Drugs for Anesthesia Flashcards by Karishma Khetani

Stages of anesthesia

stage 1- analgesia stage- dec awareness of pain, may have some anmesia, decreased consciousness

stage 2- disinhibition. loss of consciousness to regular respiration, excitation and delirium may occur, amnesia occurs, vomiting and incontinence may occur

stage 3- surgical stage
regular respiration to respiratory arrest
unconscious, no reflexes. respiration and blood pressure maintained

stage 4- medullary paralysis stage- resp arrest to death. req’s mechanical and pharmacological support

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conscious sedation

iv and/or local agents for brief procedures

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balanced anesthesia

combination agents for major surgery

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inhalable anesthetics

very controllable, readily reversible

disadvantage- not as fast or smooth as fixed agents

depress spontaneous and evoked neuronal activity
may involve actions at various ion channels- voltage gated K+ channels, GABAa receptor Cl- channel resulting in hyperpolarization

agents vary in potency, rate of induction, effect of cv fxn, degree of muscle relaxation produced

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nitrous oxide

inhalable anesthetic, gaseous
insufficient potency for surgical anesthesia
analgesic activity
potential toxicity- chronic exposure can cause megaloblastic anemia

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volatile inhalable anesthetic

halothane, enflurane, desflurane, isoflurane (most widely used), sevoflurane

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pharmacokinetics of inhaled anesthetic

rate at which a given concentration of anesthetic in brain is reached depends on:
1) anesthetic concentration in inspired air- gasses flow from high pressure to low partial pressure–> high pp in lungs results in rapid achievement of anesthetic conc in blood
2) solubility- blood:gas partition coefficient (otswald coefficient)- solubility in blood
lower–> less soluble–> more rapid rise in pp in blood–> faster equilibration with brain
3) brain:blood partition coefficient- solubility in lipid- adequate for all agents, so doesn’t contribute to significant differences between clinically useful anesthetics

4) pulmonary ventilation- better ventilation=rapid onset of anesthetisa
5) pulmonary blood flow- partial pressure rises faster with low blood flow, slower with high blood flow

6) artereovenous concentration gradient- uptake into highly perfused tissue may decrease gas tension in mixed venous blood
7) elimination- reverse of process for uptake- less soluble–> faster elimination (based on blood:gas partition coefficient)

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low solubility in blood

less soluble–> more rapid rise in pp in blood–> faster equilibration with brain–> reach anesthetic concentrations in brain more rapidly

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elimination dependent on

blood:gas partition coefficient- less soluble–> faster elimination

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minimum alveolar concentration (MAC)

concentration of anesthetic in inspired air at equilibrium when there is no response to skin inscision in 50% of pts
high MAC= less potent
nitrous oxide= highest MAC, never anesthetic

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inhalable anesthetics that cause vasodilation and tachycardia

desflurane, isoflurane

causes decreased bp

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inhalable anesthetic that causes vasodilation

sevoflurane

causes dec bp

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inhalable anesthetic that depresses myocardium

nitrous oxide
halothane
enflurane
cause dec BP and dec CO

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inhaled anesthetics with rapid rate of induction

nitrous oxide, sevoflurane, desflurane

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lowest MAC

halothane

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IV or fixed anesthetics

quick, easy, smooth induction

slow elimination

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barbiturates

iv or fixed anesthetic
thiopental (redistributes to other tissues, can accumulate in adipose leading to long doa)
methohexital (used for ECT)
short and fast acting barbiturates
no analgesia
decrease in respiration at anesthetic doses
difficult to control level of anesthesia

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propofol

iv or fixed anesthetic
actions at GABAa receptor (inc channel open time)
more rapid recovery than barbiturates due to faster hepatic metabolism
maintenance of anesthesia as well as induction
good for out patient because no hangover and those effects
less post op nausea and vomiting

can dec bp and blunts baroreceptor reflex

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etomidate

iv
used for induction esp for pts at risk for hypotension
no analgesia
high incidence of nausea and vomiting, pain on injection, myoclonus

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ketamine

iv anesthesia
dissociative anesthesia- noncompetitive antagonist at NMDA glutamate receptor ion channel
catatonia, analgesia, amnesia without loss of consciousness
short acting, pain on injection
cardiac stimulation

produces emergence phenomenon- hallucinations and disorientation, can be decreased by benzodiazepines so usually used with scmall children and pts at risk for hypotension or bronchospasm

experimental treatment for depression

midazolam

benzo
shortest acting benzo and least irritating for iv
used for maintenance of anesthesia because induction too slow to induce anesthesia
good amnestic effects
rapid onset and recovery
antagonist flumazenil can accelerate recovery

flumazenil

antagonist for midazolam

fentanyl

opioid
cna achieve anesthesia with sufficient dose or in combo with benzos
-excellent post op analgesia
useful in pts with compromised CV fxn
can cause truncal rigidity and impair ventilation

pre-anesthetic and adjunct medication reasons

inc rate of induction
decrease anxiety
decrease pre and postop pain
decrease side effects of general anesthetics
reduce amt of general anesthesia required

scopolamine

anticholinergics to decrease salivation and gut motility and antiemetic

neuromuscular blocking agents- paralytics

minimize anesthetic use good for orthopedics should not be used as a substitute for inadequate anesthesia

competitive neuromuscular blocking agents

at nicotinic ach receptors- antagonists inhaled anesthetics and certain antibiotics increase potency of agent isoquinolines- -d-tubocurarine causes large increase in histamine release- 80 min duration mivacurium - 10 min duration rocuronium- steroid derivative: 20 min duration

depolarizing- nicotinic agonist

succinylcholine stimulates motor end plate leading to persistent partial depolarization so that muscle cannot contract anymore will cause initial fasciculation leading to muscle soreness shortest duration of action

d-tubocurarine

competitive antagonist neuromuscular blocking agent | cause histamine release leading to hypotension and bronchospasm

drug interactions of neuromuscular blocking agents

mainly with aminoglycosides and isoflurane increase potency and duration of competitive antagonists

local anesthetics

block sensory transmission from a local area of body to cns use- infiltration, field block, spinal block, topical application

local anesthetic mechanism

block nerve conduction by blocking voltage gated Na+ channels- preventing depolarization and conduction of cation potential also blocks K+ channels at higher concentrations higher frequency of stimualation- higher membrane potential- higher anesthetic block

clinical effects of local anesthetics

- pain blocked first along pre and post ganglionic sym fibers (Adelta, B and C fibers) - then cold, warmth, touch, deep pressure (C fibers) - then muscle tone, proprioception, and motor fxn (Aalpha, Abeta, A y fibers) (may be different experimentally)

cocaine

esters, local anesthetics- - vasoconstrictor, medium acting, used topically for nasal and ophthalmic procedures bc penetrates membranes- minimizes bleeding

benzocaine

ester, local anesthetic surface use only, lipophilic used for burns, bites, hemorrhoids, catheter and endoscope palcement

lidocaine

amides, local anesthetic most widely used, medium acting doa ~2 hrs, when administered with epinephrine (to vasoconstrict to minimize diffusion)

Mepivicaine

medium acting, amide, local anesthetic | vasoconstricts, longer acting than lidocaine

bupivicaine and ropivicaine

``` longer acting (3-15 hrs) ropivicaine- less cardiotoxic ```

amides

local anesthetics | used for infiltration, peripheral nerve block, epidural block

potency of local anesthetics affected by

pH -local anesthetics are weak bases, and the cation interacts with Na+ channel, but unprotonated form is req'd to penetrate membrane to gain access to channel inside cell membrane potency decreased at low pH

duration of action of local anesthetic proportional to

time the drug is in contact with nerve use vasoconstrictor (epinephrine) to increase duration and reduce systemic absorption

CNS adverse effects for local anesthetics

low concentrations- sleepiness, light headedness, visual and auditory disturbance, metallic taste high levels- nystagmus, myoclonus, leading to tonic-clonic seizures (esp esters) direct neurotoxicity with spinal administration due to pooling in cauda equina

CV adverse effects of local anesthetics

depression of myocardial conduction and peripheral vascular tone hypotension cocaine- hypertension, arrhythmias, myocardial failure

allergic reaction of local anesthetics in

esters | due to p-aminobenzoic acid metabolites

cauda equina syndrome

neural injury due to localized toxicity from continuous spinal anesthesia most likely to occur with lidocaine

transient neurologic symptoms

transient paina fter spinal and epidural anesthesia w/o loss of sensation, motor, or bowel fxn most common with lidocaine

pharmacokinetics for local anesthetic

readily diffuse for site of injxn and cause systemic effects

metabolism of esters

rapidly hydrolyzed by pseudocholinesterases

metabolism of amides

in liver and or blood followed by urinary excretion