Older individuals are prone to develop heart failure (HF) because of the combination of age-related changes in the cardiovascular system and the high prevalence of cardiovascular diseases. Approximately 80% of all cases of HF occur in individuals 65 years and older,¹ and because of the aging of the population, it is anticipated that the number of older adults with HF will double during the next 25 years in the United States.² In this group, HF accounts for more hospital admissions than any other condition.³

Excessive noise is becoming a significant problem for intensive care units (ICUs). This paper first reviews the impact of noise on patients' sleep in ICUs. Five previous studies have demonstrated such impacts, whereas six other studies have shown other factors to be more important. Staff conversation and alarms are generally regarded as the most disturbing noises for patients' sleep in ICUs. Most research in this area has focused purely on noise level, but work has been very limited on the relationships between sleep quality and other acoustic parameters, including spectrum and reverberation time. Sound-absorbing treatment is a relatively effective noise reduction strategy, whereas sound masking appears to be the most effective technique for improving sleep. For future research, there should be close collaboration between medical researchers and acousticians.

Introduction: Sleep disturbances are common in critically ill patients and when sleep does occur it traverses the day-night periods. The reduction in plasma melatonin levels and loss of circadian rhythm observed in critically ill patients receiving mechanical ventilation may contribute to this irregular sleep-wake pattern. We sought to evaluate the effect of exogenous melatonin on nocturnal sleep quantity in these patients and, furthermore, to describe the kinetics of melatonin after oral administration in this patient population, thereby guiding future dosing schedules. Methods: We conducted a randomised double-blind placebo-controlled trial in 24 patients who had undergone a tracheostomy to aid weaning from mechanical ventilation. Oral melatonin 10 mg or placebo was administered at 9 p.m. for four nights. Nocturnal sleep was monitored using the bispectral index (BIS) and was expressed in terms of sleep efficiency index (SEI) and area under the curve (AUC). Secondary endpoints were SEI measured by actigraphy and nurse and patient assessments. Plasma melatonin concentrations were measured in nine patients in the melatonin group on the first night. Results: Nocturnal sleep time was 2.5 hours in the placebo group (mean SEI = 0.26, 95% confidence interval [CI] 0.17 to 0.36). Melatonin use was associated with a 1-hour increase in nocturnal sleep (SEI difference = 0.12, 95% CI -0.02 to 0.27; P = 0.09) and a decrease in BIS AUC indicating 'better' sleep (AUC difference = -54.23, 95% CI -104.47 to -3.98; P = 0.04). Results from the additional sleep measurement methods were inconclusive. Melatonin appeared to be rapidly absorbed from the oral solution, producing higher plasma concentrations relative to similar doses reported in healthy individuals. Plasma concentrations declined biexponentially, but morning (8 a.m.) plasma levels remained supraphysiological. Conclusion: In our patients, nocturnal sleep quantity was severely compromised and melatonin use was associated with increased nocturnal sleep efficiency. Although these promising findings need to be confirmed by a larger randomised clinical trial, they do suggest a possible future role for melatonin in the routine care of critically ill patients. Our pharmacokinetic analysis suggests that the 10-mg dose used in this study is too high in these patients and may lead to carryover of effects into the next morning. Reduced doses of 1 to 2 mg could be used in future studies. Trial registration: Current Controlled Trials ISRCTN47578325.

The diaphragm is normally the main inspiratory muscle and diaphragm strength in chronic obstructive pulmonary disease (COPD) is therefore of interest. We assessed diaphragm strength in 20 patients with severe stable COPD (mean FEV1 0.61, mean thoracic gas volume [Vtg] 5.31) and seven normal control subjects, measuring both maximal sniff transdiaphragmatic pressure (sniff Pdi(max)) and twitch transdiaphragmatic pressure (Tw Pdi) elicited by cervical magnetic stimulation (CMS) of the phrenic nerve roots at FRC. Acute-on-chronic hyperinflation was examined in four patients. Mean Tw Pdi in patients and control subjects was 18.5 cm H2O and 25.4 cm H2O, respectively (p < 0.01), and mean sniff Pdi was 81.9 cm H2O and 118 cm H2O, respectively (p < 0.001). Reduction in mean intrathoracic pressures was more marked; twitch esophageal pressure (Tw Pes) was -7.3 cm H2O and -16.3 cm H2O, respectively (p < 0.001) and sniff Pes was -67 cm H2O and -97.8 cm H2O (p < 0.001). During acute-on-chronic hyperinflation there was a linear negative correlation of Tw Pdi with increasing lung volume of 3.5 cm H2O/L. The ability of the diaphragm to generate transdiaphragmatic, and particularly a negative intrathoracic, pressure is reduced in COPD and these changes are exaggerated with acute-on-chronic hyperinflation.