Chemical Properties of Local Anesthetics
The most common local anesthetics we use for nerve blocks the the ones below.
Agent
Lipid
Solubility
Mepivacaine 1
4
Lidocaine
Bupivacaine 28
Ropivacaine Not established
Relative Potency Protein Binding% Duration pKa Onset
Time
2
75
Medium 7.6 Quick
4
65
Medium 7.7 Quick
16
95
Long
8.1 Moderate
16
94
Long
8.1 Moderate
Systemic Vascular Absorption of Local Anesthetic from Different Regional Techniques.
Intercostal nerve block>Caudal>Epidural>Brachial Plexus>Sciatic-Femoral>Subcutaneous
Onset Times of Local Anesthetics for Specific Peripheral Nerve Blocks
Local Anesthetic
Regional Block Approximate Time To Surgical
Anesthesia
10 – 15mins
Mepivacaine or Lidocaine 1.5% Interscalene
Interscalene
15 – 20mins
Ropivacaine 0.5%
15 – 30mins
Mepivacaine or Lidocaine 1.5% Axillary
Axillary
20 – 40mins
Ropivacaine 0.5%
Sciatic
30 – 45mins
Ropivacaine 0.5%
Femoral
15 – 20mins
Ropivacaine 0.5%
Maximum Doses of Local Anesthetics
Local Anesthetic
Dose (mg/kg) without
epinephrine
5
5
3–4
2.5
Dose (mg/kg) with
epinephrine
7
7
3–4
2.5
Lidocaine
Mepivacaine
Ropivacaine
Bupivacaine
Systemic Toxicity
Systemic toxicity is a result of local anesthetic overdose with subsequently high serum levels.
The potential for systemic toxicity is directly proportional to the intrinsic potency of the local
anesthetics:
Lidocaine < Mepivacaine < Ropivacaine < Bupivacaine
Most toxic reactions to local anesthetics involve the central nervous system (CNS).
Cardiovascular depression occurs at much higher blood levels, produces more severe
consequences, and is more difficult to manage than CNS toxicity. Bupivacaine is the most
cardiotoxic of all the local anesthetics agents due to its strong affinity for the cardiac
calcium channel and intravascular injection of bupivacaine may result in cardiovascular
collapse prior to the onset of CNS toxicity.
CNS Toxicity
 Local anesthetics produce CNS toxicity proportional to their potency. When combining
local anesthetics the potency is additive. With bupivacaine seizures occur at venous
blood levels of 2 – 4mcg/mL, with lidocaine at venous blood levels of 10mcg/mL.
Cardiovascular Toxicity
 Toxic blood levels of local anesthetics affect vessel tone, myocardial contractility,
cardiac rhythm and conduction. CNS toxicity usually precedes CV toxicity however,
with a drug such as bupivacaine myocardial depression can occur before CNS
manifestations appear. At equipotent doses bupivacaine depresses cardiac conduction
more than lidocaine. This is due to the five fold greater potency of bupivacaine as a
calcium channel antagonist.
Caution:
 Hypoxia and acidosis increase the cardiac toxicity of local anesthetics, bupivacaine in
particular.
 Both newborns and pregnant females are more susceptible to bupivacaine toxicity.
Resuscitation Algorithm for Local Anesthetic Toxicity
 Establish an airway and assure adequate ventilation.
 Administer 100% oxygen.
 Promptly control convulsions by administering: midazolam (2 – 5mg) or propofol (5mg
increments).
 Establish EKG and blood pressure monitoring.
 Control ventricular arrhythmias with amiodarone and cardioversion (never use lidocaine).
 Treat myocardial depression with ephedrine or small doses of epinephrine (10 – 20mcg
increments).
 Treat severe bradycardia or asystole with epinephrine. Bupivacaine induced asystole
will require administration of large doses of epinephrine (1mg increments).
For refractory malignant cardiac arrhythmias (ventricular tachycardia and fibrillation) associated
with intravenous bupivacaine injection, which are unresponsive to cardioversion and
amiodarone, consider emergency cardiopulmonary bypass.