JORGE MOTTA, M.D.; CHRISTIAN GUILLEMINAULT, M.D.; JOHN S. SCHROEDER, M.D.; WILLIAM C. DEMENT, M.D., Ph.D.
▸Requests for reprints should be addressed to Christian Guilleminault, M.D., Sleep Research Center, Stanford University School of Medicine; Stanford, CA 94305.
MOTTA J., GUILLEMINAULT C., SCHROEDER J., DEMENT W.; Tracheostomy and Hemodynamic Changes in Sleep-Induced Apnea. Ann Intern Med. 1978;89:454-458. doi: 10.7326/0003-4819-89-4-454
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Published: Ann Intern Med. 1978;89(4):454-458.
Because pulmonary hypertension and systemic hypertension occur during sleep-induced obstructive apnea, six patients underwent overnight hemodynamic monitoring before and after tracheostomy. Variables studied included heart rate, pulmonary artery pressure, femoral artery pressure, and arterial oxygen tension (PO2). After tracheostomy, significant reductions were noted during sleep in mean pulmonary artery pressure from 45 ± 6 mm Hg (mean ± SEM)to 22 ± 2 mm Hg (P < 0.05) and in mean femoral artery pressure from 137 ± 6 mm Hg to 97 ± 3 mm Hg (P < 0.005). There was also a significant increase for the group in arterial PO2 recorded during the apneic episodes from 38 ± 3 mm Hg before tracheostomy to 71 ± 2 mm Hg (P < 0.001) after tracheostomy. We conclude that tracheostomy improves the hemodynamic abnormalities and hypoxemia that occur during sleep in patients with sleep-induced obstructive apnea.
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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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