes. This overlap may be a causal association or due to shared risk factors of chronic sleep deprivation and disrupted sleep architecture. Overlap can be observed between risk factors and outcomes in the form of metabolic and cardiovascular disorders. This overlap may represent reciprocal causal association or noncausal association due to shared risk factors.
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 7 CHAPTER 1 Sleep-Related Breathing Disorder PAP therapy. Effective PAP titration can result in the elimina- tion of apnea events and normalization of oxygen saturation. Long-term effects of effective PAP therapy include improved sleep efficacy and architecture, improved neurocognitive func- tion, and reversal of many of the metabolic and cardiovascular effects of OSA. Adherence to PAP therapy is the major limitation of its effectiveness. Initial acceptance rates of PAP therapy of 70% might decrease to 50% or less over time. Complications of PAP therapy are uncommon and can be managed with therapy modification. The most common complications are mechanical and include nasal obstruction or stuffiness, facial pressure ulcers, and skin rash. Other complications are social or psychological in nature and are related to self-image and intimacy. The goal of PAP titration is to select the lowest airway pres- sure that eliminates all respiratory events, including apneas, hypopneas, arousals, and snoring, so that the RDI decreases to less than 5 per hour, with acceptable oxygenation (SpO2 ≥ 90%), and an acceptable mask leak level (Fig. 1.7). 21:49 W R 1 2 3 4 B R F L 90 80 70 60 50 Des 20 AHI=108 AHI=11.7 AHI=9.5 AHI=4.0 8 7 6 5 4 CPAP 3 2 1 Hours 16 12 8 4 0 100 HYP APN 22:49 23:49 00:49 01:49 Sleep Stages Position Apneas and Hypopneas Sao 2 02:49 03:49 04:49 05:37 Fig. 1.7 All-night hypnogram demonstrating optimal continuous positive airway pressure ( CPAP ) titration. This is an all-night hypnogram of about 8-h duration that represents a split-night PSG study, in which the first half of the study is used for diagnosis and the second half for therapeutic titration of CPAP . The time in hours is listed at the bottom of the graph. The first panel from the bottom shows the CPAP level. During the first half of the study, the diagnostic PSG study yielded an AHI of 108/h. Toward the middle of the study, CPAP titration started at 6 cm H2O, then increased to 8 cm H2O, which resulted in reducing the AHI to 11.7/h; progressive increases in CPAP and decreases in AHI follow. The second panel from the bottom shows the oxygen satura- tion ( Sa O 2 ) during the night and demonstrates the frequent desaturation episodes during the first half of the night to Sa O 2 levels of 75%, and resolution during CPAP titration. The third panel from the bottom shows the apnea and hypopnea events, with frequent occurrence of these events during the first half of the night (AHI 108/h) and the significant resolution of these events by CPAP (AHI 4/h). The fourth panel from the bottom shows the patient position, which demonstrates that the patient avoided the supine position ( labeled B for back ) during the first half of the night and only maintained the supine position during the last period of sleep during the CPAP titration. The top panel shows the sleep stage with the REM sleep period indicated in black. It shows that CPAP titration achieved adequate resolution of the respiratory events even during the REM sleep period. The patient was not able to achieve any deep sleep (N3) during the first half of the night, while compensatory N3 sleep was reached during CPAP titration. N3 normally occurs during the first third of the night. This CPAP titration is considered optimal because it was the lowest level of CPAP that reduced AHI to 5/h or less and achieved that reduction during all sleep positions, including supine, and during all stages of sleep, including REM.
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 8 CHAPTER 1 Sleep-Related Breathing Disorder Suggested mechanisms of action of PAP therapy include (1) increasing the pharyngeal transmural pressure (pneumatic splint effect), (2) reducing pharyngeal wall thickness and airway edema, (3) increasing airway tone by mechanoreceptor stimula- tion, and (4) increasing end-expiratory lung volume and pro- ducing a tracheal tug effect. Manual in-laboratory, PSG-guided, full-night titration of fixed PAP is considered the standard. APAP is an acceptable alternative for the treatment of uncom- plicated moderate-to-severe OSA that is associated with snor- ing. APAP consists of a single variable PAP that is maintained during both inhalation and exhalation, with variation from breath to breath according to the presence or absence of apnea, hypopnea, or snoring. APAP mode may improve patient adher- ence and may minimize the average airway pressure by allowing higher PAP during periods of greater obstruction, such as in the supine position and during REM sleep, and lower PAP during periods of lesser obstruction. Depending on the examined outcome, four levels of evidence are found in the literature regarding the efficacy of PAP therapy in OSA. There is clear evidence for reducing AHI; strong evi- dence for increasing deep sleep and decreasing EEG arousals; less clear evidence for improved sleep architecture; and equivo- cal evidence for improved daytime sleepiness, neurobehavioral performance, psychological functioning, quality of life, and car- diovascular outcomes, especially HTN. One example of estab- lishing the efficacy of CPAP therapy in increasing deep sleep is through the demonstration of CPAP-induced restoration of the nocturnal surge in the release of growth hormone (GH) during deep sleep, also known as slow-wave sleep or non-REM sleep stage 3 (N3). Oral Appliance Therapy for OSA Oral appliance (OA) therapy is considered a second-tier treat- ment in the management of OSA. The most common forms of OA are mandibular advancement devices (MADs) and tongue retaining devices (TRDs). MADs are usually custom-made devices that are fitted to the teeth like a mouth guard and act to advance and stabilize the mandible to increase upper air- way capacity. TRDs advance and retain the tongue in an ante- rior position by holding it with a suction cup placed over the front teeth. OA therapy is indicated for the treatment of snor- ing, mild-to-moderate OSA, and select cases of moderate-to- severe OSA, such as predominantly supine OSA or OSA due to a proportionally large tongue relative to oral cavity capacity. OA therapy is less effective than PAP therapy in reducing AHI, but may be better tolerated and preferred by patients, and has been shown to be effective in reducing sleep interruption, EDS, neurocognitive impairment, and cardiovascular complications. Side effects include excessive salivation, temporomandibular joint discomfort, and long-term occlusion changes. OA therapy should be provided jointly by a qualified dentist and sleep medi- cine physician with appropriate follow-up testing to document maintained efficacy. Other Device Therapy for Obstructive Sleep Apnea Many forms of device therapy continue to be introduced for the treatment of OSA, with a wide range of complexity, invasiveness, price, and need for medical prescription and application. Nasal expiratory PAP is a diaphragm-like membrane applied to both nares to provide resistance to exhalation and stent the upper airway. Oral pressure therapy is a mouthpiece attached to a vac- uum source, which pulls the soft palate forward and increases the size of the pharyngeal cavity. In the postoperative setting, in patients with untreated moderate-to-severe OSA, a combi- nation of high-flow nasal cannula (20 L/min with 40% oxygen) and 30-degree head of bed elevation was found to have a high acceptance rate (96%) and efficacy (38% reduction in AHI and improved nadir SpO2 by 5%). Airway Surgical Therapy for OSA Currently, airway surgical therapy for OSA in adults is consid- ered third tier. Airway surgical therapy includes tracheostomy, maxillomandibular advancement (MMA), laser-assisted uvu- lopalatoplasty (LAUP), uvulopalatopharyngoplasty (UPPP), radiofrequency ablation, and palatal implants. Most of these procedures are considered options for the treatment of OSA when other treatment options are lacking, have failed, or are refused, with the exception of LAUP, which is graded as not routinely recommended. MMA may be associated with better safety and efficacy than UPPP. Implantable hypoglossal nerve stimulation consists of implant- ing a hypoglossal nerve stimulator in the chest with sensing leads between the internal and external intercostal muscles. The leads detect breathing and signal the device to stimulate the hypoglos- sal nerve during inhalation, which results in the enlargement of upper airway capacity. The system is turned on by the patient before going to sleep and turned off upon awakening. Bariatric Surgery for OSA Bariatric surgery aims to restrict caloric intake, absorption, or both. Bariatric surgery can be a sole therapy or adjunct to PAP therapy in patients with severe obesity associated with OSA or obesity hypoventilation syndrome (OHS). Screening for OSA should be performed in all patients undergoing bariatric surgery. Adjunct Medical Therapy for OSA Adjunct medical therapy for OSA can be considered with any of the three tiers of OSA treatment: PAP therapy, OA, or surgery. Adjunct therapy includes diet, exercise, positional therapy, avoidance of alcohol and sedatives before sleep, supplemental oxygen, and pharmacologic therapy. Positional therapy consists of devices that discourage or prevent the patient from sleeping in the supine position. Coexisting medi- cal conditions should be treated, including hypothyroidism and acromegaly. In hypothyroidism, hormonal therapy can attenuate EDS, OSA, respiratory insufficiency, and bradycar- dia. CNS stimulants such as modafinil and pitolisant can be used to treat residual EDS only in conjunction with effective PAP therapy and in the absence of an identifiable cause of residual EDS. Patients may often self-medicate with caffeine to treat EDS. Supplemental oxygen should be used to treat residual hypoxia ( ≤ 88%) that persists despite adequate treat- ment of OSA. In the perioperative setting, the use of analgesic
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 9 CHAPTER 1 Sleep-Related Breathing Disorder modalities that produce minimal CNS depression is preferred, in conjunction with providing postoperative supplemental oxygen, continuous SpO2 monitoring, and, preferably, ventila- tion monitoring. Gabapentinoids, as analgesic adjuncts in the perioperative period, do not significantly reduce opioid use or CNS depression. In addition, they are associated with the risk of significant respiratory depression. Pediatric Obstructive Sleep Apnea An age cutoff for applying pediatric or adult rules for OSA is not clearly established. In general, pediatric rules are used for children below the age of 12 years and adults above the age of 18 years; either adult or pediatric rules apply for those 13 to 18 years of age. In children, OSA diagnosis can be based either on clinical findings alone or a combination of clinical and PSG findings. PSG findings are used to support the clinical diagnosis, assess the severity of OSA, and provide a basis for treatment recom- mendations. When clinical criteria alone are used to diagnose OSA, they must include one of these three findings: snoring, labored or obstructed breathing, or daytime consequences such as sleepiness, hyperactivity, or impaired performance. When PSG is performed for OSA assessment, there are dif- ferences between children and adults in terms of recommended modes of monitoring for the respiratory events, scoring respi- ratory events, and using PSG data to establish the OSA diag- nosis, grade its severity, and provide recommendations for treatment. When monitoring for respiratory events, it is rec- ommended that PSG in children include either end-tidal PCO2 (PETCO2) or transcutaneous PCO2 (PTCCO2) using properly calibrated and validated equipment. In children, a duration of two missed breaths is used to define a respiratory cycle, instead of the 10-second duration that is used in adults. Therefore an obstructive apnea event is defined as a 90% or greater reduc- tion in the amplitude of airflow (Flow) as measured by an oral/ nasal thermal sensor that lasts 90% of a respiratory cycle of two missed breaths, with continued respiratory effort throughout the period of decreased airflow. In defining hypopnea events in children, the 50-3a rule is used exclusively and is modified to include awakening in addition to EEG arousal. Awakening may occur in children before EEG arousal owing to the increased threshold for EEG arousal in children. Thus the 50-3a rule in children could be called the 50-3aa rule, with one a standing for arousal and another a for awakening . Using the two missed breaths duration and the 50-3aa rule, an obstructive hypopnea event is defined as a drop of 50% or more in the amplitude of airflow as measured by the nasal pressure sensor that lasts for 90% or more of the hypopnea event and is associated with either a 3% or greater drop in SpO2 or EEG arousal (or awakening). PSG criteria for OSA diagnosis in children consist of either of two findings: 1. One or more obstructive events per hour of sleep (i.e., an AHI ≥ 1), with an obstructive event being defined as obstruc- tive or mixed apnea or obstructive hypopnea. 2. Obstructive hypoventilation, manifested by PaCO2 greater than 50 mm Hg for more than 25% of sleep time, coupled with snoring, paradoxical thoracoabdominal movement, or flattening of the nasal airway pressure waveform. Proxies for PaCO2 include properly calibrated and validated PETCO2 or PTCCO2 monitors. Severity assessment of OSA in children is based on a com- bination of AHI, SpO2, and clinical findings. Severity of OSA is used as a basis for the necessity of treatment. 1. Mild OSA: AHI greater than 4 and no drop in SpO2. Treatment is indicated if there are daytime consequences, such as sleepiness, hyperactivity, or decreased performance. 2. Moderate OSA: AHI 5 to 10 and/or SpO2 less than 85%. Most children should be treated. 3. Severe OSA: AHI greater than 10, with SpO2 less than 85%, and clinical consequences. Treatment is strongly recommended. Common causes of OSA in children include enlarged tonsils and adenoids, obesity, and congenital abnormalities that affect the head and neck. These include laryngomalacia, Pierre-Robin syndrome, Down syndrome, achondroplasia, spinal muscle atrophy, Prader-Willi syndrome, Klippel-Feil syndrome, and Arnold-Chiari malformation type II. Overall frequency of OSA in children is similar to that in adults. Peak prevalence of about 2% to 3% occurs in the age group 2 to 6 years, coinciding with the period of lymphoid hyperplasia, which increases the likeli- hood of adenotonsillar hypertrophy. Pathophysiologic and clin- ical consequences of OSA in children include increased risk for poor growth, failure to thrive, developmental delays, decreased cognitive function, behavioral problems, hyperactivity, obesity, and pulmonary and systemic HTN. Treatment of OSA in children includes surgery, PAP therapy, and adjunct measures. In children, the variety of congenital syn- dromes and their comorbidities may require concurrent use of different modes of therapy and may present unique challenges. Surgical Therapy for OSA in Children In children, surgical therapy in the form of tonsillectomy and adenoidectomy is a first-line therapy because enlarged tonsils and adenoids are the most common cause of OSA. Additional orthopedic or plastic surgery may be required to correct ana- tomic abnormalities in certain congenital syndromes such as correction of the small mandible in Pierre-Robin syndrome or correction of anatomic abnormalities in Klippel-Feil syndrome, which include fusion of cervical vertebrae, cleft palate, and kyphoscoliosis. Positive Airway Pressure Therapy for OSA in Children Desensitization to PAP therapy in children is important in improving compliance and may have to be initiated prior to pressure titration. Proper functioning of the PAP therapy can be challenged by anatomic difficulties such as a short neck in Klippel-Feil syndrome, which can interfere with the proper fit- ting of the PAP device-patient interface. Adjunct Medical Therapy for OSA in Children Adjunct therapy includes diet, exercise, avoidance of seda- tives, supplemental oxygen, and pharmacologic therapy. In
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 10 CHAPTER 1 Sleep-Related Breathing Disorder Prader-Willi syndrome, the use of GH therapy for the treatment of small stature may worsen OSA and necessitate additional titration of the PAP therapy. CENTRAL SLEEP APNEA (CSA) SYNDROMES Central sleep apnea (CSA) refers to cessation or decrease in airflow in conjunction with absence or decrease in respiratory effort. This definition of CSA does not differentiate between lack of respiratory muscle activity due to neuronal dysfunction, neu- romuscular disease, or musculoskeletal deformities. Because of this lack of differentiation, CSA describes a variety of sleep apneas that are unrelated in their etiology and pathophysiology and can coexist with each other or with other forms of SRBD. In some forms of CSA, there is heightened chemoreceptor sensitivity that produces periodic oscillation between periods of apnea and hyperpnea; these types of CSA tend to attenuate or resolve during REM sleep when chemoreceptor sensitivity is blunted. Treatment of CSA can be quite varied due to the large variety of disorders that can cause CSA. Adjunct medical therapy for treatment of the underlying disorder is the first line of therapy in many medical conditions, including CHF, AF, and chronic renal failure (CRF). Different modes of noninvasive positive pressure ventilation (NIPPV), and even invasive positive pressure ventilation, may be required for the treatment of CSA due to neurologic, neuromus- cular, or musculoskeletal disorders. ASV mode is usually effec- tive in patients with respiratory control system instability due to increased respiratory drive or in complex (treatment-emergent) CSA. Surgical therapy or other device therapy can be required to treat other underlying disorders of CSA. CSA With Cheyne-Stokes Breathing Cheyne-Stokes breathing (CSB) refers to a periodic breathing pattern in which periods of apnea are followed by periods of hyperpnea, during which tidal volume waxes and wanes in a crescendo-decrescendo pattern. It occurs both during wakeful- ness and sleep. CSA with CSB is a CSA that has a CSB pattern, particularly as it appears on PSG. The central nature of the apnea event is determined based on concurrent reduction or absence both in airflow (Flow), as detected by oral or nasal thermal sensor, and in respira- tory effort, as detected on thoracic and abdominal movement (Mvmt) channels. Identifying CSB depends on detecting a cre- scendo-decrescendo pattern both in the airflow and respiratory effort channels, which reflect tidal volume, as well as on calcu- lating the frequency of apnea events and the duration of the pat- tern. The criteria are: • Three or more consecutive cycles of crescendo-decrescendo pattern on the Flow and Mvmt channels plus either one of the following: • A frequency of five or more central apnea or hypopnea events per hour of sleep (i.e., an AHI ≥ 5) • A duration of 10 minutes or more of crescendo-decre- scendo pattern on the Flow and Mvmt channels (Fig. 1.8) Common causes of CSA with CSB include CHF, AF, and stroke. Other causes of CSA with CSB include brain injury, CRF, and high-altitude periodic breathing (HAPB). In CRF, CSA with CSB is caused mainly by acid-base disturbances and compensa- tory hyperventilation. CSA with CSB in CHF has distinctive diagnostic and prog- nostic features. While CSA with CSB is common in CHF, it is not the only SRBD that is encountered. In general, the rule of thirds applies to SRBD in CHF—one-third of CHF patients have CSA with CSB, one-third have OSA, and one-third have nei- ther. Risk factors for CSA in CHF include male sex, age over 60 years, and baseline hypocapnea. In CHF, the pathophysiologic basis for CSA with CSB consists of a long circulation time due to decreased left ventricular function, decreased oxygen stores due to pulmonary edema, and respiratory center instability attribut- able to heightened chemoreceptor responsiveness to CO2 and O2. These pathophysiologic features lead to alternating periods of hyperventilation and hypocarbia, and apnea and hypoxemia. These periodic oscillations are reflected on the PSG by (1) prominent crescendo-decrescendo pattern of the hyperpnea period, (2) hyperpnea periods that are two to three times as long as apnea periods, (3) duration of the breathing cycle of apnea plus hyperpnea that is 60 seconds or more, and (4) 25 or more breaths per breathing cycle. Correlations exist between physiologic and PSG features. Severity of left ventricular dysfunction correlates with promi- nence of the crescendo-decrescendo pattern of the hyperpnea period, duration of hyperpnea period, length of apnea plus hyperpnea cycle, and the delay of nadir SaO2 to the peak of the hyperpnea period, which also coincides with peak work of breathing (WOB) and EEG arousals. Severity of pulmonary edema correlates with tachypnea (number of breaths per cycle of apnea plus hyperpnea) and severity of heightened chemosen- sitivity to CO2 and O2, and with the likelihood of REM sleep- induced resolution of CSA with CSB. There is also an increased risk of death from CHF if CSB is present. Pathophysiologic consequences of CSA with CSB are the result of prolonged periods of severe hypoxia and severe sleep disrup- tion due to EEG arousal events and periodic leg movement (PLM). CHF and CRF are associated with high rates of PLMs, and the CRF-associated restless leg syndrome (RLS) is usually difficult to treat. The resulting hypoxia and sleep disruption may increase left ventricular dysfunction, which may further worsen CSA and sleep disruption and result in a vicious perpetuating cycle. Treatment of CSA with CSB consists of adjunct medical therapy for the treat- ment of the underlying condition, PAP therapy, and supplemental oxygen. In CSA with CSB due to CHF, first-tier therapy consists of CPAP therapy and nocturnal oxygen supplementation. This can be augmented with BPAP or drug therapy with acetazolamide and theophylline after medical optimization of CHF. In CSA with CSB due to CRF, treatment includes CPAP, supplemental oxygen, use of bicarbonate during dialysis, and nocturnal dialysis. Iron supple- mentation in patients with iron deficiency is an effective adjunct medical therapy in the treatment of RLS. CSA due to a Medical Disorder Without Cheyne-Stokes Breathing Medical conditions associated with this type of CSA include Shy-Drager syndrome, familial dysautonomia, diabetes mel- litus, post-polio syndrome, muscular dystrophy, myasthenia
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 11 CHAPTER 1 Sleep-Related Breathing Disorder gravis, cerebral palsy, spinal muscle atrophy, and kyphoscolio- sis. Multiple causes of CSA can coexist as well as multiple types of SRBD. CSA due to High-Altitude Periodic Breathing CSA due to HAPB is usually encountered at altitudes of 7600 m (25,000 ft) or more (but occasionally less). It usually has a peri- odic pattern of alternating periods of apnea and hyperpnea of 35-second cycle length or less (apnea plus hyperpnea). If the periodic breathing pattern of HAPB meets the criteria of CSB, then it is called CSA with CSB due to HAPB. CSA due to a Medication or Substance CSA due to a medication or substance is caused by a medica- tion or substance that suppresses the chemical or neural control of breathing. Long-term opioid use ( ≥ 2-month use of long- acting opioid [e.g., methadone]) is the most common cause of this CSA. Opioids suppress both the chemical and neural con- trol of breathing through μ -opioid receptors in the medullary pre-Botzinger complex, the main autonomic respiratory pace- maker. Opioid-induced CSA is more prominent during NREM sleep and may resolve during REM sleep. The severity of opi- oid-induced CSA correlates with a daily morphine milligram equivalent of 200 mg or more and with low to normal body mass CHIN(1) 250 V C3-A2 125 V O2-A1 125 V ROC-A1 125 V LOC-A2 125 V ECG 2.5 mv LEG(L) LEG(R) THOR RES x1 ABD RES x1 PULSE bpm Pco 2 mm Hg AIRFLOW 62.5 V –4 30 3295 3370 3445 3520 Period Period Period 5 min/page 3447 30 sec/page Cursor: 23:35:58 Epoch: 115 - STAGE 2 3445 3442 3440 3437 3435 3432 3430 3427 3425 3422 Period Period Period Period Period Period Period Period Period 120 40 85 100 Sao2 % Fig. 1.8 Polysomnography (PSG) features of central sleep apnea with Cheyne-Stokes breathing in a patient with congestive heart failure (CHF). This PSG display is split into upper and lower windows of different dura- tions. The upper window is a 30-s epoch that displays the channels that are used for the recording and stag- ing of sleep: electromyography, electroencephalography (EEG), electrooculography, and electrocardiography (ECG). The lower window is a 5-min epoch that displays the channels that are used to document movement disorders and breathing disorders. Starting from the bottom of the lower window, the airflow channel shows a flow pattern of periodic oscillation between periods of apnea that last more than 10 s and periods of hyper- pnea that have a crescendo-decrescendo pattern. The P cO 2 channel shows that P cO 2 recordings very slightly lag behind airflow recordings and display an identical periodic oscillation between periods of apnea and hyper- pnea. The pulse channel shows heart rate changes that are most prominent at the peak of hyperpnea periods, which usually corresponds with nadir Sp O 2 and EEG arousal. The abdominal and thoracic resistance channels show that the apnea events are central apneas since there is no respiratory effort during the apnea periods. These respiratory effort channels demonstrate the same crescendo-decrescendo pattern during the hyper- pnea periods, which reflect tidal volume. The Sp O 2 channel shows that the nadir Sp O 2 level corresponds with the peak of the hyperpnea period and the recovery of Sp O 2 occurs during the apnea period. The LEG channels record the occurrence of periodic leg movements (PLMs), which are common in CHF . In the upper window, the ECG channel shows wide complex paced beats and narrow complex irregular beats that represent an underlying atrial fibrillation.
Order your copy of Stoelting’s Anesthesia and Co-Existing Disease, 9th Edition at elsevierhealth.com/9780443286841 12 CHAPTER 1 Sleep-Related Breathing Disorder index (BMI). The two main types of breathing patterns associ- ated with opioid-induced CSA are periodic Biot breathing and irregular ataxic breathing. Biot breathing consists of abruptly alternating periods of apnea and hypopnea (low tidal volume), with background bradypnea (respiratory rate [RR] < 10) and periodic hypoxia. It is also encountered in pontine injury and brainstem herniation. Ataxic breathing consists of irregular variations both in tidal volume and RR, with prolonged apneas and profound hypoxia. Treatment of opioid-induced CSA con- sists of reducing long-term opioid use and may require provid- ing PAP therapy with ASV mode (Fig. 1.9). Primary CSA Primary (idiopathic) CSA is of unknown cause, but it is more common in middle-aged males and possibly associated with nasal obstruction, anxiety, reduced arousal threshold, and insomnia. The pathogenesis includes heightened chemorecep- tor response to CO2 and O2, which leads to hyperventilation during wakefulness and to ventilatory control system instability during sleep, manifesting as periodic alteration between periods of apnea and hyperpnea. Therefore, REM sleep, by decreasing chemoreceptor sensitivity to CO2, may attenuate primary CSA. PSG features that distinguish primary CSA from CSA with CSB due to CHF include (1) EEG arousal occurring at the end of the apnea period instead of the peak of the hyperpnea period, (2) hyperpnea periods having a more abrupt onset and offset pat- tern instead of the crescendo-decrescendo pattern, (3) duration of a breathing cycle of apnea plus hyperpnea of 30 to 40 seconds instead of 60 to 90 seconds, and (4) number of breaths per cycle usually in the teens instead of 20 or 30. Because of heightened chemoreceptor response to CO2 and O2 in primary CSA, treat- ment consists of supplemental oxygen, acetazolamide, and PAP therapy with ASV mode, which can compensate for the respi- ratory control system instability due to increased respiratory drive. Primary CSA of Infancy Primary CSA of infancy refers to apnea episodes that either last 20 s or longer or are associated with bradycardia or hypoxia in a newborn infant who is older than 37 weeks of gestational age. Under 37 weeks of gestational age, this disorder is called primary CSA of prematurity. Differential diagnosis includes normal breathing pauses of newborns, periodic breathing of infancy, congenital central alveolar hypoventilation syndrome (CCAHS), and apparent life-threatening event (ALTE). Normal breathing pauses of newborns are short central apnea events that are not associated with bradycardia or hypoxia and are common in healthy newborns, especially during active sleep. Periodic breathing of infancy has a CSB pattern, with apnea periods of 3 to 10 seconds and cycle length (apnea plus hyperpnea) of 10 to 18 seconds. It is considered a normal variant if not associated with bradycardia or hypoxia. CCAHS is one of the types of SRHV disorders that is associated with apnea and erratic breathing, which lead to hypoxemia and hypercarbia. ALTE refers to the occurrence of one or more of the quartet of apnea, pallor, hypotonia, or choking during the first 6 months of infancy. Common etiologies of ALTE include gastroesophageal reflux disorder, respiratory infections, seizures, other infections, or unknown (20%–30%). Hospital admission is recommended after an ALTE to rule out serious conditions. Home apnea moni- toring is not recommended as it has not been shown to decrease the risk of sudden infant death syndrome. Treatment depends on clinical and PSG findings and may include theophylline and supplemental oxygen. Sao2 % THOR RES x1 ABD RES x1 PULSE bpm Pco2 mm Hg 0 50 40 120 80 100 AIRFLOW 62.5 V Fig. 1.9 Polysomnography (PSG) features of opioid-induced central sleep apnea (CSA). This is a 5-min epoch of PSG displaying CSA in a patient with long-term opioid use. The central nature of the apnea events is evident from the coupling of the airflow and respiratory effort. Features of opioid-induced CSA include significant brad- ypnea (4–5 breaths per minute), prolonged apnea periods ( ≥ 30 s), followed by a few breaths (2–3) per cycle length (apnea plus subsequent hypopnea). The nadir oxygen saturation coincides with the breathing periods, and the recovery of oxygen saturation occurs during the apnea period.