Investigation of Sleep-disordered Breathing
Given the prevalence of SDB inpatients with HF, a high index of suspicion is appropriate. In the general population, questionnaires designed to screen for daytime somnolence, such as the Epworth sleepiness questionnaire are frequently used. However, patients with HF tend to report low daytime somnolence even in the presence of significant SDB,11 possibly due to increased sympathetic nervous activity. It is therefore usually necessary to take a confirmatory history from a partner where possible or to proceed to formal investigation where SDB is suspected. However, those with SDB do have increased measures of sleepiness when assessed objectively.34
Simple screening for SDB may be performed by overnight pulse oximetry. Using desaturations of ≥3 % at a cut off of 12.5 events/ hour for significant SDB, Ward et al. reported a sensitivity of 93 % and specificity of 77 % compared with formal polysomnography.35 With this approach, few patients with SDB would be missed, but pulse oximetry alone is unable to differentiate between OSA and CSA and further investigation is mandatory in patients with a high desaturation index or anyone in whom suspicion remains high despite a negative test.
Several non-contact bedside monitors are available which use ultra- low power radiowaves to detect respiratory movement during sleep. These can diagnose significant SDB with a sensitivity and specificity of around 90 %,36 but are not yet common in clinical practice.
The gold-standard test for SDB remains in-hospital polysomnography. This involves the patient spending a night in a monitored sleep laboratory while the equipment monitors the respiratory pattern, oxygen saturation, electrocardiogram, electroencephalogram and, in some cases, electromyogram and oculogram. This test provides unparalleled detail on the severity and type of SDB, as well as phases and architecture of sleep. It is, however, relatively expensive and laborious and therefore SDB is commonly diagnosed by more limited sleep polygraphy in the patient’s home. This test usually incorporates elastic effort straps around the chest and abdomen, a finger saturation probe and tubing under the nostrils to measure airflow. A thermistor may be included to estimate oral airflow and a snore sensor is also available. This is easily portable and can be fitted by the patient; it may provide more useful data in that sleep is less likely to be disrupted by the hospital environment and the data are relatively simple to interpret. Research has shown that polygraphy correlates well with polysomnography for the diagnosis of SDB in HF.37
Over the past 10 years, there has been interest in whether pacemaker respiratory sensors can be used to accurately diagnose and monitor SDB. Both simple and complex devices are now available that incorporate algorithms that use changes in transthoracic impedance with ventilation to give a respiratory disturbance index, akin to the AHI. In one study, a commercially available pacemaker algorithm showed a sensitivity of 88.9 % and a specificity of 84.6 % for the diagnosis of severe SDB.38 Evaluation of the accuracy of other available algorithms is currently underway (NCT02204865). At pacemaker download, up to 3 months of data on AHI are available and, with remote monitoring, changes in AHI could be a useful early indicator of HF decompensation. Further research is required.
Treatment of Sleep-disordered Breathing in Heart Failure
Optimal pharmacological therapy of HF, including careful attention to maintaining euvolaemia, would be expected to improve SDB of both sorts by reducing pharyngeal oedema, sympathetic drive and pulmonary congestion, although specific data are lacking. While OSA and CSA share many pathophysiological mechanisms and may co-exist in the same patient to varying degrees, the role of non- invasive ventilation (NIV) and some novel therapies are very different between the two.
Obstructive Sleep Apnoea
The approach to patients with OSA and HF includes advice regarding weight loss and sleep hygiene, including avoidance of excess alcohol or other sedatives as appropriate.39,40 This is relatively less useful in the HF population as OSA is less frequently associated with these factors than in the general population, but should be considered on an individual patient basis.
Non-invasive ventilation, particularly with CPAP, is well-established in current guidelines for non-HF patients with moderate to severe OSA and daytime somnolence (40). In this population, CPAP significantly improves the AHI and Epworth sleepiness score, but has not been consistently shown to improve hypertension, mortality or quality of life measures.40,41
The evidence for CPAP use in the HF population is based on fewer and smaller studies than the general population. In a randomised controlled trial of 24 patients with HF and OSA, Kaneko et al.42 found that 1 month of CPAP therapy improved left ventricular EF (LVEF) from 25.0 ± 2.8 % to 33.8 ± 2.4 % (p<0.001), reduced LV end systolic diameter from 54.5 ± 1.8 mm to 51.7 ± 1.2 mm (p=0.009) and reduced heart rate and blood pressure in parallel with a significant decrease in AHI (37.1 ± 6.4/hour to 8.3 ± 2.8/hour; p<0.001). There was no significant change in these parameters in the control group. Mansfield et al. randomised 55 patients with HF and OSA to CPAP for 3 months or control. Those receiving CPAP had a greater improvement in LVEF (5.0 ± 1.0 % versus 1.5 ± 1.4 %; p=0.04), reduced urinary noradrenaline and improved quality of life scores.43 In a larger non-randomised trial, Kasai et al. followed 88 patients with HF and moderate to severe OSA for around 2 years.44 They demonstrated that those not treated with CPAP had a significantly higher risk of death or hospitalisation (HR 2.03, 95 % CI 1.07–3.68; p=0.030) than those receiving CPAP. Those with poor CPAP compliance also had significantly worse outcomes. Physiologically, OSA has been shown to acutely reduce stroke volume and cardiac output overnight and that this reduction is ameliorated by CPAP therapy.45 Measures of cardiac sympathetic tone are also reduced by CPAP in those with OSA.46
There are conflicting reports regarding the impact of cardiac resynchronisation therapy (CRT) on OSA.47,48 The majority of research has demonstrated no significant improvement in AHI with CRT, in contrast to those with CSA. In some patients with retrognathism or tongue enlargement, mandibular advancement devices have been shown to be effective.49 Hypoglossal nerve stimulation is a novel technique aimed at maintaining pharyngeal tone during sleep. A non-controlled study of 126 general OSA patients demonstrated a 68 % reduction in AHI with this technique, but the role in patients with HF is not known.50