Factors Associated with and Prognosis Impact of Perceived Sleep Quality and Estimated Quantity in Patients Receiving Non-Invasive Ventilation for Acute Respiratory Failure.

Background. The objectives of this study were (1) to determine factors associated with impaired sleep and (2) to evaluate the relationship between impaired sleep and the outcome. Methods. Secondary analysis of a prospective observational cohort study in 54 intensive care units in France and Belgium. Sleep quality was quantified by the patients with a semi-quantitative scale. Results. Among the 389 patients included, 40% reported poor sleep during the first night in the ICU and the median (interquartile) total sleep time was 4 h (2−5). Factors independently associated with poor sleep quality were the SOFA score (odds ratio [OR] 0.90, p = 0.037), anxiety (OR 0.43, p = 0.001) and the presence of air leaks (OR 0.52, p = 0.013). Factors independently associated with short-estimated sleep duration (<4 h) were the SOFA score (1.13, p = 0.005), dyspnea on admission (1.13, p = 0.031) and the presence of air leaks (1.92, p = 0.008). Non-invasive ventilation failure was independently associated with poor sleep quality (OR 3.02, p = 0.021) and short sleep duration (OR 0.77, p = 0.001). Sleep quality and duration were not associated with an increase in mortality or length of stay. Conclusions. The sleep of patients with ARF requiring NIV is impaired and is associated with a high rate of NIV failure.

Prolonged mechanical ventilation worsens sepsis-induced diaphragmatic dysfunction in the rat.

BACKGROUND: Short-term mechanical ventilation (MV) protects against sepsis-induced diaphragmatic dysfunction. Prolonged MV induces diaphragmatic dysfunction in non-septic animals, but few reports describe the effects of prolonged MV in sepsis. We hypothesized that prolonged MV is not protective but worsens the diaphragmatic dysfunction induced by a mild sepsis, because MV and sepsis share key signaling mechanisms, such as cytokine upregulation. METHOD: We studied the impact of prolonged MV (12 h) in four groups (n = 8) of male Wistar rats: 1) endotoxemia induced by intraperitoneal injection of Escherichia coli lipopolysaccharide, 2) MV without endotoxemia, 3) combination of endotoxemia and MV and 4) sham control. Diaphragm mechanical performance, pro-inflammatory cytokine concentrations (Tumor Necrosis Factor-α, Interleukin-1ß, Interleukin-6) in plasma were measured. RESULTS: Prolonged MV and sepsis independtly reduced maximum diaphragm force (-27%, P = 0.003; -37%, P<0.001; respectively). MV and sepsis acted additively to further decrease diaphragm force (-62%, P<0.001). Similar results were observed for diaphragm kinetics (maximum lengthening velocity -47%, P<0.001). Sepsis and MV reduced diaphragm cross sectional area of type I and IIx fibers, which was further increased by the combination of sepsis and MV (all P<0.05). Sepsis and MV were individually associated with the presence of a robust perimysial inflammatory infiltrate, which was more marked when sepsis and MV were both present (all P<0.05). Sepsis and, to a lesser extent, MV increased proinflammatory cytokine production in plasma and diaphragm (all P<0.05); proinflammatory cytokine expression in plasma was increased further by the combination of sepsis and MV (all P<0.05). Maximum diaphragm force correlated negatively with plasma and diaphragmatic cytokine production (all p<0.05). CONCLUSIONS: Prolonged (12 h) MV exacerbated sepsis-induced decrease in diaphragm performance. Systemic and diaphragmatic overproduction of pro-inflammatory cytokines may contribute to diaphragm weakness.

Diaphragmatic function is preserved during severe hemorrhagic shock in the rat.

BACKGROUND: Acute diaphragmatic dysfunction has been reported in septic and cardiogenic shock, but few data are available concerning the effect of hemorrhagic shock on diaphragmatic function. The authors examined the impact of a hemorrhagic shock on the diaphragm. METHODS: Four parallel groups of adult rats were submitted to hemorrhagic shock induced by controlled exsanguination targeting a mean arterial blood pressure of 30 mmHg for 1 h, followed by a 1-h fluid resuscitation with either saline or shed blood targeting a mean arterial blood pressure of 80 mmHg. Diaphragm and soleus strip contractility was measured in vitro. Blood flow in the muscle microcirculation was measured in vivo using a Laser Doppler technique. Muscle proinflammatory cytokine concentrations were also measured. RESULTS: Hemorrhagic shock was characterized by a decrease in mean arterial blood pressure to 34 ± 5 mmHg (-77 ± 4%; P< 0.05) and high plasma lactate levels (7.6 ± 0.9 mM; P < 0.05). Although tetanic tension of the diaphragm was not altered, hemorrhagic shock induced dramatic impairment of tetanic tension of the soleus (-40 ± 19%; P < 0.01), whereas proinflammatory cytokine levels were low and not different between the two muscles. Resuscitation with either blood or saline did not further modify either diaphragm or soleus performance and proinflammatory cytokine levels. The shock-induced decrease in blood flow was much more pronounced in the soleus than in the diaphragm (-75 ± 13% vs. -17 ± 10%; P = 0.02), and a significant interaction was observed between shock and muscle (P < 0.001). CONCLUSION: Diaphragm performance is preserved during hemorrhagic shock, whereas soleus performance is impaired, with no further impact of either blood or saline fluid resuscitation.