Here's something that's been bugging me that I just can't figure out and figured someone will know. Valley says one of the treatments we can do to try and decrease seizures from local anesthetic toxicity is to hyperventilate the patient--you decrease CO2 levels which causes vasoconstriction to the brain, and also you decrease K+ levels which hyperpolarizes cells/ causes resting potentials to become more negative. Makes sense except . . .

Don't we hyperventilate patients to make it easier to induce seizures--ie ECT cases? Hyperventilation would cause transient hypocalcium, which increases excitability by decreasing the action potenitals, and alkalosis causes the inhibition of GABA and the potentiation of NMDA, both of which would increase the chance to have a seizure.

Am I mixing up something or is it just one thing trumps another here???