Pathophysiology

Patients with OSA experience intermittent upper airway obstruction above the epiglottis generally of the pharynx. The pharyngeal musculature attempts to keep the upper airway open to permit ventilation and opposes subatmospheric pressure in the pharynx that results from turbulent flow during partial upper airway obstruction. The genioglossus muscles also keep the upper airway clear of obstruction by pulling it forward. Anatomic factors (e.g., adipose tissue, tongue size, mandibular configuration, uvula, and tonsils) as well as neuromuscular factors (e.g., sleep state affecting the pharyngeal muscles and alcohol) contribute to increasing, maintaining or reducing upper airway patency (11).

Obstructive events result from the completely or partially obstructed upper airway during sleep may lead to cessation (apnea) (Fig. 1) or reduction (hypopnea) (Fig. 2) of airflow. Partial obstruction can also lead to snoring without a reduction in airflow. Partial or complete cessation of respiratory effort leads to central apneas (Fig. 3) or hypopneas. Mixed events start with a central component and end with an obstructive component. Mixed apneas (Fig. 4) and hypopneas are considered to be obstructive in behavior.

FIGURE 1 A series of obstructive apneas (no airflow with continued respiratory effort) from a Level III portable monitoring system used unattended in the patient's home. Note the severe cyclical arterial oxygen desaturations associated with the apneas. The patient was instructed in the outpatient area of the medical center, took home the system, attached it to himself just before retiring for the night, and brought the system back the next day for analysis. The epoch is 10 minutes in duration. Note that the events were occurring so frequently that the labels "Desaturation" and "Obstructive Apnea" are partially obscured on the record. Abbreviations: SpO2, pulse oximetry; HR, heart rate; FLOW from a nasal/oral pressure cannula; EFFOR(T) from the movement of a chest wall belt; POS(ition) is supine (S).

FIGURE 1 A series of obstructive apneas (no airflow with continued respiratory effort) from a Level III portable monitoring system used unattended in the patient's home. Note the severe cyclical arterial oxygen desaturations associated with the apneas. The patient was instructed in the outpatient area of the medical center, took home the system, attached it to himself just before retiring for the night, and brought the system back the next day for analysis. The epoch is 10 minutes in duration. Note that the events were occurring so frequently that the labels "Desaturation" and "Obstructive Apnea" are partially obscured on the record. Abbreviations: SpO2, pulse oximetry; HR, heart rate; FLOW from a nasal/oral pressure cannula; EFFOR(T) from the movement of a chest wall belt; POS(ition) is supine (S).

FIGURE 2 An obstructive hypopnea associated with snoring and ending in an arousal. The airflow is reduced but not absent and is associated with continued respiratory effort with a paradox of the abdominal and thoracic movement (respiratory excursions are out of phase) and an arterial oxygen desaturation to 82%. The hypopnea is occurring in rapid eye movement (REM) sleep (REMs seen at the beginning and end of the epoch). The hypopnea ends with a snore associated with a brief arousal noted by an increase in chin electromyogram tone and an increase in the electroencephalogram signal frequency. The record also demonstrates electrocardiogram artifact in several leads. The epoch is 30 seconds in duration. Abbreviations: LOCA2, left eye electro-oculogram referenced to the right (A2) ear; ROCA1, right eye electro-oculogram referenced to the left (A1) ear; CHIN, electromyogram recorded from chin muscles; C3A2, O1A2, electroencephalogram electrodes placed centrally or occipitally, respectively, and referenced to the right (A2) ear; EKG, electrocardiogram; LEGS, sensors placed on each leg and linked to provide a single signal for leg movement; SNOR, snoring intensity by microphone; FLOW, airflow measured by oronasal thermistor; THOR and ABDM, thoracic and abdominal movement, respectively, measured by strain gauges; SaO2, pulse oximetry from a finger sensor.

FIGURE 2 An obstructive hypopnea associated with snoring and ending in an arousal. The airflow is reduced but not absent and is associated with continued respiratory effort with a paradox of the abdominal and thoracic movement (respiratory excursions are out of phase) and an arterial oxygen desaturation to 82%. The hypopnea is occurring in rapid eye movement (REM) sleep (REMs seen at the beginning and end of the epoch). The hypopnea ends with a snore associated with a brief arousal noted by an increase in chin electromyogram tone and an increase in the electroencephalogram signal frequency. The record also demonstrates electrocardiogram artifact in several leads. The epoch is 30 seconds in duration. Abbreviations: LOCA2, left eye electro-oculogram referenced to the right (A2) ear; ROCA1, right eye electro-oculogram referenced to the left (A1) ear; CHIN, electromyogram recorded from chin muscles; C3A2, O1A2, electroencephalogram electrodes placed centrally or occipitally, respectively, and referenced to the right (A2) ear; EKG, electrocardiogram; LEGS, sensors placed on each leg and linked to provide a single signal for leg movement; SNOR, snoring intensity by microphone; FLOW, airflow measured by oronasal thermistor; THOR and ABDM, thoracic and abdominal movement, respectively, measured by strain gauges; SaO2, pulse oximetry from a finger sensor.

Although the above distinctions are made, the vast majority of patients with sleep apnea have predominantly obstructive apneas and hypopneas (continued respiratory effort with absence or reduction in airflow, respectively) even if there are elements of central or mixed events. Central apneas are seen more commonly in patients with congestive heart failure (in association with Cheyne-Stokes respiration), underlying neurologic disorders (such as stroke), or in individuals who reside at higher altitudes (1,12).

A variant is known as the upper airway resistance syndrome (UARS) (1), in which the pathologic events are respiratory effort-related arousals (RERAs). RERAs as defined by the American Academy of Sleep Medicine (AASM) (13) are due to partial upper airway obstruction with an increase in amplitude of negative intratho-racic pressure (increase in respiratory effort), leading to minimal reduction in airflow and arterial oxygen saturation but terminating in an arousal. The gold standard for assessing RERAs is by esophageal manometry (i.e., pressure measurements), which typically uses either a water-filled catheter or balloon placed in the esophagus inserted via the nose. Esophageal pressure assesses respiratory effort or work of breathing by estimating transmitted intrathoracic pressure, and can be useful in

FIGURE 3 A central apnea, probably from a postarousal hyperventilation apnea from an in-laboratory polysomnogram. The chest and abdominal effort are lacking, there is no airflow and there are cardiac oscillations observed on the airflow channel from small amounts of airflow resulting from contraction and relaxation of the heart causing the lungs to slightly compress and decompress. The patient had a modest 4% reduction in arterial saturation (not labeled except as "Desat"). The sleep stage is non-rapid eye movement stage 1 with a frequency of electroencephalogram (EEG) activity of 4 to 6 cycles/second after the arousal (EEG frequency > 8 cycles/second, a subtle increase in chin electromyogram activity and a leg movement from the arousal) that occurred at the beginning of the epoch. The epoch is 60 seconds in duration. Abbreviations: LEOG, left eye electro-oculogram; REOG, right eye electro-oculogram; CHIN EMG, electromyogram recorded from chin muscles; C3A2, O2A1, electroencephalogram electrodes placed centrally or occipitally and referenced to the right (A2) or left (A1) ear, respectively; L&R LEGS, sensors placed on each leg and linked to provide a single signal for leg movement; EKG, electrocardiogram; SONOGRAM, snoring intensity by microphone; AIRFLOW, airflow measured by oronasal thermistor; THORACIC and ABDOMINAL, thoracic and abdominal movement, respectively, measured by strain gauges; OXIMETRY, pulse oximetry from a finger sensor.

helping the sleep specialist to identify and distinguish abnormal breathing events (Figs. 5 and 6). Alternatively, a RERA may be inferred from repetitive snoring increasing in amplitude followed by an arousal (Fig. 7). An arousal is an EEG event characterized as an abrupt shift in EEG frequency (excluding delta waves and spindles) lasting more than three seconds and preceded by at least 10 seconds of sleep. An arousal is frequently accompanied by an increase in chin muscle tone, particularly during rapid eye movement (REM) sleep (14).

Cardiac arrhythmias are common in patients with OSA. The most common is sinus arrhythmia but atrial fibrillation, bradycardia, premature atrial and ventricular contractions, and nonsustained and sustained ventricular tachycardia occur more frequently than in control patients (15).

FIGURE 4 A mixed apnea with a central component (no airflow or respiratory effort) followed by an obstructive component (no airflow with continued respiratory effort) from Level III portable monitoring system used unattended in the patient's home. The patient was instructed in the outpatient area of the medical center, took home the system, attached it to himself just before retiring for the night and brought the system back the next day for analysis. The epoch is 60 seconds in duration. Note that the start of arterial oxygen desaturation occurs at about 20 seconds after the start of the apnea. This time delay is due to a combination of arterial circulation lag time from lungs to finger and the oximetry machine electronic lag time from time of sensing to display. Abbreviations: SpO2, pulse oximetry; HR, heart rate; FLOW from a nasal/oral pressure cannula; EFFOR(T) from the movement of a chest wall belt; Pos(ition) is supine (S).

FIGURE 4 A mixed apnea with a central component (no airflow or respiratory effort) followed by an obstructive component (no airflow with continued respiratory effort) from Level III portable monitoring system used unattended in the patient's home. The patient was instructed in the outpatient area of the medical center, took home the system, attached it to himself just before retiring for the night and brought the system back the next day for analysis. The epoch is 60 seconds in duration. Note that the start of arterial oxygen desaturation occurs at about 20 seconds after the start of the apnea. This time delay is due to a combination of arterial circulation lag time from lungs to finger and the oximetry machine electronic lag time from time of sensing to display. Abbreviations: SpO2, pulse oximetry; HR, heart rate; FLOW from a nasal/oral pressure cannula; EFFOR(T) from the movement of a chest wall belt; Pos(ition) is supine (S).

Sleep Apnea

Sleep Apnea

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