Episode 152: Keywords Part 7: MH and Hepatic Disease for the Basic Exam

Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Episode 152: Keywords Part 7: MH and Hepatic Disease for the Basic Exam

In this 152nd episode I welcome Dr. Gillian Isaac back for another 2 ABA keywords. We discuss malignant hyperthermia and the portion of hepatic disease that is covered by the Basic Exam. We’ll do the portion covered by the Advanced Exam on the next keywords episode.

CME: https://earnc.me/NU3JPS

Malignant Hyperthermia Website: www.mhaus.org

Great review website where Dr. Isaac gets her questions: http://www.anesthesiahub.com

Atlantic Article: https://www.theatlantic.com/entertainment/archive/2012/03/what-do-fact-checkers-and-anesthesiologists-have-in-common/253838/#note

6 thoughts on “Episode 152: Keywords Part 7: MH and Hepatic Disease for the Basic Exam”

  1. I’m not a GI specialist, but I think we made a mistake with our reasoning with the last question (But still managed to come to the correct answer!)

    Patient with jaundice, minimally elevated AST, markedly elevated alkaline phosphatase, normal PT received muscle relaxant. Which of following is most likely?

    o Increased intubating dose of pancuronium
    o Increased intubating dose of atracurium
    o Prolonged duration of succinylcholine
    o Prolonged durationof vecuronium
    o Shortened duration of tubocurarine

    This patient has a normal PT indicating that he has normal liver function; Factor VII has a half-life of only a few hours so the PT would be prolonged if there was a synthesis problem.

    AST which is found primarily in the hepatocyte mitochondria is only mildly elevated, indicating a mild degree of hepatocyte damage. On the other hand, ALP, which is produced primarily by the bile duct epithelium, is significantly elevated. The elevated ALP along with the jaundice suggests that he has an obstructive jaundice from something like a billiary stone. I don’t think this is a picture of cirrhosis.

    If the patient had impaired liver function, like in cirrhosis, there should be prolongation of both succinylcholine and vecuronium. Succinylcholine is metabolized by pseudocholinesterase, which is synthesized by the liver, and vecuronium is primarily metabolized by the liver.

    I think the key thing that was missed is that vecuronium is excreted primarily through the billiary system. Thus, a patient with an obstructive jaundice won’t be able to get rid of the vecuronium which would lead to its accumulation and prolonged duration.

    However, I could be TOTALLY wrong. What do you think?

  2. Hi Jed,

    I thought hypercapnia increased splanchnic vascular resistance, which would decrease portal vein flow and hepatic blood flow. But it sounds like hypercapnia actually causes vasodilation and increases hepatic blood flow?

    How does hypoxia affect hepatic blood flow?


    1. Yes, hyoercapnea increases flow. I’m not aware of the liver being able to regulate flow based on oxygen levels but it will extract more oxygen in the presence of hypoxia.

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