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Cardiac diastolic function and hypercapnic ventilatory responses in central sleep apnoea

Depts of ¹ Respiratory Medicine and ² Cardiology, The Alfred Hospital and Monash University Medical School, Melbourne, Victoria, Australia

CORRESPONDENCE: M.T. Naughton, Dept of Respiratory Medicine, Alfred Hospital, Commercial Road, Melbourne, Victoria, 3004, Australia. Fax: 613 92763601. E-mail: m.naughton@alfred.org.au

Keywords: central apnoea, chemoreceptors, diastolic heart function, pulmonary vascular pressure

Received: January 31, 2002
Accepted April 2, 2002

P. Solin is a recipient of a National Health and Medical Research Council scholarship.

Hyperventilation is the key factor contributing to the development of idiopathic nonhypercapnic central sleep apnoea (ICSA), where left ventricular systolic function is normal. ICSA is reported to occur in 20% of patients with left ventricular diastolic dysfunction, in whom elevated pulmonary vascular pressures and resultant increased pulmonary vagal afferent traffic may contribute to hyperventilation. The contribution of the two potential mechanisms responsible for the hyperventilation seen in the following ICSA was measured: 1) left ventricular diastolic dysfunction-induced pulmonary hypertension; and 2) increased peripheral and central hypercapnic ventilatory responses (HCVR).

The pulmonary artery pressure, left ventricular diastolic function and chemosensitivity to hypercapnia were measured during wakefulness in 16 subjects with ICSA.

All subjects had systolic pulmonary artery pressures <3.99 kPa (<30 mmHg) and only four had diastolic dysfunction. All subjects had elevated peripheral and central HCVR compared with historical normal control subjects. Diastolic dysfunction correlated with increasing age but not with HCVR or markers of central sleep apnoea severity.

Idiopathic nonhypercapnic central sleep apnoea is likely to be dependent upon raised hypercapnic ventilatory responses, and not pulmonary hypertension due to left ventricular diastolic dysfunction.

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