The American Academy of Sleep Medicine (AASM) Sleep Apnea Definitions Task Force reviewed the current rules for scoring respiratory events in the 2007 AASM Manual for the Scoring and Sleep and Associated Events to determine if revision was indicated. The goals of the task force were (1) to clarify and simplify the current scoring rules, (2) to review evidence for new monitoring technologies relevant to the scoring rules, and (3) to strive for greater concordance between adult and pediatric rules. The task force reviewed the evidence cited by the AASM systematic review of the reliability and validity of scoring respiratory events published in 2007 and relevant studies that have appeared in the literature since that publication. Given the limitations of the published evidence, a consensus process was used to formulate the majority of the task force recommendations concerning revisions.The task force made recommendations concerning recommended and alternative sensors for the detection of apnea and hypopnea to be used during diagnostic and positive airway pressure (PAP) titration polysomnography. An alternative sensor is used if the recommended sensor fails or the signal is inaccurate. The PAP device flow signal is the recommended sensor for the detection of apnea, hypopnea, and respiratory effort related arousals (RERAs) during PAP titration studies. Appropriate filter settings for recording (display) of the nasal pressure signal to facilitate visualization of inspiratory flattening are also specified. The respiratory inductance plethysmography (RIP) signals to be used as alternative sensors for apnea and hypopnea detection are specified. The task force reached consensus on use of the same sensors for adult and pediatric patients except for the following: (1) the end-tidal PCO(2) signal can be used as an alternative sensor for apnea detection in children only, and (2) polyvinylidene fluoride (PVDF) belts can be used to monitor respiratory effort (thoracoabdominal belts) and as an alternative sensor for detection of apnea and hypopnea (PVDFsum) only in adults.The task force recommends the following changes to the 2007 respiratory scoring rules. Apnea in adults is scored when there is a drop in the peak signal excursion by ≥ 90% of pre-event baseline using an oronasal thermal sensor (diagnostic study), PAP device flow (titration study), or an alternative apnea sensor, for ≥ 10 seconds. Hypopnea in adults is scored when the peak signal excursions drop by ≥ 30% of pre-event baseline using nasal pressure (diagnostic study), PAP device flow (titration study), or an alternative sensor, for ≥ 10 seconds in association with either ≥ 3% arterial oxygen desaturation or an arousal. Scoring a hypopnea as either obstructive or central is now listed as optional, and the recommended scoring rules are presented. In children an apnea is scored when peak signal excursions drop by ≥ 90% of pre-event baseline using an oronasal thermal sensor (diagnostic study), PAP device flow (titration study), or an alternative sensor; and the event m...

We conducted a serological study to define correlates of immunity against SARS-CoV-2. Relative to mild COVID-19 cases, individuals with severe disease exhibited elevated virus-neutralizing titers and antibodies against nucleocapsid (N) and the receptor binding domain (RBD) of spike protein. Age and sex played lesser roles. All cases, including asymptomatic individuals, seroconverted by 2 weeks post-PCR confirmation. Spike RBD and S2 and neutralizing antibodies remained detectable through 5-7 months post-onset, whereas α-N titers diminished. Testing of 5882 members of the local community revealed only 1 sample with seroreactivity to both RBD and S2 that lacked neutralizing antibodies. This fidelity could not be achieved with either RBD or S2 alone. Thus, inclusion of multiple independent assays improved the accuracy of antibody tests in low seroprevalence communities and revealed differences in antibody kinetics depending on the antigen. We conclude that neutralizing antibodies are stably produced for at least 5-7 months after SARS-CoV-2 infection.

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Because patients who fail a trial of weaning from mechanical ventilation experience a marked increase in respiratory load, we hypothesized that these patients develop diaphragmatic fatigue. Accordingly, we measured twitch transdiaphragmatic pressure using phrenic nerve stimulation in 11 weaning failure and 8 weaning success patients. Measurements were made before and 30 minutes after spontaneous breathing trials that lasted up to 60 minutes. Twitch transdiaphragmatic pressure was 8.9 +/- 2.2 cm H2O before the trials and 9.4 +/- 2.4 cm H2O after their completion in the weaning failure patients (p = 0.17); the corresponding values in the weaning success patients were 10.3 +/- 1.5 and 11.2 +/- 1.8 cm H2O (p = 0.18). Despite greater load (p = 0.04) and diaphragmatic effort (p = 0.01), the weaning failure patients did not develop low-frequency fatigue probably because of greater recruitment of rib cage and expiratory muscles (p = 0.004) and because clinical signs of distress mandating the reinstitution of mechanical ventilation arose before the development of fatigue. Twitch pressure revealed considerable diaphragmatic weakness in many weaning failure patients. In conclusion, in contrast to our hypothesis, weaning failure was not accompanied by low-frequency fatigue of the diaphragm, although many weaning failure patients displayed diaphragmatic weakness.

To determine whether sleep quality is influenced by the mode of mechanical ventilation, we performed polysomnography on 11 critically ill patients. Because pressure support predisposes to central apneas in healthy subjects, we examined whether the presence of a backup rate on assist-control ventilation would decrease apnea-related arousals and improve sleep quality. Sleep fragmentation, measured as the number of arousals and awakenings, was greater during pressure support than during assist-control ventilation: 79 +/- 7 versus 54 +/- 7 events per hour (p = 0.02). Central apneas occurred during pressure support in six patients; heart failure was more common in these six patients than in the five patients without apneas: 83 versus 20% (p = 0.04). Among patients with central apneas, adding dead space decreased sleep fragmentation: 44 +/- 6 versus 83 +/- 12 arousals and awakenings per hour (p = 0.02). Changes in sleep-wakefulness state caused greater changes in breath components and end-tidal CO2 during pressure support than during assist-control ventilation. In conclusion, inspiratory assistance from pressure support causes hypocapnia, which combined with the lack of a backup rate and wakefulness drive can lead to central apneas and sleep fragmentation, especially in patients with heart failure.

Abnormalities of sleep are extremely common in critically ill patients, but the mechanisms are poorly understood. About half of total sleep time occurs during the daytime, and circadian rhythm is markedly diminished or lost. Judgments based on inspection consistently overestimate sleep time and do not detect sleep disruption. Accordingly, reliable polygraphic recordings are needed to measure sleep quantity and quality in critically ill patients. Critically ill patients exhibit more frequent arousals and awakenings than is normal, and decreases in rapid eye movement and slow wave sleep. The degree of sleep fragmentation is at least equivalent to that seen in patients with obstructive sleep apnea. About 20% of arousals and awakenings are related to noise, 10% are related to patient care activities, and the cause for the remainder is not known; severity of underlying disease is likely an important factor. Mechanical ventilation can cause sleep disruption, but the precise mechanism has not been defined. Sleep disruption can induce sympathetic activation and elevation of blood pressure, which may contribute to patient morbidity. In healthy subjects, sleep deprivation can decrease immune function and promote negative nitrogen balance. Measures to improve the quantity and quality of sleep in critically ill patients include careful attention to mode of mechanical ventilation, decreasing noise, and sedative agents (although the latter are double-edged swords).

Background Insomnia has been associated with mortality risk, but whether this association is different in subjects with persistent versus intermittent insomnia is unclear. Additionally, the role of systemic inflammation in such an association is unknown. Methods We used data from a community-based cohort to determine whether persistent or intermittent insomnia, defined based on persistence of symptoms over a six-year period, were associated with death during the following 20-years of follow-up. We also determined whether changes in serum C-reactive protein (CRP) levels measured over two decades between study initiation and insomnia determination were different for the persistent, intermittent, and never insomnia groups. The results were adjusted for confounders such as age, sex, body mass index, smoking, physical activity, alcohol and sedatives. Results Of the 1409 adult participants, 249 (18%) had intermittent and 128 (9%) had persistent insomnia. During a 20-year follow-up period, 318 participants died (118 due to cardiopulmonary disease). In adjusted Cox proportional-hazards models, participants with persistent insomnia (adjusted Hazards Ratio [HR] 1.58, 95%CI: 1.02-2.45) but not intermittent insomnia (HR 1.22, 0.86-1.74), were more likely to die than participants without insomnia. Serum CRP levels were higher and increased at a steeper rate in subjects with persistent insomnia as compared with intermittent (p=0.04) or never (p=0.004) insomnia. Although CRP levels were themselves associated with increased mortality (adjHR: 1.36, 1.01-1.82, p=0.04), adjustment for CRP levels did not notably change the association between persistent insomnia and mortality. Conclusions In a population-based cohort, persistent, and not intermittent, insomnia was associated with increased risk for all-cause and cardiopulmonary mortality and was associated with a steeper increase in inflammation.

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