NS: 75 Local Anesthetics
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What is a local anesthetic?
- an agent that interrupts pain impulses in a specific region of the body without a loss of patient consciousness
- the process is completely reversible
- no residual effect on nerve fibers
What was the first anesthetic?
- isolated from Coca leaves by Albert Niemann in Germany in the 1860s
- used by Karl Kollar for clinical opthalmology anesthesia in 1884
What was the first local synthetic anesthetic?
Procaine-made in 1907
What is the target of all local anesthetics?
Sodium Voltage Gated Channels (NOT PUMPS!)
What are the 3 distinct stages of a voltage-gated sodium channel?
What are the speeds between the three stages of voltage-gated Na+ channels?
- C-O is fast
- O-I is fast
- I-C is a little slower
How long does a current exist in an action potential?
A few miliseconds or less
How many segments and domains are there per voltage gated sodium channel?
- 4 domains
- 6 segments/domain
What is the voltage sensing segment on voltage-gated sodium channels?
Where does the pore lie in voltage-gated sodium channels?
between 5 and 6 segment
What is the guarded Receptor Theory of Ion Channels?
When can a LA reach the anesthetic binding site?
- When the receptor is in an activated state
- or if the drug is sufficiently lipophilic enough, it can reach when the channel is in the inactivated state
What is the percentage of non-ionized LA in vitro?
- Remember 7.5=8.5*log(base/charged) --> base/charged=10-1
- Also remember Le Chatlier's Principle when discussing this
What form of the drug actually holds the Na+ channel in the inactive state?
LAs with a lower pK or higher pK will have a more rapid onset of action? why?
lower pK --> aka LAs that are more uncharged will have a more rapid diffusion to the cytoplasmic side of the Na+ channel
What are the 5 mechanisms of action of LAs? What is NOT a mechanism of action of LA?
- Reduce height of AP
- Reduce rate of rise of AP
- Slow axonal conduction
- Ultimately prevent propagation of AP
- Increase activation threshold
- DO NOT alter the resting membrane potential
Functional Consequence of Na+ Channel Blockade by LAs
Vascular Smooth Muscle
- Nerves: decrease or abolition of conduction
- Vascular Smooth Muscle: vasodilation
- Heart: decreased excitability (reduced pacemaker activity, prolongation of effective refractory period)
- CNS: increased excitability, followed by generalized depression
What are the four characteristics of LAs?
- Blockade of sensory transmission to brain from a localized area
- Blockade of voltage-gated Na+ channels
- Use-dependent block
- Administer to site of action
What is the basic structure of an LA and what is the importance of each?
- Aromatic Ring: Lipophilicity
- Connecting Chain: ?
- Amino Terminus: Amine can become charged
What are the 2 classifications of LAs? What is the basis of the classification?
- Benzoic Acid Derivatives: Ester connecting chain
- Aniline Derivatives: Amide connecting chain
What determines potency and rate of onset of LAs?
- Lipid Solubility (obviously) the more lipophilic a LA is, the more potent the LA is
- LAs are weak bases pKas of 7.5-9.0
Why are LAs less effective in infected tissues?
several reasons, the most important being that pH is lower/more acidic causing a decrease in lipophilicity of the drug as a whole
What LAs are esters?
Which type of LA is more likely to produce an allergic affect and what is the cause of this effect?
- caused by the metabolism via pseudocholinesterase into paraaminobenzoic acid, which CAN cause allergic reactions
What LAs are amides?
Where are amides metabolized?
in the liver
What LAs are applied topically?
What LAs are administered via infiltration?
What drugs are administered via nerve block?
What LAs are administered via spinal?
What LA is commonly given as an epidural?
What LAs are given via caudal administration?
What are some toxicities of LAs?
- CNS sedation
- cardiovascular-cardiac block
- allergic reactions
What is common effect of LAs on vascular smooth muscle? How do we counter act this effect?
- by using a vasoconstrictor which can cause prolongation of anesthetic action, decreased risk of toxicity, and decrease in bleeding from surgical manipulations
What is a conventional vasoconstrictor used with LAs?
- Adrenaline (used in variuos concentrations expressed in grams/mL, ex. 1g:100,000mL)
What adrenergic receptor(s) do these vasoconstrictors work on and hence what is the effect produced when administered?
- Epinephrine: a, B1, B2 increase HR, increase BP
- Norephinephrine: a, B1 increase BP
- Levonordefrin: a increase BP
What is the order of sensory function block of LAs?
- deep pressure
What factors influence a neuron's susceptibility to blockage by LAs?
What does AP duration have to do with LA susceptibility?
the longer the AP, the more probability that Na+ channels are open, meaning more LA activity.....so PAIN is longest (3ms), therefore greatest action on pain
Is myocardium more or less susceptable to LAs? Why?
more susceptible because of extended duration in AP
What are the 7 classes of nerve fibers and what do they do?
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