Susceptibility to periodic breathing with assisted  ventilation during sleep in normal subjects

Meza, Sonia; Méndez, Manuel Sánchez; Ostrowski, Michele; Younes, Magdy

doi:10.1152/jappl.1998.85.5.1929

Cited by 145 publications

(88 citation statements)

References 27 publications

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“…When delivering high VT values through a ventilator, neuromechanical inhibition may occur (33,36). Although approximately the same VT was used under all three conditions, it may not have necessarily caused a comparable degree of neuromechanical inhibition at the three FI O 2 levels (8).…”

Section: Discussionmentioning

confidence: 99%

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Xie¹,

Skatrud²,

Puleo³

et al. 2006

Journal of Applied Physiology

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Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Jerome A. Dempsey. Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep. J Appl Physiol 100: 171-177, 2006. First published September 22, 2005 doi:10.1152/japplphysiol.00440.2005.-To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired PO 2. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O 2 saturation ϭ 78 -80%), and hyperoxia (inspired O2 fraction ϭ 50 -52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 Ϯ 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 Ϯ 0.8 s; P Ͻ 0.05), whereas hyperoxia prolonged it (71.5 Ϯ 13.8 s; P Ͻ 0.01). The apneic threshold end-tidal PCO 2 (PETCO 2 ) was defined as the PETCO 2 at the onset of apnea. During hypoxia, the apneic threshold PET CO 2 was higher (38.9 Ϯ 1.7 Torr; P Ͻ 0.01) compared with normoxia (35.8 Ϯ 1.1; Torr); during hyperoxia, it was lower (33.0 Ϯ 0.8 Torr; P Ͻ 0.05). Furthermore, the difference between the eupneic PET CO 2 and apneic threshold PET CO 2 was smaller during hypoxia (3.0 Ϯ 1.0 Torr P Ͻ 001) and greater during hyperoxia (10.6 Ϯ 0.8 Torr; P Ͻ 0.05) compared with normoxia (8.0 Ϯ 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO 2 below the eupneic PETCO 2 was increased by hypoxia (3.44 Ϯ 0.63 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) and decreased by hyperoxia (0.63 Ϯ 0.04 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) compared with normoxia (0.79 Ϯ 0.05 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors. apnea threshold THE RELATIVE CONTRIBUTION of peripheral vs. central chemoreception in initiating the posthyperventilation apneas remains an unresolved question. The importance of peripheral chemoreception in mediating the rapid ventilatory response to hypocapnia has been supported using animal models. Carotid body denervation either eliminated or prolonged the time course for the development of apnea after the administration of augmented breaths (6, 39). However, carotid body denervation profoundly alters central chemoreception as indicated by the substantial CO 2 retention after denervation. Our laboratory has previously demonstrated the complex effect of hypoxia in t...

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Section: Discussionmentioning

confidence: 99%

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Xie¹,

Skatrud²,

Puleo³

et al. 2006

Journal of Applied Physiology

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“…A commonly used analogy is the regulation of room temperature, whereby temperature will be prone to oscillation in a situation where there is a particularly sensitive thermostat and an overly powerful heater (i.e., high loop gain) (52). Techniques have been developed to measure loop gain of the respiratory system, such as the proportional assist ventilation (PAV) technique (53,54). Studies using PAV have demonstrated that patients with OSA do in fact have an elevated loop gain and suggest that ventilatory instability is an important mechanism contributing to sleep-disordered breathing (55,56).…”

Section: Ventilatory Control Stabilitymentioning

confidence: 99%

Pathophysiology of Adult Obstructive Sleep Apnea

Eckert¹,

Malhotra²

2008

Proceedings of the American Thoracic Society

513

321

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Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive narrowing or collapse of the pharyngeal airway during sleep. The disorder is associated with major comorbidities including excessive daytime sleepiness and increased risk of cardiovascular disease. The underlying pathophysiology is multifactorial and may vary considerably between individuals. Important risk factors include obesity, male sex, and aging. However, the physiological mechanisms underlying these risk factors are not clearly understood. This brief review summarizes the current understanding of OSA pathophysiology in adults and highlights the potential mechanisms underlying the principal risk factors. In addition, some of the pathophysiological characteristics associated with OSA that may modulate disease severity are illustrated. Finally, the potential for novel treatment strategies, based on an improved understanding of the underlying pathophysiology, is also discussed with the ultimate aim of stimulating research ideas in areas where knowledge is lacking.

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“…1 During sleep in PSV mode, inspiratory efforts are constant but tidal volume (V T ) oscillates, intermittently decreasing the P aCO 2 level below the apneic threshold, which is not very different from the P aCO 2 value in eupnea. 2 The apneic P aCO 2 threshold is physiologically lower during stage 1 sleep than during wakefulness.…”

Section: Introductionmentioning

confidence: 99%