Week 4 - Pediatric Physiology and Development Flashcards

1
Q

What happens with the cardiovascular system at birth?

A

First breath –> decrease in pulmonary vascular resistance –> increases pulmonary blood flow –> increasing LV preload

Constriction of umbilical vessels increases SVR –> functional closure of the foramen ovale (increase in LA pressure greater than RA pressure closes flap over foramen ovale)

PaO2 increases –> decrease in prostaglandins –> constriction of Ductus Arteriosus

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2
Q

What will cause reversion back to fetal blood flow?

A

Conditions of stress (decrease PaO2, increase CO2, decrease pH, lung collapse, septic mediators (LT, TXA, PAF))

Causes contraction of smooth muscles of pulmonary vasculature –> increase in PVR –> right to left shunt via PDA, PFO bypassing the lungs –> desaturation

*must overcome R–>L shunt to reperfuse

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3
Q

How is cardiac output different in infants?

A

They have relatively fixed stroke volume so cardiac output is heart rate dependent

*Frank-Starling curve – lower ability to augment CO at any LVEDP

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4
Q

What is the effect of maturation of SNS innervation later than PSN innervation in infants?

A

PNS predominates while the SNS is still developing in infants

This imbalance can be seen as marked bradycardia or even asystole (during laryngoscopy, orogastric tube placement, tracheal suctioning)

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5
Q

What occurs with the pulmonary vasculature at birth?

A

Low number of thick media walled arterioles (causes high PVR) – 20:1 ratio of Alveoli to artery (adult ratio is 6:1)

Maturation to many thinner arterioles and continue to remodel as they age - lowering PVR

PVR reaches adult levels by 6 months under normal conditions (unless exposed to chronic stress conditions, ie. hypoxemia or volume overload)

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6
Q

What increases PVR in infants? **

A
  • PEEP
  • High airway pressures
  • Atelectasis
  • Low FiO2
  • Respiratory and metabolic acidosis
  • Increased hematocrit
  • Sympathetic stimulation
  • Direct surgical manipulation
  • Vasoconstrictors (ie. phenylephrine)
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7
Q

What decreases PVR in infants? *****

A
  • No PEEP
  • Low airway pressures
  • Lung expansion to FRC
  • High FiO2
  • Respiratory and metabolic alkalosis
  • Low hematocrit
  • Blunted stress response (deep anesthesia)
  • Nitric oxide (vasodilates only pulmonary arterioles that are perfused)
  • Vasodilators (ie. milrinone, prostacyclin, others)
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8
Q

What are vascular access options in neonates?

A

PIV, a-line, central line, IO – can be difficult

Cannulation of umbilical vessels (up to 20 days post partum) is relatively easy
-proper catheter position reduces serious complications such as arterial thrombosis w/ organ ischemia, vasospasm, portal vein thrombosis, pulmonary infarction

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9
Q

What is the proper placement of an umbilical vein catheter (UVC) and an umbilical artery catheter (UAC)?

A

UVC = tip at the IVC-right atrium junction

UAC = tip at either L3-5 or T7-9

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10
Q

What is the most common cause of neonatal bradycardia?

A

Hypoxia

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11
Q

How is the lung water removed during birth of the neonate?

A

Squeezing through birth canal

Lymphatics

Absorption into pulmonary vasculature

*high negative inspiratory pressure with first breaths – 1% pulmonary air leak

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12
Q

How is pediatric lung tissue and compliance different than an adult?

A
  • Pliable rib cage due to lots of cartilage — intercostal indrawing
  • Decreased compliance of lung parenchyma
  • Abdominal breathing
  • Horizontal ribs
  • High diaphragm
  • High chest wall compliance
  • Low lung tissue compliance
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13
Q

Describe how the infant’s body shape affects their respiratory system

A

They have a large abdomen which causes cephalad displacement of the diaphragm

  • the closing capacity of the alveoli is near the FRC
  • overcome this by auto PEEP (airway resistance, partial closure of the vocal cords, inspiratory muscles during expiration)
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14
Q

Why are infants respiratory rates so high?

A

Their metabolic demands are so high

-O2 consumption in neonates is 2x that of an adult –> Minute ventilation is very high –> Minute ventilation is the product of RR and tidal volume –> tidal volume is equal between neonate and adult thus RR is the only factor that can be augmented

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15
Q

What respiratory parameters are increased in infants compared to adults? Which are decreased?

A

Increased:

  • O2 consumption (I: 5-8; A: 2-3)
  • Respiratory Rate (I: 40-60; A: 12)
  • Minute Ventilation

Decreased:

  • Total Lung Capacity (I: 53mL/kg; A: 85mL/kg)
  • Airway Diameter (I: 5mm; A: 14-16mm)
  • Trachea/Bronchus/Bronchiole

*Tidal Volume is equal (I: 6-8mL/kg/min; A: 7mL/kg/min)

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16
Q

Describe the anatomy of an infant airway

A

Nasal Breathing

Large Tongue

Epiglottis = large, floppy, Ω-shape

Cephalad Larynx (Level C3) – funnel shaped larynx

“Anterior” airway

Narrowest point is the cricoid level (up for debate)

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17
Q

What are the purpose of fontanels/open sutures?

A

Enable head passage through narrow birth canal and for rapid brain growth postnatally

Evaluation of hydration status

18
Q

Why is apnea common in neonates?

A

Immature respiratory center in the brain stem with poor integration of proprioceptor and chemoreceptor input

*Apnea periods <5 seconds are common

19
Q

What exaggerates apnea episodes in the neonate?

A

Hypothermia

Hypoglycemia

Hypocalcemia

Anesthetics

*Paradoxical respiratory depression with hypoxia

20
Q

What is post-operative apnea in the neonate a result of? How is it treated

A
  • Prolonged anesthetic action
  • Shift of CO2 response curve
  • Immaturity of respiratory center**
  • Muscle fatigue
  • *Risk factors = prematurity and anemia
  • can occur after GA and also regional

Treatment: caffeine citrate 10 mg/kg

21
Q

At what age should a neonate be admitted for post-op apnea monitoring?

A

44 week post conceptual age if healthy

60 weeks if risk factors are present

22
Q

What spinal level does the conus medullaris and dural sac end in an infant?

A

Conus Medullaris: L3

Dural Sac: S3-S4

23
Q

Up to what age do pediatrics have hemodynamic stability with a neuraxial block?

A

Children less than 6

  • small venous capacitance of lower extremities
  • lack of resting sympathetic peripheral vascular tone
24
Q

What is the most common cause of neonatal hypotension?

A

Hypovolemia

25
Q

How does a spontaneously breathing neonate prevent alveolar collapse at expiration?

A

PEEP

  • airway resistance
  • partial closure of vocal cords
  • inspiratory muscles during expiration
26
Q

Describe the GI system in a neonate

A
  • Higher gastric pH
  • Short GI transit times
  • Decreased esophageal sphincter tone (reflux common)
  • Colics up to 3 months
27
Q

What is the mechanism behind Jaundice of the newborn?

A
  • High Hct
  • Short life span of fetal erythrocytes (80 days)
  • Decreased conversion of unconjugated bilirubin to urobilinogen by decreased intestinal flora
  • Breastfeeding

**Increased unconjugated bilirubin serum levels in 50-60% of neonates

28
Q

What is a complication of Jaundice in the newborn? What is the treatment of Jaundice?

A

Complication = Kernicterus

Treatment = UV-phototherapy and exchange transfusions

29
Q

What is neonatal liver function impaired by?

A

Immature enzyme of biotransformation

Low hepatic blood flow

Different speed of enzyme maturation of Phase 1 and 2 reactions

30
Q

Why are neonates prone to hypoglycemia? What factors increase this risk?

A

Limited glycogen stores and gluconeogenesis

Increased risk in neonates who are Small for Gestational Age, Preterm, or had Diabetic Mothers

31
Q

What are the symptoms and treatment for hypoglycemia for pediatrics?

A

Infant Hypoglycemia = <40

Symptoms: irritability, seizures, tremors, sweating

Treatment: 2-4 mL/kg of D10W plus increased basal infusion
*avoid hypertonic glucose boluses – can cause intraventricular hemorrhage in the preterm baby

32
Q

How is the renal function in a neonate? When are nephrons formed?

A
  • Immature renal function at birth
  • Low GFR
  • Immature tubulus system (max 600 mosmol/L)
  • All nephrons formed at 36 weeks – just immature
  • Problems to handle high water and sodium load

*renally excreted drugs can accumulate

33
Q

How does fetal hemoglobin effect the oxyhemoglobin saturation curve?

A

It is shifted to the LEFT

  • facilitates O2 loading in the placenta
  • needs to shift back to the right to unload O2 from Hbg –> reason why neonates have hypercarbia, acidic, and hyperthermia
  • Have high Hbg at birth, slow replacement by Hgb A
  • Physiological anemia at about 2 months is normal
34
Q

What is the WBC count at birth?

A

High – 20k

Steadily declines

35
Q

What is the total blood volume in mL/kg for premature, term neonate, infant, and adult?

A

Premature: 106 mL/kg

Term Neonate: 86 mL/kg

Infant: 90 mL/kg

Adult: 55-60 mL/kg

36
Q

What are the modes of heat exchange?

A

Radiation (39%)

Convection (37%)

Evaporation (31%

Conduction (3%)

37
Q

How does general anesthesia affect temperature regulation?

A

Causes vasodilation

Suppression of hypothalamic center

Decreases shivering

38
Q

Why are neonates poor at temperature regulation?

A
  • Non shivering thermogenesis
  • Unfavorable surface/mass ratio
  • Decreased subQ tissue
  • Immature thermoregulatory center
39
Q

What can you do to help temperature regulation in the neonate?

A
  • Increase OR temperature (85*F)
  • Radiant heaters
  • Bair hugger blankets
  • Warmed fluids
  • Heat moisture exchangers
  • Warm blankets for transport, head covers
  • Incubators for transport
  • Plastic drapes
40
Q

What is non-shivering thermogenesis?

A
  • SNS stimulation enhances the metabolism of brown fat to increase heat production
  • Uncoupling of Oxidative Phosphorylation – lets the proton pass through the membrane without generation of ATP, produces heat – regulated by norepi, activated by fatty acids, and inhibited by nucleotides
  • In brown fat – has central nucleus, increased mitochondria, increased vessels
  • Forms around 26-30 weeks
  • Distribution: scapulae, axillae, mediastinum, around adrenals, internal mammary & neck vessels
41
Q

At what age does UDP-GT reach adult levels?

A

6-18 months

-Conjugates: chloramphenicol, MORPHINE, acetaminophen, valproic acid, lorazepam, dexmedetomidine