Myocardial injury associated with hyperinflation of the lung

Abstract

A recent study [1], conducted in an animal model of acute lung injury, compared a ventilation strategy in which lungs were inflated by brief application of 50 cmH2O pressure followed by increased positive end-expiratory pressure (recruitment strategy) versus conventional ventilation. The study identified an increased inflammatory reaction in liver sinusoids, and increased serum aspartate aminotransferase (AST) and hyaluronate levels with the recruitment strategy. The authors speculated that deficient oxygen delivery and increased sinusoidal pressures may have caused liver injury. The findings of the study suggest an origin of AST outside the liver because there was no elevation in alanine aminotransferase levels, hepatocellular necrosis, or liver dysfunction. Animals in the group receiving the recruitment strategy required volume support and had temporarily reduced cardiac output. This indicated that the origin of AST elevation was a myocardial injury. Previous studies found that patients with acutely elevated intrapulmonary pressure resulting from bronchospasm [2] and severe respiratory syncytial viral lung disease leading to hyperinflation [3] exhibited evidence of myocardial injury, such as elevated cardiac troponin levels; this was probably due to strain imposed on the right ventricle by pulmonary hypertension. Ventricular strain has previously also been associated with elevated hyaluronate levels [4]. The increase in hepatic neutrophils may be due to a hyperoxia-induced increased inflammatory response found in patients with increased positive end-expiratory pressure and fractional inspired oxygen (FiO2) [5]. Future studies need to use specific markers for myocardial injury such as cardiac troponin T in order to discriminate between myocardial and hepatic injury associated with the various ventilation strategies.