Heart
Myocardial function is severely altered in human and porcine MH.
Tachycardia and arrhythmias are followed by hypotension, decreased cardiac output,
and eventual cardiac arrest. Porcine data suggest that these alterations are secondary;
increased myocardial oxygen consumption during MH is related to β-agonist stimulation
of sympathetic activation without the lactate production or potassium efflux that
suggests a primary MH response.[62]
Porcine MH
myocardium does not respond abnormally to exaggerated concentrations of calcium,
digoxin, potassium, or carbon dioxide.[52]
Overall,
the heart appears to be affected primarily by the tremendous, potentially ischemic
demands placed on it by exaggerated whole-body metabolism.[63]
Central Nervous System
Central nervous system involvement during fulminant human MH appears
to result from increased temperature, acidosis, hyperkalemia, hypoxia, and hypo-osmolality
related to fluid shifts as factors in acute cerebral edema. The extreme picture
includes coma, areflexia, and fixed, dilated pupils. Recovery varies and is related
to the duration and severity of the MH episode. Severe fever (to 42.5°C [108.5°F])
may result in a virtually flat electroencephalogram and coma, but recovery is still
possible.[64]
MH is not a central nervous system disorder, as demonstrated by
the fact that a tourniquet-isolated limb remains flaccid during the whole-body rigidity
of an acute episode.[65]
Cerebral oxygen consumption
and lactate production are not increased in swine during MH episodes.[66]
Kochs and colleagues[67]
observed early profound
electroencephalographic depression during porcine MH and improvement with dantrolene,
which they interpreted as primary brain involvement. Hofer and coworkers[68]
contradicted this opinion by correlating alteration of electroencephalographic and
cerebral metabolites with beginning whole-body MH episodes.
