Nocturnal Hypoxemia in Sleep Apnea

Nocturnal Hypoxemia in Sleep Apnea

Nocturnal Hypoxemia in Sleep Apnea Since nocturnal hypoxemia plays a key role in the pathogenesis of sleep apnea, it is important to understand the ...

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Nocturnal Hypoxemia in Sleep Apnea

Since nocturnal hypoxemia plays a key role in the

pathogenesis of sleep apnea, it is important to understand the determinants of nocturnal hypoxemia in these patients. These determinants include: (1) the length and number of apneas during sleep; (2) baseline oxyhemoglobin saturation (SaOJ; and (3) the rate of fall of 8a02 during each apnea (a balance between oxygen stores and oxygen uptake). Little is known about what determines the number and length of apneas during sleep. Body weight and obesity affects both the number and length of apneas. 1 Drugs such as alcohol may increase the number of apneas during sleep by depressing the eNS or increasing upper airway resistance.v" Hypoxic ventilatory drive may affect apnea length during sleep, for supplemental oxygen may increase the length of apneas in some patients." In addition, receptors sensitive to inspiratory muscle fatigue may affect the length of apneas," Finally, sleep state affects apneas, for REM sleep is associated with increased number and length of apneas in patients with obstructive sleep apnea." The baseline Sa02 of patients determines their position on the oxyhemoglobin dissociation curve and will affect the rate of fall in Sa02 during apneas. If the baseline Sa02 is low, the rate of fall in Sa02 will be increased during apneas. Increasing baseline Sa02 by supplemental oxygen decreases the rate offall in Sa02, although the apneas may become longer. 7 The rate of fall in Sa02 during an apnea will depend on a balance between the oxygen stoi es before and the oxygen uptake during an apnea. Oxygen stores is the amount of alveolar oxygen available for gas exchange during an apnea. These stores are determined by the alveolar gas volume, partial pressure of oxygen of alveolar gas (PAOJ and the gas exchange efficiency of the lung. The lower the lung volume, the higher the rate at which Sa02 will fall during apnea. 8,9 Depressed PA0 2 due to hypercapnia or other causes will increase the rate at which Sa02 will fall. Finally, a shunt or other lung disorder inhibiting gas exchange will decrease available oxygen stores and increase the rate at which Sa02 falls. The oxygen uptake from the lung during apnea is determined by mixed venous oxygen (SV02) and oxygen consumption. The lower the SV02 level, the greater the amount of oxygen

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required to reoxygenate the venous blood and the greater the fall in Sa02 during apnea (see Fletcher et al, p 717).10 A higher oxygen consumption during apnea might rapidly deplete oxygen stores and cause a rapid fall in Sa02 during apneas. Small increases in oxygen consumption probably have little effect, since vigorous respiratory maneuvers during apnea do not affect the rate of Sa02 fall during apneas,"-" However, measurements of oxygen consumption have not been related to the rate of fall of Sa02 during apneas in sleeping humans. The effect of cardiac output on oxygen uptake may be variable. A chronically low cardiac output may lower SV02 and increase the rate at which saturation falls during apnea. In contrast, acute declines in right ventricular cardiac output may decrease uptake from the lung oxygen stores and decrease the rate of fall of Sa02 during apnea. lLlrry J Findley, M.D. Charlottesville, VA Pulm~nary

Division, University of Virginia Health Sciences Center.

Repnnt requests: Dr. Findley, University a/Virginia Medical Center.

Box 225, Charlottesville 22908

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REFERENCES

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Suratt ~ McTier R, Findley L, Pohl S, Wilhoit S. Changes in breathing and the pharynx after weight loss in obstructive sleep apnea Chest 1987; 92:631-37 Taasan Block A, Boysen ~ Wynne J. Alcohol increases sleep apnea and oxygen desaturation in asymptomatic men. Am J Moo 1981; 71:240-45 Robinson R, White D, Zwillich C. Moderate alcohol ingestion increases upper airway resistance in normal subjects. Am Rev Respir Dis 1985; 132:1238-41 Motta J, Guilleminault C. Effects of oxygen administration in sleep-induced apneas. In: Guilleminault C, Dement ~ OOs. Sleep apnea syndromes. New York: Alan R Liss, 1977:134-44 Vincken ~ Guilleminault C, Silvestri L, Cosio M, Grassino A. Inspiratory muscle activity as a trigger causing the airways to open in obstructive sleep apnea. Am Rev Respir Dis 1987; 135:372-77 Findley L, Wilhoit S, Suratt P Apnea duration and hypoxemia during REM sleep in patients with obstructive sleep apnea. Chest 1985; 87:432-36 Strohl K, Altose M. Oxygen saturation during breath-holding and during apneas in sleep. Chest 1984; 85:181-86 Findley L, Ries A, Tisi G, Wagner E Hypoxemia during apnea in normal subjects: mechanisms and impact of lung volume. J Appl Physiol 1983; 55:1777-83 Bradley T, Martinez D, Rutherford R, Lue F, Grossman R, Moldofsky H, et ale Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnea. J Appl Physioll985; 59:1364-68 Fletcher E, Kass R, Thornby J, Rosborough J, Miller T. Central venous O2 saturation and rate of arterial desaturation during obstructive sleep apnea. J Appl Physioll989; 66:1477-85

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