Pharmacology for Pediatric Anesthesia Flashcards

1
Q

how to roughly estimate weight (calculation)

A
50th percentile (kg)=(age x 2) + 9
<1: age (mo)/2+4
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2
Q

neonates and TBW, fat, muscle mass

A

higher total water content (75%)
reduced % of fat
rrerduced amounts of lean muscle mass

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3
Q

ECF Vd in neonates versus adults

A

ECF Vd proportionally higher than that of an adult (ex most abx and succ)

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4
Q

water soluble drugs and neonates implications

A

larger initial doses of water soluble drugs are required
potentially delayed excretion
succinylcholine, bupivicaine, many antibiotics

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5
Q

fat soluble drugs and neonates implications

A

decreased Vd of fat soluble drugs related to decreased fat and muscle mass
increased DOA r/t less tissue mass into which drug can distribute
includes thiopental, fentanyl

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6
Q

at what age does high membrane permeability (BBB) start to improve

A

by age 2

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7
Q

protein binding drugs and neonates

A

reduced total serum protein concentrations
more of administered drug is free in plasma to exert clinical effect (ex lidocaine and alfenanil)
reduced dosing may be needed for drugs such as barbiturates and local anesthetics

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8
Q

hepatic metabolism and neonates

A

hepatic enzymes usually convert medications from a less polar state to a more polar, water soluble compound
this ability is generally reduced in neonates
ability to metabolize a conjugate medication improves with age with both increased enzyme activity and increased delivery of drugs to the liver
ex) diazepam takes longer to metabolize (conjugation)

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9
Q

renal excretion and neonates

A

renal function is less efficient than in adults. incomplete glomerular development, low perfusion pressure, inadequate osmotic load
GFR and tubular function develop rapidly in first few months of life
ahminoglycosides and cephalosporins have a prolonged elimination half life in neonates (may have reduced per kg dosing)

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10
Q

inhalation agents concentration in relation to age

A

concentration of inhaled anesthetics in alveoli increase more rapidly with decreasing age infants>children>adults
more rapid inhalation induction

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11
Q

inhalation agents with infants/children and excretion/recovery/overdose

A

excretion and recovery of inhaled anesthetics is also more rapid
overdose occurs quickly and is leading cause of serious complications

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12
Q

determinants of the wash in of inhalation agents

A

impaired concentration
alveolar ventilation
FRC
CO
solubility (wash in inversely related to blood solubility)
alveolar to venous partial pressure gradient

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13
Q

the pediatric population has these three things that increase wash in of inhalation anesthetics

A

increased RR (higher MV)
decreased FRC
increased CO distribution to vessel rich groups

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14
Q

blood pressure is very sensitive to volatiles in neonates because

A

of lack of compensatory mechanisms, immature myocardium, reduced calcium stores

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15
Q

when does MAC peak

A

around 3 months of age

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16
Q

all inhalationals do what to NDMR’s

A

potentiate

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17
Q

MAC values of gases in neonates

A

sevoflurane 3.2
isoflurane 1.6
desflurane 9.2

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18
Q

MAC values of gases in infants

A

sevoflurane 3.2
isoflurane 1.8
desflurane 10

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19
Q

MAC values of gases in small children

A

sevoflurane 2.5
isoflurane 1.4
desflurane 8.2

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20
Q

describe stage 2 anesthesia

A

stage of excitement or delirium, from loss of consciousness to onset of automatic breathing. eyelash reflex disappear but other reflexes remain intact and coughing, vomiting, and struggling may occur. respiratory rate can be irregular with breath holding

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21
Q

nitrous oxide can achieve what 2 a’s

A

analgesia and amnesia

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22
Q

when is N2O contraindicated

A

pneumothorax, necrotizing enterocolitis, bowel obstructions, anywhere where air can accumulate. contraindicated in PONV as well because may contribute

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23
Q

MAC of N2O

A

104%

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24
Q

70% N2O doubles the size of pneumothorax in

A

12 minutes

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25
Q

which law encompasses the second gas effect

A

daltons law of partial pressure

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26
Q

sevoflurane specs

A

agent of choice for inhalation inductions. dose related depression of RR and TV. Common to begin with N2O then add sevoflurane in stepwise fashion

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27
Q

Blood:gas solubility of sevoflurane

A

.68

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28
Q

types of induction with sevoflurane

A

single capacity breath induction versus steal induction

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29
Q

sevoflurane used with which type of absorbents can increase the production of compound A?

A

barium hydroxide or soda lime

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30
Q

isoflurane blood: gas solubility

A

1.43

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31
Q

islflurane onset, price, NDMR

A

slower and more pungent (major disadvantage)
appropriate to use in pedes especially after inhalation induciton
potentiate NDMR to a greater extent than sevoflurane and desflurane
least costly inhalation agent

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32
Q

desflurane blood gas coefficient

A

.42

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33
Q

desflurane and LMA, emergence

A

most pungent, causes airway irritation (50% incidence of laryngospasm if used during induction)
better use is maintenance
use with LMA is controversial
emergence is rapid (could contribute to emergence delirium in a (+) or (-) way)

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34
Q

propofol induction dose, elimination half life, plasma clearrance

A

requires larger induction doses related to increased volume of distribution, elimination half life is shorter, higher rates of plasma clearance

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35
Q

propofol MOA

A

sedative hypnotic effects through interaction with GABA, principle inhibitory NT of CNS

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36
Q

propofol effects on Cv system

A

produces decerase in SVR and systolic BP.

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37
Q

propofol effects on ventilation

A

produces dose dependent depression of ventilation

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38
Q

propofol induction and TIVA dose in infants

A

1-3mg/kg, TIVA 25mcg-200mcg/kg/min

IONM: <120-130mcg/kg/min

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39
Q

ketamine MOA

A

dissociation of cerebral cortex. produces dissociative anesthesia. may resemble cataleptic state. patients eyes may remain open with slow nystagmus gaze.
analgesic and amnestic

40
Q

ketamine effects on CV system

A

resemble SNS stimulation-increased BP, pulmonary pressures, HR, and CO

41
Q

ketamine effects of ventilation

A

does not produce significant respiratory depression unless given by rapid IV dose. does produce bronchodilator and is useful in asthmatic patients.
laryngospasms may still occur

42
Q

ketamine side effects

A

secretions, vomiting, hallucinations. consider supplementing with glycopyrrolate .01mg/kg IV to precent excessive secretions

43
Q

ketamine PO, IM, IV induction, IV pain, IM induction dose

A
PO 6-10mg/kg
IM 2-5mg/kg (sedation)
IV induction 1-2mg/kg
IV pain .5mg/kg bolus, 4mcg/kg/min infusion
IM induction: 5-10mg/kg
44
Q

etomidate MOA

A

presumed to produce CNS depression via an ability to enhance the inhibitory neurotransmitter GABA. hypnotic steroid based induction agent

45
Q

etomidate effects on CV system

A

produces minimal changes in HR and CO

46
Q

edomidate effects on ventilation

A

produces dose dependent depression of ventilation

47
Q

etomidate main advantage and main disadvantage

A

main advantage: cardiovascular stability in hypovolemic patients
main disadvantage: adrenocortical suppression not well tolerated in critically ill children

48
Q

etomidate dose

A

.2-.3mg/kg

49
Q

opioids have more potent effects in pedes because

A

considered to be a result of immature BBB

50
Q

morphine dose

A

.025-.05mg/kg IV

51
Q

morphine 3 considerations

A

histamine release
hepatic conjugation is reduced
renal clearance is decreased

52
Q

fentanyl DOA

A

increased DOA in high doses r/t decreased fat/muscle. 30-60 minutes is usual
neonates and preterm infants may metabolize fentanyl more slowly

53
Q

fentanyl MOA

A

acts at stereospecific opioid receptors in CNS

used to produce analgesia and to blunt circulatory response to direct laryngoscopy

54
Q

fentanyl dose

A

.5-1mcg/kg IV to start
1mcg/kg on induction
.5mcg/kg redone
.5-2mcg/kg/hour indusion

55
Q

how long before dependence on fentanyl can occur

A

as little as 7 days

56
Q

hydromorphone class

A

semi synthetic opioid agonist. derivative of morphine, 5x more potent than morphine

57
Q

hydromorphone onset, duration, common routes of administration

A

onset: 5 minutes
duration: 2-3 hours
routes of administration: IV and epidural

58
Q

hydromorphone and compromised renal function

A

patients with compromised renal function are at risk for metabolite accumulation and neuro excitatory symptoms (tremor, agitation, cognitive dysfunction)

59
Q

naloxone antagonizes opioids and reduces

A

respiratory depression, n/v, pruritus, urinary retention

60
Q

naloxone dosing for reversal of opioid induced respiratory deperssion

A

.25-.5mcg/kg repeated until effect
max 2mg
always titrate slowly

61
Q

naloxone onset, elimination

A

rapid onset 30 seconds to one minute

elimination half life 1.5-3 hours

62
Q

naloxone overdosing can lead to

A

systemic HTN, cardiac arrhythmias, and pulmonary edema

63
Q

midazolam dosages PO, Intranasal, IV

A

.5mg/kg PO (onset 20 minutes)
.2-.3mg/kg intranasal
.05mg/kg IV (onset 5 minutes)

64
Q

midazolam PICU sedation

A

.4-2mcg/kg/min

65
Q

midazolam DOA

A

1-6 hours

66
Q

flumazenil MOA, onset, dose, elimination half life

A

GABA receptor competitive antagonist
rapid onset 5-10 minutes
10mcg/kg IV
elimination half life approximately 1 hour

67
Q

clonidine MOA

A

presynaptic alpha agonist. binding decreases calcium levels, thus inhibiting release of norepinephrine. used before precedex was a thing!

68
Q

clonidine dose PO and onset

A

4mcg/kg, 60-90 minute onset

69
Q

clonidine dose adjunct for regional anesthesia

A

1-2mcg/kg epidural/caudal. prolongs analgesia by approximately 3 hours

70
Q

clonidine side effects

A

residual sedation postoperatively

can see bradycardia and HoTN from clonidine in blocks

71
Q

dexmedetomidine MOA

A

8x more specific for alpha 2 adrenergic receptors than clonidine with anxiolytic, sedative, and analgesic properties. sedation without respiratory deperssion

72
Q

dexmedetomidine elimination half life

A

approx 2 hours

73
Q

dexmedetomidine doses PO, intranasal, IV, infusion

A

PO 1mcg/kg onset ~45 minutes
intranasal 1mcg/kg
IV .25-1mcg/kg over 10-15 minutes
infusion .2-2mcg/kg/hour

74
Q

why doe neonates have an increased sensitivity to NDMB’s?

A

reduction in release of Ach and reduced muscle mass
exntrajunctional receptors
fetal receptors have a greater opening time, allowing more sodium to enter the cell

75
Q

onset of muscle relaxants in kids

A

all relaxants have shorter onset (up to 50%) because of faster circulation times

76
Q

rocuronium doses

A

.6mg/kg and 1.2mg/kg IV

77
Q

cisatracurium doses

A

.15mg/kg IV

78
Q

vecuronium doses

A

.1mg/kg IV

79
Q

reversal of muscle relaxants: glycopyrrolate and neostigmine doses

A

.01mg/kg IV glycopyrrolate
.05mg/kg IV neostigmine
do this instead of sugammadex for female teens

80
Q

reversal of muscle relaxants: sugammadex

A

2-4mg/kg IV (16mg/kg IV for 1.2mg/kg IV rocuronium dose)

81
Q

why do infants require larger doses of succinylcholine

A

because of the increased ECF Vd. fastest onset. recovery time is similar to that of an adult

82
Q

pediatrics are at increased risk for these things when administered succinylcholine

A
cardiac arrhythmias
hyperkalemia
rhabdomyolysis
myoglobinuria
masseter muscle spasm
malignant hyperthermia
83
Q

succinylcholine doses: IV induction, IM, laryngospasm IV

A

IV: <10kg; 2mg/kg, >10mg; 1-2mg/kg
IM: 4mg/kg
IV laryngospasm: .25-.5mg/kg

84
Q

if cardiac arrest occurs after succinylcholine, what is the recommendation

A

treat for hyperkalemia.

85
Q

what to administer in pedes in conjunction with succinylcholine?

A

atropine .02mg/kg IV/IM to prevent bradycardia

86
Q

sugammadex MOA

A

cyclodextrins are rigid, ring shaped molecules composed of sugar units. the outside of the cyclodextrin is hydrophilic, which makes the molecule water soluble. the hole in the middle of the cyclodextrin ring is hydrophobic, which allows lipophilic molecules, like steroids, to enter this cavity, creating water soluble complexes

87
Q

ketorlac class, elimination half life, age limit

A

NSAID, half life 4 hours, may be reserved for children less than 1 year

88
Q

ketorlac dose

A

.5mg/kg IV

89
Q

ketorlac: caution in

A

impaired renal, increased risk for bleeding, impaired bone healing

90
Q

neonates and glycogen stores

A

neonates have very low glycogen stores and are prone to hypoglycemia during NPO and stress (such as periods of illness and injury)

91
Q

symptoms of hypoglycemia

A

jitteriness, convulsions, apnea

92
Q

acute hypoglycemia management

A

10% dextrose 1-2mL/kg
never administer bolus of D50% due to risk of vessel necrosis and high osmolarity
maintenance on supplemental IV dextrose infusions
minimize operative fasting

93
Q

percent of drug per 100mL of fluid in grams: D50% example

A

50 grams of dextrose per 100mL=.5grams/mL

94
Q

epinephrine resuscitation dose

A

1mcg/kg to tx HoTN, 10mcg/kg IV for cardiac arrest

repeat q3-5minutes PRN

95
Q

atropine resuscitation dose

A

20mcg/kg IV for symptoms of bradycardia. max dose 1mg for child and 2mg for adolescent

96
Q

adenosine resuscitation dose

A

100mcg/kg IV rapid bolus and flush, max 6mg IV, second dose 200mcg/kg IV rapid bolus and flush, max 12mg IV