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64 Cards in this Set
- Front
- Back
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definition of general anesthetic
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reversible loss of consciousness and awareness to stimuli.
Includes: 1. Amnesia 2. lack of somatic and autonomic responses to pain 3. skeletal muscle relaxation |
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types of anesthetics
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inhalation
injectable |
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3 phases of anesthesia
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induction
maintenance Emergence/recovery |
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Phases of Descending anesthesia
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slight impairment of thinking
Strong sedation stupor loss of consciousness deep anesthesia paralysis of respiration death |
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How anesthetics affect the brain
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top to bottom (correlates to stages of descending anesthesia)
cerebral cortex (thinking) midbrain/brainstem (consciousness) medulla (CV and respiration) |
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Guedels stages
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Illustrates descending
Stage 1 - analgesia Stage 2 - Disinhibition Stage 3 - Surgical anesthesia Stage 4 - Medulary depression |
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Describe Analgesia (Stage 1)
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decreased awareness of pain
still conscious, but drowsy blurred thinking amnesia begins |
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Describe disinhibition (Stage 2)
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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 |
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Theories to explain disinhibition
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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 |
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Describe surgical anesthesia (Stage 3)
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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 |
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Describe medullary depression (Stage 4)
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Resp slows, becomes shallow, ceases
BP down Cardiac action stops Death |
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4 Goals of anesthesia
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Pleasant loss of consicousness
Amnesia Analgesia (no non-relex based response to pain) Muscle relaxation (loss of tone) Last 2 are common to NOT acheive with analgesia alone |
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Types of ancilliary drugs
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Preoperative meds
Induction Agents Muscle relaxants Intraoperative meds |
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Goals of preop meds
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Reduce apprehension
Pre/intra op analgesia Reduce SE's of anesthesia (antiemetics, anticholinergics) Reduce vol and acidity of gastric contents |
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Induction Agents
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barbiturates
etomidate propofol ketamine selected opiods |
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Inhalational anesthetics
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mainly volatile liquids but Nitric oxide is gas
Mainly just for maintenance |
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MAC
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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 |
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Pharmacokinetics of Inhaled anesthetics
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excreted thru lung
metabolism is minor, but can make toxic metabolites |
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Blood-gas partition coefficient
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low value = rapid onset, recovery
blood acts as reservoir for entry/exit |
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Lipid solubility
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need some to cross BBB
too much = slow recovery |
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Intra-Op SE's
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hypotension
cardiac arrhythmias (halothane) Increased intracranial pressure due to vasodilation (halothane) malignant hyperthermia |
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IntraOp ADE - hypotension
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not with NO
can be severe |
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IntraOp ADE - cardiac arrhythmias
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not as common
Not with NO, extra with halothane drugs sensitize heart to sympathetic fx |
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IntraOp ADE - intracranial pressure
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cerebral vasodilation -->up cerebral blood flow -->up pressure
all drugs up cerebral blood flow, esp. halothane |
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IntraOp ADE - malignant hyperthermia
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can be triggered by any anes. except NO
extra with halothane, succinylcholine more with both together. |
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PostOp SE's -
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N&V
Liver damage (halothane) |
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PostOp SE's - Nausea and vomitting
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most common
varies by drug, person, procedure, duration |
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PostOp SE's - liver damage
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"halothane hepatitis"
very rare, even with hepatitis either a toxic metabolite or immune rxn |
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Anesthetic Mech of Action
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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 |
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Membrane perturbation theory
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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 |
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Protein binding theory
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drug binds hydrophobic domain on membrane pro
Most common theory, but still not complete |
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lipid-protein interface theory
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drugs dissolve in membrane, but only work at membrane/protein junction
newest theory |
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Synaptic effects of anesthetics
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potentiate GABA-A and glycine = up inhibition
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What happens when Gen Anesthetic binds glycine/GABA receptor
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up affinity of receptor for GABA/gly
increases affect (coupling)of GABA - assures channels opens at high dose, can open channel on its own HYPERpolarization |
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Other effects of Gen Anesthetics
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inhibits ACh, 5HT, glutamate
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Gen Anes effects on ion channels
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opens K --> K out = HYPERpolarization
blocks Na --> prevent depolarization block some Ca --> prevent NT release |
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Sensory input pathways
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Sensory input --> Reticular activating system --> thalmic relay nuclei -->cerebral cortex
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Site of action for effects:
Amnesia Consiousness Movement inhibition |
Amnesia - hippocampus
consciousness - reticular activating system, thalmic relay nuceli, cerebral cortex movement inhibition - spinal cord |
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early anesthetics
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Ether, Nitrous oxide, chloroform
only NO is still used Ether- irritating, explosive Chloroform- liver damage, cardiac depression |
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Halothane properties
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largely replaced by others in US
significant metabolism to toxic metabolites hypotension, arrythmias liver toxicitiy (halothane hepatitis) increased intracranial pressure |
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Enflurane properties
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less hypotension, hepatitis
can cause transient seizures |
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Isoflurane properties
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best choice for inhaled anes.
down SEs, no SZ |
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Desflurane properties
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faster onset/recovery (down blood/gas partition)
irriation problems mean you need injection to induce it |
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Sevoflurane properties
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best approximation to anesthesia
cost is biggest problem fast, few SE's |
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Common anesthetics
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halothane
enflurane isoflurane desflurane sevoflurane nitous oxide |
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Nitrous oxide properties
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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 |
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Nitric oxide abuse
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laughing gas
NOT a major social issue PSYCH dependence, not physical mostly a party drug B12 dependecne |
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Injectable Anesthetics
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mainly IJ, but ketamine can be lots of routes
Used for induction/short surgery use is increasing, esp propofol TIVA - total intravenous anesthesia |
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barbiturates
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thiopental, methohexital, thiamylal
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general characteristics of barbiturates
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classified by duration - ultra-short, short, moderate, long
mainly induction/short procedures, extensive in vet med |
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Kinetics of ultrashort barbiturates
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onset = 10-30 sec -->high lipid solubility
duration = 5-8 min determined by redistribution to muslces, not metabolism |
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distribution of barbiturates
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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 |
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Context sensitive half-life
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t1/2's vary based on drug, metabolism, infusion time, accumulation in fat, etc
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advantages of barbiturates
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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 |
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disadvantages of barbiturates
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not good for long procedures
Resp depression hypotension (dose dependent) no analgesia activity |
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Barbiturate mech of anesthesia
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same GENERAL mech as inhalationals
BUT Some have GABAnergic inhibition |
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propofol properties
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non-barbiturate structure
oil - inject as emulsion onset/duration similar to thiopental (short, redistribution) Mech of action: same as barbiturates |
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propofol pros and cons
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pros- fast onset/ recovery, minimal postop N&V
cons- significant HYPOtension, strong resp depression, pain at IJ site, no analgsia |
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Ketamine routes, onset
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IV or IM usual, but can be any route
similar onset to thiopental, but longer duration (slower redistribution) |
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dissociative anesthesia
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EKG looks normal, eyes open, but fully anestetized
dissociates physiology from anesthesia |
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symptoms of dissociative anesthesia
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more anesthesia than NO
amnesia 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) |
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Uses of ketamine
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minor surgery/diagnostic procedures for kids
wide use in vet med |
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Mech of Action for Ketamine
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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 |
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Ketamine abuse
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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 |
