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Pharm > E4 > Flashcards

E4 Flashcards

1
Q

What is LTA

A

Laryngotracheal topical anesthetic

Comes in 4 mL of 4% Lidocaine

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2
Q

Which LA contributes to ventilatory response to hypoxia

A

Lidocaine

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3
Q

peripheral nerve effects at LA offset

A

Most distal/peripheral portion of block returns sensation FIRST
More central/proximal, return of sensation LAST

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4
Q

Which LA has highest incidence of cardio/neuro-toxic effects and why?

A

Bupivacaine

D/t high lipid solubility

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5
Q

Can LAs be used in combination for regional anesthesia, why?

A

YES

Because short-acting in conjunction w/ long-acting decreases onset and prolongs duration

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6
Q

Which LAs cross the placenta the greatest

A

prilocaine > lido > bupivacaine

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7
Q

Elimination 1/2 life for edrophonium, neostigmine, pyridostigmine
physostigmine

A

edrophonium-
neostigmine
pyridostigmine
Physostigmine

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8
Q

What is LA OOA dependent upon?

OOA of Lidocaine and bupivacaine

A

LA pKa
Lido = 3 min
bupiv = 15 min

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9
Q

Procaine metabolite and excretion

A

metabolite: PABA
excretion: unchanged in urine

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10
Q

What are side-effects when giving ACh-ases

A

D/T INC ACh in NMJ

There is INC nicotinic or muscarinic activity

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11
Q

Which nerve fiber stimulates SNS

A

Preganglionic B fibers

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12
Q

How are side effects blunted with the use of ACh-ases

A

By giving anti-cholinergic (anti-muscarinic) agents

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13
Q

Prilocaine metabolism. Effects of metabolite?

A

Metabolite: orthotoluidine

Converts hgb to methemoglobin

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14
Q

What is anterior spinal artery syndrome?

What may cause this?

A

Lower extremity paresis
Variable sensory deficit

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

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15
Q

Most CV toxic to least CV toxic agents

A

Bupivacaine > ropivacaine > lidocaine

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16
Q

Difference in neural tissue and systemic toxicity?

A

Neural tissue toxicity occurs at the neuron level of injection

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17
Q

What may the plasma lido concentration be if a pt has seizures and becomes unconscious

A

10-15 mcg/ml

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18
Q 
PRILOCAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 time-
A 
% Unionized 7.4/7.6 pHs- 24/33
Lipid solubility- 0.9
Vd- 191 L
Cl- 
E 1/2 time-96 min
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19
Q

What drug class should be avoided when treating cocaine induced MI?

A

Beta blockers

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20
Q

What is the onset for epidurals, use of vasoconstrictor and loading options

A

Onset = 15-30 minutes slow diffusion

Vasoconstrictor - epi has no advantage, consider absorption in venous outlets

Loading dose and intermittent boluses utilized

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21
Q

Which NMBD are most or least responsive to sugammadex

A

Rox > Vec&raquo_space; Panc

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22
Q

What is the corresponding plasma lido concentration when someone experiences tinnitus, systemic hypotension, circumoral numbness, twitching or myocardial depression

A

5-10 mcg/ml

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23
Q

Chemical composition of LAs

A

HCl salts
pH 6
because LAs are normally basic

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24
Q

Side effect of atropine

A

Tachycardia

Miosis

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25
Q 
MEPIVACAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 time-
A 
% Unionized 7.4/7.6 pHs- 39/50
Lipid solubility- 1
Vd- 84 L
Cl- 9.78 L/min
E 1/2 time- 114 min
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26
Q 
CHLOROPROCAINE
Classification-
Onset-
Duration-
MAX plain dose-
pK-
protein binding-
A 
Classification-ESTER
Onset-RAPID
Duration-30-45 min
MAX plain dose-600 mg
pK-8.7
protein binding
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27
Q

Tetracaine metabolism and comparison to other esters

A

metabolism: hydrolysis
Slower than procaine

chloroprocaine (fast) > procaine > tetracaine (slowest)

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28
Q

Renal excretion for neostigmine, pyridostigmine and edrophonium

A

Neostigmine = 50%

Pyridostigmine and edrophonium = 75%

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29
Q

Types of preparations of EMLA

A

Tetracaine 4% gel
Lidocaine 7%
Tetracaine 7%

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30
Q

Cocaine MOA/use as topical anesthetic

A

Localized vasoconstriction
Decreases blood loss
Improves surgical visualization
Nasal mucous membranes

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31
Q

Causes of hepatotoxicity when using LA?

What is the treatment?

A

Causes:
continuous or intermittent epidural bupivacaine to treat postherpetic neuralgia

Treatment:

  • stop infusion
  • normalize liver transaminase enzymes
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32
Q

How does pregnancy effect LAs. How is this incorporated in the plan of care?

A

DEC level of plasma ch-ase

avoid or decrease ester dose

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33
Q

LA effects in pregnancy and feturs

A

-Significant transplacental transfer (amides > esters)
-Ion trapping
(maternal pH [union]> fetal[ion])

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34
Q

Most common anesthetics used for SAB

A 
Tetracaine
Lidocaine
Bupivacaine
Ropivacaine
levobupivacaine
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35
Q

CV effect of vasoconstrictors w/ LA

A

Enhanced cardiac irritability especially w/ inhaled anesthetics

Systemic absorption can lead to HTN

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36
Q

Importance of alpha-adrenergic effects from LA-vasoconstrictor?

A

a-adrenergic effects may have some analgesic ability

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37
Q

What type of block is produced w/ Bier block

A

BOTH motor and sensation block

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38
Q

Foal for treatment of LA systemic toxicity

A

Prompt airway management
Circulatory support
Remove LA from receptors

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39
Q

Spinal anesthesia block is

A

Direct injection of LA into SA

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40
Q

How are the vasodilatory effects of LAs blunted?

A

Addition vasoconstrictor (epi, neo) to LA

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41
Q

How does enantiomerism affect the action of bupivacaine, levobupivacaine, and ropivacaine

A

Bupivacaine is racemic mixture and more neuro/cardio-toxic

Levobupivacaine/ropivacaine are (R) left-handed enantiomers and are less neuro/cardio-toxic

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42
Q

What are other etiologies that may cause anterior spinal artery syndrome?

A
  • effects of HToN or vasoconstrictors drugs
  • PVD
  • SC compression d/t epidural abscess or hematoma
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43
Q

Where is the epidural space

A

Between the dura and spinal cord

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44
Q

LA MOA

A
  • Binds to VG-Na channels
  • Blocks Na+ passage in post-synaptic nerve
  • Slows rate of depolarization, unable to reach threshold potential
  • NO propagation fo AP
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45
Q

Neuromuscular monitoring AKA and most common monitoring technique

A

Acceleromyography

Train-of-four

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46
Q

How does pK to pH level affect LA pharmacokinetics and why? Effects on action?

A

pK closest to physiologic pH
Most Rapid OOA
b/c most nonionized form

Ionized LA won’t pass through channel and block it

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47
Q

Where does the LA bind on the VG-Na channel

A

On the inner gate

aka H-gate

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48
Q 
Cocaine 
Metabolism
Duration
Populations to avoid use
Elimination
A

Metabolism: liver > plasma Ch-ase
DOA: 60 min post peak
Populations: fetal, parturients, elderly, hepatic Dx
Elimination: Urine (24-36 hrs)

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49
Q

pK of LAs and % ionization

A

Weak bases
Above physiologic pH
Only 50% in lipid-soluble nonionized form

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50
Q

Purpose of local infiltration w/ LA
Duration alterations
C/Is

A

Purpose:
Extravascular LA in SQ injection

Duration alterations:
DOUBLE DOA w/ Epi 1:200,000

C/I:
w/ Epi NO
fingers, toes, ears, nose or penis

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51
Q

Benefits of additives to epidurals/SABs?

A

Opioids are beneficial for pain control w/ synergistic effects

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52
Q

Purpose of magnesium as adjunct w/ LAs

A

INC duratin of SAB w/ or w/o opioids

d/t small muscle relaxation

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53
Q

How are beta-blockers/dig/CCBs and epi/phenyleph a predisposing factor to LA toxicity

A

B-blockers/Dig/CCB:
Alters conduction

Epi/phenyleph:
IV use to treat CV effects can compound CV issues

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54
Q

Molecular structure of LAs and difference in classifications

A

1) lipophilic portion (aromatic) connected by
2) hydrocarbon chain to the
3) hydrophilic portion (quaternary amide)

Bond between (1) & (2) classifies it as ester or amide

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55
Q 
LEVOBUPIVICAINE
Classification-
Onset-
Duration-
MAX plain dose-
pK-
protein binding-
A 
Classification-AMID
Onset-SLOW
Duration-240-480 min
MAX plain dose-175 mg
pK-8.1
protein binding->97%
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56
Q 
LIDOCAINE
Classification-
Onset-
Duration-
MAX plain dose-
pK-
protein binding-
A 
Classification-AMIDE
Onset-RAPID
Duration-60-120
MAX plain dose-300 mg
pK-7.9
protein binding-70%
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57
Q

How does location affect the possibility of systemic toxicity

A

Highest blood concentration

IV
Tracheal
Caudal
Paracervical
Epidural 
Brachial
Sciatic
SQ

Lower blood concentration

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58
Q 
BUPIVACAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 time-
A 
% Unionized 7.4/7.6 pHs- 17/24
Lipid solubility- 28
Vd- 73 L
Cl- 0.47 L/min
E 1/2 time- 210 min
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59
Q

What is dosing of SAB based on?

A

Height of patient determines volume of SA space

Segmental level of anesthesia desired
Duration of anesthesia needed

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60
Q

LA of choice for Bier block

A

Esters or amides

Most common = lido

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61
Q

Which NMB does not have the risk of recurarization

A

Suggamadex

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62
Q

Importance of 100% O2 in the treatment of LA toxicity

A

To inhibit hypoxemia and metabolic acidosis

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63
Q

At what levels are SNS and motor block with SAB

A

SNS = 2 spinal segments cephalad of sensory

Motor = 2 spinal segments below sensory

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64
Q

What is the ventilatory response to hypoxia when LA agents are in use?
Which pts are susceptible to this problem?

A

Lidocaine depresses the ventilatory response to arterial hypoxemia

CO2 retainers are most susceptible

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65
Q

Most common technique when monitoring for twitches?

A

Train-of-four

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66
Q

What are associated issues of cauda equina syndrome?

What is the cause of CES?

A

Associated
• large lumbar disc herniation
• prolapse or sequestration w/ urinary retention.

Cause:
unknown

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67
Q

What can hyperpyrexia lead to in the cocaine toxic patients?

A

Seizures

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68
Q

Describe difference in dosing and blockade of epidural vs SAB

A

For epidural
There is no differential zone of SNS, sensory and motor blockade

Generally block is at the same level

Dosing = epidural is much greater volume/dosing

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69
Q

How does specific gravity affect LA action

A

Determines the spread of drug

solute concentration of LA compared to CSF

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70
Q

Sugammadex dosing for all block types

A

Moderate (TOF 2 twitches) = 2 mg/kg

Deep (1-2 PT and NO TOF twitch) = 4 mg/kg

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71
Q

How do vasoconstrictors affect LA DOA in relation to nerve fivers?

A

Prolongs duration of contact w/ nerve fiber by decreasing systemic absorption

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72
Q

What determines the rate of clearance of LAs

A 
CO
Protein binding (% bound inversely r/t % plasma)
-more bound = longer clearance?
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73
Q

significance of liposomes in LA use

A

They are used to upload higher amount of LA into molecule

Then have a consistent release of LA in tissue

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74
Q

Where is tumescent infiltration used

A

Thigh
abdomen
hips
buttocks

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75
Q

Duration of action of LA is proportional to what?

A

The amount of time the drug is in contact with nerve fiber

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76
Q

Order of “speed” based on nerve type

A

B fibers (fastest) > A fibers > C unmyelinated fibers (small/slow)

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77
Q

Sugammadex side-effects

A

anaphylaxis
marked bradycardia
doesn’t work

Dose-realted:
N/V
pruritis
urticaria

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78
Q

Which ester LA is not metabolized by plasma cholinesterases

A

Cocaine

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79
Q

What can occur with an SNS block from SAB at the level of T4. What drugs are CI? What drugs are used for treatment?

A

Can knock out cardiac accelerator nerve function leading to bradycardia or asystole

CI drugs = ephedrine, antimuscarinics (atropine, glycopyrolate)

Treatment= beta-1 agonist like epinephrine

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80
Q

What is the MOA of NMBD reversal agents

A
  • Acetylchoinesterase inhibitors
  • Prevents hydrolysis of of ACh in the NMJ
  • INC ACh concentration in NMJ
  • Out-competes ND-NMBD displacing drugs from a-subunit of ACh-Rs
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81
Q

Alkalinization enhances depth of block, what is the drawback to that?

A

This can shorten the duration of action

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82
Q

Affect of infection on LA action

A

Local infection pH ionizes LA and it won’t work

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83
Q

Purpose of clonidine/ketamine in conjunction w/ LAs

A

Prolong duration in peds

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84
Q

Mcg of epi
• 1:200,000
• 1:500,000
1:10,000

What is more concentrated

A
  • 1:200,000 (1,000,000/200,000) = 5 mcg/ml
  • 1:500,000 (1,000,000/500,000) = 2 mcg/ml

1:10,000
(1,000,000/10,000) = 100 mcg/ml

most concentrated 1:10,000

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85
Q

Lidocaine Metabolism. Metabolite? Hepatic effects?

A

Metabolism: oxidative dealkylation in liver THEN hydrolysis

Metabolite: Xylidide

Hepatic Dx: will affect metabolism and elimination
-Give less

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86
Q

What is the elimination 1/2 time and major route/time of elimination of sugammadex

A

E 1/2 time = 2 hrs
Route = URINE
6 hrs = 70%
24 hrs = 90%

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87
Q

Anti-cholinergic dose of atropine and glycopyrolate in conjunction w/ NMBD reversal

A 
Atropine = 7-10 mcg/kg
Glycopyrolate = 7 - 15 mcg/kg
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88
Q

What is the MOA of cocaine toxicity?

A

SNS stimulation by blocking presynaptic uptake of NE and dopamine
• HIGH postsynaptic levels

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89
Q

PNB MOA and S/Sx

A

MOA:
diffusion (NOT osmosis) from outer mantle to central core of nerve along a concentration gradient

S/Sx:
peripheral affected FIRST
THEN central second

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90
Q

CV effects with accidental IV bupivacaine

A

Precipitous hypotension, AV block

Cardiac dysrhythmias
SVTs, ST-T wave changes
PVCs, widening of QRS, V-tach

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91
Q

Ester metabolism

A

Hydrolysis by cholinesterase enzymes in the plasma
Plasma metab > liver
Metabolize faster than amides

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92
Q

Bier block process

A 
	IV start
	Exsanguination
	Double cuff
	LA injection
	IV D/C
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93
Q

Liposome duration of bupiviacaine ER

A

DOA up to 96 hrs

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94
Q

Baillard follow-up study on vec w/ reversal results

A

Postop residual NM blockade 4%

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95
Q

Sugammadex dose for deep NMB

A

8-16 mg/kg

effective even w/o twitches

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96
Q

By what percent can epinephrine mixed w/ LA decrease systemic absorption

A

33.33%

1/3

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97
Q

Lidocaine
uses
Max plain dose
Clearance

A

Uses: anti-dysrhythmic
MAX dose: 300 mgs
Clr: prolonged w/ PIH

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98
Q

Effects of vasoconstrictor use in combo w/ LAs

A 
Vasoconstriction
INC neuronal uptake of LA
alpha-adrenergic effects
No change to onset of LA
Prolong duration
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99
Q

What is EMLA cream?
LA used?
Dosing?

A

Eutectic mixture of LA

LA:
Lidocaine 2.5% and Prilocaine 2.5% - 5% LA total

Dose:
1 to 2 gms/cm2 area

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100
Q

Amide metabolism

A

Microsomal enzymes in the liver
Fastest to slowest metab
Prilocaine > lido/mepiv > etido/bupiva/ropivacaine

Metabolize slower than esters

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101
Q 
PROCAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 ytime-
A 
% Unionized 7.4/7.6 pHs- 3/5
Lipid solubility- 0.6
Vd- 65 L
Cl- 
E 1/2 time- 9 min
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102
Q

Classification of NMBD reversal agents

A

aka-ACh-ase
aka-Cholinergic agents
aka-Competitive antagonist

103
Q

Bupivacaine metabolism, and protein binding

A

Metabolism: LIVER
aromatic hydroxylation, N-dealkylation, amide hydrolysis, and conjugation

Protein binding site
α1-Acid glycoprotein

104
Q

Prilocaine
Toxic dose
S/Sx
Treatment

A

Toxic dose: >600 mg

s/sx: cyanosis d/t DEC O2 carrying capacity

Tx: Methylene blue

105
Q

Use of epidurals in OB and CS
Placenta and fetal effects?
How is that affected by lipid solubility, onset, and protein binding capacity?

A

LA crosses placental barrier when absorbed systemically

Fetus - effects for 24 -48 hrs

Solibility = lido > bupiv
onset = lido < bupiv
higher protein binding = lido < bupiv

106
Q

When is the best time to check for baseline twitch

A

Before NMBD given

107
Q

How are nerves identified for PNB

A
  • Nerve stimulator
  • mA 0.1-1
  • Pinpoint needles
  • Ultrasound guided
  • In plane vs out-of-plane
108
Q 
PROCAINE
Classification
Onset
Duration
MAX plain dose
pK
protein binding
A 
Classification-ESTER
Onset-SLOW
Duration-45-60 min
MAX plain dose: 500 mg
pK: 8.9
protein binding: 6%
109
Q

When full CV depression occurs following LA use, what is the plasma lido concentration likely at?

A

> 25 mcg/ml

110
Q

Which nerve fiber stimulates pain and temperature, proprioception etc

A

Myelinated A-delta

Unmyelinated C fibers

111
Q

Treatment for CNS toxicity from LAs (5)

A 
100% O2
Hyperventilation
Barbiturates
Benzodiazepines
Epi as additive
112
Q

Do vasoconstrictors affect the OOA w/ LAs

A

No effect on OOA

113
Q

What is tumescent liposuction? What agent and dosing is used?

A 
SQ infiltration of large volumes-->5 L or more
Solution:
	LR base fluid
	Diluted Lidocaine  = 0.05% to 0.10%
	Epinephrine 1:100,000 (10 mcg/ml)
114
Q

Importance of un/ionization of LAs. What is this based on?

A

Unionized passes through VG-Na channel
Becomes ionized once it passes through and blocks channel

Based on the LA pK compared to physiologic pH

115
Q

Anti-cholinergic administration considerations in CV pts

A

Glycopyrolate preferred

Administer slowly: over 2-4 min

116
Q

What is the treatment and recovery time for transient neurologic symptoms?

A

Treatment:
• Trigger point injections and NSAIDs

Recovery:
• 1 to 7 days.

117
Q

Mg dose of epinephrine or phenylephrine when mixed with LA

A 
Epi = 0.2 mg
Phenylephrine = 2 mg
118
Q

Problem w/ combination of chlorprocaine and bupivacaine? Due to?

A

Problem:
Tachyphylaxis
The addition chlorprocaine can possibly reduce sensitivity to following doses
Lessened effect on following doses

Due to:
Desensitized receptors

119
Q

Order of nerve effects w/ PNB

A

FIRST - Smallest sensory and ANS fibers

SECOND/LAST - Large motor and proprioceptive axons

120
Q

Sugammadex structure and physical properties

A

Structure = y-cyclodextin
Dextrose units from starch
Highly H2O soluble

121
Q

LA Systemic toxicity management for seizures (5)

A
  • Supplemental O2
  • Benzodiazepine = midazolam or diazepam
  • Propofol = if hemodynamically stable
  • Muscle relaxant = SCh or NMDA
  • Intralipid = lipid emulsion
122
Q

What effect does dilution have on tumescent dosing?

Theory of tumescent LA absorption and name?

A

B/c anesthetic is highly diluted lido/epi can go up to 35-55 mg/kg

Tissue buffering system
Theory = 1 gm SQ can absorb 1 gm of lido

123
Q

Purpose of dexmedetomidine in conjunction w/ LAs

A

IV dex INC duration of motor and sensory block

Inc duration of time before 1st analgesic requested following spinal anesthesia

124
Q

Lidocaine use as topical anesthetic

A

Use:
Surface anesthetic
Inhaled anesthetic (doesn’t change airway resistance BUT does vasodilate)

125
Q

When is the best time to check for twitches?

A

Baseline

Before giving NMBD

126
Q

What is ACh-ase purpose in NMBD use?

A

Rapid hydrolysis of ACh
Inhibition = MORE ACh available
INC amounts of ACh out-competes NMBD and displaces them from alpha-subunit of ACh-R

127
Q

Which anti-cholinergic may be contraindicated in CV disease? Which agent should be used?

A

Atropine d/t tachycardia

Glycopyrolate preferred

128
Q

What medication in conjunction w/ EMLA can aid in arterial cannulation?

A

NTG
Can decrease pain?
Vasodilate vessel for better cannulation

129
Q

Types/Locations of PNB

A
  • Interscalene = shoulder
  • Axillary = lower arm
  • Femoral = Upper leg/knee
  • Sciatic = back of knee/lower leg
130
Q 
LIDOCAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 time-
A 
% Unionized 7.4/7.6 pHs- 25/33
Lipid solubility- 2.9
Vd- 91 L
Cl- 0.95 L/min
E 1/2 time- 96 min
131
Q

Locations of topical anesthetic use

A

Mucous membranes
Nose, mouth, tracheobronchial tree
esophagus or GU tract

132
Q

What are the 2 alterations of specific gravity for LAs and purpose?
Compare to CSF?
What is used?

A

Hyperbaric, so LA “sinks”
LA sp gr > CSF
5% glucose additive

Hypobaric, so LA “floats”
LA sp gr < CSF
Distilled water

133
Q

What are 4 things that systemic absorption depends on

A
  • Dose
  • Vascularity of site
  • Epinephrine use
  • Physicochemical properties (pKa)
134
Q

Treatment for cocaine associated CP

A

IV NTG (NO donors)

135
Q

What are the 3 categories of neural tissue toxicity

A

Transient neurologic symptoms
Cauda equina syndrome
Anterior spinal artery syndrome

136
Q

Cautions when administering sugammadex

A

Back up contraception for 7 days if on BCP
-binds to progesterone
Toremifene
-Non-steroidal anti-estrogen that displaces NMBD from sugammadex
Coagulopathy/bleeding
-Heaprin/LMWH = INC aPTT, PT, INR

137
Q

Why are LAs w/ epi c/i in digital appendages

A

C/i
fingers, toes, ears, nose, penis

Vasoconstriction -> ischemia -> necrosis

138
Q

Significance of nodes of ranvier when using LAs

A

Must cover at least, preferably 3 nodes
Equal to 1 cm
So that AP can’t skip nodes

139
Q

Side-effects of vasoconstrictor use in combo w/ LAs

A

Enhanced cardiac irritability

Systemic absorption

140
Q

CV effects of LA toxicity are due to what occurring?

How does this affect conduction?

A

High plasma concentrations that block cardiac Na+ channels

  • Slows conduction of cardiac impulses
  • prolonged PR interval & QRS widening
141
Q

In conjunction w/ LAs this electrolyte can promote szs

A

Hyperkalemia

142
Q

EMLA readiness

Altered time frame

A

45 min OOA

10 mins in setting of
genital wart cautery
veni/lumbar puncture
Art line w/ NTG
Myringotomy
143
Q 
TETRACAINE
Classification-
Onset-
Duration-
MAX plain dose-
pK-
protein binding-
A 
Classification-ESTER
Onset-SLOW
Duration-60-180 min
MAX plain dose-100 (topical)
pK-8.5
protein binding-76%
144
Q

Pulm side effects of ACh-ases

A

Bronchoconstriction
INC airway resistance
INC salivation

145
Q

Epinephrine IV dose in the presence of LA toxicity, following lipid emulsion?

A

10 - 100 mcg

146
Q

Ropivacaine metabolism, metabolites, altered effects and protein binding

A

Metabolism: hepatic P450
Metabolite: Accumulate in uremic pts

effects: less toxicity

Protein binding: a1-acid glycoprotein

147
Q

When reversing NMBD, which agent is given first?

A

Anticholinergic FIRST

THEN anticholinesterase

148
Q

What drug class is sugammadex

A

Selective relaxant-binding agent

To non-depolarizing NMBD

149
Q

Most common nerve monitored

A

Ulnar nerve

150
Q

Reversal drugs that are not anti-cholinergics? Which drugs do they work with?

A 
Purified human plasma cholinesterase
-Mivacurium
Cysteine
-Gantacurium
Sugammadex
-Selective binding w/ aminosteroids non-depolarizing NMBD
151
Q

Cocaine cautions when using as LA

A 
Coronary vasospasm
•Causes vascoconstriction
ventricular dysrhythmias
HTN
Tachycardia
CAD
152
Q

What is the most important factor of dosing of SAB

A

Dose is more important than concentration of drug(%) or volume (mls) of injection

153
Q

5 uses of LAs

A 
Treat dysrythmias
Analgesia
ANS blockade
Sensory block
Motor block-skeletal muscle paralysis
154
Q

What is the product of tumescent infiltration?

Effects?

A

Product:
Causes taut stretching of overlying blanched skin d/t large volume & vasoconstriction

Effects
 Local anesthesia with bloodless aspirates
•prolonged postoperative analgesia

155
Q

Dibucaine metabolism, MOA and use

A
  • Metabolism: hepatic
  • MOA: inhibits activity of plasma cholinesterases by >70%

Use: to test for atypical cholinesterase issues

156
Q 
Benzocaine
Use
pK
OOA
DOA
Dose/MAX
Adverse effects
A

Use-topical anesthesia of mucous membrances
(endo, intub, TEEs)

pK: 3.5 (weak acid)
OOA: rapid
DOA: 30-60 min
Dose/MAX: 20%/200-300 mgs
Adverse: methemoglobinemia
157
Q

How are LA systemic absorption limited?

A

By the use of vasoconstrictors which keep the LA LOCAL

By keeping drug concentration in the vicinity of nerve fiber

158
Q

What action of the LAs affect the potency and DOA. Why?

A

Intrinsic vasodilator activity

Vasodilation INC systemic absorption DECreasing local effects of anesthetic thus decreasing the DOA

159
Q

How long can cocaine toxicity effects last

A

Up to 6 weeks

160
Q

How does sugammadex work in NMBD reversal

A 
Binds to free drug in plasma
Uses intermolecular (vdW) forces for a very tight reversal
161
Q

Problem with LA preservatives and allergic reactions.

What cautions should be taken?

A

Methylparaben is similar in structure to PABA
It is used in both esters and amides

Cautions take
Use preservative free LA for methylparaben allergy

162
Q

How does protein binding alter LA in parturient

A
  • INC protein binding
  • determine rate and degree of diffusion
  • DEC concentration and diffusion
  • LESS LA crosses the placenta
163
Q

When is EMLA cream C/I

A

Amide allergy

Not for skin wounds

164
Q

4 Adjuvants w/ LAs

A

Dexmedetomadine
Magnesium
Clonidine/Ketamine
Dexamethasone

165
Q

Which reversal agent can be used when no twitches are present on deep NMB

A

Suggamadex

166
Q

Neuromuscular monitoring a.k.a.

A

acceleromyography

167
Q

CNS effects of LA systemic toxicity

A

Drowsiness, facial twitch before sz

168
Q 
What effects correspond to the following plasma lido concentrations?
1-5
5-10
10-15
15-25
>25
A

1-5:
Analgesia

5-10:
Circumoral numbness, tinnitus
skeletal muscle twitching
systemic hypotension, myocard depression
10-15:
Sz, unconsciousness

15-25:
Apnea, coma

> 25:
CV depression

169
Q

NMBD (roc or vec) re-administration after sugammadex administration

A

5 min = 1.2 mg/kg roc
4 hrs = 0.6 mg/kg roc or 0.1 mg/kg vec
Use nonsteroidal NMBD

170
Q

Use of IV regional anesthesia

A

Total extremity anesthesia

Produces sensation and motor block

171
Q

What are transient neurologic symptoms r/t neural toxicity?

What can cause this?

A

TNS:

  • Moderate to severe pain
  • lower back, buttocks & posterior things
  • Occurs W/in 6 to 36 hrs s/p single-shot SAB
Causes:
1-Unknown
2-Lidocaine > other Las
3-positioning?
4-addition of vasoconstrictor?
172
Q

What is the alkalinizing agent used w/ LAs?

Dose/Ratio?

A

8.4% sodium bicarbonate
1 mL

Dose/Ratio:
1 mL NaHCO3 + 30 mL LA

173
Q

Baillard et al initial study on vecuronium results

A

Postop residual NM blockade in 33% of pts (n-568)

Causing recurarization

174
Q

Factors affecting blockade by LAs

A

Lipid solubility/unionized form
Repetitively stimulates nerve (better block)
Diameter of nerve

175
Q

What is the function of alkalinization of LA solutions?
Benefits?
Average pKa?

A

Function:
INC in % of lipid-soluble form

Benefit:
Shortens onset by 3-5 min
Enhances depth (shorten duration)
INC the spread

AVG pKa = 8

176
Q

How is IV regional anesthesia performed

A
  • IV injection of LA into extremity
  • Extremity isolated from systemic circulation w/ tourniquet
  • Block dependent on tourniquet
177
Q

Effects of transmission from B fiber nerve

A

SNS stimulation

178
Q

Effects of first-pass of 3 LAs

A

-Pulmonary extraction
-Will release LA as concentrations decrease
3 LAs:
Lido, bupiv, prilocaine

179
Q

What is the treatment of methemoglobinemia?

Timeframe for reversal of metHgb?

A

Treatment:
• Methylene blue 1 to 2 mg/kg over 5 mins (max. 7 to 8 mg/kg)

Time frame:
• Reversal from metHgb (Fe3+) to Hgb (Fe2+) is within 20 to 60 min

180
Q

What is the drug of choice for the tachycardic and hypertensive cocaine-induced MI pt

A

Nitroprusside

why not NTG?

181
Q

What is methemoglobinemia and it’s causes?

A

complication d/t LOW O2 carrying capacity (metHgb > 15%).
• Potentially life-threatening

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

182
Q 
LEVOBUPIVACAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 time-
A 
% Unionized 7.4/7.6 pHs- 17/24
Lipid solubility- 
Vd- 55 L
Cl- 
E 1/2 time- 156 min
183
Q

What may result w/ the administration of vasoconstrictor-LA and inhaled anesthetic?

A

Inhaled anesthetic & vasoconstrictor can inc risk for dysrhythmias

184
Q

How is dosing done based on height

A

5 ft = 1 mL of 0.75 %
+0.1 mL for every inch above 5ft

MAX is 2 ml total for 1.5 - 2 hrs

185
Q

Rapid acting esters and amides

A

ESTERS:
Chlorprocaine

AMIDE:
Lidocaine

186
Q

How are ACh-ases cleared primarily and secondarily

A 
Primary = renal
Secondary = hepatic (30-50%) if no renal fxn
187
Q

What is the primary determinant of potency and distribution for LAs? How does this effect DOA

A

HIGH lipid solubility

Shortens DOA

188
Q

Order of potency of esters and amides

A

ESTERS
Procaine < chlorprocaine < tetracaine

AMIDES
Lido/prilo/mepiv < bupiv/levobupiv/ropiv

189
Q

Uptake of LA based on site of administration; highest to lowest LA concentration

A

IV > tracheal > caudal > paracervical > epidural > brachial > sciatic > SQ

190
Q

What factors may effect excretion of neostigmine, pyridostigmine, and edrophonium

A

Renal failure DEC plasma clearance

Prolongs action

191
Q

What is the MOA for lipid emulsion use in LA toxicity

A

 creates lipid compartment

 provides for fat for myocardial metabolism

192
Q

Chemical composition of LA w/ epinephrine

A

Addition of Sodium bisulfate to make weak acid

193
Q

what are 5 underlying factors that could lead to LAST

A 
	Patient co-morbidities
	Medications
	location &amp; technique of block
	LA used
	dose
194
Q

Most common muscle monitored

A

Adductor policis

195
Q

4 Factors that influence absorption

A

Site of injection
Dosage (% concentration)
Use of epi
Pharmacologic characteristics of the drug

196
Q

Which pts should not receive ropivacaine and why

A

Renal pts

Metabolite accumulation

197
Q

Sensory transmission of A and C fibers

A

Pain, temperature, touch, proprioception, motor

198
Q

Max dose of neostigmine and edrophonium d/t ceiling effect

A

Neostigmine: 60-80 mcg/kg (5 mg MAX)
Edrophonium: 1-1.5 mg/kg

199
Q 
Edrophonium and neostigmine 
Class
Dose
Onset
Duration
A

Acetycholine-esterase inhibitors

Edrophonium
Dose: 0.5-1 mg/kg
Onset: 1-2 min
Duration: 5-15 min

Neostigmine
Dose: 40-70 mcg/kg
Onset: 5-10 min
Duration:

200
Q

How is SAB confirmed and what is principal site of action

A

Confirmation = CSF

Site of action: Preganglionic fibers
Which are the ANS site for relay of transmissions

201
Q

What is LA allergy attributed to?

A

Excess plasma levels that manifest as allergic reaction

202
Q

What is cauda equina syndrome (CES)?

A

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

203
Q

Purpose of dexamethasone as adjunct w/ LAs

A

INC duration

either IV or mixed w/ LA

204
Q

What occurs to preservative metabolite of esters?

A

Turns into Paraminobenzoic acid (PABA)

Can cause sever allergic reactions

205
Q

What is the plasma lido concentration range if a pt becomes apneic or comatose after LA use

A

15-25 mcg/ml

206
Q

DOA of LA depends on what?

A

DOSE (concentration) of LA
Mixtures increase DOA of LA w/:
epi, fenta, clonidine, decadron

207
Q

CV side effects of ACh-ases

A

Bradycardia
Dysrhythmias
Asystole
DEC SVR

208
Q

How does combination LA affect toxicity of the agents?

A

Toxic effects are additive

Combine ratios in proportion

209
Q

What is LAST?

Caused by?

A

Local anesthetic systemic toxicity
•d/t excess plasma concentration of the drug

Causes

  1. Entrance into systemic circulation
    - -from inactive tissue redistribution and clearance metabolism
  2. Accidental direct IV injection
210
Q

Purpose of cholinergic agents in anesthesia

A

Accelerate recovery from NMBD

211
Q 
PRILOCAINE
Classification-
Onset-
Duration-
MAX plain dose-
pK-
protein binding-
A 
Classification-AMIDE
Onset-SLOW
Duration-60-120
MAX plain dose-400 mg
pK-7.0
protein binding-55%
212
Q

Cautions of use with EMLA cream

A

Methemoglobinemia (if prilocaine used)
NOT recommended for skin wounds (vasodilation)
C/I w/ amide allergies

213
Q

What are the adverse effects of cocaine toxicity?

A 
CV effects:
HTN, tachycardia
coronary vasospasm
MI
Ventric dysrhythmias
214
Q

Describe the symptoms and possibilities for cross sensitivity of agents.

What mediates the anaphylactic reaction?

A

Symptoms:
Rash, urticaria, laryngeal edema, hypotension?, bronchospasm, IgE anaphylaxis

Cross sensitivity:
NO cross sesnsitivity between ester and amides

Anaphylaxis mediated by IgE

215
Q

When are neostigmine and edrophonium not effective against NMBD reversal

A

Deep block

NO twitches

216
Q

Benefits of continuous infusion blocks

A 
Benefits
•	Improved pain control
•	less nausea
•	greater satisfaction
Additives may be used
217
Q

GI side effects of ACh-ases

A

Hyperperistalsis (diarrhea)

NO PONV

218
Q

Sugammadex use in renal and dialysis patients

A

Avoid in renal impairment if Crt clr < 30 ml/min

Not used in HD pts.

219
Q

Mepivacaine metabolism, DOA, differences, action in parturients

A
  • Metabolism sim to lidocaine (oxidative dealkylation)
  • INC DOA
  • LACK vasodilator activity
  • parturients: prolonged elminiation (fetal/mom)
220
Q 
TETRACAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 time-
A 
% Unionized 7.4/7.6 pHs- 7/11
Lipid solubility- 80
Vd- 
Cl-
E 1/2 time-
221
Q

What is the treatment of choice for nonresponsive LA systemic toxicity?

A

Cardiopulmonary bypass (CPB)

222
Q 
Time to maximum block:
Pancuronium
Rocuronium
Vecuronium
Atracurium
Cisatracurium
Mivacurium
A 
Pancuronium- 2.9 min
Rocuronium- 1.7 min
Vecuronium- 2.4 min
Atracurium- 3.2
Cisatracurium-5.2
Mivacurium-3.3
223
Q

Chlorprocaine metabolism and changes in pregnancy

A

Metab: plasma ch-ase (3.5 x faster)
Pregnancy: Give less b/c lower Ch-ase

224
Q

How does nerve size affect LA action

A

Larger nerve requires higher concentration of LA

225
Q

Most common muscle and nerve monitored w/ nerve stimulator?

A 
Muscle= Adductor Policis
Nerve = Ulnar
226
Q

Other sites of action targets of LA

A

K+ channel
Ca ion channel
GPCRs

227
Q

Effects of anesthetic gases on NMBD reversal

A

Can impede reversal if MAC hasn’t been decreased

228
Q 
ROPIVACAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 time-
A 
% Unionized 7.4/7.6 pHs- 17
Lipid solubility-
Vd- 59 L
Cl- 0.44
E 1/2 time- 108 min
229
Q

Which NMB reversal agents match with which anti-cholinergic drug

A 
Edrophonium = atropine
Neostigmine/Pyridostigmine = glycopyrolate
230
Q

What agent helps reduce complications of adverse reactions to LAs

A

Adding epinephrine to mixture

231
Q

How are pregnancy and arterial hypoxemia/acidosis a predisposing factor to LA toxicity

A

Pregnancy:
LOW plasma ACH-ase

Hypoxemia/Acidosis:
Alters PERCENT ionized

232
Q

5 factors of NMB reversal depend upon

A
  1. Depth of NMB
  2. ACh-ase inhibitor choice
  3. Dose administered
  4. Rate of plasma clr of NMBD
  5. Anesthesia agent choice and depth
233
Q

Cocaine toxicity effects on parturients

A

DECREASED UBF leading to fetal hypoxemia

234
Q

Purpose of peripheral nerve blocks w/ LA (PNB)

A

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

235
Q 
CHLORPROCAINE
% Unionized 7.4/7.6 pHs-
Lipid solubility-
Vd-
Cl-
E 1/2 time-
A 
% Unionized 7.4/7.6 pHs- 5/7
Lipid solubility- 
Vd- 35 L
Cl-
E 1/2 time- 7 min
236
Q 
ROPIVACAINE
Classification-
Onset-
Duration-
MAX plain dose-
pK-
protein binding-
A 
Classification-AMID
Onset-SLOW
Duration-240-480 min
MAX plain dose-175 mg
pK-8.1
protein binding-94%
237
Q

What part of nerve is the goal for spinal anesthetization

A

Anterior portion of nerve

238
Q

Effects of liposomes with LA

A

Prolong DOA and DEC toxicity of lido, tetracaine and bupivacaine

239
Q

Cautions following tumescent infiltration?

A

LA Plasma Peak at 12 to 14

Monitor for cardiac and neuro toxicity post injection

240
Q

Slow acting esters and amides

A

ESTERS:
Procaine, tetracaine

AMIDES:
Prilocaine, bupiavaine, Levobupivicaine, ropivacaine

241
Q

What level is affected by a SAB

A

Sensory effect is on SAME level of innervation

242
Q

What is the rate of allergic reactions to LAs and which agents are more likely to cause the reaction and why?

A

Rate = < 1%

Agent
Esters > Amides
B/c esters have PABA metabolite

243
Q

What is the recommended dose for tumescent liposuction and how does it differ from regional?

A

•Regional Anesthesia
Lidocaine with Epi=7mg/kg
•500 mg TOTAL

Tumescent
•Highly diluted Lidocaine w/ Epi Tumescent=35 to 55 mg/kg

244
Q

Most and least common agents used for epidurals and why

A

Most
Lidocaine - good diffusion through tissues and safer
Bupivacaine - be aware of toxicity

Lesser
Levobupivacaine/ropivacaine - still has potential for toxicity

245
Q

4 predisposing factors for systemic toxicity from LAs

A

Pregnancy
Arterial hypoxemia, acidosis
Beta blockers, digitalis, CCBs
Epi/Phenylephrine

246
Q

At what point should plasma concentration levels of lido be monitor

A

When more than 900 mgs of

247
Q

What is the standard of care for LA removal from receptors?

Dosing for bolus, infusion, and first 30 minutes max?

A

Standard:
Intralipid ~ Lipid Emulsion

Bolus: 1.5 mL/kg of 20% lipid emulsion
Infusion: 0.25 mL/kg/minute for at least 10 min
1st 30 min: 3.8 mL/kg (1.2 to 6 mL/kg)

248
Q

How is fetus affected by epidural LA lipid solubility, onset, and protein binding capacity between lido and bupivacaine? Which is least likely to reach fetus?

A

Solubility = lido > bupiv
Onset = lido < bupiv
higher protein binding = lido < bupiv

Least likely - Bupivacaine
Lidocaine crosses placenta more than bupivacaine

249
Q

Which LAs may need to be treated with methylene blue and why? Dosing?

A

Benzocaine
Prilocaine
Metabolite orthotoluidine converts hgb into methemoglobin

Dose:
1-2 mg IV over 5 min
TOTAL: 7-8 mg/kg

250
Q 
Bupivicaine
Classification-
Onset-
Duration-
MAX plain dose-
pK-
protein binding-
A 
Classification-AMIDE
Onset-SLOW
Duration-240-480 min
MAX plain dose-175 mg
pK-8.1
protein binding-95%
251
Q

Renal elimination and clearance

A
  • Poor H2O solubility
  • 5% unchanged in urine
  • 10-12% unchanged cocaine in urine
  • PABA excreted in urine
252
Q

NMBD reversal ceiling effect?

A

Neostigmine and edrophonium will not work w/ deep NM blockade

253
Q

Most used topical anesthetic and doses

A

Cocaine (4-10%)
THEN
Tetracaine (1-2%)
Lidocaine (2-4%)

Pharm (4 decks)

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