Local Anesthesia
Definition
Local anesthesia (regional anesthesia) technique depends
on a group of local anesthetics that produce transient loss
of sensory, motor and autonomic function in a discrete
portion of the body
It includes:
Infiltration anesthesia
Nerve and nerve plexus block
Topical anesthesia
Intrathecal anesthesia
1. Pharmacology
1.Mechanism
Na+ channel blockade—
nerve propogation interrupted---
loss of sensation
2.Chemical Structure and
Classification
All commonly used local anesthetics consist of a three-
part structure: aromatic benzene ring, intermediate chain
and chain-amino group
Classification
As the intermediate chain contains either an ester or an
amide linkage, they may conveniently be divided into
esters and amides
Aminoesters : procaine, tetracaine
Aminoamides: lidocaine, bupivacaine, ropivacaine
Classification
Long duration agents: bupivacaine, ropivacaine, tetracaine,
and so on.
Medium duration agents: lidocaine, prilocaine, and so on.
Short duration agents: procaine, chloroprocaine, and so on.
3. Physiochemical Properties and
Clinical Anesthesia Characteristics
Physicochemical property Clinical property
pKa pKa Onsetofofanesthesia
Onset anesthesia
Liposolubility
Liposolubility Potency
Potency
Protein Binding
Protein Binding Rate
Rate Duration
Duration of
of ansethesia
anesthesia
Ⅰ. pKa - Onset of Action
The pH at which the amount of ionized and nonionized
drug is equal is the pKa of the local anesthetic. The pKa of
a compound determines the portion of ionized and
nonionized when inject into body.
The higher the pKa, the less of the unionized base form is
present at body pH. As only unionized drug can penetrate
nerve membranes, the pKa will affect the onset speed of
the drugs; the lower the pKa is, the faster the onset.
Ⅱ. Lipid Solubility - Anesthetic Potency
Lipid solubility is the main determinant of local
anesthetic potency: the higher the lipid/water partition
coefficient, the more potent the drug is likely to be.
Ⅲ. Protein Bonding - Duration of Action
Protein binding determines the duration of drugs,
presumably because high protein bounding drugs can stay
longer in the lipoprotein of nerve membranes .
4. Pharmacokinetics
Ⅰ. Absorption
Site of given
Dosage and speed
Presence of vasoconstrictors or vasodilators
Ⅱ. Distribution
Most of the local anesthetics bind to plasma proteins,
and then distribute to other tissues
The tissue with abundant blood vessels that are highly
perfused also have a faster redistribution
Ⅲ. Biotransformation and Excretion
The metabolism of local anesthetics varies defined by their
chemical structure
The aminoester drugs undergo hydrolysis in plasma
by the pseudocholinesterase enzymes
The aminoamide agents undergo enzymatic
degradation primarily in the liver
5. Side effects of Local
Anesthetics
Ⅰ. Toxic reaction
concentration of LAs > tolerance of body
Causes :⑴ overdose
⑵ injection into blood vessels
⑶ abundant blood supply, and no addition of
vasoconstriction drugs
⑷ decrease in tolerance
Central Nervous System Toxicity
Mild Toxicity
Symptoms: dizzy, tinnitus, tingling of the tongue,
circumoral numbness, slurred speech, Bp increased,
pulse increased, drowsy, light-headed anxious
Management:
⑴ Stopping anesthetic agent
⑵ Supplemental oxygen
Moderate Toxicity
Symptoms: restlessness, Bp increased, HR decreased
Management:
stopping anesthetic agent
supplemental oxygen
diazepam iv
Severe Toxicity
Symptoms: muscle spasm, convulsion
Management:
Relieve convulsion
Endotracheal intubation immediately
Cardiovascular System Toxicity
Cardiovascular system symptoms occur often after CNS
Arrhythemia ,cardiac output decrease , cardiac arrest
Cardiovascular toxicity caused by bupivacaine is
difficult to rescue
Toxic Reaction - Prevention
Within the maximum dose
Withdrawal before injection
Addition of epinephrine
Premedication: barbiturate, benzodiazepines
Ⅱ. Allergic Reactions
Allergic reactions of local anesthetic are rare, Indeed, it
is estimated that fewer than 1% adverse reactions of
local anesthetics are due to allergic mechanisms
The vast majority of adverse responses that are
attributed to allergic reactions which are in fact
systemic toxicity manifestations caused by excessive
plasma concentrations of the local anesthetic
We should distinguish between the toxicity and allergic
reactions of local anesthetic
6. Commonly Local Anesthetics
Ⅰ. Procaine
Short duration
Low efficiency
Less toxic
Ⅱ. Tetracaine
Efficiency is ten times larger than Procaine
Toxic is higher than Procaine
Can not uesd in Infiltration Anesthesia
Ⅲ. Lidocaine
Medium duration
Rapid onset
Wild dispersion
Strong penetration
No obvious vascular dilation effect
Can be used for all kinds of local anesthesia
Ⅳ. Bupivacaine
Strong and long-acting local anesthetic
Adult safety dose is 150mg
Cardiac toxicity
Ⅴ. Ropivacaine
Separation of movement and sensation
Less cardiac toxicity
2. Application of local anesthesia
Application of Local Anesthesia
Ⅰ.Surface anesthesia
Appliacation: eye, nose, mouth, throat, trachea, urethra,
anal canal skin; superficial surgery or examination
Lidocaine and Tetracaine
Ⅱ. Infiltration Anesthesia
Definition : Inject local anesthetics into the operation
tissue to block nerves and then achieve anesthetic effect.
Attention
Suction before injection
Don't exceed the limit dose
Increase volume or concentration in the surface of the
film, the film, the periosteum
The needle should enter slowly, if change the direction,
the puncture needle should be withdrawed to the
subcutaneous first to avoid needle bending or breaking
Brain has no sense of pain
Can not used in Infection or tumor location
Ⅲ. Regional Anesthesia
Around the tissue to be resected
Ⅳ. Nerve and Nerve Plexus Block
Injection of local anesthetics around the nerve cord,
nerve plexus, and the ganglion ,block the nerve impulse
conduction, which contribute to regional anesthetic effect,
called nerve block
1. How to Locate the Nerve?
Feeling different like electricity-paresthesia
Nerve stimulator
Ultrasound
2. Cervical Plexus Block
Now are less and less
C1-C4
Superficial Cervical Plexus Block
Deep Cervical Plexus Block
Complications
Diaphragmatic nerve block
Laryngeal recurrent nerve block
Epidural or subarachnoid block
Toxic reaction
Horner’s syndrome
Vertebral artery injury
3. Brachial Plexus
Brachial plexus is derived from the anterior rami of the
fifth, sixth, seventh, eighth cervical nerves and the first
thoracic nerve. After leaving their intervertebral foramina,
they course anterolaterally and inferiorly lie between the
anterior and middle scalene muscles, where they formed
brachial plexus. Then these nerves course along the upper
surface of the first rib to enter axilla and form medial
nerve, ulnar nerve, radial nerve and musculocutaneous
nerve. Brachial plexus control the sensation and movement
of upper extremities.
Ⅰ. Supraclavical Brachial Nerve Block
Main complications are hemothorax and pneumothorax
Ⅱ. Interscalene Brachial Plexus Block
Advantages: this technique is easy to grasp, and even
small dose of local anesthetics may achieve perfect
anesthetic effect of upper arm and shoulders blockade
meanwhile with less risk of pheumothorax
Ⅲ. Axillary Brachial Plexus Block
Advantages:
It is easy to localize the insertion site because axillary
arterial pulse is easy to palpate and the nerve plexus
are within the axillary sheath.
It is possible to perform continuous block through the
catheter placed in the sheath.
Low complication rate.
Ⅳ. Lumbar Plexus Block
Used in lower limb surgery of lumbar plexus area
Complications:
Epidural block
Total spinal anesthesia
Renal hematoma
Ⅴ. Sciatic Nerve Block
Used in lower limb surgery
Advantage: No blocking sympathetic nerve
Ⅵ. Intercostal Nerves Block
Commonly used in the treatment of intercostal nerve
pain, rib fracture pain ,postoperative of chest (abdomen)
surgery and herpes zoster.
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