The effect of an improved ICU physical environment on outcomes and post-ICU recovery-a protocol.

BACKGROUND: Intensive care medicine continues to improve, with advances in technology and care provision leading to improved patient survival. However, this has not been matched by similar advances in ICU bedspace design. Environmental factors including excessive noise, suboptimal lighting, and lack of natural lights and views can adversely impact staff wellbeing and short- and long-term patient outcomes. The personal, social, and economic costs associated with this are potentially large. The ICU of the Future project was conceived to address these issues. This is a mixed-method project, aiming to improve the ICU bedspace environment and assess impact on patient outcomes. Two innovative and adaptive ICU bedspaces capable of being individualised to patients' personal and changing needs were co-designed and implemented. The aim of this study is to evaluate the effect of an improved ICU bedspace environment on patient outcomes and operational impact. METHODS: This is a prospective multi-component, mixed methods study including a randomised controlled trial. Over a 2-year study period, the two upgraded bedspaces will serve as intervention beds, while the remaining 25 bedspaces in the study ICU function as control beds. Study components encompass (1) an objective environmental assessment; (2) a qualitative investigation of the ICU environment and its impact from the perspective of patients, families, and staff; (3) sleep investigations; (4) circadian rhythm investigations; (5) delirium measurements; (6) assessment of medium-term patient outcomes; and (7) a health economic evaluation. DISCUSSION: Despite growing evidence of the negative impact the ICU environment can have on patient recovery, this is an area of critical care medicine that is understudied and commonly not considered when ICUs are being designed. This study will provide new information on how an improved ICU environment impact holistic patient recovery and outcomes, potentially influencing ICU design worldwide. TRIAL REGISTRATION: ACTRN12623000541606. Registered on May 22, 2023. https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=385845&isReview=true .

A validation study of a ballistocardiograph sleep tracker against polysomnography.

STUDY OBJECTIVES: Consumer home sleep trackers provide a great opportunity for longitudinal objective sleep monitoring. Nonwearable sleep devices cause little to no disruption in the daily life routine and need little maintenance. However, their validity needs further investigation. This study aims to evaluate the accuracy of sleep outcomes of EMFIT Quantified Sleep (QS), an unobtrusive nonwearable sleep tracker based on ballistocardiography, against polysomnography. METHODS: 62 sleep-lab patients underwent a single clinical polysomnography with measures simultaneously collected through polysomnography and EMFIT QS. Resting heart rate, total sleep time, wake after sleep onset, sleep onset latency, and duration in sleep stages, collected from the 2 devices, were compared using paired t-tests and their agreement analyzed using Bland-Altman plots. Additionally, continuous heart rate and sleep stages in 30-seconds epochs were evaluated. RESULTS: EMFIT QS data loss occurred in 47% of participants. In the remaining 33 participants (15 women, with mean age of 53.7 ± 16.5 years), EMFIT QS overestimated total sleep time by 177.5 ± 119.4 minutes (p<0.001) and underestimated wake after sleep onset by 44.74 ± 68.81 minutes (P < .001). It accurately measured average resting heart rate and was able to distinguish sleep onset latency with some accuracy. However, the agreement between EMFIT QS and polysomnography on sleep-wake detection was low (kappa = 0.13, P < .001), EMFIT QS failed to distinguish sleep stages. CONCLUSIONS: A consensus between polysomnography and EMFIT QS was found in sleep onset latency and average heart rate. There was significant discrepancy and lack of consensus in other sleep outcomes. These findings indicated that further development is necessary before using EMFIT QS in clinical and research settings. CLINICAL TRIAL REGISTRATION: Registry: Australian New Zealand Clinical Trials Registry; Name: Sleep parameter validation of a consumer home sleep monitoring device, EMFIT Quantified Sleep (QS), against Polysomnography; URL: https://www.anzctr.org.au/ACTRN12621000600842.aspx; Identifier: ACTRN12621000600842. CITATION: Kholghi M, Szollosi I, Hollamby M, Bradford D, Zhang Q. A validation study of a ballistocardiograph sleep tracker against polysomnography. J Clin Sleep Med. 2022;18(4):1203-1210.

Multiple Sleep Latency Test: when are 4 naps enough?

STUDY OBJECTIVES: The Multiple Sleep Latency Test (MSLT) is central to the diagnosis of narcolepsy and idiopathic hypersomnia. This study is the first to assess the impact of a 5-nap protocol on meeting MSLT-derived diagnostic criteria in a general cohort referred for MSLT, without selection bias. METHODS: Data for all MSLTs performed at 2 tertiary sleep units in Australia between May 2012 and May 2018 were retrospectively assessed for the impact of the fifth nap on mean sleep latency (MSL) and sleep onset rapid eye movement periods. RESULTS: There were 122 MSLTs included. The MSL was 8.7 ± 5.1 minutes after 4 naps, compared with 9.2 ± 5.2 minutes for 5 naps (P < .0001). In 8 cases, inclusion of the fifth nap changed the MSL to a value above the diagnostic threshold of 8 minutes. There were no instances in which the MSL moved to ≤ 8 minutes based on fifth nap data. A sleep onset rapid eye movement period occurred in the fifth nap in 9 patients and altered the interpretation in 2 cases. CONCLUSIONS: The fifth nap in an MSLT is associated with an increased MSL, although this difference is rarely clinically significant. In patients with borderline MSL or 1 sleep onset rapid eye movement period after 4 naps, a fifth nap can alter the outcome and should be performed. However, for many cases, a 4-nap MSLT protocol will suffice, potentially allowing resource savings without compromising diagnostic accuracy. We propose the adoption of a conditional 4-nap or 5-nap protocol based on specific criteria.

CPAP combined with oral appliance therapy reduces CPAP requirements and pharyngeal pressure swings in obstructive sleep apnea.

Oral appliance (OA) therapy is the leading alternative to continuous positive airway pressure (CPAP) for obstructive sleep apnea (OSA). It is well tolerated compared with CPAP. However, ≥50% of patients using OA therapy have incomplete resolution of their OSA. Combination therapy with CPAP and oral appliance (CPAP + OA) is a potential alternative for incomplete responders to OA therapy. This study aimed to determine the extent to which combination therapy reduces therapeutic CPAP requirements using gold-standard physiological methodology in those who have an incomplete response to OA therapy alone. Sixteen incomplete responders [residual apnea/hypopnea index (AHI) > 10 events/h] to a novel OA with a built-in oral airway were recruited (3 women:13 men, aged 31-65 yr, body mass index: 22-38 kg/m2, residual AHI range: 13-63 events/h). Participants were fitted with a nasal mask, pneumotachograph, epiglottic pressure catheter, and standard polysomnography equipment. CPAP titrations were performed during non-rapid eye movement (NREM) supine sleep in each participant during three conditions (order randomized): CPAP only, CPAP + OA (oral airway open), and CPAP + OA (oral airway closed). OSA was resolved at pressures of 4 ± 2 and 5 ± 2 cmH2O during CPAP + OA (oral airway open) and CPAP + OA (oral airway closed) conditions versus 8 ± 2 cmH2O during CPAP only (P < 0.01). Negative epiglottic pressure swings in oral airway open and closed conditions were normalized to CPAP only levels [-2.5(-3.7, -2.6) vs. -2.3(-3.2, -2.4) vs. -2.1(-2.7, -2.3) cmH2O]. Combined CPAP and OA therapy reduces therapeutic CPAP requirements by 35%-45% and minimizes epiglottic pressure swings. This combination may be a therapeutic alternative for patients with incomplete responses to OA therapy alone and those who cannot tolerate high CPAP levels.NEW & NOTEWORTHY Combined CPAP and oral appliance therapy has been suggested as an alternative for incomplete responders to oral appliance therapy. We used a novel oral appliance incorporating an oral airway together with CPAP to show that pharyngeal pressure swings were normalized at reduced CPAP levels. Our findings demonstrate that using CPAP and oral appliance together may be a beneficial alternative for incomplete responders to oral appliance therapy and intolerant CPAP users due to high-pressure requirements.

Efficacy of a novel oral appliance and the role of posture on nasal resistance in obstructive sleep apnea.

STUDY OBJECTIVES: High nasal resistance is associated with oral appliance treatment failure in obstructive sleep apnea (OSA). A novel oral appliance with a built-in oral airway has been shown to reduce pharyngeal pressure swings during sleep and may be efficacious in those with high nasal resistance. The role of posture and mandibular advancement on nasal resistance in OSA remains unclear. This study aimed to determine (1) the effects of posture and mandibular advancement on nasal resistance in OSA and (2) the efficacy of a new oral appliance device including in patients with high nasal resistance. METHODS: A total of 39 people with OSA (7 females, apnea-hypopnea index (AHI) (mean ± standard deviation) = 29 ± 21 events/h) completed split-night polysomnography with and without oral appliance (order randomized). Prior to sleep, participants were instrumented with a nasal mask, pneumotachograph, and a choanal pressure catheter for gold standard nasal resistance quantification seated, supine and lateral (with and without oral appliance, order randomized). RESULTS: Awake nasal resistance increased from seated, to supine, to lateral posture (median [interquartile range] = 1.8 [1.4, 2.7], 2.7 [1.7, 3.5], 3.4 [1.9, 4.6] cm H2O/L/s, P < .001). Corresponding measures of nasal resistance did not change with mandibular advancement (2.3 [1.4, 3.5], 2.5 [1.8, 3.6], 3.5 [1.9, 4.8] cm H2O/L/s, P = .388). The median AHI reduced by 47% with oral appliance therapy (29 ± 21 versus 18 ± 15 events/h, P = .002). Participants with high nasal resistance (> 3 cm H2O/L/s) had similar reductions in AHI versus those with normal nasal resistance (61 [-8, 82] versus 40 [-5, 62] %, P = .244). CONCLUSIONS: Nasal resistance changes with posture in people with OSA. A novel oral appliance with a built-in oral airway reduces OSA severity in people with OSA, including in those with high nasal resistance. CLINICAL TRIAL REGISTRATION: Registry: ANZCTR; Title: Combination therapy for obstructive sleep apnoea; Identifier: ACTRN12617000492358; URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=372279.

Impaired pulmonary diffusing capacity and hypoxia in heart failure correlates with central sleep apnea severity.

BACKGROUND: Heart failure (HF) is often associated with interstitial pulmonary edema and structural changes, resulting in thickening of the alveolar-capillary membrane and reductions in diffusing capacity of the lung for carbon monoxide (Dlco). Reduced Dlco reflects an impaired efficiency of gas exchange, which may increase plant gain, influence ventilatory control stability, and result in central sleep apnea (CSA). In this study, we test the hypothesis that reductions in Dlco would be associated with increased apnea-hypopnea index (AHI) in patients with CSA. METHODS: Overnight polysomnography, pulmonary function tests, and arterial blood gas analyses were performed in 45 patients with chronic, stable HF. Univariate and multivariate regression analyses were performed in those patients with predominant CSA to test which variables were associated with AHI. RESULTS: Patients had a mean (+/-SD) age of 52.7+/-8.9 years, a mean left ventricular ejection fraction of 26.5+/-9.9%, and a mean AHI of 22.0+/-17.4 events per hour. In CSA patients, Dlco and Pao2 both correlated with total AHI (r=-0.43, p=0.046 and r=-0.53, p=0.011, respectively) and with supine AHI (r=-0.56, p=0.009 and r=-0.60, p=0.004, respectively). In a forward stepwise estimation model, Dlco, Pao2, and body mass index were independent predictors of total AHI, explaining 51% of variability, as was supine AHI, explaining 64% of variability. Dlco and Pao2 accounted for 37% of the variability in total AHI and 49% of the variability in supine AHI. CONCLUSIONS: In patients with HF and CSA, reductions in Dlco and Pao2 are independently associated with respiratory disturbance during sleep. The increase in ventilatory instability may be due to plant gain effects.

Sleep apnea in heart failure increases heart rate variability and sympathetic dominance.

AIMS: Sleep disordered breathing (SDB) is common in heart failure and ventilation is known to influence heart rate. Our aims were to assess the influence of SDB on heart rate variability (HRV) and to determine whether central sleep apnea (CSA) and obstructive sleep apnea (OSA) produced different patterns of HRV. METHODS AND RESULTS: Overnight polysomnography was performed in 21 patients with heart failure and SDB. Two 10-minute segments each of SDB and stable breathing from each patient were visually identified and ECG signal exported for HRV analysis. SDB increased total power (TP) with very low frequency (VLF) power accounting for the greatest increase (1.89+/-0.54 vs 2.96+/-0.46 ms2, P <0.001); LF/HF ratio increased during SDB (1.2+/-1.0 vs 2.7+/-2.1, P <0.001). Compared to OSA, CSA was associated with lower absolute LF (2.10+/-0.47 vs 2.52+/-0.55 ms2, P = 0.049) and HF power (1.69+/-0.41 vs 2.34+/-0.58 ms2, P = 0.004), increased VLF% (78.9%+/-13.4% vs 60.9%+/-19.2%, P = 0.008), decreased HF% (6.9%+/-7.8% vs 16.0%+/-11.7%, P = 0.046) with a trend to higher LF/HF ratio. CONCLUSIONS: SDB increases HRV in the setting of increased sympathetic dominance. HRV in CSA and OSA have unique HRV patterns which are likely to reflect the different pathophysiological mechanisms involved.

Lateral sleeping position reduces severity of central sleep apnea / Cheyne-Stokes respiration.

INTRODUCTION: The influence of sleeping position on obstructive sleep apnea severity is well established. However, in central sleep apnea with Cheyne Stokes respiration (CSA-CSR) in which respiratory-control instability plays a major pathophysiologic role, the effect of position is less clear. STUDY OBJECTIVES: To examine the influence of position on CSA-CSR severity as well as central and mixed apnea frequency. METHODS: Polysomnograms with digitized video surveillance of 20 consecutive patients with heart failure and CSA-CSR were analyzed for total apnea-hypopnea index, mean event duration, and mean oxygen desaturation according to sleep stage and position. Position effects on mixed and central apnea index, mean apnea duration, and mean desaturation were also examined in non-rapid eye movement sleep. RESULTS: Data are presented as mean +/- SEM unless otherwise indicated. Group age was 59.9 +/- 2.3 years, and total apnea-hypopnea index was 26.4 +/- 3.0 events per hour. Compared with supine position, lateral position reduced the apnea-hypopnea index in all sleep stages (Stage 1, 54.7 +/- 4.2 events per hour vs 27.2 +/- 4.1 events per hour [p < .001]; Stage 2, 43.3 +/- 6.1 events per hour vs 14.4 +/- 3.6 events per hour [p < .001]; slow-wave sleep, 15.9 +/- 6.4 events per hour vs 5.4 +/- 2.9 events per hour [p < .01]; rapid eye movement sleep, 38.0 +/- 7.3 events per hour vs 11.0 +/- 3.0 events per hour [p < .001]). Lateral position attenuated apnea and hypopnea associated desaturation (supine 4.7% +/- 0.3%, lateral 3.0% +/- 0.4%; p < .001) with no difference in event duration (supine 25.7 +/- 2.8 seconds, lateral 26.9 +/- 3.4 seconds; p = .921). Mixed apneas were longer than central (29.1 +/- 2.1 seconds and 19.3 +/- 1.1 seconds; p < .001) and produced greater desaturation (6.1% +/- 0.5% and 4.5% +/- 0.5%, p = .003). Lateral position decreased desaturation independent of apnea type (supine 5.4% +/- 0.5%, lateral 3.9% < or = 0.4%; p = .003). CONCLUSIONS: Lateral position attenuates severity of CSA-CSR. This effect is independent of postural effects on the upper airway and is likely to be due to changes in pulmonary oxygen stores. Further studies are required to investigate mechanisms involved.

Effect of surface tension of mucosal lining liquid on upper airway mechanics in anesthetized humans.

Upper airway (UA) patency may be influenced by surface tension (gamma) operating within the (UAL). We examined the role of gamma of UAL in the maintenance of UA patency in eight isoflurane-anesthetized supine human subjects breathing via a nasal mask connected to a pneumotachograph attached to a pressure delivery system. We evaluated 1). mask pressure at which the UA closed (Pcrit), 2). UA resistance upstream from the site of UA collapse (RUS), and 3). mask pressure at which the UA reopened (Po). A multiple pressure-transducer catheter was used to identify the site of airway closure (velopharyngeal in all subjects). UAL samples (0.2 microl) were collected, and the gamma of UAL was determined by using the "pull-off force" technique. Studies were performed before and after the intrapharyngeal instillation of 5 ml of exogenous surfactant (Exosurf, Glaxo Smith Kline). The gamma of UAL decreased from 61.9 +/- 4.1 (control) to 50.3 +/- 5.0 mN/m (surfactant; P < 0.02). Changes in Po, RUS, and Po - Pcrit (change = control - surfactant) were positively correlated with changes in gamma (r2 > 0.6; P < 0.02) but not with changes in Pcrit (r2 = 0.4; P > 0.9). In addition, mean peak inspiratory airflow (no flow limitation) significantly increased (P < 0.04) from 0.31 +/- 0.06 (control) to 0.36 +/- 0.06 l/s (surfactant). These findings suggest that gamma of UAL exerts a force on the UA wall that hinders airway opening. Instillation of exogenous surfactant into the UA lowers the gamma of UAL, thus increasing UA patency and augmenting reopening of the collapsed airway.

Heterogeneous activity of the human genioglossus muscle assessed by multiple bipolar fine-wire electrodes.

Genioglossus (GG) electrical activity [measured by electromyogram (EMGgg)] is best measured by intramuscular electrodes; however, the homogeneity of EMGgg is undefined. We investigated the relationships between EMGgg and the site from which activity was measured to determine whether and to what extent inhomogeneity in activity occurred. Eight healthy human volunteers underwent ultrasound to determine GG depth and width. Four pairs of electrodes were then inserted percutaneously into the left and right GG muscle, anteriorly and posteriorly. Additional configurations were obtained by connecting electrodes across the midline and along each muscle belly. EMGgg activity was simultaneously recorded from these 10 configurations at rest and during various respiratory maneuvers. Heterogeneous behavior of the GG was evidenced by 1) the variable presence of phasic EMGgg at rest, which was undetectable in two subjects but evident in 65% of configurations in six subjects and present in all configurations in all subjects during voluntary hyperventilation; 2) a greater amplitude of EMGgg response to pharyngeal square-wave negative pressure in anterior than posterior configurations (14.1 +/- 7.1 vs. 8.5 +/- 5.1% of maximum, P < 0.05); and 3) variable (linear and alinear) relationships between EMGgg and lingual force within and between subjects. We hypothesize that regional differences in density and type of muscle fiber are the most likely sources of heterogeneity in these responses.

Collapsibility of the upper airway during anesthesia with isoflurane.

BACKGROUND: The unprotected upper airway tends to obstruct during general anesthesia, yet its mechanical properties have not been studied in detail during this condition. METHODS: To study its collapsibility, pressure-flow relationships of the upper airway were obtained at three levels of anesthesia (end-tidal isoflurane = 1.2%, 0.8%, and 0.4%) in 16 subjects while supine and spontaneously breathing on nasal continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (11.8 +/- 2.7 cm H(2)O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. The site of collapse was determined from simultaneous measurements of nasopharyngeal, oropharyngeal, and hypopharyngeal and esophageal pressures. RESULTS: The airway remained hypotonic (minimal or absent intramuscular genioglossus electromyogram activity) throughout each study. During flow-limited breaths, inspiratory flow decreased linearly with decreasing mask pressure (r(2) = 0.86 +/- 0.17), consistent with Starling resistor behavior. At end-tidal isoflurane of 1.2%, critical pressure was 1.1 +/- 3.5 cm H O; at 0.4% it decreased to -0.2 +/- 3.6 cm H(2)O ( < 0.05), indicating decreased airway collapsibility. This decrease was associated with a decrease in end-expiratory esophageal pressure of 0.6 +/- 0.9 cm H(2)O ( < 0.05), suggesting an increased lung volume. Collapse occurred in the retropalatal region in 14 subjects and in the retrolingual region in 2 subjects, and did not change with anesthetic depth. CONCLUSIONS: Isoflurane anesthesia is associated with decreased muscle activity and increased collapsibility of the upper airway. In this state it adopts the behavior of a Starling resistor. The decreased collapsibility observed with decreasing anesthetic depth was not a consequence of neuromuscular activity, which was unchanged. Rather, it may be related to increased lung volume and its effect on airway wall longitudinal tension. The predominant site of collapse is the soft palate.

Comparison of upper airway collapse during general anaesthesia and sleep.

Measurement of the collapsibility of the upper airway while a patient is awake is not a good guide to such collapsibility during sleep, presumably because of differences in respiratory drive, muscle tone, and sensitivity of reflexes. To assess whether a relation existed between general anaesthesia and sleep, we measured collapsibility of the upper airway during general anaesthesia and severity of sleep-disordered breathing in 25 people who were having minor surgery on their limbs. Anaesthetised patients who needed positive pressure to maintain airway patency had more severe sleep-disordered breathing than did those whose airways remained patent at or below atmospheric pressure. Such an association was strongest during rapid-eye-movement (REM) sleep. Our findings suggest that sleep-disordered breathing should be considered in all patients with a pronounced tendency for upper airway obstruction during anaesthesia or during recovery from it.