1 2 3 Corresponding author's email: geeta.mehta@utoronto.ca Rationale Patients in the intensive care unit (ICU) experience qualitative and quantitative sleep disruption. The consquences are sleep deprivation, and possibly adverse physiological and psychological sequelae. Patient-related factors (eg. illness, pain), environmental factors (eg. light, noise), and health support techniques (eg. mechanical ventilation, sedation) all contribute to sleep disruption. The current study reports patients' perspectives regarding sleep in the ICU. Methods Since June 2009, all patients admitted to the Mount Sinai Hospital Medical/Surgical ICU for ≥ 1 night were approached within 72 hours of discharge.Patients were asked to complete a sleep questionnaire if they passed an assessment of orientation and if they were able to communicate. The questionnaire explored the patients' quality and quantity of sleep in the ICU and following discharge from the ICU, ICU-related factors contributing to poor sleep, and possible changes in the ICU that could improve patients' sleep. Patient demographics (age, gender) as well as admission data (mechanical ventilation, sedation, APACHE II scores) were collected from patients' charts. ResultsThe target N is 100. In the first 48 patients (25 M:23 F), mean age ± SD was 56 ± 19 years (range 20-94), and mean APACHE II score was 18 ± 8. Of the sample, 33% were mechanically ventilated, and 62% received intravenous (IV) sedatives (intermittent or continuous). The average ICU length of stay was 4 nights. Sleep quality in the ICU was rated as poor or very poor by 69% of patients; and sleep quantity rated as poor or very poor by 58%. The 5 most frequently cited reasons for poor sleep were: noise (40%), pain (40%), presence of IV lines (35%), time disorientation (35%), and discomfort (30%). Patients most commonly identified the following as potentially improving sleep in the ICU: closing doors/blinds at night (42%), no unnecessary interruptions (40%), sleeping pills (33%), and dimmed lights (27%). Following ICU discharge, in-hospital sleep quality improved, primarily due to a reduction in pain (43%), fewer nocturnal interruptions (40%), and less noise (30%). Patients who received IV sedatives reported better quality of sleep (p<0.01). No significant correlations were found between perceived sleep quality and illness severity or intubation/mechanical ventilation. ConclusionsThe majority of ICU patients experience poor sleep in the ICU, regardless of whether they are intubated/mechanically ventilated. Patient-identified environmental factors to improve night-time sleep were considerable and modifiable, indicating the possibility for further development of clinical protocols. This abstract is funded by: Ontario Thoracic SocietyAm J Respir Crit Care Med

Objective. To assess the hypothesis that B27 or a gene(s) in close proximity (e.g., within or near the major histocompatibility complex [MHC]) represents a diseasecausing ankylosing spondylitis (AS) gene, and therefore contributes directly to the pathogenesis of this disorder.Methods. MHC haplotypes were determined by both serologic and molecular analyses in 15 multiplecase AS families from Toronto and Newfoundland. Segregation of MHC haplotypes with AS within these families was examined by linkage and identity-bydescent analyses. Submitted for publication October 4, 1993; accepted in revised form February 27, 1994. linkage between AS and the MHC, the maximal logarithm of odds (LOD) score being 3.48 at a recombination frequency (0) of 0.05. In a second analysis in which the population association of the MHC gene HLA-B27 with AS was taken into account, the maximal LOD score was 7.5 at 0 = 0.05. Identity-by-descent analyses showed a significant departure from random segregation among affected avuncular (P < 0.05) and cousin (P < 0.01) pairs. The presence of HLA-B40 in HLA-B27 positive individuals increased the risk for disease more than 3-fold, confirming previous reports. Disease susceptibility modeling suggested an autosomal dominant pattern of inheritance, with penetrance of approximately 20%.Conclusion. These data provide the first conclusive demonstration of linkage between the MHC region and AS, and confirm that genes within this region contribute directly to the genetic susceptibility for AS.

IntroductionCardiac troponins are sensitive and specific biomarkers of myocardial necrosis. We evaluated troponin, CK, and ECG abnormalities in patients with septic shock and compared the effect of vasopressin (VP) versus norepinephrine (NE) on troponin, CK, and ECGs.MethodsThis was a prospective substudy of a randomized trial. Adults with septic shock randomly received, blinded, a low-dose infusion of VP (0.01 to 0.03 U/min) or NE (5 to 15 μg/min) in addition to open-label vasopressors, titrated to maintain a mean blood pressure of 65 to 75 mm Hg. Troponin I/T, CK, and CK-MB were measured, and 12-lead ECGs were recorded before study drug, and 6 hours, 2 days, and 4 days after study-drug initiation. Two physician readers, blinded to patient data and drug, independently interpreted ECGs.ResultsWe enrolled 121 patients (median age, 63.9 years (interquartile range (IQR), 51.1 to 75.3), mean APACHE II 28.6 (SD 7.7)): 65 in the VP group and 56 in the NE group. At the four time points, 26%, 36%, 32%, and 21% of patients had troponin elevations, respectively. Baseline characteristics and outcomes were similar between patients with positive versus negative troponin levels. Troponin and CK levels and rates of ischemic ECG changes were similar in the VP and the NE groups. In multivariable analysis, only APACHE II was associated with 28-day mortality (OR, 1.07; 95% CI, 1.01 to 1.14; P = 0.033).ConclusionsTroponin elevation is common in adults with septic shock. We observed no significant differences in troponin, CK, and ECGs in patients treated with vasopressin and norepinephrine. Troponin elevation was not an independent predictor of mortality.Trial registrationControlled-trials.com ISRCTN94845869

In patients with septic shock, inter-rater agreement of electrocardiogram interpretation for myocardial ischemia was fair, and improved with troponin knowledge.