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117 Cards in this Set
- Front
- Back
regional anesthetic techniques produce transient loss of
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sensory, motor, and autonomic function
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The thicker the fiber
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the harder it is to block
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A -alpha
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6-22 (Microns)
Motor efferent (skeletal muscle) |
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A-beta
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Proprioception afferent (small motor, touch & pressure)
6 - 22 (Microns) |
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A-gamma
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Muscle Spindle efferent (muscle tone)
1 - 4 (Microns) |
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A·delta
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Sensory roots & afferent
Peripheral Nerves (pain, temperature, touch) |
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Beta fiber
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Preganglionic Autonomic (SNS)
(vasomotor, visceromotror, sudomotor, pilomotor) <3 (Microns) min Myelin |
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C fiber
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Postganglionic autonomic (SNS) Sensory roots & afferent peripheral nerves
(pain, temperature, touch) 0.3 -1.3 |
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What allowd for a differential blockade?
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Local Anesthetic agent & concentration
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Possible to block pain & temperature sensation
How? |
(A-delta and C fiber) without significant motor blockade (A-alpha fibers)
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reflection of the arrangement of fibers within peripheral nerve
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outermost layer blocked first with a concentration gradient toward the center
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Development of an action potential
eIectrical excitability is due to |
voltage sensitive ion channels
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Development of an action potential
In response to voltage fluctuations, these |
channels open and close sequentially in a gate-like fashion
Allowing rapid diffusion of specific ions along their concentration gradient _ |
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Development of an action potential
resultant ionic current flux across cell membrane and |
depolarizes and repolarizes it·
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Most important for Local Anesthetics mechanism of action is the
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Properties of Sodium Channels
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Development of an action potential .
Wave of depolarization activates |
successive Na+ ion channels of successive membranes as it travels
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myelinization
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increases speed of neural transmission as the action potential jumps from one node of Ranvier to the next
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Local Anesthetics interact with specific receptors on the
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Na Channel
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Sodium channels exist in one of three states
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(Closed, Open, and Inactivated)
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Local Anesthetics bind to
(what does this do) |
inactivated Na+ channels
Preventing subsequent channel activation and the large transient sodium influx Does not alter resting membrane potential or threshold DEPOLORAZATION RATE SLOWED The action potential is not propagated (threshold is never reached) |
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Sequence of Neural blockade
1st fibers |
B fibers
sympathetic block with peripheral vasodilation and skin temperature elevation |
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Sequence of Neural blockade
2nd to be blocked |
C and A·delta fibers
loss of pain and sensation |
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Sequence of Neural blockade
3rd to be blocked |
A- gamma fibers
muscle tone |
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Sequence of Neural blockade
4th to be blocked |
A·beta fibers
loss of touch and pressure (proprioception) |
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Sequence of Neural blockade
5th to be blocked |
A alpha fibers
motor paralysis |
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the amount of the local anesthetic that reaches a nerve depends on
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its proximity of injection
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spinal nerve roots float
and require |
freely in the CNS
and require small amounts of local |
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Brachial plexus & sciatic nerves surrounded by
and require |
fascial sheaths and adipose tissue .
large amounts of local anesthetic |
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lipid solubility and LA
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lipid solubility increases potency, the ability of the local anesthetic to penetrate the nerve terminal
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Local anesthetics are prepared as
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hydrochloride salts
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LA which in aqueous solution dissociate
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into ionized and nonionized forms
both involved in the blockade. |
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Anesthetic molecules traverse the cell membrane by
2X |
Passive non ionic diffusion in the uncharged state
Binding to the Na+ channel in the charged state |
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LA Nonionized Interact with Na+ channels by
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passing thru lipid environment of the axon membrane
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LA Ionized Gain access to specific receptors on the interior of the sodium channel
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thru the aqueous pathway of the sodium channel pore
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pKa determines
why |
the speed on onset of neural blockade
the pKa of all local anesthetics are higher than the physiologic pH (most of the injected anesthetic ionized) |
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Acidosis due to local infection decreases
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surrounding pH increases ionization of Local anesthetics.
this increases the ionization of the local anesthetic |
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drugs that have a ________ pka work longer
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lower
(closer to physiologic ph) |
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protein binding determines:
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amount available to produce an effect and the duration of effect
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a high degree of protein binding will have
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a prolonged duration of action.
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Systemic circulation LA
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Absorbed Local anesthetics undergo pulmonary first-pass effect
this limits the drug that reaches systemic circulation |
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intermediate chain connects
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benzene ring and quaternary ring
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Intermediate chain determines
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the type of Local anesthetic:
Amide vs. Ester |
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Intermediate Chain connects
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connects the lipophilic head and the hydrophilic tail
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Intermediate Chain contains either an
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ester or amide linkage
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subdivides local anesthetics: into
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amino esters
amino amides |
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Ester linkage cleaved by _
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liver and plasmacholinestersis
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Reduced cholinesterase activity may
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lead to increased toxicity
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Esters Degradation product
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aminobenzoic acid (PABA)
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Esters Half life
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is very short about 1 minute
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Amides metabolized in the
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liver, amide linkage is cleaved via n-dealkation followed by hydrolysis
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Severe hepatic disease may increase likelihood of adverse reaction
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from amide local anesthetics
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Amides half life
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is 2-3 hours
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decreases in CO reduce the
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Vd (volume of distribution) and the plasma clearance
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decrease in CO and LA
2X |
reflects decrease in hepatic bloodflow
prolonges elimination halftime of all amines |
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age and LA
3X |
Does not alter initial dose
Subsequent doses in elderly should be decreased to avoid cumulative drug effects Elimination half-time of aminoamides is prolonged 2-3x in neonates (norm in 6 mnths) |
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Fetal acidosis results in
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greater transfer of Local anesthetic from mother to fetus
no evidence that an acidotic fetus IS more susceptible to local anesthetic induced toxicity |
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Concentration of a LA
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Dependant on diameter of nerves to be blocked
-large diameter nerves (epidural) require higher concentration than peripheral nerves |
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quality of blockade
intrathecal intensity of motor block |
Tetracaine>Bupivicaine
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quality of blockade
intrathecal duration of sensory block |
bupivicaine > Tetracaine
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Quality of blockade
Brachial Plexus block |
Mepivicaine >lidocaine (motor blockade & longer sensory anesthesia)
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cocaine 3 points
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naturally occuring
produces clinically significant vasoconstriction used as a topical |
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Cocaine blocks
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reuptake of norepinepherine
Dopamine |
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Cocaine stimulatory effects
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on the CNS and Cardiovasaular system
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Cocaine CNS effects: 3
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euphoria
agitation seizures |
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Cocaine Cardiovascular system effects:
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htn
tachycardia cardiac dysrhymthias MI |
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Cocaine .Plasma cholinesterase deficiency =
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Increased risk for sudden death
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Cocaine ·· Duration of action:
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60 minutes
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Cocaine Safe dose
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150-200mg
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Cocaine .Used only topically b/c of
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its addictive properties & increased potential to produce system toxicity
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Procaine duration
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fast onset, short duration of action
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Procaine infrequently produces
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b/c of its low potency and rapid plasma hydrolysis, Procaine infrequently produces systemic toxicity
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Chloroprocaine 2 keys
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rapid onset short duration
Low potency, very low toxicity |
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Chloroprocaine Rapid hydrodrolysis by
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plasma cholinesteraise
Accounts for its low toxicity & short duration of action |
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Chloroprocaine used for
3x |
local infiltration
nerve blocks epidurals |
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Chloroprocaine Maximum safe clinical dose
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800 mg
1000 mg with Epinephrine added |
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Chloroprocaine
Popular for Obstetric Epidural Anesthesia: b/c 4X |
rapid onset
incomplete motor block low toxicity ability of the fetus to metablize the drug |
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Tetracaine used primary for
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spinal anesthesia
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Tetracaine blockade
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Motor blockade = Sensory blockade
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Tetracaine (Pontacaine) duration
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very long duration of action
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Hyperbaric solution
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mix with equal volumes of 10 dextrose
heavier so it sinks |
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Lidocaine Maximum safe clinical dose
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5 mg/kg w/o epi
7 mg/kg with epi |
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Mepivacaine (Carobcaine) local infiltrating dose
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400mg solution w/o epi
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Mepivacaine (Carobcaine) max safe dose
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do not exceed> 4 mg/kg without adding epinephrine
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bupivicaine and epi
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do not add epi to it
can add fentanyl |
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Bupivicaine and block
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sensory greater than motor block
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Bupivicaine max safe dose
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2 mg/kg
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Combining local anesthetics
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Systemic toxicity of combination's appears to be additive
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EMLA cream is
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Ljdocaine and Prilocaine mixture
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EMLA cream onset is
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60 minutes
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EMLA cream formation concern
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methemohemoglobin formation concern in infants younger than 3 months
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EMLA cream maximum depth
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of anesthesia is 5mm , restricting usefulness to superficial operation
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Epinephrine Prolongs duration of action
More effective for (what regional) 3x |
lidocaine and tetracainea
than bupivicaine |
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Epinephrine solutions must be acidified because
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alkaline solutions promote oxidation of catacholamines
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Parabens
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are preservatives in Ester locals
may be responsive to reaction to local anesthetics |
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Epinephrine Decreases
2X |
systemic toxicity
(decreases the rate of absorbtion) Decreases surgical bleeding .. |
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Epinephrine increases the
2X |
intensity the block (denser block),
duration of action |
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Epinephrine component of epidural test dose
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3 ml 1.5%
dose contains 15 ug, intravascular injection indicated by increase in HR of at least 20% |
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Epinephrine 1:200,000 con
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5mcg/ml
-Add 0.1 ml of 1 : 1000 Epinephrine (wI TB syringe) to 20 ml of Local anesthetic |
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test dose blunted if receiving
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beta blockers
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positive test dose
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dose contains 15 ug, intravascular injection indicated by increase in HR of at least 20%
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Epinephrine Maximum dose
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1.5 mcg/kg
or 200-250 mcg . |
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Absorbed Epinephrine produces
3X |
predominantly beta effects
increased HR and CO decreases SVR |
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Sodium Bicarbonate with LA
3x |
Raises pH
Increases % of nonionized drug· (increases rate of diffusion adn speed of onset) |
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Sodium Bicarbonate added to LA
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1 meq/1 Oml of lidocaine or Mepivacaine
1 meq/10mi of Bupivicaine |
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Ester-type local anesthetics have more reactions than aminoamides because of
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PABA
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Local hypersensitive reactions may manifest as:
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local erythemia
uticaria edema dermitis |
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Neurotoxicity can occur secondary to unintentional subarachnoid injection of (3)
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large volumes
high concentrations chemically contaminated solution |
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Most commonly occurs during nerve blockade in areas
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Accidental intravascular injection
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CNS toxicity
9X with progression |
lightheadnessness
tinnitus metalic taste visual disturbance numbness of the tongue of lip progress to severe neurological symptoms, muscle twitching, LOC, seizure, coma |
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CNS toxicity is exacerbated by
3X |
hypercarbemia
hypoxia acidosis |
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How to min intravascular injection
4 helps |
aspirate before dose
proper technique test dose small volume |
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Treatment of CNS Toxicity
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1. apply oxygen at first sign of toxicity
arterial hypoxemia and acidosis develop rapidly and further accentuate the toxicity of local anesthetics |
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Cardiovascular toxicity Manifested by: 4X
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Decreased ventricular contractility
Decreased conduction Dysrhythmias Loss of peripheral vasomotor tone |
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local anesthetics produce a dose-dependent
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delay in transmission of cardiac impulses
Action on cardiac Na and ion channels |
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bupivicaine cardiotoxicity > lidocaine
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bupivicaine is 70x more potent in blocking cardiac conduction than lidocaine at same heart rates
|
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Cardiovascular toxicity increased by:
4X |
hypoxia
acidosis pregnancy hyperkalemia |
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toxic manifestations
in order |
lightheadness, tinnitus, tongue numbness
visual disturbances muscle twitching unconsciousness convulsions coma respiratory arrest cardiovascular collapse |