TY - CHAP M1 - Book, Section TI - Hepatic Physiology & Anesthesia A1 - Ramsay, Michael A2 - Butterworth IV, John F. A2 - Mackey, David C. A2 - Wasnick, John D. Y1 - 2022 N1 - T2 - Morgan & Mikhail’s Clinical Anesthesiology, 7e AB - KEY CONCEPTS The hepatic artery, coming directly off the celiac trunk, supplies approximately 30% of the blood supply and 50% to 70% of the liver’s oxygen requirements, and the portal vein supplies 70% of the blood supply and the remaining 50% or less of oxygen requirements. All coagulation factors, with the exception of factor VIII and von Willebrand factor, are produced by the liver. Vitamin K is a necessary cofactor in the synthesis of prothrombin (factor II) and factors VII, IX, and X. Many “liver function” tests, such as serum transaminase measurements, reflect hepatocellular necroinflammatory activity more than hepatic function. Liver tests that measure hepatic synthetic function include serum albumin, prothrombin time (PT) or international normalized ratio (INR), serum cholesterol, and plasma pseudocholinesterase. Serum bilirubin reflects liver excretory function. Albumin values less than 2.5 g/dL are generally indicative of chronic liver disease, acute stress, or severe malnutrition. Increased losses of albumin in the urine (nephrotic syndrome) or the gastrointestinal tract (protein-losing enteropathy) can also produce hypoalbuminemia. The PT, which normally ranges between 11 and 14 s, depending on the control value, measures the activity of fibrinogen, prothrombin, and factors V, VII, and X. A prolonged INR reflects a dysfunctional liver. The effect on coagulation will depend on the balance between coagulation and anticoagulation factors. If production of protein C, protein S, and antithrombin 3 are affected more than the coagulation factors, a normal or hypercoagulable state might exist. The INR was developed to monitor the effect of warfarin, which only affects clotting factors made in the liver, not hepatic-synthetized anticoagulant factors. So if a patient has an INR of 3 and is not taking warfarin, the liver clotting mechanism is dysfunctional. Such a patient could have a potential bleeding tendency, as most will have, but some will have an increased clotting potential. This is because the pro-coagulation factors may not be impeded as much as the anticoagulation factors, so additional assessment should be done in this situation before withholding venous thromboembolism (VTE) prophylaxis or administering fresh frozen plasma. Operative procedures near the liver can reduce hepatic blood flow up to 60%. Although the mechanisms are not clear, they most likely involve sympathetic activation, local reflexes, and direct compression of vessels in the portal and hepatic circulations. The neuroendocrine stress response to surgery and trauma is characterized by elevated circulating levels of catecholamines, glucagon, and cortisol and results in the mobilization of carbohydrate stores and proteins, causing hyperglycemia and a negative nitrogen balance (catabolism). All opioids can potentially cause spasm of the sphincter of Oddi and increase biliary pressure. When liver tests are abnormal postoperatively, the usual cause is underlying liver disease or the surgical procedure itself. Liver cirrhosis may result in portal hypertension, bleeding varices, and major organ dysfunction. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/10/04 UR - accessanesthesiology.mhmedical.com/content.aspx?aid=1190607925 ER -