Abstract
Low tidal volume ventilation is beneficial in patients with severe pulmonary dysfunction and would, in theory, reduce postoperative complications if implemented during routine surgery. The study aimed to investigate whether low tidal volume ventilation and high positive end-expiratory pressure (PEEP) in a large animal model of postoperative sepsis would attenuate the systemic inflammatory response and organ dysfunction. Thirty healthy pigs were randomized to three groups: Group Prot-7h, i.e. protective ventilation for 7 h, was ventilated with a tidal volume of 6 mL x kg-1 for 7 h; group Prot-5h, i.e. protective ventilation for 5 h, was ventilated with a tidal volume of 10 mL x kg-1 for 2 h, after which the group was ventilated with a tidal volume of 6 mL x kg-1; and a control group that was ventilated with a tidal volume of 10 mL x kg-1 for 7 h. In groups Prot-7h and Prot-5h PEEP was 5 cmH2O for 2 h and 10 cmH2O for 5 h. In the control group PEEP was 5 cmH2O for the entire experiment. After surgery for 2 h, postoperative sepsis was simulated with an endotoxin infusion for 5 h. Low tidal volume ventilation combined with higher PEEP led to lower levels of interleukin 6 and 10 in plasma, higher PaO2/FiO2, better preserved functional residual capacity and lower plasma troponin I as compared with animals ventilated with a medium high tidal volume and lower PEEP. The beneficial effects of protective ventilation were seen despite greater reductions in cardiac index and oxygen delivery index. In the immediate postoperative phase low VT ventilation with higher PEEP was associated with reduced ex vivo plasma capacity to produce TNF-α upon endotoxin stimulation and higher nitrite levels in urine. These findings might represent mechanistic explanations for the attenuation of systemic inflammation and inflammatory-induced organ dysfunction.
Highlights
Ever since the polio epidemic, mechanical ventilation has been of indisputable value for the survival of many patients with acute respiratory failure [1]
With low tidal volume (VT) ventilation and positive end expiratory pressure (PEEP) titration based on inspiratory oxygen fraction (FiO2), has been shown to reduce mortality and morbidity in patients with acute respiratory distress syndrome (ARDS) [2]
Imai et al reported that an injurious ventilator strategy might lead to end-organ epithelial cell apoptosis and organ dysfunction [6] and O'Mahony et al demonstrated that mechanical ventilation together with endotoxin-enhanced pulmonary inflammation promoted liver and kidney injury [7]
Summary
Ever since the polio epidemic, mechanical ventilation has been of indisputable value for the survival of many patients with acute respiratory failure [1]. With low tidal volume (VT) ventilation and positive end expiratory pressure (PEEP) titration based on inspiratory oxygen fraction (FiO2), has been shown to reduce mortality and morbidity in patients with acute respiratory distress syndrome (ARDS) [2]. The main effect of protective ventilation is to reduce ventilation-induced lung injury and subsequent spread of inflammation to the systemic compartment, which could reduce the risk of multiple organ failure (MOF) [4]. The effect of ventilator regimes on non-pulmonary organ dysfunction has been investigated in a few animal studies. A retrospective study [11] found that high VT ventilation was associated with a higher occurrence of ARDS and higher mortality in patients with a need for prolonged ventilatory support after surgery
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