Using The Pathophysiology of Obstructive Sleep Apnea To Teach Cardiopulmonary Integration
Using The Pathophysiology of Obstructive Sleep Apnea To Teach Cardiopulmonary Integration
Using The Pathophysiology of Obstructive Sleep Apnea To Teach Cardiopulmonary Integration
doi:10.1152/advan.90137.2008.
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PATHOPHYSIOLOGY OF OBSTRUCTIVE SLEEP APNEA
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Fig. 1. Estimated changes in arterial PO2 and PCO2 during 30 s of apnea. Slopes
of changes were modeled after the breathhold data of Lanphier and Rahn (16)
but start at an arterial PO2 of 100 mmHg and a PCO2 of 40 mmHg instead of
after hyperventilation as in the original. A patient with obstructive sleep apnea
(OSA) is likely to begin the apneic period at a lower arterial PO2 and a higher
arterial PCO2 than those shown.
Fig. 2. Estimated effects of changes in arterial PO2 and PCO2 on carotid body
activity. Carotid bodies are much more sensitive to changes in PCO2 than PO2
near the normal range.
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Fig. 3. Representation of a normal polysomnogram. EEG, electroencephalogram; EMG, electromyogram; ECG, electrocardiogram; BP, arterial blood
pressure; Abd, abdominal motion; Chest, rib cage motion; Vt, air flow. Note
that abdominal and rib cage motion are in phase during breathing.
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Fig. 5. Representation of alveolar, intrapleural, and upper airway pressure at end expiration (left) and during a strong inspiratory
effort (right). Note the potential collapse of
the upper airway during the strong inspiratory
effort.
Fig. 6. Common sites of upper airway obstruction during OSA events (right).
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reflex, as well as other protective respiratory reflexes, is depressed. The response to arterial hypoxia is depressed as well.
REM sleep decreases the tone of the intercostal and accessory
muscles, but it has less effect on diaphragm. The depression of
minute volume and the increase in arterial PCO2 are not as great
as occur during NREM sleep, but the depression of the response to arterial hypoxia is greater. These changes in the
mechanics and control of breathing that occur during sleep in
people that do not have OSA predispose those with OSA to
obstruction during sleep.
Pathophysiology of Other Symptoms and Signs of OSA
Fig. 9. Representation of the effects of arterial PO2 and PCO2 on cerebral blood
flow. Cerebral blood vessels are much more sensitive to changes in arterial
PCO2 than arterial PO2 near the normal range.
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PATHOPHYSIOLOGY OF OBSTRUCTIVE SLEEP APNEA
Hypersomnolence or excessive daytime sleepiness. The repeated arousals precipitated by upper airway obstruction,
which may occur as many as hundreds of times per night,
interfere with normal sleep architecture, especially REM sleep.
Abnormal sleep architecture leads to daytime somnolence,
decreased attentiveness, blunted mentation, depression, and
personality changes; hypersomnolence greatly increases the
risk of motor vehicle accidents (9, 11, 13, 25).
Ethanol consumption exacerbates OSA. Ethanol depresses
the respiratory responses to hypoxia and hypercapnia as well as
depressing the activity and tone of the genioglossal and pharyngeal dilator muscles (10). Ethanol also depresses other
protective respiratory reflexes, which can lead to aspiration and
other problems not directly related to OSA. Ethanol consumption may also interfere with normal sleep architecture.
Treatment of OSA
OSA can be treated a number of ways, depending on the
cause and severity of the problem in the individual patient and
whether or not the patient is compliant with the treatment.
Lifestyle changes. Because the supine position predisposes
upper airway obstruction, changing to another body position
during sleep may decrease or eliminate obstructions. Simple
solutions such as sewing a tennis ball into the back of the
patients pajama top, body belts that make the supine position
uncomfortable, or the use of special pillows may prevent
patients from assuming the supine position during sleep.
Weight loss can help patients for whom adipose tissue around
the upper airway is a contributing factor to upper airway
obstruction during sleep. Decreased consumption of ethanol
will help many OSA patients for the reasons described above.
Fig. 10. Representation of the effects of continuous positive airway pressure (CPAP) in opposing upper airway obstruction in OSA.
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Summary
OSA is a common disorder of upper airway obstruction
during sleep. Discussion and explanation of the pathophysiology of the disorder and its symptoms and signs involves many
aspects of pulmonary and cardiovascular physiology and can
be used to demonstrate the integration of the cardiovascular
and respiratory systems. Topics that can be discussed include
the mechanics of breathing, alveolar ventilation, pulmonary
blood flow, oxygen transport by the blood, acid-base balance,
control of breathing, systemic and pulmonary hypertension,
right ventricular hypertrophy, and cor pulmonale. Sleep physiology, renal physiology, interpretation of electrocardiograms,
and lifestyle and social issues can be added to the discussion,
particularly in the context of problem-based learning.
ACKNOWLEDGMENTS
The author thanks Betsy Giaimo for preparing the figures in this article.
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