Local Anesthetics:
onset determined by…
- lower pKa = faster onset (50% ionized/nonionized)
- higher agent concentration/dose = faster onset
Local Anesthetics:
duration determined by…
- increased protein binding = longer duration
- increased lipid solubility = longer duration
- presence of adjuncts (epi) = longer duration
Local Anesthetics:
What does epinephrine adjunct do? (6)
produces local vasoconstriction
- limit systemic absorption
- decrease rate of LA metabolism
- prolong duration of LA action
- decrease possibility of systemic toxicity from LA
- decrease bleeding
- provides evidence of IV injection (increase HR, etc.)
Local Anesthetics:
what are cons to using an adjunct like epi?
- increase risk of arrhythmias, HTN
- can cause ischemia in areas lacking collateral blood flow
Where should you not use an adjunct like epi with local anesthetics?
areas lacking collateral blood flow = fingers, toes, nose, ears, penis
Systemic toxicity of local anesthetics? (LAST)
CNS: lightheadedness, dizziness, tinnitus, visual changes, LOC, seizures
CV: myocardial depression, hypotension, vasodilation, circulatory collapse
due to excessive plasma concentrations of LA
Treatment of LAST?
IV lipid emulsion (sink for LA)
IV access, airway management, treat seizures (BZDs)
Major adverse effect of bupivicaine?
cardiotoxicity
Local Anesthetics: order of loss of sensation?
pain –> temp –> touch –> pressure
block small > large and myelinated > unmyelinated
General principles of anesthetics:
decrease solubility in blood = ?
increase solubility in lipids = ?
decrease solubility in blood = rapid induction/recovery times
increase solubility in lipids = increased potency (1/MAC)
MAC
minimal alveolar concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimuli
nitrous oxide has low blood and lipid solubility –> ?
halothane has high blood and lipid solubility –> ?
nitrous oxide has low blood and lipid solubility –> fast induction/recovery, low potency
halothane has high blood and lipid solubility –> slow induction, high potency
Effects of inhaled anesthetics? (3)
myocardial depression
nausea/emesis
INCREASED cerebral blood flow (decreased cerebral metabolic demand)
adverse effects of inhaled anesthetics? (3)
- halothane = hepatotoxicity
- nephrotoxicity = methoxyflurane
- proconvulsant = enflurane
Barbiturates (Thiopental)
high potency, high lipid solubility, rapid entry into brain
- used for induction
- rapid termination of effect 2/2 rapid redistribution into tissue/fat
**Decreases cerebral blood flow
GABA-a potentiator (increase duration of opening)
Benzos (Midazolam)
GABA-a potentiator (increase frequency of channel opening)
can cause severe post-op respiratory depression
- decrease BP
- anteriograde amnesia
TX OD w/flumazenil
Ketamine
blocks NMDA receptors
- PCP analog, dissociative amnesia
- CV STIMULANT, INCREASE cerebral blood flow
- disorientation, hallucination, unpleasant dreams
Propofol
- GABA-a potentiator
- used for ICU sedation, rapid anesthesia induction
- less post-op nausea than thiopental
Succinylcholine
ACh receptor agonist (depolarizing agent)
-produces sustained depolarization –> prevent muscle contraction
-adverse effects = hyperCa, hyperK, malignant hyperthermia
Rocuronium
non-depolarizing agent
- competitive ACh receptor antagonist
- can reverse with neostigmine (AchE inhibitor) + atropine (to prevent muscarinic effects like bradycardia)
predictors of a difficult airway? (5)
1) high mallampati classification (I-IV)
2) small mouth opening
3) prominent upper incisors
4) thyromental distance < 6 cm
5) decreased neck extension
