Local Anesthetics Flashcards

Question

Other Actions when LAs Admin Centrally:

Answer 1

o Na channel blockade o K, Ca channels: dorsal horn of spinal cord, altered sensory processing o Substance P binding (tachykinin), evoked increase iCa o Glutaminergic transmission --> decreased NMDA, neurokinin-mediated transmission o Targeting of large nerves, nerve trunk (BP, LST): somatosensory arrangement of nerve fibers also affects progression of block

Answer 2

 Lipophilic aromatic (benzene) ring  Hydrophilic amine group (tertiary or quaternary amine)  Intermediate chain linkage - ester or amide

Answer 3

O-C; hydrolyzed by plasma esterases (one i) o Procaine o Tetracaine o Chloroprocaine

Answer 4

Metabolized by liver (two is) o Lidocaine o Ropivacaine o Bupivacaine, levobupivacaine o Mepivacaine

Answer 5

mostly racemic mixture that 50:50 R-, S-

Answer 6

1. Tetracaine 2. Prilocaine 3. Lidocaine

Answer 7

Levobupivacaine, ropivacaine

Answer 8

o R-enantiomers assoc with greater in vitro potency, greater therapeutic efficacy but also increased CV, CNS toxicity

Answer 9

Diffusion coefficient, MW not important factors in determining activity  MW very similar btw LAs, 220-228Da

Answer 10

**WEAK BASES** Formulated as acid solutions

Answer 11

acidic HCl solutions (pH 4-7)  Formulation in acidic solutions increases CHECK THIS ionized portion --> improves H2O solubility

Answer 12

 Increased pKa --> increased BH+ at physiologic pH (7.4) (increased ionization) --> slow onset  Higher pKa, more drug ionized at physiologic pH – ionized form = ACTIVE * More ionized form, more drug to interact with receptor * BUT moves more slowly across hydrophobic cell membrane, thus slower onset

Answer 13

(eg lidocaine): more uncharged base, faster onset o Once intracellular, becomes ionized – interact with R

Answer 14

determines penetration of nerve cell membrane  **Increased lipid solubility --> increased potency**, decreased concentration needed for blockade  More lipid soluble, better penetration through lipid membrane, faster onset in unmyelinated nerves

Answer 15

delayed onset DT trapping in myelin, other lipid compartments * Net effect of ing lipid solubility = delayed onset of LAs * Increased duration due depot for slow release of drug

Answer 16

Only free drug active: **increased protein binding --> increases duration of action** Don’t know why: Likely related to membrane or extracellular proteins in membrane

Answer 17

**pKa**, lipid solubility, concentration, volume, frequency of membrane stimulation, pH of site  Addition of HCO3 to increase pH --> promotes more un-ionized base to be present to hasten onset B > BH+ (contradicting studies  Ex: LAs will not work around infected abscess with acidic pH

Answer 18

Correlates to lipid Solubility

Answer 19

**Protein binding** site of administration, vasomotor tone

Answer 20

fiber size, length, myelin, frequency of stimulation, concentration, drug properties

Answer 21

Amides Increased pKa Decreased lipid solubility More potent blockade of C fibers than fast-conducting A fibers

Answer 22

 More differential blockade, more sparing of certain types of nerve fibers  At higher concentrations, drug properties become less important for differential blockade * High concentration of ANY LA, differential blockade goes away B > C = Adelta > Agamma > Abeta >Aalpha Drink Good Beer Always

Answer 23

 Site of injection, vascularity  Intrinsic lipid solubility  Vasoactivity of agent  Dose admin  Additives, other formulation factors that modify local drug residence, release  Influence of nerve block in region (VD)  Pathophysiologic state of patient

Answer 24

Lower systemic absorption, greater margin of safety

Answer 25

Increased absorption  Increased peak plasma concentration (Cmax)  Decreased time to peak plasma concentration (Tmax)  **Intercostal > epidural > brachial plexus > femoral/sciatic** * Study only done using those sites * Related to differences in vascularity * Intrathecal much lower systemic absorption than epidural

Answer 26

**Intercostal > epidural > brachial plexus > femoral/sciatic** * Study only done using those sites * Related to differences in vascularity * Intrathecal much lower systemic absorption than epidural

Answer 27

--Decreased lipid solubility, decreased protein binding Lidocaine, mepivacaine > bupivacaine, ropivacaine Increased lipid sol, increased protein binding = less absorption – bind to neural, non-neural lipid-rich tissues so less systemic absorption

Answer 28

 Most LAs cause vasodilation, which decreases time to peak plasma concentrations (increases Tmax)  Ropivacaine, levobupivacaine = vasoconstriction, Tmax

Answer 29

lower Tmax (less time to reach peak plasma concentration), higher Cmax (higher peak plasma concentrations)  Greatest risk systemic toxicity: Tmax arterial blood, 5-45’ after inj depending on site of block, speed of inj, drug  Risk of systemic toxicity coincides with Tmax, independent of dose  Faster speed of injection, increased Cmax (peak plasma concentration

Answer 30

Degree of tissue distribution, protein binding related to apparent volume of distribution at steady state (Vdss): free fraction governs tissue concentration Usually paralleled by degree of protein binding

Answer 31

rapid plasma hydrolysis by pseudocholinesterases, limited distribution

Answer 32

Widely Distributed -Can be affected by a1-acid glycoprotein (AAG) concentrations -pulmonary first pass effect

Answer 33

* Increased AAG --> increase TOTAL LA concentration, but NOT free (active) fraction (amides) * AAG = acute phase reaction protein produced by the liver in response to inflammation * Normally low in plasma, serum concentrations can increase 2-5x * Academic > clinical

Answer 34

risk of toxicity with R-->L cardiac shunts Normal: temporarily increases plasma concentration of drug, lungs able to attenuate toxic effects after accidental IA injection * Mostly dependent on lipid solubility, pKa o More lipid soluble agents --> more pulmonary uptake o Lower pKas = greater unionized form, which accumulates in the lung

Answer 35

* Some of drug will bypass first pass due to shunt * Increased toxicity so increase dose ***CLINICALLY RELEVANT*** * Most pulmonary first pass: bupivacaine > etidocaine > lidocaine, levobupivacaine > ropivacaine

Answer 36

Milk, muscle

Answer 37

relatively lipophilic, unionized (Lower pKa), not strongly protein bound, low MWs FARAD: recommends 24hr meat, milk withhold on lidocaine

Answer 38

Limited for esters due to rapid metabolism, enhanced for amides by “ion trapping” Unionized form rapidly crosses placenta --> once in more acidic fetal circulation, ionized drug forms more readily --> gets “stuck” in fetal circulation Back transfer from fetus to mother occurs with bupivacaine, NOT lidocaine

Answer 39

* Only unbound, free drug crosses placenta * Fetal AAG content, binding < maternal, F:M of highly protein-bound LAs lower than less-protein bound o Ex: bupivacaine F:M 0.36, lidocaine F:M 1.0

Answer 40

Fetus/neonate able to metabolize, eliminate lidocaine better than bupivacaine * If high plasma concentrations of local in maternal blood likely, potentially delay delivery if bupivacaine to allow bup to transfer back to maternal circulation * Do not have to delay delivery if lidocaine bc ion trapped, can eliminate just fine

Answer 41

Limited renal excretion

Answer 42

Hydrolyzed by plasma pseudocholinesterases, excreted in urine * Additional contributions from esterases in RBCs, liver, synovial fluid * Chloroprocaine = most rapid clearance, fast hydrolysis rate * Procaine IV admin in horses: t1/2 = 50’, Vd 6.7L/kg * Hydrolysis products of procaine, chloroprocraine, tetracaine = pharmacologically inactive

Answer 43

* Illegal use in race horses, dogs * Ester hydrolysis in plasma; N-demethylation in liver to norcocaine, which undergoes further hydrolysis

Answer 44

para-aminobenzoic acid metabolite  allergic reaction * Why esters more assoc with allergic reactions than amides

Answer 45

metHb in people, dogs, cats * Proposed MOA: direct oxidation of heme

Answer 46

Metabolized by CYP-450 system, excreted urine/bile * Phase I: hydroxylation, N-dealkylation, N-demethylation * Phase II reactions: metabolites conjugated with amino acids or glucuronide into less active, inactive metabolites

Answer 47

Small portion excreted unchanged in urine * Humans: 4-7% lidocaine, 6% bupivacaine, 16% mepivacaine * 1.7-29% lidocaine in horses

Answer 48

Prilocaine > etidocaine > lidocaine > mepivacaine > ropivacaine > bupivacaine * In humans, prilocaine cleared most rapidly: blood clearance values exceed hepatic blood flow, indicating extrahepatic metabolism

Answer 49

O-toluidine (orthotoluidine) --> oxidizes Hgb to metHb

Answer 50

MEGX/GX --> toxicity after prolonged infusions (esp renal failure, diabetes) * Hydroxylation, demethylation in liver * MEGX = monoethylglycinexylidide o Activity 70% of lidocaine, potentially contributes to toxicity after long infusions * GX = glycinexylidide (also active) * Metabolites NOT detected in cows

Answer 51

(mepi, ropi, bupi): N-dealkylation, hydroxylation * Produce less toxic metabolite pipecoloxylidide (PPX) * Bup dealkylated metabolite: N-desbutylbupivacaine = ½ cardiotoxic, less CNS toxic vs bup  Some further conjugated to glucuronides before eliminated in urine, bile

Answer 52

 Neonates: increased absorption, in decreased Vd, increased t1/2, decreased plasma esterase activity  Geriatrics: decreased hepatic clearance, increased t1/2

Answer 53

 increased nerve sensitivity (faster onset of blockade) * Unlikely to be direct effect of progesterone on cell membrane  increased hepatic blood flow: faster lido clearance  decreased hepatic enzyme activity: slower bupivacaine, ropivacaine clearance  decreased plasma esterase activity

Answer 54

Decreased metabolism of amides, decreased plasma esterases, decreased clearance  Do not need to adjust for single dose but should for CRIs, repeated dosing, dosing intervals

Answer 55

 hepatic blood flow (any condition that decreases CO) = slower clearance, esp **lido bc dependent on HBF for clearance**  Mep, bup – metabolism more dependent on activity of hepatic enzymes, effect of decreased hepatic blood flow less pronounced

Answer 56

 Decreased plasma pseudocholineresterase activity  decreased amide metabolite excretion/increased amide metabolite (MEGX/GX)

Answer 57

Increased hepatic clearance of lidocaine, decreased excretion of MEGX

Answer 58

Decreases lidocaine clearance

Answer 59

increased plasma concentration, decreased elimination  Any that decreases plasma esterase activity (neostigmine, acetazolamide)  CYP1A2, CYP3A4 inhibitors (erythromycin): decreased hepatic clearance of amides  Adrenergic R blocking agents that decrease liver perfusion, inhibit activity of hepatic microsomal metabolizing enzymes responsible for metabolism of amides

Answer 60

Cooling increases pKa so more active, ionized form

Answer 61

one of most important physical properties during IT/subarachnoid admin  Affects distribution, spread of solution  impact characteristics of block calculated ratio of density of solution to density of CSF both measured at same temp (37*C)  Density: weight in grams of 1mL of solution, inversely related to temp

Answer 62

(= 1) – most LAs at room temp Density of CSF = Density of LA

Answer 63

(<1) goes to **non-dependent site** bc **density lower than CSF** * LAs warmed to body temp or diluted with water * Addition of opioids will also make hypobaric

Answer 64

– >1 -goes to dependent site (greater density than CSF), preferential blockade on sx side * Decreased temp or dilute with dextrose or hypertonic solution or add epi

Answer 65

Procaine, chlorprocaine

Answer 66

Mepivicaine, lidocaine, etidocaine

Answer 67

Procaine, chloroprocaine (6-7%)

Answer 68

Tetracaine, ropivaine, bupivacaine, levo, etidocaine

Answer 69

Procaine, chloroprocaine

Answer 70

Tetracaine Bup/levo bup etidocaine

Answer 71

Procaine, Chloroprocaine < lidocaine, prilo, mepivacaine

Answer 72

Ropivcaine

Answer 73

Lidocaine Mepivacaine Prilocaine

Answer 74

Bup/levobup < tetracaine < etidocaine

Answer 75

Bupivacaine

Answer 76

procaine, Chloroprocaine < lido< mepivacaine, prilocane

Answer 77

1. Procaine 2. Benzocaine 3. Chloroprocaine 4. Tetracaine

Answer 78

 Prototypical ester  Fastest onset, 30-60’ duration  CNS stimulant – illegal use in race horses  Infiltration, NBs, +/- IT for short procedures  Not very effective topically  PABA --> allergic reaction

Answer 79

Ester  Fast onset  TOPICAL ONLY  PABA --> allergic reactions  MetHb  Fish anesthesia (MS-222)

Answer 80

 Ester: Fast onset, 30-60’ duration  Human OB ax, not used regularly in vetmed  Highest pKa, fast onset due to highly concentrated form

Answer 81

 AKA amethocaine  Slow onset, except when admin intrathecal  High toxicity potential, not used in vet med  Humans: fast onset (3-5’) via IT, 2-3hr duration  Lido + tetracaine latch = better, faster dermal ax than EMLA cream  Rapid absorption from MM (fatalities in human med), excellent topical anesthesia

Answer 82

 Prototypical amide, fast onset, 1hr duration * Low pKa, not highly protein bound, can cause local VD * Prolonged up to 3h with epi  Infiltration, NBs, epidural, IT, IVRA  Some topical: mucosal (lido spray for larynx), EMLA, lidocaine patches (+/- tetracaine) Also administered systemically

Answer 83

Lidocaine 2.5%, prilocaine 2.5%

Answer 84

 Systemic: analgesia, anti-inflammatory, anti-arrhythmic (class 1b), MAC sparing in dogs, cats, goats, horses, calves * Analgesia MOA: thought to include action of Na, Ca, K channels, NMDA R * +/- Improve intestinal motility in horses, prevent POI esp if reperfusion injury

Answer 85

Cattle: * Epidural: 1d meat, 24hr milk * Infiltration (inverted L block): 4d meat, 72hr milk * Lido + epi for epidural, infiltration: 1d meat, 24hr milk Goats * Infiltration, epidural – single or multiple doses: 1d meat, 24hr milk Sheep * Infiltration, epidural – single or multiple doses: 1d meat, 24hr milk

Answer 86

One paper in humans, not validated in vet med

Answer 87

* Cats 3-5mg/kg * Dogs 6-10mg/kg * Sheep 6mg/kg

Answer 88

 Fast onset, 1-2h duration due to less VD compared to lidocaine  Infiltration, NB  Poor topical efficacy  Drug of choice for diagnostic NBs in horses DT decreased neurotoxicity  Very slow metabolism in fetus, newborn

Answer 89

* Cats 2-3mg/kg * Dogs 5-6mg/kg * Sheep 5-6mg/kg

Answer 90

Slow onset (20-30’), 3-10hr duration  high pKa, highly protein bound, highly lipophilic, minimal VD so sticks around at block site longer Infiltration, NB, epidural, IT Poor topical efficacy Not recommended for IV DT cardiotoxicity, FATAL

Answer 91

S-enantiomer of bupivacaine, decreased CV toxicity

Answer 92

Intrinsic differential blocking properties, esp at low concentrations – indicated when sensory accompanied by minimal motor blockade required

Answer 93

* Cats 1-1.5mg/kg * Dogs 2mg/kg * Sheep: 2mg/kg

Answer 94

 S-enantiomer, decreased CV toxicity vs R-enantiomer  Similar onset to bupivacaine  Differential blockade: motor blockade less affected at equipotent doses of bup  Infiltration, NB, epidural, IT  Up to 6hr duration

Answer 95

>1% vasodilation, <0.5% vasoconstriction

Answer 96

* Cats 1.5mg/kg (2) * Dogs 3mg/kg (4.4)

Answer 97

o Expectation: best of both worlds --> fast onset from lido, long duration from bupiv o Reality: conflicting studies  Similar onset to bupivacaine alone  Shorter duration that bupivacaine alone  Decreased depth of block? Increased post-op analgesia requirements

Answer 98

Nocita ® by Elanco o Other formations: polylactide microspheres, cyclodextrin inclusion complexes o Long-acting LA, up to 72hr

Answer 99

o Labeled for:  Incisional infiltration after CCL sx 5.3mg/kg  Nerve block for feline onychectomy 5.3mg/kg/forelimb o Used extra-label for many px in dogs, cats

Answer 100

discard after 4h, Carlson et al Vet Surg: up to 4d

Answer 101

 Decreased absorption, decreased Cmax (decreases potential for systemic tox), increases duration in short-acting LAs – lido, mepiv  Local VC delays absorption of LA * decreases in peripheral nerve or spinal cord blood flow --> nerve, SC ischemia * IT: regional dural VC, no decrease in SC or CBF  decreases dose required, prolongs duration

Answer 102

1gm (1000mg)/200,000mL epi = 0.005mg/mL

Answer 103

may enhance analgesia: inhibition of presynaptic NT release from C, Adelta fibers in substania gelatinosa in DH of SC * Also modify certain K channels in axons of peripheral nerves

Answer 104

systemic absorption: flushed area, increased HR, increased SV, increased CO, decreased SVR, (tachy)arrhythmias  Avoid VCs for blockade of areas with erratic blood supply, without good collateral perfusion --> VC-induced tissue ischemia, necrosis (eg ring blocks)

Answer 105

lower pH vs plain or freshly prepared solutions --> lower amt of unionized, slower onset of action

Answer 106

significant decreases in sciatic N, skeletal m blood flow when admin w/ lidocaine

Answer 107

**non-selective aR antag,** approved for reversal of soft tissue ax, associated functional deficits resulting from local dental ax in humans Can reverse effects of LAs potentiated with epi

Answer 108

 Depolymerization interstitial HA (main cement of interstitum), improves tissue penetration  **Increased pH, increased B (increasedd amount of unionized drug), shorter onset/increased spread of block**  May increase Cmax (increase toxicity) Possibly better quality of peribulbar, retrobulbar blocks in humans

Answer 109

 Opioid R on sensory neurons  Increase depth, duration of blockade  Ex: Synder 2016: bupivacaine, buprenorphine for infraorbital NB in dogs prolonged blockade duration 48-96hr * Buprenorphine can block VG Na channels, prolong LA

Answer 110

 Increased pH, increased un-ionized fraction of drug --> in theory causes faster diffusion across lipid bilayer and then becomes ionized inside cell, shorter onset  Ion trapping: Increases density, duration  Decreased pain on injection, insertion of EC

Answer 111

 Most studies fail to show efficacy with intradermal admin, NB * No effect of onset, extent, duration of skin ax in humans  Greater effect when LA admin into acidic environment * Ex: intravesicular instillation provided LA of bladder submucosa in human patients with interstitial cystitis  Buffered LAs: greater effect when topically applied to cornea

Answer 112

 0.1mEq/1mL LA – more than that will cause precipitation

Answer 113

 Decreased onset, improve quality of block possibly DT decreased intracellular pH/ion trapping

Answer 114

Effect isn’t particularly DT a2 effect - no change in presence of alpha 2 reversal agents  Clonidine extensively used in people to prolong duration of IT, epidural, PNBs

Answer 115

 **Hyperpolarization of C fibers** * Blockade of so-called hyperpolarization activated cation currents in C fibers  Shorter onset, increase duration, increase quality

Answer 116

 0.5-2mcg/mL LA  Xylazine, detomidine: epidurals in LA  Dexmed, medetomidine: regional NB in SA

Answer 117

o Decrease in duration, segmental spread, intensity of regional block despite repeated constant dosages  Not related to: structural/pharmacological properties, technique, mode of admin o Promoted by longer interanalgesic intervals btw injections  Did not occur if inj repeated at intervals short enough to prevent return of pain, or at intervals with pain <10’

Answer 118

local edema Increased epidural protein concentration Changes in LA distribution in epidural space Decrease in perineural pH (limits diffusion of LA from epidural space to binding sites in Na channels) Increased epidural blood flow Increase in local metabolism (favors clearance of LA from epidural space)

Answer 119

antagonistic effects of nucleotides, increased [Na], increased afferent input from nociceptors, receptor downregulation of Na channels

Answer 120

 Drugs that prevent hyperalgesia at spinal sites (NMDA R antag, NO-synthase inhibitors) prevent development of tachyphylaxis

Answer 121

Increased lipid solubility, increased potency --> increased potential for toxicity (bup >> lido, mep) o Most common cause: inadvertent IV (IA) inj during PNB  Incidence unknown in vet med  Humans: 1 in 10,000 with PNBs highest incidence 7.5 in 10,000

Answer 122

S enantiomers

Answer 123

 Route of administration  Speed of administration  Species  Acid-base balance  Concurrent drugs/anesthesia

Answer 124

 Low doses: effective anticonvulsants, sedative effects  Humans: tongue numbness, light-headedness, dizziness, drowsiness, acute anxiety  Horses: changes in visual function, rapid eye blinking, mild sedation, ataxia  Inhibition of inhibitory IN

Answer 125

* Inhibit inhibitory cortical neurons in temporal lobe or amygdala --> faciliatory IN function in unopposed fashion --> increased excitatory activity --> m twitching --> grand mal sz * As plasma concentrations , LAs can inhibit both inhibitory, facilitatory pathways --> CNS depression, unconsciousness, coma

Answer 126

CNS depression (cyanosis, bradycardia, unconsciousness)

Answer 127

significant difference btw rate of sz development * Caudal > brachial plexus > epidural

Answer 128

Conscious sheep: dose, plasma concentrations assoc with CV collapse (disappearance of pulsatile BP) calculated as CV:CNS ratio * Supports notion that CNS tox precedes CV tox

Answer 129

**DECREASES** seizure threshold * Hypercapnia: increases CBF --> increases drug delivery to brain +/- decreases in plasma protein binding of LAs (increase in free drug)

Answer 130

Decreased sz threshold, increased CNS/CV Tox

Answer 131

Lido 21-22mg/kg Bup 4-5 Rop 5

Answer 132

Lido 12 Bup 5

Answer 133

Lido 6.8 Bup 1.6 Ropiv 3.5

Answer 134

 Toxic effects complex, non-linear  Cardiac Na channel blockade: decreased max rate of phase 0 depolarization * Pronounced, evolving inhibition of cardiac conduction  Prolongation of PR, QRS intervals and refractory period

Answer 135

myocardial depression, increase HR slightly, widen QRS complexes, no effect on BP, CO * Long-acting LAs, R-enantiomers more arrhythmogenic than short-acting, pure S-enantiomers

Answer 136

profound sympathetic response, reverses induced myocardial depression --> increase HR, BP, CO --> arrhythmias, vtach/vfib * Short acting LAs less arrhythmogenic than long acting * Slower unbinding rates even though binding rates similar * R > S (R-enantiomers = more arrhythmogenic)

Answer 137

bradycardia, hypotension, decreased contractility, asystole  CNS toxic effects possibly involved: onset of resp failure accompanied by hypoxia, bradycardia, hypercapnia, acidosis

Answer 138

**INCREASES** toxicity * Potassium gradient most important in establishing membrane potential in cardiac myocytes * Cardiotoxic doses of lido, bupivacaine halved when K >5.4mEq/L in dogs

Answer 139

 Concentration dependent  Proposed MOA: injury to Schwann cells, inhibition of fast axonal transport, disruption of blood-nerve barrier, decreased neural blood flow with assoc ischemia, disruption of cell membrane integrity DT detergent property of LAs Spinal cord, nerve roots more prone to injury Most LAs increase spinal BF

Answer 140

 Procaine

Answer 141

 Concentration-dependent, generally regenerative, clinically imperceptible  Bupivacaine most myotoxic * Dysregulation of intracellular [Ca] +/- changes in mitochondrial bioenergetics  Pigs: bupivacaine, ropi = irreversible skeletal m damage * Calcific myonecrosis 4wks after PNB

Answer 142

 Time, concentration-dependent * Greater risk for chrondolysis with longer exposure to higher [LA] * Mepivacaine = best  Intact articular surface not protective

Answer 143

Mepivacaine < ropivacaine < bupivacaine = lidocaine (chondrocyte necrosis)

Answer 144

Oxidative damage to hemoglobin molecule: iron (Fe2+) oxidized to ferric form, Fe3+ Cannot bind oxygen, decreases carrying capacity Oxidative denaturation --> Heinz body formation --> irreversible, decreases lifespan of RBCs * Only sign if chronic * Chocolate-brown blood, not responsive to O2 therapy

Answer 145

Benzocaine, prilocaine * Benzocaine: nasopharyngeal MM, IN, dermal admin * Prilocaine: MHb in mother, fetus following epidural

Answer 146

Physiologic

Answer 147

Well tolerated

Answer 148

Clinical Signs of Hypoxia

Answer 149

lethargy, stupor, shock

Answer 150

1% methylene blue, dextrose * Dogs: 4mg/kg * Cats: 1-2mg/kg, avoid repeated doses DT markedly aggravated subsequent hemolysis * Requires NADPH to be effective, dextrose = major source of NADH

Answer 151

Amino-esters metabolized to PABA --> allergic reactions Can also have preservatives in amide preparations = PABA * Methylparaben * Sodium metabisulfite Anaphylaxis: bronchospasm, upper airway edema, vasodilation, increased capillary permeability, cutaneous wheal/flare

Answer 152

 Lidocaine, tetracaine, benzocaine – ingestion of topical preparations, laryngeal spray prior to intubation  Prolonged sedation, VD/hypotension, arrhythmias, resp depression, sz, death

Answer 153

concerns for neurotoxicity  Sodium metabisulfite  Chlorobutanol  Methyparaben  Disodium EDTA  Benzathonium chloride **MUST USE PF FREE ON BOARDS FOR EPIDURAL ADMIN**

Answer 154

o Discontinue local use o Intubation, oxygen therapy, benzodiazepine for CNS toxicity o CPR, epi, defibrillation if warranted for CPA o Amiodarone for ventricular arrhythmias – class III, K+ channel blocker o 20% lipid emulsion o Insulin, dextrose

Answer 155

 Low dose epi <1mcg/kg  High dose epi + lipid therapy = higher incidence ventricular arrhythmias, hyperlactatemia, hypoxia, acidosis, pulmonary edema

Answer 156

Amiodarone for ventricular arrhythmias – class III, K+ channel blocker

Answer 157

No, bc only 10% lipid

Answer 158

Decrease outward potassium current

Answer 159

lidocaine/procainamide, vasopressin, Ca channel blockers (IV, diltiazem), beta blockers

Answer 160

increases risk of pulmonary hemorrhage, worse outcome in rats when admin alone or with epi

Answer 161

exaggerated cardiodepressant effects