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Peri test 3

WilliamWallace Peri test 3

QuestionAnswer
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
Created by: williamwallace