Abstract
BackgroundThere is mounting experimental evidence that hypercapnic acidosis protects against lung injury. However, it is unclear if acidosis per se rather than hypercapnia is responsible for this beneficial effect. Therefore, we sought to evaluate the effects of hypercapnic (respiratory) versus normocapnic (metabolic) acidosis in an ex vivo model of ventilator-induced lung injury (VILI).MethodsSixty New Zealand white rabbit ventilated and perfused heart-lung preparations were used. Six study groups were evaluated. Respiratory acidosis (RA), metabolic acidosis (MA) and normocapnic-normoxic (Control - C) groups were randomized into high and low peak inspiratory pressures, respectively. Each preparation was ventilated for 1 hour according to a standardized ventilation protocol. Lung injury was evaluated by means of pulmonary edema formation (weight gain), changes in ultrafiltration coefficient, mean pulmonary artery pressure changes as well as histological alterations.ResultsHPC group gained significantly greater weight than HPMA, HPRA and all three LP groups (P = 0.024), while no difference was observed between HPMA and HPRA groups regarding weight gain. Neither group differ on ultrafiltration coefficient. HPMA group experienced greater increase in the mean pulmonary artery pressure at 20 min (P = 0.0276) and 40 min (P = 0.0012) compared with all other groups. Histology scores were significantly greater in HP vs. LP groups (p < 0.001).ConclusionsIn our experimental VILI model both metabolic acidosis and hypercapnic acidosis attenuated VILI-induced pulmonary edema implying a mechanism other than possible synergistic effects of acidosis with CO2 for VILI attenuation.
Highlights
There is mounting experimental evidence that hypercapnic acidosis protects against lung injury
These “protective” ventilation strategies may lead to the development of hypercapnic acidosis (HA), a fact initially viewed as an undesirable side
Myocardial [11], brain [12] and liver [13] protection have been shown to be effectively mediated by metabolic acidosis. Having these considerations in mind, we evaluated the effects of hypercapnic versus normocapnic acidosis in an ex-vivo rabbit lung model of ventilator-induced lung injury (VILI)
Summary
There is mounting experimental evidence that hypercapnic acidosis protects against lung injury. The ARDS Network study [1] documented that a low tidal volume (VT) of 6 ml/kg has beneficial effects on outcomes compared to the traditionally used volume of 12 ml/kg These “protective” ventilation strategies may lead to the development of hypercapnic acidosis (HA), a fact initially viewed as an undesirable side. Hickling et al [3] adopted a low tidal volume ventilation strategy and reported that the presence of acidemia (mean pH: 7.2) was related to increased survival This suggestion was further supported by data originating from a 10-year study [4]. The authors concluded that hypercapnic acidosis resulted in reduced 28-day mortality even in patients ventilated with the injurious VT of 12 ml/kg This finding was not demonstrated when analysis was applied in the low VT (6 ml/kg) group
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