Central Sleep Apnea

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Pathophysiologic classification of central sleep apnea

CSA is often classified as hypercapnic or nonhypercapnic central apnea according to the level of alveolar ventilation, as shown in Box 1 [1].

Development of central apnea

Central apnea does not occur as an isolated event but as periodic breathing consisting of cycles of recurrent apnea or hypopnea alternating with hyperpnea. Conversely, experimentally induced central apnea (such as following passive mechanical ventilation) occurs as a single event, with resumption of spontaneous breathing on termination of apnea (see later discussion). Therefore, although hypocapnia can produce the initial event, additional factors are required to sustain breathing instability

Clinical presentation

Patients who have hypercapnic CSA present with the underlying ventilatory insufficiency and features of sleep apnea hypopnea syndrome. Thus, presenting symptoms may include those of the underlying disease in addition to morning headache, peripheral edema, dyspnea, daytime sleepiness, snoring, and poor nocturnal sleep.

The presenting symptoms in patients who have nonhypercapnic central apnea are variable. Patients can present with symptoms similar to obstructive sleep apnea, including snoring and

Management

Management of CSA reflects the heterogeneity of the condition. The approach to the treatment of hypercapnic CSA differs from treatment of nonhypercapnic CSA, given the difference in etiology. The decision to treat a patient who has central apnea is based on the combination of clinical picture, polysomnographic findings, and clinical judgment. The lack of prospective outcome data or accepted metrics of severity precludes the implementation of simple algorithms. In addition, comorbid conditions

Approach in selected cases

The heterogeneity of CSA dictates an individualized approach to therapy, and several considerations must be taken into account.

For CSA associated with sleep onset, it is critical to determine pathology versus physiology. Central apnea may occur only at sleep onset and resolve with consolidation of sleep. This may not require treatment in an asymptomatic individual who is free of significant comorbidity.

Treatment options for CSA associated with CHF (CHF–CSR) begin by ensuring optimal CHF

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References (61)

  • M.S. Badr et al.

    Post-hyperventilation hypopnea in humans during NREM sleep

    Respir Physiol

    (1996)
  • P.R. Eastwood et al.

    Effect of upper airway negative pressure on inspiratory drive during sleep

    J Appl Physiol

    (1998)
  • C.A. Harms et al.

    Negative pressure-induced deformation of the upper airway causes central apnea in awake and sleeping dogs

    J Appl Physiol

    (1996)
  • P.M. Simon et al.

    Role of airway mechanoreceptors in the inhibition of inspiration during mechanical ventilation in humans

    Am Rev Respir Dis

    (1991)
  • A.M. Leevers et al.

    Apnea after normocapnic mechanical ventilation during NREM sleep

    J Appl Physiol

    (1994)
  • A. Xie et al.

    Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea

    Am J Respir Crit Care Med

    (1994)
  • T.D. Bradley et al.

    Clinical and physiologic heterogeneity of the central sleep apnea syndrome

    Am Rev Respir Dis

    (1986)
  • A. Berssenbrugge et al.

    Mechanisms of hypoxia-induced periodic breathing during sleep in humans

    J Physiol

    (1983)
  • G. Warner et al.

    Effect of hypoxia-induced periodic breathing on upper airway obstruction during sleep

    J Appl Physiol

    (1987)
  • S. Javaheri et al.

    Occult sleep-disordered breathing in stable congestive heart failure

    Ann Intern Med

    (1995)
  • T.D. Bradley et al.

    Sleep apnea and heart failure: Part II: central sleep apnea

    Circulation

    (2003)
  • D. Georgopoulus et al.

    Respiratory short-term poststimulus potentiation (after-discharge) in patients with obstructive sleep apnea

    Am Rev Respir Dis

    (1992)
  • F.L. Eldridge

    Central neural stimulation of respiration in unanesthetized decerebrate cats

    J Appl Physiol

    (1976)
  • M.S. Badr et al.

    Determinants of poststimulus potentiation in humans during NREM sleep

    J Appl Physiol

    (1992)
  • A.M. Leevers et al.

    Apnoea following normocapnic mechanical ventilation in awake mammals: a demonstration of control system inertia

    J Physiol

    (1993)
  • B. Phillips et al.

    Sleep apnea: prevalence of risk factors in a general population

    South Med J

    (1989)
  • S. Ancoli-Israel et al.

    Sleep-disordered breathing in community-dwelling elderly

    Sleep

    (1991)
  • A.I. Pack et al.

    Correlation between oscillations in ventilation and frequency content of the electroencephalogram

    J Appl Physiol

    (1992)
  • E.O. Bixler et al.

    Prevalence of sleep-disordered breathing in women: effects of gender

    Am J Respir Crit Care Med

    (2001)
  • D.D. Sin et al.

    Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure

    Am J Respir Crit Care Med

    (1999)
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