Andres E. Carrillo

Non-invasive ventilation after extubation in hypercapnic patients with chronic respiratory disorders: randomised controlled trial

BACKGROUND Non-invasive ventilation can prevent respiratory failure after extubation in individuals at increased risk of this complication, and enhanced survival in patients with hypercapnia has been recorded. We aimed to assess prospectively the effectiveness of non-invasive ventilation after extubation in patients with hypercapnia and as rescue therapy when respiratory failure develops. METHODS We undertook a randomised controlled trial in three intensive-care units in Spain. We enrolled 106 mechanically ventilated patients with chronic respiratory disorders and hypercapnia after a successful spontaneous breathing trial. We randomly allocated participants by computer to receive after extubation either non-invasive ventilation for 24 h (n=54) or conventional oxygen treatment (n=52). The primary endpoint was avoidance of respiratory failure within 72 h after extubation. Analysis was by intention to treat. This trial is registered with clinicaltrials.gov, identifier NCT00539708. FINDINGS Respiratory failure after extubation was less frequent in patients assigned non-invasive ventilation than in those allocated conventional oxygen therapy (8 [15%] vs 25 [48%]; odds ratio 5.32 [95% CI 2.11-13.46]; p<0.0001). In patients with respiratory failure, non-invasive ventilation as rescue therapy avoided reintubation in 17 of 27 patients. Non-invasive ventilation was independently associated with a lower risk of respiratory failure after extubation (adjusted odds ratio 0.17 [95% CI 0.06-0.44]; p<0.0001). 90-day mortality was lower in patients assigned non-invasive ventilation than in those allocated conventional oxygen (p=0.0146). INTERPRETATION Early non-invasive ventilation after extubation diminished risk of respiratory failure and lowered 90-day mortality in patients with hypercapnia during a spontaneous breathing trial. Routine implementation of this strategy for management of mechanically ventilated patients with chronic respiratory disorders is advisable. FUNDING IDIBAPS, CibeRes, Fondo de Investigaciones Sanitarias, European Respiratory Society.

Acute and Short-term Effects of Secondhand Smoke on Lung Function and Cytokine Production

RATIONALE The acute effect of secondhand smoke (SHS) on lung function and the duration of system disruption remain unknown. OBJECTIVES To assess the SHS effects and their duration on lung function and inflammatory markers. METHODS In a randomized single-blind crossover experiment data were obtained from 16 (8 women) nonsmoking adults at baseline and at 0, 1, and 3 hours after a 1-hour SHS exposure set at bar/restaurant SHS levels. MEASUREMENTS AND MAIN RESULTS Serum and urine cotinine, lung function, and cytokines IL-4, IL-5, IL-6, tumor necrosis factor (TNF)-alpha, and IFN-gamma. At 0 hours most lung function parameters were significantly reduced (indicative: FEV(1), 4.3 +/- 0.4 vs. 3.8 +/- 0.3 L; FEV(1)/FVC, 0.9 +/- 0.1 vs. 0.8 +/- 0.1; P < 0.05) but at 3 hours they were at baseline levels. In contrast, cotinine (serum, 8.9 +/- 3.2 vs. 35.5 +/- 10.2 ng x ml(-1)), IL-4 (41.3 +/- 5.8 vs. 44.2 +/- 4.5 pg x ml(-1)), IL-5 (36.1 +/- 3.2 vs. 60.1 +/- 7.0 pg x ml(-1)), IL-6 (2.5 +/- 0.3 vs. 7.6 +/- 1.4 pg x ml(-1)) and IFN-gamma (0.3 +/- 0.2 vs. 0.6 +/- 0.2 IU x ml(-1)) at 3 hours were higher than at baseline (P < 0.05). IL-4 and TNF-alpha increased only in men, whereas IL-5, IL-6, and IFN-gamma were different between sexes after exposure (P < 0.05). Regression analyses revealed inverse associations of FEV(1) and FEV(1)/FVC ratio with IL-5 (P < 0.05) in men and with IL-5 (P = 0.01), IL-6 (P < 0.001), IFN-gamma (P = 0.034) and serum cotinine (P < 0.001) in women. CONCLUSIONS We conclude that 1 hour of SHS exposure at bar/restaurant levels is accompanied by significant decrements on lung function and marked increases in inflammatory cytokines, particularly in men. More importantly, whereas most smoke-induced effects on lung function appear to recede within 60 minutes, inflammatory cytokines remain elevated for at least 3 hours after exposure to SHS.

Noninvasive Ventilation in Acute Hypercapnic Respiratory Failure Caused by Obesity Hypoventilation Syndrome and Chronic Obstructive Pulmonary Disease

RATIONALE Noninvasive ventilation (NIV) is widely used in episodes of acute hypercapnic respiratory failure (AHRF) in patients with chronic obstructive pulmonary disease (COPD). However, there is no evidence on the efficacy of NIV during similar episodes in obesity hypoventilation syndrome (OHS). OBJECTIVES To compare the efficacy of NIV in episodes of AHRF caused by OHS and COPD. METHODS We prospectively assessed 716 consecutive patients (173 with OHS and 543 with COPD) with AHRF (arterial pH < 7.35 and Pa(CO(2)) > 45 mm Hg) treated with a similar protocol of NIV. We defined successful NIV as avoidance of intubation and intensive care unit survival at least 24 hours in the ward. Hospital survivors were followed for 1 year to assess hospital readmission and survival. MEASUREMENTS AND MAIN RESULTS Both groups had similar (mean ± SD) baseline respiratory acidosis (arterial pH, 7.22 ± 0.08; Pa(CO(2)), 86 ± 21 mm Hg). Patients with OHS were older (74 ± 11 vs. 71 ± 10 yr; P < 0.001); were more frequently female (134, 77% vs. 66, 12%; P < 0.001); had less late NIV failure (12, 7% vs. 67, 13%; P = 0.037); had lower hospital mortality (10, 6% vs. 96, 18%; P < 0.001); and had higher 1-year survival (odds ratio, 1.83; 95% confidence interval, 1.24-2.69; P = 0.002). However, survival adjusted for confounders (adjusted odds ratio, 1.41; 95% confidence interval, 0.70-2.83; P = 0.34), NIV failure (11, 6% vs. 59, 11%; P = 0.11), length of stay, and hospital readmission were similar in both groups. Among patients with COPD, obesity was associated with less late NIV failure and hospital readmission. CONCLUSIONS Patients with OHS can be treated with NIV during an episode of AHRF with similar efficacy and better outcomes than patients with COPD.

Caloric restriction and longevity: Effects of reduced body temperature

Caloric restriction (CR) causes a reduction in body temperature (T(b)) which is suggested to contribute to changes that increase lifespan. Moreover, low T(b) has been shown to improve health and longevity independent of CR. In this review we examine the connections between CR, T(b) and mechanisms that influence longevity and ageing. Recent findings regarding the overlapping mechanisms of CR and T(b) that benefit longevity are discussed, including changes in body composition, hormone regulation, and gene expression, as well as reductions in low-level inflammation and reactive oxygen species-induced molecular damage. This information is summarized in a model describing how CR and low T(b), both synergistically and independently, increase lifespan. Moreover, the nascent notion that the rate of ageing may be pre-programmed in response to environmental influences at critical periods of early development is also considered. Based on current evidence, it is concluded that low T(b) plays an integral role in mediating the effects of CR on health and longevity, and that low T(b) may exert independent biological changes that increase lifespan. Our understanding of the overlap between CR- and T(b)-mediated longevity remains incomplete and should be explored in future research.

Impact of vitamin D supplementation during a resistance training intervention on body composition, muscle function, and glucose tolerance in overweight and obese adults.

BACKGROUND & AIMS The impact of vitamin D supplementation in overweight and obese adults during resistance training on body composition, muscle function, and glucose tolerance was investigated. METHODS Twenty-three overweight and obese (age: 26.1±4.7 y; BMI: 31.3±3.2 kg/m(2); 25-hydroxyvitamin D: 19.3±7.2 ng/mL) adults were recruited for participation in a double-blind, placebo-controlled trial. Participants were randomly divided into vitamin D (VitD, 4000 IU/d; 5 females, 5 males) and placebo (PL; 7 females, 6 males) groups. Both groups completed 12 weeks of resistance training. 25-hydroxyvitamin D, parathyroid hormone, body composition, and glucose tolerance were assessed at baseline and 12 weeks. Muscle function (strength and power) was assessed at baseline, 4, 8, and 12 weeks. RESULTS During the intervention, 25-hydroxyvitamin D increased and parathyroid hormone decreased in the VitD group (P<0.05). Peak power was significantly increased at 4 weeks in the VitD group only (P<0.05). Regression analysis revealed an inverse association between the change in 25-hydroxyvitamin D with the change in waist-to-hip ratio (R(2)=0.205, P=0.02). No other improvements were observed with supplementation. CONCLUSIONS Vitamin D supplementation in overweight and obese adults during resistance training induced an early improvement in peak power, and elevated vitamin D status was associated with reduced waist-to-hip ratio. CLINICAL TRIAL REGISTRATION NUMBER NCT01199926.

Exercise Training Modifies Ghrelin and Adiponectin Concentrations and Is Related to Inflammation in Older Adults

The purpose of this study was to observe exercise training-induced effects on adiponectin, leptin, and ghrelin. Twenty-nine older, healthy participants were classified as physically active (comparison group: N = 15, 70.9 ± 1.2 years) or physically inactive (exercise group: N = 14, 70.5 ± 1.4 years). Exercise group participants completed 12 weeks of combined aerobic and resistance exercise training, whereas comparison group participants maintained their current level of exercise and served as a physically active comparison group. Monocyte phenotype, as well as serum ghrelin, leptin, adiponectin, and soluble tumor necrosis factor receptor II were analyzed prior to and following the 12-week period. Ghrelin and adiponectin increased 47% and 55%, respectively, in exercise group participants following exercise training. Percent change in ghrelin (post and pre) was negatively correlated with the percent change in CD14+CD16+ monocytes (post and pre) in exercise group participants. Despite no changes in body mass, these data contribute to evidence for the anti-inflammatory effects of exercise.

A novel model to predict cutaneous finger blood flow via finger and rectal temperatures.

Please cite this paper as: Carrillo, Cheung, and Flouris (2011). A Novel Model to Predict Cutaneous Finger Blood Flow Via finger and Rectal Temperatures. Microcirculation18(8), 670–676.

Effects of Secondhand Smoke on Thyroid Function

Growing evidence suggests that the effects of second hand smoke (SHS) exposure contribute to disruptions in thyroid function. Toxic elements contained in cigarette smoke, such as thiocyanate, may be partially responsible for impaired thyroid hormonogenesis. SHS-induced inflammatory stress, namely interleukin 1beta (IL-1beta), impairs thyroid hormonogenesis and iodine uptake; initiates interleukin 6 (IL-6) production from thyroid epithelial cells and stimulates the expression of molecules that exacerbate thyroid autoimmunity. The link between SHS exposure and thyroid autoimmune disease is not well documented and thus, remains to be fully understood. Elevated inflammatory stress and thyroid hormone secretion in response to SHS exposure initiates catabolic processes that alter body composition via lean body mass breakdown; translating to an elevation in resting energy expenditure of approximately 10%. The combination of certain biological factors, such as sex and/or existing thyroid disease may stimulate differential SHS-induced effects on thyroid function. Nevertheless, exposure to SHS disturbs vital human processes via thyroid disruption.

Autonomic nervous system modulation during accidental syncope induced by heat and orthostatic stress.

BACKGROUND Heart rate variability (HRV) indices (LF, HF, LF/HF, RMSSD, and pNN50) under combined heat and orthostatic stress leading up to and during accidental syncope (EXP group: one man, two women; age: 23.7 +/- 2.9 yr) were compared with data collected from subjects who did not experience syncope (CON group: one man, two women; age: 22.3 +/- 1.5 yr). METHODS Minute averages of HRV indices were collected during 5 min at baseline (Base), 5 min leading up to syncope (PRE), and 5 min during syncope (Syncope) (i.e., 2 min leading up to, 1 min during, and 2 min post-syncope). Data were individually analyzed as 1-min means during Syncope as well as 5-min means during Base, PRE, and Syncope. RESULTS Between-group results revealed that LF and LF/HF were significantly higher and HF was significantly lower in EXP compared to CON subjects at minutes 1, 2, and 3 during Syncope. Further, RMSSD (CON: 161.1 +/- 37.0 ms; EXP: 17.5 +/- 13.3 ms) and pNN50 (CON: 26.4 +/- 36.3%; EXP: 1.3 +/- 1.2%) were significantly lower in EXP compared to CON subjects at minute 3 during Syncope. During Syncope, 5-min averages of LF (CON: 46.1 +/- 13.9 nu; EXP: 77.5 +/- 6.6 nu) and LF/HF (CON: 1.0 0.5; EXP: 3.8 +/- 1.7) were significantly higher, and HF (CON: 53.9 +/- 13.9 nu; EXP: 22.5 +/ 1 6.6 nu) was significantly lower in EXP subjects compared to CON. DISCUSSION Our findings show that autonomic nervous system modulation leading up to and during accidental syncope induced by heat and orthostatic stress is characterized by an exaggerated suppression of parasympathetic and elevation of sympathetic activity. Thus, elevated LF and LF/HF, and lower HF, RMSSD, and pNN50 may represent risk factors for accidental syncope.

Heart rate variability during high heat stress: a comparison between young and older adults with and without type 2 diabetes

We examined whether older individuals with and without Type 2 diabetes (T2D) experience differences in heart rate variability (HRV) during a 3-h exposure to high heat stress compared with young adults. Young (Young; n = 22; 23 ± 3 yr) and older individuals with (T2D; n = 11; 59 ± 9 yr) and without (Older; n = 25; 63 ± 5 yr) T2D were exposed to heat stress (44°C, 30% relative humidity) for 3 h. Fifty-five HRV measures were assessed for 15 min at baseline and at minutes 82.5-97.5 (Mid) and minutes 165-180 (End) during heat stress. When compared with Young, a similar number of HRV indices were significantly different (P < 0.05) in Older (Baseline: 35; Mid: 29; End: 32) and T2D (Baseline: 31; Mid: 30; End: 27). In contrast, the number of HRV indices significantly different (P < 0.05) between Older and T2D were far fewer (Baseline: 13, Mid: 1, End: 3). Within-group analyses demonstrated a greater change in the Young groups HRV during heat stress compared with Older and T2D; the number of significantly different (P < 0.05) HRV indices between baseline and End were 42, 29, and 20, for Young, Older, and T2D, respectively. Analysis of specific HRV domains suggest that the Young group experienced greater sympathetic activity during heat stress compared with Older and T2D. In conclusion, when compared with young, older individuals with and without T2D demonstrate low HRV at baseline and less change in HRV (including an attenuated sympathetic response) during 3 h high heat stress, potentially contributing to impaired thermoregulatory function.