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Regional Anesthesiology > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

5th vital sign:

A

pain

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2
Q

What creates pain?

A

noxious stimulus

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3
Q

2 components of pain:

A

perception, reaction

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4
Q

What component of pain is the same bw people:

A

perception

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5
Q

La will not work in this case:

A

hot tooth

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6
Q

4 ways to stop pain pw:

A

initiation, propagation, integration, stimulation of descending inhibitory pw

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7
Q

How does la intercede in pain pw?

A

prevent propagation

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8
Q

poorly myelinated fibers, diffuse pain, la will interact well with:

A

C

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9
Q

fibers for sharp pai, huge myelinated nerves, more difficult to anesth with la

A

A beta, a delta

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10
Q

LA must cross:

A

he ct, epinerum, perinerum, endoneureum, middle of nerve bundle:

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11
Q

Fraction of mandibular blocks that will not be effective even when good, due to alterations in pt anatomy

A

1/5

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12
Q

anelgesics and narcotics intercede in the part of the pain pw:

A

Integration: still sense pain (not as much), you just don’t care, brain nad s.c.

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13
Q

drug for stimulation of the descending pain inhibitory pw:

A

serotonin, increase cns serotonin levels to decrease pain

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14
Q

A-delta/ beta fibers:

A

fast, sensitive to mechanical stimuli, small, myelinated, high conductance speed, acute, sharp, well localized pain

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15
Q

c fibers:

A

slow, sensitive to many stimuli, small, unmyelinated, slow conductance speed, dull, achy, poorly localized

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16
Q

What explains the phenomenon of double pain?

A

2 sets of pain fibers: a-delta and C

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17
Q

Which type of pain fibers do we want to knock out?

A

All 3: A-d, A-beta and C

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18
Q

Most heavily myelinated nerves:

A

Motor nerves

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19
Q

Pain travels up via:

A

spinothalamic track (anterior/ ventral and lateral)

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20
Q

Anterior/ ventral spinothalamic track:

A

immediate warning of the presence, location, and intensity of an injury

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21
Q

Lateral spinothalamic track:

A

slow, aching reminder that tissue damage has occured

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22
Q

Where do the lateral and anterior/ ventral spinothalamic tracks decusate?

A

level of sc

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23
Q

Pain ends here in the brain:

A

Somatosensory cortex

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24
Q

Responsible for affective sensation:

A

descending pathways

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25
Q

Ex of affective sensation:

A

compulsion to act

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26
Q

anelgesia:

A

pain relief

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27
Q

Ways to produce local pain:

A

Mechanical trauma, low temperature, low O2, chemical irritants, neurolytic agents, chemical agents

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28
Q

Ex’s of neurolytic agents:

A

alcohol, phenol (inject alcohol so it can no longer transmit)

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29
Q

Ex’s of chemical agents:

A

local ensthestics

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30
Q

Only la with intrinsic vasoc props:

A

cocaine

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31
Q

Koller first use cocaine to:

A

anesthetize the cornea

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32
Q

Benefit of the vasoc properties of cocaine:

A

absorption, duration, absorption rate, decrease chance of systemic serum levels, diffusion

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33
Q

First synthesized local anesthetic:

A

procaine

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34
Q

What type of anesthetic is procaine?

A

ester anesthetic

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35
Q

First non-ester type la used in dentistry:

A

lidocaine (amide)

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36
Q

What type of anesthetic is lidocaine:

A

amide

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37
Q

Lidocaine is aka:

A

xylocaine

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38
Q

3 parts of la:

A

aromatic ring, amine group, ester or amide linkage

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39
Q

La’s with ester linkages (5):

A

cocaine, procaine, tetracaine,2-chlorprocaine, benzocaine

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40
Q

La’s with amide linkages:

A

mepivicaine, lidocaine, prilocaine, bupivacaine, etidocaine, ropivacaine

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41
Q

What determines the classifiaction of La?

A

linkage

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42
Q

lipophilic portion of La’s:

A

aromatic ring

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43
Q

hydrophilic portion of La’s:

A

3’/ 4’ amine

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44
Q

We need to the hydrophilic end to:

A

diffuse through interstitial tissue

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45
Q

We need the hydrophobic end to:

A

pass through myelin and L.B.

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46
Q

Properties of an ideal anesthetic:

A

Reversible, non-irritating, low systemic toxicity, rapid onset, required duration, high potency, absorb through skin/mucosa for topical use, free from allergic reactions, stable in solution, readily metabolized, sterile or capable of being sterilized

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47
Q

TF? Some LA’s permanently interfere with the ability of a nerve to produce an AP.

A

T

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48
Q

Ion channels that Ap’s depend upone:

A

Na, K, Cl, Ca

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49
Q

Ion channel that la’s primarily work on:

A

Na

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50
Q

States of the Na channel that la’s work on:

A

resting, open, inactivated

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51
Q

Which are open for a longer duration, Na channels or K channels?

A

K

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52
Q

Chemicals that inhibit Na channels besides La:

A

Toxins, CCBA’s, Alpha-2 adrenergic agents, meperdine, volatile anesthetics

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53
Q

la’s are classified based on:

A

How strong they are (potency), how long they work, how fast they work, what they block

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54
Q

Potency of La tends to increase with:

A

increasing molecular size

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55
Q

Potency is directly proportional to:

A

lipid solubility

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56
Q

Duration of action is related to:

A

lipid solubility

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57
Q

Higher lipid solubility,

A

longer lasting effects

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58
Q

Duration of action is indirectly related to:

A

protein-binding

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59
Q

Speed of onset is inversely related to:

A

pKa (ionization constant) and lipid solubility

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60
Q

Only form of La that can interact w membrane:

A

non-ionized, uncharged form

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61
Q

Highly lipid soluble La:

A

etidocaine

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62
Q

La with a high pKa:

A

chlorprocaine

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63
Q

Rate of onset is controlled by:

A

aqueous diffusion

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64
Q

How fast LA works is inversely related to:

A

molecular size

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65
Q

Two local anesthetics that are “relatively” selective for sensory blockade:

A

bupivicaine, ropivacaine

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66
Q

Additional factors that affect la activity:

A

Dosage, site of administration, additives (same as preservatives?) - vasoconstrictor, temperature, pregnancy

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67
Q

Properties of all la’s:

A

synthetic (weak B, strong A), tertiary amino groups, form salts with strong acids, salts are water soluble, weak alkaloid base is soluble in lipids, reversible, compatible with vasoc’s, incompatible with metal salts, little to no direct irritating affects on tissue, similar systemic toxic effect, all metabolized in the body

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68
Q

3 moa of La:

A

receptor binding, membrane swelling, channel blockade

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69
Q

Salts fo weak base w strong acid:

A

stable, soluble in water, the farther the pH from the pKa, the more water soluble and less lipid soluble

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70
Q

La is present in these 2 forms in the tissues:

A

ionized and un-ionized (same as associated/ dis?)

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71
Q

More of the ionized form will be present if:

A

higher pKa of La or lower pH of body

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72
Q

higher pKa or lower pH are good for this and bad for this:

A

water solubility, anesthesia

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73
Q

Required to produce a nerve blockade:

A

free, uncharged base, diffuse into nerve, bind receptor

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74
Q

Effectiveness of a local anesthetic depend on:

A

Chemical structure, concentration, rate of diffusion of the salt and free base, vasoconstrictors, anatomy of nerve

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75
Q

Toxic effects of local anesthetics:

A

Mutagenicity, carcinogenicity, fetotoxicity, effect on geriatric/pediatric populations, A, D, M, E, Drug interactions, adverse reactions

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76
Q

Is absorption a factor in La?

A

not really

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77
Q

Proteins that La bind:

A

alpha 1 acid glycoprotein, albumin

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78
Q

What does protein binding effect?

A

duration of action

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79
Q

Distribution is dependent upon:

A

direct application, dose, vasculature, vasoconstrictor

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80
Q

Effect of metabolism on la:

A

convert lipid soluble agents to water soluble agents for excretion by the kidneys

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81
Q

These are involved in ester hydrolysis of la’s:

A

cholinesterases

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82
Q

This is responsible for allergic reactions in ester hydrolysis:

A

PABA

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83
Q

How are amide La’s metabolized?

A

liver

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84
Q

Liver enzymes for la metabolism:

A

cytochrome P450 system

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85
Q

Toxic by-products metabolism of La’s can produce:

A

O-toluidine and methemoglobinemia

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86
Q

Clearance of amide LA’s depends on (3):

A

Hepatic blood flow and extraction, cytochrome P450 enzyme system function

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87
Q

Factors/drugs that can reduce hepatic blood flow:

A

Beta adrenergic blocking agents, Histamine-2 blocking agents, Heart failure, Liver failure

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88
Q

What can increase the chance of LA toxicity?

A

reduced blood flow to the liver

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89
Q

Toxic effects of LA’s:

A

CNS, Cardiovascular, allergic (usually to the preservative, right?), direct neurotoxic

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90
Q

What type of response is there to LA?

A

biphasic, CNS stimulation/ depression, seizures/ respiratory depression or arrest

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91
Q

Seizure generating ability of LA is directly related to:

A

potency

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92
Q

Factors that would make a person have seizures at a lower dose:

A

elevated CO2 levels (COPD), Acidosis (from aspirin use)

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93
Q

Which requires higher doses to produce, seizures ro CV depression?

A

CV depression, 3X more

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94
Q

There is a higher incidence of CV depression with this LA:

A

bupivicaine (one of the 2 sensory specific)

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95
Q

How do La’s depress the CV system:

A

bind and inhibit myocardial Na channels

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96
Q

Which isomer binds to myocardial Na channels more strongly?

A

right handed

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97
Q

Left-handed La’s:

A

levobupivacaine (is this sensory specific?) and ropivacaine (one of two sensory specific)

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98
Q

Are true allergic reactions to LA common?

A

no

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99
Q

Anaphylaxis related to LA:

A

IgE mediated anaphylaxis to esters or amides (allergy to preservative)

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100
Q

How to test for allergic reactions to LA:

A

skin testing

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101
Q

Tx for minor allergic reaction:

A

nothing

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102
Q

Tx for non-minor allergic reactions:

A

Benadryl, epi, steroids

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103
Q

Benadrly is aka:

A

diphenhydramine

104
Q

Injection techniques:

A

Standard mandibular block, Gow-gates and akinosi

105
Q

Standard mandibular block:

A

Jorgensen modification of Halsted tech, aim for w/in 1mm of target, 80% success

106
Q

Landmarks for Stan Man block:

A

coronoid notch, pterygomandibular raphe, occlusal plane posteriorly, premolar dentition

107
Q

how to give a stan man block:

A

Aim for lingula, midpoint of medial surface of ramus in both A-P and S-I directions, 2/3 - 3/4 of needle, may hit bone, may not

108
Q

Why might the stan man block not work?

A

Lingula not in the middle, nerve branching variation

109
Q

How to increase the success rate of the stan man block:

A

aim high (cephalad), Gow-Gates Technique

110
Q

Gow-Gates Technique provides sensory anesthesia to:

A

entire man division of CN V

111
Q

Advantages of Gow-Gates Technique:

A

Higher success rate, lower rate of positive aspiration, anesthetizes (7) inferior alveolar, lingual, mylohyoid, mental, incisive, auriculotemporal, buccal nerves – only one injection

112
Q

Name all nerves anesthetized with Gow-Gates Technique

A

nferior alveolar, lingual, mylohyoid, mental, incisive, auriculotemporal, buccal nerves – only one injection

113
Q

When to not use Gow-Gates Technique:

A

Patient can’t open wide, must open 50-55mm

114
Q

Pt positioning for Gow-Gates Technique:

A

reclines, supine position

115
Q

Why is there a higher success rate with the Gow-Gates Technique?

A

uses extraoral landmarks as well, commisure of lip, tragus/intertragic notch

116
Q

Explain Gow-Gates Technique:

A

inject lateral to raphe but medial to temporalis tendon from opposite commissure, along visualize commissure-intertragus line and parallel with angulation of ear to face, go until bone/ condyle, about 25mm, deposit after negative aspiration or “walk” the needle toward the medial

117
Q

Closed mouth technique:

A

Akinosi Technique

118
Q

Primary indication to use the Akinosi technique:

A

pts with trismus

119
Q

Explain Akinosi technique:

A

buccal mucogingival junction of the maxillary second/third molar, intraoral reference: coronoid notch, teeth in occlusion, syringe parallel with maxillary occlusal plane

120
Q

three operative factors:

A

Avoid (issue), recognize, manage (if it occurs)

121
Q

This is when action taken is not action intended:

A

Technical error, ie intra-vascular administration

122
Q

Are system errors common with LA?

A

no

123
Q

Anesthesai complications: Recognition:

A

NETCC: Necessary, efficacy, toxicity, compliance, cost (?)

124
Q

What to check when monitoring and managing anesthesia complications:

A

ABC’s, BP, P, RR, OMI/ MONA

125
Q

CN V originates from these three sensory nuclei in the midbrain:

A

Mesencephalic, principle sensory nucleus, spinal nucleus

126
Q

What merge to form the sensory root?

A

sensory nuclei

127
Q

Where do the sensory nuclei merge to form the sensory root?

A

pons

128
Q

What forms the motor route?

A

motor nucleus

129
Q

The trigeminal ganglion is in this fossa:

A

middle cranial fossa

130
Q

The trigeminal ganglion is adjacent to:

A

cavernous sinus

131
Q

The trigeminal ganglion is aka:

A

Gasserian ganglioin

132
Q

Trigeminal ganglion is at the level of the:

A

pons

133
Q

In which portion of the brainstem is the mesencephalic nuceus?

A

midbrain (m-m)

134
Q

In which portion of the brainstem is the Principle sensory nucleus?

A

Pons (p-p)

135
Q

In which portion of the brainstem is the spinal nucleus?

A

medulla

136
Q

The opthamlic division exits via the:

A

superior orbital fissure

137
Q

Terminal branches of the opthalmic dividision:

A

Frontal, lacrimal, and nasociliary

138
Q

Besides the main three terminal brances, what else does the opthalimic division carry?

A

Also carries postganglionic parasympathetic fibers from the pterygopalatine ganglion (via facial nerve) which initially travel with the zygomatic branch of the maxillary division then join the lacrimal branch of the ophthalmic division

139
Q

Which branch of the opthalmic division carries parasympathetic fibers?

A

lacrimal

140
Q

What does the opthalmic division innervate?

A

skin and mucous membrane derivatives of the frontonasal process: Forehead and scalp, Frontal and ethmoid sinuses, Upper eyelid and conjunctiva, Cornea, Dorsum of nose

141
Q

Maxillary division of the trigeminal nerve exits the skull via:

A

the foramen rotundum

142
Q

How many branches does the maxillary division give rise to?

A

14

143
Q

Maxillary division innervates:

A

the skin, mucous membranes and sinuses that are derived from the maxillary prominence of the first pharyngeal arch

144
Q

Does the maxillary branch carry parasympathetic?

A

Yes, to the lacrimal and the nasal glands

145
Q

7 of the 14 maxillary branches that we care about:

A

Anterior superior alveolar nerve, middle superior alveolar nerve, posterior superior alveolar nerve, infraorbital nerve, nasopalatine nerve, greater palatine nerve, lesser palatine nerve(s)

146
Q

Sensory branches of V3 innervate:

A

skin, mucous membranes and striated muscle derivatives of the mandibular prominence of the first pharyngeal arch Mucous membranes and floor of the oral cavity, external ear, lower lip, chin, anterior 2/3 of the tongue with special taste sensation from the chorda tympani branch from the facial nerve, all lower teeth, gingiva and bone

147
Q

4 terminal branches of V3:

A

Buccal, Inferior alveolar (mental nerve/incisive nerve extensions), Auriculotemporal, Lingual

148
Q

How many muscles does V3 supply motor innervation to? and name:

A

8: Muscles of mastication (masseter, temporalis, Internal/medial pterygoid, external/lateral pterygoid), anterior belly of the digastric, mylohyoid, tensor veli palatini, tensor tympani

149
Q

What innervation does the mylohyoid often carry?

A

accessory sensory innervation to mandible

150
Q

Does the mandibular branch carry parasympathetic?

A

Yes, supply to the salivary glands – sublingual, submandibular, parotid

151
Q

Infraobital block:

A

MaxRCI to MR2P and the MB aspect of MR1M, including the lip in that area

152
Q

Anterior superior alveolar block:

A

MaxLCI to the MaxLC and the lip area

153
Q

Middle superior alveolar block:

A

MaxL1P and MaxL2P, the MB aspect of the MaxL1M AND the lip of that area

154
Q

Posterior superior alveolar block:

A

The Max L molars except the MB aspect of the Max1M and the surrounding gingiva

155
Q

Nasopalatine block:

A

Hard palate region from canine to canine, comes to a point on the hard palate

156
Q

Greater palatine block:

A

MaxL hard palate from Max1P and posterior

157
Q

inferior alveolar block:

A

All man R teeth, right half of tongue, lips from the D aspect of the 2nd premolar to the midline

158
Q

Incisive block:

A

ManLCI to the Man2P and the lip in that region

159
Q

Buccal block:

A

The gingiva and lip adjacent to the mandibular molars

160
Q

What does the anterior superior alveolar nerve supply?

A

pulp & investing structures & labial mucoperiosteum of anterior teeth

161
Q

What does the middle superior alveolar nerve supply?

A

The pulp & investing structures & buccal mucoperiosteum of mromoplars and MB root of 1st molar

162
Q

What does the greater palatine nerve supply?

A

palatal mucoperiosteum of maxillary molars and premolars

163
Q

What does the nasopalatine nerve supply?

A

palatal mucoperiosteum of maxillary anterior teeth

164
Q

Which is more anterior on the lateral side of the ramus, the inferior alveolar nerve or artery?

A

nerve

165
Q

You want the needle to be bw these structures:

A

medial surface of the ramus and medial pterygoid muscle/ lingual nerve

166
Q

Injection point in the mucosa:

A

pterygomandibular raphe

167
Q

How can local anesthetics interfere with the excitation process?

A

Alter the resting membrane potential, alter the threshold potential, decrease the rate of depolarization, prolong the rate of repolarization

168
Q

80-58% of LA work in this manner:

A

Interfering with depolarization, decrease rate of polarization, let it leak in slowly

169
Q

Which LA’s alter the threshold potential?

A

none

170
Q

Which LA’s arrest the membrane potential?

A

none

171
Q

Does LA prevent Na from entering or leaving the cell?

A

entering

172
Q

Which ion does LA not really affect?

A

chloride

173
Q

Where is the specific Na channel receptor that LA reacts with?

A

either outer or inner cell membrane surface

174
Q

Primary mechanism of action of LA:

A

via specific receptor binding at the Na channel, decreasing permeability of Na channel, slight decrease in K conductance (insignificant)

175
Q

Where does venom interact with the cell?

A

inside of cell membrane

176
Q

Do most LA’s react with the outer or inner membrane?

A

outer

177
Q

Typical anesthetics react with specific receptor sites here:

A

within the channel itself

178
Q

Snake venom react with specific receptor sites here:

A

outer surface of the channel

179
Q

Scorpion venoms react with specific receptor sites here:

A

the fast or slow sodium gates

180
Q

Class A:

A

receptor on external surface of membrane

181
Q

Class B:

A

receptor on internal surface of membrane (not clinically usable, venoms)

182
Q

Class C:

A

receptor independent

183
Q

Class D:

A

combination of receptor dependent and independent mechanisms

184
Q

Topical anesthetic is what class anesthetic?

A

3

185
Q

Recommended injection rate for anesthetic:

A

1mL per minute

186
Q

Why is it painful for pt if you inject quickly?

A

Rippinng interstitial tissue

187
Q

Class C drugs exist only in this form:

A

uncharged dissociated form

188
Q

Ex of Class C drug:

A

benzocaine

189
Q

Class D drugs exist in this form:

A

both charged, undissociated form and the uncharged dissociated form

190
Q

Most acitivity of Class D drugs is due to:

A

uncharged form and 10% is due to the charged form

RNH+ or RN

191
Q

Which form of LA has the most effect?

A

Uncharged dissociated form (check) (due to pH the charged form is what has the efffect?)

192
Q

TF? The moa is dependent onthe nerve fiber itself.

A

T

193
Q

Where does LA interact with my nn.?

A

Na channels in the nodes

194
Q

TF? Na channels are only found at the nodes of Ranvier.

A

F. mainly found there

195
Q

All LA’s are toward this end of the pH scale:

A

basic end (7.6-8.0)

196
Q

Is the body’s pH higher or lower than LA?

A

lower, more acidic

197
Q

We need to silence about this many nodes in order to stop the AP:

A

6-12 (1 cm or more of distance) at LEAST 3 adjacent nodes, can be up to 8-10mm

198
Q

If you inject LA 1 cm away from the intended target will it work?

A

no, not enough to get the desired effect

199
Q

Small, unmyelinated nerves have about __ sodium channels per square micrometer.

A

35

200
Q

Nodes of Ranvier may contain sodium channels per square micrometer.

A

20,000

201
Q

Why won’t the AP be stopped if you block only one node?

A

saltatory conduction

202
Q

Which has more nodes, a small unmy n. or or node or ranvier?

A

node

203
Q

TF? The goal in anesthesia is to block the transmission of all nerve fibers.

A

F. This will never happen

204
Q

Even if pain is blocked a pt may still experience these senses:

A

proprioception, sense of direction

205
Q

What effect is calcium bound in the membrane thought to exert?

A

regulatory effect on movement of sodium ions across membrane

206
Q

Proposed mech of LA:

A

LA displaces Ca rom Na channel (competitive antagonism), LA then binds receptor, blocking it (conduction blockade)

207
Q

Whether the A is short or long duration depends on:

A

it’s structure

208
Q

Short acting LA’s last:

A

30 min

209
Q

Lidocaine without vasoconstrictor will only give pulpal A for:

A

5min

210
Q

Lidocaine with vasoconstrictor will give pulpal A for:

A

1.5-2hours

211
Q

TF? The rate of LA metabolism is altered with the addition of vasoconstrictor.

A

T

212
Q

Where are amide A’s metabolized?

A

liver

213
Q

If a pt has liver disease what LA should you not gibe?

A

any amide

214
Q

Hw are ester LA’s metabolized?

A

enzyme in blood, pseudocholinesterase in serum, ester is metabolized by esterase, Some ppl have hereditary issues with esterases. Know MxHistory

215
Q

A LA will be less lipid soluble if:

A

the pH is fa from the pKa (more ionized, more water soluble)

216
Q

90% of molecuels of LA are in this form:

A

undis charged form, highly water soluble, poorly lipid soluble (other 10% can’t get to n.)

217
Q

Would infection drive the equation to the charged or uncharged side?

A

uncharged (highly water soluble)

218
Q

pH of infected tissue:

A

4-5 (check)

219
Q

2 competing factors of LA:

A

diffusibility and binding

220
Q

Which factor of LA is more important clinically, diffusibility or binding

A

difusibiity

221
Q

LA with pKa of 7.9 will have this % water and lipid soluble:

A

75% water, 25% lipid

222
Q

What happens as a local anesthetic diffuses into a nerve?

A

increasingly diluted by tissue fluids and absorption, tissue/protein binding

223
Q

nerve blockade:

A

free, uncharged base must interact with the nerve membrane, diffuse into and bind receptor site

224
Q

3 factors that decrease effectivity as the LA diffuses

A

Decease volume, decreased concentration, protein binding

225
Q

Related to intrinsic potency of LA:

A

Lipid solubility

226
Q

LA with low lipid solubility, La with high lipid solubility:

A

Procaine = 1, etidocaine = 140

227
Q

This is related to the duration of action of LA:

A

protein binding

228
Q

TF? Increased protein binding to receptor = decreased duratio

A

F. increased

229
Q

factors that influence the clinical effectiveness of LA:

A

Chem struct, diffusibility, vasoc, conc, anatomy of n., location of n.

230
Q

Will mepevocaine be present more in the assoc or disocciated form?

A

dis

231
Q

Lipid solubility theoretically leads to:

A

more rapid onset of action, longer duration, slower recovery

232
Q

What differs bw each LA?

A

carrier protein molecules

233
Q

All LA’s bind this:

A

albumin

234
Q

TF? The more LA binds to protein, the better,

A

T

235
Q

TF? Most LA’s have intrinsic vasodilating abilities.

A

T. except coke

236
Q

Moderate duration anesthetic lasts:

A

up to 3 hours

237
Q

Long lasting anesthetic lasts:

A

up to 12 hours

238
Q

Why is recovery slower than the onset of action?

A

because LA is bound to receptor and is released more slowly than it is bound

239
Q

Posterior sup alveolar artery, thin or thick fibers?

A

very thin, to upper premolar

240
Q

Sequence of sense loss with anesthesia:

A

Pain and temp lost at same time, then touch/ prop, then motor

241
Q

If prop sensors are still there they will feel:

A

pressure and vibrations

242
Q

in what order do you gain sense back as anesthesia wears off?

A

reverse

243
Q

What to do if you accidentally anesthetize CN 7:

A

nothing, it will come back in minutes

244
Q

physiologic effects of local anesthesia are dependent on :

A

concentration

245
Q

Amt of fluid in each carpule:

A

1.7ml

246
Q

3 components in each carpule:

A

LA, vasoc, preservative

247
Q

When is a preservative needed?

A

if there is vasoc

248
Q

1% solution =

A

1gm in 100 ml, 1000 mg in 100 ml, 00 mg in 10 ml, 10 mg in 1ml

249
Q

1.7 ml of a 1% solution =

A

17 mg

250
Q

1.7 ml of a 2% solution =

A

34mg

251
Q

1.7 ml of a 3% solution =

A

51 mg

252
Q

How is LA conc reported?

A

weight/volume molar solution

253
Q

How is vasoc concentration reported?

A

fraction in weight/volume

254
Q

In one 1.7 ml carpule how much epinephrine is injected if everything is delivered?

A

0.017 mg of

255
Q

In very ml of 2% lidocaine with .. Epi there will be __mg of lido in every ML of the injection and __ mg of epi in every ml of the injection

A

20, 0.01

256
Q

Be aware of this with a patient that has COPD:

A

Increased likelihood of seizure at lower dose of LA

Regional Anesthesiology (3 decks)

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