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Pediatric Anesthesia > Exam2:fluid, blood, CHD, congenital heart surgery > Flashcards

Exam2:fluid, blood, CHD, congenital heart surgery Flashcards

1
Q

what is the incidence of congenital heart issues

A

7-10/1000

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2
Q

what is risk of congenital heart defet in premature compared to normal

A

2-3x higher

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3
Q

what percent of congenital diseases are heart diseases

A

30%

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4
Q

what percent of congenital heart disease survive to adulthood without treatment

A

15%

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5
Q

R to L shunts are (cyanotic/acyanotic)

A

cyanotic

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6
Q

L to R shunts are (cyanotic/acyanotic)

A

acyanotic

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7
Q

what kind of cardiac anomalies require a simple repair

A

PDA, AD, VSD

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8
Q

what kind of cardiac anomalies require a complex repair with baffles and conduits

A

tetralogy of fallot
severe AS
severe PS
mitral stenosis

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9
Q

a shunt is a (resp/blood) problem

A

resp

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10
Q

deadspace is a (resp/blood) problem

A

blood

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11
Q

what kind of repair is curative meaning that cyanosis is fixed

A

anatomic

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12
Q

what kind of repair is cyanosis relieved

A

physiologic repair

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13
Q

what kind of repair is usually univentricular or reversed ventricles

A

physiologic

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14
Q

what kind of repair is for single ventricles that ar overloaded

A

physiologic repair

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15
Q

how is anesthesia in anatomic repair post repair

A

normal

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16
Q

how is anesthesia in physiologic repair

A

significant changes in anesthesia care with increased perioperative risk

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17
Q

what kind of repair has increase perioperative risk

A

physiological

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18
Q

what type of repair is palliative in nature

A

physiological

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19
Q

shunt is all _______ with no ______

A

blood
air

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20
Q

dead space is all ________ with no _______

A

air
blood

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21
Q

what is communication between systemic and pulmonary circulation

A

shunting

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22
Q

what is mixing of arterial and venous blood

A

shunting

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23
Q

what kjnd of shunting is PVR and SVR less important

A

small communication

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24
Q

what is an example of a small shunt where flow is limited

A

ASD/VSD or small PDA

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25
Q

what kind of shunt dose size and direction depend on PVR and SVR

A

dependent shunt

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26
Q

what kind of shunt is between two nearly equal pressures

A

dependent shunt

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27
Q

what kind of shunt can anesthesia control by manipulating SVR and PVR

A

dependent

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28
Q

what kind of shunt is a PDA (dependent vs obligatory)

A

dependent

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29
Q

what kind of shunt is SVR/PVR pressure significant so is no longer dependent of PVR/SVR relationsip

A

obligatory

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30
Q

what kind of shunt is AV canal Defect (obligatory vs dependent)

A

obligatory

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31
Q

what can we give to manipulate SVR

A

phenylephrine, phentolamine

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32
Q

what way does blood ravel if PVR>SVR

A

R to L

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33
Q

what way does blood travel if SVR> PVR

A

L to R

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34
Q

what direction of shunt is cyanotic

A

R to L

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35
Q

what kind of shunt is deoxygenated blood bypassing the lungs and entering systemic circulation

A

cyanotic (R to L)

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36
Q

what kind of shunt is an Acyanotic shunt

A

L to right

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37
Q

what kind of shunt does oxygenated blood recirculated into pulmonary circulation

A

acyanotic shunt

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38
Q

what are acyanotic shunts with increased pulmonary blood flow

A

ASD
VSD
PDA
AV canal defect
(L to R shunts)

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39
Q

what are acyanotic shunts from obstructions to blood flow from ventricles

A

coarctation of the aorta
aortic stenosis
pulmonic stenosis
(outflow obstructions)

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40
Q

what are cyanotic shunts with decreased pulmonary blood flow

A

tetralogy of fallot
tricuspid atresia

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41
Q

what are cyanotic shunts with mixed blood flow

A

transposition of great arteries
total anomalous pulmonary venous return
truncus arteriosus
hypoplastic L heart syndrome

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42
Q

what is the HCT limit afterwhich there is decreased oxygen carrying capacity, sludging, increased workload on heart, and clotting

A

65%

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43
Q

what factors affect shunt

A

size of shunt orifice
pressure gradient
LV and RV compliance
PVR to SVR ratio
Blood viscosity (Hct)

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44
Q

when PVR is > SVR this is a ______ to _____ shunt

A

R to L

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45
Q

when SVR > PVR this is a _____ to _____ shunt

A

L to R

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46
Q

what is PVR calculation

A

PVR= (mPAP-PAOP)/CO x 80

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47
Q

what is normal PVR

A

150-200 dynes/sec/cm-5

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48
Q

what is SVR calculation

A

SVR= (MAP-CVP)/CO x80

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49
Q

what is normal SVR

A

800-1500 dynes/sec.cm-5

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50
Q

increased decreased PVR

A
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51
Q

increased decreased SVR

A
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52
Q

what shunt bypasses pulmonary circulation

A

cyanotic shunt

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53
Q

what are examples of cyanotic shunt

A

tetralogy of Fallot
transposition of great arteries
epsteins anomaly
truncus arteriosus
totally anomalous pulmonary venous connection

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54
Q

what is patho of cyanotic shunt

A

decreased pulmonary flow
hypoxemia
LV volume overload
LV dysfunction

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55
Q

what are hemodynamic goals of cyanotic shunts

A

Maintain SVR
Decrease PVR (hyperoxia, hyperventilation, avoid lung hyperinflation)

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56
Q

how is inhalation induction in cyanotic shunt

A

slowed

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57
Q

how is IV induction in cyanotic shunt

A

faster

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58
Q

how do children with cyanotic cardiac defects compensate for chronic hypoxia

A

increased erythropoiesis (polycythemia increased SVR/PVR)
increased circulating blood volume
vasodilation

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59
Q

T/F coagulopathies are common in cyanotic shunts

A

true

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60
Q

T/F keep child with cyanotic shunt NPO

A

F, do not want dehydration 2/2 increased viscosity of blood

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61
Q

transposition of great arteries

A
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62
Q

what congenital heart defect has
aorta connected to RV
PA connected to LV
PFO
may have VSD and subpulmonic stenosis
characterized by recirculation of systemic and pulmonary blood

A

transposition of great arteries

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63
Q

what does survival of transposition of great arteries rely on

A

communication between circuits
PFO
VSD
PDA
ASD

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64
Q

what meds do we avoid in Transposition of Great arteries because they may close PFO/VSD/PDA/ASD

A

NSAIDS

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65
Q

what meds do we give in Transposition of Great arteries because they keep PFO/VSD/PDA/ASD open

A

prostaglandin

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66
Q

in transposition of Great Arteries, what kind of shunt does VSD and PDA allow

A

R to L

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67
Q

in transposition of great arteries what kind of shunt does PFO and ASD allow

A

L to R

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68
Q

transposition of great arteries shunts

A
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69
Q

what is O2 of TGA at birth

A

<70%

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70
Q

what infusion do we give to maintain PDA in TGA

A

PGE1

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71
Q

how do we manage vent in transposition of great arteries

A

hyperventilation to decrease PVR

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72
Q

what are treatments at birth for TGA

A

PGE1 infusion
Balloon Atrial Septoplasty
ECMO may be necessary

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73
Q

what is the physiologic correction procedure for TGA

A

Mustard and Senning procedure

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74
Q

describe Mustard and Senning procedure for TGA

A

atrial switch
atrial baffles direct systemic blood to LV and PA and pulmonary blood to RV then Aorta

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75
Q

Mustard and Senning Procedure for TGA

A
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76
Q

what is the anatomic repair for the TGA

A

jatene switch

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77
Q

Jatene switch for TGA

A
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78
Q

what is risk of Jatene Switch for TGA

A

single RCA-> risk of postop MI/death

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79
Q

what is Anesthetic Management of TGA

A

maintain CO, HR, preload
maintain adequate intercirculatory mixing
AVOID
decrease PVR and hypocarbia/alkalosis
increased PVR (compromise venous return and mixing)

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80
Q

how long do we continue PGE1 infusion in TGA

A

until shortly before CPB

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81
Q

what anesthetic do we avoid in anesthesia induction and maintanence in TGA

A

inhalational induction and maintenance (cause myocardial depression)

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82
Q

what is anesthesia management of TGA

A

high dose fentanyl or sufenta
small doses of benzos
low dose volatiles
Volume expansion
inotropic support (dopamine)

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83
Q

what is risk of sufenta

A

bradycardia

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84
Q

what is dose of fentanyl for TGA

A

75 mcg/kg

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85
Q

what is dose of sufenta for TGA

A

25 mcg/kg

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86
Q

what is anesthetic management for post CPB of TGA

A

maintain HR (pacing)
controlled BP to reduce bleeding at suture lines
milrinone
watch for myocardial ischemia (aggressive)

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87
Q

what is the most common congenital heart defect

A

Tetrology of Fallot

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88
Q

what are characteristics of Tetralogy of Fallot

A

VSD
Overridig aorta
RV hypertrophy
Pulmonic Stenosis
RVOT stenosis

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89
Q

what does an increased RVOT stenosis lead to

A

increased shunt through VSD
erythropoesis???

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90
Q

tetralogy of fallot

A
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91
Q

what are s/s tetralogy of fallot

A

cyanosis
LSB ejection murmur (stenotic pulm valve)
Squatting in older children

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92
Q

what does squatting with ToF lead to

A

increases SVR
decreases R to L shunt
increases pulmonary blood flow
improved oxygenation

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93
Q

what is hypercyanotic/hypoxic episode with TOF

A

TET spells

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94
Q

what are causes of TET spells

A

stress
exercise
crying
defecation
IV placement
Induction
taking kid from parent in preop

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95
Q

what are S/S Tet Spells

A

paroxysmal hyperpnea
deleterious effects
cyanosis
increased O2 consumption
decreased SVR 2/2 cyanosis
increased venous return
increased shunt

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96
Q

how do we treat TET spell

A

100% O2
knee to chest position
manual compression of abd aorta
morphine 0.1 mg/kg (sedation/depress ventilation)
crystalloid 15 ml/kg
phenylephrine (increase SVR)
reduce SNS stimulation
BB (esmolol)
Avoid inotropes
ECMO

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97
Q

when does surgical correction of TOF occur

A

2-10 months of age

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98
Q

what is goal of TOF sx

A

reduce RV pressure
avoid RV overload (regurg)
close VSD

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99
Q

what is anesthetic management of TOF

A

avoid dehydration
premedicated before IV placement
IV induction preferred
Sevo induction is ok
avoid systemic hypotension
Fentanyl or Ketamine induction
volume expansion

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100
Q

what is dose of ketamine induction for TOF

A

ketamine 102 mg/kg IV

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101
Q

anesthesia for TOF

A
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102
Q

tx of TOF

A
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103
Q

truncus arteriosus

A
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104
Q

describe truncus arteriosus

A

single great vessel
VSD
complete intracardiac mixing
increase in flow to one vessel will reduce flow to the other

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105
Q

what is normal SpO2 in Truncus arteriosus pre fontan procedure

A

75-80%

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106
Q

what happens to pulmonary blood flow and PVR at first breath

A

increases blood flow, decreases PVR

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107
Q

what happens at birth with TA

A

PBF is high-CHF signs with mild cyanosis (metabolic acidosis)
risk of pulmonary veno-occlusive disase (PVOD) which is a type of pulmonary HTN

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108
Q

what is repair of TA

A

Rastelli repair with patched septum and new pulm valv/artery

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109
Q

describe rastelli repair

A

patch to the VSD
Graft PA to RV
Valvuplasty

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110
Q

what is management of Truncus Arteriosus similar to

A

same as single ventricle physiology/hypoplastic L heart syndrome

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111
Q

what can happen post CPB of Truncus Arteriosus

A

RV dysfunction likely
LV overload may occur
TX;
maintain HR, reduce PVR, inotropic support

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112
Q

what is the most common congenital defect of tricuspid valve

A

ebsteins anomaly

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113
Q

describe ebsteins anomaly

A

abnormality of the tricuspid valve, leaflets are down in RV,
0atrialized RV
-stenotic or rregurgitant TV
-ASD, PFO with R to L shunt

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114
Q

ebsteins anomaly

A
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115
Q

what issues occur in RV with ebsteins anomally

A

sludging and bloodclots in RV

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116
Q

what does magnitude of R to L shunt from ASD or PFO in ebsteins anomaly depend on

A

RV dysfunction and tricuspid severity

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117
Q

what are s/s Ebsteins anomaly in neonate

A

CHF
systemic venous congestion
cyanosis after PDA closure

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118
Q

what are s/s ebsteins anomaly in adults

A

asymptomatic

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119
Q

what are risks of ebsteins anomaly with PFO

A

paradoxical emboli
brain abscess
CHF
sudden death

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120
Q

what is single ventricle physiology

A

complete mixing of pulmonary venous and systemic venous blood

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121
Q

what is formula for output of single ventricle physiology

A

output= pulmonary bf+systemic bf

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122
Q

what is distribution of blood flow in single ventricle physiology dependent on

A

resistance to flow

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123
Q

in single ventricle physiology the oxygen saturation in the PA is __________ as the Aotra

A

the same

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124
Q

what congenital heart issues have single ventricle physiology with two well formed ventricles

A

tet of fallot with pulmonary atresia
truncus arteriosus
sever aortic stenosis with PDA suppling system flow

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125
Q

tricuspid atresia

A
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126
Q

HLHS (hypoplastic left heart syndrome)

A
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127
Q

where does HLHS get aortic blood flow from

A

PDA

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128
Q

where does HLHS get pulmonary BF from

A

RV

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129
Q

where does sever neonatal aortic stenosis get aortic blood flow from

A

PDA

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130
Q

where does Severe neonatal aortic stenosis get pulmonary BF from

A

RV

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131
Q

where does Tetralogy of fallot with pulmonary atresia get aortic blood flow from

A

LV

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132
Q

where does Tetralogy of fallot with pulmonary atresia get pulmonary BF from

A

PDA

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133
Q

where does truncus arteriosus get aortic blood flow from

A

LV/RV

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134
Q

where does truncus arteriosus get pulmonary BF from

A

aorta

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135
Q

where does tricuspid atresia 1b/1c get aortic blood flow from

A

LV

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136
Q

where does tricuspid atresia 1b/1c get pulmonary BF from

A

LV through VSD to RV

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137
Q

what is anesthesia management of single ventricle (three steps)

A

1-optimization of systemic oxygen delivery and perfusion (blalock shunt)
2- reducing the volume load on the ventricle (superior cavopulmonary connection or bidirectional glenn procedure)
3- acheiving a series circulation with fully saturated systemic arterial blood (fontan procedure)

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138
Q

what is norwood procedure for HLHS

A

aortic arch reconstruction
atrial septectomy
Blalock Taussig shunt (BTS)

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139
Q

blalock shunt for HLHS

A
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140
Q

when is Bidirectional Glenn procedure completed

A

6-8 months

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141
Q

what does blalock taussig shunt connect

A

SCL (from aorta) to PA

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142
Q

what does Bidirectional Glenn conect

A

IVC to CA

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143
Q

bidirectional Glenn

A
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144
Q

when is fontan procedure completed

A

2-3 years

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145
Q

describe fontan procedure

A

add tube from IVC to PA
creates completely pasive blood flow into RA

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146
Q

what is important with fontan procedure and PVR

A

has to have a very low PVR, flow is completely dependent on preload
IF PVR is too high, blood will back up systemically

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147
Q

what is management of SV physiology BEFORE CPBP

A

-PGE1 infusion (maintain sats)
-induce with high dose narcotic, muscle relaxant, versed
-Target PaO2 40-45 and PaO2 70-80
-SpO2 70-80
-Increase PVR with hypercarbia (45-55)
-21% FiO2 (avoid high FiO2 decreases PVR)
-may require inotropes
-avoid tachycardia >140-150

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148
Q

T/F do inhalation induction in SV physiology

A

F

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149
Q

what are major problems with SV physiology AFTER CPBP

A

hypoxemia
hypotension
low systemic perfusion
gas exchange dsfxn
bleeding (suture lines, coagulation factors/PLT consumption)
high PVR
reduced pulm BF
hypoxemia
myocardial/tissue edema
myocardial dysfunction is common (low CO)

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150
Q

what happens if there is too large of a shunt after CPBP

A

pulmonary overload

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151
Q

what happens if there is too small of a shunt after CPBP

A

cyanosis

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152
Q

how do you treat myocardial/tissue edema after CPBP

A

maintain open chest?

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153
Q

what special medication may be necessary after CPBP

A

NO (nitric oxide)

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154
Q

myocardial dysfunction from low CO is common after stage 1 HLHS, how do we treat

A

may require dopamine of epinephrine

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155
Q

what happens with too large of shunt after CPBP

A

too much pulmonary blood flow= no enough to the body
high SpO2
hypotension
hypoperfusion
EKG= ischemia

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156
Q

how do we treat too large shunt after CPBP

A

increase PVR, increase inotropic support, Narrow the shunt

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157
Q

what happens with too small shunt after CPBP

A

low SaO2
normal or elevated systemic BP

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158
Q

how do we treat to small shunt after CPBP

A

decrease PVR
improve ventilation
increase systemic SVR

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159
Q

which is more common, too large or too small shunt after CPBP

A

too small

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160
Q

what is most common complication after CPBP

A

los SaO2 or hypotension

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161
Q

how do we treat low SaO2 or Hypotension after CPBP

A

optimize

vent parameters

HCT 35-40

CO

Arterial BP

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162
Q

tricuspid atresia

A
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163
Q

describe tricuspid atresia

A

atretic tricuspid valve
hypoplastic RV
ASD
VSD
restricted pulm BF
R to L shunt
single ventricle physiology
complete obstruction to RV outflow
obligatory ASD or PFO

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164
Q

what are S/S tricuspid Atresia

A

cyanosis
dyspnea
hypoxic spells
clubbing in childhood
harsh ejection systolic murmur
EKG: LAD, LVF, abnormal P-wave
R atrial overload

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165
Q

what causes abnormal P wave in tricuspid atresia

A

2/2 no RV

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166
Q

what is treatment for tricuspid atresia

A

PGE 1
atrial septostomy & BT shunt
Fontal procedure (18-30 months)
hemi fontan 6 months

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167
Q

tricuspid atresia with blalock shunt

A
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168
Q

tricuspid atresia fontan procedure

A
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169
Q

what is anesthetic management of tricuspid atresia

A

-IV induction
-opioids, low concentration volatile, muscle relaxant
-ductal dependent for pulmonary BF
-preserve cardaic contractility /CO balanced PVR/SVR to maintain SaO2 70-80%

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170
Q

what happens with an increased R to L shunt in tricuspid atresia

A

hypoxemia, cyanosis

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171
Q

what happens with an increased L to R shunt in tricuspid atresia

A

increased arterial oxygen, wide pulse pressure, hypotension (compromised systemic perfusion)

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172
Q

what is SaO2 after BT shunt

A

75-85%

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173
Q

what would cause a lower SaO2 after BT shunt

A

high PVR, R-L shunt

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174
Q

what is management after BT shunt

A

may need inotropes
controlled ventilation post op
potential for excessive PBF
-support systemic CO
-prevent increase in PBF
-avoid increase FiO2 and hypocarbia

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175
Q

hypoplastic L heart

A
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176
Q

hypoplastic L heart

A
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177
Q

describe hypoplastic L heart

A

-hypoplasia of all L heart structures
-possible Mitral/Aortic Atresia
-Hypoplasia of aorta, coarctation
-PDA provides blood flow to systemic circulation and retrograde to coranaries
-single ventricle with complete mixing

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178
Q

what are s/s hypoplastic L heart

A

grayish-blue skin color
rapid-difficult breathing
poor feeding
cold hands and feet
lethargy
failure to thrive

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179
Q

what are signs of worsening congenital heart defect

A

nutritional status
poor feeding
FTT

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180
Q

what is goal management of hypoplastic left heart with single ventricle physiology

A

-optimization of systemic O2 delivery and perfusion pressure
-prevent end-organ ischemia/injury
-balanced systemic/pulmonary circulation

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181
Q

what is treatment Hypoplastic left heart with single ventricle physiology

A

PGE1 infusion to maintain PDA
atrial septoplasty if there is resitriction
palliative procedure (BT shunt, aortic arch reconstruction)

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182
Q

norwood, bi directional glenn, fontan for HLHS

A
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183
Q

what does bidirectional glenn connect in HLHS

A

SVC to R PA

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184
Q

when is bidirectional glenn done for HLHS

A

3-8 months (when PVR decreased)

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185
Q

bidirectional glenn for HLHS

A
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186
Q

what is an indicator for outgrowing BDG and having a decreased PBF

A

baseline O2 saturation is a good indicator

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187
Q

when can HLHS who have had BDG procedure get CPBP

A

infants have grown and gain weight (less likely to develop excess PBF after induction)
BUT if outgrown BG shunt, may have decreased PBF

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188
Q

what are managment for LHS who have had BDG procedure before CPBP

A

IV induction with etomidate or ketamine
volume expansion prior to induction
may need inotropic support

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189
Q

what is post-CPB managment of BDG patients

A

SVC need unimpeded flow and pressure for forward flow
control HR, NSR, contractility
appropriate preload
inotropic support (dopamine, milrinon)
normocarbia (avoid hypercarbia)
SaO2 goal of 76-85 (same as before BDG)

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190
Q

when is fontan procedure completed

A

2-3 years

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191
Q

what is fontan procedure

A

total cavopulmonary connection
final staged correction to a series or normal circulation
passive flow from IVC/SVC to PA

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192
Q

what are absolute contraindications for fontan procedure

A

early infancy
pulmonary htn
sever PA hypoplasia
EF<30%

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193
Q

fontan procedure

A
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194
Q

what is pre-fontan anesthetic management

A

same as post BDG
SaO2-75-85%
IV induction with opioids and benzos
KEY:
maintain filling and function of systemic ventricle

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195
Q

how do we maintain filling and function of systemic ventricle pre fontan

A

adequate preload
low PVR
low intrathoracic pressure
SR
normal vent function
low afterload

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196
Q

what is versed dose for prefontan procedure

A

20-30 mg PO (1 mg/kg)

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197
Q

do kids <6 need pre meds for fontan procedure

A

no, they have had major surgeries before

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198
Q

do older kids need pre meds for fontan procedure

A

yes, anxiety

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199
Q

what causes of increased PVR do we avoid pre fontan

A

stress
hypercarbia
hypoxia
acidosis
atelectasis
increased intrathoracic pressure

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200
Q

what is induction for pre fontan

A

volume expansion
etomidate
high opioids
benzos
etomidate
muscle relaxer

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201
Q

what is maintanence for pre fontan

A

opioids
benzos
low dose volatiles
MR

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202
Q

what lines do we want for pre fontan

A

art line
IJ CVC

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203
Q

what is post fontan management

A

maintain HR, contractility, preload to maintain CO
need volume
inotropic support

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204
Q

how is pt oxygenation post fontan

A

patients are fully saturated (unless fenestrated where deoxygenated blood is crossing over)

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205
Q

what are examples of acyanotic shunts

A

VSD, ASD, PDA, coarctation of aorta, PFO, AV canal defect

206
Q

what shunt does oxygenated blood recirculate back to lungs

A

acyanotic, L to R

207
Q

what is patho of acyanotic shunt

A

decreased systemic blood flow
low cardiac output
hypotension
increased pulmonary blood flow
pulmonary htn
RVH
CHF

208
Q

what are hemodynamic goals of acyanotic shunt

A

avoid increased PVR
avoid decreased PVR (decrease FiO2, hypoventilation)

209
Q

what is the most common CHD

A

VSD

210
Q

what CHD is detected in 1/3 of adults

A

ASD

211
Q

what CHD is common in premies

A

PDA

212
Q

what congenital issue has more CHD

A

trisomy 21

213
Q

what are effects of L to R shunt

A

increased pulmonary blood flow
increased PAP
increased PVR
increased volume overload
increased LA pressure/volume
pulmonary congestion/edema
BiVentricular failure

214
Q

what kind of shunt is ASD

A

L to R

215
Q

what are direction and magnitude of ASD shunt dependent on

A

size of the defect
relative compliance of the ventricles

216
Q

if a heart chamber has INCREASED compliance, how is its pressure

A

decreased

217
Q

what are s/s ASD

A

systolic ejection murmur at pulmonic valve (increased flow)
split/fixed second heart shound
EKG: RAD, imcomplete BBB, Afib, SVT

218
Q

what causes afib in ASD

A

atrial dilation from increased pressure stretches nerves, causing AFIB

219
Q

what is is the most common congenital cardiac abnormality in infants and children

A

VSD

220
Q

when do most VSDs spontaneously close

A

by 2 years

221
Q

ASD

A
222
Q

VSD

A
223
Q

what happens with PVR after birth

A

PVR falls, pulmonary overcirculation and congestive heart failure (CHF)

224
Q

what are s/s VSD

A

tachypnea
increased work of breathing
poor feeding
poor growth
hepatomegaly

225
Q

what is treatment for VSD

A

closed with patch

226
Q

what is eisenmengers syndrom

A

L to R shunt from VSD, if unrepaired, leads to high PVR, R to L shunt, low pulmonary flow, and cyanosis

227
Q

how does body respond to cyanosis from eisenmengers syndrome

A

bobe marrow compensatory erthrocytosis

228
Q

what are systemic effects of cyanosis from eisenmengers

A

leucocytosis (infection)
platelets (bleeding)
skin (acne)
cholelithiasis
gout
bones (scoliosis)

229
Q

eisenmengers

A
230
Q

what is a narrowing of the aorta

A

Coarctation of the aorta

231
Q

what is coarctation of the aorta usually associated with

A

aortic stenosis
bicuspid aortic valve
VSD

232
Q

what is most common cause of aortic stenosis

A

bicuspid aortic valve and calcification; calcifies earlier than tri-leaflet valve

233
Q

what are tx for coarctation of the aorta

A

PGE1 infusion
inotropes
preload
increase PVR (to maintain R to L shunt)

234
Q

what at surgeries for coarctation of the aorta

A

balloon angioplasty
resection
flab

235
Q

what is induction for coarctation of the aorta

A

benzos
high dose narcotics

236
Q

what drug do we avoid in coarctation of the aorta

A

ketamine

237
Q

T/F neonates are canditates for volatiles for coarctation of the aorta

A

False

238
Q

what are som preop assessments for children undergoing heart sx

A

prescriptions
create relationship with parent/child
formulate a plan
nutritional state
aprotonin dose

239
Q

what is poor growth and development associated with

A

severe CHD

240
Q

what is a consideration if a patient is having a repeat sternotomy

A

may require peripheral CPB

241
Q

if patient BT shunt is being placed on L, where do we place a-line

A

on right to avoid SC cross clamping

242
Q

where do we put preductal pulse ox

A

R side

243
Q

where do we put post ductal pulse ox

A

foot, tests perfusion to see how shunts are doing

244
Q

do we premedicate <6 months

A

no

245
Q

do we premedicate older kids with no anxiety

A

no

246
Q

do we premedicate older kids with multiple sxs, anxiety, parental anxiety

A

yes

247
Q

do we premedicate in severe CHF

A

avoid or judicial use

248
Q

do we premidicate in dynamic outlet obstruction or tetralogy of fallot

A

premedicate to avoid increase cyanosis 2/2 crying/struggling on induction

249
Q

what is rule of thumb with elective cardiac surgeries in a patient with URI

A

postpone

250
Q

URI and cardiac patient

A
251
Q

why do glenn shunt and fontan have increased risk of URI

A

increased PVR

252
Q

what does cyanosis lead to systemically

A

erythropoiesis

253
Q

what are complications of erythropoiesis

A

increased viscosity leads to sludging, thrombosis, increased PVR> SVR

254
Q

how does NPO affect erythropoiesis

A

makes it worse, do not limit clear liquids for long periods

255
Q

at what HCT does viscosity outweigh benefit of increased oxygen carrying capacity

A

Hct>65%

256
Q

what is anesthesias biggest concern with shunting

A

control of shunting via hemodynamics and control of vascular resistance is anesthesias biggest concern

257
Q

what are side effects of CPBP

A

hemodilution
consumption of clotting factor
immature coagulation factor synthesis
decreased vitamin-K dependent coag factors

258
Q

what is priming dose of CPBP in children

A

3x the blood volume of child

259
Q

what is tx of hemodilution and hypocoag state of CPBP

A

plt 10ml/kg
cryo
txa
desmopressin

260
Q

what does FFP lead to

A

hemodilution

261
Q

what factors does DDAVP help replace

A

factor 8
vWF

262
Q

what do we monitor in CPBP

A

ionized calcium (Ca++ used by heart)
temperature (cooling and rewarming)
art line
TEE

263
Q

what is the best core temp

A

swan then esophagus

264
Q

what is best brain temp

A

nasopharyngeal

265
Q

what is issue with trisomy 21 and art line

A

altered anatomy

266
Q

what is side effect of protamine

A

vasodilation

267
Q

how does art line read in CPBP

A

flat line, shows map

268
Q

what is equivalent to CO on pump

A

flow rate

269
Q

what medication should be given before going on pump

A

heparin

270
Q

what is ACT goal of hepranization for bypass

A

ACT 3x baseline

271
Q

why do we avoid nitrous oxide in CPBP

A

enlarge emboli
increases PBR
microbubbles

272
Q

what does ketamine cause

A

SNS activation

273
Q

what induction is preferred for CPBP

A

IV induction (not propofol)

274
Q

on and off pump meds

A
275
Q

when is pediatric hemoglobin formed

A

6 months

276
Q

T/F fetal hgb is the same as adult hgb

A

false

277
Q

what is changed in fetal hgb

A

beta unit is switched for gamma unit (2 each)

278
Q

fetal hgb holds on to O2 (more/less) than adult hgb does

A

more (so that it does not release O2 to mother)

279
Q

a left shift in oxy hgb curve means it holds onto O2 (more/less)

A

more

280
Q

what factor is absent in fetal hgb

A

binding site for 2, 3 DPG

281
Q
A

B is normal adult
A is fetal shift

282
Q

what is P50 at term

A

19mmhg

283
Q

what is P50 at 6 months

A

26mmhg

284
Q

when does hgb begin to increase in peds

A

4 months

285
Q

what blood complication are premis ar risk for

A

anemia

286
Q

blood types and antigens

A
287
Q

what do we ask if child needs blood

A

have they had a blood transfusion before?

288
Q

what blood types can A receive

A

A O

289
Q

what blood types can b receive

A

B O

290
Q

what blood types can AB receive

A

A, B, AB, O

291
Q

what blood types can O receive

A

O

292
Q

what happens when an Rh- receives Rh + blood

A

produce anti Rh antibodies
if mother has anti-Rh antibodies and fetus is Rh positive, antibodies will cross placenta and damage fetal RBGs

293
Q

T/F Rh antibodies affect first pregnancy

A

F, second

294
Q

what is treatment for Rh Antibodies

A

RhoGAM

295
Q

when do we give RhoGAM

A

between 26-28 weeks
3 days after delivery

296
Q

T/F only Rh+ moms receive RhoGAM

A

F, only Rh- moms, then if baby is Rh + then they get additional shot after birth

297
Q

what population may refuse RhoGAM

A

JW, contains blood protiens

298
Q

what kind of blood do all infants receive

A

Type O Rh - OR
ABO and RH D compatible

299
Q

blood component effect table

A
300
Q

what is dose of PRBCs

A

10-15 ml/kg

301
Q

what is effects of PRBCs

A

increases HGB by 2-3 g/dl

302
Q

what is HCT of PRBCs

A

60%

303
Q

what is dose of platelets

A

5-10 ml/kg

304
Q

what is effect of platelet admin

A

increase platelet count by 50-100,000/mm3

305
Q

what is dose of FFP

A

10-15 mL/kg

306
Q

what is effect of FFP

A

factors increase 15-20%

307
Q

what is dose of Cryo

A

1-2 units/kg

308
Q

what is effect of cryo

A

increase fibrinogen by 60-100 mg/dl

309
Q

what is dose of fibrinogen concentrate

A

70 mg/kg

310
Q

what is effect of fibrinogen concentrate

A

increase level of 120 mg/dL

311
Q

what is trigger for blood transfusion for <3 months old healthy patient

A

25% hct

312
Q

what is trigger for >3 months old if post op bleeding is not expected

A

20% hct

313
Q

transfusion ars rarely indicated when Hgb is >

A

10 g/dL

314
Q

transfusions are always indicated when Hgb is <

A

6 g/dL

315
Q

what other factors do we consider when hgb is 6-10 to determine if transfusion is needed

A

ongoing blood loss, evidence of organ ischemia (kidneys), risk of complications from inadequate oxygenation, shunting

316
Q

what is calculations for allowable blood loss

A

EBV x ( Hct- minimal Hct)/ (avg of hct)

317
Q

what is EBV of premature infant

A

90-100 ml/kg

318
Q

what is EBV of term newborn

A

80-90 ml/kg

319
Q

what is EBV of infants younger than 1 yr

A

75-80 ml/kg

320
Q

what is EBV of older children

A

70-75 mL/kg

321
Q

what is normal minimal accepted HCT

A

24%

322
Q

what is formula for age based weight in Kg <12 months old

A

age in months +9/2

323
Q

what is formula for age based weight for 1-5 years yr

A

age in years +5 x2

324
Q

what is formula for age based weight for 5-14 years

A

age x4

325
Q

what is formula for volume of PRBCs to give

A

EBVx (desired HCT-present HCT) (HCT of PRBCs (60))

326
Q

what hgb do we want cyanotic congenital heart disease at

A

13-18

327
Q

what are examples of cyanotic heart disease

A

Tet of Fallot
Transposition of Great Arteries
Tricuspid Atresia
total anomalous pulmonary vein connection

328
Q

what are risks of transfusion of blood

A

viral infections
bacterial infections
hyperkalemia
TRALI

329
Q

what is chance of getting HIC, HEP C from blood

A

1 in 1.1 million

330
Q

what are s/s TRALI

A

ARDS- dyspnea, hypoxia, pulmonary edema, onset 4-6 hours after transfusion

331
Q

what type of plasma donors helps prevent TRALI

A

male

332
Q

what do you do if you start having transfusion reaction

A

surgeon and nurse
blood bank- send blood back to blood bank for testing

333
Q

risks of massive transfusion chart

A
334
Q

what are risks of acidosis from blood transfusion

A

poor oxygen delivery
lactate

335
Q

what are risks of alkalosis from blood transfusion

A

citrate metabolism to bicarb by liver

336
Q

what are risks of hypocalcemia from blood transfusion

A

citrate binding of calcium

337
Q

what are risks of hyperglycemia from blood transfusion

A

dextrose preservation in packed RBC

338
Q

what are risks of hypothermia from blood transfusion

A

transfusion of cold blood products

339
Q

what are risks of hyperkalemia from blood transfusion

A

multifactorial

340
Q

what are s/s bleeding risk

A

easy bruising
petechia
nose bleeds
mucusal bleeding
heavy period
excessive bleeding with umbilical stump
bleeding after circumcision
bleeding after dental work
low factory 8

341
Q

what do you do if you have a patient with high bleeding risk getting a tosillectomy

A

contact hematology, possibly reschedule

342
Q

what do you give for severe bleeding with VWF

A

factor 7

343
Q

what do we give to increase VWF (8)

A

DDAVP

344
Q

what are preopconsiderations for patients with VWF disease

A

-Consultation with hematologist: establish correct diagnosis and response to desmopressin (DDAVP);
administer DDAVP or viral attenuated factor concentrates containing factor VIII and von
Willebrand factor (vWF) such as Humate-P for severe vWD or for those types not responsive to
DDAVP186
-Determination of actual and desired factor concentrations and expected duration of postoperative
therapy191
-Discontinuation of any platelet-inhibiting medication (e.g., aspirin)

345
Q

what are intraop considerations for patients with VWF disease

A

-Judicious use of regional anesthesia, intramuscular medications, nasogastric tubes, nasal intubation,
and other procedures that may cause bleeding
-Limited use of medications with potential bleeding risk (e.g., ketorolac)
-Coagulation profiles, including platelet counts for more invasive surgeries
-Treatment of bleeding with appropriate blood products
-Consider use of antifibrinolytic agents (i.e., ε-aminocaproic acid, tranexamic acid)190
-Possible use of recombinant factor VIIa for severe bleeding episodes in severe vWD type 3 or
patients with inhibitors

346
Q

what are postop considerations for patients with VWF disease

A

-Follow factor concentrations (i.e., factor VIII and vWF)
-Availability of blood products and factors
-Appropriate treatment of bleeding episodes
-Monitor for thromboembolism in children receiving multiple concentrates or antifibrinolytic agents,
or both186

347
Q

what factor is hemophilia A

A

factor 8

348
Q

what factor is hemophilia B

A

factor 9

349
Q

what are signs of hemophilia A B

A

bleeding from heel sticks, circumcision, delivery intracranial hmmged
isolated prolonged aPTT
normal PT, thrombin time, platelet count, and bleeding time

350
Q

table 10.13

A
351
Q

when do we treat patient with ITP

A

below 10-20,000?

352
Q

what is ITP

A

low platelets 2/2 life span of only a few hours

353
Q

what do we want patient with G-6-PDD to aboid

A

stressors
pain, anxiety
infection, triggering things like prilocaine, benzocaine, sodium nitroprusside, hydralazine, procainamide, ASA, methylene blue, sulfa drug (10.8)

354
Q

table 10.8

A
355
Q

what is anesthetic management of thalassemia

A

facial deformities
osteoporosis
hyperdynamic circulation
cardiac dysfunction
hepatic disease
pulm htn
thrombosis risk

356
Q

what do we do preop for patient with SCD

A

Screening if unknown status in at-risk children
Primary management by hematology service (in most circumstances)
History of acute chest syndrome, vasoocclusive pain crises, hospitalizations, transfusions,
transfusion reactions
Neurologic assessment (e.g., strokes, cognitive limitations)
History of analgesic and other medication use
Hematocrit
Oxygen saturation (on room air), chest radiograph
Pulmonary function tests (when appropriate)
Practice incentive spirometry at home
Work with child-life specialist if indicated
Echocardiography (when appropriate)
Neurologic imaging (for recent changes)
Renal function studies
Transfusion crossmatch (e.g., antibody-matched, leukocyte-reduced, sickle-negative)
Transfusion to correct anemia (in most circumstances)
Parenteral hydration for nil per os (NPO) status
Pain management
Aggressive bronchodilator therapy
Appropriate antibiotic therapy, including presplenectomy antibiotics and immunizations (as
indicated)

357
Q

what are intraop consideration for SCD

A

Maintenance of oxygenation, perfusion, normal acid-basis status, temperature, hydration
Availability of appropriately prepared blood (as indicated)
Replacement of blood loss
Anesthetic technique appropriate for procedure and postoperative analgesic requirements
Attention to physiologic effects of laparoscopy on circulatory and respiratory function
Appropriate antibiotic therapy
Judicious use of tourniquets, cell saver, and cardiopulmonary bypass

358
Q

what are postop considerations for SCDs

A

Management by hematology service
Monitoring for complications, especially acute chest syndrome and vasoocclusive pain crises
Maintenance of oxygen saturation monitoring and supplementation as needed, including
prophylactic supplemental oxygen the first 24 hours regardless of oxygen saturation
Appropriate hydration (oral plus parenteral)
Appropriate antibiotic therapy
Aggressive pain management—must ensure ability to breathe deep and do incentive spirometry
Early mobilization
Incentive spirometry (possibly with continuous or bilateral positive airway pressure) and
bronchodilator therapy

359
Q

what does sickle cell trait produce

A

Hb A HbS (hetero)

360
Q

what does sickle celll anemia produce

A

only Hb S

361
Q

which type of sickle patient has crisis

A

sickle cell anemia (HbS)

362
Q

what is the hallmark signs of sickle cell anemia

A

chronic hemolytic anemia
hgb 5-9
hgb S
sickled hgb

363
Q

what can lead to sickle cell crisis

A

hypoxia
emotional stress
pain
infection
surgical stress
hypothermia
dehydration
leukocytosis
inflammation
acidosis
thrombosis

364
Q

what surgery is common for sickle cell anemia

A

cholecystectomy-have gallstones

365
Q

what is life span of sickled RBCs

A

10-12 days

366
Q

what are complications of sickle cell anemia

A

vaso occlusive crisis
gallstones
organ dysfunction
pulm htn
priapism
skin ulcers
reactive airway from decreased nitric oxide
stroke
acute splenic sequestration
pulmonary and neurological complications

367
Q

what med is helpful in sickle cell crisis

A

NO

368
Q

what do we avoid in sickle cell anemia to avoid stroke

A

hyperventilation

369
Q

what are the leading causes of morbidity and mortality in sickle cell anemia

A

pulmonary and neurologic complications

370
Q

ACS

A
371
Q

what is a new pulmonary inflitrate of at least one complete lung segment on chest X-ray and is the leading cause of death with SCD

A

acute chest syndrome

372
Q

what are triggers of acute chest syndrome

A

infection, fat embolism from bone marrow infarction, pulmonary infarction, surgery induced stress

373
Q

what are s/s acute chest syndrome

A

chest pain, fever, tachypnea, wheezing, coughing, and hypoxemia

374
Q

what is treatment of acute chest syndrome

A

broad-spectrum ABX
O2
adequate analgesia
bronchodilators
incentive spirometry

375
Q

what is hallmark of pain pattern in SCD

A

occlusion-> pain and pain-> more occlusion

376
Q

what is treatment for pain from acute chest syndrom?

A

APAP
NSAIDS
Steroids
opioids
psychotropics
regional anesthesia

377
Q

what are indicators for transfusion of SCD

A

correction of preexisting anemia
dilution of HGB S (to less than 30%)

378
Q

what factors are in FFP

A

2, 7, 8, 9, 10, 11

379
Q

what factors are in PCC

A

2,7,9, 10, 12, proteins C and S

380
Q

what factors are in cryo

A

vWF
fibrinogen

381
Q

table 12.7

A
382
Q

FFP must be transfused with _______ hours of thawing

A

24

383
Q

what is dose of FFP

A

20ml/kg will replace 50% of factors
10-15 will increase by

384
Q

what is used for the reversal of warfarin in emergencies

A

FFP

385
Q

what is platelet level for surgery

A

50,000

386
Q

T/F give platelets through platelets through filter and warmer system

A

F, will destroy them

387
Q

MAC of volatiles is (higher/lower) in peds

A

higher

388
Q

Highly water soluble drugs are confined to the __________ space and as such have a (larger/smaller) volume of distribution

A

intravenous
smaller

389
Q

lipophilic drugs have a (smaller/larger) volume of distribution as they can disseminate into the _________

A

larger
tissues

390
Q

neonates and infants have larger distribution volumes for _________ soluble drugs

A

water

391
Q

neonates and infants have smaller distribution volumes for _________ soluble drugs

A

lipid

392
Q

neonates have more _________ weight

A

water

393
Q

what are examples of water soluble drugs

A

antibiotics
anectine
digoxin

394
Q

a greater water soluble Vd in infants means an (increased/decreased) loading dose

A

increased

395
Q

although infants/neonates have a higher Vd, they are (more/less) sensitive to medication effects

A

more

396
Q

T/F preterm infants are more sensitive to medication effects

A

true

397
Q

what is the most important organ for water-soluble drug elimination

A

kidney

398
Q

what is GFR in neonate

A

5ml/min

399
Q

what is GFR in preterm

A

1ml/min

400
Q

when does GFR mature by

A

20 weeks

401
Q

as age increases, GFR _________

A

increases/matures

402
Q

what determines renal drug clearance

A

GFR, active tubular secretion, active and passive tubular reabsorption

403
Q

what drugs are metabolized by liver

A

sedatives

404
Q

what leads to greater volume of distribution of hydrophilic drugs in infants

A

greater total body water and larger extracellular fluid spaces= larger volume of distribution and lower intravascular drug concentrations

405
Q

how are lipophilic drugs effected by maturation

A

increases in volume of distribution of fat-soluble drugs as propofol and thiopental

406
Q

what drug class causes rapid induction of hypnosis with minimal relaxation or analgesia

A

barbiturates

407
Q

neonates have a (increased/decreased) ability to metabolize barbiturates

A

decreased

408
Q

what are examples of barbiturates

A

thiopental
methohexital (brevital)
Diazepam (valium)
Midazolam (versed)

409
Q

T/F give barbiturates in prophyria

A

false

410
Q

what barbiturate do we use for ECT

A

methohexital

411
Q

what is benefit of methohexital

A

fast on and off

412
Q

how does methohexital effect BP

A

high BP after

413
Q

what do you watch for in methohexital

A

watch airway

414
Q

what barbiturate do we avoid in preterm

A

versed

415
Q

what oral drugs are good for special needs

A

versed and benadryl

416
Q

which barbiturate has the lowest clearance in preterm

A

versed

417
Q

versed has extensive __________ metabolism

A

hepatic

418
Q

what is reversal for benzos

A

Flumazenil

419
Q

what is dose of flumazenil

A

0.01 mg/kg

420
Q

what are SE of flumazenil

A

nausea
vomiting
blurred vision
sweating
anxiety
emotional lability

421
Q

what two sedatives do we avoid in seizures

A

etomidate and lidocaine (lower the seizure threshold)

422
Q

what sedative do we avoid in addisons and congenital adrenal hypoplasia

A

etomidate

423
Q

what three conditions do we avoid etomidate in

A

addisons
congenital adrenal hypoplasia
seizures

424
Q

what can we give with etomidate to help offset adrenocorticotropic supression

A

versed

425
Q

what are SE of etomidate

A

myoclonic movements
pain
adrenocorticol suppression
N/V?

426
Q

what procedure can you do before giving propofol in peds

A

baby-beer block- give lidocaine and squeeze arm to numb vein before giving propofol

427
Q

how do you treat hypotension from propofol

A

fluids

428
Q

what are rates of propofol infusion to cause PRIS

A

> 4 mg/kg/hr or 67 mcg/kg/hr over a long period of time

429
Q

what are s/s PRIS

A

bradycardia = one or more: lipemic plasma, hepatomegaly, metabolic acidosis with or without increase in serum lactate, rhabdomyolysis with myoglobinuria
green urine?

430
Q

what is metabolism of propofol

A

redistribution, hepatic/lung/kidney clearance

431
Q

what are SE of propofol

A

involuntary motor movements
pain on injection
hypotension

432
Q

which has less NV etomidate or propofol

A

propofol

433
Q

what sedative is an NMDA antagonists that causes dissociation of the cerebral cortex from the limbic system

A

ketamine

434
Q

what can we give to dry up secretions from ketamine

A

atropine, robinol

435
Q

what can we give to stop PTSD from ketamine

A

versed

436
Q

what are SE of ketamine

A

increased HR, SBP

437
Q

T/F ketamine causes resp depression

A

no

438
Q

what are contraindications for ketamine

A

increased ICP, full stomach

439
Q

what is drug class of precedex

A

selective a2 agonists

440
Q

what is ratio of a2 to a1 in precedex

A

1600:1

441
Q

precedex causes (hyper/hypo) polarization of noradrenergic neurons in the locus coeruleus

A

hyper

442
Q

T/F precedex causes resp depression

A

false

443
Q

what stage of anesthesia do we not touch kids during

A

stage 2 (delirium)

444
Q

what can happen when kid is moved in stage 2

A

laryngospasm

445
Q

T/F use des for inhalation induction in peds

A

F, causes spasms

446
Q

what 6 things affect the uptake of anesthetic gases

A

1-inspired concentration
2- alveolar ventilation
3-FRC
4- CO
5-solubility
6-alveolar to venous partial pressure gradient

447
Q

how does a decrease in CO affect FA/FI

A

increases FA/FI ratio, causing a buildup in alveoli, gas is not carried away

448
Q

Fa/FI equilibrates (faster/slower) in children than adults

A

faster

449
Q

wash in of volatiles is (faster/slower) in adults than children

A

slower

450
Q

what four factors cause a faster uptake (FE/FI) in neonates/ infants

A

1VA:FRC 5:1 in child compared to 1:4:1 in adults
-tissue solubility is decreased
-CO increased to vessel rich group
-blood gas solubitlity coefficient lower in infants and neonates (except sevo)

451
Q

wash out increases as blood solubility (increases/decreases)

A

decreases

452
Q

what is the preferred anesthetic gas for peds

A

sevo

453
Q

what volatile has the fastest wash in of all volatiles

A

des

454
Q

what cases do we avoid Nitrous Oxide in

A

neuro

455
Q

what effects is caused by Nitrous Oxide

A

second gas

456
Q

what SE does Nitrous Oxide cause

A

N/V

457
Q

use a (higher/lower) concentration of oxygen in premature

A

lower

458
Q

what can high concentrations of oxygen cause in premature

A

retinopathy of prematurity

459
Q

what are risk factors for retinopathy of prematurity

A

Gestational diabetes
bright light
maternal antihistamine before delivery

460
Q

what opioid do we use precaution on in peds

A

sufentanil

461
Q

what opioids cause the most post op N/V

A

morphine/dilaudid

462
Q

T/F giv meperidine for seizures

A

false

463
Q

what opioid is good for shivering

A

merperidine

464
Q

if a patient is bradycardic and you want give fentanyl, what do you pretreat patient with

A

atropine/robinol

465
Q

what is dose of Naloxone

A

0.01 mg/kg repeated every 2-3 minutes

466
Q

what is opioid reversal

A

naloxone

467
Q

when do we avoid NSAIDS

A

asthma
bleeding
kidney problems
allergies to aspirin

468
Q

what is dose of IV APAP

A

7.5-15 mg/kg IV

469
Q

what is max dose of APAP for <2 yo

A

60 mg/kg/day

470
Q

what is max dose for APAP > 50 kg

A

4 gm day and 1 gm doses

471
Q

which anticholinergics cross the BBB

A

atropine and scopolamine

472
Q

which anticholinergic does not cross the BBB

A

robinol

473
Q

what is dose of succs for laryngospasm

A

0.1-0.2 mg/kg

474
Q

what parlytic has a blackbox warning in peds

A

succs

475
Q

what can happen with succs and undiagnosed duchennes muscular dystrophy

A

intractable, unexpected cardiac arrest with 50% mortality

476
Q

what are SE succs

A

sinus brady
increased intragastric pressure
increased ICP

477
Q

T/F it is routine to give parlytic in peds

A

false

478
Q

what are absolute contraindications for succs

A

patient or FH of MH
suspected myopathy
burn victims
disuse atrophy

479
Q

what are relative contraindications of succs

A

plasma cholinesterase deficiency
hypercarbia
intraabdominal sepsis
hyperkalemia

480
Q

what paralytic is good for renal patient

A

nimbex

481
Q

where do we check TOF for reversal

A

adductor pollicus

482
Q

what is blood volume of preemie

A

90ml/kg

483
Q

what is blood volume of infants <6 months

A

80ml/kg

484
Q

what is blood volume of 6months-2 years

A

75 ml/kg

485
Q

what is blood volume of 2-12 years

A

72 ml/kg

486
Q

what is blood volume in adulthood

A

60 ml/kg

487
Q

why are young children more susceptible to severe hyponatremic encephalopathy

A

larger brain-to skull

488
Q

what is best fluid for peds

A

LR or plasmalyte (balanced)

489
Q

what is fluid calculation 4-2-1

A

4 ml/kg/hr first 10 kg
2 ml/kg/hr second 20 kg
1 ml/kg/hr for kgs >20kg

490
Q

what is loss of minimal incision

A

3-5 ml/kg/hr

491
Q

what is loss of moderate incision

A

5-10 ml/kg/hr

492
Q

what is loss of large incision

A

8-10 ml/kg/hr

493
Q

what is total hourly requirement for fluid

A

estimated hourly requirement + estimated deficit + insensible loss + EBL

494
Q

how do we treat mild dehydration (<10%)

A

oral rehydration with pedialyte

495
Q

what kind of fluids do we avoid until dehydration is corrected

A

hypotonic like 0.45 NS and 0.22 NS

496
Q

what is process for correcting dehydration

A

20-40 ml-kg of balanced salt solution (NS, LR, plasmalyte)
40ml/kg of 0.9 NS over 2-4 hours
reamainder of deficit as 0.9% Na over 24 hours

497
Q

what kind of induction do we do for dehydration

A

no inhalation
RSI
have a reactive airway

498
Q

Morphine dose

A

IV 0.1 mg/kg

499
Q

fent dose

A

IV bolus analgesic 1-2 mcg/kg
IV loading dose 5-10 mcg/kg
IV infusion 1-3 mcg/kg/hr

500
Q

robinol dose

A

0.01 mg/kg (5 mcg/kg for reversal)

501
Q

atropine dose

A

0.02 mg/kg (7-10 mcg/kg for reversal)

502
Q

neostigmine dose

A

50 mcg/kg

503
Q

narcan dose

A

0.01 mg/kg every 2-3 minutes

504
Q

romazicon (flumazenil) dose

A

0.01 mg/kg

505
Q

succs dose

A

infants 3-4 mg/kg
children 2 mg/kg
laryngospasm 0.1-0.2 mg/kg

506
Q

BG coefficient Sevo

A

0.59

507
Q

BG coefficient Des

A

.42

508
Q

BG coefficient Iso

A

1.4

509
Q

BG coefficient nitrous oxide

A

.46

510
Q

rate of increase in FA/FI in (inversely/directly) related to CO

A

inversely

Pediatric Anesthesia (5 decks)

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