Pediatrics I Flashcards
Premature
< 37 weeks gestation
Low Birth Weight
< 2,500g
Very-Low Birth Weight
< 1,500g
Extremely-Low Birth Weight
< 1,000g
Pediatric Airway Differences
Larger tongue in proportion to oral cavity → easy obstruction
Narrow nasal passages
↑salivary secretions
Large tonsils & adenoids
Larynx
- Higher, more cephalad (neonates to 2yo)
- Anterior
- C3-C4
- Oblong/football shaped
Epiglottis narrow omega shaped & angled away (more difficult to lift)
Vocal cords lower, more caudad attachment anterior → difficult to pass ETT twist
Trachea shorter 4-5cm (infant)
Subglottic = narrowest portion
- Funnel shaped
Subglottic Stenosis
90% acquired results from ETT & prolonged intubation
Often requires smaller ETT placement
Tracheal Stenosis
Often occurs at carina
Creates additional resistance to ETT
Tracheobronchomalacia
Intrathoracic airway collapses during exhalation
PEEP or CPAP helpful to stent airway open
Surfactant Production
Begins b/w 23-34 weeks
Inadequate concentration until 36 weeks post-conception
Type 1 Muscle Fibers
Low numbers 10-25%
- Marathon muscles
- Slow twitch muscles
- Used for prolonged activity
- Do not develop adequate type 1 fibers until >6-8 mos
↓muscle strength → fatigue
Apnea risk
Chest Wall
Horizontal & pliable
Minimal vertical movement ↓lung expansion room
Vaginal Squeeze
Approximately 90mL or 30mL/kg fluid forced from lungs
Compression relieved after delivery & air sucked into lungs
C-section infants more residual fluid in lungs
Oxygen Consumption
↑2-3x
6-10mL/kg/min
Respiratory System
↓FRC ↑closing capacity
Immature hypoxia & hypercapnia drive
↑metabolic rate ↑CO2 ↑RR
Premature infant response to hypoxia?
Initially ↑ventilation
After several minutes (fatigue)
↓minute ventilation → bradycardia or apnea
Decreased ventilatory response to hypothermia & carbon dioxide
What are increased risks associated with premature infants in the postop period?
↑hypoxia, hypercapnia, & apnea risks
What factors contribute to premature infants risks?
Immature respiratory control system
Immature intercostal & diaphragmatic muscles
BPD
Bronchopulmonary Dysplasia
Chronic lung disease that occurs in neonates who survive severe lung disease
BPD Cause
Uncertain
Potentially r/t ↑end-inspiratory lung volumes & frequent collapse & re-opening alveoli
Oxygen toxicity, barotrauma (PPV), inflammation, ETT intubation, premature lungs
BPD S/S
Hypoxia Lower airway obstruction Air trapping CO2 retention Atelectasis Bronchiolitis Bronchopneumonia
BPD Treatment
4-6mL/kg TV ↑RR PEEP Minimize FiO2 ICU therapy ↑calories to meet energy demand d/t WOB, respiratory support, diuretics, bronchodilation, & alternative ventilation support (ECMO or HFOV)
RDS
Respiratory distress syndrome
Breathing disorder that affects newborns
Common in premature infants born < 34 weeks (6 weeks early)
Apnea inversely r/t _____
Post-conceptual age
= conceptual age + post-natal age
= 23&6 + dol 138
= 45 weeks corrected
RDS Cause
2° lack surfactant production
Results in airway collapse w/ hypoxia
RDS Complications
Treatment → BPD Anemia Apnea history Residual chronic respiratory disease Impaired gas exchange Prolonged ventilation history Residual subglottic stenosis d/t long-term ETT
Apneic Episodes
> 15 seconds
→ bradycardia & desaturations
Central Apnea
Failure to breath
Obstructive Apnea
Failure to maintain patent airway
Apnea Risk Factors
Low birth weight Anemia Hypothermia Sepsis* Neurological abnormalities Surgical procedure (even w/ regional)
When does apnea & periodic breathing risk decrease?
After 44 weeks corrected
Neonates < 2,500g 25% risk
< 1,000g 85% risk
Apnea Management Post-Anesthesia
Common up to 48 hours postop
Admit all premature infants < 60wks
Continuous apnea & bradycardia monitoring
IV caffeine 5-10mg/kg
Nasal CPAP or tracheal intubation w/ mechanical ventilation
Defer elective surgery until > 44-50 weeks corrected
Cardiovascular System
Immaturity & ↓myofibrils #
↓contractility ↓relaxation
↑risk CV collapse during anesthesia & surgery
Fetal heart ↑connective tissues, less organized contractile elements, & ↑dependence on extracellular Ca2+
Less compliant tissues
↓catecholamine sensitivity
Autoregulation not well-developed
HR unable to compensate hypovolemia → impaired blood flow & cerebral oxygen delivery
R & L ventricle are equal size
Micropreemie EBV
110mL/kg
Preemie EBV
100mL/kg
Full-Term Neonate EBV
90mL/kg
Infant EBV
80mL/kg
Child EBV
70mL/kg
How do neonates tolerate fluid shifts?
POORLY ↓contractility & relaxation ↑afterload poorly tolerated ↓preload poorly tolerated Dependent on serum ionized Ca2+ Immature Frank-Starling curve ↓volume load response
_____ innervation well-developed
Parasympathetic
Vagus → bradycardia
Sympathetic innervation = poorly developed
PDA Failure to Close
↑CV collapse risk during major surgery
PDA promotes pulmonary HTN & CHF
R → L Shunt
Blue or cyanotic lesions
Occurs w/ ↑PVR
Venous blood ejected systemically ↓pulmonary blood flow
→ hypoxia, hypercarbia, & acidosis
ASD or VSD w/ pulmonary HTN
Tetralogy of Fallot during Tet spell
L → R Shunt
Pink or acyanotic lesions
Occurs w/ ↑SVR
↑pulmonary blood flow
→ hypotension & pulmonary volume overload
PDA, ASD, & VSD
Normal Fetal Circulation
AVA
Umbilical arteries x2 originate from fetal internal iliac arteries & deliver fetal blood to the placenta
Umbilical vein x1 carries oxygenated blood from the placenta to the fetus
1° umbilical vein blood supply bypasses the liver via the ductus venous & empties into the IVC where mixes w/ less oxygenated blood from LE
IVC blood enters R atrium via Eustachian valve across foramen ovale into the L atrium
L ventricle pumps blood to UE via aortic arch great vessels
Deoxygenated SVC blood enter R atrium & crosses tricuspid valve into R ventricle
↑PVR → R ventricular output → systemic circulation via ductus arteriosus
Ductus Arteriosus
Originates from pulmonary artery & inserts into the aorta at point distal to L subclavian artery origin
Fetal Circulation Characterizations
↑PVR
↓SVR
Oxygenated blood from umbilical vein → perfuse brain & heart via ductus venosus shunt across the liver
Foramen ovale connects R & L atrium
Umbilical Vein PaO2
30-35mmHg
Fetal Hemoglobin
LEFT SHIFT
P50 = 19mmHg
↑Hgb (polycythemia) levels in utero ↑CaO2
When do neonates transition from fetal to adult circulation?
Umbilical cord clamping & lung inflation
What happens when the lungs inflate w/ air?
↑PaO2 ↓PVR
Vasomotor tone relaxation
↑pulmonary blood flow ↑L atrium blood flow via the pulmonary vein
↑L atrium pressure > R atrium → closes atrial septum over the foramen ovale
What happens when the OB places the umbilical cord clamp?
Removes the low resistance placenta
↑SVR
↓IVC blood flow & R atrium pressure
Reverse flow via ductus arteriosus
↑O2 concentration ↓PGEs → ductus arteriosus closure
Closures prevent blood from bypassing pulmonary circulation
Neonatal blood able to become oxygenation in newly operational lungs
Foramen Ovale
Functional closure quick
Anatomic closure usually requires weeks
Ductus Arteriosus
Remains open d/t hypoxia, mild acidosis, & placental PGEs
Functional closure when these factors are removed
Reverse flow pressure & ↑PaO2 >50-60mmHg causes muscular wall to constrict
When does permanent PDA anatomic closure complete?
5-7 days
Potential to persist until 3 weeks
What physiological stressors cause the newborn to revert to fetal circulation?
Hypothermia Hypercarbia Acidosis Hypoxia Sepsis ↑PVR
Delayed PDA closure common in premature infants < 34wks
PDA S/S
Low diastolic pressure
Congestive heart failure
Pulmonary edema → pulmonary HTN
Central Nervous System
Incomplete myelination
Cerebral cortex less developed
Immature blood-brain barrier (more vulnerable to drugs or toxins)
Neural pathways present
Impaired cerebral autoregulation → blood flow = pressure dependent
IVH
Fragile cerebral vessels susceptible to rupture → intra-cerebral hemorrhage & intraventricular hemorrhage
Spontaneous bleeding into & around lateral ventricles
IVH Predisposing Factors
Small birth weight & preterm (1/3 micropreemies)
RDS - hypoxia, hypercarbia Acute BP fluctuations Acidosis Hypernatremia ↓Hct Over transfusion Stress/trauma Rapid admin hypertonic fluids (NaHCO3 or dextrose)
IVH S/S
Hypotonia Apnea Seizures Loss sucking reflex Bulging anterior fontanelle
ROP
Retinopathy of prematurity
Normal retinal vascular development stops
Neovascularization & fibrous tissue formation in the retina → retinal detachment, fibrosis, & blindness
ROP Associated w/
Low birth weight < 1,000g Prematurity Oxygen exposure Apnea Blood transfusions Sepsis CO2
*Fluctuating oxygen levels or rapid swings
Anesthesia Goal Saturation
90-94%
Titrate based on pre-ductal saturation
Why are pediatric patients more susceptible to hypothermia?
↑surface are per kg
Thin skin
↓fat content
↑heat loss risk
Radiation > convection > evaporation > conduction
Heat Production Mechanisms
Non-shivering thermogenesis (up to 3mos) Brown fat metabolism Volatile anesthetics inhibit thermogenesis Crying Movement Stress → poor weight gain
Volatile Anesthetics Impact on Temperature
Depress the hypothalamus
- Reduction in already impaired ability to maintain body temperature
Cutaneous vasodilation
Pediatric hypothermia results in…
Delayed awakening from volatile anesthetics Cardiac instability Respiratory depression ↑PVR Altered drug response
How to prevent hypothermia?
Transport isolette and/or heating pad Room temp 70-80°F Fluid warmer Limit skin exposure Cover infant head Forced air warmer Heat lamps
Renal System
↓ability to compensate volume swings
Glomeruli continue to develop until 40 days postnatal
Prolonged duration/half-life drugs dependent on GFR excretion
↓proximal tubular Na+/H2O reabsorption
Monitor Na+ & electrolytes
Impaired glucose production
Hepatic System
Immature
CYP450 phase 1 metabolism 50% adult values at birth
Phase 2 impaired until 1yo
Limited glycogen stores & ability to handle large protein loads
↓albumin synthesis ↑unbound drug available
Bilirubin & ABO incompatibility
Calcium
Infant dependent on extracellular Ca2+ & reserves
Parathyroid function not fully established
Vitamin D stores inadequate
Anticipate hypocalcemia especially in preterm, severe neonatal illness, & after blood transfusions
Calcium gluconate or chloride infusions to treat symptomatic hypocalcemia
Central line preferred