Article

Crossing the apnoeic threshold: Causes and consequences

John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, 1300 University Avenue, Rm. 4245 MSC, Madison, WI, USA.
Experimental Physiology (Impact Factor: 2.87). 02/2005; 90(1):13-24. DOI: 10.1113/expphysiol.2004.028985
Source: PubMed

ABSTRACT This brief review addresses the characteristics, lability and the mechanisms underlying the hypocapnic-induced apnoeic threshold which is unmasked during NREM sleep. The role of carotid chemoreceptors as fast, sensitive detectors of dynamic changes in CO2 is emphasized and placed in historical context of the long-held debate over central vs. peripheral contributions to CO2 sensing and to apnoea. Finally, evidence is presented which points to a significant role for unstable, central respiratory motor output as a significant contributor to upper airway narrowing and obstruction during sleep.

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    • "Transient cessations in breathing rhythm (apneas), or in breath amplitude (hypopneas), sufficient to cause significant arterial hypercapnia and hypoxemiam activate a feedback circuit (loop gain) that is stable unless the PaCO 2 thresholds of apnoea and of eupnoea are very close: in this condition the loop gain becomes unstable and patients are predisposed to repetitive episodes of apnoea/hypopnea [54] [55] [56] [57] [58]. If breathing efforts persist, the SDB is classified as ''obstructive'' – OSA; in absence of brain stem respiratory motor output it is instead classified as ''central'' sleep apnea – CSA. "
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    • "Behavioral influences and neurocompensatory responses strongly inhibit apnea, even in the presence of marked decreases in PaCO2 during wakefulness, but this is not the case during sleep. Indeed, during sleep, all individuals are susceptible to breathing cessation when PaCO2 falls below a critical threshold known as the apnea threshold.13–15 The apnea threshold is usually 2–6 mmHg below the eucapnic sleeping PaCO2 level. "
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    • "More specifically, enhancement of peripheral and possibly central chemoreflex sensitivity , particularly during wakefulness (see Point A – Fig. 2), would likely induce profound hypocapnia, resulting in carbon dioxide levels that are significantly below the apneic threshold. This enhanced sensitivity, which might be coupled with a reduction in the carbon dioxide reserve [i.e. the difference between the carbon dioxide value that demarcates the apneic threshold and normal resting values – see Fig. 2 in (Dempsey, 2005) or Fig. 4 in (Mateika and Narwani, 2009) for additional clarification of carbon dioxide reserve if required], could ultimately result in a prolonged central and obstructive apnea during sleep because of the time required for carbon dioxide to build and exceed the apneic threshold . Alternatively, if respiratory muscle activity was enhanced by a mechanism that was independent of chemoreflex input (see Respiratory Plasticity for this discussion) and continued to persist in the presence of hypocapnia (Point B – Fig. 1), the development of a central apnea could be prevented. "
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