Peds pt 2 Flashcards
What increases the risk of neonatal intracerebral hemorrhage
htn, immature cerebral autoregulation, fragile cerebral vasculature
Normal ICP
2-4 mmhg
Cushing response in peds
absent cushing response
Where does the spinal cord end in peds
L3 and is normal by age 8
Consider sinus brady____ until proven otherwise
hypoxia
CO is derived form ___ and ____
HR and volume
Explain peds being HR dependent
-Peds don’t have the startlings law; the ability to increase force of contraction to maintain CO.
-The under developed myocardium/ immature contractile elements = decreased contractility
- Poorly compliant ventricles; can’t increase contractility to overcome elevated afterload.
- with increased SVR in an underdeveloped heart it cant compensate for the increased pumping needs/ increased workload
- maximum contracltity in neonates because of increased beta stimulation and thyroid hormone
- have a higher resting tesion but develop less stress during transition
What is the primary determinant of SBP
HR
In the setting of hypovolemia + bradycardia what is the medication of choice
epi because it augments contractility
Which vasopressor should be avoided in peds
Phenylephrine because the HR needs to be able to adjust to the increased SVR
How does the ventricle eventually become more compliant
SVR increases with age -> LV pumps against higher SVR -> develops stronger contractile elevments= better adjust contractlity
Normal CO
200 ml/kg/min
Normal SVR in peds
Low
Explain where the PFO is
R to left atrium. R-> left shunt.
How does the PFO close
when blood returns to the heart from the pulmonary veins increases the pressure in the LA and above that of the RA -> closure.
When is PFO usually closed
closes between 3 months - 1 year. 10-30% of ppl have a PFO.
Risk of PFO
Venous air embolism.
PDA location
Between the pulm artery and the aorta.
When does the PDA close
10-15 hrs of life and anatomical closure takes place in 4-6 weeks.
Premature Ductus arteriosus closure causes
NSAIDs, preterm bitht, inc PAP, dec PBF.
During stress / hypoxia what changes does the heart make
hypoxemia, hypercarbia, and acidosis the heart reverts back to utilizing the vessels; R->L shunting, arterial hypoxia- > further increases PVR -> worsening shunting and persistent pulm htn.
Parasymathatic nervous system -> hypotension
Baroreceptors in neonates
baroreceptor reflex is poorly developed in neonates = reflex fails to increase the HR in the setting of hypovolemia.
Stroke volume in neonates
static/ doesn’t move
peds and the BBB
immature, allows the passage of drugs that would otherwise not be able to enter the brain -> higher sensitivity to sedative- hypnotics.
Exogenous catecholamines in neonates
they are less effective because they have a higher endogenous catecholamine level.
Herring–Breuer inflation reflex
over lung inflation -> stimulate stretch receptors -> vagal afferents in apenustic center -> inhibition of apneustic center -> inhibits inspiration -> prolonged expiration.
FRC in children
FRC is lower in children 30 ml/ kg vs adults 34 ml/kg,
Chest wall vs lung compliance in peds
highly compliant thoracic wall and poorly compliant lung tissue
Peds accommodation for air trapping from compliant airways
sustained tonic activity of inspiratory muscle, narrowing of the glottis during expiration, shorter expiratory time w. Faster RR = end-expiratory pressure
Risks with increased closing capacity in neonates
less outward recoil, lungs have a tendency to collapse (increased closing capacity)-. vq mismatch, increased A-a gradient and risk of hypoxemia.
Peds dead space
2 ml/kg
Why are peds nose breathers?
up to 5 months of age. convert to oral breathing w/ nasal obstruction. Becuase they have long epiglotis and absence of paranasal sinus -> decrease riststance in the nasal passages.
Peds O2 consumption vs adults
6ml/kg/min (double that of adults=3.5ml/kg/min) -> inc CO2 production = inc RR/MV. Newborn = 9 ml/kg/min
Managed by inc RR not VT
VT remains normal
normal neonate alveolar ventilation
130 ml/kg/min
because increased O2 consumption and decreased SA = increased need for alveolar ventilation
normal VT peds
6-8 ml/kg
How is surfactant produced
starting at 20 weeks gestation from type 2 pneumocytes
surfactant lowers the air liquid interfacial tension and reduces the opening pressure necessary to aerate the alveoli and prevent alveolar collapse.
usually adequate in neonates borns after 35 weeks.
What is inspiration dependent on
diaphragmatic descent
because intercostal muscles are poorly developed and less effective as accessory muscles
Muscle type on the diaphragm peds
they have more type 2 muscle fibers (fast twitch/ short bursts of heavy workload/ tire easily) and less type 1 (slow twitch/ endurance/ resistance to fatigue/ 25% vs adults usually have 55%)
How to detect R-> L shunting
-Preductal and postductal oxygen saturation by simultaneous use of two pulse oximeters, RUL (preductal) and and lower limb (postductal).
-Preductal arterial saturation of at least more than 3% above the postductal saturation = R-> L shunting.
-This results in decreased oxygen delivery to peripheral tissue and hypoxia and slows uptake of volatiles-> prolonged inhalation induction
Neonates respiratory control
ventilatory response to hypoxia/ hypercarbia is impaired. takes weeks to develop
Fetal hbg structure
2 alpha and 2 gamma subunits
increased affinity for O2
adult hbg 2 alpha and 2 beta
Binding site for DPG on hbg
beta chain of adult hbg
Life span of fetal hbg
70-90 days
lifespan of adult hbg
120 days
HBF relationship to 23DPG
they won’t bind -> L shift in oxyhb curve/ higher affinity for O2
HBF P50
19 mmhg vs adults 26.5
When will there be physiologic anemia from the transition of HBF to HBA
9-12 weeks.
CO2 set point for spont ventilation
50-55 mmhg
Role and number of umbilical artery
return of deoxygenated blood form the fetus to the placenta
2 arteries
Role and number of umbilical vein
take blood from the placenta to the fetus
1 vein
Ductus venosus role
connects from the umbilical vein to the inferior vena cava and bypasses the liver
Portal vein role
where blood enters the umbilical vein and joints the deoxygenated blood coming form the lower half of the body
Risks associated with passive transfusion
hypocalcemia (binding of calcium by citrate), metabolic acidosis/ or metabolic alkalosis (due to citrate metabolism to bicarbonate in the liver), and hyperkalemia (due to administration of older blood), hypothermia (transfusion of cold blood). Hyperglycemia (due to dextrose additive to stored blood)
Transfusion threshold for < 4 months
< 4 months old = transfuse at 12 g/dL w/ severe cardiopulmonary dz
Transfusion trigger < 10 g/dL in children w/ major surgery or with moderate cardiopulmonary dz.
dose for transfusion
10-15 ml/kg
10 ml/kg will rase hbg 1-2 g/dl
Threshold for transfusion > 4 months old
Transfuse if hbg < 6g/dL
or if
Intraoperative blood loss > 15% blood volume
Tranfusion dose for platelets
Dose 5 ml/kg or If pooled 1 pack/10 kg
One pooled plat will increase plat by 10-50 /L
Maintain platelet > 50,000
Peds dont have teeth if they are _____
< 6 months
peds laryxn positioning
superior/cephalad/ rostral
not anterior
Cervical positioning of larynx
Full term = C3-4 (apex info)
Infants = C1-2 (dr ernst info)
Adults - C4-6 (achieved at 5-6 yo)
vocal cord attachment in peds
Vocal cords are attached LOWER anteriorly than posteriorly = ETT gets caught on the anterior commissure (anterior slant)
Bronchi takeoff in peds
Both bonchi take off at 55 degrees on both sides from the midline. Risk of R or L mainstem up to age 3. (adult R mainstem = 25 degrees, L = 45)
Normal infant larynx radius
Normal infant larynx = 4 mm vs adults 8 mm (consider pousielles Law Resistance = 8x viscosity x length / pie radius to the 4th )
Parasympathetic nervous system in children
more developed/ prevalent than SNS
Stress in adults = sns stim
Stress in baby = psns stim -> bradycardia w/ hypoxia/hypotension
When is the SNS developed
4-6 months
Areas of resistance in the small airway
bronchi because of small diameter of airways and greater compliance of the trachea and bronchi -> obstuctuion
trachea in infants is short and narrow and more compliant because of the presence of immature cartilage
Child’s airway flow
turbulent flow
Premies skin
Thin keratin layer -> increased evalopartive loss
forms of heat loss
conduction
convection
radiation
evaporation
What is the major mechanism of heat loss
radiation
what is conducting heat loss
contacting cold objects
what is convection heat loss
air moving over and around the body
uncovered head = 60% of heat loss
what is radiation heat loss
warm air from the body that is trying to warm the cooler environment.
What is evaporation heat loss
skin and lungs. each gm of water evaporation carries -.58 kcal.
Consequences of heat loss
decreased metabolism/ drug distribution -> narcotize, paralyse, slow wake-up
blood coagulopathy is slowed -> bleeding risk
Shivering -> imparied wound healing
cardiac arrhythmias
Explain brown fat metabolism with shivering
Increase brown fat metabolism -> lipase release that splits trig into glycerol and fatty acids = increase heat/ NE production -> VC -> increase PA pressure -> R to L shunt thru PFO & ductus arteriosus -> hypoxemia. (also hard to place IV)
neonates and bilirubin
decreased glucouronic transferase; enzyme that breaks down bilirubin -> increased bilirubin levels
The neonate cannot conjugate bilirubin due to a reduction in glucosyl transferase -> this is the same enzyme that metabolizes acetaminophen.
Neonates and glucose stores
Neonates still need glucose because they have low glycogen stores and impaired gluconeogenesis and depend on carbohydrates and free fatty acids for fuel. (D5, D7.5, D10)