Sleep-Disordered Breathing and Scoring

FIGURE 4.1 Obstructive sleep apnea.
A 10-minute compression is shown in a 47-year-old man. Overt and repetitive obstructive respiratory events with associated oxygen desaturations are seen. Following a larger arousal, postarousal central apneas and respiratory instability are seen. Periodic tibialis motor activations occur associated with respiratory arousals. However, note that many of the events, especially the fourth to seventh events from the left, have a nearly identical timing of 30 seconds. Such timing characteristics (short, metronomical) can reflect strong respiratory chemoreflex modulation of sleep breathing, but by any criteria the events shown here need to be scored as obstructive hypopneas.

FIGURE 4.2 Complex sleep apnea.
The same subject as in Figure 4.1 while on continuous positive airway pressure (CPAP). A 10-minute compression is shown. Note the emergence of central apneas at low to moderate CPAP pressures. This pattern persisted through much of non–rapid eye movement sleep. In this snapshot the patient is nonsupine.

FIGURE 4.3 Stabilization effects of rapid eye movement (REM) sleep on chemoreflex-modulated sleep apnea.
The same subject as in Figures 4.1 and 4.2. A 10-minute compression is shown. Note the excellent response to therapy. The body position is supine, and thus positional effects cannot explain the non-REM (NREM) versus REM sleep differences. The NREM-dominant sleep apnea phenotype is readily recognizable and confers a high risk for conversion to the “complex” phenotype.

FIGURE 4.4 Short cycle obstructive apneas in non–rapid eye movement sleep.
A 10-minute compression is shown in a 32-year-old woman. The events are clearly obstructive yet have few recovery breaths after individual events. The return of oxygen saturation levels to the baseline after arousals suggests that there is no hypoventilation, but end-tidal CO₂ monitoring would be required. Note the robust cardiac accelerations and decelerations, but these do not exactly match the timing of arousal/recovery breaths.

FIGURE 4.5 Classic periodic breathing/Cheyne-Stokes pattern during continuous positive airway pressure titration.
A 59-year-old man with clinical symptoms consistent with sleep apnea, with no other comorbidities. The vertical lines are 30 seconds. The pattern during the diagnostic assessment was identical. This readily recognizable pattern reflects unstable and exaggerated respiratory chemoreflex influences.

FIGURE 4.6 Bradypnea.
A 30-second epoch snapshot from a 22-year-old with mixed sleep apnea. Respiratory rate is about 8 breaths/min, with prolonged expiration phases that show some variability. The rate while awake was 14 breaths/min, and this pattern was seen during continuous positive airway pressure application. Unexplained sleep bradypnea (which will be designated central apneas if the rate slows down enough) or ataxic respiration in the absence of opiate use in a young individual could raise the possibility of a craniovertebral junction abnormality.

FIGURE 4.7 Increased upper airway resistance with consequences.
A 26-year-old woman, 10-minute screen compression. The stage is rapid eye movement sleep, with variable degrees of flow limitation (PTAF channel) and arousals characterized by transient chin electromyographic tone increases and recovery breaths. There is no oxygen desaturation.

FIGURE 4.8 Ataxic respiration and opiates.
A 77-year-old woman with spinal stenosis and methadone use. Note the unpredictable variability of the expiratory phase.

FIGURE 4.9 Dynamism in sleep-breathing disorders.
A 10-minute screen compression from a 66-year-old male patient with long-standing sleep apnea and a new diagnosis of myasthenia gravis. Repetitive obstructive respiratory events and respiratory instability occur and lead relatively abruptly to a switch to stable non–rapid eye movement (NREM) sleep. Such periods of stability are intrinsic to NREM sleep and in this case occur in stage N2.

FIGURE 4.10 Respiratory events while awake.
A 10-minute compression from a 60-year-old man with stable congestive heart failure. Note that even though the epochs are scored “wake” by conventional criteria, there are repetitive central apneas on continuous positive airway pressure and fluctuating electroencephalographic (EEG) amplitudes and frequency (see EEG channels) associated with these events. The problem reflects limitations of the current epoch-based scoring system. These events may be preventing a proper transition to sleep.

FIGURE 4.11 Respiratory events while awake.
A 10-minute compression from a 56-year-old man with chronic obstructive pulmonary disease. Note that even though the epochs are scored “wake” by conventional criteria, there are repetitive central apneas during this diagnostic assessment. The electroencephalogram less clearly shows state transitions than in Figure 4.10, there are no slow eye movements of drowsiness, but the oxygenation fluctuations and respiratory cycling suggest that these events are pathological and related to sleep state or at least the transition to it. Note that the oxygen saturation levels remain low during recovery phases, likely because of reduced lung functional reserve.

FIGURE 4.12 Stable non–rapid eye movement sleep during adaptive ventilation.
A 10-minute screen compression during titration of adaptive ventilation and dead space use in a 58-year-old male patient with congestive heart failure and Cheyne-Stokes respiration. Note overall stability of sleep and respiration. The respiratory signals from top are servo ventilation (SV) pressure (pressure output from the ResMed VPAP Adapt SV), nasal pressure (mask pressure), chest and abdominal effort, and mainstream end-tidal CO₂ (maximum is 38.4 mm Hg).

FIGURE 4.13 Unstable non–rapid eye movement sleep during adaptive ventilation.
A 10-minute screen compression during titration of adaptive ventilation and dead space in the same patient as in Figure 4.12. The respiratory signals from top are spontaneous ventilation (SV) pressure (pressure output from the ResMed VPAP Adapt SV), nasal pressure (mask pressure), chest and abdominal effort, and mainstream end-tidal CO₂ (maximum is 38.4 mm Hg). Note the “pressure cycling” profile of the servo ventilation (SV) pressure that signifies adaptive responses to ongoing periodic breathing. Conventional scoring can be challenging during adaptive ventilation: effort signals reflect machine plus patient, and the flow signals can be continuously undulating—with a reduction in pressure during recovery breaths, exactly the opposite relative to continuous positive airway pressure titration. However, the ongoing arousals suggest that these events need to be scored as hypopneas with arousals.

FIGURE 4.14 Sleep apnea and parasomnias.
A 25-year-old man presents with what could be nocturnal seizures or non–rapid eye movement (NREM) parasomnias. There is no snoring or daytime sleepiness. The diagnostic polysomnogram shows repetitive nonhypoxic respiratory events, no clear epileptiform activity, and vigorous arousals. Sleep apnea may be asymptomatic (no sleepiness) in those with NREM parasomnias, whereas treatment of sleep apnea can stop clinical expression of NREM parasomnias.

FIGURE 4.15 Obstructive sleep apnea—but where are the arousals?
This 10-minute compression shows typical obstructive sleep apnea—maintained effort, variable-duration respiratory events, recovery breaths, electromyographic tone fluctuations—but there is a paucity of electroencephalographic (EEG) arousals. This 26-year-old is using clonazepam for anxiety disorder; benzodiazepines can inhibit the full expression of EEG arousals. In this instance the 30-second compression (not shown) did show brief alpha intrusions, but these did not reach the threshold of conventional arousal scoring.

FIGURE 4.16 Pseudoperiodic breathing during rapid eye movement (REM) sleep.
Periodic breathing (at sea level or high altitude) is rare or absent during REM sleep. Phasic REM events can inhibit respiration, and well-timed phasic REM phenomena can cause sufficient respiratory inhibition to cause this oscillatory pattern. In this sample from a continuous positive airway pressure titration study, the “abnormality” seems to be associated with no significant pathophysiological consequences such as arousals or oxygen desaturations.

FIGURE 4.17 Rapid eye movement–dominant obstructive sleep apnea.
A 10-minute screen compression from a 33-year-old obese woman. Repetitive respiratory events and severe oxygen desaturation are noted. In this case, contrary to the patient in Figure 4.15, the electroencephalographic responses are vigorous but chin tone elevations are minimal to absent.

FIGURE 4.18 Rapid eye movement (REM)-related pressure cycling during adaptive ventilation.
Phasic REM sleep-related tidal volume fluctuations can trigger the adaptive algorithms in the ResMed VPAP Adapt SV and “cause” periodic breathing during REM sleep. In this snapshot note that the PAP Pressure channel, which is the ventilator pressure output in this study, shows increases shortly after a cluster of phasic eye movements. No intervention is required. Some increase in phasic motor activity is also seen in the tibialis electromyographic channels (R and L Legs) time synchronized with phasic REM bursts.

FIGURE 4.19 Central apneas during phasic rapid eye movement sleep.
A normal phenomenon, along with other features of respiratory variability and instability.

FIGURE 4.20 Ambulatory recording of periodic breathing.
This metronomical pattern can be characteristic enough on an ambulatory monitoring study that the patient can be triaged to sleep laboratory management and not initiated on auto–continuous positive airway pressure.

FIGURE 4.21 Rapid eye movement (REM) sleep effects on opiate-induced sleep apnea.
Opiate-induced sleep apnea has several features that in aggregate form a relatively unique polysomnographic picture: ataxic respiration and central apneas during non-REM sleep, mild hypercapnia, and relative respiratory stability during REM sleep. This 10-minute compression from the same patient as in Figure 4.8 shows stable breathing during REM sleep and end-tidal CO₂ levels that go as high as 50 mm Hg.

FIGURE 4.22 Normal respiratory variability during rapid eye movement sleep.
This 10-minute compression shows prominent but normal tidal volume and respiratory rate variability. There are no consequences to the reductions in airflow (i.e., no arousals or oxygen desaturations), and these events therefore cannot be scored.

FIGURE 4.23 Obstructive sleep apnea during ambulatory recording.
Information on airflow, effort, and oximetry are typically considered sufficient to confirm sleep apnea in subjects with high clinical probability. In selected instances, oximetry and airflow alone may be sufficient (even if not reimbursable). When the signal quality is acceptable and the abnormality is obvious, as in this figure, the diagnosis is straightforward.

FIGURE 4.24 Obstructive sleep apnea during ambulatory recording.
A 10-minute compression showing, from top, nasal pressure, thermistor, thoracic and abdominal effort, sum of effort, snoring, pulse oximetry, finger pulse plethysmogram, and derived pulse rate. Does this patient have sleep apnea? By many sets of criteria, no (absent oxygen desaturation). However, the flow limitation and recovery breaths associated with plethysmographic amplitude reductions are suggestive of respiratory effort–related arousals. Note that the heart rate change with presumptive arousal is small in this patient.

FIGURE 4.25 Non–rapid eye movement (NREM)-dominant obstructive sleep apnea during NREM sleep.
A 10-minute compression from a 37-year-old man with otherwise typical symptoms of sleep apnea. Repetitive obstructive hypopneas with arousal and relatively minor oxygen desaturation. The events are not particularly short cycle (not less than 30 seconds) and are of variable length, with well-maintained effort. The body position is supine.

FIGURE 4.26 Non–rapid eye movement (NREM)-dominant obstructive sleep apnea changes during rapid eye movement (REM) sleep.
The same patient as in Figure 4.25, still supine, now during REM sleep. Note the complete absence of abnormal respiration.

FIGURE 4.27 “Banding” of oximetry and nonobstructive sleep apnea.
An 84-year-old woman with atrial fibrillation and congestive heart failure. The integrated snapshot shows part of the hypnogram, with oxygen desaturations that are nearly identical and the associated periodic breathing/Cheyne-Stokes pattern.

FIGURE 4.28 Ataxic breathing caused by narcotics.
A 240-second excerpt taken from the bilevel titration study in a 53-year-old woman on large doses of oxycodone (OxyContin, 260 mg daily) for chronic severe lower back pain associated with lumbosacral disk disease. This epoch shows several episodes of Biot’s breathing (a type of ataxic breathing characterized by recurrent central apneas followed by two to three breaths) accompanied by oxygen desaturation in stage N2. This is a characteristic finding that may be noted in patients on chronic narcotics ingestion, as well as in those with brainstem lesions destabilizing the central respiratory controllers. Top four channels: electroencephalograms (international nomenclature); E1-M1 and E2-M1, right and left electro-oculograms; CHIN1-CHIN2, mentalis muscle electromyogram (EMG); ECG, electrocardiogram; HR, heart rate; Tib, tibialis anterior muscle EMGs; Lt, left; Rt, right; CFLOW and effort, channels 12 to 14; Sao₂, arterial oxygen saturation by finger oximetry. Also included is a snore channel.

FIGURE 4.29 The effect of stage on Cheyne-Stokes respiration.
Epochs of 600 seconds from the overnight polysomnogram (PSG) of an 82-year-old man with a history of atrial fibrillation and stroke. His PSG showed evidence of central sleep apnea with Cheyne-Stokes respirations (apnea-hypopnea index, 40.1/hr, and arterial oxygen saturation [SaO₂], nadir of 89%), characterized by crescendo-decrescendo pattern of hyperventilation and central apneas, with longer hyperpneic than apneic phase and prolonged circulation time (measured from the termination of apnea to the lowest SaO₂ toward the end of the hyperpneic phase). A, An epoch of stage N2 sleep. Cheyne-Stokes respiration with the characteristics described earlier persisted throughout non–rapid eye movement sleep. B, Note improvement of Cheyne-Stokes respiration as the patient transitions to rapid eye movement sleep. Top eight channels: electroencephalograms (international nomenclature); E1-M1 and E2-M1, right and left electro-oculograms; Chin1-Chin2, mentalis muscle electromyogram (EMG); ECG, electrocardiogram; HR, heart rate; LtTib, RtTib, left and right tibialis anterior EMG; LGAST, RGAST, left and right gastrocnemius EMG; INTRC, intercostal EMG (right 8th space); airflow and effort, channels 19 to 22; Sao₂, arterial oxygen saturation by finger oximetry.

FIGURE 4.30 The effect of position on Cheyne-Stokes respiration.
Epochs of 480 seconds from the bilevel titration of a 68-year-old man with a history of myocardial infarction and congestive heart failure. His spouse reported irregular breathing and witnessed apneas in sleep, and he had excessive daytime sleepiness. He also had hypertension and asthma. A previously performed polysomnogram showed severe central sleep apnea (apnea-hypopnea index, 48/hr) with a mean arterial oxygen saturation (SaO₂) of 84% and an O₂ saturation nadir of 74%. A, Note the presence of Cheyne-Stokes respirations in stage N2 sleep with the patient in the supine position The patient is on a pressure of 12/9 cm. B, Improvement of Cheyne-Stokes respirations when the patient assumes the lateral position. He remains in stage N2 sleep at the same bilevel pressure. Top four channels, electroencephalograms (international nomenclature); LOC-A2, ROC-A1, elecro-oculogram; CHIN, chin electromyogram (EMG); LtTib, RtTib, right and left lower limb EMGs; CFLOW, CPAP airflow channel; THORAX, ABD, thoracic and abdominal respiratory belts; Sao₂, arterial oxygen saturation by finger pulse oximetry. Also included are channels for ECG, heart rate, and snoring.