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Introduction The clinical relevance of preclinical sepsis research has been questioned [1]. This may in part be the result of varying degrees of experimental infl ammatory insults. The objective of this study was to quantify infl ammation based on plasma TNFa levels after exposure to two diff erent bacterial loads and after diff erent lengths of bacterial incubation in the peritoneal cavity. Methods We retrospectively evaluated plasma TNFa concentrations measured before and 24 hours after fecal peritonitis induced by 1 g/ kg autologous feces (16 anesthetized pigs median weight: 40.0 kg) and after 6 12 and 24 hours of fecal peritonitis induced with 2 g/kg autologous feces (24 anesthetized pigs (n = 8/group); median weight: 41.0 kg). All animals were resuscitated with fl uids norepinephrine and antibiotics and were mechanically ventilated according to standardized protocols. Diff erences along time after fecal peritonitis induced with 2 g/kg feces were assessed by ANOVA for repeated measures. Comparison between the two models (1 g/kg vs. 2 g/kg) after 24 hours of peritonitis was performed with an independent t test. Results TNFa increased from baseline to 6 12 and 24 hours of peritonitis induced with 2 g/kg feces (P

Muscle weakness and atrophy due to critical illness polyneuromyopathy (CIPM) is common in long-stay intensive care patients. Recent nerve excitability studies suggest that the recovery cycle after a single supramaximal stimulus provides useful information about axonal membrane potential and ion channel function in neuropathies. We previously found that critical illness polyneuropathy is associated with nerve depolarization, and that this depolarization is strongly correlated with serum potassium in patients with renal failure [1]. We have adapted this method to human muscle fibres, by measuring the changes in conduction velocity of muscle fibres [2]. The muscle relative refractory period (RRP) increases and supernormality (SN) decreases in ischaemia, suggesting that these measures may be indicators of membrane potential also in the muscle [2]. The aim of this study was to evaluate muscle RRP and SN in patients with CIPM.

Neurally adjusted ventilatory assistance (NAVA) delivers pressure (Paw) in proportion to the electrical activity of the diaphragm (EAdi). It is not known whether EAdi adequately reflects the respiratory drive in patients with critical illness polyneuromyopathy (CIPM) and would be sufficient to deliver assistance using NAVA.

Introduction Experimental and clinical studies have shown a reduction in intrapulmonary shunt with spontaneous breathing during airway pressure release ventilation (APRV) in acute lung injury. This reduction was related to reduced atelectasis and increased aeration. We hypothesized that spontaneous breathing will result in better ventilation and aeration of dependent lung areas and in less cyclic collapse during the tidal breath. Methods In this randomized controlled experimental trial, 22 pigs with oleic-acid-induced lung injury were randomly assigned to receive APRV with or without spontaneous breathing at comparable airway pressures. Four hours after randomization, dynamic computed tomography scans of the lung were obtained in an apical slice and in a juxtadiaphragmatic transverse slice. Analyses of regional attenuation were performed separately in nondependent and dependent halves of the lungs on end-expiratory scans and end-inspiratory scans. Tidal changes were assessed as differences between inspiration and expiration of the mechanical breaths. Results Whereas no differences were observed in the apical slices, spontaneous breathing resulted in improved tidal ventilation of dependent lung regions (P < 0.05) and less cyclic collapse (P < 0.05) in the juxtadiaphragmatic slices. In addition, with spontaneous breathing, the end-expiratory aeration increased and nonaerated tissue decreased in dependent lung regions close to the diaphragm (P < 0.05 for the interaction ventilator mode and lung region). Conclusion Spontaneous breathing during APRV redistributes ventilation and aeration to dependent, usually well-perfused, lung regions close to the diaphragm, and may thereby contribute to improved arterial oxygenation. Spontaneous breathing also counters cyclic collapse, which is a risk factor for ventilation-associated lung injury.

We summarize all original research in the field of respirology and critical care published in 2003 and 2004 in Critical Care. Articles were grouped into the following categories to facilitate a rapid overview: pathophysiology, therapeutic approaches, and outcome in acute lung injury and acute respiratory distress syndrome; hypoxic pulmonary arterial hypertension; mechanical ventilation; liberation from mechanical ventilation and tracheostomy; ventilator-associated pneumonia; multidrug-resistant infections; pleural effusion; sedation and analgesia; asthma; and techniques and monitoring.