This chapter will cover clinical considerations concerning hepatic and biliary physiology as they pertain to the practice of anesthesia. Appreciation of normal physiology, as well as pathological states of the hepatic and biliary anatomy, is paramount to ensure a safe anesthetic and in management of patients with complex related disease states. Common diseases and conditions such as alcoholism, obesity, inflammatory bowel disease, and gastroesophageal reflux are discussed in detail in this chapter.
CLINICAL ANESTHESIA CONSIDERATIONS OF LIVER DISEASE
The liver’s role in the body ranges from producing plasma proteins, detoxifying the body of toxins and drugs, absorbing nutrients, and metabolizing carbohydrates.1,2 Related to its many roles, a dysfunctional liver leads to consequential systemic deleterious effects.
The liver receives a dual afferent blood supply which consists of about 25% of cardiac output. Seventy percent comes from the portal vein and 30% from the hepatic artery.3 The portal vein and hepatic artery each contribute to half of the liver’s oxygen supply under normal conditions. The portal vein is greatly affected by decreases in cardiac output and systemic hypotension because its blood flow is not regulated.
Intrinsic Determinants of Hepatic Blood Flow
Liver perfusion is maintained via changes in hepatic artery tone in situations of decreased portal blood flow. Changes in hepatic tone are stimulated by low pH, low O2 content, and increased pCO2 content.1
Extrinsic Determinants of Hepatic Blood Flow
Hepatic blood flow is determined by splanchnic vascular resistance and hepatic perfusion pressure. The sympathetic nervous system provides vasomotor innervation to the splanchnic vessels. When the splanchnic nerves are stimulated by pain, surgical stress, or hypoxemia, splanchnic vascular resistance increases, resulting in reduced hepatic blood flow.4
The magnitude of hepatic blood flow change depends on surgical stress and location of the operation. While liver perfusion pressure is directly proportional to total hepatic blood flow, increased splanchnic vascular resistance is inversely proportional to total hepatic blood flow. Liver cirrhosis has been shown to increase resistance to blood flow during the administration of general anesthesia, leading to increased hepatic venous pressure and increased central venous pressure.
Glucose storage and release are mainly regulated by the liver.5 Glucose is stored as glycogen in the liver and extracted via insulin by hepatocytes. Normal blood glucose levels are maintained by glycogenolysis and glycogen catabolism mediated by glucagon. Glycogenolysis is stimulated by starvation, activation of the sympathetic nervous system, and surgical stress.
Antithrombin III, protein C, protein S, and most other procoagulant proteins are synthesized by liver hepatocytes.6 However, factor VIII is partially produced by endothelial cells. Vitamin K catalyzes several procoagulants into factors II, VII, IX, and X. Absorption of ...