Peds 4

• –Placenta – organ of respiration
• –Umbilical Vein carries oxygenated blood (max PaO2 = 30-35mm) from the placenta to
• The liver and via the Ductus Venosus to the IVC
• –To the RA, oxygenated blood preferentially flows through the Foramen Ovale to the LA and LV
• Into the ascending aorta to the carotid arteries (PaO2 is now about 26-28 mm)

• –Deoxygenated blood from the SVC
• flows to the RV and PA where high pressures limit flow to lungs to about 10%
• The other 90% passes through the Ductus Arteriosus into the aorta
• –Both paths send deoxygenated
• blood through the aorta and Umbilical Arteries and back to the Placenta

umbilical vein

• •Prematurity
• •Pulmonary Disease (pneumonia*)
• •Hypoxia* & Hypercarbia
• •Congenital Heart Disease
• •Sepsis
• •Acidosis*
• •Hypothermia*
• •High Altitude
• •Prolonged Stress

• •Loss of tremendous blood flow
• through the placenta
• •SVR doubles at birth – increase in aortic pressure,
• left atrial and left ventricular pressure
• •Decrease in pulmonary vascular resistance (x 5) due to expansion of the lungs – oxygen initiated vasodilation takes place when aeration of the
• lungs eliminates HPV
• •Decrease in PA pressure, right atrial and right ventricular pressure
• •Blood attempts to flow backward
• through the foramen ovale from left atrium (higher
• pressure) to right atrium (lower pressure) – small valve over the foramen ovale on the left side of the atrial septum closes over the opening preventing further flow through the foramen ovale (fibrous closure in a few months)

• •Functional closure of the ductus arteriosus (DA)-
• blood attempt to flow from aorta (higher pressure) to PA (lower pressure)
• however the muscle wall of the DA constricts (initiated by ápaO2)
• within 1-14 days and becomes fibrous by 4 months (structural closure)

• Tetralogy of Fallot
• Transposition of great vessels
• Truncus arteriosus
• Tricuspid atresia
• Total anomalous pulmonary venous return
• HLH
• Pulmonary stenosis

• Acyanotic defects (left-to-right shunt)
• VSD
• ASD
• PDA
• Pulmonary stenosis
• Aortic stenosis
• Coarctation of aorta
• atrioventricularseptal defect

• blood attempts to flow from aorta (higher pressure) to PA (lower pressure) however the
• muscle wall of the DA constricts (initiated by increased paO2) within 1-14

DA becomes fibrous at 4 months (structural closure)

• Prematurity.
• Any factor that increases PVR:
• Pulmonary Disease (pneumonia*)
• Hypoxia** & Hypercarbia, CHD, Sepsis
• Acidosis* Hypothermia*High Altitude
• Prolonged Stress

shunting occurs through the foramen ovale and PDA

• •N20, Desflurane ≥ 1.6 MAC
• Ketamine ???,
• PPV, peep, high TV & PIP
• Hypoxia, hypercapnia , acidosis & atelectasis
• SNS stimulation, pain, light anesth
• hypothermia

• increased pO2, hypocarbia, alkalosis
• Nitric Oxide
• Prostacyclin and Prostaglandin (PGE1, also keeps
• PDA open)
• Propofol
• Volatile inhalation agents (not N2O)
• Spontaneous or HFJ vent
• Surfactant

• –Increased by
• Pain, light anesthesia
• SNS stimulation
• Vaso-constricting drugs (phenylepherine)

–Decreased by

• •Volatile inhalation agents (not N2O)
• Vasodilating drugs (nitroprusside)
• Neuraxial regional anesthesia
• Most IV anesthetics (except Ketamine and Etomidate)
• Morphine (& all histamine releasers)

2 big things (corpulmonale/reversal shunt)

• 2 big negative consequences
• RVH & CHF

• Ventricular septal defect (VSD)
• Pulmonic stenosis
• Dextroposition (right side) and overriding of
• aorta
• Right ventricular hypertrophy

• Prone
• knee-chest position/squatting (­ SVR by kinking arteries)
• supplemental O2
• narcotic, propranolol, phenylephrine

• a)
• Cyanosis
• clubbing of the digits
• normal pulses
• systolic murmur
• loud 2nd heart sound
• boot-shaped heart (RVH)
• diminished pul. vascular markings
• right axis deviation
• RVH

amoxicillin 50mg/kg

• ­
• increased PVR (hypoxia, hypercarbia, hypothermia, PNA, N2O, desflurane > 1.6 MAC, high
• altitude)

fragile vessels

• what makes it worse
• Prematurity
• is the most important risk factor for intracranial hemorrhage

• respiratory complications (RDS)
• impaired autoregulation of CBF (rapid ­¯ CBF during induction & intubation)
• ­increased CVP
• immature cerebral blood vessels
• bicarb administration (­ CO2 vasodilates & rapid infusion hyperosmolar
• stressed neonates (arterial hypoxemia & hypercapnia)

• •Appropriate monitoring: five-lead
• EKG, 2 pulse oximeters, multiple site temperature
• measurement, radial or femoral (>1y) Aline, CVP, ABGs, ionized Ca++, TEE

• CHARGE with choanal atresia
• Colobomas (hole in iris)
• Heart abnormalities
• Atresia (choanal)
• Retardation
• GU
• anomalies
• Ear abnormalities

VACTERL with TEF (TEF type D most common)

• TEF/EA occur together
• vertebral anomalies
• anus (imperforate)
• cardiac anomalies
• tracheoesophageal fistula or esophageal atresia;
• renal anomalies;
• limb anomalies

• CV abnormalities 25%
• Hypoplastic lung
• Pul hypoplasia & pul HTN (medical
• emergencies)

• Oomphacele – cardiac defects, Beckwith
• Weidermean & GI anomalies

Gastrochisis - other congenital anomalies

Undescended testicles

Urinary tract anomalies

• its not an anomaly, it is an illness
• contributing factors:
• Mucosal ischemia (secondary to splanchnic vasoconstriction, Bacterial invasion of immature bowel,Immature immune system, Early enteral
• feeding, Umbilical vessel cannulation and
• Cardiac or pulmonary disease

• Mortality 10-30%
• Early signs of NEC include
• feeding problems, vomiting, jaundice, lethargy
• bloody stools, fever, or hypothermia
• The abdomen may be distended tender

Significant abnormalities of electrolytes (hyperglycemia, hyperkalemia) and coagulation (DIC, thrombocytopenia) & anemia may be present

• increased paO2, hypocarbia, alkalosis
• Nitric Oxide
• Prostacyclin and Prostaglandin (PGE1, also keeps
• PDA open)
• Propofol
• Volatile inhalation agents (not N2O)
• Spontaneous or HFJ vent
• Surfactant

L to R shunt defects (acyanotic defects)

• Awake or asleep intubation (IV* or inhalational induction)
• Rotate the ETT during intubation so the bevel faces anteriorly to avoid fistula intubation
• Deliberate RIGHT mainstem intubation then retract
• ETT until equal BBS heard
• Tip of the ETT is above carina but below the fistula
• Choose the largest ETT possible for frequent suctioning

• ETT should NOT have a Murphy eye so that the posterior wall of the tube will block the fistula opening
• ETT should be cuffed and inflating the cuff will help to block the fistulous opening

• Tape precordial stethoscope
• to the LEFT axilla –helps in diagnosis of ETT migration
• Avoid increased­ airway pressures – will cause gastric distention, especially during induction.
• N2O; avoid ­FiO2 (O2/AIR OK)

• Opioid anesthetic (fentanyl 10-25 mcg/kg)
• low dose IA
• Epidural (via caudal or thoracic)
• Intercostal Nerve block for analgesia

extubation in OR if stable, warm, awake & pain free

• Complications
• Aspiration,anastomosisleakage,tracheomalacia,
• strictures, apnea, hypoventilation, metabolic acidosis, hypothermia,

• fluid & heat loss
• prevent infection
• cover viscera
• IV access for fluids/abx
• NGT/RSI after suctioning the stomach
• GA
• Epidural asleep
• Muscle relaxation
• NO N2O
• aggressive fluid replacement (10 mL/kg/hr LR or 5% Albumin)
• avoid effects of ­ increase abd. Pressure

repair is undertaken as soon as possible after birtrh while an unruptured imphalocele is repaired only after evaluation for other associated anomalies

• MANAGEMENT
• Pulmonary HTN & hypoplasia are medical emergencies
• CDH is managed medically
• until respiratory & CV status is stabilized
• then the surgery is scheduled within several days of birth (done 1st or 2nd day old)

• Initial AIRWAY control is priority:
• Awake intubation –(or RSI)
• NGT to decompress stomach & intestines
• Position infant with the affected side down for intubation (max ventilation of good lung)
• Pneumothorax at anytime
• Rapid, low TV ventilation (HFOV or low PIP/high RR PCV)

Hypocarbia, narcotics, inhaled nitric oxide, ECMO

AVOID hypoxemia and acidemia, all decrease PVR

prevent pul HTN & R to L shunting

• IRDS(hyaline membrane disease)
• Apnea of prematurity
• Hypoglycemia
• Hypocalcemia
• Hypomagnesemia
• Hyponatremia
• Hyperkalemia
• Hyperbilirubinemia
• Polycythemia
• Thrombocytopenia
• Congenital anomalies
• Infections
• Acidosis

• hyperkalemia d/t immature distal tubule function and relative hypoaldosteronism
• hypocalcemia caused by parathyroid hormone insufficiency and peripheral resistance to PTH, inadequate CA supplementation, altered distribution of calcium by transfusions, diuretics
• hypoglycemia(decreased glycogen stores)
• hypomag

correct hypomag, 100mg/kg calcium gluc by slow IV infusion, maintenance CA++

Etiology

1. Caused by alteration in development of retinal vasculature

• 2. Arterial hyperoxia (PaO2 >80 mmHg) leads to retinal vasoconstriction disturbing normal retinal development
• Retinal vasoconstriction, angiogenesis &
• growth of vessels & scarring
• When PaO2 returns to normal, abnormal vascularization of retina continues, scarring develops

Normal PaO2 @ birth = 60-80 mmHg

• #1 is prematurity(< 44 wkspostconceptual age)
• birth weight <1500 gm

• avoid factors that can precipitate hemorrhage; maintain BP within normal limits, avoid hypoxia, hypercapnia, avoid alteration in cerebral blood flow,
• hyperventilation, vigilant monitoring

• Choanal atresia (surgical emergency)
• TEF (surgical emergency)
• Gastrochisis (surgical emergency)
• Imperforate anus (surgical emergency)

• NEC (medical management first)
• Oomphalacele (medical management)
• CDH ( medical management first)
• Pyloric stenosis(medical)
• BPD (medical management first)

• Most pts arrive to OR intubated, sedated and
• ventilate
• Unintubated pts- NGT before induction
• RSI or awake intubation
• IV atropine 0 .02 mg/kg as premed before induction to avoid bradycardia
• NO mask ventilation (stomach distention)
• NO N2O
• avoid worsening of pul. HTN (will ­ increase PVR and cause R toL cyanotic shunt)
• High dose opiods (fentanyl 10-20 mcg/kg vs. normal
• 1-2mcg/kg) if tolerated

• Vigilant monitoring: pre & post-ductal SpO2 (will reflect degree of shunting)right radial Aline CVP, Temprature (avoid hypothermia),ACTs if on ECMO, Frequent ABGs if on HFOV (end-tidal CO2 is hard to monitor), foley,
• Position supine, transabdominal approach
• After reduction of viscera from chest, the diaphragmatic defect is closed primarilyor with a prosthetic patch
• Chest tubes are not used routinely
• Muscle paralysis is maintained
• Infants remain intubated postop and transported to NICU
• Morphine IV infusion to avoid responses to stress

• Do not attempt to inflate hypoplastic lung after repair – may lead to tension pneumothorax on unaffected side (hypoplasia (not atelectasis) is
• the problem)
• Keep PIP < 25 cm H2O use pressure mode ventilation!!

• Correct metabolic abnormalities due to chronic diuretic therapy
• Optimize respiratory & CV status.
• Pts may have a cardiomyopathy due to steroid
• therapy (inflammatory component of BPD)

• Vigilance with fluids
• Diuretics (long term use = hypoKalemia, hypoChloremia, ­ serum bicarb)
• NO N2O
• bronchodilators, theophylline, caffeine, steroids
• Anxiolysis for severe BPD (avoid BPD spell -
• bronchospasm & cyanosis likely during phys. Stimulation
• SPinal anesthesia

• increase Expiratory time, Avoid excessive PPV
• chose LMA instead of ETT if possible

deep extubation to avoid bronchospasm monitor for postop apnea.

• decrease glycogen stores = hypoglycemia
• infant ­ increase BMR = use up glucose quickly
• hepatic immaturity (where glycoNEOgenesis
• occurs)
• infants of maternal diabetics

• multiple blood draw), doesn’t’ cause disturbances in electrolytes, even though increase volume, baby cannot replace RBC's quickly= blood draws primarily effect ANEMIA
• Also due to decrease EPO
• decrease RBC lifespan

Electrolyte disturbances will be due to immature production of electrolytes or problems with renal retention

• oropharyngeal suctioning
• selective tracheal intubation & suctioning of meconium from the lungs (infants with Apgars <7),
• chest physiotherapy
• warmed humidified oxygen
• Bronchial lavage is contraindicated (NO squirting saline down lungs)

Leukocyte function is immature:pt prone to sepsis, bacterial infections

• Normal SPO2 93-95% (preductal)
• Normal PaO2 60-80 mmHg (> 80= retinal vasoconstriction in ROP)
• Intra-op PaO2 < 150 safe

• Pneumothorax @ anytime(Sudden hypotension &
• desaturation)
• Hypoventilation
• Hypothermia
• Metabolic acidosis (toxin release from bowel)
• increase PVR
• CHF

• CHARGE workup (25% have other congenital
• anomalies)
• Airway emergency – intubated in delivery room
• right away
• Arrive to surgery – what changes need to be made
• Laser compatible ETT (Surgery involves LASER:
• (malleable aluminum metal)PVC tubing if hit by laser will melt & burn

• lowest possible FiO2 – compressed air instead; NO N2O
• be aware of the hazard of airway fire

• Begins @ 13 weeks (notes – first lecture)
• Type II pneumocytes appear @ 22 weeks
• Viability @ 24 weeks
• Functional/ ”satisfactorily” @ 30-36 weeks

• Shunting @ PFO/PDA
• Things that ­ increase PVR will contribute to PFC

R to left(cyanotic)

Left to right (acyanotic)

Prostacyclins(PGE1) keeps open 0.1mck/kg IV

Cox inhibitors (indomethacin, ibuprofen) closes