Case Studies in Sleep Medicine

CASE ONE

History of Present Illness

A 47-year-old male presented with a several-year history of heroic snoring and witnessed apneas. He complained of excessive daytime somnolence with passive activities, becoming drowsy while driving, and fatigue. He reports nonrefreshing sleep and early morning headaches. He has no history of alcohol, tobacco, or drug use. Family history is noncontributory. He has no known history of cardiovascular disease.

Physical Examination

Blood pressure was 118/88. Height was 5 feet 7 inches. Body mass index was 32.3 kg/m². Cardiovascular examination was normal. Pulmonary auscultation was normal. Neurological examination was also normal.

Discussion

This gentleman has several symptoms consistent with obstructive sleep apnea (OSA). Patients who present with snoring, witnessed apneas, and excessive daytime somnolence are likely to have obstructive sleep apnea. However, other entities must also be considered. Primary snoring is defined as snoring that does not create disruptions in sleep patterns, insomnia, or excessive daytime sleepiness.[1] Upper airway resistance syndrome (UARS) is a form of sleep-disordered breathing characterized by a high resistance to airflow in the upper airway associated with increased respiratory effort that leads to an increase in arousals, sleep fragmentation, and ultimately excessive daytime somnolence. This increased respiratory effort minimizes change in the tidal volume and usually avoids the hypoxemia that is typical of OSA.[2] Central sleep apnea (CSA) is a condition in which the absence of respiratory effort leads to the cessation of breathing. Central sleep apnea has a variety of causes, and the clinical presentation will often differ based on the underlying cause. Unlike OSA, CSA is more likely to present with insomnia. Patients with CSA also have arousals associated with gasping for air, inability to sleep in a horizontal position, snoring, and sometimes excessive daytime somnolence.[3]

This case illustrates several educational points about patients with OSA. This patient had a diagnostic polysomnogram (PSG), which revealed a respiratory disturbance index (RDI) of 90 (normal ≤ 5) associated with severe oxygen desaturation to a minimum of 57% (Table [1]). His sleep is very fragmented as indicated by the number of stage shifts and frequent arousals. These factors combined are a likely explanation for his apparent sleepiness as demonstrated by the very short sleep latency of 1.5 minutes. The most profound hypoxemia occurred in the first and only rapid eye movement (REM) sleep period in the baseline portion of this study (see* Fig. [1]). This is likely explained by the increased respiratory variability and respiratory depression, which is due to the relative hypotonia of the upper airway and intercostal muscles seen during REM sleep. In addition, there is widespread skeletal muscle hypotonia that serves as a protective mechanism to prevent the acting out of dreams. This leaves the diaphragm as the only active respiratory muscle during REM sleep. Ventilatory responses to hypoxia and hypercapnia are also reduced.[4]

Table 1 Results From the Nocturnal Polysomnogram in Case One Polysomnogram Recording time 451.0 minutes Total sleep time 420.0 minutes Latency to sleep 1.5 minutes REM latency 90.0 minutes Number of stage shifts 269 Sleep efficiency 93.1% Wake time 28.5 minutes Stage 1 sleep 117.0 minutes 27.9% Stage 2 sleep 131.5 minutes 31.3% Stage 3/4 sleep 19.0 minutes 4.5% Stage REM sleep 152.5 minutes 36.3% Total NREM sleep 267.5 minutes 63.7% TST/position Prone 0 minutes Supine 339 minutes Left 80 minutes Right 0 minutes Respiratory analysis of the baseline portion Total sleep time (h:min) 2:42 Number of apneic episodes 243 Number of apneic episodes/h of sleep 90.0 Number of apneic episodes/h of NREM 80.9 Number of apneic episodes/h REM 30.0 Minimum SaO2 57% Baseline SaO2 94% Number of events Obstructive apneas 41 NREM 1 REM Mixed apneas 5 NREM 0 REM Central apneas 0 NREM 0 REM Hypopneas 167 NREM 1 REM Wake apneas 28 NREM Snoring: frequent loud Arousals: frequent Leg movement analysis: There were 21.0 periodic leg movements per hour of sleep with rare associated arousals TST, total sleep time Figure 1 Sleep hypnogram depicting the baseline portion of a spilt night polysomnogram (PSG). (A) Repeated hypoxemia [oxygen saturation of 60%, worse during REM sleep (*)] and sleep fragmentation associated with the apneic episodes during the baseline portion of the study (solid arrow). (B) The CPAP portion of the study (dashed arrow). Obstructive sleep apnea improves once positive pressure (CPAP) is introduced. As higher CPAP levels are used (5 cm → 7 cm → 9 cm → 11 cm → 13 cm water), the sleep becomes less fragmented and hypoxemia is normalized. Incidentally, as higher CPAP pressures are utilized the patients has more frequent periodic leg movements (PLMs).

When treated with positive pressure therapy, long periods of REM sleep can occur in some patients (see♢ Fig. [1]). This REM rebound probably develops as a result of cumulative REM sleep deprivation due to the repeated arousals associated with untreated OSA.

Illustrated in Fig. [2] (60-second epoch) is a period of prolonged sinus pause (arrow) and its relationship to the obstructive apnea and resulting hypoxemia. A closer view of the arrhythmia is provided in Fig. [3] (10-second epoch). Marked sinus bradycardia and sinus arrest are the most common arrhythmias observed in patients with OSA.[5] These arrhythmias occur in association with the obstructive event and are likely vagally mediated. The increased vagal tone is caused by fluctuations in intrathoracic pressure and stimulation of the carotid body receptors by hypoxemia. Hypoxemia in the absence of an apnea induces an increase in respiratory rate that causes lung distention, which then inhibits vagal activity. During apnea, lung distention does not occur, and the increased vagal tone induced by hypoxia leads to bradycardia.[6]

Figure 3 A 10-second epoch from the baseline portion (A) of the study. Note in this figure the view of the prolonged sinus pause as shown in the electrocardiogram (arrow). Channels are as follows: electrooculogram (left: LOC-A2; right: ROC-A1), chin EMG, EEG (left central, right central, left occipital, right occipital), electrocardiogram, limb EMG (left leg, right leg), snoring, nasal-oral airflow, respiratory effort (thoracic, abdominal), nasal pressure, and oxygen saturation.

Severe OSA, morbid obesity, REM sleep, and the severity of the oxygen desaturations are independent predictors of heart block developing during apneic episodes.[7] In this case, the sinus pause took place during the only REM episode in the baseline portion of the study, when the oxygen saturation fell. Continuous positive pressure (CPAP) therapy frequently eliminates the nocturnal episodes of sinus arrest and heart block in patients with OSA. The arrhythmias resolved with the use of CPAP in this gentleman (Fig. [1], B).

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