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Ch. 31-34 Disease Book

__________ _________ 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