Apnoeic Events Research Articles

Association Between Patent Foramen Ovale and Obstructive Sleep Apnoea

Background: Previous small epidemiological studies have suggested a possible association between patent foramen ovale (PFO) and obstructive sleep apnoea (OSA). Obstructive sleep apnoea (OSA) is an independent risk factor for stroke; and nocturnal apnoeic events can provoke right to left shunting (RLS) via a PFO. Our aim was to assess prospectively the association between PFO and OSA. Methods: A case–control study was performed to evaluate the prevalence of RLS in subjects with and without OSA. Subjects with OSA (n = 85) without history of stroke, migraine, decompression illness, lung disease or heart failure were recruited from a tertiary hospital sleep laboratory. Control subjects (n = 41) proven to have no significant OSA were age-matched in 2:1 ratio. Presence of RLS was assessed by contrast enhanced transcranial Doppler examination with Valsalva manoeuvre. Results: In the OSA group, mean age was 51 ± 13 years, 70.1% were males, mean body mass index was 33.2 ± 6.7 kg, and mean apnoea–hypopnoea index was 39 ± 30 events/h. Prevalence of RLS was significantly higher in the OSA group compared to controls (44.7% versus 24.4%; odds ratio, 2.51; CI, 1.10–5.68; p = 0.032). There was a trend towards a higher proportion of medium to large RLS (>10 microembolic signals) in OSA subjects compared to controls (63.2% versus 30%, p = 0.13). Conclusion: An increased prevalence of RLS occurs in OSA subjects. This may lead to worse desaturation and symptoms of OSA. Further studies could address the pathophysiological and treatment implications of this potentially significant association.

Outcomes of upper airway reconstructive surgery for moderate to severe obstructive sleep apnea syndrome based on upper airway pressure measurements

To assess the effect of upper airway reconstructive surgery for moderate to severe obstructive sleep apnea-hypopnea syndrome (OSAHS) with the obstructive sites determined by pressure measurements, and to evaluate the clinical value of upper airway manometry in localizing the obstructive sites. Fifty-one moderate to severe OSAHS patients were examined using whole night recording, including airway continuous pressure measurements (ApneaGraph, MRA-Medical Ltd, UK). ApneaGraph (AG) transducer catheter contains two pressure and two temperature sensors used for obstruction site determination and detection of apnoeic events during sleep. Obstructive sites were divided into upper (retropalatal region) and lower level (retroglossal region). The lower limit of obstruction was determined by AG pressure pattern. Using constituent ratio to reflect the obstructive proportion of different levels. All patients were divided into two groups (retropalatal or retroglossal) according to the primary obstructive level. The patients of retropalatal group were treated with modified uvulopalatopharyngoplasty (UPPP), or plus hard palate shortening. The patients of retroglossal group underwent tongue and palatal surgical procedures such as UPPP, hyoid suspension, radiofrequency ablation of tongue base, genioglossus advancement etc. All patients were followed-up at least 6 months using Apneagraph. Clinical outcomes included the Epworth sleeping scale (ESS), apnea-hypopnea index (AHI) and lowest arterial oxygen saturation (LSaO2). Five patients had moderate OSAHS and 46 were severe. Four patients had experienced UPPP failures. The ESS reduced from average 17.6 ± 4.7 to 4.3 ± 4.3 (x(-) ± s, t = 15.195, P < 0.001). The AHI reduced from average 52.4 ± 17.5 to 16.3 ± 18.2 (t = 10.873, P < 0.001). The LSaO2 increased from 0.706 ± 0.099 (x(-) ± s) to 0.823 ± 0.092 (t = -8.396, P < 0.001). The success was defined as a ≥ 50 percent reduction and final apnea-hypopnea index < 20/h, the total success rate was 76.5%. Retropalatal group had 27 patients and 24 cases were in retroglossal group.Their success rate were 81.5% and 75.0% respectively. The upper airway pressure measurements can identify the level of obstruction accurately and prove to be effective in the treatment of OSAHS.

Complex paroxysmal nocturnal behaviors in Parkinson's disease

Complex paroxysmal nocturnal motor behavioral disorders (CPNBs) are frequently reported in patients with Parkinson's disease (PD). REM sleep behavior disorder (RBD) is reported in at least a third of PD patients, although CPNB episodes can also occur on arousal from NREM sleep. It is important to establish the nature of CPNBs occurring in PD, as the different types have different neurobiological significance and clinical importance, and also different treatments. Ninety-six PD patients with and without CPNBs were submitted to overnight in-hospital video-polysomnography. Of these, 76 (47 men) were included in the study analysis: these were patients in whom it was possible to establish the presence or absence of CPNBs and to obtain a clear-cut diagnosis of the nature of the CPNBs reported. The CPNBs were found to be RBD episodes in 39 cases (87%) and nonRBD episodes in 6 (13%) (arousal-related episodes arising from NREM sleep in 3 cases and from REM sleep in 2 cases, parasomnia overlapping syndrome in 1 case). In 4 of the 6 subjects with nonRBD episodes, these occurred upon arousal at the end of an obstructive apnoeic event. Our data confirm that CPNBs in PD are, in most cases, RBD episodes. However, arousal-related episodes accounted for 13% of the CPNBs observed in our sample and occurred in close temporal association with sleep-disordered breathing (SDB). The arousal system is defective in extrapyramidal diseases due to neurodegenerative changes involving the brain stem reticular network; against this background, a trigger effect of SDB on CPNBs, through induction of abrupt arousal, may be hypothesized.

Investigation of Pulse Transit Time Characteristics During Single and Recurrent Obstructive Respiratory Events

Conventional overnight polysomnography (PSG) used to determine the respiratory behaviour during sleep can be a complex and expensive procedure. Pulse transit time analysis (PTT) has shown potential to detect obstructive apnoeic and hypopnoeic events (OE) in adults. Due to abnormalities in central ventilatory control, recurring OE may occur. This study was undertaken to determine the potential of PTT to differentiate responses during upper airway obstruction in the paediatric population. This preliminary study included 11 children (10 male; aged 7.5 +/- 3.8 year) recruited to investigate PTT trend during single and recurrent OE. PTT measurements were evaluated against the corresponding PSG results pre-scored by two blinded observers. A total of 110 valid OE (47 single and 63 recurrent) were observed during these PSG studies. There were distinct PTT responses observed for these two types of OE with respect to those of tidal breathing (P < 0.05). For the tidal breathing events, the mean absolute standard deviation (SD) and maximal percentage (%) decrease (MAX) were 7.71 ms and 3.88% respectively. For the recurrent OE, the absolute SD, SD (%) and MAX were 52.21 ms, 8.52% and 55.08% accordingly while for the single OE, the absolute SD, SD (%) and MAX were 12.23 ms, 5.27% and 13.56% respectively. The findings herein can suggest that PTT can be a valuable clinical tool in the paediatric respiratory sleep studies.

Evaluation of ApneaGraph in the diagnosis of sleep-related breathing disorders

ApneaGraph relies on measuring pressure and airflow simultaneously at different levels in the pharynx identifying the segment of airway obstruction and providing baseline respiratory parameters. This study aims to evaluate ApneaGraph and correlate results with both sleep nasendoscopy and polysomnography. This was a prospective study of 49 patients with snoring and/or obstructive sleep apnoea. Thirty of the these patients underwent a PSG and an ApneaGraph study simultaneously in the Sleep Lab. Nineteen patients attended the day surgery unit and had a sleep nasendoscopy with a 10-min ApneaGraph analysis. Polysomnography was used to validate the ApneaGraph system. There are no significant differences (independent t test, P > 0.15) between ApneaGraph compared to Polysomnography based on the apnoea-hypopnoea index, total number of apnoeic events, average oxygen saturations and maximum desaturation. This suggests that the ApneaGraph can be used to assess OSA. Statistically, there is poor correlation between the two groups (Spearman's rho 0.29). In the cases of discordance, ApneaGraph places greater emphasis on a lower pharyngeal contribution. This unique study analyses the ApneaGraph system in the diagnosis of obstructive sleep apnoea and snoring. It demonstrates the benefits of this new system and highlights certain limitations in localizing the site and level of pharyngeal obstruction in patients with sleep disorders.

Simulated apnoeas induce serotonin-dependent respiratory long-term facilitation in rats.

Long-term facilitation (LTF) is a form of respiratory neuroplasticity frequently induced by acute intermittent isocapnic hypoxia (AIH, three 5 min isocapnic hypoxic episodes). Although repetitive apnoeas are a frequent natural occurrence producing brief (< 30 s) episodes of hypoxia and hypercapnia, it is unknown if repetitive apnoeas also elicit LTF. Apnoea-induced LTF may preserve upper airway patency during sleep, thereby limiting further apnoeic events. We tested the hypothesis that repeated, brief ventilator-induced apnoeas are sufficient to induce serotonin-dependent phrenic and hypoglossal (XII) LTF in anaesthetized rats. Anaesthetized, male Sprague-Dawley rats were exposed to three or six 25 s ventilator apnoeas with 5 min intervals, and compared to time control and AIH-treated rats. Three and six ventilator apnoeas induced phrenic and XII LTF with a magnitude similar to AIH. Both apnoea-induced and AIH-induced LTF were associated with a decreased CO(2) recruitment threshold for phrenic and XII activity (approximately 4 mmHg). Spinal methysergide, a serotonin receptor antagonist, blocked apnoea-induced LTF but not changes in the CO(2)-recruitment threshold. Thus, brief ventilator apnoeas elicit phrenic and XII LTF. Similar to AIH-induced LTF, apnoea-induced LTF is serotonin dependent, and the relevant serotonin receptors for phrenic LTF are located in the cervical spinal cord. Apnoea-induced LTF may have implications for the maintenance of breathing stability, particularly during sleep.

Neural respiratory drive during apnoeic events in obstructive sleep apnoea

For a given neural drive, oesophageal pressure during apnoeic episodes may differ from that during airflow, since inspiratory airflow and increased lung volume both reduce pressure generation. It was, therefore, hypothesised that diaphragm electromyography (EMG) may provide additional data to oesophageal pressure when used for the assessment of neural drive in patients with obstructive sleep apnoea, whose breathing is associated with variable airflow and changes in lung volume. Neural respiratory drive was assessed using diaphragm EMG recorded from multipair oesophageal electrodes in 12 patients with obstructive sleep apnoea. Oesophageal pressure was also recorded. The mean+/-sd inspiratory oesophageal pressure swing was 11.0+/-3.7 cmH(2)O during wakefulness, 38.2+/-15.7 cmH(2)O at the end of the apnoea and reduced to 28.5+/-10.4 cmH(2)O at the beginning of arousal. The mean peak inspiratory diaphragm EMG signal was 21.8+/-6.5 muV during wakefulness, 38.6+/-14.0 muV at the end of the apnoea and further increased to 59.6+/-32.0 muV at the beginning of arousal. It was concluded that the pattern of neural drive assessed by oesophageal pressure differs from that measured by diaphragm electromyography during apnoeic events and, therefore, that diaphragm electromyography may be a useful adjunct to measurement of oesophageal pressure for the assessment of neural drive in patients with obstructive sleep apnoea.

Routine neonatal postextubation chest physiotherapy: A randomized controlled trial

To test the effects of a neonatal postextubation programme on the incidence of postextubation collapse and adverse outcomes. A randomized controlled trial was carried out at the Mater Mothers' Hospital, Brisbane. Mechanically ventilated infants were randomized into one of two groups, physiotherapy group--which involved a regimen of chest wall percussion and oropharyngeal suctioning and control group - which involved suctioning without the percussion unless indicated. Chest X-rays were taken at 6 h and at 24 h postextubation. The primary outcome measure was postextubation collapse as determined by a paediatric radiologist blinded to the group allocation. One hundred and seventy-seven neonates were enrolled in the trial between 1997 and 1999. After an interim analysis, the trial was stopped early. No statistically significant difference was shown in the rate of postextubation collapse (15 of 87 (17.2%) physiotherapy group and 17 of 86 (19.8%) control group (P = 0.85)). No differences were shown between the groups in the number of apnoeic or bradycardic events, duration of requirement for supplemental oxygen or the need for re-intubation within 24 h postextubation. The results of this trial suggest that a routine neonatal postextubation chest physiotherapy programme for all infants is not indicated. There was no evidence that chest physiotherapy is associated with any adverse outcomes.

Interaction of chemoreceptor and baroreceptor reflexes by hypoxia and hypercapnia – a mechanism for promoting hypertension in obstructive sleep apnoea

Asphyxia, which occurs during obstructive sleep apnoeic events, alters the baroreceptor reflex and this may lead to hypertension. We have recently reported that breathing an asphyxic gas resets the baroreceptor-vascular resistance reflex towards higher pressures. The present study was designed to determine whether this effect was caused by the reduced oxygen tension, which affects mainly peripheral chemoreceptors, or by the increased carbon dioxide, which acts mainly on central chemoreceptors. We studied 11 healthy volunteer subjects aged between 20 and 55 years old (6 male). The stimulus to the carotid baroreceptors was changed using graded pressures of -40 to +60 mmHg applied to a neck chamber. Responses of vascular resistance were assessed in the forearm from changes in blood pressure (Finapres) divided by brachial blood flow velocity (Doppler) and cardiac responses from the changes in RR interval and heart rate. Stimulus-response curves were defined during (i) air breathing, (ii) hypoxia (12% O(2) in N(2)), and (iii) hypercapnia (5% CO(2) in 95% O(2)). Responses during air breathing were assessed both prior to and after either hypoxia or hypercapnia. We applied a sigmoid function or third order polynomial to the curves and determined the maximal differential (equivalent to peak sensitivity) and the corresponding carotid sinus pressure (equivalent to 'set point'). Hypoxia resulted in an increase in heart rate but no significant change in mean blood pressure or vascular resistance. However, there was an increase in vascular resistance in the post-stimulus period. Hypoxia had no significant effect on baroreflex sensitivity or 'set point' for the control of RR interval, heart rate or mean arterial pressure. Peak sensitivity of the vascular resistance response to baroreceptor stimulation was significantly reduced from -2.5 +/- 0.4 units to -1.4 +/- 0.1 units (P < 0.05) and this was restored in the post-stimulus period to -2.6 +/- 0.5 units. There was no effect on 'set point'. Hypercapnia, on the other hand, resulted in a decrease in heart rate, which remained reduced in the post-stimulus period and significantly increased mean blood pressure. Baseline vascular resistance was significantly increased and then further increased in the post-control period. Like hypoxia, hypercapnia had no effect on baroreflex control of RR interval, heart rate or mean arterial pressure. There was, also no significant change in the sensitivity of the vascular resistance responses, however, 'set point' was significantly increased from 74.7 +/- 4 to 87.0 +/- 2 mmHg (P < 0.02). This was not completely restored to pre-stimulus control levels in the post-stimulus control period (82.2 +/- 3 mmHg). These results suggest that the hypoxic component of asphyxia reduces baroreceptor-vascular resistance reflex sensitivity, whilst the hypercapnic component is responsible for increasing blood pressure and reflex 'set point'. Hypercapnia appears to have a lasting effect after the removal of the stimulus. Thus the effect of both peripheral and central chemoreceptors on baroreflex function may contribute to promoting hypertension in patients with obstructive sleep apnoea.

Is heart rate variability the simple solution to diagnose sleep apnoea?

Early in the investigation of obstructive sleep apnoea it was recognised that the events of apnoea and hypopnoea are accompanied by concomitant cyclic variations in heart rate 1. The pattern of brady/tachycardia is closely linked to the time course of apnoeic events. As a consequence, this pattern had been used successfully to detect sleep apnoea in patients with clinical symptoms for sleep apnoea. Dedicated devices were developed over the past 15 yrs to detect sleep apnoea at an early stage of the disease using recordings of heart rate, snoring, oxygen saturation and body position 2. These devices were used successfully to stratify the individual risk of patients suffering from sleep-disordered breathing before they were referred to cardiorespiratory polysomnography. Sleep laboratories have limited capacity for cardiorespiratory polysomnography and are expensive in terms of personal costs due to continuous attendance during the night. The sensitivity and specifity of these simplified four channel-based recording systems had been evaluated in many studies giving results for specific systems. A recent systematic review compiled the results of these studies in a comparative overview 3. The review revealed the value and the limitations of systems with respect to the accepted criteria for the diagnosis of sleep apnoea 4. In conclusion, a satisfactory standardisation of terms and of diagnostic criteria regarding the portable diagnosis of sleep apnoea could not be achieved. In parallel with efforts to define evidence-based criteria for the simplified diagnosis of …

Activity of dorsal medullary respiratory neurons in awake rats.

Sleep disordered breathing (SDB) is a major clinical disorder affecting 2-4% of the middle-aged [Young et al., 1993] and is a major public health problem [Phillipson, 1993]. It is characterized by multiple episodes of collapse of the upper airway (UA) during inspiration when the negative pressure in the UA is not adequately counteracted by contraction of UA dilator muscles (obstructive sleep apnoea, OSA) or more rarely by episodic central hypopnoea or apnoea i.e. reduced neural drive to the respiratory muscles [Deegan and McNicholas, 1995]. This results in sleep fragmentation and asphyxia and is associated with hypersomnolence, impaired cognitive function and increased risk of pulmonary and systemic hypertension, congestive heart failure, cardiac arrhythmias, myocardial infarction, stroke and vehicular accidents [Deegan and McNicholas, 1995; Peter et al., 1995]. OSA is caused by collapse of the UA during sleep because of a reduction in tone of the UA muscles that dilate and stabilize the UA during inspiration [Remmers et al., 1978]. However, the cause of the reduction in UA muscle tone occurring in OSA is not known but there is evidence suggesting that it is due to a withdrawal of serotonergic or noradrenergic facilitation of the hypoglossal motor nucleus (XHn), in the dorsal medulla, that contains the motoneurons to the UA muscles (see Horner, 2000, for review). An understanding of the activity of this nucleus is fondamental to understanding the cause of OSA and opens the possibility of pharmacological intervention to treat or prevent OSA [Horner, 2000]. There is some evidence implicating alterations in this central control of respiration in the pathophysiology of SDB [Horner, 1996; Pack, 1995] and histochemical brainstem abnormalities have been identified in patients who have died of sleep apnoea [Sullivan et ai, 1990]. The Xlln receives crucial inputs from other central areas involved in the integration of responses to chemoreceptors and mechanoreceptors, such as the nucleus tractus solitarius (NTS) [Ono et al., 1994; Peever et al., 2002]. However, little is known about the premotor inputs to the XIIn. During apnoeas, there is systemic hypoxia and hypercapnia and the UA muscle responses to systemic hypoxia and hypercapnia play a crucial role in the prevention of apnoea during sleep normally [Parisi et al., 1987; Brouillette and Thach, 1980; Gleeson et al., 1989; Bowes et al., 1981] and in the termination of apnoeic events in SDB [Parisi et al., 1987; Gleeson et al., 1989].

Computerised audiovisual event recording for infant apnoea and bradycardia.

Event recording, by differentiating between true and false events, has advanced the diagnosis and management of infants on home cardiorespiratory monitors; however, the pathogenesis of many events remains obscure. To clarify infant behaviours around the time of apnoea/bradycardia alarms, a computerised audiovisual event recording system (CAVERS) triggered by the apnoea/bradycardia recorder, has been developed. The audiovisual recording can begin up to 3 min before the alarm and can continue for up to 3 min after the alarm. CAVERS information is recorded for a total of 65 events in 13 infants. The CAVERS proves most helpful in documenting infant position and the wide variety of behaviours associated with bradycardic events. These behaviours range from sleep or quiet wakefulness to crying and generalised movements. Post-event activity is also highly variable. Interestingly, 20 of 65 events appear to terminate when the infant wakes to the audible monitor alarm. Nursing intervention is documented for 14 of 42 bradycardic events but only one of 23 apnoeic events. The CAVERS, by elucidating infant behaviours, provides information complementary to that given by cardiorespiratory event recording. It is suggested that infant monitors of the future should incorporate both audiovisual and cardiorespiratory data to elucidate optimally apparent life-threatening events, apnoeas and bradycardias.

Sleep bruxism in patients with sleep-disordered breathing

The aim was to test the hypothesis of a direct association between sleep-disordered breathing and sleep bruxism. The frequency of masseter contraction (MC) episodes and rhythmic jaw movements (RJM) was measured in patients with mild and moderate obstructive sleep apnoea (OSA). The diagnosis of sleep bruxism was made from a combination of questionnaire, clinical observation and all-night polysomnographic recording which included masseter electromyography. A total of 21 patients (19 males/two females, mean age 40.0 years±9.2 SD) were randomly selected from a provisional diagnosis of snoring and OSA by a sleep physician. In the patients with mild OSA [ n=11, mean apnoea hypopnoea index (AHI)=8.0±4.1 SD, body mass index (BMI)=29.1±5.0], the diagnosis of sleep bruxism was made in six out of 11 patients (54%); similarly, four out of 10 patients (40%) with moderate OSA ( n=10, mean AHI=34.7±19.1, BMI=30.6±5.0) were identified as bruxists. Although the combination of clinical, subjective estimation and nocturnal electromyographic recording of masseter muscle might provide a more solid base for the diagnosis of sleep bruxism, the result is biased by the variation in the bruxing activity. MC episodes were associated with the termination of apnoea or hypopnoea episodes in only 3.5% of the mild group and 14.4% of the moderate group ( p<0.05). It appears that sleep bruxism is rarely directly associated with apnoeic events, but is rather related to the disturbed sleep of OSA patients.

Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study

Objective: To assess whether sleep apnoea syndrome is an independent risk factor for hypertension.Design: Population study.Setting: Sleep clinic in Toronto.Participants: 2677 adults, aged 20-85 years, referred to the sleep clinic...

Nasal pressure recording in the diagnosis of sleep apnoea hypopnoea syndrome

BACKGROUNDNasal pressure tracing is now being used to measure breathing in ambulatory screening devices for sleep apnoea but it has not been compared with other methods of assessment.METHODSSleep induced breathing...

Haemodynamic responses to obstructive sleep apnoeas in premenopausal women.

Obstructive apnoeas during sleep are associated with marked cyclical blood pressure fluctuations in men with obstructive sleep apnoea (OSA). Haemodynamic responses to OSA in women are largely unknown. We aimed to investigate haemodynamics during apnoeic events in women with OSA and to assess the influence of the menstrual cycle on these responses. Full overnight polysomnography and continuous non-invasive blood pressure monitoring was performed in 13 women with OSA during follicular and luteal phases of the menstrual cycle. Change in blood pressure (deltaBP) from pre- to post-apnoea termination was measured for each apnoeic cycle. Only 10 of 13 subjects ovulated. In women who ovulated, pressor responses to apnoea termination occurred in both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep, but substantially increased during the luteal phase of ovulatory cycles [NREM change in mean arterial pressure (deltaMAP) 12 +/- 3 mmHg during the follicular phase and 20 +/- 3 mmHg during the luteal phase, P < 0.001; REM deltaMAP 11 +/- 3 mmHg during the follicular phase and 23 +/- 3 mmHg during the luteal phase, P < 0.001]. Sleep apnoea severity did not change during the cycle in NREM sleep, but was reduced in REM during the luteal phase. Changes in pressor responses were absent in non-ovulating subjects. Obstructive apnoeas in women were associated with marked blood pressure changes, similar to those previously reported in men. While respiratory events improved slightly in the luteal phase, blood pressure responses to these events increased by approximately 100%. Thus, the menstrual cycle has discordant effects on the respiratory and cardiovascular effects of OSA in women.

Flumazenil antagonizes midazolam-induced airway narrowing during nasal breathing in humans

We measured nasal resistance (Rn) while awake, during midazolam-induced sedation and after antagonism with flumazenil (n = 9). Nasal and oral airflow were measured. Rn was calculated by dividing the difference between maximal nasal mask and oropharyngeal pressures by inspiratory airflow at minimum pharyngeal pressure. During sedation, two subjects developed obstructive apnoeic events and four subjects had snoring events. Each apnoea was ended by mechanisms other than a change in breathing route. After antagonism with flumazenil, apnoeic and snoring events were abolished. Rn during midazolam sedation (median 1.46 (25th percentile 1.00, 75th 2.61) kPa litre-1 s) was significantly greater than before midazolam (0.29 (0.25, 0.48) kPa litre-1 s) and after flumazenil (0.41 (0.25, 0.58) kPa litre-1 s) (P < 0.01 in each subject). We conclude that midazolam increased Rn, sometimes leading to obstruction, and flumazenil abolished this increase in Rn.

Evaluation of a non-invasive respiratory monitoring system for sleeping subjects

In a previous paper we introduced a non-invasive respiratory monitoring system (NIRMS) for monitoring respiratory movements during sleep. Unlike standard sleep laboratory methods, the NIRMS can be used in frail older adults to describe breathing patterns during sleep that will mark individuals with declining neurological function. The present study evaluates the use of the NIRMS as a respiratory monitor and identifies variables that can reliably detect changes in breathing patterns and the presence of other body movements. Data were obtained from eleven healthy adults (six women, five men) whose body mass indices ranged from 20 to , and whose baseline respiratory rates ranged from 4 to 19 breaths per minute. We evaluated three variables derived from frequency and amplitude measurements of the NIRMS: (1) the interval between breathing cycles (the interbreath interval or IBI); (2) the period between breathing cycles (the interbreath frequency or IBF); and (3) the amplitude of breath cycles (AMP). The frequency of NIRMS waveform deflections correlated highly with the frequency of visually observed chest movements ( r = 0.99). Compared with a subject's baseline, a standard deviation of IBI > 3.0 s consistently identified time segments with three or more apnoeic events. The IBF and AMP differentiated respiratory from other body movements. An IBF > 20 cycles/s or an AMP > 0.4 V identified experimentally introduced body movements much more accurately than wrist accelerometry (NIRMS detected 99% of events, ; WA detected 50%, ). These findings support the use of the NIRMS in monitoring changes in breathing patterns during sleep, especially in frail and cognitively impaired subjects. Keywords: breathing, movements, non-invasive monitoring device, sleep, older adults

Spectral analysis of wakefulness and REM sleep EEG in patients with sleep apnoea syndrome.

Neuropsychological investigations of patients with obstructive sleep apnoea syndrome (OSAS) have shown impairments in such basic functions as memory, attention and executive control. Since executive functions are known to be dependent on the integrity of the frontal lobe, it was hypothesized that OSAS may be associated with hypoxaemic frontal lobe dysfunction. To test this hypothesis, 21 apnoeic patients and 10 normal controls were studied with quantitative electroencephalographic (EEG) methods during rapid eye movement (REM) sleep, when most apnoeic events occur and during wakefulness. In apnoeic patients, EEG slowing in REM sleep was observed over frontal, central and parietal regions, while EEG slowing during wakefulness was observed over all cortical regions examined. A positive correlation was found between EEG slowing during wakefulness and oxygen desaturation during the night. Contrary to the hypothesis, these electroencephalographic changes were not localized only to the frontal region. This result may explain the wide range of neuropsychological deficits noted in patients with obstructive sleep apnoea syndrome, in addition to their poor performance in tasks of executive functioning.

Systemic arterial blood pressure during obstructive sleep apnoea

The cardiovascular changes that accompany obstructive apnoeic events are now well recognized, but their relationship to other processes during the apnoea, whether mechanical, chemical or neurophysiological remains unclear. These relationships have been examined by focusing on arterial blood pressure measured non-invasively using the Finapres device, gas tensions (SaO2, ETCO2), intrathoracic effort (Ppl) and the median EEG frequency (derived from off-line FFT analysis). Eighteen patients with OSA were studied (mean age 43.7 y, BMI 31.2, A + HI 41.2) during stable NREM sleep. However, not all variables were measured for each patient. Data were analysed for the breath before, at the start, mid and end of the apnoea and immediately afterwards. Mean blood pressure initially fell with the onset of apnoea, remained stable until mid-apnoea but rose acutely with apnoea termination. The mean systolic and diastolic pressures were greater during inspiration for the initial and mid-apnoeic efforts, but this difference was reversed at apnoea termination, possibly reflecting the onset of the arousal response. The change in blood pressure over the apnoea was unrelated to apnoea duration and only weakly associated with the intensity of the peak pleural pressure. The rise in blood pressure at end apnoea was related to the fall in SaO2, but not to changes in ETCO2. There was no correlation between the change in EEG frequency and blood pressure over the apnoea as a whole but the increase in blood pressure from the final effort to the first breath correlated with the change in EEG frequency. These data suggest that the change in arterial pressure during an obstructive apnoea are only weakly dependent on the intensity of inspiratory effort made, but are modified by chemical factors and especially changes in sleep state. The close relationship between arousal and change in blood pressure in NREM events confirms the usefulness of cardiovascular markers of arousal responses in OSA.