Flashcards in Anesthetics Deck (38):
Drugs with increased solubility in lipids do what to the potency?
Increased potency = 1/MAC
What is the MAC?
minimal alveolar concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (i.e. skin incision)
Decreased blood and lipid solubility, and thus fast induction and low potency.
Halothane has increased lipid and blood solubility and thus high potency and slow induction
What are the inhaled anesthetics?
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
mech of inhaled anesthetics
What is the effect of inhaled anesthetics?
Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)
Toxicity of inhaled anesthetics?
Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gsa in a body cavity (nitrous oxide). Can cause malignant hyperthermia - rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene
Describe the potency and lipid solubility of IV barbiturates (Thiopental)
high potency, high lipid solubility and therefore rapid entry into brain
What is the use of Thiopental?
Induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (i.e. skeletal muscle) and fat. Decrease cerebral blood flow.
What is the most commonly used benzodiazepine for endoscopy?
Midazolam; used adjunctively with gasous anesthetics and narcotics.
What is the risk of Midazolam?
may cause severe postoperative respiratory depression, decrease BP (treat overdose with flumazenil), and anterograde amnesia
What is an Arylcyclohexylamine?
What is ketamine?
PCP analog that act as dissociative anesthetic. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. Increase cerebral blood flow
Which opiods are used during anesthesia?
Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less postoperative nausea than thiopental. Potentiates GABA(A)
What are the IV anesthetics?
Barbiturates (thiopental), Benzos (midazolam), ketamine, opioids (morphine, fentayl), propofol
What are the two classifications of local anesthetics?
Esters and amides
What are the Esters?
Procaine, Cocaine, Tetracaine
What are the Amides?
lidocaine, mepivacaine, bupivacaine (amides have 2 I's in name)
What is the mech of local anesthetics?
Block Na+ channels by binding to specific receptors on INNER portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons.
How do the tertiary amines bind?
Penetrate membrane in uncharged form, then bind to ion channels as charged form
What can be given with the local anesthetics to enhance local action?
vasoconstrictors (usually epinephrine) - decrease bleeding, increase anesthesia by decreasing systemic concentration.
In infeted tissue, why must more anesthetic be delivered?
In acidic tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively
Order of Nerve blockade?
Small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small small unmyelinated > large yelinated fibers > large unmyelinated fibers
Order of pain loss?
1) pain 2) temp 3) touch 4) presssure
What is the clinical use of local anesthetics?
Minor surgical procedures, spina anesthesia. If allergic to esters, give amides.
Toxicity of local anesthetics
CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine)
What are the neuromuscular blocking drugs used for?
muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor
What are the Depolarizing neuromuscular blocking drugs?
What is the mech of succinylcholine
strong Ach receptor agonist; produces sustained depolarization and prevents muscle contraction.
Describe the reversal of blockade of succinylcholine:
Phase I: (prolonged depolarization) - no antidote. Block potentiated by cholinesterase inhibitors
Phase II: (repolarized but blocked; ACh receptors are available, but desensitized) - antidote consits of cholinesterase inhibitors
What are the complications of Depolarizing neuromuscular blocking drugs?
Hypercalcemia, Hyperkalemia, and Malignant Hyperthermia
What are the nondepolarizing neuromuscular blocking drugs?
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
What is the mech of the nondepolarizing neuromuscular blockers?
competitive antagonists - compete with ACh for receptors.
What is the reversal of blockade for the non depolarizing neuromuscluar blocking drugs?
Neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.
Prevents the release of Ca++ from the SR of skeletal muscle