Local Anesthetics Flashcards by Jackson Jones

Hyperpolarization

Increase in cells resting membrane potential

Generally by diffusion of K to extracellular compartment

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Depolarization

Decrease in cells resting membrane potential

Diffusion of sodium to intracellular compartment

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Action potential generation

Trigger zone- initial segment, high concentration of sodium channels

Voltage gated triggered at -50mV

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Action potential termination

NA channels inactivated, opening of K channels and hyperpolarization

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Refractory period

Both Na and K channels are inactivated- no AP possible

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Purpose to myelination

Increases speed of conduction, AP only conducted at nodes of Ranvier

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MOA of Local Anesthetics

Antagonists at Voltage gated Na channels

Must penetrate nerve sheaths

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Ionization of locals

Most pKas are slightly higher than physiologic pH= non-ionized on injection

Once local has entered cell it converts to ionized form which allows binding to Nav

Converts NAv to inactive state

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Locals and duration of action

Direct relationship with degree of protein binding

Higher binding= longer duration

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Vasoconstrictors (epi) and locals

Slow vascular uptake, prolonging effect

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Variables in quality of block

Concentration
Volume
Potency

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Characteristics of nerve fibers and type of block

Sympathetic/sensory nerves are typically easier to block because they are unmyelinated and smaller

Motor- larger and myelinated- more difficult

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BICEPS

Highest to lowest rate of absorption

B lood
I ntercostal
C audal
E pidural
P lexus
S ubcutaneous

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Metabolism of Locals

Ester- plasma esterases

Amide- hepatic

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Elimination of amide local anesthetics

Amides are excreted via kidneys so higher risk of toxicity in renal failure

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Toxicity of locals

Concentration and absorption time frame

IV injection- venous or arterial?
Arterial-undiluted brain bolus :(
Immediate cardiovascular collapse

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Local CNS toxicity symptoms

Mild: anxiety, dizziness, tinnitus

Severe: seizure, twitching, altered LOC

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Local Cardiac toxicity mechanism

Blockade of cardiac sodium channels- neg inotropy- lethal arrhythmias or arrest

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Which locals are more cardiotoxic?

Higher potency, lipophilic

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Cardiovascular considerations in neuraxial

Sympatholytic- blockade of sympathetic nerve fibers

Blockade above T-4 dermatome blocks cardiac accelerator nerves=hypotension/bradycardia

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Treating LAST

Support circulation and cardiac function

Seizure- midazolam/lorazepam/propofol

ACLS with severe bradycardiawith following adjustments:
Epi bolus < 1mcg/kg

Lipid emulsion in LAST

Lipids act as a “sink” sequestering local from cardiac myocytes

> 70kg- bolus 100 ml lipid emulsion 20% over 2-3 min, then 200 ml over 20min

<70kg 1.5ml/kg emulsion bolus
Then 0.25 ml/kg/min infusion over 20 min

Why types of solutions do we use for neuraxial anesthesia??

PRESERVATIVE free

Cocaine

Only naturally occurring local

Current use as topical

Only local that causes vasoconstriction

Sympathomimetic effects if absorbed systemically

Benzocaine

Low potency topical- slow onset/short duration Can lead to methemoglobinemia- just use lidocaine

Chloroprocaine

Extremely short plasma half-life Common in neuraxial for rapid onset/ short duration Often combined with longer acting amides to set up the block

Amide locals

Two I’s Lidocaine Prilocaine Mepivacaine Bupivacaine Levobupivacaine Ropivacaine

Ester Locals

One I Procaine Chloroprocaine Tetracaine Cocaine Benzocaine

Tetracaine

Very potent, slow onset, long acting

Lidocaine

IV/topical/peripheral never block No longer used in neuraxial Anti-arrhythmic effects with IV as well as systemic analgesia although mechanism unknown

Bupivacaine

Prolonged/intense sensory analgesia Concentrations greater than 0.5% are no longer used due to LAST

Levobupivacaine

Reduced CNS and CV toxicity Similar profile- significantly more expensive

Ropivacaine

Structurally similar to Bupivacaine but less potent Neuraxial- greater block differentiation/ selectivity for sensory over motor block

Locals with low potency/ short duration

Procaine, Chloroprocaine

Locals with intermediate potency/duration

Mepivacaine, lidocaine

Locals with high potency/long duration

Bupivacaine, Ropivacaine, Tetracaine

Block onset based on nerve fiber/type

B- autonomic C- sympathetic/dorsal root=pain/temp/touch A- Motor

Why are type B fibers blocked before unmyelinated C fibers?

Only have to block 3 nodes instead of the entire unmyelinated fiber

Normal Sodium/potassium concentrations in and out of cell

Na out- 140 Na in- 14 K out- 4 K in- 140

Explain action potential

RMP= -70 Stimulus- influx of Na to reach -50 Threshold reached= opening of voltage gated Na channels and depolarization Repolarization- closure of Na and opening of K voltage gated channels allow rapid outflow of K Hyperpolarization=refractory period

Normal epi concentration

1:200,000 Or 5mcg/ml

Treating ventricular arrhythmias in LAST

Preferential to Amiodarone

Ion trapping in LAST

May develop acidosis in setting of resp depression =local becomes more ionized and less likely to diffuse across membranes =trapped in brain or by placental barrier

Exparel

Controlled release local anesthetic Liposomal suspension of Bupivacaine 72hr release Max dose- 266mg Specific guidelines if using in combination with other locals

Hyperkalemia risk in local anesthetic

Raises RMP, neurons more likely to depolarize-seizure

Metabolic acidosis with locals

Favors ion trapping- in cns

LAST treatment

Manage airway Benzos for seizures Modified ACLS, <1mcg/kg epi, amiodarone for vent dysrhythmias, avoid vaso/other locals Emulsion therapy

PABA

Metabolite of ester anesthetics, known to be immunogenic

This local causes methemoglobinemia

Benzocaine

Anti-emetics acting on vestibular center

Anticholinergics and H1