• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/14

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

14 Cards in this Set

  • Front
  • Back
anesthesia triad and phases
1. triad: amnesia, relaxation, analgesia
2. phases - induction, maintenance, emergence
types anethesia
1. general - lost sensory perception of entire body
2. regional - loss sensory over specific part of body
3. local - loss sensory over small area of body
anestheisa side effects
1. nausea
2. incomplete pain relief
3. nerve injury
4. malignant hyperthermia - all inhalation agents and succinycholine can cause this
Malignant hyperthermia
1. caused by inhalation agents (halothane, sevoflurane, isoflurane, desflurane) and succinylcholie
2. AD hypermetabolic state where massive amount Ca released in SR due a drug administration
3. defect of ryanodine receptor (Ca release channel)
4. correct with Dantroline which inhibits SR Ca release
w/out affecting reuptake
5. rapidly increased temp and extreme acidosis
multimodal targeted anesthesia
1. advantages - reduce pain intensity, reduce opioid use
2. disadvantages - requires knowlege drug, may increase drug-drug interactions, requires specialized skill
3. combination analgesic modalities results better analgesia with concomitant reduction adverse SE
4. faster revocery adn earlier discharge
local anesthetic classes
1. amino amides - lidocaine, etidocine, prilocaine, mepivacaine, ropivacaine, bupivacaine
2. amino esters - procaine, 20chloroprocaine, tetracaine
Local anesthetics MoA
1. inhibit influx Na ions prevent conduction of nerve impulse
-bind specific receptor on inner portion channel
-bind active Na channels, most effective firing neurons
-3* amines cross uncharged, bind channels charged
MAC
1. minimal alveolar concentration at which 50% of population is anesthetized
2. potency = 1/MAC
lipid solubility of LA
1. determines anesthetic potency, more lipsoluble = more potent
2. all CNS drugs must be either lipid soluble actively transported
degree protein binding of LA
1. determine duration of action, more bindings = longer duration
2. increased solubility in blood or less protein binding = more rapid induction and recovery time
pKa of LA
1. all are weakly basic with pKa around 8
2. infected tissue is acidic and alkaline anesthetics will be charged and thus unable penetrate membrane - need more anesthetic
potency/duration of LA
1. low - procaine, chloroprocaine (amino esters)
2. intermediate - lidocaine, mepivacaine, prilocaine
3. high - bupivacaine, ropivacaine, etidocaine, tetracaine
-epi prolongs duration of LA by vasoconstricting
LA allergic reaction
1. if allergic to ester may still give amides
2. small % population allergic via PABA release from esters
3. PABA liberated by metabolism of amino ester anesthetics
intercostal block
1. associated with highest blood levels
2. intercostal > caudal > epidural
3. order nerve block small myelinated > small unmyelinated > large myelinated > large unmyelinated
4. order sensation loss pain - temp - touch - pressure
5. high plasma levels LA produce CNS and/or cardio toxicity including death