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Pediatrics > KN Exam 2 (Part 2) > Flashcards

KN Exam 2 (Part 2) Flashcards

1
Q

Cell saver Hct

A

recovered and washed blood will have a Hct of 50-60%

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1
Q

Precedex uses:

A
  • Anxiolysis, analgesia, decrease HR, decrease emergence delirium
  • Procedural sedation
  • anesthetic adjunct
  • in neonates and children: prevention of ED, postoperative pain management, invasive and noninvasive procedural sedation, and the management of opioid withdrawal
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2
Q

How to Minimize the risks of infection and immunologic risk with cell saver

A

give the reinfusion in the OR

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3
Q

Cell saver in peds is useful to minimize allogenic blood transfusion in what type of surgery?

A

spine

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4
Q

Cell saver
Cons

A
  • pediatric sizes challenging to obtain
  • not appropriate if surgical field contaminated
  • or if clotting agents, antibiotics or other foreign materials have been used on the surgical field
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5
Q

Too small airway

A

tip will line up well above the AOM and exacerbate airway obstruction by kinking the tongue

too short: may rest against the base of the tongue, forcing it posteriorly against the roof of the mouth, further aggravating airway obstruction

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6
Q

An LMA that is too small will pass easily but

A

may not seal against the laryngeal inlet

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7
Q

the most common cause of failure to place LMA

A

wrong size

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8
Q

An oral airway that is too small places the tip in the ____ of the tongue

A

middle

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9
Q

How can too small of an airway cause damage?

A

obstruct the lingual vein and cause tongue swelling

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10
Q

Nasal airway should be _____ than the correct oral airway

A

2-4 cm longer

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11
Q

T/F:
If you don’t have a nasal airway small enough for the child, you can cut an ETT to the appropriate length

A

True

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12
Q

Too small an uncuffed tube

A

won’t provide a seal and can prevent positive pressure ventilation

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13
Q

Deep extubation

A

With ‘deep’ extubation, the ET tube is removed before wake-up and before the return of upper airway reflexes

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14
Q

indicates return of upper airway reflexes

A

Cough and gag

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15
Q

T/F:
There are no absolute indications for deep extubation

A

True

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16
Q

When to deep extubate

A

if coughing during wake-up could be detrimental

e.g. in some cases of intracranial or head and neck surgery

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17
Q

T/F:
By deep extubating, we can assure that the pt will not cough.

A

FALSE
Deep extubation does not guarantee that a patient won’t cough during wake-up

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18
Q

T/F:
LMAs are routinely removed while still deep

A

True!

presence of a supraglottic airway during wake-up can trigger laryngospasm
esp. since peds have more ‘lively’ upper airway reflexes compared to adults

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19
Q

goal during ‘deep’ extubation

A

have the patient sufficiently anesthetized to suppress any upper airway reflexes such as coughing and gagging

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20
Q

Patients less suited for a deep extubation

A
  1. (Some) patients with difficult airways; surgery of or near the airway.
  2. Obese patients: tend to not breathe very well unsupported under general anesthesia, i.e. just after ‘deep’ extubation.
  3. at risk of aspiration
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21
Q

Steps for deep extubation

A
  1. Inspect & suctioning the upper airway meticulously (direct vision under layngoscopy)
  2. Make sure they are deep: at least 1 MAC
  3. NO response to suctioning of the oral cavity and hypopharynx.
  4. established, more or less ‘normal’ spontaneous respiratory pattern and rate
  5. Consider nasopharyngeal airway (better tolerated than oral)
  6. Pre-oxygenate
  7. Extubate, turn off the gas; give high flow O2
  8. Maintain airway patency: In most patients you will initially require basic airway maneuvers to maintain airway patency
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22
Q

It is very common, even for adequately anesthetized patients, to breath-hold for a brief period immediately after ‘deep’ extubation.
Wyd?

A

Do not rush into administering bag-mask ventilation!
Since you have pre-oxygenated your patient, it should be safe to wait at least 40 seconds or so for spontaneous breathing to resume while maintaining airway patency and providing 100% oxygen insufflation.

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23
Q

evidence of partial airway obstruction

A

stridor
tracheal ‘tugging’
‘see-saw’ breathing pattern

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24
Q

After ‘deep’ extubation, do not transfer the patient out until ….

A

they are able to maintain their own airway without basic airway maneuvers

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25
Q

EBV

A
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26
Q

Appropriate heart rate for age

A
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27
Q

BP measured in
lower extremity
vs.
upper extremity

A

BP measured in lower extremity is lower

“lower is lower”

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28
Q

These infants will have a lower BP

A

birth asphyxia & those who need mechanical ventilation

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29
Q

Average SBP increases in neonates & infants

A

First 12 hr of life: 65 mmHg
4 days: 75 mmHg
6 weeks: 95 mmHg

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30
Q

Normal BP

A
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31
Q

Normal RR

A
  • 0-12 months: 30-53
  • 1-3 years: 22-37
  • 4-5 years: 20-28
  • 6-12 years: 18-25
  • 13-18 years: 12-20
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32
Q

What consistent respiratory rate …… in ANY child is abnormal & needs investigation

A

< 10 or > 60

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33
Q

CO range in full-term & preterm neonates

A

220-350 mL/kg/min

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34
Q

FT and preemies have (lower/higher) CO than adults due to…

A

2-3x HIGHER than adults

Reflects greater metabolic rate (per weight) and O2 consumption

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35
Q

Baseline O2 sats < 95% on RA

A

suggest pulmonary or cardiac compromise

need investigation

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36
Q

Normal Hgb for FT and preemies

A

neonate: 14 - 20 g/dL

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37
Q

MABL & MAH

A

EBV (Hct - min acceptable Hct) / Hct

MAH:
Healthy kid - 30%
3 months old - 25%
Older child - 20%

Remember: child with severe pulmonary disease or cyanotic congenital heart disease may need a higher Hct (~30%) even if aren’t in that age range

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38
Q

RBC transfusion must be ABO ____
Whole blood must be ABO ___

A

RBC: ABO compatible
Whole blood: ABO identical

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39
Q

Blood products with a large amount of plasma (whole blood, FFP, apheresis platelets) must be compatible with…

A

A or B surface antigens on recipients RBC

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40
Q

Platelets (apheresis & whole blood derived) should be ABO ____ for children

A

compatible

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41
Q

Whole blood derived platelets match…..

A

Rh status (+/-) if able to

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42
Q

ABO Compatibility of Blood Components

A
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43
Q

Indication for PRBC

A

symptomatic deficits of O2 carrying capacity

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44
Q

How much will PRBCs increase H&H?
Hct of a PRBC?

A

10-15 mL/kg = ↑Hbg 2-3, Hct 1%/mL/kg

1 unit PRBC average Hct 60%

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45
Q

PRBC infusion rate:

A

3-5 mL/kg/hr

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46
Q

formula to estimate the volume of PRBCs needed to achieve a final hematocrit of 35%

ex: hematocrit of a 10-kg child has decreased to 23% and the intraoperative blood loss is expected to continue postoperatively

A
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47
Q

Platelets ____ increases count by 50,000-100,000

A

5-10 mL/kg
or
0.1-0.3 units/kg

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48
Q

How fast can u give Platelets

A

finish within 30 min
if volume not > 5-10 mL/kg

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49
Q

Plt count of _____ is adequate to prevent spont. bleeding or bleeding from minor invasive procedures

A

40,000-50,000

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50
Q

FFP ___ mL/kg increases Factor levels by 15-20%

A

10-15

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51
Q

Cryo 1-2 units/kg – increases fibrinogen by

A

60-100 mg/dL

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52
Q

Fibrinogen Concentrate & and fibrinogen increases

A

70 mg/kg = ↑ fibrinogen 120 mg/dL

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53
Q

Blood product Filters

A

Standard adult/pedi transfusion filter (170-260 microns)

SQ40 microaggregate filter (40 microns)
Protects against microaggregates (leuks, fibrin, plts) and non blood component matters

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54
Q

T/F:
Hypokalemia is a possible complication of blood transfusions

A

False
HYPER

55
Q

Hyperkalemia

A

K > 5.5
but
upper normal limit in preterm/young infants can be up to 6.5

Complication of blood transfusion

56
Q

Monitor EKG when rate of transfusion (whole blood or PRBC) >

A

1.5-2 mL/kg/min

57
Q

When giving Whole blood/PRBC, you notice ventricular arrhythmias w/ peaked T waves. wyd?

A

Consider

  • Calcium chloride
  • Bicarb
  • Glucose & Insulin
  • Hyperventilation
  • Inhaled Beta Agonist (albuterol)
58
Q

K range and effects on EKG

A

5.5-6.5 = tall peaked T waves
6.5-7.5 = loss of P waves
7-8 = widening QRS
8-10 = sine wave, ventricular arrhythmia, asystole

59
Q

MTP is defined as…

A

> 40 mL/kg of total blood components in 24 hours
or
20 mL/kg of RBC over 4-6 hours

60
Q

Adult & pedi mass hemorrhage mortality: most deaths due to traumatic hemorrhage occur within…

A

the first 6 hours
⅔ of pts

61
Q

T/F:
Pedi mass hemorrhage 28 day mortality is the highest in trauma patients

A

False
medical patients (65%)
trauma (36%)
cardiac surgery (24%)

62
Q

T/F:
MTP has not improved 30 day mortality rate

A

True :(

63
Q

T/F:
Children experience more allergic, febrile, and hypotension reactions

A

True

64
Q

IV Size & Flow

A
  • 14G = 240 ml/min (1L in 4 min)
  • 16G = 180 ml/min (1L in 5.5 min)
  • 18G = 90 ml/min (1L in 11 min)
  • 20G = 60 ml/min (1L in 17 min)
  • 22G = 36 ml/min (1L in 28 min)
  • 24G = 20 ml/min (1L in 50 min)
  • 26G = 13 ml/min (1L in 77 min)

chode got the flo

65
Q

Avoid these products in 22-24G

A

dextrose 10% or higher,
K, Ca, and bicarb

66
Q

How to combat fluid deficit & metabolic abnormalities

A

Minimize fasting time
1-2% dextrose if needed
( < 6 months, TPN dependent, malnutrition, endocrinopathies)

67
Q

The Holliday - Segar 4-2-1 Rule

A

4 mL/kg/hr (first 10 kg) +
2 mL/kg/hr (second 10 kg) +
1 mL/kg/hr (every kg left)

68
Q

The Holliday - Segar 4-2-1 Rule
is based on…

A

metabolic rate
1 mL of water needed for each kcal of energy expended

69
Q

Maintenance fluid rates

A

Example: 5 kg infant
(4 mL)(5 kg) = 20 mL/hr
20 mL/hr x 24 hours = 480 mL/day

Example: 15 kg kid
40 mL + (2mL)(5kg) = 50 mL/hr
50 mL/hr x 24hr = 1200 mL/day

70
Q

How much fluid to give for marginal to moderate hypovolemia?
(ex: after fasting for surgery)

(no significant heart or kidney disease)

A

20 to 40 mL/kg of isotonic fluids
during the surgery and PACU

(as rapidly as 10–20 mL/kg/hr).

71
Q

Larger fluid deficit (after a bowel prep) may require how much fluid?

(no significant heart or kidney disease)

A

40-80 mL/kg

preop fasting usually give 20 to 40 mL/kg

72
Q

Resuscitation ranges
by agent

A
  • Crystalloid: 10-20 mL/kg (up to 3 boluses)
  • Colloid: 20 mL/kg
  • RBC or FFP: 10-20 mL/kg

when in doubt, pick 20 mL/kg

73
Q

Limitations of the Immature kidney

A
  • cannot concentrate urine
  • Limited ability to: reabsorb Na & bicarb + excrete K
  • Places neonates & risk for dehydration, hyponatremia, hyperkalemia & hypervolemia
74
Q

Neonates are at risk for which elec. imbalances d/t immature kidneys

A

hyponatremia, hyperkalemia
+
hypervolemia & dehydration

75
Q

Even during hypotensive anesthesia, kidneys should produce ____ of urine

A

0.5-1.0 mL/kg/hr

76
Q

Signs of moderate
vs
Severe
hypovolemia

A

moderate: urine output < 0.5 mL/kg/hr

severe: anuria

0.5-1.0 mL/kg/hr is the goal

77
Q

___ is the primary extracellular (+) charged ion (cation)

A

Na

78
Q

Hyponatremia can cause

A

cerebral edema & encephalopathy

79
Q

T/F:
Mild hypernatremia is common post op

A

False
hyponatremia

80
Q

common manifestation of advanced hyponatremia

A

Respiratory arrest (or irregularity)

81
Q

How fast can we correct Na

A

MAX 0.5 mEq/L/hr
or
25 mEq/L in 24-48H

82
Q

T/F:
Water moves from areas of high Na → low Na

A

FALSE
low → high Na
water follows the solute

83
Q

Rapid correction of hyponatremia can cause

A

central pontine myelinolysis

84
Q

Asymptomatic hyponatremia treatment:

A

free water restriction
1L isotonic fluids/day if needed for CV support

85
Q

Symptomatic hyponatremia treatment:

A
  • Medical emergency - could be irreversible neuro injury
  • 2-3 mL/kg of 3% saline over 20-30 min to stop seizures
  • Slowly correct after that, not to exceed 0.5 mEq/L/hr or 12-25 mEq/L total in 24-48 hr
86
Q

Speed of induction
Depends on
(5)

A
  1. Wash-in (PK)
  2. Potency/MAC of agent
  3. Rate of increase of inspired concentration
  4. Maximum inspired concentration
  5. Respiration (including airway irritability/spontaneous vs controlled)
87
Q

“Wash in”

A

ratio of alveolar to inspired anesthetic partial pressure (FA/FI)

88
Q

(Lower/higher) blood solubility = faster wash in

A

Lower

89
Q

Why is Wash/In faster in neonates than adults

A
  • Greater alveolar ventilation to FRC - 5:1 (adults 1.5:1)
  • Greater % of CO distributed to vessel rich groups
  • ½ the tissue/blood solubility
  • Reduced blood/gas solubility
90
Q

alveolar ventilation to FRC
neonates vs adults

A

neonates 5:1
adults 1.5:1

91
Q

T/F:
Gene mutations & hypothermia can change MAC requirements

A

True

92
Q

Morphine potency

A

1

93
Q

T/F:
Morphine is poorly lipid soluble

A

True

94
Q

Morphine
Activates the ___ receptor

A

Mu-1

95
Q

Morphine
metabolites

A
  • morphine-3-glucuronide (M3G) & morphine-6-glucuronide (M6G) - both active
  • M6G: analgesia, nausea, respiratory depression
  • M3G: antagonizes morphine, contributes to tolerance development
96
Q

The liver enzyme for morphine metab

A

UGT2B7

97
Q

M6G T ½ Keo

t½ke0: time to achieve 50% effect-site concentration when the plasma levels are maintained at steady state.

A

4-8 hours

98
Q

Morphine with reduced liver & renal function

A

build up of M3G + M6G leading to increased respiratory suppression in children & neonates relative to adults

99
Q

Morphine Clearance

A
  • Sulfation & renal clearance are more dominant pathways in neonates (minor in adults)
  • Metabolites are cleared by the kidney and biliary excretion
100
Q

Codeine is AKA

A

methylmorphine

101
Q

Codeine has low affinity for opioid receptors and is ___ the potency of morphine

A

1/10th

102
Q

Codeine analgesia depends on

A

how much is metabolized to morphine

103
Q

How much codeine is excreted unchanged vs metabolized

A

5-15% excreted unchanged in urine
85-95% undergoes liver metabolism

104
Q

Codeine liver metabolism

85-95% undergoes liver metabolism

A

Glucuronidation (main)
O-demethylation
N-demethylation

105
Q

Up to 11% of codeine is metabolized to ____. 5-15% undergoes O-demethylation to _____ via CYP2D6

A

11% hydrocodone

15% morphine

106
Q

How does codeine become morphine?

A

O-demethylation via CYP2D6

107
Q

Codeine in pts with CYP2D6 issues (polymorphisms)
Poor metabolizers:

A
  • CYP2D6 barely works & they can’t break down codeine into morphine
  • little/no analgesia, but still have side effects
  • 10% caucasians, 30% hong kong chinese
108
Q

Codeine in pts with CYP2D6 issues (polymorphisms)
Intermediate/extensive metabolizers (EM):

A

relatively normal - convert codeine into morphine slowly

109
Q

Codeine in pts with CYP2D6 issues (polymorphisms)
Ultra-rapid metabolizers (UM):

A
  • extra CYP2D6 - high enzyme activity
  • codeine into morphine fast & in large amounts
  • more potent effects, morphine toxicity, & resp depression even at normal doses
  • 29% ethiopian
110
Q

CYP2D6 (polymorphisms):
Amount of morphine metabolite produced in order of least to most

A

Poor → intermediate → ultra-rapid metabolizers

111
Q

T/F:
Giving Codeine to a pt with a CYP3A4 poly oprhism can lead to accidental overdose

A

False
CYP2D6

112
Q

Codeine is not recommended for children. Why?

A

variety of things can affect how they metabolize codeine depending on where they’re at in life

113
Q

desaturation WITHOUT upper airway obstruction is most likely due to…

A

ventilation-perfusion mismatch due to segmental atelectasis

114
Q

Desaturation d/t segmental atelectasis (not upper airway obstruction) is ocurring. Wyd?

A

Recruit alveoli using sustained inflation of the lungs to 30 cm H2O for 30 seconds. If the stomach inflates, stop.

115
Q

UAO from hypopharyngeal collapse or mild laryngospasm. Wyd?

A
  1. tight mask fit, close APL, 5 to 10 cm PEEP
  2. distending pressure of the bag stents the airway open until anesthetized and can place OPA.
  3. Cephalad pressure to the superior pole of the condyle of the mandible to sublux the TMJ (opens the mouth and pulls the tongue off the posterior and nasopharyngeal walls, opening the laryngeal inlet)
116
Q

digital pressure to the soft tissues of the submental triangle

A

pushes the tongue and soft tissues into the hypopharynx, occluding the oropharynx and nasopharynx

117
Q

UAO
If the child develops symptomatic bradycardia

UAO: upper airway obstruction

A
  1. oxygenation and ventilation must FIRST be established
  2. IV atropine (0.02 mg/kg)
  3. if necessary, chest compressions and IV epinephrine
118
Q

T/F:
Halothane causes more upper airway obstruction than Sevoflurane at 1 MAC.

A

False
1 MAC of Sevo causes more

119
Q

How does a dose of 0.5-1.5 MAC sevoflurane affect the airway?

A

decreases cross-sectional area of the airway by 1/3 mostly anteroposteriorly (pharyngeal wall collapse)

easily offset with PEEP

120
Q

T/F:
most drugs or inhalation agents contribute to upper airway obstruction

A

True

decrease muscle tone of the upper airway = UAO = more labored breathing, fatigue, and subsequent apnea

121
Q

T/F:
Propofol narrows the upper airway but it may still remain patent

A

True
narrows it the hypopharyngeally especially

higher doses may obstruct

122
Q

T/F:
Airways effects of higher propofol doses may cause UAO, but it reverses on emergence.

A

True

123
Q

Which agent can cause UAO via direct inhibition of genioglossus muscle

A

Prop

124
Q

Prop has these 3 effects on the airway that contribute to UAO

A

direct inhibition of:
genioglossus muscle, centrally mediated airway dilatation, & airway reflexes

125
Q

T/F:
ketamine does not cause airway obstruction, but midazolam does

A

True

126
Q

An IV Versed dose of ____ is enough to cause central apnea & UAO by reducing pharyngeal muscle tone

A

0.1 mg/kg

127
Q

Children sedated with Versed for dental procedures are at higher risk for UAO. Why?

A

mouth opening may increase upper airway collapse

(Versed reduces pharyngeal muscle tone)

128
Q

T/F:
Dexmedetomidine does not tend to cause UAO in OSA and non-OSA

A

True
always take precautions ofc

129
Q

The tongue is a larger contributor of UAO in which age group

A

infants & neonates

the tongue may still contribute to obstruction in all ages

130
Q

obstruction in older children is more likely d/t

A

nasopharynx and epiglottis collapse

infants and neonates is most likely tongue

131
Q

Obstruction of the extrathoracic upper airway can occur with…

A

epiglottitis,
laryngotracheobronchitis,
or an extrathoracic foreign body

132
Q

T/F:
Airway obstruction during anesthesia/LOC is mostly from the tongue against the posterior pharyngeal wall.

A

False!
more likely loss of muscle tone in the pharyngeal and laryngeal structures

133
Q

sniffing position

A

Extension of the head at the atlantooccipital joint with anterior displacement of the cervical spine

134
Q

The sniffing position improves hypopharyngeal airway patency but does not reposition the tongue. This tells us that…

A

upper airway obstruction is not primarily caused by changes in tongue position but rather by collapse of the pharyngeal structures.

135
Q

OPA sizing
too small vs too large

A
  • too large: tip posterior to AOM and obstruct the glottic opening by pushing the epiglottis down
  • too small: tip above AOM and exacerbate airway obstruction by kinking the tongue

Pediatrics (2 decks)

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