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Neonatal
Ch. 31-34 Disease Book
| Question | Answer |
|---|---|
| __________ _________ are the leading causes of admission to the neonatal intensive care unit. | respiratory disorders |
| what is the axiom that is essential to the understanding of respiratory distress of the neonate? | "oxygen is the primary nutrient of the human body" |
| what are the clinical manifestations presented by a baby in EARLY respiratory distress? | lethargy, cyanosis, tachypnea, nasal flaring, expiratory grunting, intercostal/substernal retractions, tachycardia, hypertension, acute alveolar hyperventilation w/ hypoxemia |
| what are the clinical manifestations presented by a baby in LATE respiratory distress? | bradypnea, gasping respirations, apnea, bradycardia, hypotension, acute ventilatory failure w/ both CO2 retention and hypoxemia |
| the compliance of the infant's thorax is ____; however, the respiratory disorders make compliance io the lungs ____. | high; low |
| what must the infant do in an effort to offset the decreased lung compliance? | generate more negative intrapleural pressures during inspiration |
| what does this condition cause? | 1. retraction of soft tissues b/t ribs 2. substernal retractions/protruding abdominal area during inspiration (seesaw) 3. cyanosis in thoracic/abdominal areas |
| what is the cause behind nasal flaring during respiratory distress? | facial reflex to facilitate the movement of gas in the TBT |
| what is the muscle responsible for this movement? | dilator naris (originates from maxilla, inserts into ala of the nose) |
| what is the mechanism behind nasal flaring? | dilator naris pulls alae laterally and wides the nasal aperture (more room for gas) |
| what does expiratory grunting do to help the infant during RDS? | generates high positive pressure in the alveoli which counteracts the hypoventilation |
| how does an expiratory grunt occur? | epiglottis abruptly opens, gas rushes past vocal cords and produces grunt or cry |
| what is apnea of prematurity described as? | cycles of short pauses in respiration followed by an increased breathing rate |
| what is apnea of prematurity defined as? | cessation of breathing effort >20 secs in baby <37 wks (causes bradycardia, cyanosis, or both) |
| about ___% of premature babies weighing less than ____ g experience severe apnea. more than ___% of infants weighing more than ____ g manifest severe apnea. | 75, 1250; 25, 1500 |
| why are premature infants believed to be susceptible to apneic episodes? | immature functioning of chemoreceptors, receptors in airways, and CNS |
| what else is thought to play an important role in causing sleep apnea? | rapid eye movement sleep |
| what are the control of ventilation factors that trigger the apnea? | REM sleep, decreased hypoxic/hypercapnic response, ondine's curse (idiopathic alveolar hypoventilation) |
| what are the reflex stimulation conditions that trigger apnea? | suctioning of nasopharynx/trachea, laryngeal stimulation, bowel movements, hiccups |
| what are the environmental conditions and neurologic disorders that trigger apnea? | ambient temp changes; seizures, intracranial hemorrhage, meningitis |
| what are the drug depression and respiratory diseases that trigger apnea? | sedatives, analgesics, prostaglandins; RDS, pneumona, TTN, MAS, BPD, DH |
| what are the cardiac disorders and systemic processes that trigger apnea? | patent DA, CHF, R-L intracardiac shunt; hypothermia, hypoglycemia, hyponatremia, hypocalcemia, sepsis |
| what is the body position and anatomic abnormalities that trigger apnea? | head flexion; micrognathia, choanal atresia, macroglossia |
| when is persistant pulmonary hypertension commonly seen in infants? | w/ underlying resp disorder such as pneumonia, MAS, or RDS |
| what is PPHN caused in part by? | reflex pulmonary vasoconstriction, activated by myriad stimuli (alv hypoxia, hypercapnia, dec pH) |
| after birth, approximately ___% of the PVR normally decreases within the first 24 hours in response to what? | 80; increased PaO2/pH, lung expansion, release of vasoactive substances |
| why does the PVR stay high in infants with PPHN? what might appear b/c of the high PVR? | pulmonary vascular hyperreactivity to irritating stimuli; cardiomegaly |
| when does PPHN usually appear and with what? | first 12 hours of life; cyanosis, tachypnea, intercostal retractions, nasal flare, grunt |
| what do the ABGs show? | shunt physiology (low PaO2 that is refractory to O2) |
| what are the maternal factors and cardiovascular factors associated with PPHN? | diabetes, C-section, hypoxia; systemic hypotension, congenital heart disease, shock |
| what are the hematologic factors associated with PPHN? | increased hematocrit, septicemia, maternal-fetal blood loss, acute blood loss |
| what are the respiratory diseases and fetal factors associated with PPHN? | MAS, RDS, pneumonia; intrauterine stress, hypoxia, dec pH, placental vascular abnormalities |
| what are the other factors associated with PPHN? | CNS disorders, hypoglycemia, hypocalcemia, neuromuscular disorders |
| what ABGs are commonly seen in newborn babies with pulmonary disorders? | acute alveolar hyperventilation w/ hypoxemia and acute ventilatory failure |
| what are the 3 major mechanisms responsible for the decreased PaO2 observed in the disorders of the newborn? | 1. pulmonary shunting and venous admixture 2. PPHN 3. infant fatigue |
| what is the apgar score? | rating system for the rapid identification of infants requireing immediate intervention or NICU |
| when is the apgar evaluation performed? | 1 minute after birth and again 5 minutes later |
| what are the 5 factors that are evaluated from a score of 0-2? | heart rate, respiratory effort, muscle tone, reflex irritability, color |
| what does the scoring system represent? | 0-3: severe distress, 4-6: moderate distress, 7-10: absence of difficulty in adjusting |
| what does a low 1-minute score require? what is required for a remaining low score at 5 minutes? | immediate intervention, O2, oral/nasal suctioning; NICU, CPAP, umbilical cath, MV |
| what is MAS? | clinical entity seen primarily in full-term or postterm infants w/ hypoxemia prenatally or during birth |
| what is meconium? | material that collects in the intestine of fetus and forms first stools of newborn; odorless, thick, sticky, blackish green |
| what are the 3 complications of MAS? | upper airway obstruction at birth, chemical pneumonitis, pulmonary arterial vasoconstriction and vasospasm (pulm HTN) |
| airways that are partially obstructed by meconium are affected by what? and what is this? | "ball-valve" effect; air can enter but cannot readily leave the distal airways and alveoli |
| in mild conditions meconium can be found where? in severe conditions meconium can be found where at birth? | smaller airways; distal airways |
| what can this condition lead to? then leads to what? | air trapping and alveolar hyperinflation; alveolar rupture and air leak syndromes |
| what do totally obstructed airways lead to and cause? | alveolar shrinkage and atelectasis; increased FRC and decrease in air flow during exhalation |
| what is chemical pneumonitis? what does it commonly lead too? | acute inflammatory reaction & edema of bronchial mucosa and alveolar epithelium; excessive bronchial secretions/alveolar consolidation |
| when does RDS complicate MAS? | when it interferes with alveolar pulmonary surfactant production |
| what are 3 major pathologic or structural changes associated with MAS? | 1. excessive bronchial secretions 2. alveolar consolidation 3. pulmonary HTN |
| how many infants are diagnosed with MAS annually? what is the overall mortality rate? | 10,000-15,000; 4% |
| what does fetal hypoxemia cause? | vagal response that relaxes anal sphincter tone and allows meconium into amniotic fluid |
| MAS is rarely seen in infants younger than ___ weeks. ___ weeks gestation postterm infants are especially at risk of MAS. | 36; 42 |
| what other infants are at risk of MAS? | small for gestational age, breech position, mothers are toxemic, hypertensive, obese |
| what are the vital signs for MAS? what are te other data obtained at bedside? | tachypnea, tachycardia, HTN, apnea; expiratory grunting, cyanosis |
| what are the chest assessment findings? | wheezes, rhonchi, crackles |
| what is the common general appearance for MAS? | meconium staining on skin, nails, umbilical cord, wrinkles and creases in skin; barrel chest |
| what is the mild-moderate ABG? severe ABG? | acute alveolar hyperventilation w/ hypoxemia; acute ventilatory failure w/ hypoxemia |
| what is shown on CXR if alveolar atelectasis and consolidation is present? what if partial airway obstruction, air trapping, and alveolar hyperinflation are present? | irregular densities; hyperlucent and diaphragm depressed |
| what is MAS difficult to differentiate from on a CXR? | pneumonia |
| what should be done if the infant is not actively breathing or crying immediately after delivery? | intubation and suction upper airways |
| what should NOT be administered until a thorough suctioning of the upper airway has been completed? | positive-pressure ventilation |
| what should be done after infant is stabilized in NICU? | vigourous bronchial hygiene; O2 therapy, and MV in severe cases |
| _________ are given for chemical pneumonitis. | antibiotics |
| meconium-stained amniotic fluid is seen in approximately ___% of all births. | 10 |
| within __-__ hours after birth, TTN produces clinical signs very similar to those associated with the early stages of ____. | 4-6; RDS |
| what does the infant with TTN have? | delay in pulmonary fluid absorption by lymphatic system and pulmonary capillaries |
| when do the anatomic alterations of the lungs associated with TTN begin to resolve? | 48-72 hours after birth |
| what are 3 major pathologic or structural changes associated with TTN? | 1. air trapping/alveolar hyperinflation 2. pulm capillary congestion 3. interstitial edema |
| TTN affects __-__% of all newborns and most often seen in ________ infants. | 1-2%; full-term |
| what are the risk factors for TTN? | elective C-section, excessive fluids to mother during labor, males, macrosomia |
| what might the infants history include with TTN? | maternal analgesia or anesthesia during labor/delivery or intrauterine hypoxia |
| what is TTN also commonly associated with? | maternal bleeding, maternal diabetes, prolapsed cord; very small infants |
| what is it believed that TTN results from? | delayed absorption of fetal lung fluid |
| how are infants with TTN at birth? | lethargic, results in depressed cough effort and accumulation of airway secretions and mucus |
| what develops after the first few hours and what are the early clinical manifestations? | RDS; tachypnea (80-120), retractions, nasal flaring, grunting, cyanosis |
| what is the hallmark clinical manifestation of TTN? | rapid and shallow breathing |
| what are the clinical signs of TTN? | tachypnea, tachycardia, HTN, intercostal retractions, expiratory grunting, cyanosis |
| what are the chest assessment findings? | wheezes, rhonchi, crackles |
| what is the mild-moderate ABG? severe ABG? | acute alveolar hyperventilation w/ hypoxemia; acute ventilatory failure w/ hypoxemia |
| what does the CXR appear initially? and what are the signs over the next 4-6 hours? | normal; perihilar streaking, air bronchograms, fluid in interlobular fissures |
| what are associated on CXR with air trapping and hyperinflation? | peripheral hyperlucency, flattened diaphragms, bulging intercostal spaces; patches of infiltrates |
| what does the treatment of TTN consist mostly of? | proper stabilization, close monitoring, and frequent and thorough evaluation |
| what are the resp. care treatment protocols? | O2 therapy, bronchopulmonary hygiene, lung expansion therapy, MV (rare) |
| what is the most common cause of respiratory failure in the preterm infant? | RDS |
| what does respiratory distress characterize? | an immature lung disorder in a preterm infant caused by in |
| what is RDS a major cause of? | morbidity and mortality in the premature infant born after <37 weeks' gestation |
| what has greatly improved the clinical course and reduced the morbidity and mortality rates? | introduction of exogenous surfactant therapy |
| what are the lungs like in RDS? | dark red and liver-like |
| what type of lung disorder is RDS? | restrictive |
| what happens if pulmonary hypoperfusion (worsens hypoxemia) does not resolve within 24 hours? | shunting will begin to flow from left to right through the patent ductus arteriosus |
| what are 3 major pathologic or structural changes associated with RDS? | 1.alveolar consolidation 2. intraalveolar hyaline membrane 3. atelectasis |
| what are the 2 reasons it is believed that the early stages of RDS develop from? | 1. pulm.surfactant abnormality or deficiency 2. pulm. hypoperfusion evoked by hypoxia |
| what is the 7 steps to the development to RDS? | 1. alveolar collapse 2. incr WOB 3. decr PAO2 4. pulm vasoconstriction 5. lung hypoperfusion 6. lung ischemia, decr lung metabolism 7. pulm surfactant decr even more |
| how many cases of RDS occur annually in the YS? and what is it the leading cause of? | 30,000; death in preterm infants |
| about ___% of the neonates born at ___ to ___ weeks' gestation develop RDS. about ___% of the babies born at ___ to ___ weeks' gestation develop RDS. | 50; 26, 28; 25; 30, 31 |
| RDS occurs more often in _____ babies and is usually more severe than in ______ babies. why is this? | male; female; increased circulating androgens in males (slows maturity of lungs) |
| what does the delayed lung maturation result in? | immature alveolar type II cells (granular pneumocytes) and a decr pulm surfactant production |
| when is RDS also commonly seen? | diabetic mothers, white preterm babies compared w/ black, C-section babies |
| what is RDS also associated with? | low birth weight (1000-1500 g), multiple births, prenatal asphyxia, prolonged labor, maternal bleeding, second-born twins |
| what are the 3 primary tests to determine lung maturity? | 1. L/S ratio 2. presence of phosphatidylglycerol (PG) 3. surfactant/albumin ratio |
| when is an L:S ratio normal and when is it likely RDS will develop? | 2:1; 1:1 |
| Lethicin is the _____ most abundant phospholipid in surfactant, PG is the ______. | first; second |
| when is their a chance for RDS without PG? | L:S ratio of <2:1 and a lack of PG |
| when does an S:A ratio indicate immature lungs, uncertain lung maturity, and adequate lung maturity? | <35; 35-55; >55 |
| what are the clinical findings for RDS? | tachypnea, tachycardia, hypertension, apnea, expiratory grunting, cyanosis |
| what is the respiratory pattern for RDS? | "hard, fast, and deep breathing" |
| what are the chest assessment findings? | bronchial (or harsh) breath sounds, fine crackles |
| what is the mild-moderate ABG? severe ABG? | acute alveolar hyperventilation w/ hypoxemia; acute ventilatory failure w/ hypoxemia |
| what is found on the CXR? | increased opacity (ground-glass appearance) - more severe RDS, whiter the x-ray image |
| what is the treatment of choice for RDS? | CPAP |
| why does CPAP work well with these patients? | 1. increases FRC 2. decreases WOB 3. works to increase the PaO2 |
| what is the normal PaO2 for newborn infants? | 40-70 mmHg |
| what should be specially be watched with an infant with RDS? | thermal environment |
| what are the 3 exogenous surfactant preparations commonly administered? | beractant (survanta), calfactant (infasurf), poractant alfa (curosurf) |
| what are the resp care treatment protocols? | O2 therapy, lung expansion therapy, MV (prolonged as long as possible) |
Created by:
christa_2008
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