Create an account
NO vs Halothane
MAC - 104% (weakest); blood gas ratio 0.5 (faster) Specific characteristics - rapid onset and recovery (inducer), may cause diffusional hypoxia so increase fiO2 with administration, spontaneous abortion
MAC - 0.8%, blood gas ratio 2.3, CV effects - sensitizes heart to catecholamines; specific characteristics - may cause malignant hyperthermia and arrythmias
thiopental - barbiturate used for induction, rapid onset so don't have to worry about P450
midazolam - benzo used for preop sedation, antergrade amnesia, induction, and outpatient surgery (give too much, flumazenil is antitode)
propofol - "looks like milk", anesthesia, antiemetic, CNS and cardiac depressant
fentanyl(s) - opiate for anesthesia and analgesia, depresses resp function
ketamine (special k) - dissociative anesthetic, NMDA receptor blocker, cause emergent delirium and hallucinations, cause cardiovascular stimulation (can maintain CV while doing surg), increase intracranial pressure
sodium channel toxins
tetrodotoxin (and saxitoxin) - block activated Na channels (Ia) and decrease sodium influx
ciguatoxin (and batrachotoxin) - bind to activated Na channels and prolong sodium influx
esters vs amides
esters metabolized by plasma and tissue esterases (Cocaine)
amides metabolized by liver amidases (i before caine is and amide) (lidocaine)
mechanism - non ionized form crosses axonal membrane and inside ionized form blocks the inactivated Na channel
nerve fiber sensitivity - smaller diameter (builds up faster) and higher firing rates more sensitive
type B and C > type Ad> type Aa (recovery in reverse order)
absorption - coadministration of alpha1 agonist (like epi) decreases the absorption into systemic circulation, prolongs effect and decreases toxicity (cocaine doesn't need an a1 agonist)
side effects - neurotoxicity, CV toxicity, allergies via esters via PABA/paraaminobenzoic acid formation
sulfonamides are PABA analogs
skeletal muscle relaxants - non depolarizing
work like myasthenia gravis, nicotinic blockers, d-tubocurarine is the prototype, reversible with AChE inhibitors, progressive paralysis (with tropism for face, limbs and resp muscle), no effects on cardiac and smooth muscle, no CNS effects
atracurium - safe in hepatic or renal impairment, spontaneous inactivation to laudanosine, (laudanosine can cause seizures)
mivacurium - shortest duration and metabolized by cholinESTERASES; can reverse block
skeletal muscle relaxants - depolarizing (non competitive)
nicotinic agonists, only way to stop block is for drug to go away
succinylcholine (may cause cholinergic crisis/flaccid paralysis)
phase I - depolarization, phase 2 - desensitization
AChE inhibitors increase phase I; have no effect on phase II
hydrolyzed by pseudocholinESTERASE
caution atypical cholinesterase aka slow therefore may need to by intubated, hyperkalemia augments depolarization, and malignant hyperthermia
a life threatening syndrome with muscle rigidity, hyperthermia, HTN, acidosis, and hyperkalemia
genotypic susceptibility may be related to mutations in the genes encoding ryanodine receptors
tx: dantrolene blocks Ca release from the SR, also used in neuroleptic malignant syndrome
Please allow access to your computer’s microphone to use Voice Recording.
Having trouble? Click here for help.
We can’t access your microphone!
Click the icon above to update your browser permissions and try again
Reload the page to try again!Reload
Press Cmd-0 to reset your zoom
Press Ctrl-0 to reset your zoom
It looks like your browser might be zoomed in or out. Your browser needs to be zoomed to a normal size to record audio.
Please upgrade Flash or install Chrome
to use Voice Recording.
For more help, see our troubleshooting page.
Your microphone is muted
For help fixing this issue, see this FAQ.
Star this term
You can study starred terms together