Central sleep apnoea, pathogenesis and treatment: an overview and perspective

Backer, W. De

doi:10.1183/09031936.95.08081372

Cited by 65 publications

(44 citation statements)

References 101 publications

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“…Schematically, two types of patients can be identified, namely hypercapnic and nonhypercapnic [12,13]. The hypercapnic group includes patients with central hypoventilation, neurological syndromes and/or impaired respiratory mechanics.…”

Section: Discussionmentioning

confidence: 99%

Central sleep apnoea in Arnold-Chiari malformation: evidence of pathophysiological heterogeneity

Rabec

Laurent²,

Baudouin³

et al. 1998

Eur Respir J

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We report on the case of two young patients with type I Arnold-Chiari malformation (ACM), as revealed by a central sleep apnoea (CSA) syndrome without any other neurological defect. Case 1 was a 14-yr-old male patient, who developed severe alveolar hypoventilation and needed long-term mechanical ventilation via a tracheostomy. Case 2 was a 39-yr-old male patient, who developed features suggestive of sleep apnoea and responded to nasal continuous positive airway pressure ventilation despite the central type of apnoeas. These two cases illustrate the different pathophysiological mechanisms involved in CSA, namely a blunted chemical drive (in hypercapnic patients) and an increased chemical drive, which destabilizes the breathing pattern during sleep (in normo/hypocapnic patients). Central sleep apnoea can be the initial manifestation of Arnold-Chiari malformation and can lead to a life-threatening condition.

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Section: Discussionmentioning

confidence: 99%

Central sleep apnoea in Arnold-Chiari malformation: evidence of pathophysiological heterogeneity

Rabec

Laurent²,

Baudouin³

et al. 1998

Eur Respir J

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“…This is generally related to high loop gain (idiopathic CSA, CSR), prolonged circulation time (CSR) or defective effector organs (hypercapnic respiratory failure). There is accumulating evidence that CSA should be considered as the end of a spectrum [57]. Mostly, CSA occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain (especially in light sleep stages) and the unmasking of a CO 2 threshold.…”

Section: Central Sleep Apnoeamentioning

confidence: 99%

Upper Airway Mechanics

Verbraecken¹,

Backer²

2009

Respiration

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This review discusses the pathophysiological aspects of sleep-disordered breathing, with focus on upper airway mechanics in obstructive and central sleep apnoea, Cheyne-Stokes respiration and obesity hypoventilation syndrome. These disorders constitute the end points of a spectrum with distinct yet interrelated mechanisms that lead to substantial pathology, i.e. increased upper airway collapsibility, control of breathing instability, increased work of breathing, disturbed ventilatory system mechanics and neurohormonal changes. Concepts are changing. Although sleep apnoea is considered more and more to be an increased loop gain disorder, the central type of apnoea is now considered as an obstructive event, because it causes pharyngeal narrowing, associated with prolonged expiration. Although a unifying concept for the pathogenesis is lacking, it seems that these patients are in a vicious circle. Knowledge of common patterns of sleep-disordered breathing may help to identify these patients and guide therapy.

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“…Cheyne-Stokes respiration (CSR) is a specific form of periodic breathing (PB) which can be observed in the setting of congestive heart failure (CHF) [6]. It occurs in y50% of patients with a left ventricular ejection fraction of v40% [7,8].…”

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confidence: 99%

Nocturnal periodic breathing in primary pulmonary hypertension

Schulz

Baseler²,

Ghofrani³

et al. 2002

Eur Respir J

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Cheyne-Stokes respiration is frequently observed in congestive heart failure. Among other factors, prolongation of circulation time, hypocapnia and hypoxia are thought to underlie this sleep-related breathing disorder. Primary pulmonary hypertension (PPH) is also characterized by reduced cardiac output and blood gas alterations. Therefore, the aim of the present study was to determine whether a nocturnal periodic breathing (PB) occurs in PPH.A total of 20 consecutive patients with PPH who had been admitted for pharmacological investigation of pulmonary vasoreactivity were investigated by lung function testing, right heart catheterization and full-night attended polysomnography.PB was detected in six patients (30%) (mean¡SEM: apnoea/hypopnoea index 37¡5 h -1 ; arterial oxygen saturation was v90% during 56¡6.5% of total sleep time). The patients with PB had more severe haemodynamic impairment than those without. They also had a more marked reduction in the pulmonary diffusion capacity and greater arterial hypoxia. PB was markedly improved or even eradicated by nasal oxygen during the night.Periodic breathing occurs in patients with advanced primary pulmonary hypertension and can be reversed by nocturnal nasal oxygen. The clinical and prognostic significance of periodic breathing in primary pulmonary hypertension needs to be determined by further studies.

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Central sleep apnoea, pathogenesis and treatment: an overview and perspective

Cited by 65 publications

References 101 publications

Central sleep apnoea in Arnold-Chiari malformation: evidence of pathophysiological heterogeneity

Central sleep apnoea in Arnold-Chiari malformation: evidence of pathophysiological heterogeneity

Upper Airway Mechanics

Nocturnal periodic breathing in primary pulmonary hypertension

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