The sleep apnoea/hypopnoea syndrome depresses waking vagal tone independent of sympathetic activation.

The modest daytime hypertension and sympathetic upregulation associated with the sleep apnoea/hypopnoea syndrome (SAHS), does not explain the relatively large increased risk of cardiac morbidity and mortality in the SAHS patients population. Therefore, efferent vagal and sympathetic activity was evaluated during wakefulness in SAHS subjects and matched healthy controls, in order to determine if vagal downregulation may play a role in the aetiology of cardiac disease in the SAHS. The awake autonomic nervous system function of 15 male subjects, with mild-to-moderate SAHS was compared to that of 14 healthy controls matched for age, body mass index, gender and blood pressure. All subjects were free from comorbidity. Vagal activity was estimated from measurements of heart rate variability high frequency power (HF) and sympathetic activity was measured from urine catecholamine excretion. The %HF power was significantly (p < 0.03) reduced in SAHS patients (10+/-1.6 (mean+/-SEM)) as compared to controls (17 +/- 3). In addition, HF power correlated with the apnoea/hypopnoea index in the SAHS subjects (R = -0.592, p = 0.02). There was no statistically significant difference in the daytime excretion of nonadrenaline between control (242 +/- 30 nmol x collection(-1)) and SAHS (316 +/- 46 nmol x collection(-1)) subjects (p = 0.38). In these sleep apnoea/hypopnoea syndrome patients there was limited evidence of increased waking levels of urine catecholamines. The principal component altering waking autonomic nervous system function, in the sleep apnoea/hypopnoea syndrome subjects, was a reduced daytime efferent vagal tone.

The effect of sulphur dioxide exposure on indices of heart rate variability in normal and asthmatic adults.

Sulphur dioxide (SO2) is an important air pollutant and causes bronchoconstriction in normal and asthmatic adults. This paper has explored the autonomic consequences of SO2 exposure using the spectral analysis of heart rate variability. Electrocardiogram recordings were made in 12 normal and 12 asthmatic adults undergoing pollutant exposures. Exposures were of a 1 h duration, double blind, in random order, > or = 2 weeks apart and included air and 200 parts per billion SO2. Spectral analysis of R-R intervals was performed. SO2 exposure was associated with an increase in total power (TP) and high (HF) and low frequency (LF) power in the normal subjects, and a reduction in these indices in the subjects with asthma. The difference in TP with SO2 exposure compared to air was +1730 ms2 in the normal group and -1021 ms2 asthmatic group (p<0.003). For HF the respective values were +964 ms2 and -539 ms2 (p=0.02) and for LF, +43 7 ms2 and -57 2 ms2 (p=0.01). No change in lung function or symptoms was observed in either group. This suggests that SO2 exposure at concentrations which are frequently encountered during air pollution episodes can influence the autonomic nervous system. This may be important in understanding the mechanisms involved in SO2 induced bronchoconstriction, and of the cardiovascular effects of air pollution.

Endogenous circadian control of the human autonomic nervous system.

To determine if an endogenous circadian rhythmicity, independent from sleep/wake cycles, exists in autonomic nervous system (ANS) function, heart rate variability analysis of electrocardiogram R-R intervals was applied to data collected during a 27-day forced desynchrony protocol. Results during wakefulness indicate that the circadian pacemaker may control both the sympathetic and vagal limbs of the ANS. Vagal tone was maximal during the circadian phase corresponding to the usual sleep episode (although these measurements were made in the absence of sleep) with an acrophase at 4 AM to 5 AM. Sympathovagal balance was minimal between 9 AM and 1 PM. These endogenous circadian rhythms in ANS function may contribute to mortality from cardiovascular disease and nocturnal asthma.

Evaluation of frequency and time-frequency spectral analysis of heart rate variability as a diagnostic marker of the sleep apnoea syndrome.

The sleep apnoea/hypopnoea syndrome (SAHS) elicits a unique heart rate rhythm that may provide the basis for an effective screening tool. The study uses the receiver operator characteristic (ROC) to assess the diagnostic potential of spectral analysis of heart rate variability (HRV) using two methods, the discrete Fourier transform (DFT) and the discrete harmonic wavelet transform (DHWT). These two methods are compared over different sleep stages and spectral frequency bands. The HRV results are subsequently compared with those of the current screening method of oximetry. For both the DFT and the DHWT, the most diagnostically accurate frequency range for HRV spectral power calculations is found to be 0.019-0.036 Hz (denoted by AB2). Using AB2, 15 min sections of non-REM sleep data in 40 subjects produce ROC areas, for the DFT, DHWT and oximetry, of 0.94, 0.97 and 0.67, respectively. In REM sleep, ROC areas are 0.78, 0.79 and 0.71, respectively. In non-REM sleep, spectral analysis of HRV appears to be a significantly better indicator of the SAHS than the current screening method of oximetry, and, in REM sleep, it is comparable with oximetry. The advantage of the DHWT over the DFT is that it produces a greater time resolution and is computationally more efficient. The DHWT does not require the precondition of stationarity or interpolation of raw HRV data.

Validation of British Thoracic Society guidelines for the diagnosis of the sleep apnoea/hypopnoea syndrome: can polysomnography be avoided?

BACKGROUND: The British Thoracic Society report on the diagnosis and treatment of the sleep apnoea/hypopnoea syndrome (SAHS) suggests that, if the pulse oximetry baseline oxygen saturation is above 90%, then 15 4% oxygen desaturation/hour in bed will diagnose SAHS requiring treatment. The diagnostic outcome of applying these guidelines has been studied. METHODS: One hundred patients referred to a district general hospital sleep clinic were recruited. After initial clinical assessment, overnight pulse oximetry measurements were performed, followed by full polysomnography at the regional laboratory. RESULTS: Sixty nine patients underwent both pulse oximetry and polysomnography. All 10 patients with more than 15 4% desaturations/hour on pulse oximetry had SAHS confirmed on polysomnography (specificity = 100%). Twenty two patients with SAHS were misdiagnosed using pulse oximetry alone (sensitivity = 31%). These patients had low apnoea scores but high hypopnoea scores. CONCLUSIONS: The BTS pulse oximetry criteria are highly specific when positive (specificity = 100%), but may miss patients with the SAHS who have hypopnoeic episodes which cause arousal but not significant oxygen desaturation (sensitivity = 31%). It should be emphasised that pulse oximetry alone does not always give sufficient information to discriminate between those patients with or without SAHS. Patients with "negative" pulse oximetry and symptoms of SAHS should undergo polysomnography or multi-channel recording.