Intro to Anesthetics Flashcards
Local anesthesia
provides numbness to a small area limited to where LA is injected
Regional anesthesia
epidural, spinal, peripheral nerve blocks; provides numbness to much larger areas then LA
Monitored anesthesia care
uses sedatives and other agents
doses low enough that patients remain responsive and breathe w/o assistance
Utilized during simple procedures and minor surgery
General anesthesia
deep state of sleep where the patient loses consciousness and sensation and usually requires assisted ventilation
Combined techniques
MAC & local/regional;
regional and general
etc
Anxiolysis
Minimal sedation
patients respond normally to verbal commands.
Cognitive fx and coordination may be impaired, ventilatory and cardiovascular functions are unaffected
Conscious sedation/ Moderate sedation/analgesia
Patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation.
No interventions are required to maintain a patent airway and spontaneous ventilation is adequate
Cardiovascular fx is usually maintained
Deep sedation/ analgesia
not easily aroused, respond purposefully following repeated/ painful stimulation. The ability to independently maintain ventilatory fx and patent airway may be impaired
Cardio fx usually maintained
General anesthesia
Not arousable, even w/ painful stimulation
Ability to independently maintain ventilatory fx impaired. Requires assistance in maintaining patient airway; pos pressure ventilation may be required
Cardio fx may be impaired
What is General anesthesia? What are some qualities of it?
Generalized, reversible CNS depression no sensory perception loss of consciousness no recall of events immobility
What are some other potential effects of GA and adjuncts?
muscle relaxation
suppression of autonomic reflexes
analgesia
anxiolysis
What are the 7 types of medication used in GA w/ an ETT Template?
- Pre-op medications/sedation
- Induction drug: IV or inhalation
- NMB
- Inhalational drug: may be IV
- Opiods/LAs, etc
- Antiemetic
- NMB reversal
Why are pre-op sedation and other meds given before GA w/ an ETT template?
patient comfort
reduce anxiety
prevent aspiration
Abx per surgeon request
Why is NMB given w/ GA?
to facilitate intubation
Why are opiods and LAs given w/ GA?
to minimize physiological effects of pain and to promote comfort at emergence
What are the 5 pharmacologic effects of Benzodiazepines?
- Anxiolysis
- Sedation
- Anterograde amnesia
- Anticonvulsant actions
- Muscle relaxation (spinal level)
what is the prototype benzo?
Diazepam
How do benzos fundamentally work?
Potentiates binding of GABA to GABA A receptor
Increases GABA potency x3
Benzos increase _________ influx, cause _________ of the membrane potential and ________ neuronal excitability.
Cl-
hyperpolarization
decrease
What are 5 ways that benzos are used in anesthesia? Which ones are rare?
pre-medication IV sedation GA induction (rare) GA maintenance (rare) post-op anxiolysis (rare)
Benzos cause a __________________ in ventilation. They can cause enhanced _________ & ________ in the presence of opiods.
dose dependent decrease
hypoxemia & hypoventilation
If used at induction dosage, benzos can cause what?
decrease in SVR
W/ benzos, __________ decreases, especially in the presence of hypovolemia.
BP
Can you use benzos in pregnant patient?
no; they cause anomalies in fetus
Opioids provide ____________ & _______________ analgesia by activation of the ______________ pain suppression system
supraspinal
spinal
endogenous
Opioids act by activating pain-modulating systems by acting as _____________ at _______________ receptors
agonists
stereospecific opioid receptors
Do opioids act at pre or post synaptic sites?
both
What tissues/organs do opioids act at?
brainstem
spinal cord
peripheral tissues
What occurs when opioids bind to a receptor?
decreased neurotransmission
Opioids cause increased _______ conductance and ______ of the membrane. The __________ channes are inactivated and there is an immediate __________ in neurotransmitter release.
K
hyperpolarization
Ca
decrease
What are some common uses of opioids in anesthesia? What is the prototype?
pre-medication intra-op pain management ( IV, epidural, spinal) GA (high doses) post-op pain management prototype: Morphine
What are some adverse effects and precautions for use of opioids?
Bradycardia (direct effect)
respiratory depression ( decreased RR, increased TV)
Miosis
Urinary retention
Physical dependence
Sedation (in higher doses, synergistic w/ other drugs)
Don’t give together w/ benzos unless already in the OR=will cause person to stop breathing
What neurotransmitter do barbituates affect?
GABA
What are 3 ways barbituates affect GABA?
- decrease the rate at which GABA dissociates from its receptor: increases the duration of GABA activated Cl- channel opening (enhances GABA activity)
- Mimics GABA at the receptor (direct activation of Cl- channels)
- Produces functional inhibition of the post-synaptic neuron
What part of the brain do barbituates depress? What is the prototype?
RAS (reticular activating system)
Thiopental
What are some uses of barbituates?
sedation and hypnosis
cerebral protection
anti-seizure (more effective then benzos)
Anesthetic uses: induction of GA in patients w/ increased ICP and/or focal brain ischemia
Barbituates cause a ___________ effect.
hang over
Barbs cause depression of the ______________ in the brain which leads to decreased _______ outflow, peripheral __________ and decreased ___________
medullary vasomotor center
SNS
vasodilation
preload
If using barbs and SBP drops, will the HR increase to compensate? Do barbs cause ventilatory depression?
yes
yes
When will you see significant decreases in BP and myocardial depression w/ barbs?
if SNS not intact OR
hypovolemia OR
large doses given to reduce ICP
What can happen if you inject a barbituate intraarterially?
gangrene/ nerve damage
What causes more preload reduction, barbs or propofol?
propofol
What can chronic use of barbs cause? What does this mean to you as a CRNA?
hepatic enzyme induction:
patient will eat up the meds you give them, you will have to increase your dosing and/or frequency
Barbs cause the increase in metabolism of what meds?
oral anticoagulants phenytoin TCAs corticosteroids Vit K
What are some other adverse effects and precautions of barbs?
- accelerated production of heme by stimulation of the enzyme: D-aminolevulinic acid sythetase: avoid in pts w/ porphyria
- allergy is rare but deadly (1:30,000)
- readily crosses placenta
How is propofol classified? What is it supplied as?
nonbarbituate IV anesthetic
supplied as: 1% solution in egg, soy, glycerol base
What type of preservatives can be in propofol?
Sodium metabisulfite vs. EDTA (etylenediamine tetraacetic acid)
How does propofol affect GABA? What receptor does it affect? What subunit?
potentiates binding of GABA to GABA “A” receptor
B1 subunit
It also decreases the rate of dissociation of GABA from the receptor
Propofol increases ___________ influx, causes _________ of the membrane and __________ neuronal activity.
Cl-
hyperpolarizatoin
decreased
What are some pharmacological effects of propofol?
dose dependent sedation & hypnosis antiemetic antipuritic anticonvulsant attentuation of bronchoconstriction (usually related to patient not being deep enough)
What are some anesthetic uses of propofol?
IV sedation induction of GA maintenance of GA (TIVA) part of balanced tecnique for maintenance of anesthesia antiemetic (small doses)
Propofol causes dose dependent _______________, __________________, & ___________
ventilatory depression
myocardial depression
vasodilation
propofol causes myocardial depression by decreasing what 3 things? How does HR respond?
SV, CO, SVR
HR remains unchanged (cant compensate)
possibility for bradycardia related death
What are some other adverse effects of propofol?
myoclonus
pain on injection
lipidemia w/ LT infusion
infection and bronchospasm
What happens on the pre-synaptic side of the NMJ?
- AP = depolarization of nerve terminal
- Ca channels open
- Ca diffuses down gradient to nerve terminal
- Ach spills out into synaptic cleft
What happens at the post-synaptic side of the NMJ?
- ACh binds at nicotinic receptors
- After both receptor spots bond to, channels open and Na & Ca diffuse into cell and K diffuses out
- motor end plate depolarizes
- AP is created
- Skeletal muscle contracts
Describe the ACh receptor
- 5 protein subunits
- Central core for cation channeling
- ACh must bind to both “a” subunits in order for the core to open
- “A” subunits are the site of agonism and antagonism
What kind of drug is Succinylcholine?
depolarizing NMB
What is the mechanism of action of succs?
- binds to nicotinic receptors: channels open and motor end plate depolarizes
- single contraction occurs
- not metabolized by true acetylcholinesterases
- channels stay open until succs diffuses back into circulation
What can not occur when succs is bound to the receptor?
further APs cannot be initiated
What is the pharmacologic effect/anesthetic use of succs?
NMB
- optimize intubating conditions
- rapid sequence
- treatment of life-threatening laryngospasm
What are some adverse effects and precautions w/ succs?
- cardiac dysrhythmias (esp. w/ kids; mix w/ atropine)
- Hyperkalemia
- muscle pains, fasciculations
- increased ICP, IOP
- potent MH triggering agent
- avoid in pts. w/ atypical acetylcholinesterase (won’t wake up for a few days bc they can’t metabolize the drug)
When is there an increased risk of hyperkalemia in succs?
burns trauma nerve damage neuromuscular disease RF
What type of drug is Vecuronium?
non-depolarizing muscle relaxant
monquaternary aminosteroid
How does vec work?
it is a competitive antagonist at pre & post NMJ nACH receptors
Vecuronium occupies __________ subunits of ________ receptors without a inducing a __________ change.
With Vec at the receptor, ____ can not be initiated
alpha
ACh
conformational
APs
What is vec used form?
muscle relaxation/ paralysis:
- facilitated ET intubation
- optimize surgical conditions
When can vec have a prolonged or unpredictable effect?
liver & kidney disease
neuromusc disease
hypothermia, e- imbalances
use of abx: aminoglycosides (metabolized similarly)
When is there risk for resistance of vec?
burn patients
What must you be on the look out for in all patients who are on muscle relaxants/paralytics? Why?
- residual NMB in all patients
- In theory, at higher risk for recall if inadequate GA given
What kind of drug is Isoflurane?
inhalational anesthetic; halogenated methyl ethyl ether
How does Isoflurane work?
Very different from IV drugs: don’t need to know specifics for this lecture!
What determines onset, duration of action, etc. of inhalational agents? How are they eliminated?
- lipid solubility
- almost entirely by lungs
What are some pharmacological effects and anesthetic uses of isoflurane?
bronchodilator
GA: sedation, hypnosis, partial muscle relaxation
-induction (usually sevo only)
-maintenance
How does isoflurane affect respiratory, cardio, and airway?
Respiratory: depression–> higher rates, lower volumes (opposite of opioids)
Cardio: depression–> decreased CO & BP, vasodilation (direct CV depressants)
Airway reflexes are abolished
What are some s/s of MH?
Ca channel interference
muscle rigidity
increased temp
increased CO2
What else can inhaled agents cause?
OR pollution
What are the 2 different types of MAC?
- Monitored anesthesia care
- Mean Alveolar Concentration: describes potency
- of a voltatile anesthetic: how much is needed to make 50% of patients not respond to a noxious stimulus
- how much gas to admin
What is the MAC of isoflurane? How much would they get if they were also on 100% O2?
1.2%
they would get 98.8% O2 and 1.2% iso
What is the only inhaled agent that will not provide 100% anesthesia by itself? What is its MAC?
N2O
104%
What is the mech of action of Local anesthetics? What is the prototype?
-block impulse conduction during depolarization phase of AP
-inhibits influx of Na (Na channel blockade)
-Blockade ONLY occurs when Na channels are in the inactivated closed state
Lidocaine
What is the pharmacologic effect of LAs?
block AFFERENT nerve transmission to produce analgeis and anesthesia w/o loss of consciousness
-autonomic, somatic sensory, somatic motor blockade
What is the class of lidocaine?
Amide: local anesthetic
What is the typical structure of an LA?
They are either amides or esters:
lipophilic molecule w/ lipophilic head (aromatic ring), intermediate chain withe either amide (NH) or ester (COO-) and hydrophilic tail (tertiary amine)
What are some s/s of LA toxicity in the CNS?
circumoral/tongue numbness tinnitus vision changes dizziness slurred speech restlessness seizure followed by CNS depression, apnea, hypotension
What are some s/s of LA toxiticy in cardio system?
MORE RESISTANT TO TOXIC EFFECTS THAN CNS?
hypotension, myocardial depression, reduced SVR & CO
Bupivicaine: arrythmias, AV heart block, hypotension, and arrest
Cocaine: massive SNS outflow, coronary vasospasm, MI, dysrhythmias including V-fib
