LA Basics
This form of a local anesthetic crosses the lipid membrane.
nonionized (base) form (B)
This property determines onset of local anesthetics.
pKa
This class is metabolized by pseudocholinesterase in plasma.
Esters
Early toxicity signs include dizziness, tinnitus, and this symptom.
circumoral numbness
This receptor is primarily responsible for analgesia and respiratory depression.
Mu
This form actually binds to the sodium channel inside the cell.
ionized (BH⁺) form
This property determines potency of local anesthetics.
lipid solubility
This class is metabolized in the liver by hepatic enzymes.
amides
Untreated toxicity progresses to this neurologic emergency.
seizures
All opioids cause this ventilatory effect.
dose-dependent respiratory depression
Local anesthetics block this ion channel to prevent depolarization.
sodium (Na⁺) channels
This property determines duration of action.
protein binding
This metabolite from esters is responsible for allergic reactions.
PABA
Severe toxicity can lead to this cardiovascular outcome.
cardiovascular collapse/asystole
This opioid metabolite is active and accumulates in renal failure.
morphine-6-glucuronide (M6G)
A local anesthetic with a pKa closer to 7.4 will have this effect.
faster onset
Local anesthetics are generally this type of drug chemically.
weak bases
This local anesthetic is an ester with strong vasoconstrictive properties.
Cocaine
This is the first-line treatment for severe LAST.
lipid emulsion (Intralipid)
This opioid is unique because it is metabolized by plasma esterases.
Remifentanil
Adding sodium bicarbonate speeds onset by increasing this form.
nonionized fraction
Increasing vascularity at injection site causes this change.
increased absorption (and toxicity risk)
This condition prolongs amide duration due to decreased metabolism.
Liver disease
Initial lipid bolus dosing is approximately this amount.
1.5 mL/kg of 20% lipid
This opioid causes histamine release leading to flushing and hypotension.
Morphine