Respiratory physiology in liver disease

Abstract

In this chapter, we will discuss hepatic-pulmonary pathophysiologic interactions in acute and chronic liver disease. Most of our understanding of how liver disease compromises the key functions of the respiratory system comes from studies of physiologic extremes. From these data, we can infer how milder manifestations of liver disease may contribute to abnormalities in ventilation and gas exchange. In liver disease, it is well established that optimal ventilation is most often perturbed by altered respiratory mechanics from ascites, hydrothorax, and hepatic cachexia. Ventilation-perfusion (V-Q) mismatching may be caused or worsened by compressive atelectasis from ascites or hydrothorax, imbalanced matching in hepatopulmonary syndrome, dynamic small airway collapse from increased pulmonary blood flow, or any of the various causes typically seen in hypoxemic hospitalized patients. Diffusion abnormalities also have myriad causes, and a low diffusion capacity (DLCO) without alternative explanation may represent the uncommon but well characterized hepatopulmonary syndrome. Additionally, acute liver failure may be complicated by the acute respiratory distress syndrome (ARDS), which itself hampers respiratory mechanics, V-Q matching, and gas diffusion. Patients with chronic liver disease are also at risk for ARDS as they are prone to sepsis and aspiration pneumonitis. Managing ARDS in these populations requires special consideration of extra-hepatic complications of liver failure such as elevated intracerebral pressure and tense ascites.