Sleep apnoea is common in patients with heart failure. While most patients have central sleep apnoea (CSA), a minority have obstructive sleep apnoea (OSA). The pathophysiology of CSA is not well understood. We hypothesized that central chemosensitivity would be an important pathophysiological factor in patients with CSA, and not in OSA. The aim of this study was to compare ventilatory responses between patients with CSA and those with OSA.Acute ventilatory responses to eucapnic hypoxia and hyperoxic hypercapnia were measured during wakefulness in 34 patients (33 males and one female, aged 59±8 yrs (mean±sd)), with stable medically-treated left ventricular dysfunction (LVD) and sleep apnoea (18 OSA and 16 CSA).Patients with CSA had a decreased awake end-tidal carbon dioxide tension (4.1± 0.5 kPa), increased ventilatory response to carbon dioxide (0.65±0.43 L·min-1·kPaPCO2-1), and eucapnic hypoxic responses in the normal range (0.6±0.4 L·min-1/% fall in arterial oxygen saturation (Sa,O2)). In contrast, patients with OSA had normal endtidal carbon dioxide tension (4.9±0.5 kPa), and normal ventilatory responses to hypercapnia (0.29±0.16 L·min-1·kPaPCO2-1) and hypoxia (0.5±0.5 L·min-1/% fall inSa,O2).These findings suggest that augmented chemosensitivity to hypercapnia may be an important factor in the pathophysiology of central sleep apnoea in patients with heart failure.

Summary We hypothesized that individuals with untreated obstructive sleep apnea (OSA) would exhibit greater vulnerability to sleep deprivation than healthy controls, due to the additional neurobiological ‘load’ of chronic sleep fragmentation. After baseline sleep with 8 h time in bed, participants remained awake for 40 h. Psychomotor Vigilance Task (PVT, mean slowest 10% 1/RT), AusEd Driving Simulator task (steering and speed deviation), and subjective sleepiness (Karolinska Sleepiness Scale, KSS) were assessed every 2 h. Nonlinear mixed‐effects models were used to characterize individual differences in baseline/average performance, the linear effect of increasing hours awake, circadian amplitude and phase. Eight participants with untreated OSA with mean (SD) age 44.6 (8.4), apnea–hypopnea index (AHI) 49.8 (24.7), Epworth Sleepiness Scale (ESS) 11.9 (4.8) and nine healthy controls age 27.8 (3.7), AHI 4.5 (2.7), ESS 7.3 (2.1) completed the protocol. Baseline KSS was significantly higher (1.4 units, P = 0.03) in the OSA group and there was a trend toward lower baseline speed deviation on the AusEd (P = 0.05). After adjusting for the significant effects of accumulated time awake, circadian amplitude and phase (all P < 0.005), there was no difference in performance decrements between those with and without sleep apnea in PVT, driving simulator performance and subjective sleepiness (P > 0.5). Random‐effects modeling confirmed the presence of significant inter‐individual variability in vulnerability to sleep deprivation. Patients with OSA did not respond differently to sleep deprivation than healthy controls. As expected, total sleep deprivation led to significant worsening in performance and subjective sleepiness in both groups.

Scientific inveStigAtionS objectives:To describe the growth in the use of state-funded (Medicare) polysomnography (PSG) in Australia since 1990 and to compare PSG growth to other common diagnostic procedures and growth in total Medicare payments. Methods: Interrogation of online database of historical census-level data routinely collected by Medicare. Results: There has been a steady rise in the number of PSGs performed in Australia since 1990; the growth has been faster than overall Medicare-spending growth and faster than growth in comparable diagnostic procedures. However, there are marked interstate differences in growth. Per capita data, available only for 1995 to 2004, shows that nationwide PSG provision has risen from 123 to 308 per 100,000 people enrolled in Medicare. conclusions:The provision of PSG in Australia has been growing steadily since publicly funded reimbursement began in 1990. This growth has been faster than the overall population growth and faster than the growth in Medicare funding for other diagnostic procedures and classes of medical interventions. However, the provision of PSG might be expected to continue to increase because the per capita provision (308 per 100,000) is still less than recent estimates from Canada and the United States (370.4 and 427.0 per 100,000, respectively).