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Lung volume available for ventilation is markedly decreased during acute respiratory distress syndrome. Body positioning may contribute to increase lung volume and partial verticalization is simple to perform. This study evaluated whether verticalization had parallel effects on oxygenation and end expiratory lung volume (EELV). Prospective multicenter study in 40 mechanically ventilated patients with ALI/ARDS in five university hospital MICUs. We evaluated four 45-min successive trunk position epochs (supine slightly elevated at 15°; semi recumbent with trunk elevated at 45°; seated with trunk elevated at 60° and legs down at 45°; back to supine). Arterial blood gases, EELV measured using the nitrogen washin/washout, and static compliance were measured. Responders were defined by a PaO2/FiO2 increase >20 % between supine and seated position. Results are median [25th–75th percentiles]. With median PEEP = 10 cmH2O, verticalization increased lung volume but only responders (13 patients, 32 %) had a significant increase in EELV/PBW (predicted body weight) compared to baseline. This increase persisted at least partially when patients were positioned back to supine. Responders had a lower EELV/PBW supine [14 mL/kg (13–15) vs. 18 mL/kg (15–27) (p = 0.005)] and a lower compliance [30 mL/cmH2O (22–38) vs. 42 (30–46) (p = 0.01)] than non-responders. Strain decreased with verticalization for responders. EELV/PBW increase and PaO2/FiO2 increase were not correlated. Verticalization is easily achieved and improves oxygenation in approximately 32 % of the patients together with an increase in EELV. Nonetheless, effect of verticalization on EELV/PBW is not predictable by PaO2/FiO2 increase, its monitoring may be helpful for strain optimization.

Objectives: a) To investigate the functional consequences of sepsis on the β-adrenergic signal transduction in human circulating lymphocytes; b) to appreciate sepsis-associated catecholamine and cytokine release. Design: Experimental, comparative study. Setting: Research laboratory in a university hospital. Subjects: Healthy controls (n = 10); critically ill patients who were not septic (n = 7); septic patients with severe sepsis or septic shock (n = 11). Measurements and main results: Experiments were carried out using freshly isolated peripheral blood mononuclear cells (PBMC). We measured β-adrenergic receptor (βAR) number and affinity, and intracellular cAMP content at baseline and after the pharmacological stimulation of each component of the β -adrenergic complex: βAR with isoproterenol, Gs-protein with sodium fluoride (NaF), adenylate cyclase with forskolin. Catecholamine (adrenaline, noradrenaline) and cytokine (TNFα, IL-1α, IL-1β, IL-6) serum levels were measured. In both septic and non-septic patients we observed a similar 40 % down-regulation of βARs compared to controls, and a reduced basal and isoproterenol-stimulated cAMP accumulation (p < 0.05). The cAMP production elicited by NaF or forskolin was lower in septic patients than in the controls (p < 0.01). Forskolin-stimulated cAMP accumulation was significantly lower in septic patients than it was in non-septic ones (p < 0.001). Catecholamine serum concentrations were increased in the two patient groups without any significant difference. Elevated cytokine serum levels were detected in 45 % of the septic patients (versus 14 % of non-septic patients p < 0.05). Conclusions: Patients presenting with severe sepsis or septic shock have extended postreceptor defects of the β-adrenergic signal transduction. This finding suggests a heterologous desensitization of adenylate cyclase stimulation.

To identify early prognostic markers of septic shock among catheterization-derived hemodynamic and metabolic data. Prospective cohort study. A medical intensive care unit in a university hospital. Thirty-two consecutive patients with septic shock, separated into two groups according to shortterm (10-day) evolution: 18 acute survivors and 14 fatalities. Usual hemodynamic and metabolic variables were measured at the onset of shock, i.e. when the catheter was inserted (T0), and 24 h later (T24). The values collected for each group at T0 and T24 and their 24-h changes were compared. On admission, no difference was found between acute survivors and eventual fatalities. After 24 h, fatalities presented with significantly lower mean arterial pressure (p

Objective: To evaluate the influence of changes in alveolar ventilation on the following tonometry-derived variables: gastric intramucosal CO2 tension (PtCO2), gastric arterial CO2 tension difference (PgapCO2), gastric intramucosal pH (pHi) and arterial pH-pHi difference (pHgap). Design: Clinical prospective study. Setting: A medical intensive care unit in a university hospital. Patients: Ten critically ill, mechanically ventilated patients requiring hemodynamic monitoring with pulmonary artery catheter. Interventions: Gastric tonometer placement. A progressive increase in tidal volume (VT) from 7 to 10 ml/kg followed by an abrupt return to baseline VT level. Measurements and main results: Tonometer saline PtCO2 and hemodynamic data were collected hourly at various VT levels: H0 and H0' (baseline VT = 7 ml/kg), H1 (VT = 8 ml/kg), H2 (VT = 9 ml/kg), H3 (VT = 10 ml/kg), H4 (baseline VT). During the “hyperventilation phase” (H0-H3), pHi (p < 0.01) and pHgap (p < 0.05) increased but PgapCO2 remained unchanged. Cardiac output (CO) was not affected by ventilatory change. During the “hypoventilation phase” (H3-H4), pHi fell from 7.27 ± 0.11 to 7.23 ± 0.09 (p < 0.01) and PgapCO2 decreased from 16 ± 5 mmHg to 13 ± 4 mmHg (p < 0.05). VT reduction was associated with a significant cardiac output elevation (p < 0.05). Conclusions: PaCO2 and PtCO2 are similarly influenced by the changes in alveolar ventilation. Unlike pHi, the PgapCO2 is not affected by ventilation variations unless CO changes are associated.

We report the case of a 29-year-old man with decompensated alcoholic cardiomyopathy who developed a Staphylococcal pulmonic valve infective endocarditis during hemodynamic monitoring, as a consequence of catheter-related bacteremia. As experimentally demonstrated, the damaging role of the pulmonary artery catheter on the endocardial surface plays a major role in the pathogenesis of related right-sided infective endocarditis. Occurrence of bacteremia in a catheterized patient should be considered as a high risk situation, and righ-heart infective endocarditis must be suspected whenever patient presents fever or bacteremia without obvious site of infection. Doppler echocardiography is the reference diagnosis procedure.