Pharmacology for Pediatric Anesthesia Flashcards
how to roughly estimate weight (calculation)
50th percentile (kg)=(age x 2) + 9 <1: age (mo)/2+4
neonates and TBW, fat, muscle mass
higher total water content (75%)
reduced % of fat
rrerduced amounts of lean muscle mass
ECF Vd in neonates versus adults
ECF Vd proportionally higher than that of an adult (ex most abx and succ)
water soluble drugs and neonates implications
larger initial doses of water soluble drugs are required
potentially delayed excretion
succinylcholine, bupivicaine, many antibiotics
fat soluble drugs and neonates implications
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
at what age does high membrane permeability (BBB) start to improve
by age 2
protein binding drugs and neonates
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
hepatic metabolism and neonates
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)
renal excretion and neonates
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)
inhalation agents concentration in relation to age
concentration of inhaled anesthetics in alveoli increase more rapidly with decreasing age infants>children>adults
more rapid inhalation induction
inhalation agents with infants/children and excretion/recovery/overdose
excretion and recovery of inhaled anesthetics is also more rapid
overdose occurs quickly and is leading cause of serious complications
determinants of the wash in of inhalation agents
impaired concentration
alveolar ventilation
FRC
CO
solubility (wash in inversely related to blood solubility)
alveolar to venous partial pressure gradient
the pediatric population has these three things that increase wash in of inhalation anesthetics
increased RR (higher MV)
decreased FRC
increased CO distribution to vessel rich groups
blood pressure is very sensitive to volatiles in neonates because
of lack of compensatory mechanisms, immature myocardium, reduced calcium stores
when does MAC peak
around 3 months of age
all inhalationals do what to NDMR’s
potentiate
MAC values of gases in neonates
sevoflurane 3.2
isoflurane 1.6
desflurane 9.2
MAC values of gases in infants
sevoflurane 3.2
isoflurane 1.8
desflurane 10
MAC values of gases in small children
sevoflurane 2.5
isoflurane 1.4
desflurane 8.2
describe stage 2 anesthesia
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
nitrous oxide can achieve what 2 a’s
analgesia and amnesia
when is N2O contraindicated
pneumothorax, necrotizing enterocolitis, bowel obstructions, anywhere where air can accumulate. contraindicated in PONV as well because may contribute
MAC of N2O
104%
70% N2O doubles the size of pneumothorax in
12 minutes
which law encompasses the second gas effect
daltons law of partial pressure
sevoflurane specs
agent of choice for inhalation inductions. dose related depression of RR and TV. Common to begin with N2O then add sevoflurane in stepwise fashion
Blood:gas solubility of sevoflurane
.68
types of induction with sevoflurane
single capacity breath induction versus steal induction
sevoflurane used with which type of absorbents can increase the production of compound A?
barium hydroxide or soda lime
isoflurane blood: gas solubility
1.43
islflurane onset, price, NDMR
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
desflurane blood gas coefficient
.42
desflurane and LMA, emergence
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)
propofol induction dose, elimination half life, plasma clearrance
requires larger induction doses related to increased volume of distribution, elimination half life is shorter, higher rates of plasma clearance
propofol MOA
sedative hypnotic effects through interaction with GABA, principle inhibitory NT of CNS
propofol effects on Cv system
produces decerase in SVR and systolic BP.
propofol effects on ventilation
produces dose dependent depression of ventilation
propofol induction and TIVA dose in infants
1-3mg/kg, TIVA 25mcg-200mcg/kg/min
IONM: <120-130mcg/kg/min
ketamine MOA
dissociation of cerebral cortex. produces dissociative anesthesia. may resemble cataleptic state. patients eyes may remain open with slow nystagmus gaze.
analgesic and amnestic
ketamine effects on CV system
resemble SNS stimulation-increased BP, pulmonary pressures, HR, and CO
ketamine effects of ventilation
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
ketamine side effects
secretions, vomiting, hallucinations. consider supplementing with glycopyrrolate .01mg/kg IV to precent excessive secretions
ketamine PO, IM, IV induction, IV pain, IM induction dose
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
etomidate MOA
presumed to produce CNS depression via an ability to enhance the inhibitory neurotransmitter GABA. hypnotic steroid based induction agent
etomidate effects on CV system
produces minimal changes in HR and CO
edomidate effects on ventilation
produces dose dependent depression of ventilation
etomidate main advantage and main disadvantage
main advantage: cardiovascular stability in hypovolemic patients
main disadvantage: adrenocortical suppression not well tolerated in critically ill children
etomidate dose
.2-.3mg/kg
opioids have more potent effects in pedes because
considered to be a result of immature BBB
morphine dose
.025-.05mg/kg IV
morphine 3 considerations
histamine release
hepatic conjugation is reduced
renal clearance is decreased
fentanyl DOA
increased DOA in high doses r/t decreased fat/muscle. 30-60 minutes is usual
neonates and preterm infants may metabolize fentanyl more slowly
fentanyl MOA
acts at stereospecific opioid receptors in CNS
used to produce analgesia and to blunt circulatory response to direct laryngoscopy
fentanyl dose
.5-1mcg/kg IV to start
1mcg/kg on induction
.5mcg/kg redone
.5-2mcg/kg/hour indusion
how long before dependence on fentanyl can occur
as little as 7 days
hydromorphone class
semi synthetic opioid agonist. derivative of morphine, 5x more potent than morphine
hydromorphone onset, duration, common routes of administration
onset: 5 minutes
duration: 2-3 hours
routes of administration: IV and epidural
hydromorphone and compromised renal function
patients with compromised renal function are at risk for metabolite accumulation and neuro excitatory symptoms (tremor, agitation, cognitive dysfunction)
naloxone antagonizes opioids and reduces
respiratory depression, n/v, pruritus, urinary retention
naloxone dosing for reversal of opioid induced respiratory deperssion
.25-.5mcg/kg repeated until effect
max 2mg
always titrate slowly
naloxone onset, elimination
rapid onset 30 seconds to one minute
elimination half life 1.5-3 hours
naloxone overdosing can lead to
systemic HTN, cardiac arrhythmias, and pulmonary edema
midazolam dosages PO, Intranasal, IV
.5mg/kg PO (onset 20 minutes)
.2-.3mg/kg intranasal
.05mg/kg IV (onset 5 minutes)
midazolam PICU sedation
.4-2mcg/kg/min
midazolam DOA
1-6 hours
flumazenil MOA, onset, dose, elimination half life
GABA receptor competitive antagonist
rapid onset 5-10 minutes
10mcg/kg IV
elimination half life approximately 1 hour
clonidine MOA
presynaptic alpha agonist. binding decreases calcium levels, thus inhibiting release of norepinephrine. used before precedex was a thing!
clonidine dose PO and onset
4mcg/kg, 60-90 minute onset
clonidine dose adjunct for regional anesthesia
1-2mcg/kg epidural/caudal. prolongs analgesia by approximately 3 hours
clonidine side effects
residual sedation postoperatively
can see bradycardia and HoTN from clonidine in blocks
dexmedetomidine MOA
8x more specific for alpha 2 adrenergic receptors than clonidine with anxiolytic, sedative, and analgesic properties. sedation without respiratory deperssion
dexmedetomidine elimination half life
approx 2 hours
dexmedetomidine doses PO, intranasal, IV, infusion
PO 1mcg/kg onset ~45 minutes
intranasal 1mcg/kg
IV .25-1mcg/kg over 10-15 minutes
infusion .2-2mcg/kg/hour
why doe neonates have an increased sensitivity to NDMB’s?
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
onset of muscle relaxants in kids
all relaxants have shorter onset (up to 50%) because of faster circulation times
rocuronium doses
.6mg/kg and 1.2mg/kg IV
cisatracurium doses
.15mg/kg IV
vecuronium doses
.1mg/kg IV
reversal of muscle relaxants: glycopyrrolate and neostigmine doses
.01mg/kg IV glycopyrrolate
.05mg/kg IV neostigmine
do this instead of sugammadex for female teens
reversal of muscle relaxants: sugammadex
2-4mg/kg IV (16mg/kg IV for 1.2mg/kg IV rocuronium dose)
why do infants require larger doses of succinylcholine
because of the increased ECF Vd. fastest onset. recovery time is similar to that of an adult
pediatrics are at increased risk for these things when administered succinylcholine
cardiac arrhythmias hyperkalemia rhabdomyolysis myoglobinuria masseter muscle spasm malignant hyperthermia
succinylcholine doses: IV induction, IM, laryngospasm IV
IV: <10kg; 2mg/kg, >10mg; 1-2mg/kg
IM: 4mg/kg
IV laryngospasm: .25-.5mg/kg
if cardiac arrest occurs after succinylcholine, what is the recommendation
treat for hyperkalemia.
what to administer in pedes in conjunction with succinylcholine?
atropine .02mg/kg IV/IM to prevent bradycardia
sugammadex MOA
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
ketorlac class, elimination half life, age limit
NSAID, half life 4 hours, may be reserved for children less than 1 year
ketorlac dose
.5mg/kg IV
ketorlac: caution in
impaired renal, increased risk for bleeding, impaired bone healing
neonates and glycogen stores
neonates have very low glycogen stores and are prone to hypoglycemia during NPO and stress (such as periods of illness and injury)
symptoms of hypoglycemia
jitteriness, convulsions, apnea
acute hypoglycemia management
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
percent of drug per 100mL of fluid in grams: D50% example
50 grams of dextrose per 100mL=.5grams/mL
epinephrine resuscitation dose
1mcg/kg to tx HoTN, 10mcg/kg IV for cardiac arrest
repeat q3-5minutes PRN
atropine resuscitation dose
20mcg/kg IV for symptoms of bradycardia. max dose 1mg for child and 2mg for adolescent
adenosine resuscitation dose
100mcg/kg IV rapid bolus and flush, max 6mg IV, second dose 200mcg/kg IV rapid bolus and flush, max 12mg IV
