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E4 Flashcards

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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
``` MEPIVACAINE % Unionized 7.4/7.6 pHs- Lipid solubility- Vd- Cl- E 1/2 time- ```
``` % 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 ```
26
``` CHLOROPROCAINE Classification- Onset- Duration- MAX plain dose- pK- protein binding- ```
``` Classification-ESTER Onset-RAPID Duration-30-45 min MAX plain dose-600 mg pK-8.7 protein binding ```
27
Tetracaine metabolism and comparison to other esters
metabolism: hydrolysis Slower than procaine chloroprocaine (fast) > procaine > tetracaine (slowest)
28
Renal excretion for neostigmine, pyridostigmine and edrophonium
Neostigmine = 50% | Pyridostigmine and edrophonium = 75%
29
Types of preparations of EMLA
Tetracaine 4% gel Lidocaine 7% Tetracaine 7%
30
Cocaine MOA/use as topical anesthetic
Localized vasoconstriction Decreases blood loss Improves surgical visualization Nasal mucous membranes
31
Causes of hepatotoxicity when using LA? What is the treatment?
Causes: continuous or intermittent epidural bupivacaine to treat postherpetic neuralgia Treatment: - stop infusion - normalize liver transaminase enzymes
32
How does pregnancy effect LAs. How is this incorporated in the plan of care?
DEC level of plasma ch-ase | avoid or decrease ester dose
33
LA effects in pregnancy and feturs
-Significant transplacental transfer (amides > esters) -Ion trapping (maternal pH [union]> fetal[ion])
34
Most common anesthetics used for SAB
``` Tetracaine Lidocaine Bupivacaine Ropivacaine levobupivacaine ```
35
CV effect of vasoconstrictors w/ LA
Enhanced cardiac irritability especially w/ inhaled anesthetics Systemic absorption can lead to HTN
36
Importance of alpha-adrenergic effects from LA-vasoconstrictor?
a-adrenergic effects may have some analgesic ability
37
What type of block is produced w/ Bier block
BOTH motor and sensation block
38
Foal for treatment of LA systemic toxicity
Prompt airway management Circulatory support Remove LA from receptors
39
Spinal anesthesia block is
Direct injection of LA into SA
40
How are the vasodilatory effects of LAs blunted?
Addition vasoconstrictor (epi, neo) to LA
41
How does enantiomerism affect the action of bupivacaine, levobupivacaine, and ropivacaine
Bupivacaine is racemic mixture and more neuro/cardio-toxic Levobupivacaine/ropivacaine are (R) left-handed enantiomers and are less neuro/cardio-toxic
42
What are other etiologies that may cause anterior spinal artery syndrome?
* effects of HToN or vasoconstrictors drugs * PVD * SC compression d/t epidural abscess or hematoma
43
Where is the epidural space
Between the dura and spinal cord
44
LA MOA
- 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
45
Neuromuscular monitoring AKA and most common monitoring technique
Acceleromyography | Train-of-four
46
How does pK to pH level affect LA pharmacokinetics and why? Effects on action?
pK closest to physiologic pH Most Rapid OOA b/c most nonionized form Ionized LA won't pass through channel and block it
47
Where does the LA bind on the VG-Na channel
On the inner gate | aka H-gate
48
``` Cocaine Metabolism Duration Populations to avoid use Elimination ```
Metabolism: liver > plasma Ch-ase DOA: 60 min post peak Populations: fetal, parturients, elderly, hepatic Dx Elimination: Urine (24-36 hrs)
49
pK of LAs and % ionization
Weak bases Above physiologic pH Only 50% in lipid-soluble nonionized form
50
Purpose of local infiltration w/ LA Duration alterations C/Is
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
51
Benefits of additives to epidurals/SABs?
Opioids are beneficial for pain control w/ synergistic effects
52
Purpose of magnesium as adjunct w/ LAs
INC duratin of SAB w/ or w/o opioids | d/t small muscle relaxation
53
How are beta-blockers/dig/CCBs and epi/phenyleph a predisposing factor to LA toxicity
B-blockers/Dig/CCB: Alters conduction Epi/phenyleph: IV use to treat CV effects can compound CV issues
54
Molecular structure of LAs and difference in classifications
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
55
``` LEVOBUPIVICAINE Classification- Onset- Duration- MAX plain dose- pK- protein binding- ```
``` Classification-AMID Onset-SLOW Duration-240-480 min MAX plain dose-175 mg pK-8.1 protein binding->97% ```
56
``` LIDOCAINE Classification- Onset- Duration- MAX plain dose- pK- protein binding- ```
``` Classification-AMIDE Onset-RAPID Duration-60-120 MAX plain dose-300 mg pK-7.9 protein binding-70% ```
57
How does location affect the possibility of systemic toxicity
Highest blood concentration ``` IV Tracheal Caudal Paracervical Epidural Brachial Sciatic SQ ``` Lower blood concentration
58
``` BUPIVACAINE % Unionized 7.4/7.6 pHs- Lipid solubility- Vd- Cl- E 1/2 time- ```
``` % 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 ```
59
What is dosing of SAB based on?
Height of patient determines volume of SA space Segmental level of anesthesia desired Duration of anesthesia needed
60
LA of choice for Bier block
Esters or amides Most common = lido
61
Which NMB does not have the risk of recurarization
Suggamadex
62
Importance of 100% O2 in the treatment of LA toxicity
To inhibit hypoxemia and metabolic acidosis
63
At what levels are SNS and motor block with SAB
SNS = 2 spinal segments cephalad of sensory Motor = 2 spinal segments below sensory
64
What is the ventilatory response to hypoxia when LA agents are in use? Which pts are susceptible to this problem?
Lidocaine depresses the ventilatory response to arterial hypoxemia CO2 retainers are most susceptible
65
Most common technique when monitoring for twitches?
Train-of-four
66
What are associated issues of cauda equina syndrome? | What is the cause of CES?
Associated • large lumbar disc herniation • prolapse or sequestration w/ urinary retention. Cause: unknown
67
What can hyperpyrexia lead to in the cocaine toxic patients?
Seizures
68
Describe difference in dosing and blockade of epidural vs SAB
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
69
How does specific gravity affect LA action
Determines the spread of drug | solute concentration of LA compared to CSF
70
Sugammadex dosing for all block types
Moderate (TOF 2 twitches) = 2 mg/kg | Deep (1-2 PT and NO TOF twitch) = 4 mg/kg
71
How do vasoconstrictors affect LA DOA in relation to nerve fivers?
Prolongs duration of contact w/ nerve fiber by decreasing systemic absorption
72
What determines the rate of clearance of LAs
``` CO Protein binding (% bound inversely r/t % plasma) -more bound = longer clearance? ```
73
significance of liposomes in LA use
They are used to upload higher amount of LA into molecule | Then have a consistent release of LA in tissue
74
Where is tumescent infiltration used
Thigh abdomen hips buttocks
75
Duration of action of LA is proportional to what?
The amount of time the drug is in contact with nerve fiber
76
Order of "speed" based on nerve type
B fibers (fastest) > A fibers > C unmyelinated fibers (small/slow)
77
Sugammadex side-effects
anaphylaxis marked bradycardia doesn't work Dose-realted: N/V pruritis urticaria
78
Which ester LA is not metabolized by plasma cholinesterases
Cocaine
79
What can occur with an SNS block from SAB at the level of T4. What drugs are CI? What drugs are used for treatment?
Can knock out cardiac accelerator nerve function leading to bradycardia or asystole CI drugs = ephedrine, antimuscarinics (atropine, glycopyrolate) Treatment= beta-1 agonist like epinephrine
80
What is the MOA of NMBD reversal agents
- 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
81
Alkalinization enhances depth of block, what is the drawback to that?
This can shorten the duration of action
82
Affect of infection on LA action
Local infection pH ionizes LA and it won't work
83
Purpose of clonidine/ketamine in conjunction w/ LAs
Prolong duration in peds
84
Mcg of epi • 1:200,000 • 1:500,000 1:10,000 What is more concentrated
* 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
85
Lidocaine Metabolism. Metabolite? Hepatic effects?
Metabolism: oxidative dealkylation in liver THEN hydrolysis Metabolite: Xylidide Hepatic Dx: will affect metabolism and elimination -Give less
86
What is the elimination 1/2 time and major route/time of elimination of sugammadex
E 1/2 time = 2 hrs Route = URINE 6 hrs = 70% 24 hrs = 90%
87
Anti-cholinergic dose of atropine and glycopyrolate in conjunction w/ NMBD reversal
``` Atropine = 7-10 mcg/kg Glycopyrolate = 7 - 15 mcg/kg ```
88
What is the MOA of cocaine toxicity?
SNS stimulation by blocking presynaptic uptake of NE and dopamine • HIGH postsynaptic levels
89
PNB MOA and S/Sx
MOA: diffusion (NOT osmosis) from outer mantle to central core of nerve along a concentration gradient S/Sx: peripheral affected FIRST THEN central second
90
CV effects with accidental IV bupivacaine
Precipitous hypotension, AV block Cardiac dysrhythmias SVTs, ST-T wave changes PVCs, widening of QRS, V-tach
91
Ester metabolism
Hydrolysis by cholinesterase enzymes in the plasma Plasma metab > liver Metabolize faster than amides
92
Bier block process
```  IV start  Exsanguination  Double cuff  LA injection  IV D/C ```
93
Liposome duration of bupiviacaine ER
DOA up to 96 hrs
94
Baillard follow-up study on vec w/ reversal results
Postop residual NM blockade 4%
95
Sugammadex dose for deep NMB
8-16 mg/kg | effective even w/o twitches
96
By what percent can epinephrine mixed w/ LA decrease systemic absorption
33.33% | 1/3
97
Lidocaine uses Max plain dose Clearance
Uses: anti-dysrhythmic MAX dose: 300 mgs Clr: prolonged w/ PIH
98
Effects of vasoconstrictor use in combo w/ LAs
``` Vasoconstriction INC neuronal uptake of LA alpha-adrenergic effects No change to onset of LA Prolong duration ```
99
What is EMLA cream? LA used? Dosing?
Eutectic mixture of LA LA: Lidocaine 2.5% and Prilocaine 2.5% - 5% LA total Dose: 1 to 2 gms/cm2 area
100
Amide metabolism
Microsomal enzymes in the liver Fastest to slowest metab Prilocaine > lido/mepiv > etido/bupiva/ropivacaine Metabolize slower than esters
101
``` PROCAINE % Unionized 7.4/7.6 pHs- Lipid solubility- Vd- Cl- E 1/2 ytime- ```
``` % Unionized 7.4/7.6 pHs- 3/5 Lipid solubility- 0.6 Vd- 65 L Cl- E 1/2 time- 9 min ```
102
Classification of NMBD reversal agents
aka-ACh-ase aka-Cholinergic agents aka-Competitive antagonist
103
Bupivacaine metabolism, and protein binding
Metabolism: LIVER aromatic hydroxylation, N-dealkylation, amide hydrolysis, and conjugation Protein binding site α1-Acid glycoprotein
104
Prilocaine Toxic dose S/Sx Treatment
Toxic dose: >600 mg s/sx: cyanosis d/t DEC O2 carrying capacity Tx: Methylene blue
105
Use of epidurals in OB and CS Placenta and fetal effects? How is that affected by lipid solubility, onset, and protein binding capacity?
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
When is the best time to check for baseline twitch
Before NMBD given
107
How are nerves identified for PNB
* Nerve stimulator * mA 0.1-1 * Pinpoint needles * Ultrasound guided * In plane vs out-of-plane
108
``` PROCAINE Classification Onset Duration MAX plain dose pK protein binding ```
``` Classification-ESTER Onset-SLOW Duration-45-60 min MAX plain dose: 500 mg pK: 8.9 protein binding: 6% ```
109
When full CV depression occurs following LA use, what is the plasma lido concentration likely at?
>25 mcg/ml
110
Which nerve fiber stimulates pain and temperature, proprioception etc
Myelinated A-delta | Unmyelinated C fibers
111
Treatment for CNS toxicity from LAs (5)
``` 100% O2 Hyperventilation Barbiturates Benzodiazepines Epi as additive ```
112
Do vasoconstrictors affect the OOA w/ LAs
No effect on OOA
113
What is tumescent liposuction? What agent and dosing is used?
``` 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
Importance of un/ionization of LAs. What is this based on?
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
Anti-cholinergic administration considerations in CV pts
Glycopyrolate preferred | Administer slowly: over 2-4 min
116
What is the treatment and recovery time for transient neurologic symptoms?
Treatment: • Trigger point injections and NSAIDs Recovery: • 1 to 7 days.
117
Mg dose of epinephrine or phenylephrine when mixed with LA
``` Epi = 0.2 mg Phenylephrine = 2 mg ```
118
Problem w/ combination of chlorprocaine and bupivacaine? Due to?
Problem: Tachyphylaxis The addition chlorprocaine can possibly reduce sensitivity to following doses Lessened effect on following doses Due to: Desensitized receptors
119
Order of nerve effects w/ PNB
FIRST - Smallest sensory and ANS fibers | SECOND/LAST - Large motor and proprioceptive axons
120
Sugammadex structure and physical properties
Structure = y-cyclodextin Dextrose units from starch Highly H2O soluble
121
LA Systemic toxicity management for seizures (5)
* Supplemental O2 * Benzodiazepine = midazolam or diazepam * Propofol = if hemodynamically stable * Muscle relaxant = SCh or NMDA * Intralipid = lipid emulsion
122
What effect does dilution have on tumescent dosing? | Theory of tumescent LA absorption and name?
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
Purpose of dexmedetomidine in conjunction w/ LAs
IV dex INC duration of motor and sensory block Inc duration of time before 1st analgesic requested following spinal anesthesia
124
Lidocaine use as topical anesthetic
Use: Surface anesthetic Inhaled anesthetic (doesn't change airway resistance BUT does vasodilate)
125
When is the best time to check for twitches?
Baseline | Before giving NMBD
126
What is ACh-ase purpose in NMBD use?
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
Which anti-cholinergic may be contraindicated in CV disease? Which agent should be used?
Atropine d/t tachycardia | Glycopyrolate preferred
128
What medication in conjunction w/ EMLA can aid in arterial cannulation?
NTG Can decrease pain? Vasodilate vessel for better cannulation
129
Types/Locations of PNB
* Interscalene = shoulder * Axillary = lower arm * Femoral = Upper leg/knee * Sciatic = back of knee/lower leg
130
``` LIDOCAINE % Unionized 7.4/7.6 pHs- Lipid solubility- Vd- Cl- E 1/2 time- ```
``` % 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
Locations of topical anesthetic use
Mucous membranes Nose, mouth, tracheobronchial tree esophagus or GU tract
132
What are the 2 alterations of specific gravity for LAs and purpose? Compare to CSF? What is used?
Hyperbaric, so LA "sinks" LA sp gr > CSF 5% glucose additive Hypobaric, so LA "floats" LA sp gr < CSF Distilled water
133
What are 4 things that systemic absorption depends on
* Dose * Vascularity of site * Epinephrine use * Physicochemical properties (pKa)
134
Treatment for cocaine associated CP
IV NTG (NO donors)
135
What are the 3 categories of neural tissue toxicity
Transient neurologic symptoms Cauda equina syndrome Anterior spinal artery syndrome
136
Cautions when administering sugammadex
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
Why are LAs w/ epi c/i in digital appendages
C/i fingers, toes, ears, nose, penis Vasoconstriction -> ischemia -> necrosis
138
Significance of nodes of ranvier when using LAs
Must cover at least, preferably 3 nodes Equal to 1 cm So that AP can't skip nodes
139
Side-effects of vasoconstrictor use in combo w/ LAs
Enhanced cardiac irritability | Systemic absorption
140
CV effects of LA toxicity are due to what occurring? | How does this affect conduction?
High plasma concentrations that block cardiac Na+ channels - Slows conduction of cardiac impulses - prolonged PR interval & QRS widening
141
In conjunction w/ LAs this electrolyte can promote szs
Hyperkalemia
142
EMLA readiness | Altered time frame
45 min OOA ``` 10 mins in setting of genital wart cautery veni/lumbar puncture Art line w/ NTG Myringotomy ```
143
``` TETRACAINE Classification- Onset- Duration- MAX plain dose- pK- protein binding- ```
``` Classification-ESTER Onset-SLOW Duration-60-180 min MAX plain dose-100 (topical) pK-8.5 protein binding-76% ```
144
Pulm side effects of ACh-ases
Bronchoconstriction INC airway resistance INC salivation
145
Epinephrine IV dose in the presence of LA toxicity, following lipid emulsion?
10 - 100 mcg
146
Ropivacaine metabolism, metabolites, altered effects and protein binding
Metabolism: hepatic P450 Metabolite: Accumulate in uremic pts effects: less toxicity Protein binding: a1-acid glycoprotein
147
When reversing NMBD, which agent is given first?
Anticholinergic FIRST | THEN anticholinesterase
148
What drug class is sugammadex
Selective relaxant-binding agent | To non-depolarizing NMBD
149
Most common nerve monitored
Ulnar nerve
150
Reversal drugs that are not anti-cholinergics? Which drugs do they work with?
``` Purified human plasma cholinesterase -Mivacurium Cysteine -Gantacurium Sugammadex -Selective binding w/ aminosteroids non-depolarizing NMBD ```
151
Cocaine cautions when using as LA
``` Coronary vasospasm •Causes vascoconstriction ventricular dysrhythmias HTN Tachycardia CAD ```
152
What is the most important factor of dosing of SAB
Dose is more important than concentration of drug(%) or volume (mls) of injection
153
5 uses of LAs
``` Treat dysrythmias Analgesia ANS blockade Sensory block Motor block-skeletal muscle paralysis ```
154
What is the product of tumescent infiltration? | Effects?
Product: Causes taut stretching of overlying blanched skin d/t large volume & vasoconstriction Effects  Local anesthesia with bloodless aspirates •prolonged postoperative analgesia
155
Dibucaine metabolism, MOA and use
- Metabolism: hepatic - MOA: inhibits activity of plasma cholinesterases by >70% Use: to test for atypical cholinesterase issues
156
``` Benzocaine Use pK OOA DOA Dose/MAX Adverse effects ```
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
How are LA systemic absorption limited?
By the use of vasoconstrictors which keep the LA LOCAL | By keeping drug concentration in the vicinity of nerve fiber
158
What action of the LAs affect the potency and DOA. Why?
Intrinsic vasodilator activity Vasodilation INC systemic absorption DECreasing local effects of anesthetic thus decreasing the DOA
159
How long can cocaine toxicity effects last
Up to 6 weeks
160
How does sugammadex work in NMBD reversal
``` Binds to free drug in plasma Uses intermolecular (vdW) forces for a very tight reversal ```
161
Problem with LA preservatives and allergic reactions. | What cautions should be taken?
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
How does protein binding alter LA in parturient
- INC protein binding - determine rate and degree of diffusion - DEC concentration and diffusion - LESS LA crosses the placenta
163
When is EMLA cream C/I
Amide allergy Not for skin wounds
164
4 Adjuvants w/ LAs
Dexmedetomadine Magnesium Clonidine/Ketamine Dexamethasone
165
Which reversal agent can be used when no twitches are present on deep NMB
Suggamadex
166
Neuromuscular monitoring a.k.a.
acceleromyography
167
CNS effects of LA systemic toxicity
Drowsiness, facial twitch before sz
168
``` What effects correspond to the following plasma lido concentrations? 1-5 5-10 10-15 15-25 >25 ```
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
NMBD (roc or vec) re-administration after sugammadex administration
5 min = 1.2 mg/kg roc 4 hrs = 0.6 mg/kg roc or 0.1 mg/kg vec Use nonsteroidal NMBD
170
Use of IV regional anesthesia
Total extremity anesthesia | Produces sensation and motor block
171
What are transient neurologic symptoms r/t neural toxicity? | What can cause this?
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
What is the alkalinizing agent used w/ LAs? | Dose/Ratio?
8.4% sodium bicarbonate 1 mL Dose/Ratio: 1 mL NaHCO3 + 30 mL LA
173
Baillard et al initial study on vecuronium results
Postop residual NM blockade in 33% of pts (n-568) | Causing recurarization
174
Factors affecting blockade by LAs
Lipid solubility/unionized form Repetitively stimulates nerve (better block) Diameter of nerve
175
What is the function of alkalinization of LA solutions? Benefits? Average pKa?
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
How is IV regional anesthesia performed
- IV injection of LA into extremity - Extremity isolated from systemic circulation w/ tourniquet - Block dependent on tourniquet
177
Effects of transmission from B fiber nerve
SNS stimulation
178
Effects of first-pass of 3 LAs
-Pulmonary extraction -Will release LA as concentrations decrease 3 LAs: Lido, bupiv, prilocaine
179
What is the treatment of methemoglobinemia? Timeframe for reversal of metHgb?
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
What is the drug of choice for the tachycardic and hypertensive cocaine-induced MI pt
Nitroprusside why not NTG?
181
What is methemoglobinemia and it's causes?
complication d/t LOW O2 carrying capacity (metHgb > 15%). • Potentially life-threatening Causes: • Prilocaine, benzocaine, lidocaine • nitroglycerine, phenytoin, & sulfonamides
182
``` LEVOBUPIVACAINE % Unionized 7.4/7.6 pHs- Lipid solubility- Vd- Cl- E 1/2 time- ```
``` % Unionized 7.4/7.6 pHs- 17/24 Lipid solubility- Vd- 55 L Cl- E 1/2 time- 156 min ```
183
What may result w/ the administration of vasoconstrictor-LA and inhaled anesthetic?
Inhaled anesthetic & vasoconstrictor can inc risk for dysrhythmias
184
How is dosing done based on height
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
Rapid acting esters and amides
ESTERS: Chlorprocaine AMIDE: Lidocaine
186
How are ACh-ases cleared primarily and secondarily
``` Primary = renal Secondary = hepatic (30-50%) if no renal fxn ```
187
What is the primary determinant of potency and distribution for LAs? How does this effect DOA
HIGH lipid solubility Shortens DOA
188
Order of potency of esters and amides
ESTERS Procaine < chlorprocaine < tetracaine AMIDES Lido/prilo/mepiv < bupiv/levobupiv/ropiv
189
Uptake of LA based on site of administration; highest to lowest LA concentration
IV > tracheal > caudal > paracervical > epidural > brachial > sciatic > SQ
190
What factors may effect excretion of neostigmine, pyridostigmine, and edrophonium
Renal failure DEC plasma clearance | Prolongs action
191
What is the MOA for lipid emulsion use in LA toxicity
 creates lipid compartment |  provides for fat for myocardial metabolism
192
Chemical composition of LA w/ epinephrine
Addition of Sodium bisulfate to make weak acid
193
what are 5 underlying factors that could lead to LAST
```  Patient co-morbidities  Medications  location & technique of block  LA used  dose ```
194
Most common muscle monitored
Adductor policis
195
4 Factors that influence absorption
Site of injection Dosage (% concentration) Use of epi Pharmacologic characteristics of the drug
196
Which pts should not receive ropivacaine and why
Renal pts | Metabolite accumulation
197
Sensory transmission of A and C fibers
Pain, temperature, touch, proprioception, motor
198
Max dose of neostigmine and edrophonium d/t ceiling effect
Neostigmine: 60-80 mcg/kg (5 mg MAX) Edrophonium: 1-1.5 mg/kg
199
``` Edrophonium and neostigmine Class Dose Onset Duration ```
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
How is SAB confirmed and what is principal site of action
Confirmation = CSF Site of action: Preganglionic fibers Which are the ANS site for relay of transmissions
201
What is LA allergy attributed to?
Excess plasma levels that manifest as allergic reaction
202
What is cauda equina syndrome (CES)?
Diffuse injury @ lumbosacral plexus • varying degrees of sensory anesthesia • bowel & bladder sphincter dysfunction, •paraplegia
203
Purpose of dexamethasone as adjunct w/ LAs
INC duration | either IV or mixed w/ LA
204
What occurs to preservative metabolite of esters?
Turns into Paraminobenzoic acid (PABA) | Can cause sever allergic reactions
205
What is the plasma lido concentration range if a pt becomes apneic or comatose after LA use
15-25 mcg/ml
206
DOA of LA depends on what?
DOSE (concentration) of LA Mixtures increase DOA of LA w/: epi, fenta, clonidine, decadron
207
CV side effects of ACh-ases
Bradycardia Dysrhythmias Asystole DEC SVR
208
How does combination LA affect toxicity of the agents?
Toxic effects are additive Combine ratios in proportion
209
What is LAST? | Caused by?
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
Purpose of cholinergic agents in anesthesia
Accelerate recovery from NMBD
211
``` PRILOCAINE Classification- Onset- Duration- MAX plain dose- pK- protein binding- ```
``` Classification-AMIDE Onset-SLOW Duration-60-120 MAX plain dose-400 mg pK-7.0 protein binding-55% ```
212
Cautions of use with EMLA cream
Methemoglobinemia (if prilocaine used) NOT recommended for skin wounds (vasodilation) C/I w/ amide allergies
213
What are the adverse effects of cocaine toxicity?
``` CV effects: HTN, tachycardia coronary vasospasm MI Ventric dysrhythmias ```
214
Describe the symptoms and possibilities for cross sensitivity of agents. What mediates the anaphylactic reaction?
Symptoms: Rash, urticaria, laryngeal edema, hypotension?, bronchospasm, IgE anaphylaxis Cross sensitivity: NO cross sesnsitivity between ester and amides Anaphylaxis mediated by IgE
215
When are neostigmine and edrophonium not effective against NMBD reversal
Deep block | NO twitches
216
Benefits of continuous infusion blocks
``` Benefits • Improved pain control • less nausea • greater satisfaction Additives may be used ```
217
GI side effects of ACh-ases
Hyperperistalsis (diarrhea) | NO PONV
218
Sugammadex use in renal and dialysis patients
Avoid in renal impairment if Crt clr < 30 ml/min | Not used in HD pts.
219
Mepivacaine metabolism, DOA, differences, action in parturients
- Metabolism sim to lidocaine (oxidative dealkylation) - INC DOA - LACK vasodilator activity - parturients: prolonged elminiation (fetal/mom)
220
``` TETRACAINE % Unionized 7.4/7.6 pHs- Lipid solubility- Vd- Cl- E 1/2 time- ```
``` % Unionized 7.4/7.6 pHs- 7/11 Lipid solubility- 80 Vd- Cl- E 1/2 time- ```
221
What is the treatment of choice for nonresponsive LA systemic toxicity?
Cardiopulmonary bypass (CPB)
222
``` Time to maximum block: Pancuronium Rocuronium Vecuronium Atracurium Cisatracurium Mivacurium ```
``` Pancuronium- 2.9 min Rocuronium- 1.7 min Vecuronium- 2.4 min Atracurium- 3.2 Cisatracurium-5.2 Mivacurium-3.3 ```
223
Chlorprocaine metabolism and changes in pregnancy
Metab: plasma ch-ase (3.5 x faster) Pregnancy: Give less b/c lower Ch-ase
224
How does nerve size affect LA action
Larger nerve requires higher concentration of LA
225
Most common muscle and nerve monitored w/ nerve stimulator?
``` Muscle= Adductor Policis Nerve = Ulnar ```
226
Other sites of action targets of LA
K+ channel Ca ion channel GPCRs
227
Effects of anesthetic gases on NMBD reversal
Can impede reversal if MAC hasn't been decreased
228
``` ROPIVACAINE % Unionized 7.4/7.6 pHs- Lipid solubility- Vd- Cl- E 1/2 time- ```
``` % Unionized 7.4/7.6 pHs- 17 Lipid solubility- Vd- 59 L Cl- 0.44 E 1/2 time- 108 min ```
229
Which NMB reversal agents match with which anti-cholinergic drug
``` Edrophonium = atropine Neostigmine/Pyridostigmine = glycopyrolate ```
230
What agent helps reduce complications of adverse reactions to LAs
Adding epinephrine to mixture
231
How are pregnancy and arterial hypoxemia/acidosis a predisposing factor to LA toxicity
Pregnancy: LOW plasma ACH-ase Hypoxemia/Acidosis: Alters PERCENT ionized
232
5 factors of NMB reversal depend upon
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
Cocaine toxicity effects on parturients
DECREASED UBF leading to fetal hypoxemia
234
Purpose of peripheral nerve blocks w/ LA (PNB)
Achieved by LA injection into tissues surrounding peripheral nerves or nerve plexuses
235
``` CHLORPROCAINE % Unionized 7.4/7.6 pHs- Lipid solubility- Vd- Cl- E 1/2 time- ```
``` % Unionized 7.4/7.6 pHs- 5/7 Lipid solubility- Vd- 35 L Cl- E 1/2 time- 7 min ```
236
``` ROPIVACAINE Classification- Onset- Duration- MAX plain dose- pK- protein binding- ```
``` Classification-AMID Onset-SLOW Duration-240-480 min MAX plain dose-175 mg pK-8.1 protein binding-94% ```
237
What part of nerve is the goal for spinal anesthetization
Anterior portion of nerve
238
Effects of liposomes with LA
Prolong DOA and DEC toxicity of lido, tetracaine and bupivacaine
239
Cautions following tumescent infiltration?
LA Plasma Peak at 12 to 14 | Monitor for cardiac and neuro toxicity post injection
240
Slow acting esters and amides
ESTERS: Procaine, tetracaine AMIDES: Prilocaine, bupiavaine, Levobupivicaine, ropivacaine
241
What level is affected by a SAB
Sensory effect is on SAME level of innervation
242
What is the rate of allergic reactions to LAs and which agents are more likely to cause the reaction and why?
Rate = < 1% Agent Esters > Amides B/c esters have PABA metabolite
243
What is the recommended dose for tumescent liposuction and how does it differ from regional?
•Regional Anesthesia Lidocaine with Epi=7mg/kg •500 mg TOTAL Tumescent •Highly diluted Lidocaine w/ Epi Tumescent=35 to 55 mg/kg
244
Most and least common agents used for epidurals and why
Most Lidocaine - good diffusion through tissues and safer Bupivacaine - be aware of toxicity Lesser Levobupivacaine/ropivacaine - still has potential for toxicity
245
4 predisposing factors for systemic toxicity from LAs
Pregnancy Arterial hypoxemia, acidosis Beta blockers, digitalis, CCBs Epi/Phenylephrine
246
At what point should plasma concentration levels of lido be monitor
When more than 900 mgs of
247
What is the standard of care for LA removal from receptors? | Dosing for bolus, infusion, and first 30 minutes max?
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
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?
Solubility = lido > bupiv Onset = lido < bupiv higher protein binding = lido < bupiv Least likely - Bupivacaine Lidocaine crosses placenta more than bupivacaine
249
Which LAs may need to be treated with methylene blue and why? Dosing?
Benzocaine Prilocaine Metabolite orthotoluidine converts hgb into methemoglobin Dose: 1-2 mg IV over 5 min TOTAL: 7-8 mg/kg
250
``` Bupivicaine Classification- Onset- Duration- MAX plain dose- pK- protein binding- ```
``` Classification-AMIDE Onset-SLOW Duration-240-480 min MAX plain dose-175 mg pK-8.1 protein binding-95% ```
251
Renal elimination and clearance
- Poor H2O solubility - 5% unchanged in urine - 10-12% unchanged cocaine in urine - PABA excreted in urine
252
NMBD reversal ceiling effect?
Neostigmine and edrophonium will not work w/ deep NM blockade
253
Most used topical anesthetic and doses
Cocaine (4-10%) THEN Tetracaine (1-2%) Lidocaine (2-4%)

Pharm (4 decks)

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