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64 Cards in this Set

  • Front
  • Back
definition of general anesthetic
reversible loss of consciousness and awareness to stimuli.

1. Amnesia
2. lack of somatic and autonomic responses to pain
3. skeletal muscle relaxation
types of anesthetics
3 phases of anesthesia
Phases of Descending anesthesia
slight impairment of thinking
Strong sedation
loss of consciousness
deep anesthesia
paralysis of respiration
How anesthetics affect the brain
top to bottom (correlates to stages of descending anesthesia)

cerebral cortex (thinking)
midbrain/brainstem (consciousness)
medulla (CV and respiration)
Guedels stages
Illustrates descending

Stage 1 - analgesia
Stage 2 - Disinhibition
Stage 3 - Surgical anesthesia
Stage 4 - Medulary depression
Describe Analgesia (Stage 1)
decreased awareness of pain
still conscious, but drowsy
blurred thinking
amnesia begins
Describe disinhibition (Stage 2)
transition to unconsciousness

Dangerous stage

incoherent speech
irregular respiration
Enhanced reflexes (involuntary urination/defecation, coughing, gagging, vomiting, breath holding, CV responses)
EPI release= HTN, tachycardia
Theories to explain disinhibition
OLD: cerebral cortex is inhibited, but lower brain is not so it does what it wants

NEW: More inhibitory neurons are affected, so excitatory neurons go wild

No data on either theory
Describe surgical anesthesia (Stage 3)
4 planes (1= low, 4= high)

No response to pain (somatic or autonomic)
Regular breath
No airway or occular protective reflexes

As progress thru planes,
Resp slows
Skeletal muscle relaxes
Describe medullary depression (Stage 4)
Resp slows, becomes shallow, ceases
BP down
Cardiac action stops
4 Goals of anesthesia
Pleasant loss of consicousness

Analgesia (no non-relex based response to pain)
Muscle relaxation (loss of tone)

Last 2 are common to NOT acheive with analgesia alone
Types of ancilliary drugs
Preoperative meds
Induction Agents
Muscle relaxants
Intraoperative meds
Goals of preop meds
Reduce apprehension
Pre/intra op analgesia
Reduce SE's of anesthesia (antiemetics, anticholinergics)
Reduce vol and acidity of gastric contents
Induction Agents
selected opiods
Inhalational anesthetics
mainly volatile liquids but Nitric oxide is gas

Mainly just for maintenance
Minimum Alveolar concentration

Measures potency and dose
Quantal dose curve similar to IC50/EC50

"alveolar concentration that prevents response to std surgical incision in 50% of patients"

steep curve --> 1.0 MAC = 50% anestitized; 1.3 MAC = 100% anest.

MAC doses are additive
Pharmacokinetics of Inhaled anesthetics
excreted thru lung
metabolism is minor, but can make toxic metabolites
Blood-gas partition coefficient
low value = rapid onset, recovery

blood acts as reservoir for entry/exit
Lipid solubility
need some to cross BBB

too much = slow recovery
Intra-Op SE's
cardiac arrhythmias (halothane)
Increased intracranial pressure due to vasodilation (halothane)
malignant hyperthermia
IntraOp ADE - hypotension
not with NO
can be severe
IntraOp ADE - cardiac arrhythmias
not as common
Not with NO, extra with halothane
drugs sensitize heart to sympathetic fx
IntraOp ADE - intracranial pressure
cerebral vasodilation -->up cerebral blood flow -->up pressure

all drugs up cerebral blood flow, esp. halothane
IntraOp ADE - malignant hyperthermia
can be triggered by any anes. except NO

extra with halothane, succinylcholine
more with both together.
PostOp SE's -
Liver damage (halothane)
PostOp SE's - Nausea and vomitting
most common
varies by drug, person, procedure, duration
PostOp SE's - liver damage
"halothane hepatitis"

very rare, even with hepatitis

either a toxic metabolite or immune rxn
Anesthetic Mech of Action
No obvious SAR

lipid solubility = act at hydrophobic domains in neurons

as partition coeff increases, so does MAC

MAINLY act at synaptic transmission, but may have some effect on conduction

up inhibitory, down excitatory

mostly affect ion-channels, but may also voltage-gated
Membrane perturbation theory
anesthetics dissolve in membrane = general change in volume/fluidity (Critical volume hypothesis/Membrane Fluidization Hypothesis)

changes affect neuron fcn by undefined mech

lots of problems = out of vogue
Protein binding theory
drug binds hydrophobic domain on membrane pro

Most common theory, but still not complete
lipid-protein interface theory
drugs dissolve in membrane, but only work at membrane/protein junction

newest theory
Synaptic effects of anesthetics
potentiate GABA-A and glycine = up inhibition
What happens when Gen Anesthetic binds glycine/GABA receptor
up affinity of receptor for GABA/gly

increases affect (coupling)of GABA - assures channels opens

at high dose, can open channel on its own

Other effects of Gen Anesthetics
inhibits ACh, 5HT, glutamate
Gen Anes effects on ion channels
opens K --> K out = HYPERpolarization

blocks Na --> prevent depolarization

block some Ca --> prevent NT release
Sensory input pathways
Sensory input --> Reticular activating system --> thalmic relay nuclei -->cerebral cortex
Site of action for effects:
Movement inhibition
Amnesia - hippocampus

consciousness - reticular activating system, thalmic relay nuceli, cerebral cortex

movement inhibition - spinal cord
early anesthetics
Ether, Nitrous oxide, chloroform

only NO is still used

Ether- irritating, explosive
Chloroform- liver damage, cardiac depression
Halothane properties
largely replaced by others in US

significant metabolism to toxic metabolites

hypotension, arrythmias

liver toxicitiy (halothane hepatitis)

increased intracranial pressure
Enflurane properties
less hypotension, hepatitis

can cause transient seizures
Isoflurane properties
best choice for inhaled anes.

down SEs, no SZ
Desflurane properties
faster onset/recovery (down blood/gas partition)

irriation problems mean you need injection to induce it
Sevoflurane properties
best approximation to anesthesia

cost is biggest problem

fast, few SE's
Common anesthetics
nitous oxide
Nitrous oxide properties
only anes that is a gas

Mec of action
-blocks NMDA and nicotinic receptors
-no effects on GABA
-endogenous opiod release

low potency - need more than 1.0MAC (>1.0atm)

low blood/gas partition = fast/pleasant onset and recovery

excellent ANALGESIA at lower doses

little resp/CV effects, low toxicity (only toxic with freq use - oxidze cobalt in B12)

only toxicity = B12 deficiency

Wide use as adjuvant anes - can help down required dose and therefore down SE's

wide use in dentistry and childbirth
Nitric oxide abuse
laughing gas
NOT a major social issue
PSYCH dependence, not physical
mostly a party drug
B12 dependecne
Injectable Anesthetics
mainly IJ, but ketamine can be lots of routes

Used for induction/short surgery

use is increasing, esp propofol

TIVA - total intravenous anesthesia
thiopental, methohexital, thiamylal
general characteristics of barbiturates
classified by duration - ultra-short, short, moderate, long

mainly induction/short procedures, extensive in vet med
Kinetics of ultrashort barbiturates
onset = 10-30 sec -->high lipid solubility

duration = 5-8 min
determined by redistribution to muslces, not metabolism
distribution of barbiturates
first: brain, heart, liver, kidney

second: skeletal muscle, skin

thrid: fat

Continuous IV - keep stores high --> duration is determined by metabolism/excretion, not distribution --> much longer t1/2
Context sensitive half-life
t1/2's vary based on drug, metabolism, infusion time, accumulation in fat, etc
advantages of barbiturates
fast onset/duration
little postop N&V
reduce intracranial pressure

good anti-SZ activity - use if person has SZ (rather than propofol/ketamine)
think phenobarbital
disadvantages of barbiturates
not good for long procedures
Resp depression
hypotension (dose dependent)
no analgesia activity
Barbiturate mech of anesthesia
same GENERAL mech as inhalationals

BUT Some have GABAnergic inhibition
propofol properties
non-barbiturate structure
oil - inject as emulsion

onset/duration similar to thiopental (short, redistribution)

Mech of action: same as barbiturates
propofol pros and cons
pros- fast onset/ recovery, minimal postop N&V

cons- significant HYPOtension, strong resp depression, pain at IJ site, no analgsia
Ketamine routes, onset
IV or IM usual, but can be any route

similar onset to thiopental, but longer duration (slower redistribution)
dissociative anesthesia
EKG looks normal, eyes open, but fully anestetized

dissociates physiology from anesthesia
symptoms of dissociative anesthesia
more anesthesia than NO
eyes open
keep the pharyngeal and laryngeal reflexes
minimal resp depression
BP and CO increase
muscle tone up
emergence reactions (generally not in kids, animals)
Uses of ketamine
minor surgery/diagnostic procedures for kids

wide use in vet med
Mech of Action for Ketamine
no action on reticular formation

acts on cerebral cortex, limbic system, spinal cord

Inhibits EXCITATORY glutamate(not up inhibitory GABA)
-High affinity binding to PCP site on NMDA
Ketamine abuse
Special K
increasing abuse, diverted from legit sources
High PSYCH dependence, low physical
Less bad than PCP/angeldust

comes as a liquid --> IJ, PO or boil and smoke/snort