The pathophysiology of SAE is highly complex and not fully understood, but proposed mechanisms include alterations in the blood–brain barrier, effects of local and systemic inflammatory cytokines, cerebral metabolism disruption and imbalance of neurotransmitters. SAE affects nearly 30% of septic patients at admission and is a known risk factor for mortality. Sepsis-associated encephalopathy (SAE), defined as a transient and reversible brain dysfunction, occurs when the source of sepsis is located outside of the central nervous system. Experimental large animal studies have shown strong associations between lower tidal volumes and decreased systemic and organ-specific inflammation, as well as decreased microbiological growth. Arguments favoring protective ventilation in patient categories other than those suffering from ARDS to prevent rather than to treat manifest lung injury have been raised. the avoidance of iatrogenic harm by the use of higher than traditional positive end-expiratory pressure (PEEP) levels and smaller than traditional tidal volumes (V T), has an established role in the care of patients with acute respiratory distress syndrome (ARDS). Mechanical ventilation (MV) carries the risks of cyclic atelectasis and overdistension of alveoli, events that add to a pro-inflammatory response. The low tidal volume group had increased cerebral blood flow, cerebral oxygen delivery and cerebral metabolism together with increased levels of markers of brain injury compared with medium–high tidal volume ventilation. ConclusionsĬontrary to the hypothesis, protective ventilation did not affect inflammatory cytokines.

Moreover, low tidal volume ventilation increased the levels of glutamate ( p < 0.01), glycerol ( p < 0.05) and showed a trend towards higher lactate to pyruvate ratio ( p = 0.08) in cerebral microdialysate as well as higher levels of S-100B ( p < 0.05) in jugular venous plasma compared with medium–high tidal volume ventilation. The low tidal volume group had increased cerebral blood flow ( p < 0.001) and cerebral oxygen delivery ( p < 0.001), lower cerebral vascular resistance ( p < 0.05), higher cerebral metabolic rate ( p < 0.05) along with higher cerebral glucose consumption ( p < 0.05) and lactate production ( p < 0.05). No differences in systemic or sagittal sinus levels of TNF-α or IL-6 were seen between the groups. Intracranial pressure, brain tissue oxygenation and brain microdialysis were sampled every hour. Systemic, superior sagittal sinus and jugular vein blood samples were analysed for inflammatory cytokines and S100B. During a 6-h experiment, the pigs received an endotoxin intravenous infusion of 0.25 µg × kg −1 × h −1. Nine animals received protective mechanical ventilation with a tidal volume of 6 mL × kg −1 and nine animals were ventilated with a tidal volume of 10 mL × kg −1. The aim of the study was to study the effect of tidal volume on cerebral inflammatory response, cerebral metabolism and brain injury. We hypothesized that protective ventilation would attenuate cerebral inflammation in a porcine endotoxemic sepsis model. In sepsis-induced encephalopathy or acute brain injury the use of protective ventilation has not been widely investigated (experimentally or clinically). Protective ventilation with lower tidal volumes reduces systemic and organ-specific inflammation.

Hippocampus injury from lung barotrauma