Call Girls Service Pune Vaishnavi 9907093804 Short 1500 Night 6000 Best call ...
Choice of Local Anesthetics for Anesthesia.pptx
1. Choice of Local Anesthetics
Dr. Biruk Abera (MD, Assistant Professor of Anesthesiology)
1
2. Choice of Local Anesthetic for Various
Regional Anesthetic Procedures
On the basis of anatomic considerations, regional anesthesia
can be divided into
infiltration anesthesia,
intravenous regional anesthesia,
peripheral nerve blockade (including plexus blockade),
central neural blockade, and
topical anesthesia
tumescent anesthesia
3. INFILTRATION ANESTHESIA
Any local anesthetic can be used for infiltration anesthesia.
Onset of action is almost immediate for all agents; however,
the duration of anesthesia varies.
Epinephrine will prolong the duration of infiltration anesthesia of all
local anesthetic drugs, although the effect is pronounced with
lidocaine
The choice of a specific drug for infiltration anesthesia largely
depends on the desired duration of action.
The dose of infiltration anesthesia depends on the extent of the area
to and the expected duration of the surgical procedure.
4. …Cont
Lidocaine is effective for infiltration in concentrations as dilute as
0.3% to 0.5%.
Patients frequently experience pain immediately after subcutaneous
injection.
Neutralization of lidocaine by sodium bicarbonate immediately
before injection reduces pain on skin infiltration and improves onset
When large surface areas have to be anesthetized, large volumes of
dilute anesthetic solutions should be used.
Infiltration analgesia and indwelling wound catheters are used
increasingly as components of multimodal postoperative analgesia.
5. INTRAVENOUS REGIONAL
ANESTHESIA
IV regional anesthesia involves the IV administration of a local
anesthetic into a tourniquet-occluded limb.
It diffuses from the peripheral vascular bed to nonvascular tissue such
as axons and nerve ending.
safety and the efficacy depend on interruption of blood flow to the
involved limb and gradual release of the occluding tourniquet.
has been used primarily for surgical procedures on the upper limbs
and shorter surgical procedures on the foot.
it should not be applied over the superficial peroneal nerve, which
can cause nerve injury.
use of an upper-leg tourniquet is preferred over lower-leg tourniquets.
6. …Cont
Prilocaine, mepivacaine,chloroprocaine, procaine, bupivacaine, and
etidocaine have also been used successfully.
Lidocaine has been the drug used most frequently for intravenous
regional anesthesia.
thrombophlebitis has been reported with chloroprocaine and
cardiovascular collapse has occurred after the use of bupivacaine.
approximately 3mg/kg (40mL of a 0.5% solution) of preservative-free
lidocaine without epinephrine is used for upper extremity procedures.
For surgical procedures on the lower limbs, 50 to 100mL of a 0.25%
lidocaine solution can be used.
7. …Cont
IV lidocaine is effective for decreasing airway sensitivity to
instrumentation by depressing airway reflexes and decreasing calcium
flux in airway smooth muscle.
Doses of intravenous lidocaine from 2 to 2.5 mg/kg are needed to
consistently blunt hemodynamic and airway responses to tracheal
instrumentation.
IV lidocaine is effective for attenuating increases in intraocular
pressure, ICP, and intra-abdominal pressure during airway
instrumentation.
8. …Cont
Intravenous lidocaine has also well-recognized cardiac
antidysrhythmic effects.
intravenous lidocaine (1 to 5 mg/kg) is an effective analgesic and has
been used to treat postoperative and chronic neuropathic pain.
9. PERIPHERAL NERVE BLOCKADE
Procedures that inhibit conduction in fibers of the peripheral nervous
system.
has been subdivided arbitrarily into minor and major nerve blocks.
Minor nerve blocks are defined as procedures involving single nerve
entities such as the ulnar or radial nerve.
major nerve blocks involve the blockade of two or more distinct
nerves or a nerve plexus or the blockade of very large nerves at more
proximal sites like femoral and sciatic nerves.
Most local anesthetic drugs can be used for minor nerve blocks.
The onset of blockade is rapid with most drugs, and the choice of
drug is determined primarily by the required duration of anesthesia.
10. …Cont
The duration of both sensory analgesia and motor blockade is
prolonged significantly when epinephrine is added
interpleural regional analgesia was described as an alternative to
multiple intercostal nerve blocks.
useful for unilateral postoperative analgesia after open
cholecystectomy,mastectomy, and nephrectomy.
Its efficacy for post-thoracotomy pain is doubtful.
It has also been used to provide analgesia for chronic pain conditions
as diverse as upper extremity complex regional pain syndromes,
pancreatitis, and cancer of the thorax and abdomen.
has been associated with risk of pneumothorax, and a subsequently
associated risk of convulsions.
11. …Cont
Currently, interpleural analgesia has largely been replaced by thoracic
epidural analgesia for the majority of thoracic and abdominal
procedures.
Two related approaches for unilateral somatic blockade in the thorax
are continuous extrapleural catheters and continuous thoracic
paravertebral somatic blockade.
One advantage of these two approaches over interpleural analgesia is
that little of the administered solution leaks from the chest into chest
tubes.
Brachial plexus blockade for upper limb surgery is the most common
major peripheral nerve block technique.
A significant difference exists between the onset times of various
agents when these blocks are used.
12. …Cont
agents of intermediate potency exhibit a more rapid
onset than the more potent compounds do.
the lumbar plexus can be approached via several routes,
including a posterior approach, an anterior perivascular
“3 in 1” approach, and an anterior fascia iliaca
compartment approach.
It is prudent to warn patients before a major nerve block
about the possibility of prolonged sensory and motor
block in the involved region.
13. PERINEURAL AND PLEXUS INFUSIONS
Local anesthetics can be administered by continuous
infusion for several days after surgery for the treatment of
chronic pain.
With prolonged infusions, there is the potential for delayed
systemic accumulation and toxicity.
Continuous bupivacaine infusions of up to 30 mg/hr in
adults for as long as 2 weeks produced no overt CNS or
Cardiac toxicity despite total plasma bupivacaine
concentrations in the range of 2 to 5 μg/mL.
14. CENTRAL NEURAL BLOCKADE
local anesthetic drugs can be used for epidural anesthesia, except
procaine and tetracaine because of their long onset times.
Drugs of intermediate potency produce surgical anesthesia of 1 to 2
hours’ duration.
Long acting drugs produce 3 to 4 hours of anesthesia.
The duration of short- and intermediate-acting drugs is significantly
prolonged by the addition of epinephrine (1:200,000)
The duration of long-acting drugs is only minimally affected by
epinephrine.
15. …Cont
The onset of lumbar epidural anesthesia occurs within 5 to 15
minutes after the administration of chloroprocaine, lidocaine,
mepivacaine, and prilocaine.
Bupivacaine has a slower onset of action.
Bupivacaine epidural bolus doses at a concentration of 0.125%
produce adequate analgesia with only mild motor deficits.
Continuous epidural infusions of bupivacaine as dilute as 0.0625% to
0.1% are useful for labor epidural analgesia in combination with
opioids.
Bupivacaine 0.25% can be used for more intense analgesia with
moderate degrees of motor block.
16. …Cont
Bupivacaine at concentrations of 0.5% to 0.75% is associated with a
more profound degree of motor block when epidural anesthesia is not
combined with GA.
High concentrations (i.e., >0.2% for bupivacaine) should generally be
avoided for continuous epidural infusions.
When concentrated bupivacaine solutions are used for infusions,
unwanted and very prolonged motor blockade will occur.
Etidocaine produces adequate sensory analgesia and profound, long-
lasting motor block.
it is primarily restricted to surgical procedures for which profound
muscle relaxation is required.
17. TOPICAL ANESTHESIA
lidocaine,dibucaine, tetracaine, and benzocaine are most commonly
used drugs.
provide effective but relatively short durations of analgesia when
applied to mucous membranes or abraded skin.
Lidocaine and tetracaine sprays are commonly used for endotracheal
anesthesia before endotracheal intubation or for mucosal analgesia for
bronchoscopy or esophagoscopy.
EMLA, which is a eutectic mixture of 2.5% lidocaine base and 2.5%
prilocaine base, is widely used for venipuncture, intravenous
cannulation, skin grafting, and a range of other uses, including
circumcision.
18. …Cont
This preparation must be applied under an
occlusive bandage
for 45 to 60 minutes to obtain effective
cutaneous anesthesia.
Longer application times increase the depth and
reliability of skin analgesia.
Topical anesthesia through cut skin is
commonly used in pediatric emergency
departments for liquid application into
lacerations that require suturing.
19. TUMESCENT ANESTHESIA
most commonly used by plastic surgeons during liposuction
procedures.
Involves the subcutaneous injection of large volumes of dilute
local anesthetic in combination with epinephrine and other drugs.
Total doses of lidocaine ranging from 35 to 55mg/kg produce safe
plasma concentrations, which can peak more than 8 to 12 hours after
infusion.
Clinicians should exercise great caution when administering
additional local anesthetics by infiltration or other routes for at least
12 to 18 hours after the use of this technique.
20. Toxicity of Local Anesthetics
Local anesthetic drugs are generally considered safe if administered
in an appropriate dosage and in the correct anatomic location.
Systemic and localized toxic reactions can occur because of
accidental intravascular or intrathecal injection or administration of an
unwanted excessive dose.
In addition, specific adverse effects are associated with the use of
certain drugs, such as allergic reactions to the aminoester drugs and
methemoglobinemia after the use of prilocaine.
Systemic reactions to local anesthetics primarily involve
the CNS and the cardiovascular system
In general, the CNS is more susceptible to the actions of systemic
local anesthetics than the cardiovascular system.
21. Central Nervous System Toxicity
initial symptoms are feelings of lightheadedness and dizziness
followed by difficulty focusing and tinnitus.
disorientation and occasional feelings of drowsiness.
Objective signs include shivering, muscular twitching, and tremors
initially involving muscles of the face and distal parts of the
extremities.
Ultimately, generalized convulsions of a tonic-clonic nature occur.
Seizure activity ceases, and respiratory depression and ultimately
respiratory arrest may occur.
22. …Cont
the potency of the local anesthetic is correlated with intravenous CNS
toxicity.
Convulsions can be terminated by small IV doses of a
benzodiazepine, such as midazolam, or by small IV doses of
thiopental.
Respiratory or metabolic acidosis increases the risks for CNS toxicity
from local anesthetics.
Hypercapnia and acidosis also decrease the plasma protein binding of
local anesthetic agents.
Seizures produce hypoventilation and a combined respiratory and
metabolic acidosis, which further exacerbates the CNS toxicity.
23. …Cont
Providing prompt assisted ventilation and circulatory support is
mandatory to prevent or correct hypercapnia and acidosis
clinicians performing major conduction blockade should make a
routine practice of having the following ready at hand.
Routine vital sign monitoring equipment
An oxygen tank or wall oxygen outlet
Airway equipment,for delivery of positive-pressure ventilation
Drugs to terminate convulsions, should they occur, preferably
midazolam, lorazepam, diazepam, or thiopental.
24. Cardiovascular System Toxicity
Local anesthetics can exert direct actions on both the heart and
peripheral blood vessels.
Indirect actions on the circulation by blockade of sympathetic or
parasympathetic efferent activity.
primary cardiac effect of local anesthetics is a decrease in the rate of
depolarization in the tissues of Purkinje fibers and ventricular muscle.
It is due to a decrease in the availability of fast sodium channels in
cardiac membranes.
Action potential duration and the effective refractory period are also
decreased by local anesthetics.
The electrophysiologic effects of various local anesthetics differ
qualitatively.
25. …Cont
the rate of recovery from block is slower in bupivacaine-treated
papillary muscles than in lidocaine-treated muscles.
ECG studies have shown that high blood levels of local anesthetics
will prolong conduction time.
This is indicated on the (ECG) by an increase in the PR interval and
duration of the QRS complex.
Extremely high concentrations of local anesthetics depress
spontaneous pacemaker activity in the sinus node, resulting in sinus
bradycardia and sinus arrest.
26. …Cont
Local anesthetics may depress myocardial contractility by affecting
calcium influx and triggered release from the SR as well as by
inhibiting cardiac sarcolemmal Ca2+ currents and Na+ currents.
All local anesthetics exert dose-dependent negative inotropic action
on cardiac muscle and is roughly proportional to conduction blocking
potency.
Bupivacaine and tetracaine are more potent cardiodepressants than
lidocaine is.
27. …Cont
Local anesthetics exert biphasic effects on peripheral vascular smooth
muscle.
Low concentrations of lidocaine and bupivacaine produced
vasoconstriction, whereas high concentrations produced vasodilation
Cocaine is the only local anesthetic that consistently causes
vasoconstriction at all concentrations.
All local anesthetics, but especially bupivacaine, can cause rapid and
profound cardiovascular depression
28. …Cont
Once toxicity occurred, basic CPR should be started immediately and
defibrillation should be performed as indicated.
low-dose epinephrine and atropine can be helpful.
Resuscitation from bupivacaine-induced cardiac toxicity is often
difficult and resistant to standard resuscitation drugs.
It is not recommended to treat bupivacaine induced ventricular
arrhythmias with lidocaine or amiodarone.
Rapid institution of extracorporeal cardiopulmonary support has been
lifesaving.
a rapid bolus of Intralipid 20%, 1.5 mL/kg (or approximately 100 mL
in adults) is recommended for those who do not respond to standard
therapy.
29. …Cont
ECG monitoring is essential during and after administration.
Negative aspiration of the syringe does not always exclude
intravascular placement.
attention to securing the airway, providing oxygenation and
ventilation, and performing chest compressions if needed
The slow reversal of Na+ channel blockade after a cardiac action
potential, which is a hallmark of bupivacaine, is considerably faster
with ropivacaine.
30. …Cont
hypercapnia, acidosis, and hypoxia potentiate the negative
chronotropic and inotropic actions of lidocaine and bupivacaine.
High levels of spinal or epidural blockade can produce severe
hypotension accompanied by bradycardia progressing to cardiac
arrest which can indirectly affect the cardiovascular system.
delays in recognition of the problem, delays in instituting airway
support (particularly in sedated patients), and delays in administration
of direct acting combined α- and β-adrenergic agonists will lead to
worse outcome.
31. Respiratory
Lidocaine depresses hypoxic drive (the ventilatory response to low Pa
O2).
Apnea can result from phrenic and intercostal nerve paralysis or
depression of the medullary respiratory center following direct
exposure to local anesthetic agents (as may occur after retrobulbar
blocks)
Apnea after administration of a “high” spinal or epidural anesthetic is
nearly always the result of hypotension, rather than phrenic block.
Local anesthetics relax bronchial smooth muscle.
Lidocaine (or any other inhaled agent) administered as an aerosol can
lead to bronchospasm in some patients with reactive airway disease.
32. Methemoglobinemia
is another side effect after the administration of large doses of
prilocaine.
600-mg doses are required for the development
Hepatic metabolism of prilocaine generates O-toluidine, which
oxidizes hemoglobin to methemoglobin.
Methemoglobinemia, if severe, can be treated with intravenous
administration of methylene blue.
EMLA (a mixture of lidocaine and prilocaine) in term newborns
produces minimal amounts of methemoglobin.
EMLA when used in this manner should thus be regarded as safe in
the great majority of newborns.
risk is increased in newborns with rare metabolic disorders and
concomitant administration of other drugs that impair reduction of
methemoglobin.
33. ALLERGIES
Aminoester drugs such as procaine produce allergic-type
reactions more commonly than the aminoamides do.
Aminoesters, are derivatives of p-aminobenzoic acid, which is
known to be allergenic.
In the rare patient for whom confirmed allergy to both
aminoamides and aminoesters precludes their use for spinal
anesthesia, meperidine can be considered as an alternative.
34. LOCAL TISSUE TOXICITY
All the clinically used aminoamide and aminoester local anesthetics
can produce direct toxicity to nerves if they achieve sufficiently high
intraneural concentrations.
application of 5% (200 mM) lidocaine in viscous, dense solutions
through narrow intrathecal catheters has been associated with a high
frequency of transient or longer-term radicular symptoms, or even
cauda equina syndrome.
concentrations of formulated local anesthetic solutions are neurotoxic
and that their dilution, in situ or in tissue, is essential for safe use
without local toxic reactions.
35. …Cont
Single-shot spinal anesthesia with commonly recommended doses
and concentrations of many different local anesthetics can produce
more limited and transient neurologic symptoms like back pain,
paresthesias, radicular
pain, or hypoesthesia
patients undergoing surgery in the lithotomy position appear to be at
increased risk for neurologic symptoms after either spinal or epidural
anesthesia.
The lithotomy position can produce neurologic sequelae and lower
extremity compartment syndrome, particularly with prolonged
surgery and use of the Trendelenburg position.
36. …Cont
Skeletal muscle changes occur after the intramuscular injection
of local anesthetics.
the more potent, longer-acting agents cause more localized
skeletal muscle damage than the less potent, shorter-acting
anesthetics.
This effect on skeletal muscle is reversible, and muscle
regeneration occurs rapidly and is complete within 2 weeks.
37. BIOLOGIC MECHANISMS OF LOCAL
ANESTHETIC FAILURE
Failure of local anesthesia is commonly ascribed to technical failure
of delivery, insufficient volume or concentration of drug, or erroneous
clinical decisions in selection of techniques.
However, there are many clinical situations in which biologic
processes contribute to failed local anesthesia, even with proper
technique and drug selection.
increased local blood flow leading to accelerated removal of drug
from perineural injection compartments
local tissue acidosis leading to a greater proportion of the drug in the
hydrochloride form, which diffuses more poorly across biologic
membranes
38. …Cont
local tissue edema, which increases diffusion distances
effects of inflammation on both peripheral sensitization of nerves and
central sensitization.
dislodgement of catheters and changes in the dermatomal origin or
intensity of nociceptive input rather than tolerance.
In a rat model, tachyphylaxis was linked to the development of
hyperalgesia
subgroup of patients with the connective tissue disorder
Ehlers-Danlos syndrome appears to have a diminished
response to topical local anesthesia.
40. References
1. Ronald, Miller D. Miller’s Anesthesiology 8th edition. Philadelphia;
2015
2. Barash, Paul G. Clinical anesthesia 7th edition. Philadelphia; 2013
3. Morgan and Mikhail's Clinical Anesthesiology 5th Ed
3/18/2024 40
An additional method of local anesthetic injection—tumescent anesthesia—is included because it is widely used in office plastic surgery practice.
Onset of action is almost immediate for all agents after intradermal or subcutaneous administration; however,the duration of anesthesia varies
Epinephrine will prolong the duration of infiltration anesthesia by all local anesthetic drugs, although this effect is mostpronounced when epinephrine is added to lidocaine.
The choice of a specific drug for infiltration anesthesia largely depends on the desired duration of action.
The dose of local anesthetic required for adequate infiltration anesthesia depends on the extent of the area to be anesthetized and the expected duration of the surgicalprocedure.
Dosing to 5 mg/kg in a 4-kg infant permits 20 mg, which is 1 mL of a 2% solution or 4 mL of a 0.5% solution.
The local anesthetic diffuses from the peripheral vascular bedto nonvascular tissue such as axons and nerve ending.
Attenuation of all these responses may be beneficial in selected clinical situations (e.g., corneal laceration or increased intracranial pressure).
Regional anesthetic procedures that inhibit conduction in fibers of the peripheral nervous system can be classified together under the general category of peripheral nerve blockade.
This procedure involves the administration of local anesthetic solution into the pleural space, either by percutaneous placement or by placementthrough the open chest by the surgeon during thoracotomy.
This technique has been associated with extremely high plasma concentrations of anesthetic, and a subsequently associated risk of convulsions.
Two related approaches for unilateral somatic blockade in the thorax are continuous extrapleural catheters55 (placed by the surgeon through the chest dorsalto the parietal pleura) and continuous thoracic paravertebral somatic blockade.
Onset times of approximately 14 minutes for lidocaine and mepivacaine have been reported, versus approximately23 minutes for bupivacaine.
It is prudent to warn patients before a major nerve block about the possibilityof prolonged sensory and motor block in the involved region
Bupivacaine 0.25% can be used for more intense analgesia (particularly during combined epidural–light general anesthesia cases) with moderate degrees of motor block.
It should be emphasized that although high concentrations of local anesthetics may be appropriate for episodic bolus dosing for surgery, these concentrations (i.e., >0.2% for bupivacaine) should generally be avoided for continuous epidural infusions.
Bolus injections produce much more cephalocaudad spread than infusions do.
When concentrated bupivacaine solutions are used for infusions, the potential exists for excessive local effect with an associated risk for unwanted and very prolonged motor blockade.
Several topical local anesthetic formulations can penetrate intact skin.
Longer application times increase the depth and reliability of skin analgesia.
Despite these seemingly huge doses, good outcomes have been reported in several case series.
Conversely, there have been several case series of cardiac arrest and death during plastic surgery procedures in which multiple risk factors,including high local anesthetic concentrations and concomitant use of sedatives, may have contributed to the patients’ instability and deterioration.
The initial symptoms of local anesthetic–induced CNS toxicity are feelings of lightheadedness and dizziness followed frequently by visual and auditory disturbances suchas difficulty focusing and tinnitus. Other subjective CNS symptoms include disorientation and occasional feelings
Objective signs of CNS toxicity are usually excitatory in nature and include shivering, muscular twitching, and tremors initially involving muscles of the face and distal parts of the extremities.
If a sufficiently large dose or rapid intravenous injection of a local anesthetic is administered, the initial signs of CNS excitation are rapidlyfollowed by a state of generalized CNS depression
In some patients, CNS depression is seen without a preceding excitatory phase, particularly if other CNS depressant drugs have been administered.
In the setting of local anesthetic toxic reactions, it is essential to provide prompt assisted ventilation and circulatory support as needed to prevent or correct hypercapnia and acidosis and to prevent or correct hypoxemia, which also exacerbates CNS toxicity.
primary cardiac electrophysiologic effect of local anesthetics is a decrease in the rate of depolarization in the fast conducting tissues ofPurkinje fibers and ventricular muscle.
this slow rate of recovery results in incomplete restoration of Na+ channel availability between action potentials, particularly at high heart rates.
These differential effects of lidocaine and bupivacaine have been advanced as explanations of the antiarrhythmic properties of lidocaine and the arrhythmogenicpotential of bupivacaine.
Cocaine is the only local anesthetic that consistently causes vasoconstriction at all concentrations because of its ability to inhibit the uptake of norepinephrine bypremotor neurons and thus to potentiate neurogenic vasoconstriction
Ropivacaine is a single (S)-stereoisomer that differs from levobupivacaine in the substitution of a propyl for the butyl group on the piperidine ring
Conversely, it appears that the (S)-enantiomers of mepivacaine and bupivacaine are metabolized by the liver more slowlythan the corresponding (R)-enantiomers, which would lead to somewhat greater systemic accumulation with prolonged infusions.
It should be noted that risk is increased in newborns with rare metabolic disorders or after the concomitant administration of other drugs thatimpair reduction of methemoglobin.various antibiotics (trimethoprim, sulfonamides, and dapsone can cause methhemoglobinemia
Aminoesters, unlike aminoamides, are derivatives of p-aminobenzoicacid, which is known to be allergenic.
Contamination of vials with latex antigen has been suspected in some allergic reactions,although it is difficult to confirm.
Local anesthetic-induced myotoxicity may involve actions on mitochondria.140
Pharmacokinetic factors include (1) increased local blood flow leading to accelerated removal of drug from perineural injection compartments;
local tissue acidosis leading to a greater proportion of the drug in the hydrochloride form, which diffuses more poorly across biologic membranes
local tissue edema, which increases diffusion distances for drug into nerves and promotes further dilution.
Pharmacodynamic factors include the effects of inflammation on both peripheral sensitization of nerves and central sensitization.