Chapter 5 Practical considerations and clinical caveats in polysomnographic interpretation in sleep-related breathing disorder
Events of abnormal breathing in sleep are characterized by snoring, apneas, hypopneas, and respiratory effort-related arousals (RERAs). These events are the result of essentially three physiologic derangements that interact to create the characteristic findings that are seen, analyzed, and summarized in polysomnography (PSG). These derangements include upper airway obstruction or flow limitation, dysregulation of respiratory control, and hypoventilation. Though apneas, hypopneas, and RERAs are seen in normal sleepers, they are rather uncommon. Nevertheless, it is the frequency of these abnormal breathing events that is pathophysiologically linked to symptoms or adverse health outcomes. Taken together, abnormal breathing events during sleep associated with clinically significant sequelae comprise many syndromes that are part of the sleep-related breathing disorder (SRBD). Aside from obstructive sleep apnea syndrome that was first defined over 30 years ago, other syndromes within SRBD include upper airway resistance syndrome (UARS), central sleep apnea syndrome (CSA), Cheyne–Stokes respiration (CSR), and alveolar hypoventilation syndrome (AHS).
It has been well established that untreated OSA has been associated with poor-quality and non-restorative sleep, excessive daytime hypersomnolence, and cognitive impairment. Furthermore, untreated OSA can adversely affect quality of life and may compromise a patient’s safety when operating machinery or driving a motor vehicle. The latter is undoubtedly fraught with both personal and public tragedy and its consequent legal ramifications should not be left unheeded. From retrospective and matched control studies, morbidity and mortality appear to be proportional to the severity of SRBD and are further influenced by underlying chronic medical conditions.
There is convincing evidence that SRBD likely plays an important causal or contributing role in the development and/or progression of hypertension, congestive heart failure (CHF), cardiac arrhythmias, stroke, and diabetes mellitus. Only a few studies have evaluated the association of SRBD in patients with coronary artery disease (CAD) with a normal percentage ejection fraction (%EF). OSA does appear to be associated with several factors that are known to contribute to the progression of CAD such as elevated sympathetic tone, increases in serum levels of inflammatory mediators (such as C-reactive protein, interleukin-6, and tumor necrosis factor-a), and a shift towards a more pro-coagulative state. Despite these striking findings, the clinical-based evidence supporting the association of SRBD with CAD is less compelling and studies that have utilized appropriate polysomnographic methodology and have attained statistical relevance have yet to be achieved.
In the last 15 years alone there has been a rapid technological evolution involving the means by which airflow and other cardiorespiratory parameters can be measured. Unfortunately, the development of many of these exquisitely sensitive physiologic monitors has yet to exhibit clinical relevance. In other words, as many sleep laboratories step up to maintain a competitive advantage by being on the ‘cutting edge’ as a technological leader, many of these new technologies are without substance as the clinical-based evidence supporting its use is often completely lacking. As such, there have been various definitions of apnea, hypopnea, and RERAs. Given that these abnormal breathing events are critical in determining the severity of SRBD, the American Academy of Sleep Medicine (AASM) has addressed this concern in its 2005 consensus guidelines on practice parameters for PSG. The recommended definitions for apneas, hypopneas, and RERAs are detailed in Table 5.1.
|Obstructive apnea||Apnea is defined as a cessation of airflow for at least 10 seconds. The event is obstructive if during apnea there is effort to breath.|
|Central apnea||Apnea is defined as a cessation of airflow for at least 10 seconds. The event is central if during apnea there is no effort to breath.|
|Mixed apnea||Apnea is defined as a cessation of airflow for at least 10 seconds. The event is mixed if the apnea begins as a central apnea, but towards the end there is effort to breath without airflow.|
|Hypopnea||Several definitions of hypopnea are in clinical use but there is no clear consensus. The Centers for Medicare and Medicaid (CMS) have approved the definition of hypopnea as an abnormal respiratory event with at least a 30% reduction in thoracoabdominal movement or airflow as compared to baseline lasting at least 10 seconds, and with ≥4% oxygen desaturation.|
|Respiratory effort-related arousal (RERA)||Clinical definition: not agreed upon. Research definition: sequence of breaths with increasing respiratory effort leading to an arousal from sleep, as shown by progressively more negative esophageal pressure for at least 10 seconds preceding an arousal with resumption of more normal pressures.|
The use of PSG for evaluating SRBD requires a minimum of the following recording: electroencephalogram (EEG), electro-oculogram (EOG), chin electromyogram (EMG), airflow, respiratory effort, arterial oxygen saturation (SaO2), and electrocardiogram (ECG) or heart rate. An anterior tibialis EMG is strongly encouraged to detect movement arousals and periodic limb movement. The AASM-recommended key items in PSG monitoring and summary reports are listed in Table 5.2. It must be noted that these recommendations are for hospital- or sleep laboratory-based PSGs. Currently, there is insufficient information from investigations using well-controlled clinical-based evidence to recommend or support unattended home PSGs in the diagnosis and management of SRBD.
|Recorded PSG parameters||Central monopolar recording|
|Occipital mono- or bipolar recording|
|R/L anterior tibialis EMG|
|ROC and LOC|
|ECG (traditionally, single lead II)|
|SaO2 (peripheral pulse oximetry)|
|pCO2, if clinically indicated:|
|Total sleep time (TST)|
|Sleep efficiency index|
|REM sleep latency|
|Wake after sleep onset (WASO)|
|Sleep stages||Total time in each stage (I, II, III/IV, REM)|
|Percent of total sleep time|
|Number and index of apneic events:||During sleep|
|• Obstructive||By body position|
|• Mixed||NREM vs. REM|
|• Central||Means and longest duration|
|Number and index of RERAs||Duration of SaO2 in percentage ranges:|
|Apnea/hypopnea index||• Wake, NREM and REM|
|Respiratory arousal/disturbance index||Mean, minimum, and maximum SaO2:|
|Minimum oxygen saturation||• Wake, NREM and REM|
|Periodic limb movements (PLMs), with and without arousal|
|Any EEG or ECG abnormalities|
|Unusual behavior observed during study|
Awareness of sleep disorders has grown immensely. In 1990, there were an estimated 110,000 office visits for SRBD. By 1998, this had risen to 1.3 million visits per year. Though the health benefits of treating SRDB are well established, the potential cost savings to healthcare providers and insurers have only recently been explored. Patients with untreated SRBD are more likely to be hospitalized and incur higher healthcare costs than matched control subjects. One study revealed that the length of stay of hospitalized patients with untreated SRBD was increased 2.8-fold and incurred excess hospital costs of $100,000–200,000. The magnitude of the medical costs correlated with the severity of the SRBD. There is only one study that details the SRBD treatment benefit on healthcare costs and utilization. In this study, patients were followed for 2 years following their diagnosis and then compared to matched control subjects over the same period of time. The SRBD-treated patients when compared to control subjects revealed an overall decrease in physician costs of 33% and a decrease in the duration of consequent hospital stays. The improvement in physician costs and hospital stay was only significant in patientsmaintaining compliance with SRBD treatment. Lastly, there are also cost advantages in including attended hospital- or sleep laboratory-based PSGs in the diagnosis of SRBD. A recent cost analysis of the benefit of a PSG in the detection of SRBD demonstrated a cost saving of $9200–13,400 per quality-adjusted life-year gained. Compared to other outpatient diagnostic tests, the cost of a PSG to diagnose SRBD is favorable. For example, the cost of a diagnostic PSG is one-fourth the cost of a standard screening for carotid stenosis in an asymptomatic patient.