Abstract
Sleep apnea syndrome (SAS) is characterized by an uninterrupted sequence of apneas recurring for long periods of sleep or throughout the night. The apneas, which are mainly of an obstructive type, are caused by a variety of anatomical and functional factors: obesity and other anatomical features restricting the upper airways, hypotonia of the oropharyngeal muscles or a lack of coordination between inspiratory and dilatory muscles of the upper airways during inspiration, or even an impaired excitability of the respiratory center. The worst consequences of apneas concern ventilation and pulmonary circulation although systemic arterial pressure is known to rise during the apneas, reaching a peak when ventilation resumes [4]. This report deals with the complex hemodynamic changes affecting the general circulation during sleep in SAS patients. The possible mechanisms responsible for the persistent arterial hypertension often encountered in these patients are also discussed.
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Coccagna, G., Cirignotta, F., Lugaresi, E. (1991). Changes in General Circulation in Sleep Apnea Syndrome. In: Peter, J.H., Penzel, T., Podszus, T., von Wichert, P. (eds) Sleep and Health Risk. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76034-1_36
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DOI: https://doi.org/10.1007/978-3-642-76034-1_36
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