Anesthetic Drugs Flashcards
How does lipid solubility impact anesthesia
CNS drugs must be lipid soluble (cross the BBB) or be actively transported
drugs with low solubility in blood = rapid induction and recovery times
drugs with high solubility in lipids = increased potency = 1/MAC
What is MAC?
minimal alveolar concentration required to prevent 50% of subjects from moving in response to noxious stimulus
Inhaled anesthetic examples
N2O has decreased blood and lipid solubility and thus fast induction and low potency
Halothane has high lipid and blood solubility and thus high potency and slow induction
Name the inhaled anesthetics
halothan, enflurance, isoflurance, sevoflurane, methoxyflurane, N2O
Effects of inhaled anesthetics
myocardial depression
respiratory depression
nausea/emesis
increased cerebral blood flow (decreased cerebral metabolic demand)
Toxicity of halothane
hepatotoxicity
Toxicity of methoxyflurane
nephrotoxicity
Toxicity of enflurane
proconvulsant
Toxicity of N2O
expansion of trapped gas in body cavity (not good for GI surgeries)
What is malignant hypertermia?
rare, life-threatening hereditary condition in which inhaled anesthetics and succinylcholine induce fever and severe muscle contractions (can see cyanotic skin mottling)
Tx: dantrolene
Properties of barbiturates as IV anesthetic
thiopental - high potency, high lipid solubility, rapid entry into brain
Use of barbiturate for IV anesthetic
induction of anesthesia and short surgical procedures
effect terminated by rapid redistribution into tissue and fat
decreased cerebral blood flow
Use of benzos for IV anesthetic
midazolam for endoscopy
adjunctively with gaseous anesthetics and narcotics
Effects of benzos for IV anesthetic
may cause severe postoperative respiratory depression, decreased BP (tx with flumazenil), anterograde amnesia
Mechanism of ketamine for IV anesthetic
PCP analogs that acts as dissociative anesthetics
blocks NMDA receptors
Effects of ketamine for IV anesthetic
cardiovascular stimulants
cause disorientation, hallucination, bad dreams
increase cerebral blood flow
Use of propofol for IV anesthetic
sedation in ICU, rapid anesthesia induction, short procedures
less postoperative nausea than thiopental
potentials GABAa
Name the local ester anesthetics
procaine, cocaine, tetracaine (one I)
Name the local amide anesthetics
lidocaine, mepivacaine, bupivacaine (two I)
Mechanism of local anesthetics
block Na+ channels by binding to specific receptors on inner portion of channel
bind to activated Na+ channels so most effective in rapidly firing neurons
3 degree amine local anesthetics penetrate membrane in uncharged form, then bind ion channels as charged form
Use of local anesthetics
minor surgical procedures, spinal anesthesia
if allergic to esters give amides
Toxicity of local anesthetics
CNS excitation, severe cardiovascular toxicity (bupivicaine), HTN, hypotension, arrhythmias (cocaine), methemoglobinemia (benzocaine)
Use of neuromuscular blocking drugs
muscle paralysis in surgery or mechanical ventilation
selective for motor (vs. autonomic) nicotinic receptors
Name the depolarizing agent and mechanism
succinylcholine
strong ACh receptor agonist
produces a sustained depolarization and prevents muscle contraction
Reversal of succinylcholine blockade
phase I - prolonged depolarization - NO ANTIDOTE
- the block is potentiated by AChE inhibitors
phase II - repolarized but blocked - ACH receptors are available but desensitized - ANTIDOTE is AChE inhibitors
Complications of succinylcholine
hypercalcemia, hyperkalemia, malignant hyperthermia
Name the nondepolarizing agents
tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
Mechanism of nondepolarizing agents
competitive antagonists - compete with ACh for receptors
Reversal of nondepolarizing blockade
neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
Mechanism of dantrolene
prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle
Use of dantrolene
malignant hypertermia and neuroleptic malignant syndrome (toxicity of antipsychotic drugs)
Mechanism of baclofen
activates GABAb receptors at spinal cord level, inducing skeletal muscle relaxation
Use of baclofen
muscle spasms (e.g. acute low back pain)
Mechanism of cyclobenzaprine
centrally acting skeletal muscle relaxant
structurally related to TCAs, similar anticholinergic side effects
Use of cyclobenzaprine
muscle spasms
