Cases reported "Cheyne-Stokes Respiration"

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1/3. Elimination of central sleep apnoea by mitral valvuloplasty: the role of feedback delay in periodic breathing.

    Central sleep apnoea is a form of periodic breathing which resembles cheyne-stokes respiration but occurs only during sleep. One mechanism in the pathogenesis is a delay in chemical feedback from the lungs to the medullary respiratory centre. We explored the relationship between circulatory feedback delay in a patient with central sleep apnoea and cheyne-stokes respiration before and after mitral valve repair. Preoperatively the patient had severe central sleep apnoea and an increased circulation time. Following mitral valvuloplasty the circulation time was decreased with resolution of central sleep apnoea. This case demonstrates the role of feedback delay in central sleep apnoea and suggests that similar haemodynamic mechanisms may lead to central sleep apnoea and cheyne-stokes respiration.
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2/3. Cheyne-Stokes breathing and systemic arterial pressure periodic pattern during sleep in central alveolar hypoventilation.

    This report refers to a 51 year old man with the clinical features of central alveolar hypoventilation (CAH). Polysomnographic recordings showed periodic breathing and central apnoeas associated with abnormal oscillations of systemic arterial pressure and heart rate during all sleep stages. oxygen administration during sleep reduced hypoxia, while the periodic breathing and arterial pressure oscillations persisted. The authors suggest that an impairment of the brain structures that play a role in homeostatic adjustment of autonomic functions in connection with the sleep-wake cycle, is responsible for the unusual sleep-related disturbances shown by this patient.
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3/3. Beneficial effect of inhaled CO2 in a patient with non-obstructive sleep apnoea.

    A 63-year-old man with severe non-obstructive sleep apnoea (apnoea index 28; apnoea duration 45-60s; O2 saturation between 72% and 98%), who did not respond to common modes of treatment, was successfully treated with CO2. A tent was perfused with compressed air (6 1/min) and increasing amounts of CO2. A concentration of 3% CO2 (180 ml/min) was sufficient to raise the PaCO2 above apnoea threshold and to suppress apnoeas completely. As a result, O2 saturation remained normal throughout the whole night and the symptoms of sleep apnoea disappeared. We hypothesize that the PCO2 ventilatory drive was intact in our patient and that hypocapnia was the major factor causing the non-obstructive sleep apnoea syndrome. Administration of CO2 with a constant flow system could be a safe and easy alternative for patients with non-obstructive sleep apnoea syndrome who present with hypocapnia and an intact respiratory feedback control system.
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keywords = apnoea
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