A consensus opinion amongst stakeholders as to benefits of obstructive sleep apnoea treatment for cardiovascular health.

BACKGROUND AND OBJECTIVE: Obstructive sleep apnoea (OSA) is a prevalent sleep disorder associated with increased cardiovascular morbidity and mortality. Whether treatment of OSA improves cardiovascular risk remains controversial. Our aim was to determine a consensus opinion of key sleep medicine stakeholder groups as to the cardiovascular benefits of treating moderate-severe OSA. METHODS: A multidisciplinary panel was assembled from representatives from the Australasian Sleep Association, Sleep Health Foundation, Australasian Sleep Technologists Association, the Sleep Health Foundation Business Council and the Sleep Disorders Australia patient support group. Three statements reflecting areas of controversy related to cardiovascular benefits of OSA treatment were created. A modified RAND/UCLA appropriateness methodology was applied determining the panel's level of consensus and agreement with each statement. RESULTS: Voting results indicated the panel: (1) remained unsure whether moderate-severe OSA treatment improves rates of cardiovascular events/death, (2) agreed that moderate-severe OSA treatment improves blood pressure in patients with hypertension and (3) mostly agreed that moderate-severe OSA treatment improves left ventricular function in patients with heart failure. Consensus of opinion was achieved for statements (1) and (2), but was narrowly missed for statement (3). CONCLUSION: The panel believed that findings from large-scale randomized trials indicate that treatment of moderate-severe OSA has not been established to improve cardiovascular event or morbidity/mortality rates. Strong evidence supports the ability of treatment to reduce blood pressure. Whilst many panel members believed that treatment improves left ventricular function, some were uncertain of the clinical significance of this secondary endpoint measure derived from lesser quality evidence.

Physician Decision Making and Clinical Outcomes With Laboratory Polysomnography or Limited-Channel Sleep Studies for Obstructive Sleep Apnea: A Randomized Trial.

BACKGROUND: The clinical utility of limited-channel sleep studies (which are increasingly conducted at home) versus laboratory polysomnography (PSG) for diagnosing obstructive sleep apnea (OSA) is unclear. OBJECTIVE: To compare patient outcomes after PSG versus limited-channel studies. DESIGN: Multicenter, randomized, noninferiority study. (Australian New Zealand Clinical Trials Registry: ACTRN12611000926932). SETTING: 7 academic sleep centers. PARTICIPANTS: Patients (n = 406) aged 25 to 80 years with suspected OSA. INTERVENTION: Sleep study information disclosed to sleep physicians comprised level 1 (L1) PSG data (n = 135); level 3 (L3), which included airflow, thoracoabdominal bands, body position, electrocardiography, and oxygen saturation (n = 136); or level 4 (L4), which included oxygen saturation and heart rate (n = 135). MEASUREMENTS: The primary outcome was change in Functional Outcomes of Sleep Questionnaire (FOSQ) score at 4 months. Secondary outcomes included the Epworth Sleepiness Scale (ESS), the Sleep Apnea Symptoms Questionnaire (SASQ), continuous positive airway pressure (CPAP) compliance, and physician decision making. RESULTS: Change in FOSQ score was not inferior for L3 (mean difference [MD], 0.01 [95% CI, -0.47 to 0.49; P = 0.96]) or L4 (MD, -0.46 [CI, -0.94 to 0.02; P = 0.058]) versus L1 (noninferiority margin [NIM], -1.0). Compared with L1, change in ESS score was not inferior for L3 (MD, 0.08 [CI, -0.98 to 1.13; P = 0.89]) but was inconclusive for L4 (MD, 1.30 [CI, 0.26 to 2.35; P = 0.015]) (NIM, 2.0). For L4 versus L1, there was less improvement in SASQ score (-17.8 vs. -24.7; P = 0.018), less CPAP use (4.5 vs. 5.3 hours per night; P = 0.04), and lower physician diagnostic confidence (P = 0.003). LIMITATION: Limited-channel studies were simulated by extracting laboratory PSG data and were not done in the home. CONCLUSION: The results support manually scored L3 testing in routine practice. Poorer outcomes with L4 testing may relate, in part, to reduced physician confidence. PRIMARY FUNDING SOURCE: National Health and Medical Research Council and Repat Foundation.

Control theory prediction of resolved Cheyne-Stokes respiration in heart failure.

Cheyne-Stokes respiration (CSR) foretells deleterious outcomes in patients with heart failure. Currently, the size of therapeutic intervention is not guided by the patient's underlying pathophysiology. In theory, the intervention needed to resolve CSR, as a control system instability (loop gain >1), can be predicted knowing the baseline loop gain and how much it falls with therapy.In 12 patients with heart failure, we administered an inspiratory carbon dioxide fraction of 1-3% during CSR (n=95 interventions) as a means to reduce loop gain. We estimated the loop gain on therapy (LGtherapy), using the baseline loop gain (using hyperpnoea length/cycle length) and its expected reduction (18% per 1% inspired carbon dioxide), and tested the specific hypothesis that LGtherapy predicts CSR persistence (LGtherapy >1) versus resolution (LGtherapy <1).As predicted, when LGtherapy >1.0, CSR continued during therapy in 23 out of 25 (92%) trials. A borderline loop gain zone (0.8

Depression may reduce adherence during CPAP titration trial.

STUDY OBJECTIVES: Depression is a risk factor for medication non-compliance. We aimed to identify if depression is associated with poorer adherence during home-based autotitrating continuous positive airway pressure (autoPAP) titration. DESIGN: Mixed retrospective-observational study. SETTING: Academic center. PARTICIPANTS: Two-hundred forty continuous positive airway pressure-naïve obstructive sleep apnea (OSA) patients. MEASUREMENTS: Patients underwent approximately 1 week of home-based autoPAP titration with adherence data downloaded from the device. Electronic hospital records were reviewed in a consecutive manner for inclusion. Three areas of potential predictors were examined: (i) demographics and clinical factors, (ii) disease severity, and (iii) device-related variables. Depression and anxiety were assessed using the Hospital Anxiety and Depression Scale (HADS). Scores on the subscales were categorized as normal or clinical diagnoses of depression (≥ 8) and anxiety (≥ 11). The primary outcome variable was the mean hours of autoPAP used per night. RESULTS: Patients were diagnosed with OSA by either attended polysomnography (n = 73, AHI 25.5[15.1-41.5]) or unattended home oximetry (n = 167, ODI3 34.0[22.4-57.4]) and had home-based autoPAP titration over 6.2 ± 1.2 nights. Mean autoPAP use was 4.5 ± 2.4 hours per night. Multiple linear regression analysis revealed that depression and lower 95(th) percentile pressures significantly predicted lesser hours of autoPAP use (R(2) = 0.19, p < 0.001). Significantly milder OSA in those requiring lower pressures may have confounded the relationship between 95(th) percentile pressure and autoPAP use. CONCLUSION: Depression was independently associated with poorer adherence during home-based autoPAP titration. Depression may be a potential target for clinicians and future research aimed at enhancing adherence to autoPAP therapy.

Clinical use of pulse oximetry: official guidelines from the Thoracic Society of Australia and New Zealand.

Pulse oximetry provides a simple, non-invasive approximation of arterial oxygenation in a wide variety of clinical settings including emergency and critical-care medicine, hospital-based and ambulatory care, perioperative monitoring, inpatient and outpatient settings, and for specific diagnostic applications. Pulse oximetry is of utility in perinatal, paediatric, adult and geriatric populations but may require use of age-specific sensors in these groups. It plays a role in the monitoring and treatment of respiratory dysfunction by detecting hypoxaemia and is effective in guiding oxygen therapy in both adult and paediatric populations. Pulse oximetry does not provide information about the adequacy of ventilation or about precise arterial oxygenation, particularly when arterial oxygen levels are very high or very low. Arterial blood gas analysis is the gold standard in these settings. Pulse oximetry may be inaccurate as a marker of oxygenation in the presence of dyshaemoglobinaemias such as carbon monoxide poisoning or methaemoglobinaemia where arterial oxygen saturation values will be overestimated. Technical considerations such as sensor position, signal averaging time and data sampling rates may influence clinical interpretation of pulse oximetry readings.

Comparison of supine-only and REM-only obstructive sleep apnoea.

OBJECTIVES: The effect of body position and sleep state on sleep apnoea have major clinical implications in the management of patients, yet are infrequently reported in the scientific literature. The aim of this study was to compare and contrast the prevalence and severity of supine-only and rapid eye movement (REM)-only obstructive sleep apnoea (OSA) in a population. METHODS: Prospective cohort analysis of the influence of supine body position and REM sleep on the severity of apnoea in 100 consecutive patients with OSA (apnoea-hypopnoea index [AHI]>5) using attended polysomnography with continuous digital monitoring in an accredited sleep laboratory. Supine-only OSA was defined as a supine:non-supine AHI ratio of >2:1 and non-supine AHI <5 events/h. REM-only OSA was defined as an REM:non-REM ratio of >2:1 and non-REM AHI <5events/h. RESULTS: Supine sleep time represented a greater proportion of total sleep time than REM sleep time (40% vs 13%). The prevalence of supine-only OSA was more than twofold greater than that of REM-only OSA (23% and 10%, respectively). The supine-only group had greater overall AHI (mean 12.6±6.1 vs 7.2±2.2 events/h; P<0.01) than the REM-only group. No significant differences in gender, age, or sleepiness were found between the two groups. CONCLUSIONS: Supine-only OSA is more common and is associated with a greater AHI than REM-only OSA.

Loop gain as a means to predict a positive airway pressure suppression of Cheyne-Stokes respiration in patients with heart failure.

RATIONALE: Patients with heart failure (HF) and Cheyne-Stokes respiration or periodic breathing (PB) often demonstrate improved cardiac function when treatment with continuous positive airway pressure (CPAP) resolves PB. Unfortunately, CPAP is successful in only 50% of patients, and no known factor predicts responders to treatment. Because PB manifests from a hypersensitive ventilatory feedback loop (elevated loop gain [LG]), we hypothesized that PB persists on CPAP when LG far exceeds the critical threshold for stable ventilation (LG = 1). OBJECTIVES: To derive, validate, and test the clinical utility of a mathematically precise method that quantifies LG from the cyclic pattern of PB, where LG = 2π/(2πDR - sin2πDR) and DR (i.e., duty ratio) = (ventilatory duration)/(cycle duration) of PB. METHODS: After validation in a mathematical model of HF, we tested whether our estimate of LG changes with CPAP (n = 6) and inspired oxygen (n = 5) as predicted by theory in an animal model of PB. As a first test in patients with HF (n = 14), we examined whether LG predicts the first-night CPAP suppression of PB. MEASUREMENTS AND MAIN RESULTS: In lambs, as predicted by theory, LG fell as lung volume increased with CPAP (slope = 0.9 ± 0.1; R(2) = 0.82; P < 0.001) and as inspired-arterial PO(2) difference declined (slope = 1.05 ± 0.12; R(2) = 0.75; P < 0.001). In patients with HF, LG was markedly greater in 8 CPAP nonresponders versus 6 responders (1.29 ± 0.04 versus 1.10 ± 0.01; P < 0.001); LG predicted CPAP suppression of PB in 13/14 patients. CONCLUSIONS: Our novel LG estimate enables quantification of the severity of ventilatory instability underlying PB, making possible a priori selection of patients whose PB is immediately treatable with CPAP therapy.

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.

The effect of successful heart transplant treatment of heart failure on central sleep apnea.

STUDY OBJECTIVE: Central sleep apnea (CSA) associated with Cheyne-Stokes respiration in patients with congestive heart failure (CHF) is thought to be an acquired pattern of respiratory control instability related, at least in part, to elevated sympathetic nervous system activity. The effect of restoring heart function to normal with heart transplantation in patients with CHF and CSA has only been reported within weeks of the transplant and with varying results. The purpose of the study was to evaluate the impact of successful heart transplant on sympathetic nervous system activity and CSA severity in patients with CHF. DESIGN: Controlled prospective trial. SETTING: University hospital. PATIENTS: Twenty-two patients with CHF (13 patients with CSA, and 9 patients with no sleep-disordered breathing [SDB]). INTERVENTIONS AND MEASUREMENTS: Polysomnography, left ventricular ejection fraction (LVEF), and overnight urinary norepinephrine excretion (UNE) were measured before and > 6 months after successful heart transplantation. RESULTS: In the CSA group, there was a fall in apnea-hypopnea index (AHI) [mean +/- SD, 28 +/- 15 to 7 +/- 6/h; p < 0.001] and UNE (48.1 +/- 30.9 to 6.1 +/- 4.8 nmol/mmol creatinine, p < 0.001) associated with normalization of LVEF (19.2 +/- 9.3% to 53.7 +/- 6.1%, p < 0.001) at 13.2 +/- 8.3 months following heart transplantation. Of the CSA group following transplantation, seven patients had no SDB (AHI < 5/h), three patients had persistent CSA (AHI, 12.3 +/- 0.9/h) and four patients acquired obstructive sleep apnea (OSA) [AHI, 11.2 +/- 7.4/h]. In comparison, none of the control group acquired CSA or OSA after transplantation. CONCLUSIONS: We conclude that CSA may persist despite normalization of heart function and sympathetic nerve activity.