Question Answer
perinatology subspecialty of obstetrics concerned with the care of the mother and fetus at high than normal risk of complications
types of disorders Perinatologist treat diabetes, premature labor, perinatal infectious disease, multiple gestation, perinatal pharmacology
what do perinatologist treat or asses in the fetus gestational age and growth, evaluation for congenital anomalies, placenta and amniotic fluid and adequacy of uteroplacental function
where does fertilization take place outer third of the fallopian tube
stage 1 aka ovum stage, what happens and how long is it conception to implantation (12-14 days),
stage 2 aka embryonic stage, what happens and how long is it end 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 it from embryonic until end of pregnancy, growing
how long does it take the ovum to reach the uterus 4-5 days
what is cleavage cell division by daughter cells inside the ovum, 1 becomes 2, 2 becomes 4
blastomeres cells produced by rapid cleavage inside the ovum, they are surrounded by a clear envelope called the zona pellucida
zona pellucida transparent envelope surrounding the blastomeres
morula blastomeres that have grown in numbers to form a ball (16-50 cells) and is what ovum is called as it enters uterus
blastocyst fluid 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
trophoblast the new outer layer of the blastocyst, takes the place of the zona pellucida
what and where are the germ layers cells 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 do it is from the germ layers that all tissues organs and organ systems will arise
what arises from the endoderm respiratory tract, epithelium of the digestive tract, bladder and thyroid, primary tissue of the liver and pancreas
what arises from the ectoderm epidermis, hair and nails, lens of the eye, central and peripheral nervous system and the skin glands
what arises from the mesoderm dermis, muscles, bone, connective tissue and lymph tissue, reproductive organs and cardiovascular system
when does the pulmonary system start to develop and when does it end starts 24 days after conception and ends around age 8
what are the 5 stages of lung development embryonic 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 tension similar 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 cause alvioli are largly liquid filled with gas, liquid is attracted inward due to the attraction causes alvioli to shrink to its smallest diameter
laplace’s law importance 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 alvioli small 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
surfactant substance 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 alveoli as 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 produced type II cells
what is surfactant made of phospholipids, 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 disorders hypoxia, hypothermia and acidosis
hypoxia, hypothermia and acidosis cause what in premature infants less than 30 weeks inhibits surfactant production and commonly leads to resp distress syndrome
L/S ratio of lung maturity fetal 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 maturity PG
what is the shake and foam test test 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 there surfactant-albumin ratio (SAR), fluorescence polarization essay
how can lung maturity be artificially induced administration of glucocorticoids
what are the limitations of glucocorticoids in inducing lung maturity must 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 maturation thyroxine thyrotropin-releasing hormone, b-adrenergic drugs, estrogen, prolactin and epidermal growth factor
do fetus of preeclamptic woman show acceleration of lung maturation no, once thought to be true, it is not.
Surfactant is vital, it enhances capillary circulation allowing for what normal V/Q ratios, protection against barotrauma (it also aids in evacuation of lung fluid)
what is the leading cause of pulmonary complications in neonates lack of surfactant or deterioration of its production following birth
what happens to lungs with little or no surfactant they become stiff and noncompliant, causing >WOB
why is support indicated for infants with little or no surfactant they will exhaust and die from combination of energy loss, hypoxia and hypoventilation
what is the fluid content of the lung at term 20-30 mL/kg, roughly equivalent of FRC
what is the composition of fetal lung fluid lower 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 fluid maintain patency of developing airways, helps in formation, size and shape of potential airways
how is lung fluid expelled prior to delivery 1/3 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 circulation 1fetal 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 heart nutrients 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 heart foramen 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 flow veins travel toward the heart, arteries travel away, in fetal veins carry o2 rich blood from mom, and arteries carry o2 poor toward mom,
baroreceptors receptors located in the bifurcaton of the carotid arteries and aortic arch, stimulation leads to bradycardia and hypotension
chemoreceptors present 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 structures placenta, umbilical cord, amnion, amniotic fluid
Placenta
chorionic villa projectiles of the trophoblast that attach to the endometrium of the uterus
inervillous spaces small pockets surrounding chorionic villa that contain maternal blood
cotyledons one of 15 to 25 segments on the maternal side of the placenta, each segment contains a villa and a inervillous space
umbilical cord lifeline between mother and fetus, 3 vessels surrounded by a tough gelatinous material caled whartons jelly, 3 vessels-2arteries, 1 vein
wharton’s jelly tough gelatinous material that surrounds and protects the umbilical cord, allowing it to bend but protecting it from collapsing, kinking and occluding blood flow
amnion sac that surrounds the growing fetus and holds the amniotic fluid, arises from trophoblast at around 7th week
amniotic fluid dynamic 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 fluid it is constanly being absorbed and replenished
where is surfactant stored in lamellar bodies, produced in type two cells
at what stage of embryologic development does the ovum enter the uterus morula
the respiratory system arises from which germ layer endoderm
the earliest development of the lung begins when 24 days
dichotomy of the airways occurs during which phase of lung development pseudoglandular (7-16 weeks)
the following statement best describes surface tension the tendency of liquid surface to contract
what is the best indicator found in ambiotic fluid of lung maturity PG
what does not appear to accelerate fetal lung maturation maternal preeclampsia
the following are true statements about lung fluid approx 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 section TTN
heart develops from what germ layer endoderm
embryologic truncus arteriosus develops into what pulm artery and aorta
path of blood that is shunted through forament ovale is right to left atruim
ductus arteriosus shunts blood where pulm artery to the aorta
the folling statement about baroreceptors is correct they are actually stretch receptors
in the placenta, the fetal vessels are cantained in the chorionic villa
polyhydramnios is defined as excessive amniotic fluid
what are the possible causes of polyhydramnios hydrocephalus, esohageal atresia, down syndrom, cleft pallate
assessment of the fetus during the first trimester is facilitated by what technique transvaginal ultrasound
can infection be detected by ultrasound no
what can be detected by ultrasound position of the fetus, position of the placenta and volume of amniotic fluid
a high level of alpha-fetoprotein found during amniocentesis indicates what neural tube defect
what test of amniotic fluid is used to help determine fetal kidney maturity creatinine level
bilirubin from amniotic fluid tests for what liver 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 is fetal scalp electrode
common cause of fetal bradycardia is asphyxia
type III decelerations are caused by compression of the umbilical cord
fetal scalp ph is the lower limit of what 7.25
the following statements are true about fetal movements greatest 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 biophysical fetal breathing, gross body movement, fetal tone, reactive NST and amniotic fluid volume (normal score 8-10)
cordocentesis removing fetal blood sample from the cord
factors of maternal history that place fetus at high risk previous miscariage, previous premature labor, asthma, maturnal obesity
Question Answer
RDS resp distress syndrome, aka HMD (hyaline membrane disease), caused by <surfactant
Primary cause of respiratory disorders in neonates RDS/HMD
risk factors that >increase incidence of RDS premature, weight, males 2:1, PDA, atelectasis, twins, prenatal complications, maternal diabetes, placenta conditions, umbilical cord problems
prenatal complications that may > risk of RDS hypoxia, hemorrhage, shock, hypotension, hypertension, anemia
abnormal placenta conditions that > risk of RDS placenta previa, abrubtio placentae
umbilical cord disorders that > risk of RDS cord 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 RDS damaged capillaries and alveolar tissue, leading to a further <surfactant and pulm vasospasm
effects of pulmonary vasospasm enhanced 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 appear appears at APGAR, RR>60, grunting, retractions, flaring, cyanosis, hypoxemia, skin w/pallor or severe edema
How is RDS diagnosed CXR, bilateral underairation, clouded opaque, reticulograndular and frost or ground-glass, >atelectasis, air bronchograms in periphery
rapid tool to diagnose RDS shake test
APGAR and RDS RDS usually appears at APGAR with >RR, skin is pallor or severe edema, flaccid muscle tone and <activity
RDS progression most cases worsening first 48-72 hours then stabilize w/slow recovery
How do we know RDS is stabilizing onset of diuresis (baby starts to pee)
If baby dies from RDS after first 72 hrs what is usual cause secondary complications, barotrauma, ICH, or infection
Ideal TX (prevention) of RDS prevent with glucocorticosteroids 48 hrs prior to birth
goal in TX of RDS maintain adequate alv ventilation with out inflicting lung damage
TX of RDS thermoregulation, low press, low FIO2 with acceptable ABG, PaO2 50-70, CO2 <60, Ph > 7.25, diuretics, LABA and parasympathetics
complications of <Ph in RDS the acidic the Ph becomes, the less surfactant is produced, organ dysfunction and >risk of IVH
Most complications of RDS are from PPV, what are they ICH, barotrauma, DIC, infection and PDA
IVH from PPV intraventricular hemorrhage, caused by positive press in the thorax is transmitted to cranial cavity, immature vasculature ruptures
Barotrauma very common in RDS, <CL requires higher pressure to maintain oxygenation and ventilation, >press leads to lung injury and air leaks, barotrauma and pneumothorax,
DIC disrupted coagulation factors causes bleeding all over body
RDS infections gram negative (very difficult to treat), from ETT cause chronic pneumonias and >tissue damage
what are the first signs of RDS nasal flaring, followed by retractions and then grunting (very bad sign)
how often does HMD occur in <28 wk preemie 1/2
how often does HMD occur in SGA and IUDR 1/3
Why is EKG given to HMD pt to rule out other causes of symptoms
pneumoparicardium CXR air completely around surrounding heart-looks like halo
pneumothorax CXR air seen around the thymus (batwings) and heart, lateral-thymus lifted
PIE CXR aka Pulmonary Interstitial Emphysema small dark streaks (air and cysts) surrounded by white tissue, black paint flicked on white
chronic hypoxia (acidosis) does what to pulm circulation pulm artery hypertrophy (swells) narrowing lumen
what is diffusion coefficient 20:1
what determines diffusion surface area, Hbg
BPD triad O2 dependence, radiologic abnormalities, resp symptoms >28 days with respiratory failure at birth
Causes of respiratory failure that lead to BPD LBW, flail chest, immature resp control, underdeveloped tone and power
single most predictive factor of BPD LBW-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 I grandular, correlates to atelectasis, HMD, lymphatic dilation
BPD CXR stage IV beyond 30 days, sponge look, correlates to emphysematous alveoli
clinical signs and symptoms of BPD tachypnea, dyspnea, wheeze, subglottic edema, intratracheal scars, polyps (cause of stridor), tracheal malacia (trach needed)
severe signs and symptoms of BPD irritable, difficult to feed and comfort, irregular sleep, digital clubbing (chronic acidemia)
BPD complications recurrent cyanosis, agitation with obstruction due to tracheal distortion or necrotising, tracheobronchitis, intermittent systemic edema, >fluid, >vasoperfusion, transient myocardial dysfunction
Olguria no pee
why xanthines and not beta agonist or parasympathetics rebound effect
BPD bottom lime forms in hyaline membrane, pulm edema, interstitial fibrosis, emphysematous, delay in lung growth episodes of pulm insufficiency
PDA and RDS R-L shunting increases hypoxemia, or during recovery can cause RHF
BPD follows the RDS, why >press & >FIO2 over time
NCLD aka neonatal chronic lung disease symptoms of BPD without confirmation of CXR
How is BPD confirmed CXR
the 4 factors of BPD pathophysiology O2 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 CXR 1. 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 DX ABG’s with chronic lung disease, hypoxia hypercapnea >HCOS
BPD & ECG DX latent 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 BPD lung parenchyma damage
best prevention of BPD press and FIO2 to maintain PaO2 50-70 and CO2 45-55
Best way to prevent tracheal stenosis in long term BPD MLT
weaning with BPD extubate ASAP, but wean slowly
best way to transition from PPV for BPD pt nasal CPAP
TX of PIE with BPD high frequency ventilation
CPT w/BPD pt frequency is dependent on amount and viscosity of secretions, suction as necessary
Theophylline and BPD drug of choice for BPD to reduce RAW and increase CL-shortens duration of weaning in pt’s <30 days
BPD hydration and urination maintain with diuretics, monitor urine output, BS and chest excursions for improving CL
PDA and BPD treat 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
ROP formation 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 serrata retina’s anterior end
vaso-obliteration constriction of vessels leading to necrosis
vitreous liquid portion of the eye
how does the eye develop 16 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 ROP immaturity, hyperoxia, blood transfusions, IVH, apnea, infection, hypercapnea, PDA, PSI, E deficiency, lactic acidosis, prenatal complications, genetics, bright lites, early intubation, hypotension, NEC
PSI prostoglandin sythetas inhibitors
Stages of ROP 1. small white demarcation line, stages progress to 5, buildup of fluid and traction leads to retina detached and blindness
4 major intracranial hemorrhages subdural, subarachnoid, intracerebellar, periventricular-intraventricular (PVH-IVH)
subdural and subarachnoid bleeds secondary to trauma or asphyxia-most often seen in term neonates during traumatic labor
IVH periventricular-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 neonates choroid plexus (lateral ventricles)
area of bleed most often seen in preemies germinal matrix
term neonate bleeds SSC-subdural, subarachnoid (trauma), choroid plexus (lateral ventricles)
why are neonates at >risk of hemorrhage immature cerebral vasculature system and inability to regulate blood flow (fluctuating blood flow)
Etiologic factors that lead to fluctuating flow shock, acidosis, hypernatremia, transfusions, seizures, rapid >blood volume, >ICP (trendelenburg or PPV)
what type of neonate has a substantially increased risk of IVH maternal alcohol use
historical factors that >risk of IVH <1500g, <34 weeks, HMD, coagulapathy, hyperviscosity, hypoxia, birth asphyxia
common signs of germinal matrix bleed apnea, hypotension, <Hct, flaccid, bulging fontanelle, tonic posturing
How are IVH diagnosed CT scan or ultrasound
IVH grades I-IV, based on extent of bleeding
stage IV, IVH bleed most 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 IVH PHH
PHH post hemorrhagic hydrocephalus caused by obstruction of the CSF outflow and impairment of CSF reabsorption in the brain
TX of PHH goal 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 shunt internal shunt from ventricle to peritoneal in abdomen that shunts CSF to abdomen for reabsorption
ventricalilostomy shunts CSF for external drainage
complications (sequelae) of IVH PHH, cerabal palsy, vision loss, hearing loss, epilepsy, mental retardation
TX of IVH supportive, 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 IVH avoid factors that cause fluctuations in cerebral blood flow, wide Bp, oxygenation or Ph, indomethacin is prophylactic
indomethacin prophylactic for IVH
asphyxia hypoxia, hypercarbia and acidosis in fetus or neonate caused by lack of perfusion
most common risk of asphyxia IUGR, breech or post maturity (trauma complication of large baby)
asphyxia inutero resulting from placental insufficiency organ of respiration not working, no O2 to baby and no CO2 back to mom
asphyxia in neonates most often results from pulm or cardiac problems
factors that contribute to fetal asphyxia maternal 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 flow shock, vasoconstriction states, inferior vena cava syndrome
dysfunction of placenta placenta previa, abrubtio placento
intrinsic fetal disorders hydrops fetalis (fetal cardiac failure), fetal hypotension secondary to hemorrhage or drugs
fetal shunting from asphyxia blood moves away from lungs muscles, liver, kidney and gut and directed to brain, heart and adrenal glands
primary fetal apnea fetal apnea caused by <Bp and <HR from uncorrected asphyxia
secondary fetal apnea follows 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 asphyxia fetal heart monitor, meconium in amniotic fluid, heart monitor-loss of base variability, late decelerations, prolonged bradycardia
major complication of prolonged asphyxia inutero hypoxic-eschemic brain injury
hypoxic-eschemic encephalopathy major 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 what PVH-IVH
periventricular leukomalacia infarction in the periventricular region
consequences of asphyxia PVL, HEL, HEE, cardiac eschemia (usually transient), tubular necrosis of the kidneys, bowel eschemia, NEC, DIC, >PVR, <surfactant and ARDS
asphyxia TX immediate reversal of hypoxemia and acidosis, rapid delivery of fetus
MAS meconium aspiration syndrome, term and post term who experience some degree of asphyxia during before or during labor causing aspiration of meconium
when does MAS occur before 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
meconium contents 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 MAS asphyxia 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 MAS 1. 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 pneumonitis inflammatory response of tracheobronchial tree epithelium to meconium causing acidic irritation of meconium, mucosal edema, <CL, further impairment of gas exchange
PPHN from MAS vasospasm of pulm vascular causes persistent pulm hypertension, blood follows fetal route, bypassing lungs and leading to >shunting and worse ABG’s
detecting PPHN cyanosis 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 test positive is PaO2 <50 that rises to >200 when pt hyperventilated to CO2 of 20-25
most accurate test of meconium aspiration green stained vocal cords at birth
TX of meconium aspiration suction 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 aspiration aspiration pneumonia, pneumothorax, pneumomediastinum, pneumoparicardium, pulm interstitial emphysema PIE, sub q emphysema,and air emboli
higher incidence of air leak syndrome in what pt’s RDS, MAS, TNN, most are from mech ventilation, few from spontaneously
TX for tension pneumo no PPV then monitor, severe do needle air removal, PPV give chest tube w/1 way valve at 15-25 cmh2o
pneumoparicardium air 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 emphysema air 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 emphysema PIE where extra alveolar air is confined to visceral pleura forming blebs
Intrapulmonary interstitial emphysema PIE where extra alveolar air remains in lung tissue
Pathophysiology of PIE air 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 TX besides preventions, mild will reabsorb in 5-7 days, lower vent pressures while maintaining ventilation and oxygenation, HFV, selective ventilation
Selective ventilation intubation and ventilation of only the affected lung or less affected lung, allowing injured lung time to heal
survivors of PIE of get what complication BPD, from aggressive mech ventilation, o2 toxicity
PFC/PPHN persistent fetal circulation aka persistent pulm hypertension of the newborn severe 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/PPHN most 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/PPHN HMD, bacterial pneumonia, myocardial dysfunction and pulm hypoplasia
what is the result from the severe v/q mismatch of PFC combined met and resp acidosis and hypoxia-causes further pulmonary vasoconstriction
why so much PFC in term and post term pulm 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 consider PLD-parenchymal lung disease, CCHL
Question Answer
what are lung volumes distinc measurements that do not overlap each other
what are lung capacities measurements containing two or more lung volumes
what volumes and capacities cannot be measured directly RV, FRC and TLC
how do we measure RV, FRC and TLC indirectly using helium dilution, nitrogen washout, body plethysmograph or radiologic estimation
TLC total lung capacity, sum of VC and RV, based on age size and gender, increased w/obstructive and decreased with restrictive
VC vital 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 FVC coaching, bad coaching is bad results
the 3 phases of the FRC are 1(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 FRC may 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 FVC by causing a slow rise in the RV
IC inspiratory capacity, measured with spirometer
FRC functional 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 <FRC pneumothorax, restrictive diseases, age, obesity (shrinks lung)
what kinds of diseases cause an >FRC emphysema, any disease that causes a loss of lung tissue, obstruction
IRV inspiratory reserve volume, measured with routine spirometer
VT tidal 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 what hypoventilation and >CO2
What is the normal RR for a pt with restrictive disease increased, because VT’s are shallow, RR must be increased proportional to loss of VT
SVC slow 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 pt VC, significant reduction in VC indicates pt is at high risk for resp failure after surgery (<20 mL/kg)
ERV expiratory reserve volume, (FRC-RV is ERV) max exhaled following passive exhalation, < obesity, poor performance and restrictive (limited clinical use)
RV residual 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 RV 25%
RV/VC, what percent of VC is normally RV 33%, >33% COPD is present
What is the significance of a reduced RV/VC none, there are no clinical states that reduce RV/VC only increase as with COPD (will be in normal range with restrictive disease state)
VE RRxVT, 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 provide contractile state of the airways, FEV1, FEV3, FEF25-75, PEF (peak flow)
FEVt forced expiratory volume timed in liters (t is commonly expressed in .5, 1, 2, 3 seconds) norm is relative to his FVC
FEV1 max 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
FEV3 looks at the 3 second point on the curve.
FEV.5 and FEV1 used 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
PEF max 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 TX PEF
spirometer positive displacement-volume, used to measure volumes and flow rates
water-seal spirometer measures volume and time
what is the best indicator of a restrictive disease? Vital Capacity
how do we measure obstructive diseases flow rates, FEV1, FEF200-1200, FEF25-75, PERF and FVC
what is the best indicator of obstructive disease FEV1
what is the best indicator of large airway obstruction FEF200-1200
what is the best indicator of a small airway obstruction FEF 25-75
what is the best indicator of airtrapping FVC that is smaller than SVC
what is a PFT determines the functional status of the lungs
what can PFT’s be used for presence 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 testing PFT that measures degree of airway hyper-responsiveness
contraindications of PFT’s recent 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 values height
at what age does a persons lung size begin to shrink 20yrs
what is the primary instrument used in PFT’s spirometer
what does a spirometer measure the lung volume compartments that exchange gas with the atmosphere
spirograph attaches to spirometer to graphically record PFT’s
spirogram the graphic tracing of the PFT
body plethysmograph for total lung capacity and airway resistance studies
what are the 2 main categories of PFT abnormalities obstructive and restrictive defects
how do obstructive disease present on PFT’s if expiratory flow is below normal
how do restrictive diseases present on PFT’s if lung volume is reduced
Upper airway obstruction will show up where on PFT reduced flow rate in initial 25% of FEC (small airways in late portion)
what portion of the flow/volume curve is effort Dependant the first 1/3
what portion of the flow/volume curve is effort independent the later 2/3
a restrictive disease is present when PFT lung volumes are reduced to less than 80% of predicted levels in spirogram or body plethsymograph
what are the two most common causes of restrictive disease atelectasis 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 disease sarcoidosis (<volumes limit airflow) and emphysema (>volumes restricts inspiratory airflow)
sarcoidosis unknown 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 PFT obstructive causes reduced expiratory flows, restrictive causes reduced lung volumes
3 ways to measure TLC body plethysmograph (body box), open-circuit nitrogen washout, or closed-circuit helium dilution
why is body box more accurate it measures communicating and non-communicating/poor communicating spaces (volumes)
what are non communicating or poor communicating lung volumes airtrapping (COPD, Asthma) or pneumothorax
(open-circuit) nitrogen washout air 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 dilution pt breaths helium for 7 minutes, when equilibrium is reached, helium is measured and lung volumes are calculated
why is helium used as a measuring gas helium is an inert gas so not significantly absorbed
what PFT equipment uses an open-circuit system nitrogen washout
what PFT equipment uses a closed-circuit system helium dilution
what is the most accurate determination of gas volumes in the chest plethsmograph/body box
MVV max 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 medications two flow volume curves superimposed on each other, one before bronchodilator and one after
FLOOPs are best used to look for patterns in what diseases restrictive (<volume), large airway obstruction (<flow, norm volume), severe COPD (hockey stick or boot)
PFT’s before and after bronchodilator 2 of 3 must improve, FVC >10%, FEV1 15%, or FEV25-75 20-30%, best in asthmatics, misleading in COPD
DLCO diffusion capacity of the lungs, <with emphysema and pulm fibrosis
RAW normal w/out ETT tube .5-3.0 cmH2O/L/sec, as airways narrow, pressure of resistance increases
compliance volume change per unit of pressure change, measured with balloon catheter
Dynamic compliance measured when gas is flowing
static compliance measured with no flow of gas
Total CL lung 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 floop stiff lungs-<CL, (less volume, more pressure)
what does a round top of the curve represent on the floop emphysema, <elastance (more volume and less press)
RQ respiratory 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
Bronchoprovocation pt inhales histamine or methacholine, cold air and exercise, used to test pt for hyperactive airways
methacholine challenge parasympathomimetic used to induce bronchospasm
most useful PFT tests as seen in table 8-1 1-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 gases no, 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 ventilation B
The tracing obtained from a PFT is called spirogram
which is the most important factor in predicting PFT measurement age, weight, height, gender height
PFT’s are effort dependent T/F True
What piece of equip is used to measure TLC and RAW body 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 tracing the initial
which is true regarding restrictive disease-<volumes on PFT, can be caused by obesity, exp flow are usually normal all
what PFT is useful in determining the need for mech ventilation FVC
Air (low density) Black (radiolucent), passes threw body and allows for more penetration
Water Water 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
Fat Shades of gray
Heart, diaphragm, & major vessels considered to have the density of water. Do not change in density but may change in size, shape, & position.
Lung consolidation Increase 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 Blebs Decrease lung density absorb fewer x-ray and result in darker areas on film
Distance from film Important to conceder, the closer the the patient is to the source, the greater the magnification and distortion of objects seen.
Indications for X-Ray Assist DX of lung pathology, determine appropriate TX, evaluating effective TX, track progress of lung disease, determine position of tubes and lines
Posterioanterior PA view into the Posterior threw to the Anterior
Lateral Side 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 view Projection is made at a 45 degree tube angulation. Sometimes required for closer look at the RML or apices’s of the lung.
Oblique views helpful 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
Pneumothorax The only time you do an expiatory film.
AP Film 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 evaluation ETT (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 film Thoracentesis, Pericardiocentesis, Bronch
CT scan Computed enhancement of x-ray shadows to give clearer look @ internal anatomy.
CT scan & Lung Tumors Superior to conventional x-ray can detect nodules 2-3mm. CT helps place biopsy needle to prevent pneumo.
CT scan & interstitial lung disease Can show considerable changes even when x-ray reads normal. Used selectively because of high cost.
CT scan & AIDS Early detection of pneumonias that occur as a result of AIDS
CT scan & Occupational lung Helpful in identifying changes in the pleura & lung parenchyma.
CT scan & Pneumonia Restricted use because of cost but they can detect pneumonia sooner.
CT scan & Bronchiectasis Has replaced invasive use of bronchogram. CT scan can detect early
CT scan & COPD Emphysema shown clear and detailed. Dx consistently in the high 90%
MRI Used 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 scan Positron emission tomography, Used to Dx and stage cancers. Compound is injected into a vein, malignant cells show >metabolic rates
Pulmonary Angiography evaluate 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) airways Tracheal mid line, carina,main stem bronchi, air bronchogram(occur with alveolar filling)
(B) bones Clavicles equal, ribs, scapulae, spine
( C) Cardiac Cardio-thoracic ratio 1/3 on PA ½ on AP, cardiac borders, aortic arch and vessels, cardio phrinic angle.
Silhouette sign Infiltrates 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 bronchogram Patent 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 Atelectasis Seen in pt w/ pleural effusion, pneumo, hemo, & any space-occupying lesion.
Obstructive Atelectasis Blockage of airway, absence of ventilation. Tumor, aspirated foreign body, fibrosis, mucus plug, mechanical obstruction, & scaring. Trachea and heart shifts toward.
X-ray & Atelectasis Shift of the fissure toward, movement of hilar toward, overall loss of volume, hemidiaphragm elevation.
X-ray & Pneumothorax Hyperlucency 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 Hyperinflation COPD, can be red as normal if mild, mod-severe large lung volumes, depressed diaphragm, small narrow heart, enlarged intercostal spaces.
X-ray Interstitial lung disease Alveolar 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 & CHF 1redistribution 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-ray film is over exposed (underexposed-cant see behind heart)
properly exposed xray thoracic vertebrae are just visualized through the heart shadow
depth of inspiration is adequate in PA film when 10 posterior ribs are seen in film
primary purpose of xrays is what identify abnormalities
why are PA views most often used less chance of pt rotation, heart size less magnified, pt must stand
xrays are normally taken on inspiration, what is the exception suspected pneumothorax
problems associated with AP (portable xrays) poor radiographic exposure, pt not centered, artifact shadows, heart magnified
xray to identify Pneumothorax lateral decubitus on expiration
ETT tube on an xray 3-5cm above Corina
what can be assessed on an xray CVP 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 what electromagnetic waves
>density causes what to an xray < penetration
radiographic density water, air, bone, fat
radiopaque white
radiolucent black
as the distance from the source (machine) and the pt decreases, what happens to the magnification? magnification increases
what is standard distance for an xray 6ft
when should an xray be taken after 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 xray lobar radiopaque pattern of infiltrates
hyperinflation xray large lung volumes, widened intercostal space bilaterally, small narrow heart
small pleural effusion xray blunted constrophrenic angle, meniscus sign, partially obscured and elevated hemidiaphragm (lateral decubitus to visualize fluid)
large pleural effusion xray complete white out on infected side, complete obscure of diaphragm
obscure heart border silhouette sign is absent, then consolidation is anterior lung segments, if silhouette is present (sharp lung borders) then consolidation is posterior
diaphragm border is obscure anterior 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 Xray fluid 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 film vertebral bodies easily seen, spineous process centered between clavicles and behind trach, ribs 10
over exposed xray lungs to black and vert to easy to see
under exposed xray vert not seen through cardiac shadow and lungs to white
clinical predisposition for pneumo trauma, broken rib, Thoracentesis, CVP line, pulm art cath, PPV, blebs, improper placement of ET, oral or NT tube
costrophrenic angle the point where diaphragm meets the chest wall (blunted with pleural effusion)
meniscus sign water 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 crackles atelectasis, pneumonia, edema, pulm edema, fibrosis
early insp crackles bronchitis, emphysema, asthma
insp & exp crackles bronchitis and resp infect
wheeze asthma, CHF, bronchitis
stridor croup, epiglotitis, post extubation
<PaO2 age, Pb, PIO2
consolidation xray minimal volume loss, usually lobar distribution, homogeneous density late in process, air bronchograms if airway leading to consolidation is open
physical findings of consolidation dull (<resonance) percussion, bronchophony (99 sounds clear), bronchial BS, crackles, whispered pectriloquay (sounds clear), egophony (E sounds like A), tachypnea, fever
clinical SS of hyperinflation barrel 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
hyperinflation most 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 space pleural effusion, transudate, exudate, blood (hemothorax), fatty (chylthorax), puss (empyema or pyothorax)
transudate pleural effusion with clear fluid, low in protein, seen in CHF and atelectasis
exudate pleural effusion w/protein, bacteria, pneumonia, pulm emboli, malignancy, virus, TB, fungal
how much fluid must be present to be seen on an x-ray 100ml
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 SS dependent 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 xray fibrotic infiltrates in LL, TB and silicosis in upper lobes, air bronchograms
clinical SS of interstitial lung disease rapid shallow breathing, <CL, crackles on Insp(usually LL), severe has hypoxemia and cyanosis, final DX via biopsy bronchoscopy
Clinical SS of CHF crackles 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
Pneumotachometers spirometer that measures flow, used continuously it can measure VE
Spirometers that measure volume and time are dry-rolling and water-sealed
Spirometers that measure flow are pneumotachometers
Calibration of body box is verified with a rotometer or pneumotach
Volume calibration and leak tests of FLOOP super syringe
Flow calibration of a FLOOP is done with a rotometer
Timing devices (kymograph X-Y recorders) are checked with stop watch
Plethysmograph is calibrated with rotometer for flows and barometer for pressures
SVC is an important measure of what restrictive disease
Decreased volumes indicate what restrictive disease
VC is the BEST INDICATOR OF WHAT RESTRICTIVE LUNG DISEASE
FVC provides what to measure obstructive disease flow rates
What is the BEST INDICATOR OF OBSTRUCTIVE DISEASE FEV1
Minimum acceptable FEV1% is 75%
Decreased FEV1/FVC OBSTRUCTIVE DISEASE
Normal FEV1/FVC not obstructive, but still may be restrictive
FEV200-1200 <with LARGE AIRWAY OBSTRUCTION
FEV25-75 <WITH EARLY STAGES OF OBSTRUCTIVE DISEASE (ASSOCIATED WITH SMALL AIRWAYS)
PEFR SOME USED TO EVAL ASTHMATICS PRE AND POST BRONCHODILATOR
IS FVC A FLOW OR VOLUME VOLUME AND SHOULD BE EQUAL TO SVC
FVC NOT COMPLETED IN 3 SECONDS OBSTRUCTION
FVC SMALLER THAN SVC OBSTRUCTIVE (AIRTRAPPING)
MVV MEASURES MUSCULAR MECHANICS OF BREATHING,
<MVV OBSTRUCTIVE DISEASE, >RAW, MUSCLE WEAKNESS, <CL AND POOR PT EFFORT
POST BRONCHODILATOR TEST MUST BE HOW HIGH TO BE SIGNIFICAN 15%
NITROGEN (N2) WASHOUT TIME >7MINUTES IS POOR DISTRIBUTION
BEST TEST FOR PARTIAL VOCAL CORD PARALYSIS (LARGE AIRWAY OBSTRUCTION) FLOOP
DISTRIBUTION OF GASSES ARE EVALUATED WITH NITROGEN WASHOUT TEST (7MIN) AND HELUIM DILUTION
DLCO CARBON MONOXIDE DIFFUSION CAPACITY
DLCO MEASURES FACTORS THAT AFFECT THE DIFFUSION OF GAS ACROSS THE A-C MEMBRANE
HOW LONG DOES A DLCO TEST LAST 1 BREATH
WHAT DISEASES HAVE A <DLCO FIBROSIS, SARCOIDOSIS, ARDS, EDEMA, EMPHYSEMA
WHAT IS THE ONLY OBSTRUCTIVE DISEASE THAT HAS A DECREASED DLCO EMPHYSEMA
POSITIVE BRONCHIAL PROVOCATION 20%DECREASE IN FEV1
PFT NORMS AND PREDICTED ACTUAL/PREDICTED IS OBSERVED 80-100% 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 VOLUMES PICT-PNNF, PLEURAL DIS, INFLAMMATORY DIS, CARDIAC DIS, THORACIC DIS, POST OP, NEUROLOGICAL NEUROMUSCULAR, FIBROTIC DIS
Question Answer
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 HFV I. 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 factors III. 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 achieved Exhalation 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 surfactant I. 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 inactivation II. 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 inspiration Cycle 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 ventilation I. 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 assessed Counting 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 stability EPAP
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 ECLS Pulsatile 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 ECLS Increase the flow of the sweep gas
Question Answer
acrocyanosis condition in the newborn characterized by a cyanotic discolorization of the hands and feet, aka peripheral acrocyanosis of the newborn
alae nasi external border at opening of nasal passage, cartilaginous, maintains patency of nasal opening during spont breathing
anencephaly genetic defect in which brain and spinal cord are absent, cranium is open, vertebral canal remains a groove
caput succedaneum localized 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
Doppler change 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
fontanelle space on a newborn cranium between cranial bones, covered by tough membrane
hydrocephaly a pathologic condition characterized by abnormal accumulation of cerebral fluid with in the cranial vault-results in dilated ventricals
hyperpnea deep, labored or rapid respiration
hypopnea shallow or slow respiration
lanugo fine, downy hair that covers fetal body, appears at 26 weeks, thins at 28, starts to disappear at 32, gone by 40
methacholine cholinergic, aerosolized and used to confirm asthma
murmur low pitched fluttering or humming heard just before, during or after the normal heart sounds
paradoxical situation or occurrence in which the outcome is the opposite of what is expected
pinna cartilage portion of the external ear
pleural iffusion abnormal fluid in the pleural space, transudate-protein free (from tissue), exudate-high protein ( from blood vascular)
pneumotachograph instrument that measures velocity of expired velocity of gas flows
rugae ridges or folds of skin, found in stomach and mature male scrotum
scaphoid sunken anterior abdominal wall
thoracic gas volume volume of gas in the thorax as measured by the body plethysmograph, may or may not include conductive airway gas
vernix off 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
Question Answer
Normal airway clearance effective mucociliary action and effective cough
increased mucus may lead to obstruction and airtrapping, atelectasis, ineffective gas exchange, inflammation and infection
*ACT airway clearance techniques
*why are premature neonate prone to atelectasis secondary to lack of pulmonary surfactant present with RDS
Severe atelectasis can lead to large areas of shunting with worsening blood gases
*why is airway clearance used to prevent atelectasis and to help reinflate those areas that are atelectic
*complications of RDS atelectasis, lung tissue damage from ventilator pressures, oxygen and lack of surfactant, leading to BPD
*BPD bronchopulmonary dysplasia
*small airways in newborns can cause what if secretions accumulate severe imbalances in ventilation/perfusion ratios
*Indications for airway clearance retained 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 secretions CF, pneumonia, asthma, bronchiolitis, bronchiectisis
*contraindications of airway clearance therapy pulm 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 drainage emesis (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 what IVH, intraventricular hemorrhage-never on baby less than 1500g
*skin integrity and percussion never on preemies less than 1200, may cause edema, excoriations (tearing of skin) and bruising
*percussion rhythmic clapping over affected lung area to loosen secretions, 1-5 mins
Why is caution used when percussioning baby with BPD may have fragile bones
*vibration rapid, constant motion, rather than rhythmic clapping. Used for loosening secretions in the airway, best done during exhalation, 30 seconds per side
Auscultation listening to the sounds produced in the lungs during the ventilatory cycle
Wheeze high pitched continuous sound
Rhonchi/course crackles continuous low pitched sound (secretions)
Crackles discontinuous sounds (fine crackles)
The goal of TX with aerosolized meds is deliver an adequate amount of med to the desired site in pulm tree with minimum side effects
*effective aerosolized TX depends on 4 factors 1. 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 what type of nebulizer used
What is the drawback of when running a jet nebulizer continuously much of medication is lost during expiration, reducing amount delivered to the lungs
*how can the loss of medication during exhalation be reduced slightly 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 growth aerosol particles grow larger when added to environment of high humidity
*what is the major characteristic of aerosol particles that affects deposition it’s ability to take on additional water-hydroscopic growth, making particle deposit higher in airway (dont make it to lungs)
*characteristics that determine aerosol deposition concentration 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 infants less 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 alveoli probably negligible, narrow airway, ett, etc are cause
*what is best ventilatory pattern for best aerosol delivery laminar 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 NICU unknown side effects and dosages in neonates (liver not functioning yet, baby can get toxic build up)
*what is the advantage of svn requires 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 svn expensive, less easily transported, cleaning and prep, inefficient dose delivery, cold, medium for bacteria,
*disadvantages of inline jet neb with ventilator high humidity may aid hydroscopic growth causing deposition in circuit or upper airway-reducing drug delivered
LVN used for continuous neb in acute asthma
Indications for aerosolized drugs bronchodilators, 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 steroids an inflammatory pulmonary process is present like BPD
*the most common nebulizer is what type updraft, used in the vertical position with a T piece attached
*what is a mainstream nebulizer and what is the advantage no 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 circuit potential 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 do turn 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 TX nosocomial 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 work compressed 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 risks riboviron 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 unit slows riboviron from entering environment on exhalation
how often should neonate be suctioned as little as possible, 4-6 hours as needed, never suction with in 20 mins of ABG
Suction Equipment cardiac, 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 sizes 2.5-4
Suction catheter size for intubated neonate 5, 6 to 8-10
Suction catheter size for nonintubated baby preemie 5, 6 neonate to 6 months 5, 6-8
What is difference in suctioning baby from adult to 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 neonate bradycardia, hypoxemia, mucosal damage, atelectasis, airway contamination, accidental extubation
What are the common causes of bradycardia when suctioning vagal 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 therapy hypoxemia
Hypoxemia in neonate (defined) PaO2 less than normal on room air (40-70mmHg)
PaO2 norms for term infant at 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 neonate retractions, expiratory grunting, nasal flaring and cyanosis
Hazards of O2 therapy in neonates ROP, O2 toxicity leading to BPD (bronchopulmonary dysplasia), cerebral vasoconstriction, fire
What is BPD and how is it caused long 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 hazard high 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 neonates keep 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 them series 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 analyzers since 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 placed in 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 humidifier aka bubble humidifier (aka diffuser), flow <10L/min and usually non heated, used with simple mask and nasal cannula
Physics of bubble humidifier as bubbles of gas rise through the sterile water, the gas picks up water molecules
wick humidifier highflow 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 do collection 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 hood at the level of the pt’s face and nose, to assure accurate FIO2 because of layering effects
*Hazards of oxygen hoods flow 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 neonate chronic need for O2 and weaning from oxygen hood
Flow for cannula always less than 1L/min
Chronic oxygen use in neonates is associated with what BPD
Flows >4L/min on cannula leads to what mucosal drying and epistaxis (nose bleed)
FIO2 for cannula are dependant on what pt age, size, VT and RR
FIO2 of NC at .25L/min 24-27%
FIO2 of NC at .50L/min 26-32%
FIO2 of NC at 1L/min 30-35%
How is NC kept in place for neonate with out causing skin damage IV site tape
Why are neonates and preemies kept in incubators temperature-controll and quit environment
How are O2 needs met with pt in incubator blended, warmed and humidified gas is blown in at desired FIO2
How is FIO2 checked for pt in incubator same as hood, as close to baby face (because of possible layer)
What is the main problem associated o2 delivery in incubators maintaining 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 incubator when pt requires >.25 FIO2 (to prevent layering)
*self inflating bag reinflate 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 bag aka 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 ports one for O2 and one for press manometer (prevent barotrauma)
On intubated pt, which port is for O2 and why is this important port that is distal to pt connection, prevents retardation of exhalation caused by direct flow of gas into end of ET tube
Indications for CPT atelectasis, CF, prolonged bed rest (never for asthma)
*do we hyperoxygenate neonate prior to CPT no
Which modality of aerosolized medication requires the least amount of pt coordination svn
Are retractions an indication for aerosolized meds no 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 what overheating of the circuit when the neb is removed
*hazards of aerosol drug therapy infection, med side effects, drug reconcentration and over hydration
What is the greatest hazard of ribavirin administration with mech vent pt precipitation and accumulation of drug on vent tubing and ETT
While suctioning pt following CPT, pt becomes bradycardic, what should RT do stop, hyperoxygenate and shorten duration of following suction attempts (always less than 10 seconds)
Anaerobic absence of oxygen
*brown fat fat 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 syndrome congenital, familial autosomal abnormality, glucuronyl transferase is deficient or absent, causes nonhemolytic jaundice, an accumulation of unconjugated bilirubin and severe disorders of the CNS
Encephalocele protrusion of the brain through a congenital defect in the skull
Enteral pertaining to the intestines, often associated with feeding or meds
Galactosemia congenital defect characterized by deficiency of enzyme galactose-1-phosphate uridyl transferase, causes hepatoplenomegaly, cataracts and mental retardation
Gastroschisis congenital defect characterized by incomplete closure of the abdominal wall with protrusion of the viscera
Guaiac wood resin used on a reagent strip to test for presence of blood in the stool or urine
hydrops fetalis massive accumulation of fluid in the fetus or newborn often associated with erythroblastosis fetalis, effusions of the pericardial, pleural and peritoneal spaces also occur
Hypersosmolar increase concentration of osmotically active components such as electrolytes and proteins
Hypotonia having a smaller concentration of solute to solution ration than that found in intravascular or interstitial fluids
*kernicterus abnormal toxic level of bilirubin that accumulates in the tissues of the CNS, can cause degenerative disorders
Lucey-driscol syndrome syndrome passed as autosomal recessive train, characterized by inhibited uridine disphosphate glucuronosyl transferase and leads to rapid progressive jaundice and kernicterus
Omphalocele congenital herniation of the intraabdominal viscera through the abdominal wall near the umbilicus
Parenteral pertaining to the uptake of substances or meds by any route other than the digestive tract
Servo-controlled any 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 corneum outer most layer of skin, composed of dead cells converted to keratin, bodies barrier to microorganisms
Turgor normal resiliency of the skin, results from outward pressure of cells and interstitial fluid
What is the most important factor in care of a neonate thermoregulation
*thermoneuteral zone temperature 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 at no 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 neonates because of the diversity of metabolic rates, gestational age and weight
*how do adults regulate body temp metabolic and physical activity (shivering) if cold, and sweating to cool.
*neonates rely on what for the production of heat relies 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 heat stimul 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 thermogenesis breakdown of brown fat with the subsequent production of heat
*what are the two gradients of physiological heat loss in neonates internal thermal gradient and external thermal gradient
*internal thermal gradient (ITG) temp difference between warm body core and cooler skin
*how is ITG regulated BSA (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 ITG large 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 ETG radiant heat loss, conductive (transfer) heat loss, convective heat loss and evaporative heat loss
*radiant heat loss dissipation 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 gain heat from the sun
*conductive heat loss transfer of heat from body to cooler surface-put blanket under baby before putting on scale or table
*convection heat loss losing 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 loss as water changes from liquid to gas, heat is released
*insensible heat loss evaporative heat loss from the skin (thin skin) and respiratory tract (normal)
*sensible heat loss evaporative heat loss from sweating from the skin
*what kind of evaporative heat loss do babies do insensible only, they do not sweat
*what is cold stress hypothermia, any lowering of the thermoneuteral temperature
*where are the most sensitive thermoreceptors located in the face (and respond the quickest)
*what is the body’s initial response to hypothermia peripheral vasoconstriction (shunts blood from surface)
*what does peripheral vasoconstriction cause and why is it dangerous anaerobic 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 hyperthermia vasodilation of peripheral vessels to allow for dissipation of heat, followed by >metabolism and >O2 consumption
causes of hyperthermia infection, 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 done maintain 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 warmer access to the pt, difficult thermal regulation and environmental control
Advantage and disadvantage of incubators advantage is controlled environment for better thermal management, quieter, barrier to handling, disadvantage is pt access
physiologic considerations of high-risk neonate nervous 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 neonate immature 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 neonate blanket over the incubator
Stimulation of the neonate should be avoided when during sleep, behavioral stress cues or physiologic stress cues are present
What are the behavioral stress cues gaze aversion, facial grimace, hiccoughs and irritability
What are the physiologic stress cues cyanosis, hyperoxemia
what is the best way for practitioner to avoid over stimulating handle 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 are low or no light (better SaO2), workers and family avoid loud talking and laughing
Physiological factors in premature neonate skin very 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 skin citrus oil, they are nontoxic
Why dont we use spray on skin barriers or traditional adhesive removal when TX preemies permeable 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 how coban wrap, fabric straps with Velcro
What is the best way to TX baby skin that has been broken or damaged from tape removal IV site dressing, will protect and allow healing and keeping microorganisms out
How is fetal fluid and electrolyte status regulated maternal and fetal mechanisms
Maternal disorders that effect fetal fluid and electrolyte balance diseases that affect uterine perfusion, and IV therapy during labor
Abnormalities in fluid and electrolytes occur with certain neonate disease states they are respiratory disorders, asphyxia, congenital heart disease, hydrops fetalis, sepsis, renal disorders, urinary tract abnormalities, endocrine disorders and <skin integrity
hydrops fetalis massive 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 how diarrhea, emesis, nasogastic tube drainage, thoracotomy tube losses, damaged skin and other factors the >insensible water loss
Assessing fluid deficit and estimating amount pt requires hx, physical exam and lab values
Signs of dehydration or hypovelemia on exam are perfusion 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 loss EGA, 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)
Bilirubin byproduct of normal breakdown of RBC’s
Life span of a RBC 120 days
How is bilirubin normally excreted passes through the liver and is excreted as bile through the intestines
*what is jaundice bilirubin 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 baby 20mg
*complications of >20mg of bilirubin deafness, cerebral palsey, brain damage (hepatitis in adults)
*types of jaundice physiological (normal) j, jaundice of prematurity, breast milk j, blood group incompatibility j
*what is a simple test for jaundice press your fingertip to babies nose or forehead, if white no problem, if yellow jaundice is present
*jaundice TX mild 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 again unlikely
*physiological jaundice 50 percent of newborns get it, due to immaturity of liver, appears at 2-4 days and disappears at 1-2 weeks
*jaundice of prematurity occurs frequently in preemies, underdeveloped liver and longer time adjusting to excreting bilirubin effectively
*breast milk jaundice 1-2 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 jaundice Rh 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) incompatibility moms 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
STABLE sugar, temp, airway, blood pressure, labs, emotion
NEC necrotizing 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 NEC prematurity, asphyxia, and formula feeding
What are the 3 main factors that lead to NEC mucosal wall injury, bacterial invasion into damaged intestinal wall and formula in the intestine
What causes injury to mucosal wall in NEC may be secondary to ischemia and or decreased blood flow to the gut and maternal cocaine use
pneumatosis intestinalis necrosis 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 what NEC
What is the first confirmatory sign of NEC guaiac-positive stools (blood in stool)
S and S of NEC abdominal distention, bile residuals and bile-tainted emesis (vomit), poor feedings, general signs of sepsis (lethargy and >fio2 requirements)
Best TX for NEC avoiding factors that lead to it
TX for NEC includes avoid 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-arginine substrate of nitric oxide that reduces intestinal injury
Gastrointestinal perforation or full-thickness necrosis requires what surgical resection
What is the first sign of NEC increased abdominal girth
How is NEC confirmed guaiac-positive stools
Active transport movement 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
Dyscrasias abnormal blood or bone marrow condition like aplastic anemia or Rh incompatibility
Extravasation a passage of blood, serum or lymph into the interstitial spaces of the tissue
Facilitated diffusion movement 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
Hydrolysis the chemical alteration or decomposition of a compound with water
Ototoxic refers to a substance having a harmful effect on the eighth cranial nerve, or on the organs of hearing and balance
Pharmacokinetic study of all aspects of drug use on the body, routes of absorption and excretion, duration of action and biotransformation
Pheochromocytoma chronic hypertension caused by a vascular tumor of the adrenal medulla or sympathetic paraganglia, characterized by hypersecretion of epinephrine and norepinephrine
Pseudocholinesterase a nonspecific cholinesterase that hydrolyses noncholine esters as well as acetylcholine
Reduction the 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 diffusion the 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
*teratogen any substance or agent that interferes with normal fetal development and causes one or more developmental abnormalities in the fetus
Ultrafiltration the 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 blood 50-100% higher
Why are fetal concentrations so much higher than maternal concentrations fetal liver immaturity
Mechanisms drugs use to cross the placenta are ultrafiltration, simple diffusion, facilitated diffusion, active transport and breaks in placental villi
Drug transfer across the placenta is determined by what concentration 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 called teratogens or teratogenic substances
*teratogens may cause what spontaneous abortions, congenital malformations, intrauterine growth retardation, mental retardation and carcinogenesis
*effects of teratogens are dependant on what factors dose 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 what pH-dependent diffusion and gastric empting time
*for a term neonate, gastric pH at birth is what 6-8, 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 reached 2 years of age
*the difference in pH of stomach for neonate may affect what normal absorption of both basic and acidic drugs like penicillin’s, Phenobarbital and phenytoin
*what is gastric emptying time in the newborn 6-8hrs, does not reach adult values until 6 months
Peristalsis digestion
Low muscle mass in neonate causes what to intramuscular absorption rates of drugs absorbs very fast
Why is absorption of drugs through the skin of newborns greatly increased newborns 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 drugs combination 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 neonates bypasses 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 body throughout 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 where to highly vascularized tissue like the heart, brain liver kidney etc
Less lipid-soluble drugs and do not readily cross cell membranes can do what gather 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 have leaves only 10% unbound or freely available to cross cell membranes and exhibit maximal pharmacologic activity
What is unconjugated bilirubin jaundice
What is drug metabolism changing or alteration of a drug to a different form, either active or inactive
Where is the primary site of drug metabolism liver (but also in plasma, kidney and GI tract)
What are the 4 types of drug metabolism that take place in the liver conjugation, oxidation, reduction, hydrolysis
Immaturity of preemie decreases drug metabolism how because all 4 metabolism functions are decreased, half life of drug or drugs is increased
Half-life amount 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 preemies increase 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 neonate because most drugs are poorly metabolized by premature liver
What is the primary route of elimination of drugs kidneys (also biliary and fecal excretion, sweat and saliva)
How is renal function measured creatinine clearance
*GFR glomerular filtration rate
*what effect does GFR have on some drugs because of immaturity of kidneys, drugs like diuretics may have to be increase due to <GFR.
*What kinds of drugs are dependent on GFR drugs 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 are penicillin’s, cephalosporin’s, aminoglycosides, macrolides, quinolones, tetracyclines, sulfonamides, antifungals and antivirals
*what kind of antibiotic is penicillin beta-lactam, kills bacteria by penetrating outer membrane of bacteria through small canals (porins)
*penicillinase aka beta-lactamase enzyme produced by some bacteria in attempt to survive, inactivates beta-lactam drugs (especially staphylococcus)
*penicillinase-resistant penicillin’s a group of penicillin drugs that are resistant to penicillinase enzyme and are effective against staphylococcus (MRSA)
*what is another name for antiviral drugs chain terminators
*ribavirin broad-spectrum antiviral specifically used in neonates for bronchiolitis caused by RSV
Because of teratogencity with exposure to ribavirin, what precautions does RT need to take delivery with SPAG 2 unit, shut off remotely, deliver only in isolation room with negative pressure and adequate air exchange to outside
Adenosine indications acute TX of sustained SVT (supraventricular tachycardia)
Adverse effects of adenosine flushing irritability and dyspnea
*epinephrine indications resuscitation for TX of acute cardiovascular collapse, subcutaneously for acute bronchospasm
*digoxin aka Lanoxin indication for neonates CHF
*Indomethacin sodium trihydrate aka Indocin hemodynamically significant PDA (indicated by resp distress, continuous murmur, hyperactive precordium, cardiomegaly
Dopamine/Intropin indications correction of hemodynamic imbalances from shock syndrome due to < cardiac function in CHF, trauma, endotoxic septicemia, renal failure and myocardial infarction
*caffeine citrate and theophylline indications TX and management of neonatal apnea, and acute or chronic bronchospasm
*fentanyl citrate used to produce analgesia, sedation and anesthesia during invasive procedures like bronchoscopy
Calcaneus heel bone
TPN aka total parenteral nutrition aka hyperalimentation admin 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 analysis measurement of different species of hemoglobin in a blood sample by determining the amount of infrared light absorbed
*when is an ABG given to a neonate better 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 drawn 1) 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 sites umbilical, 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 fussing drastically changes results, especially CO2
Transillumination light placed under wrist of neonate helps locate artery
*UAC umbilical artery catheter, is the preferred site for obtaining ABG because there is no pain for baby
*How is a suspected PDA verified right radial sample is drawn at the same time as UAC
*what is an easy (non-invasive way to detect a PDA place 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 PaO2 because 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 UAC only used for 3-4 weeks because of clotting and infections, PaO2 may be low if PDA present
What is a good alternative to UAC RAC, radial artery catheter
Why is RAC a good source for ABG preductal flow
Hazards of RAC infection, air emboli, arterial occlusion, infiltration of fluids, nerve damage
Why are arterial punctures so difficult in neonates very small arteries, pain can lead to misleading results
What are the primary complications of an arterial puncture in neonates infection, bleeding, nerve damage, embolism, hematoma
*what are capillary samples used for assessing pH and PaCo2, but not PaO2 because they have mixed venous blood (PaO2 monitoring with pulse ox or transcutaneous monitoring)
*why are capillary samples used less hazardous to pt and more easily obtained than arterial sample
*contraindications of capillary sample posterior curvature of heel, callus developing on heel, fingers of neonates, previous puncture sites, inflamed, swollen or edematous tissue, localized infection
*capillary stick procedure heat heel to 45C for 4-7 mins (no exceptions), ready equipment, wipe, puncture, avoid arteries
*complications of capillary samples puncture 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 is 50-70 mmHg
*PaCO2 norm for a neonate is 35-45 mmHg
What is PaCo2 it 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 pH 7.35-7.45 (7.30 to 7.50 is considered acceptable)
What are the disease states that most commonly cause respiratory acidosis in neonates BPD, 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 neonates mismanagement of ventilator rates or volumes, RDS, stimulation of CNS, hypoxia induced hyperventilation
What are the disease states that most commonly cause metabolic acidosis in neonates hypoxemia 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 neonates excessive 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 is 22-26
Normal BE for neonates + or – 4
how do TCM’s work Clark 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 PDA patent ductus arteriosus, ductus arteriosus fails to close after birth, R-L shunt
S and S of PDA more 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 Ph indicated to assess degree of fetal hypoxia
Normal scalp pH 7.25-7.35
*how much blood does a small preemie have can be as low as 100cc
How does RT know TCM will work check against ABG, if it closely parallels then it can easily be used
why does TCM use heat 3 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 levels because TMC measures tissue O2 too
What is the clinical use of TMC trending of PaO2 in neonate
what is the most important limitation of TCM cannot 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 changed every 2-3 hours to prevent burns
Complications and hazards of TCM burns, 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 capnometry measures exhaled CO2 with spectrophotometric infrared analysis
What are the 2 types of capnography side stream and mainstream
Side stream capnography removes a continuous sample through small tube and carries it to analysis chamber-light weight
what is downside of side stream capnography sample 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 capnography chamber 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 capnography bulky and heavy may cause accidental extubation, chamber causes increased deadspace
IUGR intra uterine growth retard
*Tolazoline aka Priscoline indications TX of persistent pulm hypertension of newborn, use when PaO2 cannot be maintained with FIO2 and or mech vent.
Question Answer
Ovum female 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)
blastomeres daughter cells produced in ovum during rapid cleavage, 2 cells become 4, 4 become 8, etc.
morula blastomeres that have grown enough to become a ball, 16-50 cells, stage of growth that ovum enters uterus
zona pellucida transparent tissue envelope surrounding blastomeres
embryo what 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.
fetus name used during 3rd stage (end of embryonic to birth), organs cont to grow, less susceptible to drugs etc, but still can affect development
neonate birth to end of first month
infant 1 month to 1 year
child pt over 1 year
chorionic villa vascular 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)
choana funnel shaped opening between posterior nares and nasopharynx
choanal atresia congenital abnormality in which membrane or bony occlusions block the choana-caused by nasopharyngeal septum failure to rupture during embryo development
chemoreceptor sensory nerve located in carotid artery, stimulated by chemical (co2-H+), signals central respiratory center to > or < ventilation
cotyledon visible segment of maternal surface of placenta, contains fetal vessels, chorionic villa and intervillous space
blastocyst ovum/embryo stage following morula, ball forms with central cavity filled w/fluid (blastoceale) with outer layer of triphoblast (becomes placenta) and embroblast (becomes embryo)
baroreceptor press sensitive nerve ending found in walls of atria, vena cava, aortic arch and carotid sinus-stretching leads to central reflex causing vasodilation or constriction
amnion membrane covering fetal side of placenta, outer umbilical cord and entire surface of uterus
dichotomy division or separation into two or more parts
ductus arteriosus vascular channel that connects pulm artery to descending aorta in fetal circulation
ductus venosus vascular channel in fetal circulation that passes through liver and connects umbilical vein to inferior vena cava
ectoderm outermost layer of the 3 germ layers, gives rise to nervous system, eyes, ears, epidermis and mucus membranes
endoderm innermost 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
Fertilization union of mail and female gametes (sperm and egg) to form zygote
foramen ovale opening in the septum separating atria in fetal heart
FRC volume of gas in lungs following normal exhalation
Intervillous space space between the chorionic villa(on placenta wall), acts as reservoir for maternal arterial blood, which exchanges nutrients and waste with fetal blood
mesoderm middle of the 3 germ layers of developing embryo, gives rise to bones, connective tissue, muscles, blood, vascular and lymph tissue
oligohydramnios abnormally small amount or absence of amniotic fluid
phosphatidylglycerol (PG) acidic phospholipids found in surfactant-presence in amniotic fluid signals mature lungs
phospholipids compound 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
polyhydramnios condition w/excess amniotic fluid (>2000 mL)
septum primum embryologic structure of developing heart, eventually becomes ventrical septum
sinus venosus embryologic structure in fetal heart eventually becomes inferior and superior vena cava and portion of right atrium
sphingomyelin a type of sphingolipid found in steady quantity in amniotic fluid, S of L/S ratio test (to determine lung maturity)
Lecithin L in L/S ratio test…….aka PC
surfactant combination of lipoproteins found in mature alveoli that reduce surface tension of pulm fluids
trophoblast one of the layers of tissue that forms wall of blastocyst, becomes placenta
truncus arteriosus embryotic tissue of developing heart, becomes aorta and pulm artery
placenta organ 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 are ductus venosus, foramen ovale, ductus arteriosus
Question Answer
Chronic Lung Disease encompasses Wilson-Mikity Syndrome Pulmonary Insufficiency in prematurity Classic BPD The “new” BPD
Other complications of neonatal respiratory care include Retinopathy of Prematurity (ROP) Intraventricular Hemorrhage (IVH)
Chronic Lung disease presents as prematurity need for ventilation/oxygenation
In chronic lung disease diagnosis is required oxygen or mechanical ventilation. Required oxygen at 36wks gestational age.
The pathophysiology of chronic lung disease includes surfactant deficiency/inactivation oxidative stress (o2 toxicity) inflammation/infection mechanical ventilation barotrauma Barotrauma and air block syndromes
The treatment for chronic lung disease is temperature oxygenation surfactant replacement resusscitation and ventilation
Wilson-Mikity Syndrome is also know as pulmonary dysmaturity
Wilson-Mikity syndrome is a disease of functional and structural pulmonary changes seen in premature neonates with no apparent underlying lung disease
The etiology of wilson-mikity syndrome is unkown and linked to low birth weight (<1500g), lung immaturity, maternal bleeding and asphyxia
The pathosphysiology of wilson-mikity syndrome presents 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 are hyperpnea 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 like RDS poor feeding and vomiting CXR: similar to stage 3 and 4 CBD changes
The treatment of wilson-mikity syndrome is support 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 includes premature 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 was 20%
The mortality of CPIP today is 0% with current standards of Care
CBD classic bronchopulmonary displasia “aka” the old bronchopulmonary displasia etiology is unknown but most incidences follow treatment of RDS with mechanical ventilation and oxygen
The pathophysiology of BPD is characterized by thickening of the alveolar membrane, necrosis of the alveolar tissues, and fibrotic changes in the interstitial spaces
air bronchograms appear as fluid 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 of hyperinflation cystic emphysema persistent oxygen requirements may suffer complications from PDA/Sepsis
The pathosphysiology of the new BPD is linked to 5 factors surfactant deficiency/inactivation oxidative stress (oxygen toxicity) inflammation/infection mechanical ventilation (barotrauma) Barotrauma and air block syndromes
In BPD the ABG will show chronic respiratory failure and hypoxemia
BPD signs/symptoms cor pulmonale (right vent. hypertrophy) pulmonary functions: increased minute ventilation requirement, increased airway resistance, decreased lung compliance
The criteria of BPD diagnosis include 36 weeks corrected gestational age need for supplemental 02 or 8wks since birth and still requires supplemental 02
What is the tx of BPD prevention 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 as Retrolental fibroplasia (RLP) (ROP)
ROP is defined as disordered vascularization and fibrovascular changes in retinas or preterm infants
With ROP scar tissue forms behind 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 as periventricular leukomalacia (PLV)
IVH occurs in 26% 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 by trauma or asphyxiation
In cerebeller tissue bleeds it is associated with prematurity
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 bleed neurodevelopmental disability (MR) Posthemorrhagic hydrocephalus (CSF) Vision/Hearing loss contralater himparesis (cerebral palsy) Death
How can IVH be prevented avoid wide fluctuations in BP, Oxygenation, and pH Avoid trendelenburg position
Respiratory distress syndrome is also known as hyaline membrane disease
RDS etiology prematurity 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 with ventilator 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 symptoms RR > 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 RDS CXR is a definitive diagnosis
IN RDS the CXR will show underaerated 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 ventilation pac02 40-50 mmhg, ph >7.25, sa02 88-94% VMS allows permissive hypercapnia; 85%-93%
Transient Tachypnea of the Newborn (TTN) is also known as Type II RDS & Wet lung syndrome
TTN is more common in boys and infants with perinatal asphyxia; also common in C-section delivery
The etiology of TTN is unkown, associated with delayed clearing of fetal lung fluid
TTN Clinical presentation tachypnea, breath sounds-rales, cyanosis, grunting, retractions, nasal flairing
In TTN the ABG will read as mild-moderate hypoxemia, hypercapnia, respiratory acidosis
With TTN the CXR will present as pulmonary 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 diagnosed R/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