Apnoeic Events Research Articles

Is non-normalized chest wall electromyogram activity a reliable index of respiratory neural drive? On the surface - yes!

Is non-normalized chest wall electromyogram activity a reliable index of respiratory neural drive? On the surface - yes!

The effect of atrial fibrillation intervention on nocturnal respiratory events in elderly patients with persistent AF.

Sleep-disordered breathing (SDB) and atrial fibrillation (AF) are associated. This study investigated the impact of AF intervention on 6-month home sleep testing data. Sixty-seven patients (aged 66 to 86, 53% male) with persistent AF were randomized (1:1:1) to direct current cardioversion (DCCV) (22 patients), permanent pacemaker (PPM) + atrioventricular node ablation (AVNA) + DCCV (22 patients) or AF ablation (23 patients). Baseline and 6-month multichannel home sleep tests with the Watch-PAT200 (Itamar Medical Lts., Caesarea, Israel) were recorded. Implantable cardiac monitors (ICMs) (Medtronic Reveal XT, Minneapolis, Minnesota) in the DCCV and AF ablation groups, and PPM Holters in the 'pace and ablate' group were utilized to assess cardiac rhythm beat-to-beat throughout the study period. The prevalence of moderate-to-severe SDB [apnoea-hypopnoea index (AHI) ≥ 15/h] was 60%. At 6months there was no change in AHI, Epworth sleepiness scale, sleep time, % REM sleep, respiratory desaturation index or central apnoeic events. Twenty-five patients (15 AF ablation, 9 DCCV and 1 following DCCV post-AVNA) maintained SR at 6months confirmed on ICMs in these patients. AHI fell from 29.8±26.6/h to 22.2±20.4/h; P=0.049. SDB is highly prevalent in patients with persistent AF. Restoration of sinus rhythm, and the associated long-term recovery of haemodynamics, is associated with a significant reduction in AHI. This implicates reversal of fluid shift from the lower limbs to the neck region, a key mechanism in the pathogenesis of SDB.

End-tidal carbon dioxide monitoring improves patient safety during propofol-based sedation for breast lumpectomy: A randomised controlled trial.

The use of sedation is becoming more commonplace. Although pulse oximetry is a standard monitoring procedure during sedation, it cannot accurately detect early hypoventilation. End-tidal carbon dioxide (EtCO2) monitoring can be an earlier indicator of airway compromise; however, the existing literature is limited to a few studies with varying outcomes. To evaluate whether EtCO2 monitoring decreases the incidences of CO2 retention and apnoeic events in propofol-based sedation. Randomised controlled study. A tertiary hospital. Two hundred women (aged 18 to 65 years, ASA physical status 1 or 2) who were scheduled for breast lumpectomy between June 2017 and August 2017. Patients were allocated randomly to receive either standard monitoring or standard monitoring and EtCO2 monitoring. The primary outcome was the incidence of CO2 retention. The secondary outcomes were the number of actions taken to restore ventilation, variations in PaCO2 and pH, the frequency of apnoea and the recovery time. CO2 retention occurred significantly less often in the EtCO2 monitoring group (10 vs. 87%; P < 0.0001). In the standard monitoring group, the mean PaCO2 was more than 6 kPa (45 mmHg) and the pH was less than 7.35 at 5, 10, 20 and 30 min after induction of anaesthesia and at the end of the procedure. Both values were within the normal range in the EtCO2 monitoring group. The number of airway interventions performed was significantly higher in the EtCO2 monitoring group (9.8 ± 1.8 vs. 1.9 ± 1.0; P < 0.0001). Apnoea occurred significantly less often in the EtCO2 monitoring group (0 vs. 10%; P < 0.0001) and recovery time was shorter (9.9 ± 1.4 vs. 11.4 ± 2.1 min; P = 0.048). The addition of EtCO2 monitoring to standard monitoring during propofol-based sedation can improve patient safety by decreasing the incidence of CO2 retention, and therefore the risk of hypoxaemia through early recognition of apnoea, and can also shorten recovery time. This trial is registered with http://www.chictr.org.cn (ChiCTR-INR-17011537).

Symbolic dynamics to enhance diagnostic ability of portable oximetry from the Phone Oximeter in the detection of paediatric sleep apnoea

Objective: This study is aimed at assessing symbolic dynamics as a reliable technique to characterise complex fluctuations of portable oximetry in the context of automated detection of childhood obstructive sleep apnoea-hypopnoea syndrome (OSAHS). Approach: Nocturnal oximetry signals from 142 children with suspected OSAHS were acquired using the Phone Oximeter: a portable device that integrates a pulse oximeter with a smartphone. An apnoea-hypopnoea index (AHI) ⩾ 5 events h−1 from simultaneous in-lab polysomnography was used to confirm moderate-to-severe childhood OSAHS. Symbolic dynamics was used to parameterise non-linear changes in the overnight oximetry profile. Conventional indices, anthropometric measures, and time-domain linear statistics were also considered. Forward stepwise logistic regression was used to obtain an optimum feature subset. Logistic regression (LR) was used to identify children with moderate-to-severe OSAHS. Main results: The histogram of 3-symbol words from symbolic dynamics showed significant differences (p < 0.01) between children with AHI < 5 events h−1 and moderate-to-severe patients (AHI ⩾ 5 events h−1). Words representing increasing oximetry values after apnoeic events (re-saturations) showed relevant diagnostic information. Regarding the performance of individual characterization approaches, the LR model composed of features from symbolic dynamics alone reached a maximum performance of 78.4% accuracy (65.2% sensitivity; 86.8% specificity) and 0.83 area under the ROC curve (AUC). The classification performance improved combining all features. The optimum model from feature selection achieved 83.3% accuracy (73.5% sensitivity; 89.5% specificity) and 0.89 AUC, significantly (p <0.01) outperforming the other models. Significance: Symbolic dynamics provides complementary information to conventional oximetry analysis enabling reliable detection of moderate-to-severe paediatric OSAHS from portable oximetry.

EFFECT OF BETA BLOCKERS ON NOCTURNAL ARRHYTHMIAS AND HEART RATE VARIABILITY IN OBSTRUCTIVE SLEEP APNOEA PATIENTS

Objective: To explore the effects of BB on nocturnal peri-apnoeic heart rate variability (HRV) and on arrhythmias in OSA patients. Design and method: Arrhythmias and increased cardiovascular V are highly prevalent in patients with obstructive sleep apneas (OSA), possibly resulting in fatal events, as showed by the significant increase of sudden cardiac death and arrhythmias during sleep in OSA patients. Data concerning drug effects on this phenomenon are scarce and the use of beta blockers (BB) has been limited by the concern that they might lead to bradyarrhythmias. However, recent evidence suggests that BB mostly reduce rhythm accelerations with trivial influence on decelerations. We enrolled 166 OSA patients (78 BB-treated and 88 BB-naïve), who performed cardiorespiratory polysomnography (PSG) between 2013 and 2015. Patients on antiarrhythmic therapy were excluded. We analysed PSG-derived ECG traces for the assessment of arrhythmias. Moreover, through an ad hoc developed software, we performed a specific analysis of HRV associated with apnoeic events. We considered HR decelerations occurring during the apnoeic phase and accelerations during the post-apnoeic phase (the first five seconds after the resumption of breathing). Statistical analysis was performed with Mann-Whitney U test. Results: We did not find any difference between BB-treated and BB-naïve groups concerning prevalence of nocturnal arrhythmias. HRV analysis showed a reduction of HR accelerations, expressed as RR length, during post-apnoeic phase in BB group (940.7 ± 121.4msec BB-treated vs 897.8 ± 122.5msec BB-naïve; P = 0.040). Moreover, BB-treated patients showed a smaller delta between HR decelerations/accelerations and mean HR during apnoeic phase (58.5 ± 28.5 vs 74.6 ± 40.2msec; P = 0.010 and75.0 ± 42.4 vs 96.7 ± 55.5msec; P = 0.018, respectively). Finally, the delta between HR accelerations and decelerations was smaller in BB-treated group (133.5 ± 63.8 vs 171.3 ± 87.7msec; P = 0.010). Conclusions: BB therapy does not worsen apnoea-induced HR decelerations nor increase the risk of bradyarrhythmias, while reducing the frequency and magnitude of apnoea-induced HR acceleration. Therefore, our study suggests that BB are safe and possibly advantageous in OSA patients, although further studies are needed to establish if in the long term they may have a role in reducing fatal events.

Le syndrome d’apnées obstructives du sommeil n’est pas mauvais que pour le cœur !

Obstructive sleep apnoea (OSA) is common in the general population, particularly in the elderly. This syndrome is frequently responsible for severe cardiovascular complications. However, the indications for its treatment in the elderly remain controversial. We report the case of a 79-year-old man with severe, undiagnosed OSA who inhaled his fixed dental bridge during sleep. The inhaled foreign body came to rest in the lumen of the left main stem bronchus. The association of obesity with a body mass index of 30kg/m2, snoring with breathing pauses reported by his partner, nocturia, morning headache and an Epworth score of 11 led to polysomnography which confirmed OSA with an apnoea/hypopnoea index of 53 per hour. This case report emphasises that OSA may constitute a risk fact for foreign body inhalation in elderly subjects due to arousal-induced hyperventilation following the apnoeic event.

Congenital myasthenic syndrome with episodic apnoea: clinical, neurophysiological and genetic features in the long-term follow-up of 19 patients

BackgroundCongenital myasthenic syndrome with episodic apnoea (CMS-EA) is a rare but potentially treatable cause of apparent life-threatening events in infancy. The underlying mechanisms for sudden and recurrent episodesof respiratory arrest in these patients are unclear. Whilst CMS-EA is most commonly caused by mutations in CHAT, the list of associated genotypes is expanding.MethodsWe reviewed clinical information from 19 patients with CMS-EA, including patients with mutations in CHAT, SLC5A7 and RAPSN, and patients lacking a genetic diagnosis.ResultsLack of genetic diagnosis was more common in CMS-EA than in CMS without EA (56% n = 18, compared to 7% n = 97). Most patients manifested intermittent apnoea in the first 4 months of life (74%, n = 14). A degree of clinical improvement with medication was observed in most patients (74%, n = 14), but the majority of cases also showed a tendency towards complete remission of apnoeic events with age (mean age of resolution 2 years 5 months). Signs of impaired neuromuscular transmission were detected on neurophysiology studies in 79% (n = 15) of cases, but in six cases, this was only apparent following specific neurophysiological testing protocols (prolonged high-frequency stimulation).ConclusionsA relatively large proportion of CMS-EA remains genetically undiagnosed, which suggests the existence of novel causative CMS genes which remain uncharacterised. In light of the potential for recurrent life-threatening apnoeas in early life and the positive response to therapy, early diagnostic consideration of CMS-EA is critical, but without specific neurophysiology tests, it may go overlooked.

Sleep apnoea is common in severe peripheral arterial disease.

BackgroundAtherosclerotic conditions have been demonstrated to be associated with sleep- disordered breathing (SDB). Peripheral arterial disease (PAD) represents severe atherosclerosis with a high mortality. In early stages of PAD a substantial prevalence of sleep apnoea has already been shown. Here, we sought to determine the frequency of undiagnosed sleep apnoea in a homogeneous group of advanced PAD patients undergoing percutaneous revascularization.Methods59 consecutive patients (mean age: 71.1 ± 9.8 years, 67.8% males) with PAD in Fontaine stages IIb-IV that underwent percutaneous transluminal angioplasty at our department were enrolled for pre-procedural polygraphy.ResultsPatients appertained to Fontaine clinical stage IIb, III and IV in 54.2%, 23.8% and 22.% of cases, respectively, and were principally intervened for femoropopliteal occlusive disease (71.2% of total study population). Polygraphy revealed sleep apnoea in 48 out of 59 patients (81.4%), of whom 60.4% offered a primarily obstructive-driven genesis. Among those patients with polygraphically confirmed sleep apnoea, mean apnoea hypopnoea index (AHI) and mean oxygen desaturation index (ODI) averaged 28.2 ± 19.5/h and 26.7 ± 18.8/h, respectively. 18 patients even offered an AHI ≥30/h that is indicative of severe sleep apnoea. For obstructive-driven apnoeic events, AHI correlated significantly with PAD severity stages (p = 0.042).ConclusionsIn our PAD collective, sleep apnoea was frequent and obstructive sleep apnoea´s severity correlated with PAD severity stages. Long-term results regarding the vasoprotective impact of CPAP treatment on PAD course remains to be determined.

Physiopathologie du syndrome d’apnées-hypopnées obstructives du sommeil et de ses conséquences cardio-métaboliques

Obstructive sleep apnoea syndrome (OSAS) is characterized by recurrent partial or complete pharyngeal collapses during sleep. The pathophysiology of OSAS is complex and multifactorial. Factors influencing upper airway patency include a reduction in upper airway dimensions that can result from both anatomical and functional alterations (obesity, fluid shift or maxillo-facial structural changes), and increased pharyngeal collapsibility owing to reduced neuromuscular compensation and lack of the pharyngeal protective reflex during sleep. Severe OSAS is associated with a high cardiometabolic risk. Obstructive apnoeic events incorporate a range of stressors that activate mechanisms contributing to the initiation and progression of cardiac, vascular and metabolic diseases. Obstructed breathing induces markedly negative intrathoracic pressure and also provokes hypoxia and hypercapnia. The hypoxaemic stress is further amplified by the subsequent reoxygenation (intermittent hypoxia), resulting in the generation of reactive oxygen species (ROS), sympathetic activation and inflammation. OSAS is able to increase the number of fatal and non-fatal cardiovascular events, including arrhythmias, myocardial infarction and stroke. OSAS is associated with dyslipidemia, type 2 diabetes, its poor control and non-alcoholic fatty liver disease. Screening, diagnosis and integrated care of OSAS should be included in an aggressive management of risk reduction in chronic cardiovascular and metabolic diseases.

Classical Music Therapy Influences Physiological Parameters in Preterm Neonates

Introduction: Neonates are unique and distinctive from the rest of pediatric population due to particular problems related to extrauterine adaptations, anatomical and physiological immaturity. The primary purpose of this study is to assess the effect of classical music therapy on physiological parameters among preterm neonates. Methods: The research approach of the study was Quasi experimental with time series design. Classical music (Instrumental Flute) was played for 50 preterm babies of 30-36 weeks of gestation with MP3 player, using head phone for a total duration of 30 minutes at 20 to 30dB-SPL. Heart rate and oxygen saturation by pulse oximeter were monitored along with respiratory rate and recorded at 5-minute intervals during the therapy period and for the pre-music and after music therapy period, the time intervals were 2.5 minutes. The study duration was 60 minutes, 15 minutes before music therapy (BMT), 30 minutes of music therapy (DMT) and 15 minutes after music therapy (AMT). 50 preterm neonates admitted in newborn nursery were selected by convenient sampling and studied for four consecutive days. Day 1 and 3 for music therapy (experimental group) and day 2 and four as the control group when no music was played through the head phone. Here the subjects act as the control group on alternate days. Results: Mean HR value on day 1 and 3 (with music were significantly lower during the music (DMT) and after music (AMT) phases compared to BMT (139.1±10.9(BMT), 128.9±10.3 (DMT) and 128.9±10.3 (AMT); BMT Vs DMT (F= 584.25, P<0.001, BMT Vs AMT (F= 295.76, P<0.001). In contrast, day 2 and 4 (control-no music), there were no differences in mean HR during the three phases of observation (139.4±11.4 (BMT), 139.9±11.4 (DMT) and 140.4±11.2 (AMT); BMT Vs DMT and BMT Vs AMT-NS). The mean respiratory rate on experimental groups (Day 1 and Day 3) with music were significantly lower during the music (DMT) and after music (AMT) phases compared to BMT (53.5±6.2 (BMT), 44.8±5.3 (DMT), 46.5±5.6 (AMT); BMT Vs DMT (F=374.12, P= <0.001), BMT Vs AMT (F= 206.12, P=<0.001). In contrast, there were no differences in the respiratory rate in the three phases on day 2 and 4 when no music was played (50.6±4 (BMT), 51±3.9 (DMT), 50.8±3.8 (AMT); BMT Vs DMT, BMT Vs AMT, NS). No apnoeic bradycardia events were noted during music therapy. Likewise mean SpO2 values on day 1 and 3 with music were significantly higher during music and after music phases than the baseline values (BMT) (96.4±1.3(BMT), 99.5±0.9(DMT), 98.6±0.8(AMT); BMT Vs DMT (F=579.42, P<0.001), BMT Vs AMT (F=283.42, P<0.001). In contrast, there were no differences in the oxygen saturation values in the three phases on day 2 and 4 when no music was played (97.1±1.4 (BMT), 96.9±1.4(DMT), 96.9±1.4 (AMT); BMT Vs DMT, NS BMT Vs AMT, NS). Conclusion: Listening to classical music as used in this study, was associated with a significant (P<0.001) lowering of resting Heart Rate and Respiratory rate and a consistent improvement of oxygen saturation was noted. These effects appear to persist beyond the music therapy for a short period and may play a useful role to achieve relaxation for babies in NICU.

Obstructive sleep apnoea: is it moving into primary care?

Periods of obstructive sleep apnoea (OSA), first properly described in 1965,1 have been shown to occur in around 25% of males and 10% of females.2 But only about a fifth will need or benefit from treatment. OSA is due to excessive collapsing forces around the pharynx that overpower the decreased muscle tone during sleep. Snoring is an early marker of this collapse, and is either partial (causing hypopnoea) or complete (causing apnoea). To prevent asphyxia such events are terminated by a brief awakening after 20 to 40 seconds or so, restoring muscle tone and airflow, but of which the patient is rarely aware. A few such events during sleep are regarded as within the normal range, but there is a continuum of severity, with the most severe cases experiencing apnoeic events every minute across the whole night, with gross sleep fragmentation and recurrent hypoxic events. The dominant risk factor is upper-body obesity, mainly around the neck, although jaw shapes that reduce pharyngeal volume are important. In children, enlarged tonsils are the main risk factor and tonsillectomy is usually curative. Excessive daytime sleepiness is the main symptom of OSA, usually then called OSA syndrome (OSAS). This may be described as tiredness or fatigue, but closer questioning usually reveals it to be more sleepiness (though in women tiredness may be the main complaint). OSAS usually develops over several years, thus the patient may not be fully aware of just how symptomatic they are. Talking to a close relative can be useful, particularly regarding any sleepiness while driving. However, many people with OSA are not sleepy and do not need treatment. The main reason for any referral will be excessive sleepiness that interferes with quality of life, or impairs a vigilance-critical activity such as …

Rebuttal from Magdy Younes.

There is really little disagreement in the two accounts (Orr et al. 2014; Younes, 2014) if one considers that I addressed the increase in loop gain (LG) when the upper airway (UA) is unstable (hereafter called Actual LG) whereas Orr et al. addressed only that component of LG that is measured when UA is stabilized, the component I called Chemical LG. To put these two loop gains in the proper perspective I refer to several investigations from the laboratory of the opposing authors. Wellman et al. (2011) and Edwards et al. (2012) measured the Actual LG in obstructive sleep apnoea (OSA) patients by relating the increase in ventilation at airway opening to the reduction in ventilation during the event. The values reported ranged from 1.4 to 14.0 (average 4.4). This is an order of magnitude greater than the Chemical LG (∼0.4; Younes et al. 2001; Wellman et al. 2004, 2008; Jordan et al. 2005). As indicated earlier (Younes, 2014), this difference results from an increased delay in getting a ventilatory response because the airway refuses to open until a threshold chemical drive, the ‘effective recruitment threshold’, is reached (Younes et al. 2007, 2012). Clearly, this increase in LG is a consequence of OSA. What is called a high LG in the absence of UA instability, and what is emphasized as a cause of OSA by Orr et al. is a Chemical LG of 0.7 with a maximum of 0.9 (Wellman et al. 2008). Even this relatively small increase in Chemical LG is the result of untreated OSA since it disappears with treatment (Loewen et al. 2009; Salloum et al. 2010). Orr et al. argue that this modest increase nonetheless contributes to the severity of OSA. I have no problem with this, and have in fact indicated so in my article (Younes, 2014). However, I believe that Orr et al. have exaggerated this clinical importance. They cite two papers in support of effectiveness of oxygen. The paper by Chowdhuri et al. (2010) simply demonstrated a reduction, with oxygen, in hypocapnic ventilatory response to CO2 in normal subjects. The study by Wellman et al. (2008) found >50% reduction in the apnoea–hypopnoea index (AHI) when breathing oxygen in only three out of six patients selected from a base of 43 patients because they had a high LG (range 0.4–0.9). Some of this AHI reduction was due to prolongation of apnoeic events and to disappearance of central/mixed events, which contributed ∼15% of baseline events. Thus the number of true obstructive events that were eliminated by oxygen must have been small. The acetazolamide evidence is also quite unconvincing. The 2013 study by Edwards et al. did not address the severity of OSA. In the 2012 study by Edwards et al. acetazolamide caused a reduction in AHI in patients already treated by continuous positive airway pressure (CPAP) and in whom Chemical LG was probably normal (Loewen et al. 2009; Salloum et al. 2010). So, it is not possible to attribute the improvement in AHI to a reduction in Chemical LG. It is important to note that both acetazolamide (Edwards et al. 2012) and oxygen breathing (Chowdhuri et al. 2010) increase baseline ventilation, and hence respiratory drive. Their helpful effects in some patients need not reflect a reduction in Chemical LG but may be because chemical drive needs to increase less to reach the effective recruitment threshold for UA opening.

Zonisamide reduces obstructive sleep apnoea: a randomised placebo-controlled study

Carbonic anhydrase inhibition reduces apnoeic events in sleep disordered breathing. Zonisamide inhibits carbonic anhydrase, and induces weight loss in obese patients. This study explored the relative influence of these two properties, which may both alleviate obstructive sleep apnoea (OSA). Continuous positive airway pressure (CPAP) was used as a standard care comparator. 47 patients with moderate-to-severe OSA and a body mass index of 27-35 kg·m(-2) were randomised to receive either zonisamide, placebo or CPAP for 4 weeks. The open extension phase (20 weeks) compared CPAP and zonisamide. Polysomnography, biochemistry and symptoms were evaluated. At 4 weeks, zonisamide reduced apnoea/hypopnoea index (AHI) by a mean±sd 33±39% and oxygen desaturation index by 28±31% (p=0.02 and 0.014, respectively; placebo adjusted). The mean compliance adjusted reduction of AHI after zonisamide and CPAP was 13 and 61%, respectively, (p=0.001) at 24 weeks. Body weight was marginally changed at 4 weeks, but reduced after zonisamide and increased after CPAP at 24 weeks (-2.7±3.0 kg versus 2.3±2.0 kg, p<0.001). Zonisamide decreased bicarbonate at 4 and 24 weeks. Side-effects were more common after zonisamide. Zonisamide reduced OSA independent of body weight potentially by mechanisms related to carbonic anhydrase inhibition. The effect was less pronounced than that obtained by CPAP.

Procedural sedation with dexmedetomidine during ablation of atrial fibrillation: a randomized controlled trial

Procedural sedation by non-anaesthesiologists with GABAergic anaesthetics has the potential risk of fatal respiratory depression. Dexmedetomidine works its sedative action via α2-adrenergic receptors, and is less associated with respiratory depression. We tested the usability of dexmedetomidine as a procedural sedative during ablation of atrial fibrillation (AF). Consecutive patients were randomized to be treated with dexmedetomidine (n = 43) or thiamylal (n = 44) as sedatives during AF ablation. Apnoeic and body movement events were monitored using a novel portable respiratory monitor, the SD-101, during the procedure. Although the majority of the patients receiving dexmedetomidine required rescue sedations with thiamylal, the respiratory disturbance index (RDI) defined as the total number of sleep-disordered breathing events divided by the recording time (10.4 ± 5.1 vs. 18.2 ± 8.1 events/h; P < 0.0001) and movement index defined as the number of body movement events per hour (7.6 ± 6.1 vs. 11.0 ± 5.5 events/h; P = 0.0098) were both significantly lower in the dexmedetomidine arm than in the thiamylal arm. A multivariate linear regression analysis including potential factors revealed that dexmedetomidine vs. thiamylal was solely and independently associated with the RDI (β = -0.62; P = 0.0031). The occurrence of hypotension [9 (21%) vs. 4 (9%); P = 0.14] and bradycardia [4 (9%) vs. 4 (9%); P = 1.0] were similar in the patients with dexmedetomidine and thiamylal. Procedural sedation with dexmedetomidine may assure safety and patient immobility during AF ablation, and therefore may be a potential alternative for that with GABAergic anaesthetics.

Sleep-wake fluctuations and respiratory events during Cheyne-Stokes respiration in patients with heart failure

Fluctuations in sleep-wake state are thought to contribute to the respiratory instability of Cheyne-Stokes respiration in patients with heart failure by promoting the rhythmic occurrence of central apnea and ventilatory overshoot. There are no data, however, on the relationship between vigilance state and respiratory events. In this study we used a novel method to detect the occurrence of state transitions (time resolution: 0.25s, minimum duration of state changes: 2s) and to assess their time relationship with apnoeic events. We also evaluated whether end-apnoeic arousals are associated with a ventilatory overshoot. A polysomnographic, daytime laboratory recording (25min) was performed during Cheyne-Stokes respiration in 16 patients with heart failure. Automatic state classification included wakefulness and non-rapid eye movement sleep stages 1-2. As a rule, wakefulness occurred during hyperpnoeic phases, and non-rapid eye movement sleep occurred during apnoeic events. Ninety-two percent of the observed central apneas (N=272) were associated with a concurrent wakefulness → non-rapid eye movement sleep → wakefulness transition. The delay between wakefulness → non-rapid eye movement sleep transitions and apnea onset was -0.3 [-3.1, 3.0]s [median (lower quartile, upper quartile); P=0.99 testing the null hypothesis: median delay=0], and the delay between non-rapid eye movement sleep→wakefulness transitions and apnea termination was 0.2 [-0.5, 1.2]s (P=0.7). A positive/negative delay indicates that the state transition occurred before/after the onset or termination of apnea. Non-rapid eye movement sleep→wakefulness transitions synchronous with apnea termination were associated with a threefold increase in tidal volume and a twofold increase in ventilation (all P<0.001), indicating ventilatory overshoot. These findings highlight that wakefulness→non-rapid eye movement sleep → wakefulness transitions parallel apnoeic events during Cheyne-Stokes respiration in patients with heart failure. The relationships between state changes and respiratory events are consistent with the notion that state fluctuations promote ventilatory instability.

Arrhythmias and conduction disturbances in obstructive sleep apnoea: the heart of the problem?

Heart rhythm disorders temporally associated with obstructive apnoeic events have been highlighted for more than 30 years. An ECG from polysomnographic recordings enables both sleep medicine specialists and cardiologists to address occasional very impressive paroxysmal atrioventricular conduction blocks or sinus pauses (of up to 10 s during rapid eye movement (REM) sleep) [1]. The pathophysiology of these disorders induced by respiratory events is obviously complex and represents an exciting challenge in the context of integrative human physiology. The role of acute and chronic imbalances in the autonomic nervous system (ANS) associated with obstructive sleep apnoeas or hypopnoeas (OSA) has been clearly demonstrated in many cellular mechanisms of myocardial adaptation to such repeated stresses [2–4]. In addition, these autonomic disorders are now recognised as independent risk factors or triggers of sudden cardiac death not only in heart failure patients [5] but also in people with preserved systolic/diastolic left ventricular function [6, 7]. Although sleep is normally a time when the parasympathetic modulation of the heart predominates and myocardial electrical stability is enhanced, OSA disturbs this quiescence, creating an autonomic profile in which both profound vagal activity leading to bradycardia and sympathetic overactivity favouring ventricular ectopy are commonly observed [8]. The authors of a review paper published in the current issue of the European Respiratory Journal [9] must be congratulated for successfully detailing of the mechanisms present during apnoea/hypopnoea that can lead to heart rhythm disturbances. This paper is, for me, a remarkable teaching tool that I will use again in the future due to its clarity and its “updated” literature review. In a second part …

Association between sleep‐disordered breathing, sleep–wake pattern, and cognitive impairment among patients with chronic heart failure

Chronic heart failure (CHF) and sleep-disordered breathing (SDB) are often co-existing problems among the elderly. Apnoeic events may cause cognitive impairment. The aim of the study was to compare sleep and wake patterns, insomnia, daytime sleepiness, and cognitive function in community-dwelling CHF patients, with and without SDB, and to investigate the association between sleep-related factors and cognitive dysfunction. In this cross-sectional observational study, SDB was measured with an ApneaLink device and defined as an apnoea-hypopnoea index (AHI) ≥15/h of sleep. Sleep and wake patterns were measured with actigraphy for 1 week. Insomnia was measured with the Minimal Insomnia Symptom Scale, daytime sleepiness with the Epworth Sleepiness Scale, and cognitive function with a neuropsychological test battery. A total of 137 patients (68% male, median age 72 years, 58% NYHA functional class II) were consecutively included. Forty-four per cent had SDB (AHI ≥15). The SDB group had significantly higher saturation time below 90%, more difficulties maintaining sleep, and lower levels of daytime sleepiness compared with the non-SDB group. Cognitive function and sleep and wake patterns did not differ between the SDB and the non-SDB group. Insomnia was associated with decreased global cognition. The prevalence of cognitive dysfunction was low in this population with predominantly mild to moderate CHF. This might have influenced the lack of associations between cognitive function and SDB. Insomnia was the only sleep-related factor significantly influencing cognition.

Effects of continuous positive airway pressure on endothelial function and circulating progenitor cells in obstructive sleep apnoea: A randomised sham-controlled study

Obstructive sleep apnoea (OSA) is characterised by reoccurring apnoeas and hypopneas, causing repetitive hypoxia and reoxygenation, and is associated with endothelial dysfunction and reduced levels of circulating progenitor cells (CPCs). The potential to improve endothelial function and CPC levels in people with OSA by preventing hypoxic episodes with Continuous Positive Airway Pressure (CPAP) was investigated in a sham-controlled CPAP study. Men with moderate-to-severe OSA (mean ± SD: age=49 ± 12 y, apnoea hypopnea index (AHI)=37.6 ± 16.4 events/h, body mass index=31.5 ± 5.7 kg/m(2)) who were CPAP naïve without diabetes mellitus were randomised in a 12-week double-blind sham-controlled parallel group study to receive either active (n=25) or sham (n=21) CPAP. CPCs, isolated from blood, were measured by flow cytometry and by co-staining cultured cells (7 days) with acetylated low-density lipoprotein (acLDL) and lectin. Endothelial function was assessed by peripheral arterial tonometry (PAT). Compared to sham, CPAP significantly decreased AHI (mean between-group difference -36.0 events/h; 95%CI, -49.7 to -22.3, p<0.0001) after 12 weeks. Despite this improvement in AHI, CPAP had no effect on change in CPC levels (including CD34(+)/KDR(+) (565 cells/mL; -977 to 2106, p=0.45), CD34(+)/KDR(+)/CD45(-) (37.0 cells/mL; -17.7 to 85.7, p=0.13), acLDL(+)/lectin(+) (-43.1 cells/field, -247 to 161, p=0.67)) or change in endothelial function (0.27; -0.14 to 0.67, p=0.19) compared to sham therapy. Despite the improvement in OSA parameters and ablation of apnoeic events by CPAP, CPC counts and endothelial function in men with moderate-to-severe OSA were not significantly improved after 12 weeks of therapeutic CPAP when compared to sham control.

P22 Do obstructive sleep apnoea (OSA) patients with normal Epworth scores comply with Continuous positive airway pressure (CPAP) therapy?

IntroductionCurrent recommendations suggest CPAP treatment in patients with OSA and excessive daytime sleepiness. The Mosaic trial showed a reduction in Epworth Sleepiness Score (ESS) in minimally symptomatic patients although there...

EEG spectral analysis of apnoeic events confirms visual scoring in childhood sleep disordered breathing

This study compared electroencephalogram (EEG) spectral analysis with standard visual scoring to assess the validity of clinical classification of arousals at respiratory event termination in children with obstructive sleep apnoea (OSA). Twenty children (six M/14F) aged 7-12years, diagnosed with moderate to severe OSA participated in this study. Overnight polysomnography was performed, and sleep stages and arousals visually scored using clinical paediatric measures. The EEG was spectrally analysed in six 5-s epochs across respiratory events, namely two consecutive 5-s epochs pre-event onset and a 5s epoch post-event onset, 5-s before event termination, and two contiguous 5-s epochs post-event termination. EEG spectral power distribution was compared across respiratory events visually categorised as full cortical arousals, subcortical activations, or non-arousals using specialised software (Sleep Research System 5.0). There was no difference in power spectra between events in REM and NREM sleep and these were combined. There was a statistically significant fall from pre-arousal baseline values in delta and theta spectral power at respiratory event terminations associated with cortical arousals only. No change in power was detected at respiratory event terminations associated with subcortical activations or non-arousals. The lack of significant EEG spectral power changes at respiratory event terminations not associated with visually identified cortical arousals indicates undetected micro-arousals are not present. The results support the validity of clinical classifications of arousals at respiratory event termination.