Local Anesthetics Flashcards
Mechanism of action for local anesthetic drugs
Bind to Na channels in nerves to block nerve transmission, inactivated and open states of Na channel
Perihpheral nerve blocks, neuraxial, subcutaneous, topical
Can be used for surgical anesthesia or to lessen post-op pain
Identify the various nerve fiber types and compare how they respond to local anesthetics
Myelinated vs non-myelinated (must be able to block 3 nodes of ranvier)
Core vs mantle (peripheral) fibers. Block onset is proximal to distal for peripheral nerve blocks
Nerve fiber types (A, B, C)
Small, myelinated fibers are easiest to block
Fiber class A alpha
Myelinated Diameter: 6-22 micmeter Conduction velocity: 30-122 m/s Location: efferent to muscles Function: Motor Block susceptibility: ++
Fiber class A beta
Myelinated Diameter: 6-22 micmeter Conduction velocity: 30-120 m/s Location: Afferent from skin and joints Function: Tactile, proprioception Block susceptibility: ++
Fiber class A gamma
Myelinated Diameter: 3-6 micmeter Conduction velocity: 15-25 m/s Location: Efferent to muscle spindles Function: Muscle tone Block susceptibility: ++++
Fiber class A delta
Myelinated Diameter: 1-4 micmeter Conduction velocity: 15-35 m/s Location: Afferent sensory nerves Function: Pain (immediate pain), cold temperature Block susceptibility: +++
Fiber class B
Myelinated
Diameter:
Fiber C SC
Unmyelinated Diameter: 0.3-1.3 micmeter Conduction velocity: 0.7-1.3 m/s Location: postganglionic sympathetic Function: various autonomic functions Block susceptibility: ++
Fiber C dyC
Unmyelinated Diameter: 0.4-1.2 micmeter Conduction velocity: 0.1-2.0 m-s Location: Afferent sensory nerves Function: Visceral pain (throbbing) Block susceptibility: +
Pharmacokinetics/Pharmacodynamics
on test
Binding occurs on cytoplasmic side, drug must traverse the membrane (uncharged crosses, charged binds)
**pH and pKa (onset time, can increase by adding sodium bicarb)
Lipid solubility (potency)
Protein binding in local tissues (duration)
Explain the local anesthetic systemic toxicity (LAST) and demonstrate how to treat it
Neurotoxicity: excitatory phenomenon, lightheadedness, peri-oral numbness, tinnitus, seizures. Acidosis makes it worse (increased blood flow to brain)
Treatment (for seizures): benzodiazepines, propofol, thiopental, succinylcholine, hyperventilation
CV: occurs at higher concentrations that neurotoxicity, Na channel blockade, vasodilator effects, inhibition of sympathetic nervous system. AV BLOCK, SLURRED QRS, V-tach and V-fib
Treatment: prevention (epi as vascular marker, monitor patient with EKG), maintain O2 and ventilation, treat seizures and arrhythmias (NO LIDOCAINE)
Name some common additive to local anesthetic and describe why the drugs are given together
Epi: vasoconstriction, add to decrease blood flow and increase the duration of the nerve block. Not effective for highly protein bound drugs. Marker for intravascular injection (if HR goes up you got the needle in a vessel and need to move your needle)
a2 agonists: Epi/dexmedetomidine/clonidine, decrease release of supstance P
Clincial uses for local anesthetics
IV: arrhythmis, beir block Epidural Caudal Intrathecal (spinal) Peripheral nerve (brachial plexus, sciatic, femoral) Topical
