Inspiratory duty cycle responses to flow limitation predict nocturnal hypoventilation

Abstract

Upper airway obstruction (UAO) can elicit neuromuscular responses that mitigate and/or compensate for the obstruction. It was hypothesised that flow-limited breathing elicits specific timing responses that can preserve ventilation due to increases in inspiratory duty cycle rather than respiratory rate.By altering nasal pressure during non-rapid eye movement (non-REM) sleep, similar degrees of UAO were induced in healthy males and females (n510 each). Inspiratory duty cycle, respiratory rate and minute ventilation were determined for each degree of UAO during non-REM sleep and compared with the baseline nonflow-limited condition.A dose-dependent increase in the inspiratory duty cycle and respiratory rate was observed in response to increasing severity of UAO. Increases in the inspiratory duty cycle, but not respiratory rate, helped to acutely maintain ventilation. Heterogeneity in these responses was associated with variable degrees of ventilatory compensation, allowing for the segregation of individuals at risk for hypoventilation during periods of inspiratory airflow limitation.Upper airway obstruction constitutes a unique load on the respiratory system. The inspiratory duty cycle, but not the respiratory rate, determine the individual's ability to compensate for inspiratory airflow limitation during sleep, and may represent a quantitative phenotype for obstructive sleep apnoea susceptibility.KEYWORDS: Nocturnal hypoventilation, obstructive sleep apnoea, sex, sleep-disordered breathing, susceptibility, ventilatory control O bstructive sleep apnoea comprises a spectrum of patients with varying degrees of upper airway obstruction (UAO) as manifested by snoring with intermittent arousals (upper airway resistance syndrome and respiratory effort-related arousals), obstructive hypopnoeas and apnoeas [1][2][3]. While male sex and obesity constitute strong risk factors for the varied manifestation of obstructive sleep apnoea [4-6], heritable factors can also play a significant role in the risk of this disorder [7][8][9][10][11][12][13], contributing to the heterogeneity in the expression of this disorder. Nevertheless, physiological mechanisms that explain the heterogeneity of sleep-disordered breathing severity are not known.UAO during sleep plays a pivotal role in the pathogenesis of obstructive sleep apnoea [14] and is caused by structural defects and disturbances in neuromuscular control [14,15]. UAO can elicit neuromuscular responses that mitigate and/or compensate for the obstruction. Under conditions of UAO (inspiratory airflow limitation), immediate responses in respiratory timing indices can help restore ventilation [16][17][18][19] and blunt disturbances in gas exchange [20]. Nevertheless the impact of respiratory pattern responses on ventilation during periods of UAO remains unclear.The purpose of the current study is to examine ventilatory responses to UAO during sleep in normal males and females. It was hypothesised that flow-limited breathing elicits specific timing responses that can preserve v...

Polysomnographic Markers in Children With Cystic Fibrosis Lung Disease

“…Third, the assessment of sleep disordered breathing was more sensitive compared with conventional methods, since IFL was classified using the unfiltered airflow signal from the nasal cannula with a novel method to assess upper-airway obstruction as previously published. 13 Limitations of our study include the small sample size because of the use of data from existing sleep studies.…”

“…These include the prevalence of inspiratory flow limitation (IFL), 10,11 determination of respiratory rate, 10,12 and measurement of inspiratory duty cycle. 10,13 The aim of the current study was to use these measures to assess gas exchange and breathing patterns in children with CF matched by age and BMI to snoring controls undergoing evaluation for obstructive sleep apnea (OSA). We hypothesized that children with CF compared with snoring controls would exhibit breathing pattern alterations and gas exchange abnormalities not reflected by conventional polysomnographic markers of sleep apnea disease severity.…”

“…We used a custom computer program that randomly generated three 3-minute samples per hour of sleep. IFL was identified as previously described 13,16,17 by visual inspection of airflow tracings during defined periods of stable NREM sleep in the absence of arousal artifacts (Fig 1). In brief, IFL was defined when inspiratory airflow showed the following characteristics: flattened contour with an early inspiratory flow maximum (VI max ), highfrequency oscillation, and prolonged inspiratory time.…”

“…In brief, IFL was defined when inspiratory airflow showed the following characteristics: flattened contour with an early inspiratory flow maximum (VI max ), highfrequency oscillation, and prolonged inspiratory time. 13 IFL was quantified as a percentage of the flow-limited breaths relative to the total number of breaths in the 3-minute samples during NREM sleep. 10 …”

The relationship between partial upper-airway obstruction and inter-breath transition period during sleep

“…In particular, patients whose airways exhibit either starling resistor (Remmers et al, 1978;Smith et al, 1988) or negative airway dependant behaviour (Isono et al, 1997) can only maintain flow during increased airway obstruction by compensating with an increase in the inspiratory duty cycle (Owens et al, 2012;Schneider et al, 2009). Our results show that patients with long transition periods during reference segments have the greatest reduction during sustained-PAO segments, suggesting that these patients have a greater capacity to increase their inspiratory duty cycle without a reduction in expiratory period.…”