local anaesthesia armamentarium Flashcards
anaesthesia
loss of sensation
analgesia
selective loss of pain sensation
how do local anaesthestics work?
block the conduction of nerve impulses in the peripheral nerves or spinal chord
mode of action of general anaesthetics
block corticol neuronal activity underlying consciousness and all sensation
historical background
1860
Albert Nieman in Germany
psychoactive alkaloid, cocaine
definition of local anaesthetics
Loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves.
Loss of sensation without inducing loss of consciousness.
classifications of LA
esters
amides
esters
procaine
cocaine
tetracaine
why are they not used anymore
addictive
amides
Bupivacaine ( Marcaine) general, long lasting
Mepivacaine (Carbocaine, Scandonest), long lasting, severe side effects
Prilocaine (Citanest) mimics birth hornmone, 7/8/9 month pregnancy
Lidocaine (Lignocaine, Xylocaine)
Articaine (Septocaine)
ideal properties of LA
I = should not be irritating to tissue
N = should not cause any permanent alteration of nerve structure
S = systemic toxicity should be low
T = time of onset of anaesthesia should be short
E = should be effective regardless of it being injected or applied topically
D = Duration of action should be long enough to complete procedure
Have the potency to give complete anaesthesia without the use of harmful concentration solutions
Should not produce an allergic reaction
Should be free in solution and undergo biotransformation in the body (should be able to be broken down and excreted from the body)
Should be sterile or capable of being sterilized by heat without deterioration
chemical structure of LA
the lipophilic aromatic ring- improves lipid solubility
whereas the tertiary amine end is relatively hydrophilic, making the molecule water-soluble
Intermediate hydrocarbon linkage – determines if the molecule is an ester or an amide
mechanism of action of local anaesthetics
Local anaesthetics block voltage-gated sodium channels
Nocicepters on the surface
conduction of nerve impulses
Nerve impulses begin in a dendrite, move toward the cell body, and then move down the axon.
depolarization → hyperpolarization → repolarization → resting potential
Local anesthetics prevent nerve impulse transmission by blocking voltage gated sodium channels without causing central nervous system depression or altered mental status
composition of local anaesthetics
local anaesthetic agent
vasoconstrictors (epinephrine)
Vasoconstrictor preservative (Sodium bisulfite,/ metabilsulfite)
Sodium Hydroxide (Buffer adjusts pH)
Sodium Chloride (Buffer creates in injectable solution)
what do you need to calculate maximum dosage?
- pt’s weight
- drug concentration
- amount of LA in cartridge
- maximum dose of anaesthetic based upon milligrams per kg
pharmacodynamics
physiological effect to the body and mechanisms of drug action
pharmacokinetics
body’s handling of the drug (absorption, distribution, metabolism and excretion; onset of action; duration; biotransformation)
pharmacokinetics (esters)
amino esters metabolised primarily by plasma esterase
PABA metabolite - causes hypersensitivity reactions (procaine)
pharmacokinetics (amides)
amino amides are metabolized primarily by hepatic cytochrome P450–linked enzymes (amidases)
Long half-life
No PABA in amides.
Metabisulphite or preservative agent, rubber stopper – allergic reaction
Indications of LA
used to anesthetize a particular part or region of the body,
are given to patients undergoing surgery
during labour and delivery
for diagnostic procedures such as gastrointestinal endoscopy.
failure of LA (pharmakinetic factors)
(1) increased local blood flow leading to accelerated removal of drug from perineural injection compartments;
(2) local tissue acidosis leading to a greater proportion of the drug in the hydrochloride form, which diffuses more poorly across biologic membranes (abcesses, must be drained or double dose); and
(3) local tissue oedema, which increases diffusion distances for drug into nerves and promotes further dilution.
failure of LA (pharmadynamic factors)
the effects of inflammation on both peripheral sensitization of nerves and central sensitization.
Infected mandibular tooth, inferior alveolar nerve block (performed proximally at a site presumably remote from the infected area) also has an unexpectedly frequent failure rate. (DS Moodley)
cocaine
first local anaesthetic to be discovered.
both local anaesthetic and CNS stimulant properties
significant vasoconstriction as a result of itssympathomimetic effect.(sympathetic nervous system, fight or flight response)
the nose, where its vasoconstrictive action highly needed.
lidocaine (lignocaine)
Available in sol. 1,5%,2%,4% and 10%
Topical and parenteral use
Most widely used anaesthetic
Cheap, autoclavable
T1/2 = 1,5hrs
Metabolised in the liver
Excreted in urine
antiarrhythmic and local anaesthetic (tachychardia and barychardia, adrenaline increases heart rate)
blockade affects all nerve fibres sequence autonomic, sensory and motor
Loss of nerve function clinically is as follows: pain, temperature, touch, proprioception, skeletal muscle
mepivacaine
Carbocaine 3%
provide profound local anaesthesia without being formulated with a vasoconstrictor
shorter duration
prilocaine
Widely available, cheap
Short half-life, quick onset
can provide excellent oral anaesthesia with or without a vasoconstrictor.
provides a slightly shorter duration of surgical anaesthesia.
bupivacaine
Slow
T1/5 - 5hrs
Expensive (4 x lignocaine)
For obstetric anaesthesia
Treatment of postsurgical pain.
causes cardiac depression more frequently than do many other local anaesthetics.
articaine
newest local anaesthetic arsenal
approved by (FDA) in April 2000.
Amide class of local anaesthetics,
available in 4% strength with 1:100,000 or 1:200,000 epinephrine.
Unique among the amide local anaesthetics
The thiophene ring increases its liposolubility
Additional ester group- biotransformation in the plasma as well as in the liver
potency 1.5 times that of lidocaine
faster onset
increased success rate
Dual metabolism
local anaesthetics and adrenaline
Reduces the blood flow
Long anesthetic time
Reduce chances of toxicity
Blue ring –adrenaline
Green ring – plain
metabolic effects of adrenalin
increases blood glucose levels
Decreases plasma potassium level arrythmias (increase heart rate and blood pressure)
unwanted effects of local anaethesia
Caused by local anaesthetic agent
Intravenous injections (aspirate before injecting, toxicity if injected into a vessel, if you see blood – withdraw)
Overdose
CNS – cerebral stimulation
Depression the medulla (resp & vasomotor centres
CVS- direct action on the heart
Action on the vascular bed
psychomotor effects
Collapse at the sight of the needle
Hysterical behavior
Need sedation
complications (CNS)
facial nerve paralysis
Paresthesia (partial numbness)
Ocular-diplopia, ptosis, mydriasis, miosis, enophthalmos, and even permanent blindness.
Horner’s mydriasis, ptosis, and diplopia
complications (CVS)
hypotensionandcardiac depression.
anaesthetics are vasodilators, and
they also block vasoconstriction induced by the sympathetic nervous system.
Most local anaesthetics haveantiarrhythmic activity,
can cause tachyarrhythmia characterized by a wide QRS complex. (bradychardia – increase heart rate) (uncontrolled hypertension!)
allergic reaction
allergies to amides is less than 1%.
methylparaben – increase shelf life – 1980 removed
esters - para-aminobenzoic acid-component (PABA)
treatment of allergic reaction
Treatment of allergic reactions depends on the severity of the reaction.
Mild form- oral or intramuscular antihistamines, such as diphenhydramine, 25 to 50 mg.
Serious signs or symptoms develop,
basic life support,
intramuscular or subcutaneous epinephrine 0.3 to 0.5 mg, and
Emergency transportation to the local hospital
toxicity due to LA
starts with excitatory phase
Manifest as tremors, muscle twitching, shivering, and tonic-clonic convulsions.
This phase is followed by generalized central nervous system depression and possible life-threatening respiratory depression.
Cardiac excitability and cardiac conduction decrease. The manifestations include ectopic rhythms, bradycardia and ensuing peripheral vasodilation, and significant hypotension.
treatment of toxicity
Treatment should address respiratory depression and convulsions.
Vital signs should be monitored
basic life support administered,
the emergency medical support
Intravenous diazepam or midazolam
emergency drugs and care
- Routine vital sign monitoring equipment
2.An oxygen tank or wall oxygen outlet
3.Airway equipment, including a bag-mask circuit for delivery of positive-pressure ventilation
4.Drugs to terminate convulsions, should they occur, preferably midazolam, lorazepam, diazepam, or thiopental.
