J U LY 2 0 1 7 O U T P A T I E N TS U R G E R Y. N E T 2 7
wished they'd known more about MH before walking into their ORs on those
fateful days.
I'll tell you just what I tell these callers. If you suspect MH, err on the side of
caution and move forward with the assumption that you're dealing with an actu-
al episode. The potential risks of not treating the patient with dantrolene —
hypoxia, cardiovascular collapse, heart attack, kidney failure and death — far
outweigh the inconvenience of overreacting to a false alarm. Here are 10 other
common questions we get at the MHAUS hotline.
1. Who's most susceptible to MH? MH-susceptible patients carry one
or more gene mutations of skeletal muscle, which, when exposed to triggering
agents, causes abnormal levels of calcium to be released in muscles. The muscles,
which may or may not contract abnormally, experience an abnormal increase in
metabolism and heat production. High metabolism increases CO
2
production and
drives increased respiration. High oxygen demand and CO
2
production cause
severe tissue hypoxemia and metabolic acidosis. Muscle cells are then depleted of
adenosine triphosphate (ATP) and die, which releases excess amounts of potassi-
um into the bloodstream. The influx of potassium into the bloodstream causes
hyperkalemia and eventually cardiac arrhythmia.
2. What triggers MH? Common triggering agents include the volatile gen-
eral anesthetics halothane, enflurane, isoflurane, desflurane and sevoflurane,
and the muscle relaxant succinylcholine, which produces immediate intense
paralysis so providers can treat life-threatening hypoxemia from airway obstruc-
tion.
3. What if we don't use inhalational agents? Patients can devel-
op MH in response to succinylcholine alone. So even if you don't use inhalation-
al agents, you still have to stock dantrolene if you carry the paralyzing agent to
treat airway emergencies.
