RESUMO
INTRODUCTION: Decompression sickness (DCS) is considered a 'bubble disease'. Intravascular bubbles activate inflammatory responses associated with endothelial dysfunction. Breathing gas has been proposed as a potential risk factor but this is inadequately studied. Different gases are used in scuba diving. Helium-containing 'trimix' could theoretically mitigate inflammation and therefore reduce DCS risk. This study determined the effect of air and trimix on the inflammatory response following dives to 50 metres of sea water, and evaluated the differences between them in advanced recreational divers. METHODS: Thirty-three divers were enrolled in this observational study and were divided in two groups: 17 subjects were included in the air group, and 16 different subjects were included in the trimix (21% oxygen, 35% helium, 44% nitrogen) group. Each subject conducted a single dive, and both groups used a similar diving profile of identical duration. A venous blood sample was taken 30 min before diving and 2 h after surfacing to evaluate changes in interleukins (IL) IL-1α, IL-1ß, IL-2, IL-4, IL-6, IL-8, IL-10, tumour necrosis factor α (TNFα), vascular endothelial growth factor (VEGF), Interferon γ (IFN-γ), monocyte chemoattractant protein 1 (MCP-1) and epithelial growth factor (EGF) after diving. RESULTS: No differences were observed between groups in demographic data or diving experience. Following the dive, IL-6 values showed a slight increase, while IL-8 and EGF decreased in both groups, without significant variation between the groups. CONCLUSIONS: In physically fit divers, trimix and air gas mixture during deep diving did not cause relevant changes in the inflammatory markers tested.
Assuntos
Doença da Descompressão , Mergulho/fisiologia , Gases , Inflamação , Biomarcadores , Doença da Descompressão/etiologia , Humanos , Água do Mar , Fator A de Crescimento do Endotélio VascularRESUMO
BACKGROUND: Fourteen adults undergoing tracheal resection and reconstruction surgery were enrolled in this prospective observational pilot study to evaluate dexmedetomidine-based sedation after tracheal surgery in an intensive care unit. METHODS: Patients remained electively intubated with an uncuffed nasal endotracheal tube, awake and exhibiting spontaneous breathing. The neck was maintained in flexion through chin-to-chest sutures. Infusion of dexmedetomidine was started from a dosage of 0.7 µg·kg-1·h-1 followed by dose titration to the target level of the sedation Richmond Agitation Sedation Scale (RASS) score -1 to -2 using a dose range of 0.2 to 1.4 µg·kg-1·h-1. RESULTS: The mean sedation levels were within the target ranges during the entire 18-hour observation period with a significant decrease in RASS (baseline RASS, 1.43 ± 0.51; 18h RASS -0.86 ± 0.95; p < 0.005). The mean arterial pressure (MAP) and heart rate (HR) were significantly decreased during dexmedetomidine infusion (baseline MAP 90.29 ± 14.33 mm Hg versus 18-hour MAP 82.50 ± 15.44 mm Hg; baseline HR 81.50 ± 12.76 beats/min versus 18-hour HR 69.29 ± 10.21 beats/min; p < 0.005). The visual analog scale (VAS) scores significantly decreased (baseline VAS 4.14 ± 0.86 versus 18-hour VAS 2.79 ± 0.67; p < 0.005). Peripheral oxygen saturation did not exhibit any significant decrease. Bradycardia occurred in 1 patient who assumed beta-blocker therapy without significant changes in blood pressure and was resolved by titration of the infusion without suspending sedation. No cases of delirium were encountered, and no additional sedative or analgesic was required. CONCLUSIONS: Dexmedetomidine provided safe and effective sedation after tracheal surgery in spontaneous breathing patients without causing respiratory depression.