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Pharm Semester 2 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What is the other name for neuromuscular monitoring

A

Acceleromyography

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2
Q

most common location, nerve, and muscle monitored

A

abductor pollicis muscle, hand, ulnar nerve

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3
Q

NMBD Reversal Agents

A

edrophonium
neostigmine

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4
Q

Anti-Cholinergic Agents

A

atropine sulfate
glycopyrrolate

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5
Q

NMBD Reversal Agents MOA

A

AcetylcholineEsterase (AchE) Inhibitors, Cholinergic Agents, COMPETITIVE ANTAGONISTS

AchE: Rapid hydrolysis (catalyze) of Ach

Inhibition = more Acetylcholine available
Ach binds to alpha subunits;

Available @:
Preganglionic (SNS & PNS)
NMJ- main focus

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6
Q

Total max neostigmine dose

A

5mg

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7
Q

Neostigmine max range

A

40 to 70 mcg/kg

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8
Q

Edrophonium max range

A

1 mg/kg

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9
Q

NMBD Reversal Agents will not work with…..

A

Will not work with deep NM blockade
because of ceiling effect

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10
Q

Reversal of NM Blockade depends on 5 factors:

A
  1. Depth of the NM Block
  2. AchE Inhibitor choice
  3. Dose administered
  4. Rate of plasma clearance of NMBD
  5. Anesthesia agent choice and depth
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11
Q

What NMBD needs to be reconstituted w/ distilled water

A

Vec - reconsitiute w/ 10 ml to make 1 ml

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12
Q

Why is pancuronium given to cardiac patients?

A

INtrinsic effects on cardiac accelerators and good for the cardiac muscle

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13
Q

Goal of NMBD reversal agents

A

Prevent postoperative residual NM blockade

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14
Q

Sugammadex dose

A

2-16 mg/kg

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15
Q

Neostigmine onset

A

5-10 min

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16
Q

neostigmine duration

A

60 mins

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17
Q

Neostigmine anticholinergic

A

glycopyrrolate 0.2 mg/ml of neostigmine

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18
Q

Sugammadex onset

A

1-4 min

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19
Q

Sugammadex duration

A

1.5-3 hrs

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20
Q

sugammadex anticholinergic

A

none

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21
Q

Edrophonium onset

A

1-2 mins

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22
Q

Edrophonium duration

A

5-15 min

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23
Q

Pyridostigminge and edrophonium are excreted by how much renaly

A

75%

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24
Q

Overall side effects of NMBD reversal agents are a result from increased…..

A

Increased Nicotinic/Muscarinic Activity

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25
Q

How much neostigmine is excreted renaly

A

50%

30-50% hepatic if no renal function

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26
Q

CRF (chronic renal failure) does what to plasma clearance

A

decrease plasma clearance= prolonged action

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27
Q

Cardiac Side effect for nmbd reversal agents

A

Bradycardia, dysrhythmias, asystole, ↓SVR

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28
Q

Pulmonary Side effect for nmbd reversal agents

A

Bronchoconstriction, increased airway resistance, increased salivation

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29
Q

GI Side effect for nmbd reversal agents

A

Hyperperistalsis, enhanced gastric fluid secretion, PONV

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30
Q

Eyes Side effect for nmbd reversal agents

A

Miosis

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31
Q

Atropine side effect and matches….

A

side effects; mydriasis and initial tachycardia

matches profile of edrophonium

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32
Q

Atropine dose

A

7-10 mcg/kg

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33
Q

Glycopyrrolate matches the profile of….

A

Neostigmine and pyridostigmine

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34
Q

Glycopyrrolate dose

A

7-15 mcg/kg (1 mg max)

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35
Q

Anti-cholinergic/ anti muscarinic agents for cardiac disease

A

Glycopyrolate is preferred over atropine
to be administered slowly over 2-5 minutes

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36
Q

mechanism for persistent NM blockade

A

Acetylcholinesterase is maximally inhibited

No further anticholinesterase is effective

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37
Q

intervention for persistent nm blockade

A

sedation and postop ventilation

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38
Q

Sugammadex MOA

A

intermolecular (van der Walls) forces, thermodynamic (hydrogen) bonds, and hydrophobic interactions* -> reversal by encapsulation.
pull paralytic form nmj to the plasma
Binds to ‘free drug” in plasma**

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39
Q

Medications that sugammadex binds to

A

Rocuronium > Vecuronium&raquo_space; Pancuronium (least), best with ROC

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40
Q

Sugammadex E1/2

A

2 hrs

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41
Q

Sugammadex Major route of elimination:

A

Urine
70% in 6 hours
90% in 24 hours
Renal impairment: C/I with dialysis by dialysis

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42
Q

Sugammadex facts

A

Selective Relaxant-Binding Agent
γ-cyclodextrin
dextrose units from starch
Highly water soluble= mainly excreted in the kidney

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43
Q

drug that does not need binding with glycopyrolate / atropine

A

sugammadex

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44
Q

Deep block sugammadex dose

A

1-2 post-tetanic counts but not twitch response = 4mg/kg

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45
Q

moderate sugammadex dose

A

2/4 twitches = 2mg/kg

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46
Q

Where is the main site of action of sugammadex

A

plasma

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47
Q

Sugammadex Dose With extreme block:

A

no post tetanic stimulation = 8-16mg/kg

Recurarization: not observed at appropriate doses

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48
Q

Reparalzation with Roc after reversal with sugammadex

A

5 minutes

give 1.2mg/kg

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49
Q

Reparalyzation with ROC after reversal with neostigmine

A

4 hours wait then give 0.6 mg/kg roc or 0.1 mg/kg with vec

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50
Q

Sugammadex Cautions

A

-Oral Contraceptives; Binds with Progesterone (7 days)
-Toremifene (non-steroidal anti-estrogen). Displaces NMBD from Sugammadex
-Coagulation/Bleeding; Heparin/LMWH; Elevated PTT, PT, INR
-Recurarization; than recommended doses.

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51
Q

Sugammadex side effects

A

Dose related; n/v, pruritis, urticaria
anaphylaxis
marked bradycardia
doesn’t work

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52
Q

S&S of recurarization

A

-dec 02 sats
-unresponsive patient
-appears “floppy” or uncoordinated
-ineffective abdominal and intercostal activity
sometimes can verbalize: suffocating feeling
unable to sustain head lift or hand grasp
worst case: pharyngeal collapse and respiratory obstruction

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53
Q

The treatment goal for recurarization

A

Treat urgently and aggressively
Re-sedate the patient
Give additional reversal agents in divided doses (Neostigmine 0.05 mg/kg IV = longer duration of action).

give antimuscarinic agents; Ropinirole?

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54
Q

First local anesthetic

A

cocaine

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55
Q

Antiarrhythmic Drug Classes:
Class I

A

Sodium-channel blockers.

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56
Q

Antiarrhythmic Drug Classes:
Class 2

A

Beta blockers

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57
Q

Antiarrhythmic Drug Classes Class 3

A

potassium channel blockers

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58
Q

Antiarrhythmic Drug Classes Class 4

A

CCB

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59
Q

Cocaine MOA

A

cerebral stimulating qualities
localized vasoconstriction: shrink nasal mucosa

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60
Q

1st synthetic ester

A

procaine

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61
Q

The standard to which all other local anesthetics are compared.

A

lidocaine; the first synthetic amide

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62
Q

LA molecular structure

A

Has a lipophilic portion connected by a hydrocarbon chain to the hydrophilic portion.
Bond between lipophilic and hydrocarbon classifies LA as ester or amide

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63
Q

Lidocaine IV dose

A

1 to 2 mg/kg IV (initial bolus) over 2 - 4 min.
1 to 2 mg/kg/hour (drip)
terminated 12 - 72 hours
Careful monitoring: cardiac, hepatic, renal dysfunction

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64
Q

Ester or amide determination is based on which portion of the LA structure?

A

the link between the lipophilic aromatic and hydrocarbon intermediate chain

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65
Q

Ph for LA

A

pH 6 (HCl salt): Weak Bases

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66
Q

Composition of LA

A

Epinephrine
Sodium Bisulfite
weak bases

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67
Q

onset procaine

A

slow

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68
Q

onset chloropocaine

A

rapid

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69
Q

tetracaine onset

A

slow

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70
Q

amides onset

A

all are slow except lidocaine is rapid

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71
Q

Duration of infiltration procaine

A

45-60 min

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72
Q

Duration of infiltration chloroprocaine

A

30-45 min

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73
Q

Duration of infiltration tetracaine

A

60-180 min

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74
Q

Duration of infiltration of lidocaine

A

60-120 min

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75
Q

Duration of infiltration prilocaine

A

60-120 min

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76
Q

Duration of infiltration mepivacaine

A

90-180 min

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77
Q

Duration of infiltration bupivicaine

A

240-480 min

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78
Q

Duration of infiltration levobupivicaine

A

240-480 min

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79
Q

Duration of infiltration ropivacaine

A

240 - 480 min

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80
Q

Procaine potency

A

1

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81
Q

chloroprocaine potency

A

4

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82
Q

tetracaine potency

A

16

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83
Q

amides potency

A

1; lido, prolocaine, mepivacaine
4; bupivacaine, levobupivacaine, ropivacaine

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84
Q

procaine pK

A

8.9

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85
Q

chloroprocaine pk

A

8.7

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86
Q

Tetracaine pk

A

8.5

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87
Q

lidocaine pK

A

7.9

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88
Q

prilocaine pK

A

7.9

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89
Q

mepivacaine pK

A

7.6

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90
Q

Bupivacaine pK

A

8.1

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91
Q

levobuvicaine pk

A

8.1

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92
Q

probivacaine pK

A

8.1

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93
Q

procaine lipid solubility

A

0.6

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94
Q

Tetracaine lipid solubility

A

80

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95
Q

lidocaine lipid solbuility

A

2.9

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96
Q

Prilocaine lipid solubilty

A

0.9

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97
Q

mepivacaine lipid solubility

A

1

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98
Q

bupivacaine lipid solubility

A

28

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99
Q

The closer the meds pK is to physiologic ph……

A

closer to physiologic = faster the onset of action

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100
Q

Lidocaine, tetracaine, and bupivacaine
have what to help prolong the DOA

A

miltivesicular liposomes upload higher amount of LA into a molecule & have a consistent release of LA in the tissues
Prolonged duration of action & decreased toxicity.

pubivacaine ER; up to 96 hours

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101
Q

LA MOA

A

-Binds to voltage-gated Na+ channels
-Block/inhibit Na+ passage in nerve membranes
-Slowed rate of depolarization
-Does not reach threshold
-No action potential

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102
Q

LA form for lipid solubility

A

nonionized = crosses to inside of cell and block na gate.

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103
Q

factors affecting blockade:

A
  1. Lipid solubility or non-ionized/unionized form
  2. Repetitively stimulated nerve
  3. Diameter of the nerve
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104
Q

LA in an acidic environment

A

becomes ionized, when ionized = won’t go through cell membrane and won’t block na gated channel.

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105
Q

Other Site of Action Targets of LA

A

Potassium channels
Calcium Ion Channels
G protein-coupled receptors

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106
Q

What component of the LA is required for a conduction block

A

non- ionized form

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107
Q

Minimal effective concentration

A

At least 2, preferably 3 Nodes of Ranvier (1 cm) blocked = 1 MAC

to prevent the propagation from being interpreted by the sc/ brain

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108
Q

Fastest fibers

A

Preganglionic B fibers - sns

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109
Q

Myelinated fibers speed

A

Myelinated A (medium) and B fibers (faster) > Unmyelinated C fibers (small)

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110
Q

touch/pressure, proprioception, & motor fibers

A

unmyelinated C fibers

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111
Q

fibers used for Pain & Temperature

A

myelinated A-δ

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112
Q

Pregnancy with LA

A

increased sensitivity

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113
Q

Last features to be blocked

A

proprioception, & motor

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114
Q

Weak bases with pKa values above physiologic pH……

A

Only 50% in lipid-soluble nonionized form

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115
Q

pKa’s closest to physiologic pH =

A

most rapid OOA

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116
Q

Intrinsic vasodilator activity reflects its

A

potency and DOA

increased vasodilation= decreased potency and DOA

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117
Q

Factors that influence absorption

A

Site of injection
Dosage
Use of Epinephrine
Pharmacologic characteristics of the drug

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118
Q

Lowest to highest blood concentration

A

SubQ
Sciatic
Brachial
Epidural
Paracervical
Caudal
tracheal
Intracenous

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119
Q

Epi effects on DOA

A

prolonged duration of action by 1/3/ limits systemic absorption by 1/3

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120
Q

primary determinant of potency

A

Lipid solubility is the primary determinant of potency

rate of tissue distribution; moa

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121
Q

Rate of clearance dependent on

A

1) Cardiac output

2) Protein binding: % bound is inversely related to % plasma

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122
Q

Procaine protein binding

A

6%

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123
Q

tetracaine protein binding

A

76%

124
Q

Lidocaine protein binding

A

70%

125
Q

mepivacaine protein binding

A

77%

126
Q

Bupivacaine protein binding

A

95%

127
Q

Levobupivacaine protein binding

A

> 97%

128
Q

Ropivacaine protein binding

A

94%

129
Q

LA with the fastest metabolism

A

Procaine (lowest protein bound)

130
Q

LA with slowest metabolism

A

Bupivacaine, levobupivacaine, ropivacaine

131
Q

Amides metabolism

A

Microsomal enzymes in the liver

132
Q

amides most rapid metabolism

A

Prilocaine

133
Q

amides intermediate metabolism

A

: Lidocaine & Mepivacaine

134
Q

amides slowest metabolism

A

Etidocaine, Bupivacaine & Ropivacaine

135
Q

Esters metabolism

A

Hydrolysis by cholinesterase enzyme in plasma > liver (except with Cocaine: Liver)

136
Q

Ester metabolite

A

ParaAminoBenzoic acid (PABA) causes allergies

137
Q

Amides are____ metabolism than esters

A

slower

138
Q

meds with First-Pass Pulmonary Extraction

A

Lidocaine, bupivacaine (dose dependent), and prilocaine

139
Q

Renal Elimination and Clearance for LA

A

Poor water solubility
Unchanged drug in urine = 5%
Cocaine is 10 to 12%
PABA through urine

140
Q

The more lipid soluble the LA is, the greater is its potency; T/F

A

true

141
Q

which LA property is most important for DOA

A

Lipid solubility

142
Q

Pregnancy Lower levels of …..

A

plasma cholinesterases

143
Q

LA effect on pregnancy

A

Significant transplacental transfer
Amides, but not significant with Esters

Ion Trapping (fetus more acidic than maternal)

Protein binding = rate and degree of diffusion

144
Q

Lidocaine protein bound

A

70%

145
Q

Bupivacaine protein bound

A

95%

146
Q

Prilocaine protein binding

A

55%

147
Q

Treatment for LA toxicity for the fetus

A

naHCO3

148
Q

Bupivacaine arterial concentration

A

0.32

149
Q

Lidocaine arterial concentration

A

0.73

150
Q

Prilocaine arterial concentration

A

0.85

151
Q

Lidocaine Metabolism

A

Oxidative dealkylation in liver, then hydrolysis.

Hepatic disease will affect metabolism and elimination

152
Q

Lidocaine metabolite

A

Metabolite: Xylidide

153
Q

Lidocaine Maximum infiltration dose

A

300 mgs plain &

500 mgs /c EPI,

154
Q

Pregnancy Induced Hypertension (PIH) does what lidocaine?

A

Prolonged clearance

155
Q

Prilocaine metabolite

A

Orthotoluidine

156
Q

Prilocaine Converts Hemoglobin to Methemoglobin causing….

A

Methemoglobinemia; cyanosis because of decreased O2 carrying capacity.

tx with methylene Blue

157
Q

Methylene Blue dose for methemoglobinemia

A

1 to 2 mgs/kg IV over 5 mins
Total dose not to exceed 7 to 8 mg/kg

158
Q

prilocaine max dose

A

> 600 mg

159
Q

Mepivacaine compared to lido

A

Longer duration of action
Lacks vasodilator activity
Prolonged elimination in fetus & newborn; no OB

160
Q

Bupivacaine metabolism

A

aromatic hydroxylation, N-dealkylation, amide hydrolysis, and conjugation in the liver

161
Q

Bupivacaine protein binding site

A

α1-Acid glycoprotein

162
Q

Ropivacaine metabolism

A

Hepatic cytochrome P450 enzymes

163
Q

Ropivacaine metabolites

A

can accumulate with uremic patients
Lesser system toxicity than Bupivacaine

164
Q

Dibucaine metabolism

A

liver

165
Q

Dibucaine MOA

A

inhibits the activity of normal butyrylcholinesterase (plasma cholinesterase) by more than 70%

166
Q

Procaine metabolite

A

PABA, excreted unchanged in urine

167
Q

Chloroprocaine metabolism

A

Plasma cholinesterase (3.5x faster)

168
Q

Pregnancy decreases _____ by 40%

A

plasma cholinesterase

169
Q

Tetracaine metabolism

A

slower than procaine

170
Q

Hydrolysis meds compared

A

chloroprocaine > procaine > tetracaine

171
Q

Benzocaine pka

A

Weak acid (pKa 3.5)

172
Q

Benzocaine use

A

Topical anesthesia of mucous membranes:
Tracheal intubation, Endoscopy, Transesophageal echocardiography (TEE), Bronchoscopy

173
Q

Benzocaine DOA

A

30-60 min

rapid onset

174
Q

Benzocaine dose

A

Brief spray (20%) = 200 to 300 mgs

se; Methemoglobinemia

175
Q

Methylene Blue dose

A

1 to 2 mgs/kg IV over 5 mins
Total dose not to exceed 7 to 8 mg/kg over 24 hrs

176
Q

Cocaine metabolism

A

Ester, metabolized by liver cholinesterase/ acts like an amide.

177
Q

Cocaine metabolism is decreased in what groups?

A

Parturients, Neonates, Elderly, Severe Hepatic Disease

178
Q

Caution in using cocaine in what circumstances

A

Coronary vasospasm, ventricular dysrhythmias, HTN, tachycardia, CAD

179
Q

Cocaine peak

A

30 to 45 mins

180
Q

Cocaine Duration

A

60 minutes after peak

181
Q

Cocaine elimination

A

Urine (24 to 36 hours)

182
Q

Cocaine risks

A

Coronary vasospasm, ventricular dysrhythmias, HTN, tachycardia, CAD

183
Q

Treatment for Methemoglobinemia

A

Methylene Blue

184
Q

Average of PkA with LA’s

A

8

185
Q

weak base with high PKA

A

more inoized, less non ionized

186
Q

Function of alkalinization of LA solutions

A

alkalinization increases the % of lipid-soluble or non-ionized form

Benefits:
Faster onset of action
Peripheral and epidural blocks by 3 to 5 mins.
Enhances the depth
Increase the spread (i.e., epidural)

187
Q

LA are acids or bases?

A

weak bases but acidic in nature.

Base = name before element
acid = element before name

188
Q

weak base with low PKA

A

more non ionized, less ionized

189
Q

Demedetomidine with LAs

A

Increased duration of:
Both motor and sensory blocks
First analgesic request after spinal anesthesia

190
Q

LA’s with PK of 9.2

A

more ionized

191
Q

LA’s with PK of 7.5

A

more ionized

192
Q

Magnesium with LA’s

A

Increased duration with SAB /c or /s opioids.

193
Q

Clonodine and Ketamine with LA’s

A

Pediatric regional anesthesia prolonged duration.

194
Q

Dexamethasone with LA’s

A

Increased duration either IV or mixed with LA.

195
Q

Chloroprocaine & Bupivacaine (ester and amide) combined cause;

A

Produce a rapid onset
Tachyphylaxis

196
Q

To alkalinize La’s use….

A

8.4% Sodium Bicarbonate (1 mL only)
Added to 30 mL of LA

Can be used with; Chloroprocaine & Bupivacaine Combo

197
Q

Toxic effects of the combination of LA’s are additive or synergistic?

A

additive

198
Q

The duration of action of a LA sub q is proportional to……

A

The duration of action of a LA is proportional to the time the drug is in contact with nerve fibers.

199
Q

What does the LA with vasoconstrictors do?

A
  • Produce vasoconstriction
  • Increased neuronal uptake of LA- soaks nerve fibers
  • α-adrenergic effects may have some degree of analgesia- block transmission
  • No effect on onset rate of LA; depends on proximity to nerve fiber
  • Enhanced cardiac irritability with inhaled anesthetics; beta 1 effect tachycardia and htn.
    -Systemic absorption -> HTN/ tachycardia
200
Q

Epi dilution dose for Bupivacaine or Lidocaine SAB

A

0.2 mg

201
Q

Phenylephrine dilution dose for Bupivacaine or Lidocaine SAB

A

2 mg

202
Q

Your surgeon injected 20 mLs of Bupivacaine 0.25% with 1:200,000 of Epi.
What are the total mgs for Bupivacaine and the total mcgs for Epinephrine?

A

bupivicaine; 2.5 mg/ ml x 20 = 50 mgs
epi; 5 mcg/ml x 20 = 100 mcg

203
Q

0.25%

A

2.5mg/ml

204
Q

1;200,000 epi

A

1,000,000 / 200,000 = 5 mcg/ ml

205
Q

Local Anesthetics (LAs) use

A

Topical
Local Infiltration
Peripheral N. Block
Intravenous
Epidural
Spinal
Tumescent Liposuction

206
Q

Lidocaine max single dose

A

300 mg or 500 with epi

spinal; 100 mg

207
Q

Mepivacaine max single dose

A

400mg or 500 mg with epi

spinal; 100 mg

208
Q

Prilocaine max single dose

A

600 mg

209
Q

Bupivacaine max single dose

A

175 mg or 225mg with epi

spinal; 20 mg

210
Q

112.5 mg of bupivacaine with epi and 250 mg of lidocaine with epi. what are the percentages of each local anesthetic based on the recommended max single dose in mgs?

A

250/500 = 50%- lido
112.5/250 = 50% - bupivacaine

211
Q

Topical Anesthesia meds ranking

A

Cocaine (4% to 10%) > Tetracaine (1% to 2%), Lidocaine (2% to 4%)

212
Q

Why are procaine and chloroprocaine ineffective as topical anesthetics

A

they don’t penetrate the mucous membrane as effectively

213
Q

effects of lidocaine as an inhalation

A

Lidocaine: great with surface anesthesia
Inhalation does not alter airway resistance, but vasodilation

214
Q

LTA stands for

A

lidocaine, trachea, anesthesia.
Localized tracheal anesthesia
laryngeal tracheal anesthesia

215
Q

(EMLA)

A

Eutectic Mixture of LA (EMLA)
Lidocaine 2.5% and Prilocaine 2.5% = 5% LA

216
Q

ELMA dose

A

1 to 2 gms/ 10 cm2 area

217
Q

ELMA onset

A

45 minutes OOA
2 hours; Skin grafting
10 minutes; Cautery of genital warts, Venipuncture, lumbar puncture, Arterial cannulation (Nitroglycerine), Myringotomy

218
Q

Side effects to ELMA

A

Caution with methemoglobinemia (w/ systemic absorption)
Not recommended for skin wounds
C/I with amide allergies

219
Q

What is local infiltration

A

Extravascular placement of LA: Subcutaneous injection

220
Q

Inguinal operative site LA’s

A

Lidocaine 1% or 2%
Ropivacaine 0.25%
Bupivacaine 0.25%

221
Q

EPI is C/I when…..

A

Not intracutaneously or into tissues at end arteries
Fingers, toes, ears, nose, and penis
vasoconstriction- >ischemia ->necrosis

222
Q

Duration of LA by adding epi 1:200,000 is…..

A

doubled

223
Q

Peripheral Nerve Block achieved by…

A

Achieved by LA injection into tissues surrounding individual peripheral nerves or nerve plexuses.

224
Q

Peripheral never block MOA

A

diffusion from outer mantle to central core of nerve along a concentration gradient.

225
Q

PNB S/S

A

proximal affected first and then distal.

@End: proximal comes back first & then distal.

226
Q

PNB nerve fibers affected

A

Smallest sensory and ANS fibers first, and then larger motor and proprioceptive axons.

227
Q

Peripheral Nerve Block OOA, lidocaine and bupivacaine

A

Lidocaine: 3 minutes
Bupivacaine: 15 minutes

228
Q

PNB duration depends on……

A

dose of local anesthetic

(e.g., Bupivacaine with epi/fentanyl/clonidine = 12 to 18 hrs)

229
Q

Regional Bier Block

A

Ester or amide LA can be used
Mepivacaine > Lidocaine but don’t want long acting so you use lidocaine.

IV start
Exsanguination
Double cuff
LA injection through IV.
IV D/C

230
Q

Neuraxial

A

central component; affects spinal subarachnoid block or epidural component

231
Q

Segmental Block in Neuraxial Anesthesia

A
  1. SNS- myelinated preganglionic B fibers (fastest) (hr/bp)
  2. Sensory- Mylinated A and B fibers > unmyelinated C fibers
  3. Motor- Pain and temperature- myelinated A -delta and unmyelinated C fibers
232
Q

Neuraxial blockade is the last reference with which assessment parameter

A

leg movement

233
Q

what is a Spinal Anesthesia Block (SAB)

A

Produced by direct injection of LA into subarachnoid; (beyond the dura)
CSF is confirmation
Preganglionic fibers: Principal site of action

234
Q

The sensory effect is on same level of ….

A

Denervation

235
Q

SNS is _______ of sensory

A

SNS is 2 spinal segments cephalad of sensory

236
Q

Motor block is ________ sensory

A

Motor is 2 spinal segments below sensory

237
Q

cardiac accelerator

A

T1-T4

block = asystole

238
Q

if the assessed sensory level after SAB is at thoracic 6, what is the SNS level and motor block

A

T8 = motor
T4 = SNS

239
Q

SAB dose is based on

A

Height of patient (volume of subarachnoid space)
Segmental level of anesthesia desired
Duration of anesthesia desired

240
Q

Subarachnoid Block (SAB) dose

A

Dose is more important than the concentration of drug (%) or the volume (mLs) of the solution injection.

241
Q

Formula for SAB dose

A

5 ft = 1 mL of 0.75% Bupivacaine
+ 0.1 mL for every inch above…. 2 cc total ( lasts; 1½ hours to 2 hours)

242
Q

_________of LA is important in determining spread of the drug.

A

Specific gravity

243
Q

Hyperbaric

A

Hyperbaric (LA sp. gr. > CSF) with glucose is additive = drug sink

244
Q

Additive to increase the specific gravity of a LA

A

glucose / dextrose = makes drug sink

245
Q

Hypobaric

A

Hypobaric with distilled water as an additive then the drug will float

246
Q

Segmental block in spinal means what for the epidural

A

epidural anesthesia is more pronounced because it soaks the area around the sc.

247
Q

Epidural Most common LA used:

A

Lidocaine
Good diffusion through tissues & safer
Levobupivacaine and ropivacaine: less than bupivacaine, but still with cardiac and CNS toxicity

248
Q

Epidural Anesthesia onset

A

Onset: 15 to 30 minutes slow diffusion/delay

249
Q

Epidural Anesthesia delivery

A

Great with loading dose and then intermittent boluses

250
Q

Epidural Anesthesia with
OB Labor and C-sections:

A

cross placental barrier
Effect on fetus at 24 to 48 hours
Bupivacaine or Lidocaine will cross more

251
Q

Epidural vs SAB

A

No differential zone of SNS, sensory, and motor blockade
Large doses required

252
Q

Epidural + Opioids

A

Opioids are acceptable as additive to both Epidural & SAB -> synergistic

253
Q

Tumescent Liposuction

A

SQ infiltration of large volumes (5 L or more)
don’t give too much fluid because will fluid overload

254
Q

Tumescent Liposuction solution

A

Diluted Lidocaine (0.05% to 0.10%)
Epinephrine 1:100,000

255
Q

Tumesent liposuction works by

A

Causes taut stretching of overlying blanched skin d/t large volume and vasoconstriction -> tumescent (blockade)
-> Local anesthesia with bloodless aspirates & prolonged postoperative analgesia

256
Q

Tumescent Liposuction Plasma peak

A

is 12 to 14 hours s/p injection

257
Q

Tumescent liposuction is done where?

A

thigh, abdomen, hips, buttocks

258
Q

Tumescent Liposuction Dose

A

Regional Anesthesia Lidocaine with Epi: 7 mg/kg
Highly diluted Lidocaine with Epi Tumescent: 35 to 55 mg/kg

259
Q

_____ of SQ tissue can absorb up to ____ of Lidocaine

A

1 gm of SQ can absorb up to 1 mg of Lidocaine
(aka: Tissue Buffering System)

260
Q

Allergic reaction frequency with LA

A

Rare < 1%

261
Q

Allergic reactions attribute to

A

to manifestations of excess plasma levels

262
Q

Causes of allergic reactions with LA

A

Esters (PABA; preservative) > Amides

Methylparaben: preservative to both esters & amides. Similar in structure to PABA. Use preservative free

263
Q

Manifestations of Allergic reactions

A

Rash, urticaria, and laryngeal edema /c or /s hypotension & bronchospasm -> IgE anaphylaxis

264
Q

Testing for allergic reactions

A

Intradermal test using preservative free LA

265
Q

LAST stands for

A

LA systemic toxicity

266
Q

Causes of systemic toxicity

A

d/t excess plasma concentration of the drug

Entrance into the systemic circulation from inactive tissue redistribution and clearance metabolism

Accidental direct IV injection

meds, co-morbidites, technique of bloc, LA used, dose

267
Q

Magnitude of systemic absorption depends on:

A

-Dose
-Vascularity of site
-Epinephrine use (VC)
-Physicochemical properties

268
Q

Systemic Toxicity CNS effect

A

Drowsiness, facial twitch prior to seizure.

269
Q

What promotes sz with LA’s

A

Hyperkalemia promotes seizures w/ LAs.

lowers sz threshold

270
Q

Lidocaine @ _____ with circumoral numbness but not CV

A

5mcg/ ml

271
Q

High LA plasma concentration causes…..

A

block cardiac Na+ channels

Slow conduction of cardiac impulses -> prolonged PR interval & QRS widening

272
Q

Accidental IV Bupivacaine causes

A

Precipitous hypotension, AV block,

Cardiac dysrhythmias: SVTs, ST-Twave changes, PVCs, widening of QRS, V-tach

273
Q

Predisposing factors for systemic toxicity CV effects

A

-Pregnancy

-Arterial hypoxemia, acidosis, or hypercarbia (in animals)

-Beta blockers, Digitalis preparations, Ca+ Channel Blockers

-Epinephrine & Phenylephrine

274
Q

Medications that cause cv effects with systemic toxicity

A

Bupivacaine > Ropivacaine > Lidocaine

275
Q

What two factors predispose our OB population to local anesthetic toxicity

A

decreased plasma esteraces
decreases plasma proteins

276
Q

Goals of treatment of systemic toxicity

A
  1. Prompt airway management
  2. Circulatory support
  3. Removal of LA from receptor sites
277
Q

Treatment of LA CNS Toxicity

A

100% O2..inhibit hypoxemia and metabolic acidosis; NRB

Hyperventilation

Barbiturates

Benzodiazepines

Epinephrine as an additive

278
Q

treatment for sz with systemic toxicity from LA

A

Supplemental oxygen
Benzodiazepine (midazolam or diazepam)

Propofol: if hemodynamically stable

Muscle relaxant (succinylcholine or NMDA)

Intralipid: lipid emulsion

279
Q

MOA for intralipid- lipid emulsion

A

creates lipid compartment; provides for fat for myocardial metabolism

280
Q

Bolus of Lipid emulsion

A

Bolus: 1.5 mL/kg of 20% lipid emulsion

281
Q

Infusion dose of intralipid

A

Infusion: 0.25 mL/kg/minute for at least 10 minutes
1st 30 minutes: max = 3.8 mL/kg (1.2 to 6 mL/kg)

282
Q

EPI dose for systemic toxicity

A

10-100 mcg

283
Q

if no response to intralipid do…..

A

Cardiopulmonary Bypass (CPB)

284
Q

meds to not use in managing LA systemic toxicity

A

no vasopressin
no prop

285
Q

60 yo 120 lb female has the vs following bupivacaine 0.5% 20 mls through the epidural catheter; Hr 38, 70/35, 40, 92%. how much intralipid in mgs would you bolus?

A

1.5 mg x 54 kgs = 84 mls
20% = 200 mgs.
84 x 200 = 16800 mgs

286
Q

Neural Tissue Toxicity categories

A

Three Categories:
1. Transient Neurologic Symptoms
2. Cauda Equina Syndrome
3. Anterior Spinal Artery Syndrome

287
Q

Neural Tissue Toxicity cause either ________ neurologic injury

A

Either transient or permanent neurologic injury

288
Q

Transient Neurologic Symptoms (TNS) manifestations

A

Moderate to severe pain (lower back, buttocks & posterior thighs) within 6 to 36 hours after uneventful single-shot SAB.

289
Q

Treatment and recovery Transient Neurologic Symptoms (TNS)

A

Treatment: Trigger point injections and NSAIDs
Recovery: 1 to 7 days.

290
Q

Causes of TNS

A

Cause: Unknown
Lidocaine > other LAs; positioning?; addition of vasoconstrictor?

291
Q

Cauda Equina Syndrome (CES) is what?

A

Diffuse injury @ lumbosacral plexus -> varying degrees of sensory anesthesia, bowel & bladder sphincter dysfunction, & paraplegia

292
Q

Cauda Equina Syndrome (CES)
is associated with

A

large lumbar disc herniation, prolapse or

sequestration with urinary retention.

293
Q

what is Anterior Spinal Artery Syndrome

A

Lower extremity paresis with a variable sensory deficit.

294
Q

What causes Anterior Spinal Artery Syndrome

A

Cause: uncertain if its thrombosis or spasm of the bilateral anterior spinal artery

effects of HypoTN or vasoconstrictors drugs;
PVD,
spinal cord compression d/t epidural abscess or hematoma

295
Q

Methemoglobinemia due to….

A

Potentially life-threatening complication d/t decreased 02 carrying capacity (metHgb > 15%).

296
Q

medications that Cause Methemoglobinemia

A

Causes: Prilocaine, benzocaine > lidocaine, nitroglycerine, phenytoin, & sulfonamides

297
Q

treatment for Methemoglobinemia

A

Treatment: Methylene blue 1 mg/kg over 5 mins (max. 7 to 8 mg/kg)
Reversal from metHgb (Fe3+) to Hgb (Fe2+) is within 20 to 60 minutes

298
Q

Ventilatory Response to Hypoxia

A

Lidocaine depresses the ventilatory response to arterial hypoxemia
Susceptible patients: C02 retainers

299
Q

Causes of hepatotoxicity

A

Cause: continuous or intermittent epidural bupivacaine to treat postherpetic neuralgia.

Stop infusion ->normalizes liver transaminase enzymes

300
Q

What is the most common first intervention, when an adverse event is ID, if for the anesthesia provider to….

A

call for help

301
Q

MOA for cocaine toxicity

A

MOA: SNS stimulation by blocking presynaptic uptake of NE and dopamine -> increased postsynaptic levels

302
Q

Cocaine adverse effects

A

Adverse effects (lasts up to 6 weeks):
CV: HTN, tachycardia, coronary vasospasm, MI (infarction & ischemia), ventricular dysrhythmias (including Vfib).

Parturient: decreased UBF -> fetal hypoxemia

Hyperpyrexia -> seizures

303
Q

Cocaine associated cp treatment

A

asa, benzos
nitro, phentolamine

esmolol, beta blockers , sodium nitropurrisize

304
Q

What NMBD needs to be reconstituted w/ distilled water

A

Vec - reconsitiute w/ 10 ml to make 1 ml

305
Q

Sugammadex E1/2

A

2 hrs

306
Q

Additive to increase the specific gravity of a LA

A

glucose / dextrose = makes drug sink

Pharm Semester 2 (6 decks)

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