lect 16 drugs and surgery Flashcards
first used anesthetic
diethyl ether
non flammable anesthetic later developped
halothane
in addition to general anesthetic other drugs used to suppress what
ANS, endocrine reflexes, somatic reflexes
mixture of other drugs to anesthetic increase both what
effectiveness of anesthesia and safety of anesthesia
how to suppress pain reflexes in surgery
anelgesics or muscle relaxants
drugs that reverse muscle relaxation so no paralyzation
reversal agents
inhalational aanesthtics examples (5)
diethyl ester prototype. halothane, isoflurane, nitrous oxide, sevoflurane
anesthesia used for short procedures
intravenous anesthetics
types of intravenous anesthetics
benzo, barbiturates, opoids. propofol
most commonly used IV anesthetic worldwide to induce anesthesia
propofol
rate of drug delivery is determined by what
partial pressure of anesthetic in gas
partial pressure of gas is proportional to what
its concentration
induction of drug gas pathway
alveoli–>blood vessels–>main arterial blood–>brain due to high flow
metabolism of inhalation anesthetic
not much so most is unchanged and breathed out
if anesthetic soluble in blood than what happens to brain
not much availability going into brain and takes longer to leave the blood
effective anesthetic that get quick to brain and less amount than halothane
nitrous oxide (lipid soluble)
does blood flow affect rate of anesthetic uptake in different locations
yes greater blood flow in brain even if its a very small proportion to the total of the body
two factors increasing affecting rate of induction
increased concentration of anesthetic and increased alveolar ventilation
two factors decreasing affecting rate of induction
increased solubility
increased cardiac output
elimination of inhalation anesthetic
via exhalation
minimal alveolor concentration meaning
amount of drug that produces anesthesia in 50% of patients
how to calculate total MAC
take each gas component in mixture since it is additive to get 1 MAC
anesthetic effect on respriration
depresse respiration, pCO2 high and minute ventilation decreases
anesthetic effect on cardiovascular
cardiovascular depression, blood pressure declines. cardiac output variable differentiates between drugs
inhalation anesthetic that is less powerful at depressing blood pressure
sevoflurane
anesthetic that does not cause pCO2 buildup and CO not badly affected. most often the choice of drug
isoflurane
has huge MAC and used as adjuvant
nitrous oxide
why was halothane replaced
unwanted effects like nausia vomiting and sensitization of CV system
why is isoflurane widely used (3)
no cardiac sensitization, good muscle relaxant, no toxic metabolites
anesthetic barbiturate that cant be used because build up in tissue and has long half life
thiopental
rapid onset and short half life intravenous anesthetic
propofol
why is diazepam not good for anesthetic
slow induction and super long half life when administered for longer
midazolam produces amnesia so mix it with what to get what phenomenon?
mix with opioid to get conscious sedation
opioids as analgesics effect on respiration and brainstem
depressed respiration, lower ventilation. more or less nausia
opioids benefits for surgery
relief of pain and anxiety reduction
total intravenous anesthesia
propofol for induction + opioid such as remifentanil + drug for amnesia such as midazolam + short acting muscle relaxant
neurolept analgesia
fentanyl opioid + droperidol (antipsychotic) for minor surgery to relieve stress but not unconsciousness
neurolept anesthesia
add also nitrous oxide
ketamine
only intravenous anesthetic that stimulates cardiovascular system
side effects of ketamine
dissociative anesthesia or dysphoria (intense hallucinations, anxiety and memories of surgery) so not favorite drug
use of ketamine
burn patients, short term procedures for kids with cardiovascular concerns
drugs that can treat nausea
ondanseron, 5HT blockers
treat cough
dextromethorphan
treat bradycardia (CV depression)
stimulants
muscle relaxation treatment and reverse by what
anticholinergics
muscarinic agonists
revrse msucle relaxation drug
muscarinic agonists
main site of action of anesthetics
synapses
presynaptic anesthetics and example
decrease transmitters release by blocking Ca channels. interfere with vescile docking/release (ex. isoflurane)
postsynaptic anesthetics
effects on ligand gated ion channels increasing inhibition (GABA) snd decreasing excitation (glutamatergic transmission NMDA, cholinergic receptors)
all anesthetics show power to increase inhibition by acting on gaba a receptors except
ketamine
ketamine mostly has effects on what and blocks what
effect on spinal cord and blocks NMDARs
neuromuscular blocking agents
blocks various reflexes and allow endotracheal intubation and ventilation so patient not fighting respirator. permit lower levels of aanesthetics
neuromuscular blocking agent permit lower levels of what
anesthetics
competitive nondepolarizing blocking agent
reversible and competitive, compete with acetylcholine for binding. can be short intermediate or long acting
metabolism of nondepolarizing agents
plasma cholinesterase inactiavtes some of them when diffused from synapse to plasma. broken down in liver, excreted in kidneys
depolarizing non competitive agents
short half life, rapid onset. binds to cholinergic receptor such that channel stays open for a long time. receptor becomes desensitized
depolarizing non competitive agent example
succinylcholine
both depolarizing and nondepolarizing neuromuscular agents dont cross BBB
TRUE
rare genetic defect that blocks inactivation succinylcholine
genetic defect in plamsa pseudocholinesterase
defect in plasma pseudocholinesterase use to inactivate succinylcholine does one
trouble breathing (apnea) increase as succinylcholine keeps getting administered
local anesthetics
smaller fibers like a delta and c fibers carrying pain so more sensitive to local anesthetics
local anesthetics target what channels
voltage gated sodium channels along the axon
local anesthetics effects on sodium
block sodium influx, blocking propagation of action potential
local anesthetics act better on which type of nerves and why
unmyelinated nerves because larger surface area of plasma membrane so easy access of anesthetic inside cell
local anesthetic is often injected with what in order to prolong their action aand why
adrenaline because it causes vasoconstriction, reduce in blood flow so longer for anesthetic to reach systemic circulation. (altered pharmacokinetics)
example of local anesthetic
lidocaine
local anesthetics are weak acids or bases
weak bases
what happens to local anesthetics if tissues ph lowered.
decrease in amount of lipid soluble drug that can enter neuron–>decrease effect of local anesthetic
two categories of local anesthetics
ester (procaine) and amides (lidocaine)
standard structure of local anesthetic
ring, linker region and amine group
local anesthetics with ester links are metabolized by what
metabolized by plasma cholinesterase and shorter half lives
local anesthetic duration with ester links in spinal fluid
longer duration because spinal fluid is low in esterase
metabolism of local anesthetic amides
metabolized in liver and longer half life so more potency
side effects of local anesthetic
large amounts can cause respiratory and cv arrest because interfering with neuronal activity.
loss of sensation of cold, heat, pain, touch, deep pressure
EMILA cream and used for what
mixture of local anesthetics in cream form to increase absorption across skin as it changes solubility
used to relieve pain associated with vaccinations so that kids dont feel anything
