Evidence Map and Systematic Review of Disinfection Efficacy on Environmental Surfaces in Healthcare Facilities.

Healthcare-associated infections (HAIs) contribute to patient morbidity and mortality with an estimated 1.7 million infections and 99,000 deaths costing USD $28-34 billion annually in the United States alone. There is little understanding as to if current environmental surface disinfection practices reduce pathogen load, and subsequently HAIs, in critical care settings. This evidence map includes a systematic review on the efficacy of disinfecting environmental surfaces in healthcare facilities. We screened 17,064 abstracts, 635 full texts, and included 181 articles for data extraction and study quality assessment. We reviewed ten disinfectant types and compared disinfectants with respect to study design, outcome organism, and fourteen indictors of study quality. We found important areas for improvement and gaps in the research related to study design, implementation, and analysis. Implementation of disinfection, a determinant of disinfection outcomes, was not measured in most studies and few studies assessed fungi or viruses. Assessing and comparing disinfection efficacy was impeded by study heterogeneity; however, we catalogued the outcomes and results for each disinfection type. We concluded that guidelines for disinfectant use are primarily based on laboratory data rather than a systematic review of in situ disinfection efficacy. It is critically important for practitioners and researchers to consider system-level efficacy and not just the efficacy of the disinfectant.

Initial orthostatic hypotension and cerebral blood flow regulation: effect of α1-adrenoreceptor activity.

We examined the hypothesis that α(1)-adrenergic blockade would lead to an inability to correct initial orthostatic hypotension (IOH) and cerebral hypoperfusion, leading to symptoms of presyncope. Twelve normotensive humans (aged 25 ± 1 yr; means ± SE) attempted to complete a 3-min upright stand, 90 min after the administration of either α(1)-blockade (prazosin, 1 mg/20 kg body wt) or placebo. Continuous beat-to-beat measurements of middle cerebral artery velocity (MCAv; Doppler), blood pressure (finometer), heart rate, and end-tidal Pco(2) were obtained. Compared with placebo, the α(1)-blockade reduced resting mean arterial blood pressure (MAP) (-15%; P < 0.01); MCAv remained unaltered (P ≥ 0.28). Upon standing, although the absolute level of MAP was lower following α(1)-blockade (39 ± 10 mmHg vs. 51 ± 14 mmHg), the relative difference in IOH was negligible in both trials (mean difference in MAP: 2 ± 2 mmHg; P = 0.50). Compared with the placebo trial, the declines in MCAv and Pet(CO(2)) during IOH were greater in the α(1)-blockade trial by 12 ± 4 cm/s and 4.4 ± 1.3 mmHg, respectively (P ≤ 0.01). Standing tolerance was markedly reduced in the α(1)-blockade trial (75 ± 17 s vs. 180 ± 0 s; P < 0.001). In summary, while IOH was little affected by α(1)-blockade, the associated decline in MCAv was greater in the blockade condition. Unlike in the placebo trial, the extent of IOH and cerebral hypoperfusion failed to recover toward baseline in the α(1)-blockade trial leading to presyncope. Although the development of IOH is not influenced by the α(1)-adrenergic receptor pathway, this pathway is critical in the recovery from IOH to prevent cerebral hypoperfusion and ultimately syncope.

The effect of time-of-day and sympathetic α1-blockade on orthostatic tolerance.

Tolerance time to a standardized orthostatic stressor is markedly reduced in normotensive individuals in the morning. However, the physiological mechanisms that underpin this phenomenon are unknown. The purpose of this study was to examine the role of α(1)-adrenergic activity on orthostatic tolerance and associated cardiorespiratory and cerebrovascular responses, and to determine whether its endogenous modulation is important in the diurnal variation of orthostatic tolerance. In a four-trial, randomized placebo-controlled crossover experiment, 12 normotensive volunteers (aged 25 ± 1 yrs; mean ± SE) completed a 60° head-upward tilt (HUT; 15 min or until onset of presyncope) at 06:00 and 16:00 h, 90 min after the administration of either α(1)-blockade (prazosin, 1 mg/20 kg body weight) or placebo. Continuous beat-to-beat measurements of middle cerebral blood flow velocity (transcranial Doppler), blood pressure (Finometer), heart rate, stroke volume, cardiac output, and end-tidal carbon dioxide were obtained. Independent of time-of-day, α(1)-blockade markedly reduced the ability to tolerate a 15-min 60° HUT; tolerance time was 229% shorter compared with the placebo condition (p ≤ .0001). Moreover, a marked diurnal variation in orthostatic tolerance was evident following α(1)-adrenergic blockade; e.g., tolerance time in the morning (176 ± 30 s) was lower than in the afternoon (354 ± 75 s; p = .04). These findings highlight an important role of α(1)-sympathetic vasoconstrictor activity in acutely regulating blood pressure and offsetting syncope, especially in the early morning.

α1-Adrenoreceptor activity does not explain lower morning endothelial-dependent, flow-mediated dilation in humans.

Early morning reduction in endothelium-dependent, flow-mediated dilation (FMD) may contribute to the high incidence of sudden cardiac death at this time of day. The mechanisms underpinning diurnal variation in FMD are unclear, but potentially relate to a circadian rhythm in sympathetic nerve activity. We hypothesized that blockade of α(1)-mediated sympathetic nerve activity would act to attenuate the diurnal variation in FMD. In a randomized and placebo-controlled design, we measured brachial artery FMD in 12 participants (mean age = 26 yr, SD = 3) at 0600 and 1600 after ingestion of an α(1)-blocker (prazosin, 1 mg/20 kg body mass) or placebo. Arterial diameter and shear rate were assessed using edge-detection software. Heart rate and blood pressure were also measured. Data were analyzed using linear mixed modeling. Following placebo, FMD was 8 ± 2% in the morning compared with 10 ± 3% in the afternoon (P = 0.04). Blockade with prazosin led to a slight but nonsignificant increase in morning FMD (P = 0.24) and a significant (P = 0.04) decrease in afternoon FMD, resulting in no diurnal variation (P = 0.20). Shear rate did not differ in the morning or afternoon under either condition (P > 0.23). Blood pressure was lower following prazosin compared with placebo (P < 0.02), an effect that was similar at both times of day (P > 0.34). Heart rate and norepinephrine levels were higher in the afternoon following prazosin. These data indicate that α(1)-adrenoreceptor activity does not explain lower morning endothelium-dependent FMD.

Hypertrophy with unilateral resistance exercise occurs without increases in endogenous anabolic hormone concentration.

We aimed to gain insight into the role that the transitory increases in anabolic hormones play in muscle hypertrophy with unilateral resistance training. Ten healthy young male subjects (21.8 +/- 0.4 years, 1.78 +/- 0.04 m, 75.6 +/- 2.9 kg; mean +/- SE) engaged in unilateral resistance training for 8 week (3 days/week). Exercises were knee extension and leg press performed at 80-90% of the subject's single repetition maximum (1RM). Blood samples were collected in the acute period before and after the first training bout and following the last training bout and analyzed for total testosterone, free-testosterone, luteinizing hormone, sex hormone binding globulin, growth hormone, cortisol, and insulin-like growth factor-1. Thigh muscle cross sectional area (CSA) and muscle fibre CSA by biopsy (vastus lateralis) were measured pre- and post-training. Acutely, no changes in systemic hormone concentrations were observed in the 90 min period following exercise and there was no influence of training on these results. Training-induced increases were observed in type IIx and IIa muscle fibre CSA of 22 +/- 3 and 13 +/- 2% (both P < 0.001). No changes were observed in fibre CSA in the untrained leg (all P > 0.5). Whole muscle CSA increased by 5.4 +/- 0.9% in the trained leg (P < 0.001) and remained unchanged in the untrained leg (P = 0.76). Isotonic 1RM increased in the trained leg for leg press and for knee extension (P < 0.001). No changes were seen in the untrained leg. In conclusion, unilateral training induced local muscle hypertrophy only in the exercised limb, which occurred in the absence of changes in systemic hormones that ostensibly play a role in muscle hypertrophy.