Decompression sickness in urban divers in France

Background: Decompression sickness (DCS) can occur in SCUBA divers. DCS is treated with oxygen, preferably given under hyperbaric conditions. Although Paris (France) is located at a distance from the sea or lakes, some injured divers require hyperbaric oxygen treatment (HBOT) in this city, sometimes within a specific time frame. Thus, this study investigated the epidemiology and outcomes of such urban divers. Aim: We conducted an observational study of SCUBA divers admitted to the Raymond Poincaré Hyperbaric centre near Paris from 1993 to 2003. Materials and methods: We prospectively enrolled 69 consecutive SCUBA divers presenting DCS. Common risk factors were reported, especially aeroplane flight and training dives. Symptoms are very often atypical (63%) and onset time of symptoms is often too long (59% after 2 h) due to denial of symptoms. First aid is generally inadequate, with only 23% of victims receiving oxygen, fluid loading and aspirin together. HBOT was given for 42 (61%) patients although their examination results were considered as normal. Conclusions: Diving pits and diving travel agencies should do more to warn divers of the need for treatment with normobaric oxygen and hydration pending HBOT. Moreover, hyperbaric physicians should better clarify HBOT indications for both symptoms of late onset and atypical presentations

Safety of hyperbaric oxygen therapy in mechanically ventilated patients

Background: To evaluate the epidemiology of patients who require mechanical ventilation during hyperbaric oxygen therapy. Materials and methods: One-hundred-fifty patients who required mechanical ventilation during hyperbaric oxygen therapy were prospectively studied during a 6-year period in a French university hyperbaric centre. We analysed the indication of hyperbaric oxygen therapy, agent used for sedation, presence of a chest tube, need for vasopressor agents and tolerance and appearance of side effects. Finally, we compared the outcomes of patients according to the presence or absence of acute respiratory distress syndrome (ARDS). Results: Eleven children and 139 adult patients were included (n = 150) in the study. In both populations, carbon monoxide poisoning (51%) and iatrogenic gas embolism (33%) were the two main causes of intubation and mechanical ventilation. The combination of midazolam and sufentanil was used in 85 (67%) patients. All of the patients were given a bolus of a neuromuscular blocker during the hyperbaric session, despite the presence of ARDS in 35 patients. Patient-ventilator asynchrony was the most frequent side effect in 6 (5%) patients and was often the consequence of suboptimal sedation. Mortality was higher in the group with ARDS (23%). Conclusions: Carbon monoxide poisoning and iatrogenic gas embolism are the two main diseases of the patients who required mechanical ventilation during hyperbaric oxygen therapy in this study. Mechanical ventilation is a safe method for patients during hyperbaric oxygen therapy. Sedation needs to be perfected to avoid patient-ventilator asynchrony.

Effet de la modulation Beta adrénergique au cours du sepsis

Les b-bloquants modulent la balance sympathique/parasympathique. Dans l insuffisance cardiaque non septique, ils restaurent la variabilité cardiovasculaire et améliorent la survie. Au cours du choc septique, des effets analogues liés à un rôle anti-inflammatoire pourraient exister. Au cours de cette recherche, un modèle porcin endotoxémique particulièrement sévère a été utilisé. Il se caractérise par la survenue d une défaillance cardiaque dès la première l heure suivant l injection de LPS. Le remplissage vasculaire était identique quelque soit le groupe. Aucun vasopresseur n était utilisé. Compte tenu du caractère contre-intuitif de l utilisation d un bétabloquant dans le choc septique, nous avons tout d abord vérifié la tolérance des b-bloquants au cours du sepsis. La diminution de 20% de la fréquence cardiaque était associée à une augmentation du volume d éjection systolique et le débit cardiaque restait stable quelque soit le groupe. Au cours de la seconde expérimentation, nous nous sommes attachés à confirmer les effets anti-inflammatoires rapportés au cours de sepsis dans des modèles murins. Ces effets n ont pas été retrouvés dans notre modèle. Le groupe d animaux traités par Esmolol présentait une aggravation de la fonction hépatique et rénale par rapport au groupe contrôle, posant notamment la question de la posologie optimale. Enfin, nous avons montré que le blocage b1 augmentatait la variabilité cardiovasculaire témoignant d une amélioration du fonctionnement global du système nerveux autonome. L analyse spectral a quant à elle révélée que l utilisation d Esmolol modifie la balance sympathique/parasympathique au profit de l activité parasympathique.Beta blockers modulate the sympathetic/parasympathetic balance. In sepsis heart failure, they restore cardiovascular variability and improve survival. During septic shock, similar effects related to anti-inflammatory role may exist. In this research, we used a porcine endotoxemic model particularly severe characterized by the occurrence of heart failure during the first hour after LPS injection. Vascular filling was the same in each groups. No vasopressor was used. Given the cons-intuitive to use a beta-blocker in septic shock, we first tested the tolerance of beta-blockers during sepsis. The 20% decrease in heart rate was associated with an increase in stroke volume. Cardiac output remained stable whatever the experimental group. In the second experiment, we try to confirm the anti-inflammatory effects reported during sepsis in mouse models. These effects were not found in our model. In addition, the group of animals treated with esmolol showed a worsening of hepatic and renal function compared to the control group, raising the issue of the optimal dosage. Finally, we showed that blocking b1 was associated with an increase in cardiovascular variability reflecting improved overall functioning of the autonomic nervous system. The spectral analysis has revealed that Esmolol alters the sympathetic/parasympathetic balance in favor of parasympathetic activity.VERSAILLES-BU Sciences et IUT (786462101) / SudocSudocFranceF

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Effects of inspiratory pause on CO2 elimination and arterial PCO2 in acute lung injury.

International audienceA high respiratory rate associated with the use of small tidal volumes, recommended for acute lung injury (ALI), shortens time for gas diffusion in the alveoli. This may decrease CO(2) elimination. We hypothesized that a postinspiratory pause could enhance CO(2) elimination and reduce Pa(CO(2)) by reducing dead space in ALI. In 15 mechanically ventilated patients with ALI and hypercapnia, a 20% postinspiratory pause (Tp20) was applied during a period of 30 min between two ventilation periods without postinspiratory pause (Tp0). Other parameters were kept unchanged. The single breath test for CO(2) was recorded every 5 min to measure tidal CO(2) elimination (VtCO(2)), airway dead space (V(Daw)), and slope of the alveolar plateau. Pa(O(2)), Pa(CO(2)), and physiological and alveolar dead space (V(Dphys), V(Dalv)) were determined at the end of each 30-min period. The postinspiratory pause, 0.7 +/- 0.2 s, induced on average <0.5 cmH(2)O of intrinsic positive end-expiratory pressure (PEEP). During Tp20, VtCO(2) increased immediately by 28 +/- 10% (14 +/- 5 ml per breath compared with 11 +/- 4 for Tp0) and then decreased without reaching the initial value within 30 min. The addition of a postinspiratory pause significantly decreased V(Daw) by 14% and V(Dphys) by 11% with no change in V(Dalv). During Tp20, the slope of the alveolar plateau initially fell to 65 +/- 10% of baseline value and continued to decrease. Tp20 induced a 10 +/- 3% decrease in Pa(CO(2)) at 30 min (from 55 +/- 10 to 49 +/- 9 mmHg, P < 0.001) with no significant variation in Pa(O(2)). Postinspiratory pause has a significant influence on CO(2) elimination when small tidal volumes are used during mechanical ventilation for ALI

Impact of acute hypercapnia and augmented positive end-expiratory pressure on right ventricle function in severe acute respiratory distress syndrome.: Hypercapnia and right ventricle during severe ARDS

The original publication is available at www.springerlink.comInternational audiencePURPOSE: To evaluate the effects of acute hypercapnia induced by positive end-expiratory pressure (PEEP) variations at constant plateau pressure (P (plat)) in patients with severe acute respiratory distress syndrome (ARDS) on right ventricular (RV) function. METHODS: Prospective observational study in two academic intensive care units enrolling 11 adults with severe ARDS (PaO(2)/FiO(2) 5 cmH(2)O). We compared three ventilatory strategies, each used for 1 h, with P (plat) at 22 (20-25) cmH(2)O: low PEEP (5.4 cmH(2)O) or high PEEP (11.0 cmH(2)O) with compensation of the tidal volume reduction by either a high respiratory rate (high PEEP/high rate) or instrumental dead space decrease (high PEEP/low rate). We assessed RV function (transesophageal echocardiography), alveolar dead space (expired CO(2)), and alveolar recruitment (pressure-volume curves). RESULTS: Compared to low PEEP, PaO(2)/FiO(2) ratio and alveolar recruitment were increased with high PEEP. Alveolar dead space remained unchanged. Both high-PEEP strategies induced higher PaCO(2) levels [71 (60-94) and 75 (53-84), vs. 52 (43-68) mmHg] and lower pH values [7.17 (7.12-7.23) and 7.20 (7.16-7.25) vs. 7.30 (7.24-7.35)], as well as RV dilatation, LV deformation and a significant decrease in cardiac index. The decrease in stroke index tended to be negatively correlated to the increase in alveolar recruitment with high PEEP. CONCLUSIONS: Acidosis and hypercapnia induced by tidal volume reduction and increase in PEEP at constant P (plat) were associated with impaired RV function and hemodynamics despite positive effects on oxygenation and alveolar recruitment ( ClinicalTrials.gov #NCT00236262)