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Peri test 3
WilliamWallace Peri test 3
| 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 |
Created by:
williamwallace
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