High oxygen extraction and slow recovery of muscle deoxygenation kinetics after neuromuscular electrical stimulation in COPD patients.

PURPOSE: It was hypothesized that patients with chronic obstructive pulmonary disease (COPD) would exhibit a slow muscle deoxygenation (HHb) recovery time when compared with sedentary controls. METHODS: Neuromuscular electrical stimulation (NMES 40 and 50 mA, 50 Hz, 400 µs) was employed to induce isometric contraction of the quadriceps. Microvascular oxygen extraction (µO2EF) and HHb were estimated by near-infrared spectroscopy (NIRS). Recovery kinetic was characterized by measuring the time constant Tau (HHb-τ). Torque and work were measured by isokinetic dynamometry in 13 non-hypoxaemic patients with moderate-to-severe COPD [SpO2 = 94.1 ± 1.6 %; FEV1 (% predict) 48.0 ± 9.6; GOLD II-III] and 13 age- and sex-matched sedentary controls. RESULTS: There was no desaturation in either group during NMES. Torque and work were reduced in COPD versus control for 40 and 50 mA [torque (Nm) 50 mA = 28.9 ± 6.9 vs 46.1 ± 14.2; work (J) 50 mA = 437.2 ± 130.0 vs. 608.3 ± 136.8; P < 0.05 for all]. High µO2EF values were observed in the COPD group at both NMES intensities (corrected by muscle mass 50 mA = 6.18 ± 1.1 vs. 4.68 ± 1.0 %/kg; corrected by work 50 mA = 0.12 ± 0.05 vs. 0.07 ± 0.02 %/J; P < 0.05 for all). Absolute values of HHb-τ (50 mA = 31.11 ± 9.27 vs. 18.08 ± 10.70 s), corrected for muscle mass (50 mA 3.80 ± 1.28 vs. 2.05 ± 1.45 s/kg) and corrected for work (50 mA = 0.08 ± 0.04 vs. 0.03 ± 0.02 s/J) were reduced in COPD (P < 0.05 for all). The variables behaviour for 40 mA was similar to those of 50 mA. CONCLUSIONS: COPD patients exhibited a slower muscle deoxygenation recovery time after NMES. The absence of desaturation, low torque and work, high µO2EF and high values for recovery time corrected by muscle mass and work suggest that intrinsic muscle dysfunction has an impact on muscle recovery capacity.

Fluid Overload and Risk of Mortality in Critically Ill Patients.

BACKGROUND: Fluid overload (FO) is a condition present in critical care units, and it is associated with clinical complications and worse outcomes for severe patients. OBJECTIVE: The aim of this study was to verify if FO is a risk factor for mortality in critically ill patients. METHODS: Retrospective study performed in a Brazilian intensive care unit, from January to March 2016, with patients older than 18 years and hospitalized for more than 24 hours. Demographic and clinical data, as well as fluid balance and overload, were analyzed to verify the risk factors for mortality. A logistic regression model was elaborated, and significance was set at P < .05. RESULTS: There were 158 patients included, of which only 13 (8.2%) presented FO. Mortality was verified in individuals 30 (18.9%), of whom only 7 (23.3%) developed FO, which was lower in survivors 6 (4.9%), P = .001. In the simple regression model, the FO was significant (odds ratio [OR], 6.23; 95% confidence interval [CI], 2.04-19.53), P = .001. However, in the multiple regression model, there were significant findings only for mechanical ventilation (OR, 5.86; 95% CI, 2.10-18.12, P = .001), acute kidney injury (OR, 4.05; 95% CI, 1.53-11; P = .001), and noradrenaline (OR, 3.85; 95% CI, 1.01-9.51; P = .041); FO was not significant (OR, 3.68; 95% CI, 0.91-15.55; P = .069). CONCLUSION: Fluid overload is higher in patients who died. Therefore, it was not considered a risk factor for mortality.