[rs] Hyperventilation And Sleep Apnea

THE RESPIRATORY SYSTEM

Hyperventilation and Sleep Apnea

Mrs. S. is a 40-year-old woman who has been obese since her early 20s. She now weighs 290 pounds and is 5 feet, 2 inches tall. For the past 6 months she has become increasingly short of breath with any exertion. On examination she appears to be a pleasant, alert woman in no apparent distress, and she breathes 24 times a minute. In addition to shortness of breath, which she feels just walking across the room, she complains of faIling asleep very easily during the day. In fact she no longer drives because a month earlier she fell asleep at the wheel but was uninjured. Her chest x-ray examination and electrocardiogram show no abnormalities. In the pulmonary function laboratory, she has the following blood gas and spirometry values (all at sea level). Arterial blood gas and hemoglobin (while she breathed room air) pH = 7.35 PaCO2 = 67 mm Hg PaO2 = 58 mm Hg SaO2 = 86% Hemoglobin content = 15 g/dl Spirometry data FVC = 78% of predicted FEV -1 = 78% of predicted FEV-1/FVC = 100%

l. How do you interpret these blood gas values? Is she hypoventilating? Why is her PaO2 low?

These blood gases are abnormal. The patient's PaCO2 is elevated, so she is hypoventilating, her pH is low as a result of the increased PaCO2. She is also hypoxemic, with a PaO2 of 58 mm Hg; this value is explained by the increased PaCO2. Using the alveolar gas equation, we calculate an alveolar PO2 of approximately 70 mm Hg; subtracting the PaO2 results in an alveolar-arterial PO2 difference of 12 mm Hg, which is within the normal range (up to 20 mm Hg).

2. How do you interpret the spirometry values? Does she have restrictive or obstructive mechanical impairment? Would you assess the impairment to be mild, moderate, or severe?

FVC and FEV-l are only slightly less than the lower limit of predicted normal (80%). Also, the ratio of FEV-l to FVC is normal and indicates no significant abnormality in air flow. Thus the patient appears to have only minimal restrictive impairment, which can be attributed to her obesity.

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3. Do you believe the degree of mechanical impairment is sufficient to explain the elevated PaCO2? If not, what is the most likely explanation?

Mrs. S. is admitted to the hospital for further evaluation and for a trial of oxygen therapy. While she receives 2 L/min of oxygen through a nasal tube, her blood analyses show the following:

pH = 7.33 PaCO2= 71 mm Hg PaO2 = 88 mm Hg SaO2 = 92%

The first night in the hospital she undergoes a sleep study. She is connected to machines that continually monitor her chest wall movements, oxygen saturation, air flow through mouth and nostrils, and electroencephalogram (EEG). Because her oxygen saturation is low while she breathes room air, she receives oxygen, at a flow rate of 2 L/min while she sleeps. Frequently while she sleeps, the following abnormal pattern is observed: air flow ceases while her chest wall movements increase. This abnormal pattern recurs throughout the night; each time it lasts between 10 and 45 seconds; each occasion ends with Mrs. S. making a loud snort or snoring sound, at which point air flow resumes. During these periods of absent air flow, her oxygen saturation falls, often to as low as 72%.

These spirometry values show no significant mechanical impairment. The patient has the mechanical ability to breathe and ventilate normally but lacks the drive to do so. The most likely explanation of her hypoventilation is an abnormality of the medullary brainstem that controls ventilation. Although she is certainly obese, most people with this body habitus do not hypoventilate or manifest this type of problem. (The pattern of obesity, hypoventilation, and daytime hypersomnolence is sometimes referred to as "Pickwickian syndrome," after Charles Dickens' novel Pickwick Papers, in which an obese character keeps falling asleep during the day.)

4. What type of sleep problem does this pattern indicate? What is the cause? What type of treatment would overcome this problem?

Two years later, Mrs. S. is admitted to the intensive care unit. She now weighs 320 pounds and has not seen a physician for at least a year. On examination she is lethargic and barely arousable. She has edema in both legs. Her hemoglobin content is increased to 19 g/dl (polycythemia). Arterial blood analyses while the patient breathes room air show the following:

pH = 7.29 PaCO2 = 70 mm Hg PaO2 = 38 mm Hg SaO2 = 74%

The features described¨Ccontinued chest wall movement with absent air flow-indicate a pattern of obstructive sleep apnea. In some obese patients, the upper airway muscles don't function normally

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during sleep to keep the airway open, so the airway closes easily. At a critical point in airway closure the patient is aroused briefly from sleep and opens the airway (in this patient, heralded by the loud sound). Although some patients may die from the obstruction during sleep, the major problem in most patients is the recurrent hypoxemia, which can lead to pulmonary hypertension. Treatment is needed to keep her airway continually open during sleep. A variety of devices have been used to increase the air pressure during sleep and thereby keep the airway open.

5. What is her current problem and its cause? Why is her hemoglobin content increased? What should the treatment be at this point?

She improves after 2 weeks of intensive care and leaves the hospital 30 pounds lighter. Her home-going regimen consists of oxygen at 2 L/min through an intranasal tube, plus a device (a continuous positive airway pressure mask) that forces air through her nostrils under pressure while she sleeps. A strict diet is also prescribed. A month after leaving the hospital, she returns to the laboratory for further evaluation. She now weighs 280 pounds. Arterial blood gases, pH, and hemoglobin are rechecked while she does not receive supplemental oxygen.

Arterial pH/blood gas and hemogzobin (while breathing room air)

pH = 7.37 PaCO2 = 60 mm Hg PaO2 = 61 mm Hg SaO2 = 89% Hemoglobin content = 15.5 g/dl

The patient now manifests severe respiratory failure, pulmonary hypertension, and right-sided heart failure. Her PaO2 is lower than predicted from hypoventilation alone. The calculated PaO2 is approximately 66 mm Hg. Hence the alveolar-arterial PO2 difference is 28 mm Hg. This increase indicates some ventilation-perfusion imbalance in addition to hypoventilation, and it is most likely caused by congestive heart failure. The heart failure and polycythemia are a result of chronic hypoxemia. Treatment is two-fold. Acutely, she needs mechanical ventilation. Long term, she will need to have her hypoxemia reversed, which will require continuous use of oxygen plus some device at night to prevent episodes of obstructive sleep apnea.

6. A CO2 response graph is plotted by having her breathe a low concentration of CO2 and measuring her minute ventilation against the exhaled, end-tidal PCO2 (which represents the arterial blood PCO2), During this test she is also given supplemental oxygen so that her PaO2 stays in a normal range. From her history, what type of CO2 response curve do you expect to see?

Her CO2 response should be subnormal. Her history indicates that she does not increase minute ventilation appropriately when PCO2 increases; a plot of her PCO2 versus minute ventilation would give a line with a subnormal slope.

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