Pharm-Local Anesthetics

Front 1

Name the 5 "ester" Local Anesthetics

Back 1

Procaine (Novacaine), Chloroprocaine (Nesacaine), Tetracaine (Pontocaine), Benzocaine (Hurricane Spray), Cocaine

Front 2

Name the 6 "amide" Local Anesthetics

Back 2

Lidocaine (Xylocaine), Mepivacaine (Carbocaine), Prilocaine (Citanest), Bupivacaine (Marcaine), Ropivacaine (Naropin), Levobupivacaine (Chirocaine)

Front 3

What type of nerve fibers are continuously encased by Schwann cells without interruption?

Back 3

Unmyelinated Fibers

Front 4

Which type of nerve fibers has a myelin covering that is interrupted by nodes of Ranvier, allowing the passage of drugs and ions?

Back 4

Myelinated nerve fibers

Front 5

In Myelinated nerve fibers, impulse propagation occurs where?

Back 5

Nodes of Ranvier

Front 6

Following a peripheral nerve block, what percentage of the dose reaches the nerve?

Back 6

<2%

Front 7

What 2 nerve characteristics result in more rapid conduction?

Back 7

increased myelination and increased nerve diameter

Front 8

Which 2 nerve fiber types are myelinated?

Back 8

Type A and Type B

Front 9

Which nerve fiber type is unmyelinated?

Back 9

Type C

Front 10

Type A nerve fiber is the only type with 4 subtypes; What are the subtypes?

Back 10

Alpha, Beta, Gamma and Delta

Front 11

What is the resting membrane potential?

Back 11

-90 mv

Front 12

What is the resting membrane potential maintained by?

Back 12

ATP dependent pump which expels Na+ in exchange for K+ via voltage-gated K+ channels

Front 13

What is the threshold potential?

Back 13

-65 mv

Front 14

What does the generation of an action potential rely on?

Back 14

Activation of voltage-gated Na+ channels in sufficient number to reach threshold potential of -65mv

Front 15

What's the general effect of Local Anesthetics on generation of an action potential?

Back 15

They don't allow enough Na+ channels to open to generate an action potential

Front 16

Are Local Anesthetics mainly weak acids or weak bases?

Back 16

Weak Bases

Front 17

Tonic or Phasic Inhibition? "Time between action potentials exceeds time for dissociation of local anesthetic from the Na+ channel"

Back 17

Tonic

Front 18

Why is it crucial for Local Anesthetics to be lipophilic?

Back 18

They must traverse the lipid membrane to affect Na+ channel from the intracellular side

Front 19

What kind of hydrophobicity results in more rapid onset of the Local Anesthetic, Poorly, moderately or extremely hydrophobic Local Anesthetic?

Back 19

Moderately hydrophobic

Front 20

Potency is directly related to ________.

Back 20

Hydrophobicity

Front 21

Which LA has a "low potency?"

Back 21

Procaine

Front 22

Which LAs have an "intermediate potency?"

Back 22

Mepivacaine, Prilocaine, Chloroprocaine, Lidocaine

Front 23

Which LAs have a "high potency?"

Back 23

Tetracaine, Bupivacaine, Etidocaine

Front 24

What form (charged, hydrophilic or lipid soluble neutral) must LA be in before it can directly inhibit the Na+ channel?

Back 24

Charged, hydrophilic form (must be reprotonated after enters through lipid membrane)

Front 25

Na+ channels have many conformations; which conformation has a low affinity for LAs?

Back 25

Resting Conformation

Front 26

What Na+ channel conformation has the highest affinity for LAs?

Back 26

Open conformation

Front 27

Which type of inhibition, tonic or phasic, is defined as "time between action potentials is less than time needed for local anesthetic to dissociate from Na+ channel?"

Back 27

Phasic

Front 28

Which type of inhibition, tonic or phasic, can more rapidly build a better block?

Back 28

Phasic Inhibition

Front 29

Which nerve fibers are MOST susceptible to local anesthetic block?

Back 29

Small, myelinated (Aγ Motor and Aδ sensory)

Front 30

Which nerve fibers are intermediately susceptible to local anesthetic block?

Back 30

Large, myelinated (Aα and Aβ)

Front 31

Which nerve fibers are LEAST susceptible to local anesthetic block?

Back 31

Small, non-myelinated (C)

Front 32

What are some situations in which rate of Neural firing is high or abnormal repetitive firing occurs?

Back 32

Tissue injury or trauma, various disease states such as neuropathic pain

Front 33

How can you use local anesthetics to treat situations in which rate of neural firing or abnormal repetitive firing occurs?

Back 33

May often be treated with local anesthetic concentrations lower than necessary to block normal nerves (by taking advantage of Phasic inhibition)

Front 34

Increasing concentrations of local anesthetic will usually produce blockade in what sequence?

Back 34

Autonomic (preganglionic sympathetics), Sensory (Pain, temperature), Motor (large motor)

Front 35

Sympathetic, sensory, and motor block will reach _____ levels following central neuraxis anesthesia

Back 35

different

Front 36

How can you determine where the SNS block is located in a particular patient?

Back 36

Run your hand lightly up the side of the patient; where skin gets "sticky" is where the SNS block is

Front 37

Sensory block is located approximately ____ Dermatomes ____ SNS block

Back 37

2 Dermatomes BELOW

Front 38

Motor block is located approximately ____ Dermatomes ____ sensory block

Back 38

2 Dermatomes BELOW

Front 39

Chemically, what do all local anesthetics consist of?

Back 39

a Hydrophobic aromatic ring joined by an ester OR amide bond to a hydrophilic amine

Front 40

What are the determinants of Local Anesthetic Onset, Duration, and Potency?

Back 40

pKa, lipid solubility, protein binding, concentration and vasoconstrictive or vasodilatory properties

Front 41

Only the _____ form of the LA may penetrate the lipid membrane

Back 41

Neutral (lipophilic)

Front 42

Percentage of LA drug in neutral (lipophilic) form is inversely proportional to the pKa; therefore, a ______ pKa equates to a more rapid onset

Back 42

LOWER

Front 43

Net result of INCREASED lipid solubility of LA drugs is ______ onset of action

Back 43

DELAYED

Front 44

Why does increased lipid solubility of LAs delay the onset of action?

Back 44

While increased lipid solubility allows the drug to pentrate the lipid membrane more rapidly, increased lipid solubility may also result in the drug being "stuck" in myelin and other lipid-soluble compartments, including the axonal membrane itself; "stuck" drug is less able to get to the site of action, delaying onset

Front 45

What factor causes an increased DURATION of action of LAs?

Back 45

Slow release of drug from the lipid depot

Front 46

Potency parallels _______.

Back 46

Lipid solubility

Front 47

The more lipid soluble the LA is, the (higher/lower) the Na+ channel receptor affinity?

Back 47

Higher

Front 48

What effect do lipid soluble LAs have on the Na+ channel?

Back 48

Ability to alter conformation of Na+ channel through direct membrane altering effects

Front 49

Increased protein binding of LAs is asscoiated with increased _________.

Back 49

Duration of action (not able to be metabolized)

Front 50

Increasing dose/concentration of LAs results in (more rapid onset, less rapid onset, or no change in onset) of action?

Back 50

More rapid onset (Ex. 3% Chloroprocaine will have a faster onset than 2%)

Front 51

Other than slow release from lipid depot and protein binding, what's another property that plays a major role in determining DURATION of ACTION of LAs?

Back 51

Vasoactive properties

Front 52

MOST are (Vasodilators, vasoconstrictors) at clinically useful concentration?

Back 52

Vasodilators

Front 53

Most LAs are vasodilators; what are 3 exceptions to this?

Back 53

Cocaine, Ropivacaine, and Levobupivacaine

Front 54

Why are Ropivacaine and Levobupivacaine vasoconstrictors?

Back 54

They are both supplied as S-enantiomers, which have inherent vasoconstrictive activity

Front 55

How does Vasodilation effect the duration of action of LAs?

Back 55

The more potent vasodilator drugs cause more blood flow, which washes out the drug more quickly

Front 56

Lidocaine is a more potent vasodilator than _______ (drug) and has a duration of 30-60 minutes; will (the other drug) have a shorter or longer duration of action than Lidocaine?

Back 56

Prilocaine; Longer duraton of action (because it's a less potent vasodilator--less washout of drug)

Front 57

What are the benefits of adding a vasoconstrictor to a LA that vasodilates?

Back 57

Decreases the rate of vascular absorption, creating a denser block (more drug reaches the site of action) and prolongs the duration of action (decreased clearance of drug from site of injection--not getting "washed" out)

Front 58

Adding vasoconstrictors to the LA (peripheral nerve block) regimen is most effective with drugs of ______ to ______ duration

Back 58

Short to moderate

Front 59

What is most commonly given as a vasoconstrictor in conjunction with LAs?

Back 59

Epinephrine (5 mcg/ml)

Front 60

What are 2 vasoconstrictors (other than Epinephrine) that are given in conjunction with LAs?

Back 60

Phenylephrine and Norepinephrine

Front 61

What sites should you avoid injecting a vasoconstrictor?

Back 61

sites which may experience vascular compromise (distal extremities, etc)

Front 62

Adjusting the pH of the LA via ALKALINIZATION may produce what effects?

Back 62

Speed up the onset of the block, provide a greater depth of block and increase the spread of epidural block

Front 63

What mechanism occurs when the pH of a LA is adjusted and made more alkaline?

Back 63

Increases the percentage of drug existing in the neutral (lipid soluble) form which may rapidly diffuse across the neural membrane

Front 64

What is the appropriate "technique" for making the LA more alkaline?

Back 64

Addition of 1 ml of sodium bicarbonate to 10 ml of Local

Front 65

What is important to remember regarding LAs prepackaged with Epinephrine in regards to pH?

Back 65

the pH of LAs prepackaged with Epinephrine is is Lower than normal to extend the shelf life of Epinephrine

Front 66

Toxicity when giving multiple LA drugs (mixture) is _______

Back 66

Additive

Front 67

When administering a "mixture" of multiple LAs, should you give (maximum dose, lower dose) of each agent in the mixture?

Back 67

You have to administer lower doses of each agent in the mixture; effects are additive and toxicity can occur

Front 68

Binding of the LA to the Na+ channel occurs primarily from the ______ side of the neural membrane

Back 68

Intracellular

Front 69

Some alteration of the Na+ channel may occur from within the lipid membrane, particularly in the case of the highly _______, highly ______ local anesthetics

Back 69

Lipophilic, Potent

Front 70

What's the problem with administering an EXTREMELY hydrophobic (lipophilic) LA?

Back 70

An extremely hydrophobic LA molecule will rapidly enter the lipid membrane, but may become "stuck" there, unable to reach the intracellular side, therefore having a SLOWER onset of action

Front 71

What's the benefit of administering a LA that is "moderately" hydrophobic?

Back 71

A moderately hydrophobic LA can enter the lipid membrane relatively quickly, and can also exit the membrane to the intracellular side to interact with the sodium channel--therefore has a faster onset of action

Front 72

A highly hydrophobic LA has a ______ affinity for the Sodium channel; what does this mean?

Back 72

HIGH; this means it stays bound to the Na+ channel longer

Front 73

Lower pKa=more non-ionized drug=???

Back 73

Faster Onset of action

Front 74

Increased lipid solubility=???

Back 74

increased duration of action and increased potency

Front 75

Increased protein binding=???

Back 75

Increased Duration of action

Front 76

Increased Concentration=???

Back 76

More rapid onset

Front 77

Increased dose=???

Back 77

Increased Duration of action

Front 78

Increased vasodilatory properties=???

Back 78

Decreased Duration (because increased blood flow and more anesthetic washout)

Front 79

Addition of Epinephrine (vasoconstrictor) is more effective in increasing the duration following infiltration and peripheral nerve blocks than following ___________.

Back 79

Central Neuraxis anesthesia (spinal, epidural)

Front 80

The injection of LA into infected (acidotic) tissue will be relatively _______

Back 80

ineffective (will become ionized fairly quickly and unable to cross the neural membrane)

Front 81

Why is alkalinizing the LA solution a good idea before injecting the LA via IV?

Back 81

Alkalinization of LA solution may also reduce the burning of injection caused by the acidic pH of the drugs (in a solution)

Front 82

Which LA is the first injectable LA?

Back 82

Procaine (Novacaine) (Ester)

Front 83

Procaine (Novacaine) is a derivative of para-aminobenzoic acid; what is significant about this fact?

Back 83

There are allergy complications with it

Front 84

Does Procaine (Novacaine) have a high or low pKa? Does it have poor or good lipid solubility?

Back 84

High pKa; poor lipid solubility

Front 85

Because Procaine (Novacaine) has a high pKa with poor lipid solubility, what does this implicate about its onset and duration of action?

Back 85

Slow onset and short duration of action (30-60 minutes)

Front 86

What are the 2 main side effects/complications of Procaine (Novacaine)?

Back 86

high incidence of nausea and increased potential for allergic reactions

Front 87

Is Procaine (Novacaine) used frequently or rarely used anymore?

Back 87

Rarely used

Front 88

Which LA is a derivative of Procaine?

Back 88

Chloroprocaine (Nesacaine) (ester)

Front 89

Which LA has the most rapid metabolism?

Back 89

Chloroprocaine (Nesacaine) (ester) (plasma half-life = <30 seconds

Front 90

Which LA is primarily used as an epidural anesthetic for C-section?

Back 90

Chloroprocaine (Nesacaine)

Front 91

Why is Chloroprocaine beneficial for epidural anesthesia for a C-section?

Back 91

Rapid onset, short duration and limited potential for systemic toxicity

Front 92

What undesirable effect does Chloroprocaine (Nesacaine) have on analgesia?

Back 92

Reduces the analgesic effect of concurrently, or subsequently administered Bupivacaine and Opioids

Front 93

Which LA is used primarily in topical (opthlamologic) and spinal anesthesia?

Back 93

Tetracaine (Pontocaine) (ester)

Front 94

Is Tetracaine (Pontocaine) highly lipophilic or poorly lipophilic?

Back 94

Highly

Front 95

Which LA has a slow rate of metabolism (for an ester)?

Back 95

Tetracaine (Pontocaine)

Front 96

Tetracaine (Pontocaine) has a long duration of action. Why?

Back 96

Highly Lipophilic, highly protein bound, slow metabolism (for an ester)

Front 97

In relation to the receptor, because Tetracaine (Pontocaine) is very lipophilic it is also highly ______

Back 97

POTENT

Front 98

What 2 things do Tetracaine (Pontcaine) block?

Back 98

Profound Sensory and Motor block

Front 99

Tetracaine (Pontocaine) is supplied as a crystalline form; this allows it to be more stable and allows for variation in ________.

Back 99

Baricity

Front 100

What makes Benzocaine (Hurricane) (ester) unique from the other LAs?

Back 100

It's a weak acid

Front 101

What's the pKa of Benzocaine (Hurricane)?

Back 101

3.5

Front 102

Which LA is best suited and most often used for topicalization of mucous membranes?

Back 102

Benzocaine (Hurricane) (ester)

Front 103

Does Benzocaine (Hurricane) have a rapid or delayed onset of action?

Back 103

EXTREMELY rapid onset

Front 104

How long is the duration of action of Benzocaine (Hurricane)?

Back 104

30-60 minutes

Front 105

Which LA has the potential to produce methemoglobinemia (esp. in neonates and doses exceeding ~300mg)?

Back 105

Benzocaine (Hurricane) (ester)

Front 106

Which ester LA produces INTENSE Vasoconstriction?

Back 106

Cocaine

Front 107

Which LA is used as a 4% or 10% solution for nasopharyngeal topicalization prior to surgery or other instrumentation?

Back 107

Cocaine

Front 108

Which ester LA has a LOW therapeutic index (least safe)?

Back 108

Cocaine

Front 109

Which ester LA has a high abuse potential?

Back 109

Cocaine

Front 110

What's the brand name for Procaine?

Back 110

Novacaine

Front 111

What's the generic name for Novacaine?

Back 111

Procaine

Front 112

What's the brand name for Chloroprocaine?

Back 112

Nesacaine

Front 113

What's ther generic name for Nesacaine?

Back 113

Chloroprocaine

Front 114

What's the brand name for Tetracaine?

Back 114

Pontocaine

Front 115

What's the generic name for Pontocaine?

Back 115

Tetracaine

Front 116

What's the brand name for Benzocaine?

Back 116

Hurricane

Front 117

What's the generic name for Hurricane?

Back 117

Benzocaine

Front 118

What's the brand name for Lidocaine?

Back 118

Xylocaine

Front 119

What's the generic name for Xylocaine?

Back 119

Lidocaine

Front 120

Is Lidocaine (Xylocaine) an amide or an ester?

Back 120

Amide

Front 121

Which amide LA was the first aminoamide introduced and most widely used?

Back 121

Lidocaine (Xylocaine)

Front 122

Is Cocaine an amide or an ester?

Back 122

Ester

Front 123

Is Procaine (Novacaine) an amide or an ester?

Back 123

Ester

Front 124

Is Chloroprocaine (Nesacaine)an amide or an ester?

Back 124

Ester

Front 125

Is Tetracaine (Pontocaine) an amide or an ester?

Back 125

Ester

Front 126

Is Benzocaine (Hurricane) an amide or an ester?

Back 126

Ester

Front 127

Which amide LA has a rapid onset, intermediate duration of action and a broad range of uses?

Back 127

Lidocaine (Xylocaine)

Front 128

Does Lidocaine (Xylocaine) have a rapid or slow onset of action?

Back 128

Rapid

Front 129

Lidocaine has many uses (including infiltration); what type of Lidocaine solution (percent) is used for infiltration and how long is the duration of action?

Back 129

0.5-1.0% solution; Duration of action is 30-60 minutes

Front 130

When Lidocaine (Xylocaine) is used as topical anesthesia of mucous membranes, what type of Lidocaine solution is used (percent) and what type of drug is administered with it?

Back 130

Typically a 4% solution; used in combination with a vasoconstrictor

Front 131

What type of surgery is "Tumescent anesthesia" associated with?

Back 131

Liposuction

Front 132

Is Lidocaine often used for epidural (central neuraxis) anesthesia?

Back 132

YES

Front 133

Which amide LA is the most commonly used drug for the Bier Block (IV regional block)?

Back 133

Lidocaine (Xylocaine)

Front 134

Does Lidocaine (Xylocaine) blunt the hemodynamic response to intubation?

Back 134

YES

Front 135

Which route of Lidocaine administration is most effective when used for intubation: Laryngotracheal spray or Intravenous? Why?

Back 135

Intravenous; spray may not have enough time to work before ET tube is placed

Front 136

In addition to blunting the HD response to intubation, what other effects are attenuated associated with tracheal instrumentation?

Back 136

attenuates increases in IOP, ICP, and intra-abdominal pressure associated with tracheal instrumentation

Front 137

What unique use does Lidocaine (Xylocaine) have in association with the heart?

Back 137

Antidysrhythmic

Front 138

How does Lidocaine (Xylocaine) help with chronic neuropathic pain?

Back 138

Low doses are effective in blocking increased ectopic discharges in a damaged nerve, possibly through inhibition of hippocampal and thalamic neurons

Front 139

What is the brand name of the LA amide Mepivacaine?

Back 139

Carbacaine

Front 140

What is the generic name for the LA amide, Carbacaine?

Back 140

Mepivacaine

Front 141

Which 2 drugs are very similar to Lidocaine (Xylocaine)?

Back 141

Mepivacaine (Carbacaine) and Prilocaine (Citanest)

Front 142

Which amide LA is very similar to Lidocaine (Xylocaine) but slightly less potent with a slightly longer duration of action?

Back 142

Mepivacaine (Carbacaine)

Front 143

Which 2 ester LAs most similar to Lidocaine (Xylocaine) produce less vasodilation, so therefore less need for a vasoconstrictor?

Back 143

Mepivacaine (Carbacaine) and Prilocaine (Citanest)

Front 144

What is Mepivacaine (Carbacaine) primarily used for?

Back 144

Peripheral nerve block

Front 145

What concentration (percent) of Mepivacaine (Carbacaine) is used for peripheral nerve block and what's the duration of action?

Back 145

1-1.5% solution; duration of action is 2-4 hours

Front 146

Which amide LA is poorly metabolized by a fetus and accumulation may lead to poor fetal muscle tone?

Back 146

Mepivacaine (Carbacaine)

Front 147

Which amide LA should you avoid using in OB as an epidural due to its negative effects on the fetus?

Back 147

Mepivacaine (Carbacaine)

Front 148

What's the Brand name of the LA amide Prilocaine?

Back 148

Citanest

Front 149

What's the generic name for Citanest?

Back 149

Prilocaine

Front 150

Is Mepivacaine (Carbacaine) an ester or an amide LA?

Back 150

Amide

Front 151

Is Prilocaine (Citanest) an Ester or an amide LA?

Back 151

Amide

Front 152

Which amide LA is very similar to Lidocaine (Xylocaine) except it is more rapidly metabolized, has decreased CNS toxicity and causes less vasodilation?

Back 152

Prilocaine (Citanest)

Front 153

What is the metabolite of Prilocaine (Citanest) that at large doses can accumulate and produce methemoglobinemia?

Back 153

Orthotoluidine

Front 154

At what dose can the metabolite of Prilocaine accumulate and cause methemoglobinemia?

Back 154

Large dose (>600 mg)

Front 155

What does Prilocaine's metabolite Orthotoluidine produce in large doses (>600 mg)

Back 155

methemoglobinemia

Front 156

Which amide LA is used most commonly in equal parts with Lidocaine (Xylocaine) as EMLA cream?

Back 156

Prilocaine (Citanest)

Front 157

What's the brand name for Bupivacaine?

Back 157

Marcaine

Front 158

What's the generic name for Marcaine?

Back 158

Bupivacaine

Front 159

Is Bupivacaine (Marcaine) and ester or an amide LA?

Back 159

Amide

Front 160

Does Bupivacaine have a fast or slow onset? Duration of action?

Back 160

Slow onset; prolonged duration of action

Front 161

With Bupivacaine (Marcaine) at concentrations below _____% sensory block is greater than motor block

Back 161

0.25%

Front 162

What are 2 indications for using 0.25% concentration of Bupivacaine (Marcaine) (causing a greater sensory block than motor block?

Back 162

Labor analgesia, Post-operative pain management

Front 163

What is considered to be the largest complication/side effect of Bupivacaine (Marcaine)?

Back 163

Cardiotoxicity

Front 164

What are the 3 uses of Bupivacaine (Marcaine)?

Back 164

Spinal anesthesia, Epidural anesthesia and peripheral nerve block

Front 165

Bupivacaine (Marcaine) has a slow onset in most all cases except ______.

Back 165

with spinal and infiltration anesthesia

Front 166

When used as spinal anesthesia, does Bupivacaine have a slow or a rapid onset of action? What is it?

Back 166

Rapid; ~5 minutes

Front 167

What is the duration of action of Bupivacaine when used as spinal anesthesia?

Back 167

~1-4 hours (dose dependent)

Front 168

Which amide LA is the most common drug used for spinal anesthesia?

Back 168

Bupivacaine (Marcaine)

Front 169

What concentration do you use with Bupivacaine (Marcaine) when using it for an epidural?

Back 169

<0.1%-0.5% depending on depth of anesthesia needed

Front 170

Which concentration of Bupivacaine (Marcaine) works for most people in keeping them comfortable (epidural)?

Back 170

0.1%

Front 171

What percentage % concentration of Bupivacaine (Marcaine) is no longer recommended due to its potential for cardiac toxicity?

Back 171

0.75%

Front 172

What is extremely important to remember regarding the injection of Bupivacaine (Marcaine)?

Back 172

INCREMENTAL injection is extremely important

Front 173

What's the brand name for Ropivacaine?

Back 173

Naropin

Front 174

What's the generic name for Naropin?

Back 174

Ropivacaine

Front 175

Is Ropivacaine (Naropin) an amide or an ester?

Back 175

Amide

Front 176

Ropivacaine (Naropin) is similar in structure to which 2 amide LAs?

Back 176

Bupivacaine (Marcaine) and Mepivacaine (Carbacaine)

Front 177

What are 4 uses for Ropivacaine (Naropin)?

Back 177

Epidural, Spinal, Peripheral Nerve Block, Brachial Plexus Block

Front 178

What is unique about Ropivacaine (Naropin) among the amides?

Back 178

causes vasoconstriction

Front 179

What's the brand name for Levobupivacaine?

Back 179

Chirocaine

Front 180

What's the generic name for Chirocaine?

Back 180

Levobupivacaine

Front 181

Is Levobupivacaine (Chirocaine) an ester or an amide LA?

Back 181

Amide

Front 182

How does Levobupivacaine (Chirocaine) relate to Bupivacaine (Marcaine)?

Back 182

It's the S(-) enantiomer of Bupivacaine

Front 183

Levobupivacaine (Chirocaine) is similar to Bupivacaine except has a slightly _____ duration.

Back 183

Longer

Front 184

Levobupivacaine (Chirocaine) is known to have decreased cardiac and CNS toxicity; why?

Back 184

Likely due to decreased affinity of Levobupivacaine for these tissues

Front 185

What is beneficial of both Ropivacaine (Naropin) and Levobupivacaine (Chirocaine)?

Back 185

both have decreased incidences of cardiac and CNS toxicity

Front 186

Potency of a given local anesthetic varies with ____; what is the significance of this fact?

Back 186

application; this may make certain drugs more appropriate for certain blocks

Front 187

Which LA do you use for infiltration anesthesia?

Back 187

Most LAs are effective

Front 188

What are the 2 most commonly used LAs for infiltration anesthesia?

Back 188

Lidocaine (xylocaine) and Bupivacaine (Marcaine)

Front 189

What concentration of Lidocaine (Xylocaine) do you typically use for infiltration anesthesia? What's the max DOSE?

Back 189

Typically 0.5-1%; Max DOSE=5 mg/kg; with epinephrine=7 mg/kg

Front 190

What's the concentration of Bupivacaine (Marcaine) used for infiltration anesthesia? What's the max DOSE?

Back 190

Typically 0.25-0.5%; Max DOSE= 2mg/kg; with epinephrine= 3mg/kg

Front 191

What can be added to infiltration anesthesia to reduce the burning on injection (particularly valuable in children)?

Back 191

Addition of Neutracaine (sodium bicarbonate)

Front 192

A plain 0.5-1% solution of Lidocaine has a duration of how long?

Back 192

30-60 minutes

Front 193

What's the max dose of Lidocaine (plain solution) in mg?

Back 193

300 mg

Front 194

An epinephrine-containing solution of Lidocaine (0.5-1%) has a duration of how long?

Back 194

120 minutes

Front 195

What's the max dose of Lidocaine (epinephrine-containing solution) in mg?

Back 195

500 mg

Front 196

Plain solution Bupivacaine (Marcaine) (0.25-0.5%) has a duration of action of how long?

Back 196

120-240 minutes

Front 197

What's the max dose of plain solution Bupivacaine (Marcaine) in mg?

Back 197

175 mg

Front 198

Epinephrine-containing solution of Bupivacaine (Marcaine) has a duration of action of how long?

Back 198

180 minutes

Front 199

What's the max dose of epinephrine-containing solution of Bupivocaine in mg?

Back 199

225 mg

Front 200

What is the most common LA used for a BIER Block?

Back 200

Lidocaine (xylocaine)

Front 201

Is Lidocaine given with or without Epinephrine when performing a BIER Block?

Back 201

Without Epinephrine

Front 202

When performing a BIER Block with Lidocaine (Xylocaine) what concentration and dosage do you use in an UPPER extremity?

Back 202

Concentration=0.5% solution;
Dosage=40-50ml

Front 203

When performing a BIER Block with Lidocaine (Xylocaine), what concentration and dosage do you use in a LOWER extremity (calf)?

Back 203

concentration=0.25% solution;
Dosage=50-100 ml

Front 204

Why do you not use ester LAs for a BIER Block?

Back 204

Potential for thrombophlebitis with the ester LAs

Front 205

What's considered a "minor" peripheral nerve block?

Back 205

blocking a single nerve

Front 206

What's considered "major" peripheral nerve blocks?

Back 206

Blocking 2 or more nerves or blocking a nerve plexus

Front 207

What determines which LA drug to use for a peripheral nerve block?

Back 207

Duration of block required

Front 208

For "single shot" epidural techniques, what is a very important consideration?

Back 208

Duration of action

Front 209

When using epidural CATHETER techniques, what are very important considerations?

Back 209

speed of onset of action, and characteristics of the block

Front 210

Which drug, when given with short and intermediate acting LAs, produces an increase in duration of action?

Back 210

Epinephrine

Front 211

Which drug, when used as epidural anesthesia, produces greater sensory than motor block at lower concentrations?

Back 211

Bupivacaine (Marcaine)

Front 212

Which drug decreases the effectiveness of concurrent or subsequent adminstration of Bupivacaine (Marcaine) or opioids via epidural?

Back 212

Chloroprocaine (Nesacaine)

Front 213

What are 3 considerations for Spinal anesthesia?

Back 213

Duration, Baricity and Toxicity

Front 214

Which is more reliable, hyperbaricity or hypobaricity?

Back 214

Hyperbaricity

Front 215

What are 3 uses of EMLA for topical anesthesia?

Back 215

IV starts, Skin grafting, Circumcision

Front 216

What are 4 indications of topical anesthesia of mucosal membranes?

Back 216

Bronchoscopy, Endoscopy, Nasal surgery, Intubation

Front 217

What does "tumescent anesthesia" include?

Back 217

Large volumes of dilute local anesthetic with epinephrine

Front 218

Which LA and concentration (%) is typically used for Tumescent anesthesia?

Back 218

Lidocaine--0.1% or less (dilute)

Front 219

What other drug is given with Lidocaine in Tumescent anesthesia? What concentration?

Back 219

Epinephrine--1:1,000,000

Front 220

What DOSE of Lidocaine (Xylocaine) do you administer with tumescent anesthesia?

Back 220

Up to 35-55 mg/kg

Front 221

Why does delayed absorption occur in tumescent anesthesia? What does this mean?

Back 221

Delayed absorption occurs because drug gets stored in the fat; peak blood levels at 11-15 hours after injection; prolonged analgesia of 18-24 hours in some patients

Front 222

What's tachyphylaxis?

Back 222

Decreased response to a repeated injection of the same dose

Front 223

True/False: If dosing intervals are short enough that pain doesn't recur, tachyphylaxis doesn't develop

Back 223

TRUE

Front 224

TRUE/FALSE: The longer the periods of pain allowed before redosing, the more slowly tachyphylaxis occurs

Back 224

FALSE; the more rapidly tachyphylaxis occurs

Front 225

What is thought to be the mechanism behind tachyphylaxis?

Back 225

thought to be due to a central mechanism, i.e. spinal cord sensitization

Front 226

Which ester LA is metabolized the fastest?

Back 226

Chloroprocaine (Nesacaine)

Front 227

Which ester LA is metabolized the slowest?

Back 227

Tetracaine (Pontocaine)

Front 228

How are ester LAs metabolized?

Back 228

hydrolysis of the ester bond by plasma cholinesterase

Front 229

How are amide LAs metabolized?

Back 229

Via enzymatic degradation in the Liver and by renal excretion of metabolites

Front 230

Because amide LAs are degraded in the Liver, what 4 things does this metabolism depend on?

Back 230

Hepatic extraction, Hepatic perfusion, Hepatic metabolism, and Protein Binding

Front 231

What's the initial step of liver metabolism of Amide LAs?

Back 231

Oxidative dealkylation

Front 232

What factors decrease clearance of Amide LAs?

Back 232

Hepatic dysfunction, PIH (Pregnancy-induced HTN), and presence of volatile anesthetics (decreases liver blood flow and therefore decreases metabolism)

Front 233

Pulmonary extraction of which 3 amide LAs limits the concentration reaching the systemic circulation?

Back 233

Lidocaine, Bupivacaine, and Prilocaine

Front 234

What does "Lung Extraction" do?

Back 234

Moderates the potential for systemic toxicity by reducing the amount reaching the cerebral and coronary vessels

Front 235

What drug inhibits Pulmonary Extraction?

Back 235

Propranolol

Front 236

Many people report _____ to local anesthetics

Back 236

Allergy

Front 237

Of the allergic reactions to LAs reported, fewer than ____% are true allergic reactions

Back 237

1%

Front 238

Which group of LAs, the esters or the amides, have the highest incidence of reported allergic reactions? Why?

Back 238

Esters; metabolism of esters results in compounds related to PABA

Front 239

Patients may experience allergic reactions from ______ in both amide and ester solutions

Back 239

preservatives

Front 240

What are 3 uses of EMLA for topical anesthesia?

Back 240

IV starts, Skin grafting, Circumcision

Front 241

What are 4 indications of topical anesthesia of mucosal membranes?

Back 241

Bronchoscopy, Endoscopy, Nasal surgery, Intubation

Front 242

What does "tumescent anesthesia" include?

Back 242

Large volumes of dilute local anesthetic with epinephrine

Front 243

Which LA and concentration (%) is typically used for Tumescent anesthesia?

Back 243

Lidocaine--0.1% or less (dilute)

Front 244

What other drug is given with Lidocaine in Tumescent anesthesia? What concentration?

Back 244

Epinephrine--1:1,000,000

Front 245

What are 3 uses of EMLA for topical anesthesia?

Back 245

IV starts, Skin grafting, Circumcision

Front 246

What are 4 indications of topical anesthesia of mucosal membranes?

Back 246

Bronchoscopy, Endoscopy, Nasal surgery, Intubation

Front 247

What does "tumescent anesthesia" include?

Back 247

Large volumes of dilute local anesthetic with epinephrine

Front 248

Which LA and concentration (%) is typically used for Tumescent anesthesia?

Back 248

Lidocaine--0.1% or less (dilute)

Front 249

What other drug is given with Lidocaine in Tumescent anesthesia? What concentration?

Back 249

Epinephrine--1:1,000,000

Front 250

Which drug, when given with short and intermediate acting LAs, produces an increase in duration of action?

Back 250

Epinephrine

Front 251

Which drug, when used as epidural anesthesia, produces greater sensory than motor block at lower concentrations?

Back 251

Bupivacaine (Marcaine)

Front 252

Which drug decreases the effectiveness of concurrent or subsequent adminstration of Bupivacaine (Marcaine) or opioids via epidural?

Back 252

Chloroprocaine (Nesacaine)

Front 253

What are 3 considerations for Spinal anesthesia?

Back 253

Duration, Baricity and Toxicity

Front 254

Which is more reliable, hyperbaricity or hypobaricity?

Back 254

Hyperbaricity

Front 255

What's considered a "minor" peripheral nerve block?

Back 255

blocking a single nerve

Front 256

What's considered "major" peripheral nerve blocks?

Back 256

Blocking 2 or more nerves or blocking a nerve plexus

Front 257

What determines which LA drug to use for a peripheral nerve block?

Back 257

Duration of block required

Front 258

For "single shot" epidural techniques, what is a very important consideration?

Back 258

Duration of action

Front 259

When using epidural CATHETER techniques, what are very important considerations?

Back 259

speed of onset of action, and characteristics of the block

Front 260

What's considered a "minor" peripheral nerve block?

Back 260

blocking a single nerve

Front 261

What's considered "major" peripheral nerve blocks?

Back 261

Blocking 2 or more nerves or blocking a nerve plexus

Front 262

What determines which LA drug to use for a peripheral nerve block?

Back 262

Duration of block required

Front 263

For "single shot" epidural techniques, what is a very important consideration?

Back 263

Duration of action

Front 264

When using epidural CATHETER techniques, what are very important considerations?

Back 264

speed of onset of action, and characteristics of the block

Front 265

What 5 things does ABSORPTION of LAs depend on?

Back 265

Vascularity of injection site, Fat content of injection site (slows absorption), Dose of Local Anesthetic, Physiochemical properties of the drug, and Presence of a vasoconstrictor

Front 266

How do they "Physiochemical Properties" of LAs effect their absorption?

Back 266

More potent agents have higher lipid solubility and protein binding resulting in less systemic absorption

Front 267

What 5 things does "ICEBS" stand for?

Back 267

I=intercostal; C=Caudal, E=Epidural, B=Brachial Plexus, S=Sciatic femoral

Front 268

What's the order of effect in regards to blood levels of LAs?

Back 268

ICEBS

Front 269

There's a new LA technique called "Liposomal Encapsulation;" What's the benefit of this technique?

Back 269

Slow, extended release; longer duration; reduced toxicity

Front 270

What mechanism causes LA neurotoxicity?

Back 270

Exposure to desheathed nerve to high concentrations of LA results in injury

Front 271

What is important to be mindful of in regards to LA injection and neurotoxicity?

Back 271

Be careful; do not inject LA into a site where parasthesias exist; back needle out

Front 272

Which is more prone to injury, peripheral nerves or spinal cord and nerve root?

Back 272

Spinal cord and nerve root

Front 273

What are the signs of LA neurotoxicity?

Back 273

Non-specific patchy numbness, Transient Neurologic Symptoms (TNS), and Cauda Equina Syndrome (it is unclear whether these are distinct entities or a spectrum of severity of the same underlying injury

Front 274

True/False: Permanent neurologic injury following regional anesthesia is a fairly common occurrence

Back 274

FALSE; it is an extremely RARE occurrence

Front 275

What are the Transient Neurologic Symptoms (TNS) after spinal anesthesia?

Back 275

Moderate to severe pain in the lower back, buttocks, and posterior thighs

Front 276

When do Transient Neurologic Symptoms (TNS) typically occur?

Back 276

Usually noted within 6-24 hours of resolution of the block (fairly quickly postop)

Front 277

When attempting to diagnose "Transient Neurologic Symptoms" is the sensory and motor exam normal or abnormal?

Back 277

NORMAL

Front 278

How long does it take to recover from Transient Neurologic Symptoms (TNS)?

Back 278

Full recovery typically within 1-7 days

Front 279

Since Transient Neurologic Symptoms (TNS) often require pain management in the interim (between onset and recovery), what types of pain management are used?

Back 279

NSAIDs, trigger point injections and Opioids

Front 280

Which LAs cause the highest incidence of Transient Neurologic Symptoms (TNS)?

Back 280

Incidence is highest following intrathecal (spinal and subarrachnoid) LIDOCAINE (Xylocaine) and Mepivacaine (Carbacaine)

Front 281

Does incidence of Transient Neurologic Symptoms (TNS)decrease by using a smaller concentration of LA?

Back 281

NO

Front 282

Usage of ______ in spinal anesthesia produces a higher incidence of Transient Neurologic Symptoms (TNS)

Back 282

spinal microcatheters

Front 283

Why is it proposed that spinal microcatheters possibly increase the incidence of Transient Neurologic Symptoms (TNS)?

Back 283

Possibly related to deposition of local in a small area without adequate mixing in CSF (not being rapidly washed away; increased concentration in a specific area over a prolonged time)

Front 284

Which "procedure" offers the lowest incidence of Transient Neurologic Symptoms (TNS)?

Back 284

C-section

Front 285

Which body positioning offers the highest incidence of Transient Neurologic Symptoms (TNS)?

Back 285

Highest incidence in Lithotomy and knee arthroscopy positions (due to increased amount of nerve stretch related to these positions)

Front 286

What are the main 3 etiologic factors in developing Transient Neurologic Symptoms (TNS)?

Back 286

Patient positioning, neural ischemia secondary to STRETCH, and Maldistribution of local anesthetic (pooling)

Front 287

What is "Cauda Equina Syndrome?"

Back 287

Diffuse injury across the Lumbosacral Plexus

Front 288

What are 3 undesirable effects from "Cauda Equina Syndrome?"

Back 288

Varying degrees of sensory loss, Bowel and bladder dysfunction and paraplegia

Front 289

What are other causes of "Cauda Equina Syndrome" other than LA administration?

Back 289

Trauma and Compression (hematoma, infection)

Front 290

Why is it important to rule out "Cauda Equina Syndrome" before instituting symptomatic treatment for "Transient Neuronal Syndrome (TNS)?"

Back 290

Don't want to mask with a bunch of Opioids and steroids in case it is an ischemic cord

Front 291

Above what concentration of Lidocaine (Xylocaine) do you get increased CNS effects?

Back 291

>5 mg/ml

Front 292

Do LAs readily cross the blood-brain barrier?

Back 292

YES

Front 293

Are LA CNS effects dose dependent?

Back 293

YES

Front 294

What CNS effects do low plasma concentrations of LAs cause?

Back 294

CNS depression

Front 295

What CNS effects do moderate to high plasma concentrations of LAs cause?

Back 295

CNS excitation, seizure activity

Front 296

What CNS effects do HIGH plasma concentrations of LAs cause?

Back 296

generalized CNS depression

Front 297

Potential for CNS toxicity ______ drug potency

Back 297

Parallels

Front 298

What factors cause an increased potential for CNS toxicity?

Back 298

Acidosis, Increased PCO2, decreased protein binding (more free drug available), decreased drug clearance, more rapid IV injection

Front 299

What 2 drug classes decrease the potential for CNS toxicity from LAs?

Back 299

Barbiturates and Benzos

Front 300

Potential for CNS toxicity varies with ___________.

Back 300

What type of block you're doing

Front 301

Which type of block appears to have the highest incidence of CNS toxicity?

Back 301

Peripheral nerve blocks (due to unintentional vascular injection)

Front 302

Cardiac toxicity from LAs generally require a higher or lower plasma concentration than CNS toxicity?

Back 302

HIGHER

Front 303

Potential for cardiac toxicity _____ anesthetic potency

Back 303

Parallels

Front 304

Higher potency, more lipid-soluble agents have a greater or smaller inherent cardiotoxicity?

Back 304

GREATER (increased affinity for Na+ channels)

Front 305

Which 3 LAs have a higher potency (lipid solubilty) and therefore higher risk for cardiotoxicity?

Back 305

Bupivacaine, Ropivacaine and Etidocaine

Front 306

When you increase doses of the LESS potent agents (e.g. Lidocaine), what 3 CV effects generally occur?

Back 306

Hypotension, Bradycardia, and Hypoxia

Front 307

What is really scary about the CV effects of the MORE potent agents (e.g. Bupivacaine)?

Back 307

The more potent agents more often result in SUDDEN cardiovascular collapse with ventricular dysrythmias which are resistant to resuscitation

Front 308

Lidocaine and Bupivacaine have equivalent effects on myocardial _______.

Back 308

contractility

Front 309

Bupivacaine has a much _____ affinity for resting and inactive sodium channels than Lidocaine

Back 309

HIGHER (it's more potent and more lipid soluble than Lidocaine)

Front 310

Bupivacaine dissociates much more _____ than Lidocaine during diastole such that sodium channels never completely recover, and conduction block by Bupivacaine accumulates

Back 310

SLOWLY

Front 311

Threshold for Bupivacaine induced cardiac toxicity is _____ in pregnancy

Back 311

REDUCED

Front 312

Which 3 cardiac drugs decrease the threshold for cardiac toxicity with LAs?

Back 312

Beta blockers, calcium channel blockers and Digoxin

Front 313

Which 2 drugs are approximately equipotent to Bupivacaine for plexus anesthesia and nerve block?

Back 313

Ropivacaine and Levobupivacaine

Front 314

Why is it that Ropivacaine and Levobupivacaine have less CNS and Cardiac toxicity?

Back 314

Preparation as single isomers may decrease affinity for brain and myocardium

Front 315

True/False: Local Anesthetic-Induced Cardiotoxicity is difficult to treat

Back 315

TRUE

Front 316

Prevention is important in preventing LA-induced cardiotoxicity; what are 2 important aspects of prevention?

Back 316

Careful assessment of appropriate dose and
Frequent aspiration=fractional injection

Front 317

What are 4 ways to treat Cardiotoxicity if it occurs?

Back 317

Maintenance of ventilation and oxygenation, pressure and rate support as necessary, management of ventricular dysrythmias, lipid therapy

Front 318

Why is management of ventricular dysrythmias problematic in cardiotoxicity?

Back 318

May be extended, may require large, and multiple doses of: Cardioversion, epinephrine, Vasopressin, and Amiodarone

Front 319

What drug is NOT indicated in treatment of ventricular dysrythmias in LA cardiotoxicity?

Back 319

Calcium channel blockers

Front 320

What's the concentration and dosing requirements of lipid therapy used for treating cardiotoxicity?

Back 320

20% lipid solution; bolus 4 ml/kg, followed by infusion of 0.5 ml/kg/min x 10 minutes