ARA G. TILKIAN, M.D.; CHRISTIAN GUILLEMINAULT, M.D.; JOHN S. SCHROEDER, M.D., F.A.C.P.; KENNETH L. LEHRMAN, M.D.; F. BLAIR SIMMONS, M.D.; WILLIAM C. DEMENT, M.D., Ph.D.
TILKIAN AG, GUILLEMINAULT C, SCHROEDER JS, LEHRMAN KL, SIMMONS FB, DEMENT WC. Hemodynamics in Sleep-Induced Apnea: Studies during Wakefulness and Sleep. Ann Intern Med. 1976;85:714-719. doi: 10.7326/0003-4819-85-6-714
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Published: Ann Intern Med. 1976;85(6):714-719.
Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial PO2, < 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.
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Pulmonary/Critical Care, Sleep Disorders.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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