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QuestionAnswer
perinatologysubspecialty of obstetrics concerned with the care of the mother and fetus at high than normal risk of complications
types of disorders Perinatologist treatdiabetes, premature labor, perinatal infectious disease, multiple gestation, perinatal pharmacology
what do perinatologist treat or asses in the fetusgestational age and growth, evaluation for congenital anomalies, placenta and amniotic fluid and adequacy of uteroplacental function
where does fertilization take placeouter third of the fallopian tube
stage 1 aka ovum stage, what happens and how long is itconception to implantation (12-14 days),
stage 2 aka embryonic stage, what happens and how long is itend of ovum until head to rump is 3cm (54-56 days), major organs develop, very vulnerable to drugs, infection etc
stage 3 aka fetus stage, what happens and how long is itfrom embryonic until end of pregnancy, growing
how long does it take the ovum to reach the uterus4-5 days
what is cleavagecell division by daughter cells inside the ovum, 1 becomes 2, 2 becomes 4
blastomerescells produced by rapid cleavage inside the ovum, they are surrounded by a clear envelope called the zona pellucida
zona pellucidatransparent envelope surrounding the blastomeres
morulablastomeres that have grown in numbers to form a ball (16-50 cells) and is what ovum is called as it enters uterus
blastocystfluid builds up inside murula and it is now called blastocyst, has a cavity inside filled with fluid consisting of uterine fluid and fluid excreted by blastomeres
trophoblastthe new outer layer of the blastocyst, takes the place of the zona pellucida
what and where are the germ layerscells inside blastocyst differentiate into 2 layers, endoderm (inside) and ectoderm (outside and thicker), short time later mesoderm forms in between.
What do the germ layers doit is from the germ layers that all tissues organs and organ systems will arise
what arises from the endodermrespiratory tract, epithelium of the digestive tract, bladder and thyroid, primary tissue of the liver and pancreas
what arises from the ectodermepidermis, hair and nails, lens of the eye, central and peripheral nervous system and the skin glands
what arises from the mesodermdermis, muscles, bone, connective tissue and lymph tissue, reproductive organs and cardiovascular system
when does the pulmonary system start to develop and when does it endstarts 24 days after conception and ends around age 8
what are the 5 stages of lung developmentembryonic period (conception-6weeks), pseudoglandular period (7-16 weeks), canalicular period (17-26 weeks), saccular period (27-32/34) alveolar period (32-34 weeks gestation to to 8years)
lung development during the embryonic period (stage 1)conception to 6weeks, lung buds appear followed by two branches, airway branches begin, pulmonary arteries perfused developing lung tissue, airways divide
lung development during the pseudoglandular period (stage 2)7-16 weeks, branching continues to term bronchi, muscle, elastic tissue and early cartilage forms in airways, mucus glands formed diaphragm develops
lung development during the canalicular period(stage 3)17-26 weeks, airways increase in length and diameter, airways end in blind pouches, few pulm capillaries present early and proliferate rapidly toward the end of period, alveolar ducts form, type I & II cells, immature surfactant
lung development during the saccular and alveolar period(stage4-5)alveoli appear, merging of alveolar epithelium and the pulmonary capillaries, appearance of mature surfactant, alveoli continue to increase in size and number
what causes surface tensionsimilar molecules attract each other from all directions, bead of water, or spider to walk on water, constant inward pull of molucules.
What causes surface tension in alvioli and what does it causealvioli are largly liquid filled with gas, liquid is attracted inward due to the attraction causes alvioli to shrink to its smallest diameter
laplace’s lawimportance of relationship between internal pressure of a sphere, it’s radius and surface tension…as the radius of the bubble (alvioli) decreases, the surface tension increases.
Apply laplace’s law to a balloon and alviolismall balloon is hard to blow up, but balloon half blown up is easy, same with alvioli, at end exhalation alvioli are small and (would if not for surfactant) require > energy and work to inflate the lungs
surfactantsubstance found in alvioli wall that reduces surface tention, unique composition and fact that it remains stable in the alveoli, allows it to exert varying influence on alveoli as they enlarge and shrink
what is the importance of the varying influence of surfactant on alveolias alveoli increase in size, surfactant thins and tension builds, aiding passive ventilation, as alveoli shrink, surfactant thickens weakening surface tension and preventing alv from collapsing
where is surfactant producedtype II cells
what is surfactant made ofphospholipids, mainly phosphatidylcholine (PC) and phosphatidyglycerol (PG), neural lipids and protein, since first surfactant only has PC, it is considered immature until PG is present around week 35
babies born befor 30 weeks are especially prone to what disordershypoxia, hypothermia and acidosis
hypoxia, hypothermia and acidosis cause what in premature infants less than 30 weeksinhibits surfactant production and commonly leads to resp distress syndrome
L/S ratio of lung maturityfetal lungs are considered mature when ratio is 2:1, two time as much lecithin (PC) as sphingomyelin, approx 35 weeks
what is amniotic fluid tested for when looking for lung maturityPG
what is the shake and foam testtest of lung maturity, mixing amniotic fluid with ethanol for 15 seconds, read 15 minutes later if there is a ring of bubble, then there is enough lecithin (PC) for lung maturity. No foam do L/S ratio
what other lung maturity tests are theresurfactant-albumin ratio (SAR), fluorescence polarization essay
how can lung maturity be artificially inducedadministration of glucocorticoids
what are the limitations of glucocorticoids in inducing lung maturitymust be administered between 27-34 weeks, at least 48 hours prior to delivery and delivery must be within 7 days
what other factors influence lung maturationthyroxine thyrotropin-releasing hormone, b-adrenergic drugs, estrogen, prolactin and epidermal growth factor
do fetus of preeclamptic woman show acceleration of lung maturationno, once thought to be true, it is not.
Surfactant is vital, it enhances capillary circulation allowing for whatnormal V/Q ratios, protection against barotrauma (it also aids in evacuation of lung fluid)
what is the leading cause of pulmonary complications in neonateslack of surfactant or deterioration of its production following birth
what happens to lungs with little or no surfactantthey become stiff and noncompliant, causing >WOB
why is support indicated for infants with little or no surfactantthey will exhaust and die from combination of energy loss, hypoxia and hypoventilation
what is the fluid content of the lung at term20-30 mL/kg, roughly equivalent of FRC
what is the composition of fetal lung fluidlower in ph, protein and bicarb than amniotic fluid, but higher in sodium and chloride, produced all through gestation until just befor birth
what is the function of fetal lung fluidmaintain patency of developing airways, helps in formation, size and shape of potential airways
how is lung fluid expelled prior to delivery1/3 is squeezed out when thorax descends maternal pelvis during delivery, the rest is absorbed with in hours of delivery
hazards of lung fluid retention(especially in cesarean section delivery) lack of thorax squeeze cause retained secretions, if not rapidly absorbed PPV can help. Failure to remove can cause transient tachypnea of the newborn (TTN) or RDS type II,
what is the first major organ to develop?heart
why is pressure in the right or venous circulation higher than the left in fetal circulation1fetal lungs have very high resistance to blood flow and high pulm vascular resistance-high pressures in right side, also becouse placenta offers little resistance to blood flow-so low resistance on left side
fetal blood flow to the heartnutrients and 02 from placenta, to umbilical vein, ductus venosus (shunt liver), inferior vena cava, right atrium (mix w/venous from superior v cava), foramen ovale (shunt r to l atrium), right atrium to pulm artery, ductus arteriosus (shunts to aorta)
fetal blood flow beyond the fetal heartforamen ovale to left vent, aorta and combines with blood from ductus arteriosus (some blood to upper organs), aorta split into two common iliac arties, further split to internal/external illiac arteries, internal illiac become umb arteries, to placenta
best way to remember fetal blood flowveins travel toward the heart, arteries travel away, in fetal veins carry o2 rich blood from mom, and arteries carry o2 poor toward mom,
baroreceptorsreceptors located in the bifurcaton of the carotid arteries and aortic arch, stimulation leads to bradycardia and hypotension
chemoreceptorspresent but not active in fetus, located in carotid arteries and orta, sensitive to PaO2, PaCO2 and PH they regulate ventilation-help initiate first breath
intrauterine structuresplacenta, umbilical cord, amnion, amniotic fluid
Placenta
chorionic villaprojectiles of the trophoblast that attach to the endometrium of the uterus
inervillous spacessmall pockets surrounding chorionic villa that contain maternal blood
cotyledonsone of 15 to 25 segments on the maternal side of the placenta, each segment contains a villa and a inervillous space
umbilical cordlifeline between mother and fetus, 3 vessels surrounded by a tough gelatinous material caled whartons jelly, 3 vessels-2arteries, 1 vein
wharton’s jellytough gelatinous material that surrounds and protects the umbilical cord, allowing it to bend but protecting it from collapsing, kinking and occluding blood flow
amnionsac that surrounds the growing fetus and holds the amniotic fluid, arises from trophoblast at around 7th week
amniotic fluiddynamic fluid that surounds fetus, serves to protect fetus from trauma, thermoregulation, and facilitation of getal movement
what is dynamic fluid mean in relation to amniotic fluidit is constanly being absorbed and replenished
where is surfactant storedin lamellar bodies, produced in type two cells
at what stage of embryologic development does the ovum enter the uterusmorula
the respiratory system arises from which germ layerendoderm
the earliest development of the lung begins when24 days
dichotomy of the airways occurs during which phase of lung developmentpseudoglandular (7-16 weeks)
the following statement best describes surface tensionthe tendency of liquid surface to contract
what is the best indicator found in ambiotic fluid of lung maturityPG
what does not appear to accelerate fetal lung maturationmaternal preeclampsia
the following are true statements about lung fluidapprox 20-30mL/kg present at birth, lower ph, protein and bicarb than ambiotic fluid, higher sodium and chloride than ambiotic, helps to maintain patency of developing airways
what is one of the biggest hazards of cesarean sectionTTN
heart develops from what germ layerendoderm
embryologic truncus arteriosus develops into whatpulm artery and aorta
path of blood that is shunted through forament ovale isright to left atruim
ductus arteriosus shunts blood wherepulm artery to the aorta
the folling statement about baroreceptors is correctthey are actually stretch receptors
in the placenta, the fetal vessels are cantained in thechorionic villa
polyhydramnios is defined asexcessive amniotic fluid
what are the possible causes of polyhydramnioshydrocephalus, esohageal atresia, down syndrom, cleft pallate
assessment of the fetus during the first trimester is facilitated by what techniquetransvaginal ultrasound
can infection be detected by ultrasoundno
what can be detected by ultrasoundposition of the fetus, position of the placenta and volume of amniotic fluid
a high level of alpha-fetoprotein found during amniocentesis indicates whatneural tube defect
what test of amniotic fluid is used to help determine fetal kidney maturitycreatinine level
bilirubin from amniotic fluid tests for whatliver maturity
monitoring fetal heart rate during labor and delivery is used to detect what?placenta insufficiency, compression of the umbilical cord and bradycardia secondary to vagal stimulation
the most accurate method of measuring fetal heart rate isfetal scalp electrode
common cause of fetal bradycardia isasphyxia
type III decelerations are caused bycompression of the umbilical cord
fetal scalp ph is the lower limit of what7.25
the following statements are true about fetal movementsgreatest activity between 28-34 weeks, destress and stillbirth are common if fetus is inactive, move can be detected as early as 7 weeks
what are the common measurements in a biophysicalfetal breathing, gross body movement, fetal tone, reactive NST and amniotic fluid volume (normal score 8-10)
cordocentesisremoving fetal blood sample from the cord
factors of maternal history that place fetus at high riskprevious miscariage, previous premature labor, asthma, maturnal obesity
QuestionAnswer
RDSresp distress syndrome, aka HMD (hyaline membrane disease), caused by <surfactant
Primary cause of respiratory disorders in neonatesRDS/HMD
risk factors that >increase incidence of RDSpremature, weight, males 2:1, PDA, atelectasis, twins, prenatal complications, maternal diabetes, placenta conditions, umbilical cord problems
prenatal complications that may > risk of RDShypoxia, hemorrhage, shock, hypotension, hypertension, anemia
abnormal placenta conditions that > risk of RDSplacenta previa, abrubtio placentae
umbilical cord disorders that > risk of RDScord compression, cord prolapse
RDS circle<surfactant, <CL, atelectasis, hypoxia, hypercapnea, resp acidosis, met acidosis, capillary and alveolar damage, <surfactant, pulm vasospasm, >hypoxemia, <perfusion, <V/Q, >hypoxemia, >atelectasis
Pathophysiology of RDS and <surfactant<surfactant causes >surface tension, and <CL (stiff lungs) and atelectasis, increasing hypoxia, hypercapnea and acidosis, this <O2 at cells leads to anaerobic metabolic acidosis
What is the net effect of combined acidosis in RDSdamaged capillaries and alveolar tissue, leading to a further <surfactant and pulm vasospasm
effects of pulmonary vasospasmenhanced by hypoxemia, leads to hypo-perfusion causing <V/Q mismatch and worsening hypoxemia—the circle
What are the clinical signs of RDS and when do first appearappears at APGAR, RR>60, grunting, retractions, flaring, cyanosis, hypoxemia, skin w/pallor or severe edema
How is RDS diagnosedCXR, bilateral underairation, clouded opaque, reticulograndular and frost or ground-glass, >atelectasis, air bronchograms in periphery
rapid tool to diagnose RDSshake test
APGAR and RDSRDS usually appears at APGAR with >RR, skin is pallor or severe edema, flaccid muscle tone and <activity
RDS progressionmost cases worsening first 48-72 hours then stabilize w/slow recovery
How do we know RDS is stabilizingonset of diuresis (baby starts to pee)
If baby dies from RDS after first 72 hrs what is usual causesecondary complications, barotrauma, ICH, or infection
Ideal TX (prevention) of RDSprevent with glucocorticosteroids 48 hrs prior to birth
goal in TX of RDSmaintain adequate alv ventilation with out inflicting lung damage
TX of RDSthermoregulation, low press, low FIO2 with acceptable ABG, PaO2 50-70, CO2 <60, Ph > 7.25, diuretics, LABA and parasympathetics
complications of <Ph in RDSthe acidic the Ph becomes, the less surfactant is produced, organ dysfunction and >risk of IVH
Most complications of RDS are from PPV, what are theyICH, barotrauma, DIC, infection and PDA
IVH from PPVintraventricular hemorrhage, caused by positive press in the thorax is transmitted to cranial cavity, immature vasculature ruptures
Barotraumavery common in RDS, <CL requires higher pressure to maintain oxygenation and ventilation, >press leads to lung injury and air leaks, barotrauma and pneumothorax,
DICdisrupted coagulation factors causes bleeding all over body
RDS infectionsgram negative (very difficult to treat), from ETT cause chronic pneumonias and >tissue damage
what are the first signs of RDSnasal flaring, followed by retractions and then grunting (very bad sign)
how often does HMD occur in <28 wk preemie1/2
how often does HMD occur in SGA and IUDR1/3
Why is EKG given to HMD ptto rule out other causes of symptoms
pneumoparicardium CXRair completely around surrounding heart-looks like halo
pneumothorax CXRair seen around the thymus (batwings) and heart, lateral-thymus lifted
PIE CXR aka Pulmonary Interstitial Emphysemasmall dark streaks (air and cysts) surrounded by white tissue, black paint flicked on white
chronic hypoxia (acidosis) does what to pulm circulationpulm artery hypertrophy (swells) narrowing lumen
what is diffusion coefficient20:1
what determines diffusionsurface area, Hbg
BPD triadO2 dependence, radiologic abnormalities, resp symptoms >28 days with respiratory failure at birth
Causes of respiratory failure that lead to BPDLBW, flail chest, immature resp control, underdeveloped tone and power
single most predictive factor of BPDLBW-low birth weight
acute O2 therapy leads to what>vascular permeability, pulm edema, acute necrotising tracheobronchitis, oxidant stress
oxidant stress<surfactant production, <biliary mobility, inactivates cellular antioxidants
complications of chronic O2 therapy (>28 days)necrosis of bronchial epithelium and type I cells, hyperplasia of type II cells, >fibroblasts and macrophages in lung interstitum
BPD CXR stage Igrandular, correlates to atelectasis, HMD, lymphatic dilation
BPD CXR stage IVbeyond 30 days, sponge look, correlates to emphysematous alveoli
clinical signs and symptoms of BPDtachypnea, dyspnea, wheeze, subglottic edema, intratracheal scars, polyps (cause of stridor), tracheal malacia (trach needed)
severe signs and symptoms of BPDirritable, difficult to feed and comfort, irregular sleep, digital clubbing (chronic acidemia)
BPD complicationsrecurrent cyanosis, agitation with obstruction due to tracheal distortion or necrotising, tracheobronchitis, intermittent systemic edema, >fluid, >vasoperfusion, transient myocardial dysfunction
Olguriano pee
why xanthines and not beta agonist or parasympatheticsrebound effect
BPD bottom limeforms in hyaline membrane, pulm edema, interstitial fibrosis, emphysematous, delay in lung growth episodes of pulm insufficiency
PDA and RDSR-L shunting increases hypoxemia, or during recovery can cause RHF
BPD follows the RDS, why>press & >FIO2 over time
NCLD aka neonatal chronic lung diseasesymptoms of BPD without confirmation of CXR
How is BPD confirmedCXR
the 4 factors of BPD pathophysiologyO2 toxicity, barotrauma, PDA, fluid overload
BPD circle of progression>O2, edema and thickening of AV membrane, Alv tissue hemorrhage and necrosis, interstitial space becomes fibrotic, new cells damaged by O2-starts over
4 stages of BPD on CXR1. Typical RDS, frosted ground-glass 2.opaque, grandular infiltrates, obscure cardiac markings 3 small cysts, visible cardiac silhouette 4. > 28 days >density, large irreg cysts
BPD lab DXABG’s with chronic lung disease, hypoxia hypercapnea >HCOS
BPD & ECG DXlatent stages, right axis deviation, hypertrophy of Right vent
PFT’s of BPD pt<VT, normal VE, >RAW, <CL
what causes RAW and CL changes in BPDlung parenchyma damage
best prevention of BPDpress and FIO2 to maintain PaO2 50-70 and CO2 45-55
Best way to prevent tracheal stenosis in long term BPDMLT
weaning with BPDextubate ASAP, but wean slowly
best way to transition from PPV for BPD ptnasal CPAP
TX of PIE with BPDhigh frequency ventilation
CPT w/BPD ptfrequency is dependent on amount and viscosity of secretions, suction as necessary
Theophylline and BPDdrug of choice for BPD to reduce RAW and increase CL-shortens duration of weaning in pt’s <30 days
BPD hydration and urinationmaintain with diuretics, monitor urine output, BS and chest excursions for improving CL
PDA and BPDtreat RHF with diuretics and Digoxin
BPD increases metabolism, what are precautions of nutrition>calories causes >O2 need (>hypoxia), metabolism of glucose >’s CO2 (>hypercapnia) worsening acidosis
Long term effects of BPD>risk of asthma, COPD in later life
ROPformation of scar tissue behind the lens, caused by capillary networks of the retina that do not develop normally
factors that lead to ROP>FOI2, retinovascular immaturity, and circulatory and respiratory instability
Ora serrataretina’s anterior end
vaso-obliterationconstriction of vessels leading to necrosis
vitreousliquid portion of the eye
how does the eye develop16 weeks gestation, capillaries start to branch from optic nerve (back of eye), toward oro-serrata (front of retina) and completes at 40 weeks
Pathophysiology of ROP>PaO2 causes vasoconstriction in retinal vessels, leads to vaso-obliteration (necrosis), remaining vessels proliferate, some into vitreous (liquid) where they hemorrhage and form scar , scar pulls and detaches retina-blindness
factors that lead to ROPimmaturity, hyperoxia, blood transfusions, IVH, apnea, infection, hypercapnea, PDA, PSI, E deficiency, lactic acidosis, prenatal complications, genetics, bright lites, early intubation, hypotension, NEC
PSIprostoglandin sythetas inhibitors
Stages of ROP1. small white demarcation line, stages progress to 5, buildup of fluid and traction leads to retina detached and blindness
4 major intracranial hemorrhagessubdural, subarachnoid, intracerebellar, periventricular-intraventricular (PVH-IVH)
subdural and subarachnoid bleedssecondary to trauma or asphyxia-most often seen in term neonates during traumatic labor
IVHperiventricular-intraventricular hemorrhage, cerebellar bleeds most often seen in preemies (24-32 weeks, and or <1500 g), and the most common type of bleed seen
area of bleed most often seen in term neonateschoroid plexus (lateral ventricles)
area of bleed most often seen in preemiesgerminal matrix
term neonate bleedsSSC-subdural, subarachnoid (trauma), choroid plexus (lateral ventricles)
why are neonates at >risk of hemorrhageimmature cerebral vasculature system and inability to regulate blood flow (fluctuating blood flow)
Etiologic factors that lead to fluctuating flowshock, acidosis, hypernatremia, transfusions, seizures, rapid >blood volume, >ICP (trendelenburg or PPV)
what type of neonate has a substantially increased risk of IVHmaternal alcohol use
historical factors that >risk of IVH<1500g, <34 weeks, HMD, coagulapathy, hyperviscosity, hypoxia, birth asphyxia
common signs of germinal matrix bleedapnea, hypotension, <Hct, flaccid, bulging fontanelle, tonic posturing
How are IVH diagnosedCT scan or ultrasound
IVH gradesI-IV, based on extent of bleeding
stage IV, IVH bleedmost severe bleed causes dilation of the ventricles and bleeding extends into brain parenchyma
sequelae(Latin for sequel) results from prior disease
most serious complication of IVHPHH
PHH post hemorrhagic hydrocephaluscaused by obstruction of the CSF outflow and impairment of CSF reabsorption in the brain
TX of PHHgoal is to maintain normal cerebral perfusion as ICP rises, done by removing CSF via lumbar puncture, if lumbar puncture fails, then V-P shunt (ventricle peritoneal) or ventricalilostomy
V-P shuntinternal shunt from ventricle to peritoneal in abdomen that shunts CSF to abdomen for reabsorption
ventricalilostomyshunts CSF for external drainage
complications (sequelae) of IVHPHH, cerabal palsy, vision loss, hearing loss, epilepsy, mental retardation
TX of IVHsupportive, not much we can do, caution with blood and plasma (slow administration) watch for >bilirubin (very common), avoid hypotension with >ICP to avoid <cerebral blood perfusion
preventing IVHavoid factors that cause fluctuations in cerebral blood flow, wide Bp, oxygenation or Ph, indomethacin is prophylactic
indomethacinprophylactic for IVH
asphyxiahypoxia, hypercarbia and acidosis in fetus or neonate caused by lack of perfusion
most common risk of asphyxiaIUGR, breech or post maturity (trauma complication of large baby)
asphyxia inutero resulting from placental insufficiencyorgan of respiration not working, no O2 to baby and no CO2 back to mom
asphyxia in neonates most often results frompulm or cardiac problems
factors that contribute to fetal asphyxiamaternal hypoxia, disrupted uteroplacenta blood flow, placenta dysfunction, compressed cord, intrinsic fetal disorder, maternal hypoxia, shock, asthma, co poison, anemia, sedation, apnea, CHF, <PIO2, pneumonia
<uteroplacenta blood flowshock, vasoconstriction states, inferior vena cava syndrome
dysfunction of placentaplacenta previa, abrubtio placento
intrinsic fetal disordershydrops fetalis (fetal cardiac failure), fetal hypotension secondary to hemorrhage or drugs
fetal shunting from asphyxiablood moves away from lungs muscles, liver, kidney and gut and directed to brain, heart and adrenal glands
primary fetal apneafetal apnea caused by <Bp and <HR from uncorrected asphyxia
secondary fetal apneafollows primary apnea, continued asphyxia causes further < in BP and HR, fetus does deep ineffective gasps until tired and stops-leads to permanent brain damage or death
detecting fetal asphyxiafetal heart monitor, meconium in amniotic fluid, heart monitor-loss of base variability, late decelerations, prolonged bradycardia
major complication of prolonged asphyxia inuterohypoxic-eschemic brain injury
hypoxic-eschemic encephalopathymajor complication of asphyxia in term neonate, results from necrosis of neurons in cerebral cortex and basal ganglia
hypoxic-eschemic necrosis in preemies is most often associated with whatPVH-IVH
periventricular leukomalaciainfarction in the periventricular region
consequences of asphyxiaPVL, HEL, HEE, cardiac eschemia (usually transient), tubular necrosis of the kidneys, bowel eschemia, NEC, DIC, >PVR, <surfactant and ARDS
asphyxia TXimmediate reversal of hypoxemia and acidosis, rapid delivery of fetus
MASmeconium aspiration syndrome, term and post term who experience some degree of asphyxia during before or during labor causing aspiration of meconium
when does MAS occurbefore or during labor, or at first breath
why are post term at >risk of MAS<amniotic fluid (to dilute meconium), diminished placenta function leading to >asphyxia
meconiumcontents of fetal bowel, thick tar-like dark green material, consists of swallowed amniotic fluid, bile salts and acids, squamous cells, vernix and interstitial enzymes
sequence of MASasphyxia in utero, blood shift leads to >peristalsis and relaxation of anal sphincter causing fetal bowel passing of meconium, gasping of apnea allows passage into resp tree
2 greatest hazards of MAS1. Obstruction and air trapping (ball-valve effect), causes >V/Q ratios and >hypoxia and hypercapnea, atelectasis, air leak of trapped gas and pneumothorax and lung rupture 2. chemical pneumonitis and infection
chemical pneumonitisinflammatory response of tracheobronchial tree epithelium to meconium causing acidic irritation of meconium, mucosal edema, <CL, further impairment of gas exchange
PPHN from MASvasospasm of pulm vascular causes persistent pulm hypertension, blood follows fetal route, bypassing lungs and leading to >shunting and worse ABG’s
detecting PPHNcyanosis not responding to >FIO2, tachypnea, retractions, systolic ejection clicks and loud 2, patchy infiltrates, hyperinflation, pleural effusion and cardiomegaly
definitive test for PPHN hypoxia-hyperventilation testpositive is PaO2 <50 that rises to >200 when pt hyperventilated to CO2 of 20-25
most accurate test of meconium aspirationgreen stained vocal cords at birth
TX of meconium aspirationsuction mouth ASAP, insert ETT and suction, replace tube and suction again and again until meconium no longer, CPT, antibiotics, keep warm vent if necessary
complications of meconium aspirationaspiration pneumonia, pneumothorax, pneumomediastinum, pneumoparicardium, pulm interstitial emphysema PIE, sub q emphysema,and air emboli
higher incidence of air leak syndrome in what pt’sRDS, MAS, TNN, most are from mech ventilation, few from spontaneously
TX for tension pneumono PPV then monitor, severe do needle air removal, PPV give chest tube w/1 way valve at 15-25 cmh2o
pneumoparicardiumair through lung into interstitum into mediastinum, rarely severe, can cause >venous return symptoms-distant crackles and heart sounds-confirm w/CSR-air around heart
PIE, pulmonary interstitial emphysemaair leaks from over distended alveoli, caused by >PEEP, >PIP, IIT, 2 types-intrapleural and intrapulmonary, either or both can be present , leads to pneumothorax, pneumomedistinum, pneumoparacardium
intrapleural interstitial emphysemaPIE where extra alveolar air is confined to visceral pleura forming blebs
Intrapulmonary interstitial emphysemaPIE where extra alveolar air remains in lung tissue
Pathophysiology of PIEair collects in interstitium, compresses small airways and vessels causing > ventilation, <perfusion, leading to worsening ABG’s, circle of > pressures to improve ABG’s causes more air leaks and >V/Q mismatch
PIE TXbesides preventions, mild will reabsorb in 5-7 days, lower vent pressures while maintaining ventilation and oxygenation, HFV, selective ventilation
Selective ventilationintubation and ventilation of only the affected lung or less affected lung, allowing injured lung time to heal
survivors of PIE of get what complicationBPD, from aggressive mech ventilation, o2 toxicity
PFC/PPHN persistent fetal circulation aka persistent pulm hypertension of the newbornsevere persistent pulm vasoconstriction causes >pressures <pulm blood flow, right side press higher than left, allowing foramen ovale and ductus arterious to stay open and shunt away from lungs
who gets PFC/PPHNmost term and post term, and pt’s with asphyxia, MAS, sepsis, CHD (congen diaph hernia), pulm hypoplasia, CHD (conj heart disease) and premature closure of ductus arteriosos
other diseases that are assoc with PFC/PPHNHMD, bacterial pneumonia, myocardial dysfunction and pulm hypoplasia
what is the result from the severe v/q mismatch of PFCcombined met and resp acidosis and hypoxia-causes further pulmonary vasoconstriction
why so much PFC in term and post termpulm arterial muscular does not form until late gestation, dysfunction of pulm vasoregulation resulting in high PVR, also connected to intrautero events (hypoxia an)
full term neonate w severe or worsening hypoxia, what are 3 diseases to considerPLD-parenchymal lung disease, CCHL
QuestionAnswer
what are lung volumesdistinc measurements that do not overlap each other
what are lung capacitiesmeasurements containing two or more lung volumes
what volumes and capacities cannot be measured directlyRV, FRC and TLC
how do we measure RV, FRC and TLCindirectly using helium dilution, nitrogen washout, body plethysmograph or radiologic estimation
TLCtotal lung capacity, sum of VC and RV, based on age size and gender, increased w/obstructive and decreased with restrictive
VCvital capacity, max exhaled volume after a deep breath (if forced it is called FVC, reflects pt ability to take a deep breath, cough and clear secretions
what is the most important part of the FVCcoaching, bad coaching is bad results
the 3 phases of the FRC are1(max inspiratory effort, 2)initial expiratory blast, 3)forceful emptying of the lungs
why do we not continue coaching and yelling during the forceful emptying portion of the FRCmay lead to airtrapping in obstructive pts
can a VC be to high?no, the higher the better, just to low
how does obstructive disease cause a decrease in FVCby causing a slow rise in the RV
ICinspiratory capacity, measured with spirometer
FRCfunctional residual capacity, (RV+ERV is FRC) resting volume in lungs following exhalation of VT
what volume represents the the force of the expanding chest wall and the contractile rebound of the lung tissue(elastic equilibrium)FRC
what kinds of diseases cause a <FRCpneumothorax, restrictive diseases, age, obesity (shrinks lung)
what kinds of diseases cause an >FRCemphysema, any disease that causes a loss of lung tissue, obstruction
IRVinspiratory reserve volume, measured with routine spirometer
VTtidal volume, exhaled or inhaled in each breath, can be reduced in both restrictive or obstr (quiet breathing)
a decrease in VT with no change in RR will result in whathypoventilation and >CO2
What is the normal RR for a pt with restrictive diseaseincreased, because VT’s are shallow, RR must be increased proportional to loss of VT
SVCslow vital capacity, test performed by having pt blow everything out slowly after max inspiration, allows for less airtrapping
what is the most important measurement for a preop ptVC, significant reduction in VC indicates pt is at high risk for resp failure after surgery (<20 mL/kg)
ERVexpiratory reserve volume, (FRC-RV is ERV) max exhaled following passive exhalation, < obesity, poor performance and restrictive (limited clinical use)
RVresidual volume, amount left in lung after pt exhales all that is physically possible, < in restrictive and >in obstructive as airtrapping occurs
RV/TLC, what percent of TLC is normally RV25%
RV/VC, what percent of VC is normally RV33%, >33% COPD is present
What is the significance of a reduced RV/VCnone, there are no clinical states that reduce RV/VC only increase as with COPD (will be in normal range with restrictive disease state)
VERRxVT, best index of ventilation when used in conjunction with ABG. Should be up with exercise, fever, pain, hypoxia and acidosis (regardless of acidosis cause)
What does the expiratory side of the FVC curve providecontractile state of the airways, FEV1, FEV3, FEF25-75, PEF (peak flow)
FEVtforced expiratory volume timed in liters (t is commonly expressed in .5, 1, 2, 3 seconds) norm is relative to his FVC
FEV1max forced exhalation during 1st second, best indicator of obstructive disease, reflects the flow in larger airways, best express as a % of FVC (FEV1/FVC is FEV1%), norm is 75% of VC, <in acute or chronic COPD, norm in restrictive
FEV3looks at the 3 second point on the curve.
FEV.5 and FEV1used along with FEV200-1200 to assess the flow rates and disorders of the large airways, will be < with airway obstruction
FEV%FEVT/FVC reduced with obstructive disorders
FEV1%75-85% <65% is is airway obstruction
FEV3%95%
FEF25-75%sensitivity test expressed in L/sec (measures flow or speed of exhalation), middle 50% of the exhalation (not 50% point but total 50%) and reflects patency of airways, best early indicator of obstructive disease
PEFmax flow rate during PFT maneuver, steepest part of FVC, can be measured with spirogram or hand-held device at home or ER. Often used by asthmatics to measure severity of asthma obstruction
PEF measurements<100 L/min is sever obstruction, 100-200 L/min is mod to severe obstruction, >200 is mild
Once treatment has been started in an asthma pt, what test can be given to help determine response to TXPEF
spirometerpositive displacement-volume, used to measure volumes and flow rates
water-seal spirometermeasures volume and time
what is the best indicator of a restrictive disease?Vital Capacity
how do we measure obstructive diseasesflow rates, FEV1, FEF200-1200, FEF25-75, PERF and FVC
what is the best indicator of obstructive diseaseFEV1
what is the best indicator of large airway obstructionFEF200-1200
what is the best indicator of a small airway obstructionFEF 25-75
what is the best indicator of airtrappingFVC that is smaller than SVC
what is a PFTdetermines the functional status of the lungs
what can PFT’s be used forpresence of pulm disease, esp which pts will be harmed by smoking, evaluating pts before surgery, eval effectiveness of therapy, documenting progression of pulm disease, effects of exercise on lung function, measures degree of airway hyper-responsiveness
what is bronchoprovocation testingPFT that measures degree of airway hyper-responsiveness
contraindications of PFT’srecent ab, thoracic or eye surgery, hemodynamic instability, symptoms indication acute sever illness, recent hypoptysis, pneumothorax, recent hx of ab thoracic or cerebral aneurysm
what tis the most important factor influencing lung size and predicted valuesheight
at what age does a persons lung size begin to shrink20yrs
what is the primary instrument used in PFT’sspirometer
what does a spirometer measurethe lung volume compartments that exchange gas with the atmosphere
spirographattaches to spirometer to graphically record PFT’s
spirogramthe graphic tracing of the PFT
body plethysmographfor total lung capacity and airway resistance studies
what are the 2 main categories of PFT abnormalitiesobstructive and restrictive defects
how do obstructive disease present on PFT’sif expiratory flow is below normal
how do restrictive diseases present on PFT’sif lung volume is reduced
Upper airway obstruction will show up where on PFTreduced flow rate in initial 25% of FEC (small airways in late portion)
what portion of the flow/volume curve is effort Dependantthe first 1/3
what portion of the flow/volume curve is effort independentthe later 2/3
a restrictive disease is present when PFTlung volumes are reduced to less than 80% of predicted levels in spirogram or body plethsymograph
what are the two most common causes of restrictive diseaseatelectasis and obesity (also seen in chest wall dysfunction, neuro diaphragm disf, absent lung tissue and interstitial lung disease)
what are two examples of combined obstructive/restrictive diseasesarcoidosis (<volumes limit airflow) and emphysema (>volumes restricts inspiratory airflow)
sarcoidosisunknown cause characterized by deposition of cicronodules called noncaseating granulomas throughout the body and lungs
what is the easiest way to distinguish between obstructive and restrictive diseases on a PFTobstructive causes reduced expiratory flows, restrictive causes reduced lung volumes
3 ways to measure TLCbody plethysmograph (body box), open-circuit nitrogen washout, or closed-circuit helium dilution
why is body box more accurateit measures communicating and non-communicating/poor communicating spaces (volumes)
what are non communicating or poor communicating lung volumesairtrapping (COPD, Asthma) or pneumothorax
(open-circuit) nitrogen washoutair in lungs is 79% nitrogen just like atmosphere, pt breaths 100% O2 for approx 7 mins, nitrogen is measured during exhalation for volume measurements
(closed-circuit) helium dilutionpt breaths helium for 7 minutes, when equilibrium is reached, helium is measured and lung volumes are calculated
why is helium used as a measuring gashelium is an inert gas so not significantly absorbed
what PFT equipment uses an open-circuit systemnitrogen washout
what PFT equipment uses a closed-circuit systemhelium dilution
what is the most accurate determination of gas volumes in the chestplethsmograph/body box
MVVmax vol vent, pt breaths as rapid/full as possible for 12-15 sec, total exhaled obtained, test is repeated 4 or 5 times and multiplied to get a max vol for 1 minute (15×4 is 60), status of resp muscles, compl and resist, used prior to surg, NOT USED MUCH
Flow volume loops (FLOOP)flow and volume on a graph paper, V is horizontal, F is vertical, Inspiration is below horizontal, expiratory is above
how are FLOOPs used to show if response to medicationstwo flow volume curves superimposed on each other, one before bronchodilator and one after
FLOOPs are best used to look for patterns in what diseasesrestrictive (<volume), large airway obstruction (<flow, norm volume), severe COPD (hockey stick or boot)
PFT’s before and after bronchodilator2 of 3 must improve, FVC >10%, FEV1 15%, or FEV25-75 20-30%, best in asthmatics, misleading in COPD
DLCOdiffusion capacity of the lungs, <with emphysema and pulm fibrosis
RAWnormal w/out ETT tube .5-3.0 cmH2O/L/sec, as airways narrow, pressure of resistance increases
compliancevolume change per unit of pressure change, measured with balloon catheter
Dynamic compliancemeasured when gas is flowing
static compliancemeasured with no flow of gas
Total CLlung tissue compliance + chest wall compliance, <CL as lungs become stiff, the more non-compliant the more stiff,
what is a flat top of the curve represent on a floopstiff lungs-<CL, (less volume, more pressure)
what does a round top of the curve represent on the floopemphysema, <elastance (more volume and less press)
RQrespiratory quotient, norm is .8-.85, ratio of CO2 produced to O2 consumed. Fatty diet RQ is .7 and RQ is 1 for carbs, best used during weaning to adjust pt diet and <WOB
Bronchoprovocationpt inhales histamine or methacholine, cold air and exercise, used to test pt for hyperactive airways
methacholine challengeparasympathomimetic used to induce bronchospasm
most useful PFT tests as seen in table 8-11-VC, 2-FEV1 and FEV1%, 3-TLC, FRC, RV, RR, VE, FEV3, FEV25-75, DLCO, RAW and CL
Do PFT’s measure the ability of the lungs to exchange resp gasesno, DLCO does and it is done in a closed circuit helium test with carbon monoxide
which of the following is least use PFT-A)documenting disease progression B) eval probability of getting a pulm disease C) exercise eval D) weaning from mech ventilationB
The tracing obtained from a PFT is calledspirogram
which is the most important factor in predicting PFT measurement age, weight, height, genderheight
PFT’s are effort dependent T/FTrue
What piece of equip is used to measure TLC and RAWbody plethysmography
which of the following are consistent with obstructive disease? > exp flows, <exp flows, <vol and flows, or >volumes and flows<exp flow
an obstruction in the upper airway will affect which portion of the spirometric tracingthe initial
which is true regarding restrictive disease-<volumes on PFT, can be caused by obesity, exp flow are usually normalall
what PFT is useful in determining the need for mech ventilationFVC
Air (low density)Black (radiolucent), passes threw body and allows for more penetration
WaterWater densities result in less exposure and therefore whitish-gray shadows on film
Bone (high density)includes ribs, clavicles,scapulae, and vertebrae. White, calcium (radiopaque) allows for less penetration
FatShades of gray
Heart, diaphragm, & major vesselsconsidered to have the density of water. Do not change in density but may change in size, shape, & position.
Lung consolidationIncrease in density because of pneumonias, tumor, or collapse, that area will absorb more x-ray and appear as a white patch on the film.
Cavities and BlebsDecrease lung density absorb fewer x-ray and result in darker areas on film
Distance from filmImportant to conceder, the closer the the patient is to the source, the greater the magnification and distortion of objects seen.
Indications for X-RayAssist DX of lung pathology, determine appropriate TX, evaluating effective TX, track progress of lung disease, determine position of tubes and lines
Posterioanterior PA viewinto the Posterior threw to the Anterior
LateralSide view (generally left) provides cardiac magnification and a sharper view of LLL. looks behind the heart
Lateral decubitus view (effusion down-Pneumo up)Pt laying on the right or left side to see whether free fluid (plural effusion or blood) is present in the chest. Can help w pneumothorax (air rises and fluid drops)
Apical lordotic viewProjection is made at a 45 degree tube angulation. Sometimes required for closer look at the RML or apices’s of the lung.
Oblique viewshelpful in delineating a pulm or mediastinal lesion from structures that override it on the PA & lateral views. pt at 45 degree angle, plate is anterior
PneumothoraxThe only time you do an expiatory film.
APFilm cassette placed behind pt back, chest x-ray passes from front (anterior) to back (posterior). Used for bedside x-ray’s.
Post procedural x-ray evaluationETT (radiopaque strip 2 in Above Carina), central (R or L subclavian or jugular vein, rest in sup vena cavae & R Atrium), swanz (check position on a daily basis in the pulm artery), picc, NG (stomach, small bowel), chest tube (tip of tube posterior
Procedures requiring AP filmThoracentesis, Pericardiocentesis, Bronch
CT scanComputed enhancement of x-ray shadows to give clearer look @ internal anatomy.
CT scan & Lung TumorsSuperior to conventional x-ray can detect nodules 2-3mm. CT helps place biopsy needle to prevent pneumo.
CT scan & interstitial lung diseaseCan show considerable changes even when x-ray reads normal. Used selectively because of high cost.
CT scan & AIDSEarly detection of pneumonias that occur as a result of AIDS
CT scan & Occupational lungHelpful in identifying changes in the pleura & lung parenchyma.
CT scan & PneumoniaRestricted use because of cost but they can detect pneumonia sooner.
CT scan & BronchiectasisHas replaced invasive use of bronchogram. CT scan can detect early
CT scan & COPDEmphysema shown clear and detailed. Dx consistently in the high 90%
MRIUsed in the evaluation of the hilar. Can better see hilar lymph node enlargement from enlarged hilar blood vessels than is CT. Also, better at seeing chest wall invasion by lung cancer specifically Pancoast tumor or superior sulcus tumor.
Lung scanning (V/Q scan)obtained by measuring gamma radiation emitted from chest after injected into bloodstream or inhaled. Useful to evaluate possible P.E. Results often inconclusive and are only suggestive,(rare use)
PET scanPositron emission tomography, Used to Dx and stage cancers. Compound is injected into a vein, malignant cells show >metabolic rates
Pulmonary Angiographyevaluate thromboembolic disease- only used if V/Q scan results are uncertain definitive dx, contrast into pulm artery, pulm emboli is proof of filling defect
X-ray interpretation(A) airways, (B) bones, (C) cardiac, (D) diaphragm, (E) extras.
(A) airwaysTracheal mid line, carina,main stem bronchi, air bronchogram(occur with alveolar filling)
(B) bonesClavicles equal, ribs, scapulae, spine
( C) CardiacCardio-thoracic ratio 1/3 on PA ½ on AP, cardiac borders, aortic arch and vessels, cardio phrinic angle.
Silhouette signInfiltrates in the lung will blur the edges of the heart or the diaphragm where the infiltrate touches them. This helps to locate w better precision where the infiltrates located.
Air bronchogramPatent airway w/ deep lung consolidation, norm bronchi are unseen (all air), bronchograms are seen if surrounded by consolidation, often seen w/pneumonia and pulm edema
Compressive AtelectasisSeen in pt w/ pleural effusion, pneumo, hemo, & any space-occupying lesion.
Obstructive AtelectasisBlockage of airway, absence of ventilation. Tumor, aspirated foreign body, fibrosis, mucus plug, mechanical obstruction, & scaring. Trachea and heart shifts toward.
X-ray & AtelectasisShift of the fissure toward, movement of hilar toward, overall loss of volume, hemidiaphragm elevation.
X-ray & PneumothoraxHyperlucency on the affected side, shift of the mediastinal away from the air-filled pleural space. Trachea shift away. <blood flow, <good lungs ability to oxygenate.
X-ray and HyperinflationCOPD, can be red as normal if mild, mod-severe large lung volumes, depressed diaphragm, small narrow heart, enlarged intercostal spaces.
X-ray Interstitial lung diseaseAlveolar pattern may lead to air bronchograms as a result of alveolar spaces becoming infiltrated/denser, air filled airway is clear and dark, the contrast between the two appear as ground glass.
X-ray & CHF1redistribution of pulm vasculature to the UL(norm in LL)2Cardiomegaly 3Kerley’s B lines(1-2cm)usually right base, (pleural lymphatic vessels filled w/fluid)4Misc. >interstitial markings, plural effusion in R hemithorax,enlarged pulm art segments
If vertebrae are easily seen in x-rayfilm is over exposed (underexposed-cant see behind heart)
properly exposed xraythoracic vertebrae are just visualized through the heart shadow
depth of inspiration is adequate in PA film when10 posterior ribs are seen in film
primary purpose of xrays is whatidentify abnormalities
why are PA views most often usedless chance of pt rotation, heart size less magnified, pt must stand
xrays are normally taken on inspiration, what is the exceptionsuspected pneumothorax
problems associated with AP (portable xrays)poor radiographic exposure, pt not centered, artifact shadows, heart magnified
xray to identify Pneumothoraxlateral decubitus on expiration
ETT tube on an xray3-5cm above Corina
what can be assessed on an xrayCVP line position, chest tube position and effectiveness, NT placement
MRI is better than CT for evaluating what?Hilar areas for lymph node and vascular enlargement
Pneumonias can cause what on lung scan<perfusion and <ventilation
xrays are produced by whatelectromagnetic waves
>density causes what to an xray< penetration
radiographic densitywater, air, bone, fat
radiopaquewhite
radiolucentblack
as the distance from the source (machine) and the pt decreases, what happens to the magnification?magnification increases
what is standard distance for an xray6ft
when should an xray be takenafter intubation, assess progression of pneumonia, check effectiveness of CPT (not with CPR)
can an xray appear normal in the presence of significant pulm disease?yes
tension pneumothorax xray>radiolucency on affected side, mediastinal shift away, >resonance to percussion on affected side, BS absent on affected side
atelectasis xray>radiopacity, hemidiaphragm elevated, hilar shift toward
CHF xray> Cardio-thoracic ratio
consolidation due to pneumonia xraylobar radiopaque pattern of infiltrates
hyperinflation xraylarge lung volumes, widened intercostal space bilaterally, small narrow heart
small pleural effusion xrayblunted constrophrenic angle, meniscus sign, partially obscured and elevated hemidiaphragm (lateral decubitus to visualize fluid)
large pleural effusion xraycomplete white out on infected side, complete obscure of diaphragm
obscure heart bordersilhouette sign is absent, then consolidation is anterior lung segments, if silhouette is present (sharp lung borders) then consolidation is posterior
diaphragm border is obscureanterior consolidation (not obscure then consolidation is posterior)
Left heart failure(lungs back up) No 1 external dyspnea, orthopnea, possible nocturnal dyspnea, cheyne stokes, pale cool skin, dysrrhythmias, fatigue, restlessness, irritability, short attention span
Right heart failure(body backs up) edema, JVD, cyanosis, dyspnea, dysrrhythmias, hepatomegaly, sometimes ascites
CHF Xrayfluid in dependent portions-enlarged vessels in upper lobes, heart >1/2 of cage, kerley B usually in right base, >interstitial marks, pleural effusion on right, >pulm artery segments
evaluating chest filmvertebral bodies easily seen, spineous process centered between clavicles and behind trach, ribs 10
over exposed xraylungs to black and vert to easy to see
under exposed xrayvert not seen through cardiac shadow and lungs to white
clinical predisposition for pneumotrauma, broken rib, Thoracentesis, CVP line, pulm art cath, PPV, blebs, improper placement of ET, oral or NT tube
costrophrenic anglethe point where diaphragm meets the chest wall (blunted with pleural effusion)
meniscus signwater moving up the chest wall, instead of diaphragm looking like upside down bowl, edges of look like bowl is right side up, water creeping up the side of a glass
late insp cracklesatelectasis, pneumonia, edema, pulm edema, fibrosis
early insp cracklesbronchitis, emphysema, asthma
insp & exp cracklesbronchitis and resp infect
wheezeasthma, CHF, bronchitis
stridorcroup, epiglotitis, post extubation
<PaO2age, Pb, PIO2
consolidation xrayminimal volume loss, usually lobar distribution, homogeneous density late in process, air bronchograms if airway leading to consolidation is open
physical findings of consolidationdull (<resonance) percussion, bronchophony (99 sounds clear), bronchial BS, crackles, whispered pectriloquay (sounds clear), egophony (E sounds like A), tachypnea, fever
clinical SS of hyperinflationbarrel chest (increased AP diameter), >resonance to percussion, <BS, limited diaphragm movement, wheezing when tired, prolonged expiration, >RR, use of accessory muscles, tripodding, pursed lipped breathing
hyperinflationmost common cause is COPD, large lung volumes, >anterior space on lateral film, flat diaphragm, narrow elongated heart, enlarged intercostal space
free fluid in the intrapleural spacepleural effusion, transudate, exudate, blood (hemothorax), fatty (chylthorax), puss (empyema or pyothorax)
transudatepleural effusion with clear fluid, low in protein, seen in CHF and atelectasis
exudatepleural effusion w/protein, bacteria, pneumonia, pulm emboli, malignancy, virus, TB, fungal
how much fluid must be present to be seen on an x-ray100ml
Pneumothorax clinical SS (w/o tension)reduced chest wall movement on affected side, <BS on affected side, >resonance to percussion on affected side, tachycardia, tachypnea, absent whispered pectriloquay, absent tactile fremitus, trach shift away
pleural effusion SSdependent on amount, pain on inspiration, dull at sight, coughing, SOB, significant amount may be dull percussion, egophony, <BS on effected side, tachypnea
interstitial lung disease xrayfibrotic infiltrates in LL, TB and silicosis in upper lobes, air bronchograms
clinical SS of interstitial lung diseaserapid shallow breathing, <CL, crackles on Insp(usually LL), severe has hypoxemia and cyanosis, final DX via biopsy bronchoscopy
Clinical SS of CHFcrackles at bases, >RR, orthopnea, JVD, >HR(may be irreg), S3, loud S2, hepatomegaly, pulses alterans, peripheral edema, noturia (nite pee)
Spirometers (positive displacement-volume)measure volumes and flow rates
Pneumotachometersspirometer that measures flow, used continuously it can measure VE
Spirometers that measure volume and time aredry-rolling and water-sealed
Spirometers that measure flow arepneumotachometers
Calibration of body box is verified with arotometer or pneumotach
Volume calibration and leak tests of FLOOPsuper syringe
Flow calibration of a FLOOP is done witha rotometer
Timing devices (kymograph X-Y recorders) are checked withstop watch
Plethysmograph is calibrated withrotometer for flows and barometer for pressures
SVC is an important measure of whatrestrictive disease
Decreased volumes indicate whatrestrictive disease
VC is the BEST INDICATOR OF WHATRESTRICTIVE LUNG DISEASE
FVC provides what to measure obstructive diseaseflow rates
What is the BEST INDICATOR OF OBSTRUCTIVE DISEASEFEV1
Minimum acceptable FEV1% is75%
Decreased FEV1/FVCOBSTRUCTIVE DISEASE
Normal FEV1/FVCnot obstructive, but still may be restrictive
FEV200-1200<with LARGE AIRWAY OBSTRUCTION
FEV25-75<WITH EARLY STAGES OF OBSTRUCTIVE DISEASE (ASSOCIATED WITH SMALL AIRWAYS)
PEFRSOME USED TO EVAL ASTHMATICS PRE AND POST BRONCHODILATOR
IS FVC A FLOW OR VOLUMEVOLUME AND SHOULD BE EQUAL TO SVC
FVC NOT COMPLETED IN 3 SECONDSOBSTRUCTION
FVC SMALLER THAN SVCOBSTRUCTIVE (AIRTRAPPING)
MVV MEASURESMUSCULAR MECHANICS OF BREATHING,
<MVVOBSTRUCTIVE DISEASE, >RAW, MUSCLE WEAKNESS, <CL AND POOR PT EFFORT
POST BRONCHODILATOR TEST MUST BE HOW HIGH TO BE SIGNIFICAN15%
NITROGEN (N2) WASHOUT TIME>7MINUTES IS POOR DISTRIBUTION
BEST TEST FOR PARTIAL VOCAL CORD PARALYSIS (LARGE AIRWAY OBSTRUCTION)FLOOP
DISTRIBUTION OF GASSES ARE EVALUATED WITHNITROGEN WASHOUT TEST (7MIN) AND HELUIM DILUTION
DLCOCARBON MONOXIDE DIFFUSION CAPACITY
DLCO MEASURESFACTORS THAT AFFECT THE DIFFUSION OF GAS ACROSS THE A-C MEMBRANE
HOW LONG DOES A DLCO TEST LAST1 BREATH
WHAT DISEASES HAVE A <DLCOFIBROSIS, SARCOIDOSIS, ARDS, EDEMA, EMPHYSEMA
WHAT IS THE ONLY OBSTRUCTIVE DISEASE THAT HAS A DECREASED DLCOEMPHYSEMA
POSITIVE BRONCHIAL PROVOCATION20%DECREASE IN FEV1
PFT NORMS AND PREDICTED ACTUAL/PREDICTED IS OBSERVED80-100% OF PREDICTED NORMAL, 60-70% OF PREDICTED MILD, 40-59% OF PREDICTED MODERATE, <40% OF PREDICTED SEVERE DISORDER
RESTRICTIVE PFT<VOLUMES, VC OR FVC
OBSTRUCTIVE PFT<FLOWS OR FEV1
OBSTRUCTIVE AND RESTRICTIVE BOTH<FLOWS AND <VOLUMES
ALWAYS USE THE “BEST TEST”HIGHEST FVC + FEV1
OBSTRUCTIVE DISEASES W/ DECREASED FLOW (CBABE)CF, BRONCHITIS, ASTHMA, BRONCHIECTASIS, EMPHYSEMA
RESTRICTIVE DISEASES W/DECREASED VOLUMESPICT-PNNF, PLEURAL DIS, INFLAMMATORY DIS, CARDIAC DIS, THORACIC DIS, POST OP, NEUROLOGICAL NEUROMUSCULAR, FIBROTIC DIS
QuestionAnswer
Full-term infants with RDS, surfactant nonresponders, and infants who cannot be extubated in the first weeks of life because of a respiratory condition should be evaluated for which of the following deficiencies?I. -Antitrypsin deficiency, III. SP-B deficiency
Which of the following terms is used to describe the variable that is responsible for terminating inspiration?Cycle variable
Which of the following cardiovascular conditions can cause surfactant inactivation?II. Pulmonary hemorrhage, III. Hemorrhagic edema
Which of the following statements refer to the Bear Cub 750vs infant ventilator?In A/C mode, mand. breaths are time or flow triggered., If mandatory breaths are pressure controlled, the resulting flow and volume waveforms are exponential,The low gas supply alarm activates if either the air or oxygen pressure falls below 24 2 psig.
Which of the following is the most common form of surfactant abnormality associated with acute lung injury?Inactivation by proteins
What does the Laplace law postulate about the alveoli in the lung?That alveoli would collapse as they got smaller
A Maquet Servo 300A ventilator has been set in such a manner that the resulting inspiratory flow exceeds the maximal flow for the selected patient range setting. What type of alarm will be activated?A technical alarm will be set off.
What are the physiologic benefits of surfactant?II. Surfactant prevents capillary leakage of fluid into alveoli, III. Surfactant optimizes surface area for gas exchange, IV. Surfactant protects the epithelium of the lung.
About a century after Laplace described the relationship of transsurface pressure and surface tension at a gas-fluid interface in a sphere, what did von Neergaard discover about the retractile force of the lung?That it was dependent on the surface tension in the alveoli
Which of the following relationships is correct regarding the composition of amniotic fluid as it relates to determining fetal lung maturity?PG and lecithin increase while sphingomyelin decreases during gestation.
With the Dräger Medical Evita 4 ventilator, how will the inspiratory pressure waveform appear for a pressure-controlled mandatory breath when the pressure rise time is set at 0?Rectangular
Which of the following terms is used to describe the variable that reaches a preset value before the end of inspiration?Pressure rise time
Which of the following factors influence the ability to wean patients with congenital diaphragmatic hernia from extracorporeal membrane oxygenation (ECMO)?II. Surfactant inactivation, III. Severe pulmonary hypoplasia
What is the role of SP-D in human pulmonary surfactant?I. Suppresses proinflammatory responses II. Enhances phagocytosis III. Enhances killing of microbes
Which of the following components comprise pulmonary surfactant?I. Dipalmitoyl phosphatidylcholine II. Phosphatidylcholine IV. Phospholipids
Which of the following terms is used to describe the variable responsible for initiating inspiration?Trigger variable
Which of the following proteins are known to comprise human pulmonary surfactant?I. SP-B II. SP-C III. SP-D
On the Maquet SERVO-i, what is the result of increasing the “inspiratory cycle off” settings?It enables expiration to occur at an earlier point in the peak flow requirements.
Which of the following pathophysiologic conditions are components of meconium aspiration?I. Surfactant inactivation II. Chemical pneumonitis
Which of the following physiologic consequences would develop if the liquid-gas interface were without surfactant?III. Every breath would require a considerable amount of pressure to expand the lung with each inspiration.IV. All the alveoli would collapse during exhalation
Which of the following conditional variables can most easily become the baseline variable?Pressure
Which of the following flow wave patterns is generated by the Puritan Bennett LP10 ventilator when the pressure limit control is inactivated?Sinusoidal
A Newport HT50 ventilator experiences an AC power outage and switches to DC power. When will the low battery alarm activate?When 30 minutes of battery life remains
Which of the following physiologic conditions result from the presence of normal amounts of pulmonary surfactant in the lung?II. Uniform gas distribution during inspiration occurs. III. The functional residual capacity is maintained.
How is the minute ventilation decreased when a patient is being weaned from HFOV?By reducing oscillatory amplitude
What is the primary therapeutic goal when a patient with lungs prone to atelectasis receives HFV?To optimize lung inflation
How can the problem of conjunctival irritation associated with NPPV be overcome?By using an appropriately sized interface
What type of monitoring should be used in the outpatient setting during NPPV for children with limited capacity to spontaneously increase minute ventilation because of an advanced neuromuscular disorder?II. Cardiorespiratory impedance monitor III. Pulse oximeter
How is the radiographic assessment of neonatal lung volume assessed?Counting the number of posterior ribs above the diaphragm
A patient is about to be switched from a conventional mode of ventilation to inverse ratio ventilation. What should the therapist recommend for this patient before instituting this mode?That the patient be sedated and paralyzed
What are the consequences of failing to quickly wean a neonatal patient from HFVI. Pulmonary over-distention IV. Impaired cardiac output
What is the primary goal of intermittent NPPV at night in children who have chronic disorders complicated by alveolar hypoventilation?To improve the quality of sleep
What is the most common complication associated with NPPV among pediatric patients?Skin irritation caused by the interface
Which of the following bilevel adjustments would the therapist need to make on the ventilator to reduce a patient’s PaCO2?Increase IPAP and maintain EPAP
Which of the following factors need to be considered for HFV ventilator circuits?I. Time for gas egress during exhalation II. Circuit compliance IV. Intrinsic timing mechanisms
Which of the following bilevel ventilator settings influences upper airway stability?EPAP
Which of the following modes of mechanical ventilation is generally absent on most portable volume-controlled ventilators used in the home?Pressure support
Which of the following issues continue to confront the practice of surfactant replacement therapy?II. Nature of surfactant to administer III. Timing of surfactant replacement IV. Method of delivery during HFV
How should a volume-controlled portable ventilator be adjusted to deliver the appropriate tidal volume (VT) to a pediatric patient during NPPV?The delivered VT should be set at twice the child’s physiologic VT.
According to the U.S. Food and Drug Administration, which of the following mechanical ventilatory rates constitutes high-frequency ventilation (HFV)?More than 150 breaths/minute
What are the primary objectives of noninvasive positive-pressure ventilation (NPPV)?II. To restore adequate carbon dioxide removal III. To decrease the patient’s work of breathing
Enhanced diffusion is a function of which of the following factorsIII. Tidal volume IV. Respiratory frequency
When NPPV is used to ventilate pediatric patients, which operating mode of ventilation is generally used?Spontaneous/timed
What effect should the therapist expect to observe after initiating continuous positive airway pressure (CPAP) on a neonate who has a restrictive lung disorder?Increased lung volume
When airway pressure release ventilation is used, what physiologic process occurs as the higher pressure is released and the lower is achievedExhalation of carbon dioxid
What is the clinical significance of the IPAP-EPAP gradient in bilevel NPPV?It determines the patient’s tidal volume.
In which of the following types of pediatric patient has NPPV been used effectively to stabilize airway function?Patients being weaned from mechanical ventilation after a laryngotracheoplasty
Which of the following steps might be involved when a therapist assesses a patient suspected of having a reduction of airway diameter while receiving HFV?I. Observe the patient’s chest wall for movement. II. Increase conventional ventilation. III. Apply ventilation via a manual resuscitation bag
What is a feared complication of long-term intermittent NPPV applied by means of a nasal mask to pediatric patients?Impaired maxillary bone growth
Which of the following terms describes the rate of increase in airway pressure from baseline at the onset of inspiration?Pressure breath
Which of the following variables is the control variable when both the volume and pressure waveforms vary considerably when the patient’s lung compliance and airway resistance change?Time
Which of the following terms is used to describe the variable responsible for initiating inspiration?Trigger variable
. On the Maquet SERVO-i, what is the result of increasing the “inspiratory cycle off” settings?It enables expiration to occur at an earlier point in the peak flow requirements.
Which of the following relationships is correct regarding the composition of amniotic fluid as it relates to determining fetal lung maturity?PG and lecithin increase while sphingomyelin decreases during gestation.
What does the Laplace law postulate about the alveoli in the lung?That alveoli would collapse as they got smaller
Which of the following conditional variables can most easily become the baseline variable?Pressure
Which of the following physiologic conditions result from the presence of normal amounts of pulmonary surfactant in the lung?II. Uniform gas distribution during inspiration occurs. III. The functional residual capacity is maintained
Which of the following motor and linkage mechanisms are used in ventilator compressors?I. Electric motor/rotating crank and piston III. Electric motor/rack and pinion IV. Direct-drive electric motor
Which of the following pathophysiologic conditions are components of meconium aspiration?I. Surfactant inactivation II. Chemical pneumonitis
With the Dräger Medical Evita 4 ventilator, how will the inspiratory pressure waveform appear for a pressure-controlled mandatory breath when the pressure rise time is set at 0?Rectangular
Which of the following settings requires that the patient breathe spontaneously?Pressure support ventilation with CPAP
What is the purpose of the optional open lung tool on the SERVO-i ventilator?To assist in determining the inflating and deflating pressures of the lung
What is the role of SP-D in human pulmonary surfactantI. Suppresses proinflammatory responses II. Enhances phagocytosis III. Enhances killing of microbes
How do synthetic surfactants compare with bovine surfactants?Bovine surfactants contain SP-B and SP-C, and synthetic surfactants contain SP-A and SP-D.
Which of the following statements characterize a ventilator’s control scheme as closed loop?I. An output variable is measured and compared with a reference. II. The input variable is modified as needed to more closely approximate the desired output.
Which of the following cardiovascular conditions can cause surfactant inactivationII. Pulmonary hemorrhage III. Hemorrhagic edema
Which of the following terms is used to describe the variable that reaches a preset value before the end of inspiration?Limit variable
How is pneumonia in a neonate believed to adversely affect surfactant?I. By bacteria directly attacking type II pneumocytes III. By microbes releasing substances altering surfactant components
Which of the following terms is used to describe the variable that is responsible for terminating inspirationCycle varaible
Which of the following physiologic consequences would develop if the liquid-gas interface were without surfactant?III. Every breath would require a considerable amount of pressure to expand the lung with each inspiration. IV. All the alveoli would collapse during exhalation.
Which of the following proteins are known to comprise human pulmonary surfactant?I. SP-B II. SP-C III. SP-D
Which of the following proteins is found to be deficient in the sputum of patients with asthma?SP-A
Which of the following statements refer to the Bear Cub 750vs infant ventilator?I. In A/C mode, mandatory breaths r time or flow triggered. III. mandatory breaths are pressure controlled,the resulting flow and volume waveforms are exponential. IV.low gas supply alarm activates if either the air or o2 pressure falls below 24 2 psig
A Newport HT50 ventilator experiences an AC power outage and switches to DC power. When will the low battery alarm activate?When approximately 2 hours of battery life remains
What is the primary therapeutic goal when a patient with lungs prone to atelectasis receives HFV?To optimize lung inflation
In which of the following types of pediatric patient has NPPV been used effectively to stabilize airway function?Patients unable to achieve adequate alveolar ventilation because of restrictive lung disorders
Which of the following steps might be involved when a therapist assesses a patient suspected of having a reduction of airway diameter while receiving HFV?I. Observe the patient’s chest wall for movement.. IV. Reduce the oscillatory amplitude.
During volume-controlled ventilation, which of the following factors influences the peak inspiratory pressure?Pulmonary compliance
Which of the following statements best describes the relationship between tidal volume and frequency during HFJV of pediatric and neonatal patients?Neonatal patients need higher frequencies and lower tidal volumes than pediatric patients.
During HFOV, manipulation of which of the following components establishes the continuous distending pressure?III. Expiratory valve aperture IV. Bias flow
A patient receiving bilevel ventilation develops a leak at the interface. What action will likely take place at this time?The ventilator will automatically compensate for this leak
What is the only absolute contraindication to a trial of NPPV in pediatric patients with acute respiratory distress?Cardiovascular instability
When NPPV is used to ventilate pediatric patients, which operating mode of ventilation is generally used?Spontaneous/timed
What is the clinical significance of the IPAP-EPAP gradient in bilevel NPPV?It determines the patient’s tidal volume.
During HFOV, which of the following factors has a direct influence on a neonate’s delivered tidal volume?II. Oscillatory amplitude
A patient is about to be switched from a conventional mode of ventilation to inverse ratio ventilation. What should the therapist recommend for this patient before instituting this mode?That the patient be sedated and paralyzed
Which of the following ventilator settings are preset during time-cycled, pressure-limited ventilationI. Inspiratory time III. Respiratory rate IV. Inspiratory-to-expiratory ratio
What are the consequences of failing to quickly wean a neonatal patient from HFV?I. Pulmonary overdistention IV. Impaired cardiac output
How is the radiographic assessment of neonatal lung volume assessedCounting the number of posterior ribs above the diaphragm
Which of the following bilevel adjustments would the therapist need to make on the ventilator to reduce a patient’s PaCO2?Increase IPAP and maintain EPAP
Which of the following bilevel ventilator settings influences upper airway stabilityEPAP
Why may HFOV not be an optimal ventilation strategy for patients who have either fresh particulate meconium aspiration or bronchopulmonary dysplasia?Gas trapping may develop.
Which of the following modes of ventilation attempt to maintain a minimal target tidal volume with a constant pressure by manipulating the inspiratory flow?Pressure-regulated volume control (PRVC)
What is the most common complication associated with NPPV among pediatric patients?Skin irritation caused by the interface
Which of the following forms of mechanical ventilation is the most efficacious method for acquired bronchopleural fistulas?High-frequency jet ventilation (HFJV)
The therapist is conducting a ventilator check for a neonate and makes the following notations on the ventilator flow sheet: PEEP: 5 cm H2O,PIP: 25 cm H2O, RR 15 breaths/min, FIO2: 0.35 what should the therapist recommend for this neonate?Weaning from mechanical ventilation
How is the minute ventilation decreased when a patient is being weaned from HFOV?By reducing oscillatory amplitude
Which of the following features characterize neonatal HFOV circuits?I. Larger diameter tubing for inspiratory gas flow II. Narrower diameter tubing for exhalation
According to the U.S. Food and Drug Administration, which of the following mechanical ventilatory rates constitutes high-frequency ventilation (HFV)?More than 150 breaths/minute
A neonate demonstrates the following clinical signs 3 hours after birth: 1 Respiratory distress, breath sounds on the left side of the thorax, and chest radiograph revealing gastrointestinal. What is the neonate most likely?Congenital diaphragmatic hernia
What are the major advantages of venovenous ECLSPulsatile flow in maintained, Potential emboli from the circuit are trapped in the pulmonary vasulature
What can be done to lower a patient’s PaCO2 when it is elevated during ECLSIncrease the flow of the sweep gas
QuestionAnswer
acrocyanosiscondition in the newborn characterized by a cyanotic discolorization of the hands and feet, aka peripheral acrocyanosis of the newborn
alae nasiexternal border at opening of nasal passage, cartilaginous, maintains patency of nasal opening during spont breathing
anencephalygenetic defect in which brain and spinal cord are absent, cranium is open, vertebral canal remains a groove
caput succedaneumlocalized pitting edema found in the scalp of a newborn that may overlie sutures, results from press of cervix on fetal head, not dangerous, last a few days
Dopplerchange in frequency when a sound is emitted by an object moving toward or away an observer, Doppler scanner-ultrasonic waves reflected from moving (heart) yield info about the structure
fontanellespace on a newborn cranium between cranial bones, covered by tough membrane
hydrocephalya pathologic condition characterized by abnormal accumulation of cerebral fluid with in the cranial vault-results in dilated ventricals
hyperpneadeep, labored or rapid respiration
hypopneashallow or slow respiration
lanugofine, downy hair that covers fetal body, appears at 26 weeks, thins at 28, starts to disappear at 32, gone by 40
methacholinecholinergic, aerosolized and used to confirm asthma
murmurlow pitched fluttering or humming heard just before, during or after the normal heart sounds
paradoxicalsituation or occurrence in which the outcome is the opposite of what is expected
pinnacartilage portion of the external ear
pleural iffusionabnormal fluid in the pleural space, transudate-protein free (from tissue), exudate-high protein ( from blood vascular)
pneumotachographinstrument that measures velocity of expired velocity of gas flows
rugaeridges or folds of skin, found in stomach and mature male scrotum
scaphoidsunken anterior abdominal wall
thoracic gas volumevolume of gas in the thorax as measured by the body plethysmograph, may or may not include conductive airway gas
vernixoff white cheese-like substance that covers the skin of the fetus and newborn, composed of sebaceous gland secretions, lanugo and epithelial cells, thermoregulation and passage through canal
QuestionAnswer
Normal airway clearanceeffective mucociliary action and effective cough
increased mucus may lead toobstruction and airtrapping, atelectasis, ineffective gas exchange, inflammation and infection
*ACTairway clearance techniques
*why are premature neonate prone to atelectasissecondary to lack of pulmonary surfactant present with RDS
Severe atelectasis can lead tolarge areas of shunting with worsening blood gases
*why is airway clearance usedto prevent atelectasis and to help reinflate those areas that are atelectic
*complications of RDSatelectasis, lung tissue damage from ventilator pressures, oxygen and lack of surfactant, leading to BPD
*BPDbronchopulmonary dysplasia
*small airways in newborns can cause what if secretions accumulatesevere imbalances in ventilation/perfusion ratios
*Indications for airway clearanceretained secretions (atelectasis, RDS, BPD, intubation), excessive secretions (CF, pneumonia, asthma, bronchitis, bronchiectisis), aspiration (meconium, foreign body), prophylaxis (post intubation)
*disease processes that cause increased lung secretionsCF, pneumonia, asthma, bronchiolitis, bronchiectisis
*contraindications of airway clearance therapypulm hemorrhage, excessive agitation or hypoxemia during TX, feeding previous 45-60 mins, hx of reflux, neonate <1200g, <32 weeks, hx of intraventricular hemorrhage > grade 1 or <7days post bleed, pheumothorax, CHF, bradycardia
*hazards of postural drainageemesis (vomiting) and aspiration (never do with in 1 hour of feeding), never with hx of reflux, >ICP (in trendelenburg)
*Increased ICP predisposes early gestation baby to whatIVH, intraventricular hemorrhage-never on baby less than 1500g
*skin integrity and percussionnever on preemies less than 1200, may cause edema, excoriations (tearing of skin) and bruising
*percussionrhythmic clapping over affected lung area to loosen secretions, 1-5 mins
Why is caution used when percussioning baby with BPDmay have fragile bones
*vibrationrapid, constant motion, rather than rhythmic clapping. Used for loosening secretions in the airway, best done during exhalation, 30 seconds per side
Auscultationlistening to the sounds produced in the lungs during the ventilatory cycle
Wheezehigh pitched continuous sound
Rhonchi/course cracklescontinuous low pitched sound (secretions)
Cracklesdiscontinuous sounds (fine crackles)
The goal of TX with aerosolized meds isdeliver an adequate amount of med to the desired site in pulm tree with minimum side effects
*effective aerosolized TX depends on 4 factors1. Size and amount of particles produced, 2 characteristics of particles, 3 anatomy of the airways, 4 pt vent pattern (cannot be altered by RT)
Jet nebulizer particle size and amount are dependant on whattype of nebulizer used
What is the drawback of when running a jet nebulizer continuouslymuch of medication is lost during expiration, reducing amount delivered to the lungs
*how can the loss of medication during exhalation be reducedslightly by adding a reservoir that collects some of the aerosol produced during exhalation and makes it available on next inspiration-spacer distal to the neb
*hydroscopic growthaerosol particles grow larger when added to environment of high humidity
*what is the major characteristic of aerosol particles that affects depositionit’s ability to take on additional water-hydroscopic growth, making particle deposit higher in airway (dont make it to lungs)
*characteristics that determine aerosol depositionconcentration and viscosity of drug and velocity it is delivered-more drug is delivered when the volume of diluent is increased
*lung deposition of aerosolized drugs to intubated infantsless than 1/20 of non intubated adult and less than 1/10 of intubated adult-implication is higher dose needed for intubated infant to achieve dose equivalent to nonintubated pt
*how much aerosolized drug makes it to infant terminal airway and alveoliprobably negligible, narrow airway, ett, etc are cause
*what is best ventilatory pattern for best aerosol deliverylaminar flow fallowed by pause-slow deep breath with inspiratory pause.
*How can RT aid in deposition of meds in mechanical vent pt>Itime, <flow and add short inspiratory pause at end inspiration
*why do aerosolized drugs have limited use in NICUunknown side effects and dosages in neonates (liver not functioning yet, baby can get toxic build up)
*what is the advantage of svnrequires little pt coordination, works well in acute distress with reduced inspiratory flows and volumes, modification of drug concentration, can aerosolize almost any liquid, effective with minimal breath hold
*disadvantages of svnexpensive, less easily transported, cleaning and prep, inefficient dose delivery, cold, medium for bacteria,
*disadvantages of inline jet neb with ventilatorhigh humidity may aid hydroscopic growth causing deposition in circuit or upper airway-reducing drug delivered
LVNused for continuous neb in acute asthma
Indications for aerosolized drugsbronchodilators, mucolytics and steroids
Indications for bronchodilator in preemie and peds<breath sounds, <chest expansion, wheeze and retractions, >RR, nasal flaring, grunting, >ventilatory pressures, increasing FIO2 requirements, and an increasing PaCO2
Indications for aerosolize steroidsan inflammatory pulmonary process is present like BPD
*the most common nebulizer is what typeupdraft, used in the vertical position with a T piece attached
*what is a mainstream nebulizer and what is the advantageno additional tubing to adapt into circuit, designed to work in horizontal position, so works well inside incubator
*what is the biggest hazard associated with aerosolized meds inline to vent circuitpotential increase in VT and peak pressures
*why do VT and peak pressures go up during inline aerosolized med TX’s during mech ventilation?nebulizer requires 6-8L/min flow (on top of what mach is already set, adds VT and PIP)
*what is the recommended solution to keep VT and PIP at manageable levels during aerosolized TX?place the nebulizer at the humidifier outlet and nebulize the med during exhalation, this allows meds to fill the expiratory limb of circuit, and deliver during pt’s next breath.
To prevent excess condensation during inline svn on mech ventilated pt, what can RT doturn off humidifier (or bypass)
If circuit has a distal temp probe, RT should place neb distal to the probe, why?if proximal, then when neb removed, then heated gas could potentially burn pt
*Hazards if SVN TXnosocomial infection, medication side effects, drug reconcentration, ventilator malfunction, excessive noise (place svn on circuit outside incubator), sticky expiratory valve from medication deposits
*what is a SPAG(small particle aerosol generator) designed and intended for admin of ribavirin to treat RSV (no other meds should be used in it)
how does a SPAG unit workcompressed gas into unit, reduced to 26psi, ½ then to flowmeter for nebulizer, ½ then to particles exiting nebulizer. 2 flows together with particles enter drying chamber (dries and reduces particle size 1.2-1.4 microns), then to pt.
What are the risks associated with administering riboviron to a vent pt, and what can we do to reduce those risksriboviron precipitates and accumulates on the walls of vent tubing and ETT tubes-<risk with highly trained, suction 1-2 hrs, monitor vent press, one-way valves to med into vent flow into spag (change often), bacteria filters
What is the purpose of bacteria filter and why do we change it often when using spag unitslows riboviron from entering environment on exhalation
how often should neonate be suctionedas little as possible, 4-6 hours as needed, never suction with in 20 mins of ABG
Suction Equipmentcardiac, O2, and/or trancutaneous monitors, stethoscope, resuscitation bag with O2 source and press manometer, saline, suction catheter kit w/gloves, suction regulator at appropriate level, water soluble jelly if needed
Neonate ETT sizes2.5-4
Suction catheter size for intubated neonate5, 6 to 8-10
Suction catheter size for nonintubated babypreemie 5, 6 neonate to 6 months 5, 6-8
What is difference in suctioning baby from adultto avoid injury, babies are suctioned only to the tip of the ET tube, hyperoxygenate at 10-15 percent high than current setting (not 100%), no more that 5seconds of suction press (total time 10 seconds for procedure)
Hazards of suctioning neonatebradycardia, hypoxemia, mucosal damage, atelectasis, airway contamination, accidental extubation
What are the common causes of bradycardia when suctioningvagal stimulation (prevent by suction time less than 10 seconds total) and hypoxemia induced (prevent with hyperoxygenate and suction press applied for only 5 seconds)
Indications for O2 therapyhypoxemia
Hypoxemia in neonate (defined)PaO2 less than normal on room air (40-70mmHg)
PaO2 norms for term infantat birth-16mmHg, 20 mins 51mmHg, 3-5 hours 75mmHg, preemie at 3 to 5hrs-60mmHg and preemie at 24 hrs 73mmHg
S and S of hypoxemia in a neonateretractions, expiratory grunting, nasal flaring and cyanosis
Hazards of O2 therapy in neonatesROP, O2 toxicity leading to BPD (bronchopulmonary dysplasia), cerebral vasoconstriction, fire
What is BPD and how is it causedlong exposure to high levels of O2 causes destruction of alveolar tissue, causing loss of surface area for gas exchange, leading to >hypoxemia and > need for O2, vicious circle
Cerebral vasoconstriction hazardhigh levels of O2 can lead to constriction of the vasculature in the brain, constriction leads to <blood flow in developing brain
Goal of O2 therapy in neonateskeep PaO2 between 50-70 mmHg, high enough to avoid hypoxemia, but low enough to avoid ROP, BPD and toxicity
what is an oxygen blender and why do we use themseries of regulators that lower wall pressure to more comfortable level, while mixing air and O2 for desired concentration (flow meter placed on outside is used to insure proper flow to pt), FIO2 IS APPROXIMATE! NOT ACCURATE! MUST ALWAYS USE O2 ANALYZER
O2 analyzerssince blenders are giving an approximate FIO2, when precise O2 is desired analyzer is place in the system to monitor babies FIO2 delivery
Where is O2 analyzer placedin the circuit, proximal to humidifier (wet gas will give erroneous readings), calibrate every 4-8 hours to ensure accuracy and prevent drifting, always document calibrations
What is a low flow humidifieraka bubble humidifier (aka diffuser), flow <10L/min and usually non heated, used with simple mask and nasal cannula
Physics of bubble humidifieras bubbles of gas rise through the sterile water, the gas picks up water molecules
wick humidifierhighflow humidifier, >10L/min, uses heated, water-saturated wick (spongey, absorbs water by capillary action) surrounded by heated tank, tank heats, evap from wick occurs, gas flow through the tank picks up heated water vapor and delivers it to pt
why do heated humidifiers create so much condensation?as heated-humidified gas flows through tubing, cold air outside tubing cools the air inside the tubing, as the air cools humidity falls out of the air-called a rain out effect, causing condensation to build up on the walls of the tubing
to prevent condensation from collecting and draining into babies lungs what must RT docollection device should be placed in the tubing at the lowest point between humidifier and pt, or heated wire circuit to keep gas temperature at desired level all the way through tubing
*oxygen hood FIO2 and Liter flow<50% at 7L/min
*where and why is FIO2 monitoring done when pt is using Oxygen hoodat the level of the pt’s face and nose, to assure accurate FIO2 because of layering effects
*Hazards of oxygen hoodsflow to low and CO2 retention inside hood (keep flow >7L/min), pt face or neck against hood or neck hole occluding airway, high or low gas temperature causing thermoregulation problems (maintain gas temp to that of incubator)
When is O2 cannula used with neonatechronic need for O2 and weaning from oxygen hood
Flow for cannulaalways less than 1L/min
Chronic oxygen use in neonates is associated with whatBPD
Flows >4L/min on cannula leads to whatmucosal drying and epistaxis (nose bleed)
FIO2 for cannula are dependant on whatpt age, size, VT and RR
FIO2 of NC at .25L/min24-27%
FIO2 of NC at .50L/min26-32%
FIO2 of NC at 1L/min30-35%
How is NC kept in place for neonate with out causing skin damageIV site tape
Why are neonates and preemies kept in incubatorstemperature-controll and quit environment
How are O2 needs met with pt in incubatorblended, warmed and humidified gas is blown in at desired FIO2
How is FIO2 checked for pt in incubatorsame as hood, as close to baby face (because of possible layer)
What is the main problem associated o2 delivery in incubatorsmaintaining FIO2 because of constant opening of doors and port holes and the large size of incubators (fio2 >.25 may cause layering)
*when should a hood be used inside an incubatorwhen pt requires >.25 FIO2 (to prevent layering)
*self inflating bagreinflate following decompression, must always have bag and O2 attached, used in emergency and short term modality, always with 100% O2 (gas in bag is entrained on each reinflation-then delivered to pt on decompression)
*flow-inflating bagaka flow-rating bags, have advantage over self inflating because exact FIO2 can be used. Flow rates are adjusted to meet the pt needs (bag fills based on flow, faster RR, needs faster flow)
*why do neonate resuscitation bags have two portsone for O2 and one for press manometer (prevent barotrauma)
On intubated pt, which port is for O2 and why is this importantport that is distal to pt connection, prevents retardation of exhalation caused by direct flow of gas into end of ET tube
Indications for CPTatelectasis, CF, prolonged bed rest (never for asthma)
*do we hyperoxygenate neonate prior to CPTno
Which modality of aerosolized medication requires the least amount of pt coordinationsvn
Are retractions an indication for aerosolized medsno indicates CPAP
*what is the advantage of a mainstream nebulizer?it can be used horizontally, so great for incubator
Placing neb in vent circuit between humidifier and the distal temp probe may cause whatoverheating of the circuit when the neb is removed
*hazards of aerosol drug therapyinfection, med side effects, drug reconcentration and over hydration
What is the greatest hazard of ribavirin administration with mech vent ptprecipitation and accumulation of drug on vent tubing and ETT
While suctioning pt following CPT, pt becomes bradycardic, what should RT dostop, hyperoxygenate and shorten duration of following suction attempts (always less than 10 seconds)
Anaerobicabsence of oxygen
*brown fatfat found in newborns, it’s unique thermogenic activity is a heat source for newborns, highly vascularized and innervated by neurons from the sympathetic NS, it is stored around the great vessels, kidneys, scapulas, axilla and nape of the neck
*crigler-najjar syndromecongenital, familial autosomal abnormality, glucuronyl transferase is deficient or absent, causes nonhemolytic jaundice, an accumulation of unconjugated bilirubin and severe disorders of the CNS
Encephaloceleprotrusion of the brain through a congenital defect in the skull
Enteralpertaining to the intestines, often associated with feeding or meds
Galactosemiacongenital defect characterized by deficiency of enzyme galactose-1-phosphate uridyl transferase, causes hepatoplenomegaly, cataracts and mental retardation
Gastroschisiscongenital defect characterized by incomplete closure of the abdominal wall with protrusion of the viscera
Guaiacwood resin used on a reagent strip to test for presence of blood in the stool or urine
hydrops fetalismassive accumulation of fluid in the fetus or newborn often associated with erythroblastosis fetalis, effusions of the pericardial, pleural and peritoneal spaces also occur
Hypersosmolarincrease concentration of osmotically active components such as electrolytes and proteins
Hypotoniahaving a smaller concentration of solute to solution ration than that found in intravascular or interstitial fluids
*kernicterusabnormal toxic level of bilirubin that accumulates in the tissues of the CNS, can cause degenerative disorders
Lucey-driscol syndromesyndrome passed as autosomal recessive train, characterized by inhibited uridine disphosphate glucuronosyl transferase and leads to rapid progressive jaundice and kernicterus
Omphalocelecongenital herniation of the intraabdominal viscera through the abdominal wall near the umbilicus
Parenteralpertaining to the uptake of substances or meds by any route other than the digestive tract
Servo-controlledany device that uses a feedback loop for control. Like a home thermostat-temp falls below set and thermostat triggers heater, in incubators probe monitors skin temp, must be kept at 36-36.5
Sodium-potassium exchange resin (kayexalate)resin contain solution administered via enema (mark says they’re his favorite,), in which sodium ions are released from solution and replace by potassium ions in the intestines, used to treat hyperkalemia
Stratum corneumouter most layer of skin, composed of dead cells converted to keratin, bodies barrier to microorganisms
Turgornormal resiliency of the skin, results from outward pressure of cells and interstitial fluid
What is the most important factor in care of a neonatethermoregulation
*thermoneuteral zonetemperature range in which the metabolic rate is at a minimum and thus O2 consumption is at it’s lowest
*what environmental temperature should neonates be kept atno exact temp recommended, should be maintained so that baby can achieve thermoneuterality, with a recommended rectal temp of 36.5 to 37.5
*why is there no exact environmental temperature for neonatesbecause of the diversity of metabolic rates, gestational age and weight
*how do adults regulate body tempmetabolic and physical activity (shivering) if cold, and sweating to cool.
*neonates rely on what for the production of heatrelies entirely on the metabolism of brown fat (do not shiver)
*at what gestational age does brown fat appear?26-30 weeks
*what is the process of brown fat to heatstimul symp NS to cold causes >norepinephrine release, >NE activates lipase, lipase breaks down brown fat to free fatty acids, acids are then hydrolyzed into glycerol and nonsterified fatty acids-oxygenation of ns fatty acids produces heat, > baby temp
*nonshivering thermogenesisbreakdown of brown fat with the subsequent production of heat
*what are the two gradients of physiological heat loss in neonatesinternal thermal gradient and external thermal gradient
*internal thermal gradient (ITG)temp difference between warm body core and cooler skin
*how is ITG regulatedBSA (body surface area), metabolic rate (crying will >), amount of subcutaneous fat, and distance from body core to the skin surface
*why do neonates have diminished capacity to maintain ITGlarge surface area to body weight (>area to lose heat), this skin, <amounts of subcutaneous and brown fat, and brown fat depletes rapidly (losing nonshivering thermogenesis), unable to take in enough calories to maintain nutrition for heat production
*external thermal gradient (ETG)temp difference between skin and environment, and is determined by the environmental factors controlled by RT
*what are the 4 factors that determine heat loss through ETGradiant heat loss, conductive (transfer) heat loss, convective heat loss and evaporative heat loss
*radiant heat lossdissipation of heat from baby to cold object-radiates from one object to another, does not have to be by contact, can be window close by or cold object placed into incubator
*what is an example of radiant heat gainheat from the sun
*conductive heat losstransfer of heat from body to cooler surface-put blanket under baby before putting on scale or table
*convection heat losslosing heat from skin by moving air, velocity and temp of air determine amount of heat loss, think convection oven (normal oven filled with heat chicken takes 1 hour, convection oven has fan to move heat-chicken takes 35 minutes)
*evaporative heat lossas water changes from liquid to gas, heat is released
*insensible heat lossevaporative heat loss from the skin (thin skin) and respiratory tract (normal)
*sensible heat lossevaporative heat loss from sweating from the skin
*what kind of evaporative heat loss do babies doinsensible only, they do not sweat
*what is cold stresshypothermia, any lowering of the thermoneuteral temperature
*where are the most sensitive thermoreceptors locatedin the face (and respond the quickest)
*what is the body’s initial response to hypothermiaperipheral vasoconstriction (shunts blood from surface)
*what does peripheral vasoconstriction cause and why is it dangerousanaerobic metab and met acidosis (lactic), leads to pulm vasoconstriction >hypoxemia and acidosis, hypoxemia then restricts babies response to cold and >acidosis, same time, nonshiv thermogenesis kicks in > metab of brown fat, <glucose (hypoglycemia)
*what is a neonates initial response to hyperthermiavasodilation of peripheral vessels to allow for dissipation of heat, followed by >metabolism and >O2 consumption
causes of hyperthermiainfection, dehydration, broken incubators, radiant warmer, humidifiers, and phototherapy lights-avoid by always monitor pt and environment
*what is the goal of thermoregulation in the delivery room and how is donemaintain environmental temp such that neonate core temp stays between 36.5-37.5, prevent evaporation (dry fast), radiant (wrap in warmed blanket and place under radiant light), convective and conductive (warm mattress and prewarmed incubator)
What is the advantage/disadvantage of an open warmeraccess to the pt, difficult thermal regulation and environmental control
Advantage and disadvantage of incubatorsadvantage is controlled environment for better thermal management, quieter, barrier to handling, disadvantage is pt access
physiologic considerations of high-risk neonatenervous system anatomically immature-chem and physiologic function is primitive, cerebral hemisphere show poor distinction between gray and white matter-neuro function is controlled by brain stem and spinal cord and existing brain function is hyperactive
What are the effects of overstimulation neonateimmature or stressed neonates have limited energy and can be exhausted by excessive stimulation-developmental handicaps and morbidity if overstimulation is increased
What is the best way to keep visual and acoustic stimulation from over stimulating a neonateblanket over the incubator
Stimulation of the neonate should be avoided whenduring sleep, behavioral stress cues or physiologic stress cues are present
What are the behavioral stress cuesgaze aversion, facial grimace, hiccoughs and irritability
What are the physiologic stress cuescyanosis, hyperoxemia
what is the best way for practitioner to avoid over stimulatinghandle only when behavioral and physiologic signs dictate, avoid clustering care giving and procedures to avoid over stimulating, delay or postpone nonemergency procedures
Environment controls to avoid stress in the nicu arelow or no light (better SaO2), workers and family avoid loud talking and laughing
Physiological factors in premature neonate skinvery permeable (potential for systemic side effects from toxins), diminished cohesion between surface epidermis and underlying dermis, very thin stratum corneum (top layer-main barrier to microorganisms)
What is the best way to dissolve adhesives from baby skincitrus oil, they are nontoxic
Why dont we use spray on skin barriers or traditional adhesive removal when TX preemiespermeable skin will allow plastic polymers in skin barrier or solvent from adhesive to absorb through skin
Trancutaneous monitors (TCM) and pulse ox can be place on skin howcoban wrap, fabric straps with Velcro
What is the best way to TX baby skin that has been broken or damaged from tape removalIV site dressing, will protect and allow healing and keeping microorganisms out
How is fetal fluid and electrolyte status regulatedmaternal and fetal mechanisms
Maternal disorders that effect fetal fluid and electrolyte balancediseases that affect uterine perfusion, and IV therapy during labor
Abnormalities in fluid and electrolytes occur with certain neonate disease states they arerespiratory disorders, asphyxia, congenital heart disease, hydrops fetalis, sepsis, renal disorders, urinary tract abnormalities, endocrine disorders and <skin integrity
hydrops fetalismassive accumulation of fluid in the fetus or newborn often associated with erythroblastosis fetalis, effusions of the pericardial, pleural and peritoneal spaces also occur
Abnormal loss of fluid in neonates occurs howdiarrhea, emesis, nasogastic tube drainage, thoracotomy tube losses, damaged skin and other factors the >insensible water loss
Assessing fluid deficit and estimating amount pt requireshx, physical exam and lab values
Signs of dehydration or hypovelemia on exam areperfusion of skin is decreased, turgur decreased (pinch skin-slow return to normal is decreased), oliguria, dry mucus membranes, sunken fontenelle, sunken eyes, extreme are signs of shock-tachycardia, hypotension, pulse, poor perfusion
Insensible water loss (IWL)evaporation from skin and respiratory tract
Why is turgor in premature neonate difficult to asses?less subcutaneous fat
Factors that increase insensible water lossEGA, resp distress, >temp above neutrothermal zone (36-37.5), > body temp, skin breakdown, congenital skin defect (spina bifida), radiant warmer, phototherapy (>heat), >motor activity or crying (>metabolic rate)
Bilirubinbyproduct of normal breakdown of RBC’s
Life span of a RBC120 days
How is bilirubin normally excretedpasses through the liver and is excreted as bile through the intestines
*what is jaundicebilirubin builds up faster than a newborns liver can break it down and pass it from the body, caused by immature liver, to much bilirubin to handle, to much bilirubin being reabsorbed from the intestines before the baby gets rid of stool
*how much bilirubin is unsafe and can cause severe complications in baby20mg
*complications of >20mg of bilirubindeafness, cerebral palsey, brain damage (hepatitis in adults)
*types of jaundicephysiological (normal) j, jaundice of prematurity, breast milk j, blood group incompatibility j
*what is a simple test for jaundicepress your fingertip to babies nose or forehead, if white no problem, if yellow jaundice is present
*jaundice TXmild to moderate levels will take care of itself by day 5-7, high levels may need phototherapy, increased feedings t help pass bilirubin
*once jaundice is treated and repaired do babies get it againunlikely
*physiological jaundice50 percent of newborns get it, due to immaturity of liver, appears at 2-4 days and disappears at 1-2 weeks
*jaundice of prematurityoccurs frequently in preemies, underdeveloped liver and longer time adjusting to excreting bilirubin effectively
*breast milk jaundice1-2 percent of breastfeed babies, caused by breast milk and bilirubin rises to >20, prevents excretion, starts at day 4-7 and last 3-10 weeks
*blood group incompatibility jaundiceRh or ABO different from moms, moms antibodies destroy infants RBC’s, increasing bilirubin, starts first day of life, preventable with Rh immune globulin to mom
*what is blood group (Rh) incompatibilitymoms blood Rh neg and fetus is Rh positive, if fetal blood gets into moms blood stream, mom will produce antibodies that could pass back to baby harming babies RBCs, first baby is fine, but subsequent babies will have problems. Can be treated with Rhogam
STABLEsugar, temp, airway, blood pressure, labs, emotion
NECnecrotizing enteroclitis (hot belly), idiopathic disorder characterized by ischemia and necrosis of the intestine, mild has abdominal distention, worst has perforation of intestines-leads to sepsis and death
Risk factors associated with NECprematurity, asphyxia, and formula feeding
What are the 3 main factors that lead to NECmucosal wall injury, bacterial invasion into damaged intestinal wall and formula in the intestine
What causes injury to mucosal wall in NECmay be secondary to ischemia and or decreased blood flow to the gut and maternal cocaine use
pneumatosis intestinalisnecrosis and the formation of gas in the intestinal wall (can be seen in x-ray), leads to bacteria getting into circulation causing sepsis or perforation of intestine allowing bacteria into abdominal cavity causing profuse peritonitis
Factors that lead to ischemia (in NEC)RDS, apgar <5, abruptio placentae, apnea, hypertonic oral meds, bowel obstruction
Factors that lead to decreased blood flow (in NEC)PDA with R-L shunting, exchange transfusion, umbilical artery catheter (UAC), polycythemia, shock
Human breast milk may enhance gastrointestinal function and has been shown to be protective against whatNEC
What is the first confirmatory sign of NECguaiac-positive stools (blood in stool)
S and S of NECabdominal distention, bile residuals and bile-tainted emesis (vomit), poor feedings, general signs of sepsis (lethargy and >fio2 requirements)
Best TX for NECavoiding factors that lead to it
TX for NEC includesavoid factors that lead to it, good hand washing, stop feeding, nasogastic suction-to rid stomach of bile, antibiotics, x-rays to monitor, >fio2, continuous infusion of L-argine
L-argininesubstrate of nitric oxide that reduces intestinal injury
Gastrointestinal perforation or full-thickness necrosis requires whatsurgical resection
What is the first sign of NECincreased abdominal girth
How is NEC confirmedguaiac-positive stools
Active transportmovement of molecules across cell membrane via chemical activity, allows for large molecules that would normally be unable to pass
Beta-lactam(penicillin’s and cephalosporin’s) group of antibiotics that inhibit bacterial cell wall synthesis
Dyscrasiasabnormal blood or bone marrow condition like aplastic anemia or Rh incompatibility
Extravasationa passage of blood, serum or lymph into the interstitial spaces of the tissue
Facilitated diffusionmovement of ions or molecules through the cell membrane by the interaction with a carrier protein that aids its passage, done by binding chemically and shuttling it through the membrane
Hydrolysisthe chemical alteration or decomposition of a compound with water
Ototoxicrefers to a substance having a harmful effect on the eighth cranial nerve, or on the organs of hearing and balance
Pharmacokineticstudy of all aspects of drug use on the body, routes of absorption and excretion, duration of action and biotransformation
Pheochromocytomachronic hypertension caused by a vascular tumor of the adrenal medulla or sympathetic paraganglia, characterized by hypersecretion of epinephrine and norepinephrine
Pseudocholinesterasea nonspecific cholinesterase that hydrolyses noncholine esters as well as acetylcholine
Reductionthe addition of hydrogen to a substance, the removal of oxygen from a substance, or a decrease in the valence of the electronegative part of a compound
Simple diffusionthe movement of fluids or particles from an area of higher concentration to an area of lower concentration through a semi permeable membrane following Brownian movement
*teratogenany substance or agent that interferes with normal fetal development and causes one or more developmental abnormalities in the fetus
Ultrafiltrationthe act of filtering large molecules from small molecules by creating a pressure gradient across a filter containing small pores
Fetal concentrations of drugs can reach what level compared to maternal blood50-100% higher
Why are fetal concentrations so much higher than maternal concentrationsfetal liver immaturity
Mechanisms drugs use to cross the placenta areultrafiltration, simple diffusion, facilitated diffusion, active transport and breaks in placental villi
Drug transfer across the placenta is determined by whatconcentration difference (across placenta), lipid solubility, degree of ionization of the drug, molecular weight of drug
*drugs that cause physical and/or mental developmental abnormalities in the embryo or fetus are calledteratogens or teratogenic substances
*teratogens may cause whatspontaneous abortions, congenital malformations, intrauterine growth retardation, mental retardation and carcinogenesis
*effects of teratogens are dependant on what factorsdose of drug that reaches embryo, length of exposure, gestational age (at time of exposure) and other drugs mother is taking at the time
Drug absorption in the gastrointestinal tract is regulated by whatpH-dependent diffusion and gastric empting time
*for a term neonate, gastric pH at birth is what6-8, but falls to 1-3 in the first 24 hours (not low in preemies-immature acid secreting mechanism), pH returns to neutral and no more acid produced for 10-15 days after birth
*when is normal adult GI acidity reached2 years of age
*the difference in pH of stomach for neonate may affect whatnormal absorption of both basic and acidic drugs like penicillin’s, Phenobarbital and phenytoin
*what is gastric emptying time in the newborn6-8hrs, does not reach adult values until 6 months
Peristalsisdigestion
Low muscle mass in neonate causes what to intramuscular absorption rates of drugsabsorbs very fast
Why is absorption of drugs through the skin of newborns greatly increasednewborns generally have thin, well hydrated skin which allows for increased permeability and enhanced absorption
Why is the neonate respiratory tract considered ideally suited for absorption of drugscombination of extensive vascularization, large surface area and thin tissue separating the airway lumen and vascular
What is the benefit of IV admin of drugs in neonatesbypasses all of the unpredictability of other methods and complications of drug absorption, allowing for more accurately calculating doses
Lipid-soluble drugs that readily cross cell membranes are distributed where in the bodythroughout all fluid areas, very rapidly into the heart, brain, liver, kidneys and other highly vascularized tissues (more slow into muscles and fat cells)
Highly lipid-soluble drugs have increased chance of side effects whereto highly vascularized tissue like the heart, brain liver kidney etc
Less lipid-soluble drugs and do not readily cross cell membranes can do whatgather in tissues at higher concentrations than in plasma
Often more than 90% of a lipid-soluble drug will be bound to plasma proteins, what effect does this haveleaves only 10% unbound or freely available to cross cell membranes and exhibit maximal pharmacologic activity
What is unconjugated bilirubinjaundice
What is drug metabolismchanging or alteration of a drug to a different form, either active or inactive
Where is the primary site of drug metabolismliver (but also in plasma, kidney and GI tract)
What are the 4 types of drug metabolism that take place in the liverconjugation, oxidation, reduction, hydrolysis
Immaturity of preemie decreases drug metabolism howbecause all 4 metabolism functions are decreased, half life of drug or drugs is increased
Half-lifeamount of time required to reduce a drug level to ½ initial value
Drugs like Phenobarbital have what kind of effect on metabolism of drug in neonates and preemiesincrease enzymatic activity in the liver-causing mediation of metabolism-dosages of other drugs will need to be reevaluated if pt is taking it
Why is drug excretion the most important factor in the termination of a drugs effects in preemie and neonatebecause most drugs are poorly metabolized by premature liver
What is the primary route of elimination of drugskidneys (also biliary and fecal excretion, sweat and saliva)
How is renal function measuredcreatinine clearance
*GFRglomerular filtration rate
*what effect does GFR have on some drugsbecause of immaturity of kidneys, drugs like diuretics may have to be increase due to <GFR.
*What kinds of drugs are dependent on GFRdrugs that are not extensively metabolized and are primarily excreted through the kidneys, doc will give drug and see how it works, then adjust
*antibiotic groups arepenicillin’s, cephalosporin’s, aminoglycosides, macrolides, quinolones, tetracyclines, sulfonamides, antifungals and antivirals
*what kind of antibiotic is penicillinbeta-lactam, kills bacteria by penetrating outer membrane of bacteria through small canals (porins)
*penicillinase aka beta-lactamaseenzyme produced by some bacteria in attempt to survive, inactivates beta-lactam drugs (especially staphylococcus)
*penicillinase-resistant penicillin’sa group of penicillin drugs that are resistant to penicillinase enzyme and are effective against staphylococcus (MRSA)
*what is another name for antiviral drugschain terminators
*ribavirinbroad-spectrum antiviral specifically used in neonates for bronchiolitis caused by RSV
Because of teratogencity with exposure to ribavirin, what precautions does RT need to takedelivery with SPAG 2 unit, shut off remotely, deliver only in isolation room with negative pressure and adequate air exchange to outside
Adenosine indicationsacute TX of sustained SVT (supraventricular tachycardia)
Adverse effects of adenosineflushing irritability and dyspnea
*epinephrine indicationsresuscitation for TX of acute cardiovascular collapse, subcutaneously for acute bronchospasm
*digoxin aka Lanoxin indication for neonatesCHF
*Indomethacin sodium trihydrate aka Indocinhemodynamically significant PDA (indicated by resp distress, continuous murmur, hyperactive precordium, cardiomegaly
Dopamine/Intropin indicationscorrection of hemodynamic imbalances from shock syndrome due to < cardiac function in CHF, trauma, endotoxic septicemia, renal failure and myocardial infarction
*caffeine citrate and theophylline indicationsTX and management of neonatal apnea, and acute or chronic bronchospasm
*fentanyl citrateused to produce analgesia, sedation and anesthesia during invasive procedures like bronchoscopy
Calcaneusheel bone
TPN aka total parenteral nutrition aka hyperalimentationadmin of nutritionally adequate hypertonic solution consisting of glucose, protein hydrolysates, minerals and vitamins through an indwelling catheter, usually in the superior vena cava
Spectrophotometric infrared analysismeasurement of different species of hemoglobin in a blood sample by determining the amount of infrared light absorbed
*when is an ABG given to a neonatebetter to get to many than not enough, some may require every 20 mins, some every 2 weeks, each is different
*what are the 4 rules that apply in determining when a neonate gets a ABG drawn1) signs of resp distress, 2) vitals, appearance or condition has changed for no apparent reason 3) 15-30 mins after any change in vent or FIO2 4) on a regular basis for vent pt to insure stable and helps document transcutaneous and pulse ox readings
*neonate ABG sitesumbilical, radial, brachial (capillary too, but reflects mixed venous blood so PaO2 not accurate)
*why do we not want to take an ABG with baby crying and fussingdrastically changes results, especially CO2
Transillumination lightplaced under wrist of neonate helps locate artery
*UACumbilical artery catheter, is the preferred site for obtaining ABG because there is no pain for baby
*How is a suspected PDA verifiedright radial sample is drawn at the same time as UAC
*what is an easy (non-invasive way to detect a PDAplace a trancutaneous monitor on the upper right chest, and another on the abdomen, a higher PaO2 in the upper right compared to the abdomen would indicate a right-to-left shunt, relative uniformity would rule out a ductal shunt (PDA)
*why do we use caution when increasing FIO2 in the presence of a PDA and low arterial PaO2because arterial blood that supplies the head is before the shunt (picture page 262), so increasing FIO2 can lead to dangerous PaO2 levels in the brain (ROP)
*problems associated with UAConly used for 3-4 weeks because of clotting and infections, PaO2 may be low if PDA present
What is a good alternative to UACRAC, radial artery catheter
Why is RAC a good source for ABGpreductal flow
Hazards of RACinfection, air emboli, arterial occlusion, infiltration of fluids, nerve damage
Why are arterial punctures so difficult in neonatesvery small arteries, pain can lead to misleading results
What are the primary complications of an arterial puncture in neonatesinfection, bleeding, nerve damage, embolism, hematoma
*what are capillary samples used forassessing pH and PaCo2, but not PaO2 because they have mixed venous blood (PaO2 monitoring with pulse ox or transcutaneous monitoring)
*why are capillary samples usedless hazardous to pt and more easily obtained than arterial sample
*contraindications of capillary sampleposterior curvature of heel, callus developing on heel, fingers of neonates, previous puncture sites, inflamed, swollen or edematous tissue, localized infection
*capillary stick procedureheat heel to 45C for 4-7 mins (no exceptions), ready equipment, wipe, puncture, avoid arteries
*complications of capillary samplespuncture of calcaneous bone (leads to osteomylitis or bone spurs), infections, burns, tibial artery laceration, pain, bleeding, hematoma, nerve damage, bruising, scarring
*PaO2 norm for a neonate is50-70 mmHg
*PaCO2 norm for a neonate is35-45 mmHg
What is PaCo2it defines the adequacy of alveolar ventilation, the byproduct of aerobic metabolism that is excreted by the lungs, >45 is indication of hypoventilation and >60 is indication of respiratory failure
*Normal neonate pH7.35-7.45 (7.30 to 7.50 is considered acceptable)
What are the disease states that most commonly cause respiratory acidosis in neonatesBPD, meconium aspiration, and transient tachypnea of newborn TTN, maternal anesthesia or any other disorder that leads to hypoventilation
What are disease states that most commonly cause respiratory alkalosis in neonatesmismanagement of ventilator rates or volumes, RDS, stimulation of CNS, hypoxia induced hyperventilation
What are the disease states that most commonly cause metabolic acidosis in neonateshypoxemia with resulting lactic acidosis, starvation, hyperalimentation, renal tubular acidosis (immature kidney cant excrete acid or reabsorb bicarb), and diarrhea (loss of bicarb)
What are disease states that most often cause metabolic alkalosis in neonatesexcessive loss of H+ from GI tract or kidneys or by addition of bicarb to blood. Gastric suctioning, vomiting, to much diuretics without potassium replacement
HCO3 norm for neonate is22-26
Normal BE for neonates+ or – 4
how do TCM’s workClark electrodes (same as blood gas monitor) heat the stratum corneum allowing faster diffusion of O2 through the skin, although it reads slightly lower than arterial blood gas, it is best used as a trending source
*what is a PDApatent ductus arteriosus, ductus arteriosus fails to close after birth, R-L shunt
S and S of PDAmore fluid in lungs, trouble breathing, >need for vent support and O2, frequent chest infections, difficult digesting food, low BP (>risk of chronic lung disease, slow growth and motor development) TX is drug therapy or surgery to close
Fetal scalp Phindicated to assess degree of fetal hypoxia
Normal scalp pH7.25-7.35
*how much blood does a small preemie havecan be as low as 100cc
How does RT know TCM will workcheck against ABG, if it closely parallels then it can easily be used
why does TCM use heat3 reasons, heat changes lipid structure of stratum corneum allowing faster diffusion through skin, heating tissue and blood causes O2 curve to shift right enhancing O2 release from RBC, heat causes vasodilation of capillaries and arterilization of blood
Why are TCM PaO2 levels lower than ABG PaO2 levelsbecause TMC measures tissue O2 too
What is the clinical use of TMCtrending of PaO2 in neonate
what is the most important limitation of TCMcannot be used without periodic correlation of ABG, also may underestimate hyperoxemia, inappropriate temp adversely affects TCM, hemodynamic status, bad site choice on infant, underestimate lung disease pt, blistering
How often should TCM site be changedevery 2-3 hours to prevent burns
Complications and hazards of TCMburns, erthema (red skin) for hrs or days, blistering, adhesive can cause epidermal stripping (use coban or Velcro), never use alone-always correlate with ABG
Capnography aka capnometrymeasures exhaled CO2 with spectrophotometric infrared analysis
What are the 2 types of capnographyside stream and mainstream
Side stream capnographyremoves a continuous sample through small tube and carries it to analysis chamber-light weight
what is downside of side stream capnographysample must pass through tubing and water trap to reach sample chamber so less responsive to high RR, in neonate excessive samples leads to < delivered VT
Mainstream capnographychamber right at airway, heated with small wire to prevent condensation (reduces errors), gives current readings (unlike side stream), much more accurate than side stream, but not used much because very bulky and heavy
What is the downside to mainstream capnographybulky and heavy may cause accidental extubation, chamber causes increased deadspace
IUGRintra uterine growth retard
*Tolazoline aka Priscoline indicationsTX of persistent pulm hypertension of newborn, use when PaO2 cannot be maintained with FIO2 and or mech vent.
QuestionAnswer
Ovumfemale germ cell extruded by ovary at ovulation, newly fertilized egg still in blastomere stage, from conception to implantation, first day to day 12-14 (beginning of cell division)
blastomeresdaughter cells produced in ovum during rapid cleavage, 2 cells become 4, 4 become 8, etc.
morulablastomeres that have grown enough to become a ball, 16-50 cells, stage of growth that ovum enters uterus
zona pellucidatransparent tissue envelope surrounding blastomeres
embryowhat fetus is called during stage II, end of ovum until growth is 3 cm head to rump, (53-56 days), major organs dev, most vulnerable to drugs, infection, radiation etc.
fetusname used during 3rd stage (end of embryonic to birth), organs cont to grow, less susceptible to drugs etc, but still can affect development
neonatebirth to end of first month
infant1 month to 1 year
childpt over 1 year
chorionic villavascular fibrils on the surface of placenta that connects placenta to uterus-place where maternal and fetal blood exchange nutrients and blood gases (formed by trophoblast)
choanafunnel shaped opening between posterior nares and nasopharynx
choanal atresiacongenital abnormality in which membrane or bony occlusions block the choana-caused by nasopharyngeal septum failure to rupture during embryo development
chemoreceptorsensory nerve located in carotid artery, stimulated by chemical (co2-H+), signals central respiratory center to > or < ventilation
cotyledonvisible segment of maternal surface of placenta, contains fetal vessels, chorionic villa and intervillous space
blastocystovum/embryo stage following morula, ball forms with central cavity filled w/fluid (blastoceale) with outer layer of triphoblast (becomes placenta) and embroblast (becomes embryo)
baroreceptorpress sensitive nerve ending found in walls of atria, vena cava, aortic arch and carotid sinus-stretching leads to central reflex causing vasodilation or constriction
amnionmembrane covering fetal side of placenta, outer umbilical cord and entire surface of uterus
dichotomydivision or separation into two or more parts
ductus arteriosusvascular channel that connects pulm artery to descending aorta in fetal circulation
ductus venosusvascular channel in fetal circulation that passes through liver and connects umbilical vein to inferior vena cava
ectodermoutermost layer of the 3 germ layers, gives rise to nervous system, eyes, ears, epidermis and mucus membranes
endoderminnermost layer of the 3 germ layers of developing embryo, gives rise to epithelium of resp tract, GI tract, urinary tract, pharynx, tonsils and thyroid gland
Fertilizationunion of mail and female gametes (sperm and egg) to form zygote
foramen ovaleopening in the septum separating atria in fetal heart
FRCvolume of gas in lungs following normal exhalation
Intervillous spacespace between the chorionic villa(on placenta wall), acts as reservoir for maternal arterial blood, which exchanges nutrients and waste with fetal blood
mesodermmiddle of the 3 germ layers of developing embryo, gives rise to bones, connective tissue, muscles, blood, vascular and lymph tissue
oligohydramniosabnormally small amount or absence of amniotic fluid
phosphatidylglycerol (PG)acidic phospholipids found in surfactant-presence in amniotic fluid signals mature lungs
phospholipidscompound of phosphoric acid, fatty acid and nitrogen base, found in most living cells (cell wall covering)
phosphatidylcholine (PC)major component of mature surfactant, compound most active in lowering surface tension (used in amniocentesis to measure lung maturity) aka DPPC
polyhydramnioscondition w/excess amniotic fluid (>2000 mL)
septum primumembryologic structure of developing heart, eventually becomes ventrical septum
sinus venosusembryologic structure in fetal heart eventually becomes inferior and superior vena cava and portion of right atrium
sphingomyelina type of sphingolipid found in steady quantity in amniotic fluid, S of L/S ratio test (to determine lung maturity)
LecithinL in L/S ratio test…….aka PC
surfactantcombination of lipoproteins found in mature alveoli that reduce surface tension of pulm fluids
trophoblastone of the layers of tissue that forms wall of blastocyst, becomes placenta
truncus arteriosusembryotic tissue of developing heart, becomes aorta and pulm artery
placentaorgan of respiration for fetus, fetus gets nutrients and O2, rids CO2 and waste, at term it is round, 1/3 of uterine surface, 1 lb or 15-20% of fetal term weight
3 shunts of fetal circulation areductus venosus, foramen ovale, ductus arteriosus
QuestionAnswer
Chronic Lung Disease encompassesWilson-Mikity Syndrome Pulmonary Insufficiency in prematurity Classic BPD The “new” BPD
Other complications of neonatal respiratory care includeRetinopathy of Prematurity (ROP) Intraventricular Hemorrhage (IVH)
Chronic Lung disease presents asprematurity need for ventilation/oxygenation
In chronic lung disease diagnosis isrequired oxygen or mechanical ventilation. Required oxygen at 36wks gestational age.
The pathophysiology of chronic lung disease includessurfactant deficiency/inactivation oxidative stress (o2 toxicity) inflammation/infection mechanical ventilation barotrauma Barotrauma and air block syndromes
The treatment for chronic lung disease istemperature oxygenation surfactant replacement resusscitation and ventilation
Wilson-Mikity Syndrome is also know aspulmonary dysmaturity
Wilson-Mikity syndrome isa disease of functional and structural pulmonary changes seen in premature neonates with no apparent underlying lung disease
The etiology of wilson-mikity syndrome isunkown and linked to low birth weight (<1500g), lung immaturity, maternal bleeding and asphyxia
The pathosphysiology of wilson-mikity syndromepresents similar to stage 3 and 4 CBD except the neonate has not been ventilated.
The early signs and symptoms of Wilson-Mikity Syndrome appear by the end of the first week and arehyperpnea expiratory grunting, nasal flaring, retractions hypoxemia transient cyanosis (comes and goes)
The acute phase of wilson-mikity syndrome appears after the first week and presents likeRDS poor feeding and vomiting CXR: similar to stage 3 and 4 CBD changes
The treatment of wilson-mikity syndrome issupport treat like bpd
What is the prognosis of Wilson-Mikity Syndrome?2/3s of neonates survive and recover by age 2
Pulmonary insufficiency in prematurity includespremature infants <1200gms normal lung function in 1st 2 days Lung function deterioration by day 7
CPIP (CHronic pulmonary insufficiency of prematurity)Required supplemental 02 with apneas but normal CXR findings
The mortality of CPIP in the 1970’s was20%
The mortality of CPIP today is0% with current standards of Care
CBD classic bronchopulmonary displasia “aka” the old bronchopulmonary displasia etiology isunknown but most incidences follow treatment of RDS with mechanical ventilation and oxygen
The pathophysiology of BPD ischaracterized by thickening of the alveolar membrane, necrosis of the alveolar tissues, and fibrotic changes in the interstitial spaces
air bronchograms appear asfluid filled tubes
CBD Stage 1 (Days 2-3)granular pattern, air bronchograms, small volume
CBD stage 2 (4-10)opacification
CBD Stage 3 (10-20)small areas of lucency, alternating w/areas of irregular density small cyst formation, visible cardiac sillhouette
Stage 4(<30 days)large cysts, hyperinflation, interstitial fibrosis, and cardiomegaly.
The New BPD clinical presentation ofhyperinflation cystic emphysema persistent oxygen requirements may suffer complications from PDA/Sepsis
The pathosphysiology of the new BPD is linked to 5 factorssurfactant deficiency/inactivation oxidative stress (oxygen toxicity) inflammation/infection mechanical ventilation (barotrauma) Barotrauma and air block syndromes
In BPD the ABG will showchronic respiratory failure and hypoxemia
BPD signs/symptomscor pulmonale (right vent. hypertrophy) pulmonary functions: increased minute ventilation requirement, increased airway resistance, decreased lung compliance
The criteria of BPD diagnosis include36 weeks corrected gestational age need for supplemental 02 or 8wks since birth and still requires supplemental 02
What is the tx of BPDprevention ventilatory support long term, low flow oxygen airway clearance bronchodilator therapy neoprofen; higher incidence of cld maintain fluid and nutrition status vitamen e therapy- increased risk of sepsis/NEC
What is the prognosis of BPD?increased risk of asthma and growth suppression.
Retinopathy of prematurity is also known asRetrolental fibroplasia (RLP) (ROP)
ROP is defined asdisordered vascularization and fibrovascular changes in retinas or preterm infants
With ROP scar tissue formsbehind the lens of the eye
What is the etiology of ROP?Primary factor: 02 use/hyperoxia it occurs in <36% if 501-1500gm birth weight
What is the pathophysiology of ROP?High Pa02 leads to constriction of retinal vessels. Constriction leads to necrosis of vessels; called vaso-obliteration vessels hemorrhage which leads to scar formation
What are some factors associated with ROP?Preterm birth, RDS, Mechanical ventilation, Chorioamnionitis, apnea, hypercarbia, surfactant deficiency, pneumonia, sepsis, CLD
How is ROP diagnosed?It develops in 5 stages opthalmologic exam
How is ROP treated?Prevention Indirect laser therapy
Intraventricular Hemorrhage is also known asperiventricular leukomalacia (PLV)
IVH occurs in26% in babies with 501-1500gm BW
What are the type of bleeds with IVH?Subdural or subarachnoid bleeding or cerebeller tissue bleeds
In subdural or subarachnoid bleeding it can be caused bytrauma or asphyxiation
In cerebeller tissue bleeds it is associated withprematurity
What is the pathosphysiology of IVH?Autoregulation (temperature) absent, puts brain at risk of hemorrhage
What are the signs/symptoms of IVH?Severe, rapid deterioration, apnea, hypotension, decreased hematocrit, flaccidity, bulging fontanelles and posturing
How is IVH diagnosed?CT scan or ultrasound
How is IVH classified?Grade 1 to Grade 4 severe to most severe
What is the tx of IVH?supportive: monitor for hyperbilirubinemia, avoid hypotension, monitor icp Correct blood loss/hypoxemia: administer osmotic agents (volume expander) Possible shunt placement
IVH complications: depends on severity of the bleedneurodevelopmental disability (MR) Posthemorrhagic hydrocephalus (CSF) Vision/Hearing loss contralater himparesis (cerebral palsy) Death
How can IVH be preventedavoid wide fluctuations in BP, Oxygenation, and pH Avoid trendelenburg position
Respiratory distress syndrome is also known ashyaline membrane disease
RDS etiologyprematurity of the lung/surfactant deficiency infants <37 weeks gestation
What is the pathosphysiology of RDS?Atelectasis leads to v/q mismatch and low FRC. Results in respiratory failure further hinders surfactant production Worsening atelectasis
RDS complications can be associated withventilator support (Development of BPD, IVH,ROP, Air leaks, development of reactive airway Disease (RAD), infection, patient ductus arteriosus (PDA), DIC, necrotizing enterocolitis (NEC)
What are RDS signs and symptomsRR > 60 bpm expiratory grunting, nasal flaring, and retractions cyanosis ABG-low pa02, combined acidosis Other-hypothermia, flaccid muscle tone, pallor skin, severe edema (kidneys shut down)
In RDSCXR is a definitive diagnosis
IN RDS the CXR will showunderaerated bilaterally, ground glass appearance, air bronchograms, stages 1-4 according to increased severity of disease
What is the treatment of RDS?Prevention:maternal steroid therapy Surfactant replacement CPAP Mechanical ventilation
CPAP (nasal prongs)neonates are obligate nose breathers 4-6 cmh20; if > 40% fi02 is needed intubation is indicated for surfactant tx, extubation within 10 minutes
Mechanical ventilationpac02 40-50 mmhg, ph >7.25, sa02 88-94% VMS allows permissive hypercapnia; 85%-93%
Transient Tachypnea of the Newborn (TTN) is also known asType II RDS & Wet lung syndrome
TTN is more common inboys and infants with perinatal asphyxia; also common in C-section delivery
The etiology of TTN isunkown, associated with delayed clearing of fetal lung fluid
TTN Clinical presentationtachypnea, breath sounds-rales, cyanosis, grunting, retractions, nasal flairing
In TTN the ABG will read asmild-moderate hypoxemia, hypercapnia, respiratory acidosis
With TTN the CXR will present aspulmonary vascular congestion, perihilar streaking, hyperexpansion, flat diaphragm, mild cardiomegaly, mild pleural effusions, mimics RDS, except better aeration and clears within 24-48 hours)
How is TTN diagnosedR/O other conditions (RDS, Group B strep pneumonia, PPHN) Lab to R/O infection- would see increased WBC w/ infection
What is the treatment of TTN?oxygen therapy and CPAP 02 hood <40%(warmed); 3-5 cmh20 cpap with increased fio2 is required mechanical ventilation antibiotics until infection is ruled out