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This study evaluated whether or not polysomnography (PSG) inter-scorer reliability (ISR) across sleep centres could be improved by external proficiency testing (EPT), or by EPT combined with method alignment training.Experienced scorers form 15 sleep centres were randomised to the following: (1) a control group, (2) a group that received a self-directed intervention of EPT reports (EPTAmong 30 scorers, there were no ISR changes in controls between baseline (BL) and 6 months (6 m). Both EPT groups showed ISR improvement from BL to 6 m for respiratory, arousal and sleep scoring (p 0.05). Respiratory scoring back-transformed mean (95CI) proportion of specific agreement (PSA) for the EPTExternal proficiency testing produced modest, statistically significant PSG inter-scorer reliability improvements among experienced scorers across sleep centres, with potential to improve clinical management of individual patients and increase research study statistical power.

There is a known association between obstructive sleep apnea (OSA) and atrial fibrillation (AF); however, how OSA affects the atrial myocardium is not well described.To determine whether patients with OSA have an abnormal atrial substrate.Forty patients undergoing ablation of paroxysmal AF and in sinus rhythm (20 with OSA [apnea-hypopnea index ≥ 15] and 20 reference patients with no OSA [apnea-hypopnea index15] by polysomnography) were studied. Multipolar catheters were positioned at the lateral right atrium (RA), coronary sinus, crista terminalis, and RA septum to determine the effective refractory period at 5 sites, conduction time along linear catheters at the RA and the coronary sinus, conduction at the crista terminalis, and sinus node function (corrected sinus node recovery time). Biatrial electroanatomic maps were created to determine the voltage, conduction, and distribution of complex electrograms (duration ≥ 50 ms).The groups had no differences in the prevalence of established risk factors for AF. Patients with OSA had the following compared with those without OSA: no difference in effective refractory period (P = .9), prolonged conduction times along the coronary sinus and RA (P = .02), greater number (P = .003) and duration (P = .03) of complex electrograms along the crista terminalis, longer P-wave duration (P = .01), longer corrected sinus node recovery time (P = .02), lower atrial voltage (RA, P.001; left atrium, P.001), slower atrial conduction velocity (RA, P = .001; left atrium, P = .02), and more widespread complex electrograms in both atria (RA, P = .02; left atrium, P = .01).OSA is associated with significant atrial remodeling characterized by atrial enlargement, reduction in voltage, site-specific and widespread conduction abnormalities, and longer sinus node recovery. These features may in part explain the association between OSA and AF.

STUDY OBJECTIVE To examine the impact of using American Academy of Sleep Medicine (AASM) recommended EEG derivations (F4/M1, C4/M1, O2/M1) vs. a single derivation (C4/M1) in polysomnography (PSG) on the measurement of sleep and cortical arousals, including inter- and intra-observer variability. DESIGN Prospective, non-blinded, randomized comparison. SETTING Three Australian tertiary-care hospital clinical sleep laboratories. PATIENTS OR PARTICIPANTS 30 PSGs from consecutive patients investigated for obstructive sleep apnea (OSA) during December 2007 and January 2008. INTERVENTIONS N/A. MEASUREMENTS AND RESULTS To examine the impact of EEG derivations on PSG summary statistics, 3 scorers from different Australian clinical sleep laboratories each scored separate sets of 10 PSGs twice, once using 3 EEG derivations and once using 1 EEG derivation. To examine the impact on inter- and intra-scorer reliability, all 3 scorers scored a subset of 10 PSGs 4 times, twice using each method. All PSGs were de-identified and scored in random order according to the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Using 3 referential EEG derivations during PSG, as recommended in the AASM manual, instead of a single central EEG derivation, as originally suggested by Rechtschaffen and Kales (1968), resulted in a mean ± SE decrease in N1 sleep of 9.6 ± 3.9 min (P = 0.018) and an increase in N3 sleep of 10.6 ± 2.8 min (P = 0.001). No significant differences were observed for any other sleep or arousal scoring summary statistics; nor were any differences observed in inter-scorer or intra-scorer reliability for scoring sleep or cortical arousals. CONCLUSION This study provides information for those changing practice to comply with the 2007 AASM recommendations for EEG placement in PSG, for those using portable devices that are unable to comply with the recommendations due to limited channel options, and for the development of future standards for PSG scoring and recording. As the use of multiple EEG derivations only led to small changes in the distribution of derived sleep stages and no significant differences in scoring reliability, this study calls into question the need to use multiple EEG derivations in clinical PSG as suggested in the AASM manual.

POLYSOMNOGRAPHY (PSG) IS PERFORMED FOR A WIDE VARIETY OF INDICATIONS, MOST COMMONLY FOR INVESTIGATION OF OBSTRUCTIVE SLEEP APNEA (OSA). OSA is characterized by repeated episodes of upper airway obstruction resulting in cessation (apnea) or reduction (hypopnea) in airflow during sleep. The apnea hypopnea index (AHI), a count of the number of apneas and hypopneas per hour of sleep, is the key measure used for case identification, for quantifying disease severity, and for defining disease prevalence in normal and clinical populations. Despite the importance of this measure, inter-laboratory variations in apnea and, in particular, hypopnea definition have been reported.1,2 Differences in hypopnea definition relate to the degree of airflow reduction and/or oxygen desaturation required and the requirement for associated EEG arousal. The effect of varying definitions of hypopnea on AHI has been examined in a number of studies3–6 and the importance of standardizing the hypopnea definition, and thereby reducing inter-laboratory variability in AHI, has been recognized.3,5,7,8 In 1999, the American Academy of Sleep Medicine (AASM) produced a consensus report,9 targeted at clinical research rather than clinical practice,10 recommending standardized scoring criteria for a range of respiratory events. These guidelines (also known as “Chicago Criteria”) described 2 types of hypopneas: (i) Those with a > 50% decrease in a valid measure of airflow without a requirement for associated oxygen desaturation or arousal, and (ii) Those with a lesser airflow reduction in association with oxygen desaturation of > 3% or an arousal. The lack of clinical practice guidelines was addressed in 2001 when the AASM, via the Clinical Practices Review Committee, published a position paper11 which described a hypopnea as an abnormal respiratory event lasting ≥ 10 sec with ≥ 30% reduction in thoracoabdominal movement or airflow, and with ≥ 4% oxygen desaturation. This is currently the approved hypopnea definition for the Centers for Medicare and Medicaid Services in the United States to determine eligibility for treatment funding.12 Nevertheless, in 2005 the AASM, via the Practice Parameters Committee, reported that, “Several clinical definitions of hypopnea are in clinical use and there is no clear consensus.”13 In a further attempt to improve standardization, the AASM recently published the Manual for the Scoring of Sleep and Associated Events.14 In this manual there is a “recommended” and an “alternative” hypopnea definition; and either can be used at the discretion of the clinician or investigator. The recommended definition is the same as the definition published in the AASM 2001 position paper: hypopnea scoring requires ≥ 30% reduction in nasal pressure signal excursions from baseline and associated ≥ 4% desaturation from pre-event baseline. The alternative definition requires ≥ 50% reduction in nasal pressure signal excursions and associated ≥ 3% desaturation or arousal. Introduction of new standards is likely to lead to a period when individual laboratories assess and change their practices and when different laboratories use different methodologies. This study aims to assist in interpretation of clinical or research results in this setting. Specifically, this study examines the impact of the 2 recently published hypopnea definitions on the AHI, compared to the previously published “Chicago” hypopnea definition, and subsequently examines the impact on the measured prevalence of OSA in a cohort of patients presenting for diagnosis or exclusion of obstructive sleep apnea. Compared to similar previous studies3–6 it is unique in its focus on published standard hypopnea definitions.

SHIPP, N. J., G. C. SCROOP, S. C. JACKSON, M. D. HOLMES, A. T. THORNTON, and C. J. GORE. Rectal Temperature Correction Overestimates the Frequency of Exercise-Induced Hypoxemia. Med. Sci. Sports Exerc., Vol. 36, No. 7, pp. 1111–1116, 2004. Exercise-induced hypoxemia (EIH) occurs in an uncertain proportion of endurance trained athletes. Whereas blood gas measurements must be corrected for core temperature at the time of sampling, the commonly used rectal temperature readings may not be the most appropriate. Ten males [mean peak oxygen uptake, VO2peak, 65.4 ± 7.0 mL·kg−1·min−1] performed incremental treadmill exercise from rest to exhaustion with radial artery blood samples collected at the end of each 2-min workload for gas analysis. The thermogenic effect of exercise was monitored with rectal, arterial blood, and esophageal temperature probes, and the values obtained at all three sites, simultaneous with blood sampling, were used to correct the standard blood gas measurements made at 37°C. The mean increase in rectal temperature across exercise (1.4 ± 0.4°C) was approximately half that recorded in radial arterial blood (2.3 ± 0.5°C) and the esophagus (2.4 ± 0.5°C). In consequence, the uncorrected fall in PaO2 across exercise of 15.4 ± 8.2 mm Hg was reduced to 8.4 ± 7.7 mm Hg when corrected for rectal temperature, and to 2.9 ± 7.4 and 2.1 ± 8.8 mm Hg when corrected for arterial blood and esophageal temperatures. Using a fall of ≥10 mm Hg as the index of EIH, the proportion in the 10 subjects in the present study fell from 80% (uncorrected) through 50% (rectal correction) to 20% (arterial blood and esophageal corrections). When correcting arterial blood gas values for the thermogenic effects of exercise, the proportion of athletes meeting the definition of EIH depends on the site of core temperature measurement.

A group of 15 competitive male cyclists [mean peak oxygen uptake, V˙O2peak 68.5 (SEM 1.5 ml · kg−1 · min−1)] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (S aO2), with all values corrected for rectal temperature. The S a O2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (P aO2) was seen at the first exercise intensity (150 W, about 40% V˙O2peak). A further significant decrease in P aO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (P aCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (V˙O2peak) P aO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P AO2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P A−aO2, r = 0.63 and r = 0.86, respectively) but not with P aCO2. At V˙O2peak P aO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P AO2 and P A−aO2 were combined in a multiple linear regression model, at least 95% of the variance in P aO2 could be explained at both 150 W and V˙O2peak. A significant downward trend in S aO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of S aO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between P aO2 and P AO2 with the first exercise intensity and at V˙O2peak led to the conclusion that inadequatehyperventilation is a major contributor to exercise-induced hypoxaemia.

Study objectives To examine the impact of using a nasal pressure sensor only vs the American Academy of Sleep Medicine (AASM) recommended combination of thermal and nasal pressure sensors on (1) the apnea index (AI), (2) the apnea-hypopnea index (AHI), where the AHI is calculated using both AASM definitions of hypopnea, and (3) the accuracy of a diagnosis of obstructive sleep apnea (OSA). Design Retrospective review of previously scored in-laboratory polysomnography. Setting A tertiary-hospital clinical sleep laboratory. Patients or participants One hundred sixty-four consecutive adult patients with a potential diagnosis of OSA, who were examined during a 3-month period. Interventions N/A. Measurements and results Studies were scored with and without the use of the oronasal thermal sensor. AIs and AHIs, using the nasal pressure sensor alone (AI(np) and AHI(np)), were compared with those using both a thermal sensor for the detection of apnea and a nasal pressure transducer for the detection of hypopnea (AI(th) and AHI(th)). Comparisons were repeated using the AASM recommended (AASM(rec)) and alternative (AASM(alt)) hypopnea definitions. AI was significantly different when measured from the different sensors, with AI(np) being 51% higher on average. Using the AASM(rec) hypopnea definition, the mean AHI(np) was 15% larger than the AHI(th); with large interindividual differences and an estimated 9.8% of patients having a false-positive OSA diagnosis at a cutpoint of 15 events and 4.3% at 30 events per hour. Using AASM(alt) hypopnea definition, the mean AHI(np) was 3% larger than the AHI(th), with estimated false-positive rates of 4.6% and 2.4%, respectively. The false-negative rate was negligible at 0.1% for both hypopnea definitions. Conclusions This study demonstrates that using only a nasal pressure sensor for the detection of apnea resulted in higher values of AI and AHI than when the AASM recommended thermal sensor was added to detect apnea. When the AASM(alt) hypopnea definition was used, the differences in AHI and subsequent OSA diagnosis were small and less than when the AASM(rec) hypopnea definition was used. In situations in which a thermal sensor cannot be used, for example, in limited-channel diagnostic devices, the AHI obtained with a nasal pressure sensor alone differs less from the AHI obtained from a polysomnogram that includes a thermal sensor when the AASM(alt) definition rather than the AASM(rec) definition of hypopnea is used. Thus, diagnostic accuracy is impacted both by the absence of the thermal sensor and by the rules used to analyze the polysomnography. Furthermore, where the thermal sensor is unreliable for sections of a study, it is likely that use of the nasal pressure signal to detect apnea will have modest impact.

Todetermine whether pulmonary hypertension (PH) can occur in obstructive sleep apnea syndrome (OSAS) in the absence of lung or primary cardiac disease, we studied 27 patients (26 males, mean age 49 ± 10 yr) with OSAS (respiratory disturbance index [RDI] > 10 events/h) in whom clinically significant lung or cardiac diseases were excluded. Pulsed Doppler measurements of pulmonary hemodynamics, pulmonary function tests, arterial blood gas analysis, and polysomnography were performed. A total of 11 OSAS pa­ tients (41%) were found to have pulmonary hypertension. The levels of PH were relatively mild (Ppa ~ 26 mm Hg). There were no differences between PH and non-PH patients in body mass index (BMI), smok­ ing history, or lung function. PH patients were more hypoxemic when awake than non-PHpatients (Pao, = 72.2 ± 7.6 versus 17.6 ± 7.3 mm Hg, respectively; p < 0.05) but did not differ in severity of sleep apnea (RDI = 51.9 ± 25.1 versus 56.8 ± 26.2 events/h, respectively; p = NS) or indices of sleep desaturation. The hypoxemia in PH patients could not be explained by impairment of lung function, greater body mass, or a higher prevalence of smoking, and Pao2 in the study population was significantly correlated with Ppa (r = -0.46, P < 0.02) but not with FEV, or BMI. We conclude that lung disease is not a prerequisite for PH in OSAS. We speculate that the development of PH in OSAS patients depends more on individual differ­ ences in the response of the pulmonary circulation to the episodic alveolar hypoxia and respiratory acido­ sis associated with sleep apneas than on differences in the frequency or severity of the apneas. Repetitive elevation of Ppa during sleep into the PH range may lead to pulmonary vascular remodeling in "responders" and thereby daytime PH and hypoxemia. Sajkov 0, Cowie RJ, Thornton AT, Espinoza HA, McEvoy RD. Pulmonary hypertension and hypoxemia in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 1994; 149:416-22.

The causes of exercise-induced hypoxemia (EIH) remain unclear. We studied the mechanisms of EIH in highly trained cyclists. Five subjects had no significant change from resting arterial[Formula: see text]([Formula: see text]; 92.1 ± 2.6 Torr) during maximal exercise (C), and seven subjects (E) had a >10-Torr reduction in [Formula: see text] (81.7 ± 4.5 Torr). Later, they were studied at rest and during various exercise intensities by using the multiple inert gas elimination technique in normoxia and hypoxia (13.2% O2). During normoxia at 90% peak O2 consumption,[Formula: see text] was lower in E compared with C (87 ± 4 vs. 97 ± 6 Torr, P < 0.001) and alveolar-to-arterial O2tension difference (a-[Formula: see text]) was greater (33 ± 4 vs. 23 ± 1 Torr, P < 0.001). Diffusion limitation accounted for 23 (E) and 13 Torr (C) of thea-[Formula: see text]( P < 0.01). There were no significant differences between groups in arterial[Formula: see text]([Formula: see text]) or ventilation-perfusion (V˙a/Q˙) inequality as measured by the log SD of the perfusion distribution (logSDQ˙). Stepwise multiple linear regression revealed that lung O2 diffusing capacity ([Formula: see text]), logSDQ˙, and[Formula: see text] each accounted for ∼30% of the variance in [Formula: see text]( r = 0.95, P < 0.001). These data suggest that EIH has a multifactorial etiology related to[Formula: see text],V˙a/Q˙inequality, and ventilation.

Sleep disordered breathing is common in patients with tetraplegia. Nocturnal arterial hypoxemia and sleep fragmentation due to sleep apnoea may be associated with cognitive dysfunction. We therefore studied the influence of sleep disordered breathing on neuropsychological function in 37 representative tetraplegic patients (mean age 34 +/- 9.7 years). Thirty percent (11 of 37 patients) had clinically significant sleep disordered breathing, defined as apnoea plus hypopnoea index (AHI) greater than 15 per hour of sleep. Most apnoeas were obstructive in type. Seven patients (19%) desaturated to < 80% during the night. Neuropsychological variables were significantly correlated with measures of sleep hypoxia, but not with the AHI and the frequency of sleep arousals. The neuropsychological functions most affected by nocturnal desaturation were: verbal attention and concentration, immediate and short-term memory, cognitive flexibility, internal scanning and working memory. There appeared to be a weak association between the presence of severe sleep hypoxia and visual perception, attention and concentration but no association was found between sleep variables and depression scores. We concluded that sleep disordered breathing is common in patients with tetraplegia and may be accompanied with significant oxygen desaturation. The latter impairs daytime cognitive function in these patients, particularly attention, concentration, memory and learning skills. Cognitive disturbances resulting from sleep apnoea might adversely affect rehabilitation in patients with tetraplegia.

obstruction (as determined by simultaneous polysomnography). Results: 20 obstructive episodes met the inclusion criteria. Mean O2 at the beginning (B) of the events was 95± 2.6%, nadir (N) 86± 4.1% and recovery (R) 95± 2.3%. ERP changes were dynamic but not different at the 3 time points (p= 0.07). CT across the CS was not different for S1, however, was significantly different for S2 (134± 30ms(B) vs. 148± 26ms(N) vs. 147± 40ms(R); p= 0.01). Lateral CT significantly changed for S1 (119± 20ms(B) vs. 126± 18ms(N) vs. 123± 20ms(R)) and S2 (177± 44ms(B) vs. 207± 38ms(N) vs. 207± 48ms(R); p= 0.03) measures. Local conduction delay (CD=A1A2−S1S2)was significantly different at the distal CS (63± 20ms(B) vs. 70± 15ms(N) vs. 74± 24ms(R); p= 0.01) and lateral RA (78± 26ms(B) vs. 97± 21ms(N) vs. 92± 30ms(R); p< 0.001). Conclusion: Acute obstruction during sleep apnoea results in significant atrial remodelling characterized by slowing of conduction during obstruction and incomplete recovery after the event. These changes may account in part for the development of AF in association with clinical OSA. doi:10.1016/j.hlc.2010.06.921

The methylxanthine derivatives are known to have respiratory stimulant properties. To determine whether these drugs would improve obstructive sleep apnea, 10 male patients with obstructive sleep apnea (OSA) (Apnea Index greater than 15/h) were given infusions of aminophylline and a saline placebo on 2 separate nights a week apart, using a randomized crossover design. There was a significant decrease during aminophylline infusion in the frequency of those apneas, which contained periods of complete respiratory inactivity (central and mixed apneas; placebo, 4.3 +/- 1.8/h; aminophylline, 0.7 +/- 0.5/h; p less than 0.05). There was no change in either the frequency (placebo, 31.8 +/- 5.9/h; aminophylline, 28.7 +/- 8.7/h; NS) or duration of obstructive apneas. Mean and minimal arterial oxygen saturation values were also unchanged. Sleep architecture was markedly disturbed by aminophylline. There was a reduction in sleep efficiency (placebo, 84.8 +/- 2.0%; aminophylline, 60.2 +/- 5.0%; p less than 0.005), an increase in sleep fragmentation (sleep stage shifts/h: placebo, 11.6 +/- 1.3: aminophylline, 21.0 +/- 2.9; p less than 0.05) and less Stage 2 and more Stage 1 non-REM sleep. We conclude that aminophylline reduces central apnea and the central component of mixed apneas but has no effect on obstructive apnea. Theophylline is therefore unlikely to be therapeutically useful in patients with OSA, and because it leads to marked sleep disruption, its long-term use could conceivably increase the propensity to upper airway occlusion during sleep.

Computer-based systems for the acquistion and treatment of data from flash photolysis, laser photolysis and pulse radiolysis experiments are described. For the flash photolysis and laser photolysis systems, data acquisition of transient optical absorbance signals takes place via a Biomation 610B transient recorder or a Digital Equipment Corp. AR-11 real-time subsystem. The digitised data are stored in a PDP-11/10 computer and treated to obtain kinetic and spectral parameters such as rate constants. For the pulse radiolysis system, data acquisition also takes place via a Biomation 610B transient recorder, and data storage and reduction is carried out with a DEC PDP-11/03 LSI computer. Auxiliary equipment for control of the data acceptance is described, together with the computer programs used for data reduction. Examples of the use of the systems are given, and the advantages of a computer-based system over a manual system discussed.

The kinetics of the Cr2+ and V2+ reductions of di-µ-hydroxo-µ-phthalato-bis[triamminecobalt(III)] complex, [(NH3)3Co·µ(OH,OH,O2CC6H4CO2H)·Co(NH3)3]3+, have been studied at temperatures in the range 9.7–40 °C, I= 1.0M(LiClO4). Comparisons are made with the Cr2+ reduction of penta-amminephthalatocobalt(III), [Co(NH3)5(O2CC6H4CO2H)]2+. Second-order rate constants for the latter exhibit an [H+]-dependence, a+b[H+]–1, where it has now been demonstrated using ion-exchange techniques that a yields the unidentate product [Cr(H2O)5(O2CC6H4CO2H)]2+, and b the chelated product [Cr(H2O)4(O2CC6H4CO2)]+. With the binuclear µ-phthalato-complex reduction of the first cobalt(III) is rate determining, and that of the second relatively rapid. Second-order rate constants conform to the [H+]-dependence, ka+kb[H+]–1, where in this instance ka corresponds to an outer-sphere process, and kb involves some form of remote attack. Evidence for the latter is that phthalate is incorporated into a binuclear chromium(III) product. Full product analyses have been carried out. With an excess of Cr2+ a second stage involving Cr2+-catalysed dissociation of primary chromium(III) products becomes increasingly important at the lower [H+] values.

To help define the place of nasal continuous positive airway pressure (n-CPAP) treatment in a general sleep apnea population we studied 12 of 13 consecutively diagnosed patients with obstructive sleep apnea syndrome (OSAS). The immediate effects of n-CPAP were tested during a nighttime sleep study divided into two approximately equal parts (control and n-CPAP). Nasal CPAP of 5-10 cm H2O decreased apnea index (apneas per hour of sleep) (control 35.1, n-CPAP 5.7; p less than 0.001) and significantly improved oxyhemoglobin saturation (SaO2). The effect was independent of body weight and the presence of cardiorespiratory complications. However, in three patients with lung disease and markedly elevated PaCO2, significant sleep-related hypoxemia persisted at the relatively low pressures required to open the upper airway. Long-term home-based n-CPAP was offered to 11 patients. (One patient was considered unsuitable because of persisting profound sleep-related hypoxemia). Seven patients consented and were followed for periods ranging from 1 to 18 months. All patients reported dramatic reversal of daytime hypersomnolence; three complained of minor nasal stuffiness but compliance was good and only one stopped using the mask (after 12 months). Apnea index decreased following home use of n-CPAP (before 35.9, after 18.1; p less than 0.01) but overall respiratory instability (apnea + hypopnea) and SaO2 were not significantly improved. It is concluded that n-CPAP is a highly effective means of preventing upper airway occlusion in OSAS and, except for some patients with coexisting lung disease, it totally reverses the accompanying gas exchange disturbance. Long-term home-based n-CPAP therapy is acceptable to a majority of patients, is free of serious side effects, and appears to result in a partial reversal of the underlying breathing disorder.

Das durch Blitzphotolyse in C1; -haltigen Losungen erzeugte Radikalanion C1; oxidiert Co(II) zu Co(III).

Luminescence lifetime measurements show that when both luminescent and quencher ions are adsorbed on cation exchange resin luminescence quenching takes place by dynamic bimolecular processes involving energy transfer or electron transfer at rates which are of the same order as those in homogeneous solution.

The radical ions I2–, Br2–, and Cl2–, generated by nanosecond pulse radiolysis of solutions containing the halide ions, oxidise vanadium(II) to vanadium(III) and chromium(II) to chromium(III). At 22 ± 3 °C and I= 0·5 mol l–1 rate constants for the reactions X2–+ V2+aq→ V3+aq+ 2X– are (1·43 ± 0·2)× 108, (1·48 ± 0·2)× 109, and (1·95 ± 0·2)× 109 l mol–1 s–1(X = I, Br, and Cl) and the reaction mechanism is outer sphere in all cases. Corresponding rate constants for the reactions X2–+ Cr2+aq→[Cr(OH2)5X]2++ X– are (1·5 ± 0·2)× 109, (1·9 ± 0·2)× 109, and (2·4 ± 0·3)× 109 l mol–1 s–1. The reaction mechanisms were established by gamma-radiolysis and flash-photolysis experiments. The reaction between the ions Cl2– and Cr2+aq proceeds by parallel inner- and outer-sphere paths with approximately equal probability. The radical ions I2– and Br2– react with Cr2+aq ions entirely by inner-sphere paths.

The radical anions Br2– and Cl2–, generated by flash photolysis of the corresponding halide solutions or of the iron(III) complexes FeBr2+ and FeCl2+, oxidize iron(II) to iron(III). The product of the reaction between the ions Br2– and Fe2+ is the FeBr2+ complex. The reaction proceeds by an inner-sphere substitution-controlled path with a rate constant of (3·6 ± 0·4)×106 l mol–1 s–1 at 25 °C (ΔH‡= 25·2 ± 2 kJ mol–1; ΔS‡=–42 ± 12 J K–1 mol–1). The reaction between the ions Cl2– and Fe2+ proceeds by two paths at 25 °C, an inner-sphere substitution-controlled path with a rate constant of (4·0 ± 0·6)× 106 l mol–1 s–1(ΔH‡= 31·5 ± 4 kJ mol–1; ΔS‡=–21 ± 15 J K–1 mol–1), and an outer-sphere path with a rate constant of (1·0 ± 0·2)× 107 l mol–1s–1(ΔH‡= 22·7 ± 4 kJ mol–1; ΔS‡=–42 ± 15 J K–1 mol–1).

The radical anion Cl2–, generated by flash photolysis of solutions containing Cl3–, oxidizes cobalt(II) to cobalt(III). At 25 °C and I= 0·3M, the rate constant is (1·4 ± 0·2)× 106 l mol–1 s–1(ΔH‡= 29 ± 4 kJ mol–1 and ΔS‡=–31 ±10 J K–1 mol–1). The reaction is inner sphere–substitution controlled, the initial product being CoCl2+ which is not labile on the time scale of the oxidation reaction.

The increased morbidity and mortality resulting from respiratory failure in patients with neuromuscular disorders and/or kyphoscoliosis can be reversed with non-invasive ventilation. Spontaneous mode bilevel pressure ventilation is preferred to other modes of ventilation, due to relative ease of use, but may not be suitable for all patients. We report a 27-year old woman with Multi-minicore disease whose respiratory failure was refractory to spontaneous mode bilevel pressure ventilation. When we altered settings and provided mandatory inspiratory rise time and respiratory rate, it augmented her respiratory efforts and improved ventilation. Our case report describes the benefit of individualising non-invasive ventilation in the management of respiratory failure due to neuromuscular weakness and kyphoscoliosis.