Week 4 - Pediatric Physiology and Development Flashcards
What happens with the cardiovascular system at birth?
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
What will cause reversion back to fetal blood flow?
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
How is cardiac output different in infants?
They have relatively fixed stroke volume so cardiac output is heart rate dependent
*Frank-Starling curve – lower ability to augment CO at any LVEDP
What is the effect of maturation of SNS innervation later than PSN innervation in infants?
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)
What occurs with the pulmonary vasculature at birth?
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)
What increases PVR in infants? **
- PEEP
- High airway pressures
- Atelectasis
- Low FiO2
- Respiratory and metabolic acidosis
- Increased hematocrit
- Sympathetic stimulation
- Direct surgical manipulation
- Vasoconstrictors (ie. phenylephrine)
What decreases PVR in infants? *****
- 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)
What are vascular access options in neonates?
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
What is the proper placement of an umbilical vein catheter (UVC) and an umbilical artery catheter (UAC)?
UVC = tip at the IVC-right atrium junction
UAC = tip at either L3-5 or T7-9
What is the most common cause of neonatal bradycardia?
Hypoxia
How is the lung water removed during birth of the neonate?
Squeezing through birth canal
Lymphatics
Absorption into pulmonary vasculature
*high negative inspiratory pressure with first breaths – 1% pulmonary air leak
How is pediatric lung tissue and compliance different than an adult?
- 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
Describe how the infant’s body shape affects their respiratory system
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)
Why are infants respiratory rates so high?
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
What respiratory parameters are increased in infants compared to adults? Which are decreased?
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)
Describe the anatomy of an infant airway
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)
What are the purpose of fontanels/open sutures?
Enable head passage through narrow birth canal and for rapid brain growth postnatally
Evaluation of hydration status
Why is apnea common in neonates?
Immature respiratory center in the brain stem with poor integration of proprioceptor and chemoreceptor input
*Apnea periods <5 seconds are common
What exaggerates apnea episodes in the neonate?
Hypothermia
Hypoglycemia
Hypocalcemia
Anesthetics
*Paradoxical respiratory depression with hypoxia
What is post-operative apnea in the neonate a result of? How is it treated
- 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
At what age should a neonate be admitted for post-op apnea monitoring?
44 week post conceptual age if healthy
60 weeks if risk factors are present
What spinal level does the conus medullaris and dural sac end in an infant?
Conus Medullaris: L3
Dural Sac: S3-S4
Up to what age do pediatrics have hemodynamic stability with a neuraxial block?
Children less than 6
- small venous capacitance of lower extremities
- lack of resting sympathetic peripheral vascular tone
What is the most common cause of neonatal hypotension?
Hypovolemia
How does a spontaneously breathing neonate prevent alveolar collapse at expiration?
PEEP
- airway resistance
- partial closure of vocal cords
- inspiratory muscles during expiration
Describe the GI system in a neonate
- Higher gastric pH
- Short GI transit times
- Decreased esophageal sphincter tone (reflux common)
- Colics up to 3 months
What is the mechanism behind Jaundice of the newborn?
- 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
What is a complication of Jaundice in the newborn? What is the treatment of Jaundice?
Complication = Kernicterus
Treatment = UV-phototherapy and exchange transfusions
What is neonatal liver function impaired by?
Immature enzyme of biotransformation
Low hepatic blood flow
Different speed of enzyme maturation of Phase 1 and 2 reactions
Why are neonates prone to hypoglycemia? What factors increase this risk?
Limited glycogen stores and gluconeogenesis
Increased risk in neonates who are Small for Gestational Age, Preterm, or had Diabetic Mothers
What are the symptoms and treatment for hypoglycemia for pediatrics?
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
How is the renal function in a neonate? When are nephrons formed?
- 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
How does fetal hemoglobin effect the oxyhemoglobin saturation curve?
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
What is the WBC count at birth?
High – 20k
Steadily declines
What is the total blood volume in mL/kg for premature, term neonate, infant, and adult?
Premature: 106 mL/kg
Term Neonate: 86 mL/kg
Infant: 90 mL/kg
Adult: 55-60 mL/kg
What are the modes of heat exchange?
Radiation (39%)
Convection (37%)
Evaporation (31%
Conduction (3%)
How does general anesthesia affect temperature regulation?
Causes vasodilation
Suppression of hypothalamic center
Decreases shivering
Why are neonates poor at temperature regulation?
- Non shivering thermogenesis
- Unfavorable surface/mass ratio
- Decreased subQ tissue
- Immature thermoregulatory center
What can you do to help temperature regulation in the neonate?
- 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
What is non-shivering thermogenesis?
- 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
At what age does UDP-GT reach adult levels?
6-18 months
-Conjugates: chloramphenicol, MORPHINE, acetaminophen, valproic acid, lorazepam, dexmedetomidine
