CCRN

• -Bil atelectasis/patchy infiltrates due to air trapping- interferes with surfactant
• -Flattened hemidiaphragms /barrel shapped
• -pneumoitis 2 to bile slats in mec
• -use a lower PEEP and inc rate to induce alkalosis to prev PPHN

• -multifactorial
• -O2 toxicity
• -excessive fluid intake
• -gestational age
• -nutritional deficits
• -Blebs in CXR

• -use steroids
• -at inc risk for RSV

• - sail sign
• - pul. air leak
• - anticipate with MAA
• - usually not tx

• -CPAP, BM vent, MEC vent
• -over distension of alveoli & rupture
• -microcystic- hyperinflated lungs & flattened diaphragm (accum. of air in lungs)
• -hypoxia and hypercapnia
• -TX- intubation of mainstem bronchus on the unaffected side
• -BPD

• -PIE
• -Pneumothorax
• -Pneumomediastinum
• -Pneuompericardium
• -Pneumoperitoneum
• -Sub Q Emphysema

- def. or inhibited growth of the lungs

• -Patho:
• -conditions that compress the lungs- CDH, CAM
• -conditions that result in oligo- renal D/O
• -congenital malforamtions- Potter syn

• - bone or memebrane protrudes into nasal passages casuing blockage or narrowing
• - obligate nose breathers
• -ass. with CHARGE
• -place prone
• -cyanosis when quiet, pink when crying

• -If pH is high, K is driven into the cell causing serum K levels to be low
• -Insulin forces K back into the cell by stimulating the Na/K pump

• -herniation of abd. organs into the thoracic cavity through a defect in the diaphragm
• -H/O polyhydram.

• -resp distress & cyanosis- worsens with BMV as intestines distend with air
• -diminished BS
• -heart tones shifted
• -Barrel chest
• -scaphoid abd
• -ECMO
• -Intubate- Avoid BMV

• - inc serum Ca
• - dec serum Ca
• - controls H2O excretion and retention in the kidneys

-For every mEq of K absorbed, kayexalate release 1 mEq of Na

• -Resp Acidosis- dec pH, inc PaCO2
• -Resp alkalosis- inc Ph, dec PaCO2

• -Meta Acidosis- dec pH, dec HCO3
• -Meta Alkalosis- inc pH, inc HCO3

B lymphocytes

• -Down's
• -IUGR
• -hypoxia
• -PIH
• -diabetes

- damage to the brain ctrs caused by inc levels of unconjug bilirubin

-yellow kern- kern=commonly affected area of the brain (nuclear region, cerebellum, hypothal.)

• -neurotoxicity secondary to unconjug bilirubin
• -bilirubin not attached to albumin is free to cross the bld brain barrier
• -most commonly found with Rh & ABO incomp.

-ass. with CP

- conversion of yellow lipid- soluble pigment into H2O soluble pigment

• -brkdn from HgB that is released from destroyed RBCs
• - not an excretable form and a potential toxin
• - found in cord blood

-excretable form

• - occurs in the 1st fews days of life
• - ass. with poor feeding and not with milk
• - encourage freq. feeding

• - related to BM that contains inc fatty acids that compete with bilirubin for binding sites on albumin
• - temp cessation of BF when bilirubin reaches 20 mg/dL

• - occurs AFTER 24 hours of life
• - acc. destruction of fetal RBC's, impaired conjug of bilirubin & inc bilirubin reabsorption
• -Normal biologic response of the newborn

- yellow color results from inc levels of unconjug bilirubin

- peak bilirubin levels- 3-5 days term; 5-7 days preterm

• - maintain neutral environment
• - monitor stools
• - encourage early fdg
• - phototherapy

• - hemolytic dis. of the newborn
• - secondary to Rh incompat.
• - Rh- or O blood type

-dec the # of albumin binding site inc bilirubin

• - breakdown of RBCs
• - ABO or RH incompatibility

• -Anemia
• -hyperbilirubinemia 24 hrs after birth
• -jaundice
• -hepatosplenomegaly
• -erythropoiesis

-Erythropoietin- stimulate RBC formation, initiation of early fdg, phototx, exchange transfusion

-Rhogam within 72 hrs of delivery

-RH- mother, RH+ baby- maternal antibodies enter fetal circulation & attach/destroy the fetal RBCs, fetal sys reponds by inc RBC prod

-erythroblasts- immature RBCs

- most sever form of erythroblastosis fetalis caused by multiple organ failure

-ABO incomp.

• - petechiae
• - hypoglycemia- inc RBC destruction stimulates insulin secretion
• - + direct Coombs test

- presence of Maternal IgG on Infants RBC

- antibodies against Infants RBC present in Maternal serum

- id's fetal Hgb in maternal bld

- form of anemia

• - vit K def.
• - vit K important in formation of Ca binding sites
• - intestinal flora req. for vit K synthesis- BF infants may prod. less vit K than that of formula fed infants

• - acquired hemorrhagic d/o
• - fibrinogen converts to fibrin

• - causes:
• -eclampsia
• -placental abnormalities
• -fetal distress
• -dead twin fetus
• -tramatic delivery
• -infection
• -thrombocytopenia
• -RH incomp.

• - plt. destruction
• - IgG crosses the placenta & destroy fetal plts

• - cessation of breathing for 20s or laonger or for < than 20s when ass. with cyanosis, pallor, & bradycardia
• - presents 2-7 days of life
• -neuronal immaturity (central apnea)

-initial cessation of resp movts as a result of asphyxia during delivery

- occurs after a period of resp as a result of prolonged asphyxia during delivery

- absence of airflow and resp effort

- ass. with blockage

• - prod postnatally in the kidneys
• - fetal life- liver, submandibular glands
• - levels inc. with anemia & low O2
• - levels dec. with hypertransfusion

• - term 60-70 days
• - preterm 35-50 days

- graft vs host dis & delayed hypersensitivity rxns.

- prod & secretion of immunoglobulins & antibodies

• - term- 80-100 ml/kg
• - preterm- 90-105 ml/kg

• HCO3 <22, Base deficit >-2 & <7.35
• - failure to retain HCO3 or an inc. in blood acid

• - HCO3 >26, BE >+2, pH>7.45
• - failure to excrete HCO3 which is controlled by kidney fxn

• - PaCO2 <35, pH>7.45
• - hyperventilation
• - dec of CO2

• - PaCO2>45, pH<7.35
• - hypoventilation
• - accumulation of CO2 the resp Acid

• pH- 7.35-7.45
• PaCO2- 35-45
• PO2- 50-80
• HCO3- 22-26
• BE- -2- +2

- depend on rate, PIP, PEEP, iT- improves oxygentation ( inc. PAO2, dec PaCO2 )

- amt of O2 delivered to the tissues in dep on CO

- delivery of O2 to tissues is inadequate

- O2 content of arterial blood is low

• - heat transfer via direct contact; ie scale, warm blankets
• - via air currents; ie incubators
• - w/o direct contact through absorption & infrared rays
• - conversion of liquid into vapor

• - effects mostly preemies
• - surfactant deficiency; c/s, DM, 2nd twin, asphyxia
• - alveolar atelectasis
• - exp. grunt- forcing air past closed glottis or PEEP
• - reticulogranular pattern- Ground glass
• - r/o pneumonia
• - metabolic acidosis- hypoxemia & acidemia
• - inc WOB- hypoglycemia
• - NaHCO3 for acidosis
• - CP

• - immature lung tissue
• - prematurity, DM, stressful delivery
• - lack of surfactant, atelectasis, resp acidosis, inc RR, retractions, exp grunt, meta acidosis
• - ground glass
• - thermoreg, admin surfactant, O2

• - inflammation of the bronchioles secondary to a viral infection
• - most commonly caused by RSV

• - wet lung disease- delayed clearance of fetal lung fluid
• - fetal lung fluid has a inc Cl concentration
• - bil perihilar
• - air trapping
• - tachypnea- 60-120 bpm
• - birth near or at term, maternal asthma, c/s, maternal sedation

• - improve CO by inc the HR
• -ie-
• - Digoxin- dec conduction through the SA & AV nodes to slow vent rate in tachyarrhythmias
• - Epi, Dopa, Dobutamine, isoproterenol
• - Epi inc BP by stimulating a1 & b1
• - Dobuta- inc CO by stimul. b1

• - most common cause of cardiac death in the 1st week of life
• - hypoplastic L vent, aortic arch, ascending aorta, mitral & aortic valves
• - obstruction of blood flow through L side of heart leads to pul congestion and edema
• - blood supply is dep on PDA
• - asymptomatic at birth
• -CHF

• - PDA closes-
• - severe mottling
• - gray pallor of skin
• - diminished pulses

- PGE, iNO

• - right hand (preductal) & right foot
• - right hand (preductal) & left hand

• - a set of s/s that reflect the heart's inability to deliver adeq O2 to meet metabolic req of the body
• - CO is unable to meet body's metab. req

• -CHF-
• - cardiac defects
• - sepsis
• - asphyxia
• - anemia
• - vol overload- twin to twin transfusin

- tachypnea, tachycardia, arrythymias, *hepatomegaly

• - maintain neutral thermal environ
• - dec vol intake, polycose or MCT oil
• - Digoxin- improves CO, HR <100 don't give
• - lasix, diuril, aldactone
• - inotropics- dopa, dobu, isoproterenol

• - R to L shunting
• - secondary to inc of PVR & PAP
• - hypoxia/asphyxia, polycythemia, CDH
• - dec PaO2, preductal/postductal
• - iNO- pul. vasodilator
• - vasopressors- inc systemic pressure grater than pul to dec R to L shunting
• - Dopa- catecholamine
• - Dobu- B1 effects
• - Nitroprusside- inc CO by dec preload & afterload
• - Epi- inc sys BP, inc HR & improve cardiac contractility

• - the arteries to the lungs remain constricted, after delivery limiting the amt of blood flow to the lungs & amt of O2 to the bloodstream
• - iNO helps to dilate the arteries
• - in utero the bld vessels to the lungs are constricted, When the cord is cut the alveoli are filled with air instead of fluid & the pul arteries dilate so bld flows through the lungs. If the don't dilate bld pressure in the pul arteries is too high (pul htn) & bld flow to the lungs is insuff & not enough O2 reaches the blood

• - a cardioresp d/o charac by systemic arterial hypoxemia secondary to elev pul vas resis. with shunting of blood flow to the sys circulation
• - the result of elev PVR so much that bld is diverted through fetal channels into the sys circ & bypassing the lungs resulting in sys areterial hypoxemia

- while in the womb there is high bld pressure in the lungs. when baby takes its 1st breath the pressure falls & the PDA closes. With PPHN the pressure stays high & the PDA remains open

• - Most common cyanotic heart lesion
• - 4 defects:
• - pul. stenosis
• - VSD
• - Aorta overriding VSD
• - R ventricular hypertrophy

• - R to L shunting
• - Boot shaped heart
• - tet spells (paroxysmal dyspnea & severe cyanosis)

• - Mngmt:
• - propranolol, PGE, surgery

• - most common cardiac cause of cyanosis in neonates
• - L to R shunt
• - Pul artery arises form the L ventricle & Aorta from the R ventricle
• - mixing of oxygenated & unoxygenated blood is req. for survival
• - oxygenated blood returns from the lungs to L atrium & ventricle then back to lungs via pul artery
• - unoxygen blood returns to R atrium & ventricle & then to the body via the Aorta

• - Egg on a string
• - cyanosis present within 1st 24 hrs
• - cardiac emergency
• -correct metabolic acidosis- due to tissue hypoxia and dec CO
• -PGE

• - single artery arises from both ventricles, overriding a VSD
• - both ventricles pump blood into the common trunk supplying the sys/pulm circulation
• - As PVR dec shunting to pulm circul occurs inc blood flow to the lugs & workload of L vent
• - CHF with bounding pulses & widened pulse pressure
• - Diuretics, digoxin, ACE inhibitors

• - pul veins drain into the R atrium
• - CHF
• - Snowman on xray
• - R to L shunt

• - CO- vol of blood ejected by the heart in 1 min
• - correcting hypovol inc blood vol, preload, SV & CO
• - as HR fluctuates so will CO
• - persis bradycardia dec CO
• - tachycardia can improve CO

- depends on preload, contractility, & afterload

• - vol of blood in the ventricles before contraction (ventricular filling)
• - dec in preload will dec SV & CO
• - measurement of pressure rather than vol
• - inc vol in the ventricles improves SV
• - infant can inc SV if there is no inc in systemic vascular resis or rapid rise in aortic pressure

• - speed of ventricular contraction
• - systole- ventricular contraction
• - diastole- ventricular relaxatio
• - contractility dec by:
• - acidosis ( inc K which inturn dec contractility)
• - Hypoxia
• - e- disturbances
• - hypoglycemia

• - the resistance to blood leaving the ventricle; if art pressure inc, afterload inc
• - dependent on sys vascular resis & pul vasc resistance; if SVR or PVR inc, afterload inc
• - afterload can be reduced by vasodilators- ie nitro, Amrinone, Nitroprusside
• - Dobutamine can be used to dec PVR

• - DM*
• - lupus
• - rubella
• - CMV
• - obesity
• - ETOH
• - sz, coagul d/o

• - mitral & tricuspid valves closing
• - Aortic & pulmonic valves closing
• - blood flow

• - SBP 56-77
• - DBP 33-50
• - MAP 42-60

• - Coarct
• - Aortic Arch abnormality

• -failure of the ductus to close within 72 hrs
• - noncyanotic
• - L to R shunt- causes inc pul artery pressure & inc L ventricular pressure & vol leading to CHF
• - bounding peripheral pulses
• - widening pulse pressure
• - dec DBP
• - metabolic acidosis

• - mngmt-
• - fluid restriction
• - diuretics
• - PEEP- reduces L to R shunt

• - L to R shunt = pul edema
• - noncyanotic
• - no surgery unless symptomatic
• - excellent prognosis

• - opening between atria
• - L to R shunt
• - noncyanotic
• - defect may be ostium primum
• ostimum secundum ( most common)
• endocardial cushion defect
• - CHF

• - Most common defect found with Down's
• - probs with Atrial septum, vent septum, mitral & tricuspid valves
• - L to R shunting
• - CHF (digoxin, diuretics)
• - think Oliver

• - seen with Turner syndrome
• - constriction of Aorta
• - CHF
• - dec or absent pulses in L ext
• - ventricular hypertrophy
• - inc BP in upper ext.
• - PGE
• - ballon angioplasty

• - oliguria
• - dec renal blood flow
• - GI bleeds

- staph aureus

- staph epi

- 50 % chance the offspring of each preg. will have the d/o

- male offspring affected & carrier females transmitting the d/o

• - epicanthal folds
• - flat face
• - protr. tongue
• - herniated umb

• - chromosome d/o/ deletion syn
• - heart defects
• - cleft palate
• - hypothyroidism
• - abnormal facies
• - short stature
• - craniofacial
• - cardiac defects
• - hypocalcemia
• - learning disabilities
• - cardiac- most common cause of death

- amt of air that moves in/out of the lungs with each single breath @ rest

- vol of air maximally inspired/expired

- vol of gas that remains in the lungs after normal expiration

- amt of air contained in the lungs after maximal inspiration

- herniation of abd. viscera into the umbilical cord

- herniation of abd contents through an abd wall defect lateral to the umbilical ring

• - obstruction of pylorus caused by hypertrophy of the pyloric musculature
• - nonbilious projectile vomiting
• - visible peristaltic waves in epigas
• - palpable pyloric "olive" in RUQ

• - congenital obstruction of the jejunum; ileum or both
• - H/O polyhyd.
• - BE shows microcolon
• - Bilious vomiting 24-28 hrs
• - Abd dis
• - no stools
• - jaundice

• - absence or closure of a normal opening (atresia)
• - double bubble
• - congenital obstruction of the duodenum (1st part of the sm. bowel. its not open & can't allow passage of stomach contents)
• - H/O polyhyd
• - Abd dis
• - no stools
• - Bilious vomiting within 1st 24 hrs

• - cyanosis
• - hepatomegaly

• - prom occiput
• - omphalocele
• - macroglossia
• - polycyth.
• - hypogly

• - Rh isoimmunization
• - fluid builds up in 2 or more fetal compartments- ascites, plueral eff, pericardial effusion, CHF (severe resp distress), & hypoxia from anemia

• - hemolytic disease when the mother & baby have different blood types. ie ABO, Rh
• - marked by anemia, jaundice, liver enlargement, spleen enlarg, & edema (hydrops)
• - erythroblasts in the blood

• - group of hereditary d/o transmitted by mutant genes, which causes an enzyme defect
• - biochemical d/o if left untreated can cause brain damage and death
• - maternally & paternally inherited- usually autosomal or X linked recessive
• - can be storage diseases or metabolism of small molecules- glucose, lactate, AA, organic acids, ammonia
• - ie- PKU- amino acid d/o; MSUD, homocystinuria, galactosemia, congenital hypothyroidism

• - most common inborn error of AA metabolism that may result in mental retardation
• - autosomal recessive trait
• - def. of the liver enzyme phenylalanine hydrolase to convert phenylalanine to tyrosine. lack of this enzyme is resp. for brain disease
• - low protein diet & use of special AA containing formula that doesn't contain phenylalanine

• - GALT def is the most common of these d/o
• - GALT blocks conversion of lactose so infants are unable to metabolize lactose
• - autosomal recessive
• - jaundice
• -E coli sepsis occurs as a complication
• - absence of the enzyme nec for breakdown & metabolism of galactose
• - lactose free diet
• - mental retardation rates remain high, speech problems

• - rare
• - Autosomal recessive trait
• - usually well at birth but become lethargic, poor fdg, high pitched cry, obtunded and coma after 2-3 days of fdgs
• - odor of maple syrup on breath

• - def in vit K & folate
• - extrinsic & intrinsic pathway is activated
• - gram - infections
• - plts dec
• - PT/PTT normal in early DIC
• - fibrinogen dec

• -mngmt-
• - FFP
• - PLT
• - cryo

• - Low L3-L4
• - High T6-T10

- just above the diaphragm

• - Gluc metabolism
• - neonatal brain is gluc dep
• - gluc levels <30- significant inc in cerebral blood flow

• - affected by pH, K, hypoxemia
• - as pH dec cerebral blood flow inc
• - as K inc cerebral blood flow inc
• - hypoxemia cerebral blood flow inc
• - cerebral blood flow inc when gluc falls <30

• - blueberry muffin rash-viral
• - ass with rubella, CMV, toxoplasmosis, syphilis, herpes

• - impairment in blie flow
• - jaundice

• - loss of all or part of one copy of X chromosome in females
• - horseshoe kidney
• - webbed neck
• - low set ears
• - coarct
• - broad nasal bridge

• - affects males
• - most common cause of hypogonadism
• - infertiltiy

• - bluish mottling or marbling disappers when rewarmed
• - diff in amt of blood flow in R & L sides of body
• - sm white or yel pustules
• - yel or pearly white papules 1mm in size- brow, cheeks, nose
• - palate

• - inflam skin d/o caused by group II staph
• - may follow upper resp infection or otitis media
• - methicillin, bacitracin

- are resp for the majority of early onset sepsis

• - serum & interstitial fluid prov immunity against viral & bacterial pathogens
• - dec levels in preterm, post term & SGA
• - placental transfer is either active or passive
• - inc gradually until 40 weeks; majority is passed in 3rd trimester

• - doesn't cross placental barrier
• - levels inc with intrauterine infection
• - levels inc after birth
• - body fluids & 1st antibody in intial exp to antigen

• - most common in GI/resp tracts, colostrum/human milk
• - found in milk, saliva, tears, resp & GI mucin- prev bacteria/viruses from invading the body through the mucosa of the GI, pul & GU tracts
• - does not cross the placental barrier
• - does not become detectable in the infant until 2-3 weeks of postnatal life

• - resp & intestinal tracts- Allergic rxns
• - major role in allergic rxns

• - BP consis > than 95th %
• - most common caused by intrinsic RF
• - coarct
• - BPD
• - cocaine/heroin
• - wilm's tumor
• - szs, ICP
• - closure of abd wall defect
• - ECMO

- hydralazine, captopril, enalapril, Na nitroprusside

• BP >90/60- term
• > 80/50- preterm

• - renal agensis, dec amniotic fluid
• - male predominance
• - epicanthal folds
• - low set ears
• - death within hrs-days secondary to RDS by pul hypoplasia

• - nutrition- 100 cal/kg with fat & carbs
• - 1-2 g/kg/day protein

• - oliguric ARF- UOP < 1ml/kg/hr
• - nonoliguric- UOP is above this level
• - azotemia with a BUN > 20 mg/dl or inc more than 1mg/dl/day
• - inc CRT > 1.5 mg/dl or inc more than 0.2 mg/dl/day

• - reabsorbs HCO3
• - inc secretion of H
• - production of Ammonia

• - excretes HCO3
• - dec prod of Ammonia
• - dec secretion of H

• - dec GFR caused by:
• - dec BP
• - dec HCT
• - renal vasoconstriction
• - dehydration
• - hypoproteinemia

- resp for regulation of systemic BP, NA & K

• - causes dec UOP, inc CRT & hyponatremia
• - inhibits prostaglandin prod
• - prostaglandin synthe. in the kidneys

• - hypoperfusion of normal kidneys
• - most common cause of ARF
• - responses of structurally intact kidneys to external processess
• - Hemmorrhage
• - sepsis
• - CHF
• - dehydration
• - NEC
• - RDS
• - Hypoxia
• - ACE inhibitors, indomethacin, Amph B

• - dispropor rise in BUN/CRT
• - tx specific causes of hypoperf.

• - renal cellular damage; structural changes within the kidneys
• - prev flow of urine from the kidney into the bladder causing a back up of urine
• - most common cause perinatal asphyxia, sepsis
• - agensis
• - renal dysplasia
• - polycystic kidney dis
• - renal vein/renal artery thrombosis
• - DIC
• - pyelonephritis
• - cardiac surgery
• - nephrotoxic drug admin

• - presence of casts, proteinuria
• - proportionate rise in BUN/CRT

- supportive care until fxn returns

• - obstruction to urinary flow distal to kidney
• - due to structural abnormalities in the ureters, bladder, urethra
• - post uretheral valves
• - bilateral ureteropelvic jxn obstruction
• - obstructive nephrolithoasis

- surgery/nephrology

• - given to r/o prerenal
• - 10/20 ml/kg NS/1 hr
• - rapid & sustained diuresis within 1-2 hrs indicates prerenal
• - UOP < 2ml/kg/hr with lasix suggests intrinsic or postrenal

• - loss of ability to maintain H2O & e- homeostasis
• - ass with abrupt & sever dec in GFR, UOP, & a progressive inc in BUN & CRT

- oligohydraminos

- inc K, dec NA, dec Ca, inc Phos

• - dilation of kidneys secondary to obstruction of blood flow
• - abd mass felt; most common cause of an abd. mass
• - reflux- cystography every 12-18 months

- comm. bet. the bladder & umbilicus causing a leakage of urine from the umbilicus

- acquired disease where plt count is dec (<150,000)

• - used to assess extrinsic
• - initiated by tissue injury

• -used to assess intrinsic
• - vascular endothelial injury

- marker for thrombin/plasmin prod

- % of RBC in a unit vol of blood

- prod of erythrocytes (RBCs)

• - major Fe- component of RBC
• - carries O2 from the lungs to the tissues

- RBCs contain 70-90% HbF ( fetal HgB) @ birth

• - HgB- 14-18
• - HCT- 45-58

- carries factor VII, XII, & Fibrinogen

- forms the Aorta & pul artery

- almost always acc. myelom

• - 2/3 through the skin
• - 1/3 via resp tract

Na- major extracellular cation

- fluid shifts into the cell causing cellular edema & intravascular dehydration

- fluid shifts into the extracellular space causing cellular dehydration & intravascular overload

- Hypoxemia, anoxia, & ischemia leading to diminished blood supply perfusing the brain, & metabolic acidosis

• - describes the relationship between available oxygen and amount of oxygen carried by hemoglobin
• - A left shift will increase oxygen's affinity for hemoglobin- In a left shift condition (alkalosis, hypothermia, etc.) oxygen will have a higher affinity for hemoglobin.SaO2 will increase at a given PaO2, but more of it will stay on the hemoglobin and ride back through the lungs without being used. This can result in tissue hypoxia even when there is sufficient oxygen in the blood.
• - A right shift decreases oxygen's affinity for hemoglobin- In a right shift (acidosis, fever, etc.) oxygen has a lower affinity for hemoglobin. Blood will release oxygen more readily.This means more O2 will be released to the cells, but it also means less oxygen will be carried from the lungs in the first place