Module 3: Sarah Flashcards
What are some multi-system effects of prematurity?
Intraventricular Hemorrhage (IVH), Patent Ductus Arteriosus (PDA), Respiratory Distress Syndrome (RDS), Necrotizing Enterocolitis (NEC), Acute Kidney Injury (AKI), sepsis, hyperbilirubinemia, hypothermia, hypoglycemia, and apnea.
What is the most common cause of respiratory distress in preterm infants?
RDS
Give examples of why the respiratory system of the preterm newborn is immature using each of the following as a guide:
lung development
The respiratory system of the newborn develops relatively late in gestation compared with other systems. Therefore, anatomy compatible with life (i.e., capable of gas exchange at the alveolar level) must exist for the newborn to be viable.
respiratory muscles
The infant must have a way to move air in and out of the lungs (pumping system). Infants do this with their chest wall muscles, diaphragm, and accessory respiratory muscles. The neonate, full term and preterm, has a circular, compliant rib cage that makes the diaphragm less effective and generally achieves less negative pressure for indrawing air. The chest wall and respiratory accessory muscles are small and tire easily. This is even more so for premature infants.
surfactant
In addition to problems with lung anatomy (in prems) and an inefficient pumping system (in neonates), the newborn needs surfactant to keep the alveoli open. Surfactant works by reducing surface tension within alveoli and thereby making the lungs easier to inflate. Remember the balloon analogy …it’s easier to inflate a balloon that has a bit of air in it. If surfactant is not present in sufficient quantities, the infant’s alveoli collapse with every exhalation (atelectasis). This makes every breath as hard as the first.
surface tension
If surfactant is insufficient and the surface tension increases enough to cause atelectasis, then lung resistance is increased. This is because lung volume is decreased from the alveolar collapse. This means that for lung expansion to happen, increased pressure is needed. The neonate is ill equipped to do this due to some of the factors described above. Clinically, the result is signs and symptoms of respiratory distress.
resistance, compliance, elasticity
Resistance, compliance, and elasticity are all terms used to describe the ease of lung distensibility. Increased resistance, decreased compliance, and decreased elasticity would all make the lungs more difficult to inflate. All of this increases the work of breathing for the infant, who will surely soon tire.
Many neonatal diseases, including many with nonpulmonary origins, may manifest with signs of respiratory distress. What does this statement mean?
This statement means that, even if you have a 12-hour old prem, you can’t just assume RDS from a respiratory distress picture. Respiratory distress is a set of symptoms from an underlying problem or disorder which requires investigation. There are many causes of respiratory distress. Respiratory Distress Syndrome is just one of the common causes of respiratory distress for premature infants.
Name other pulmonary disorders that may present with respiratory distress in preterm infants.
pneumonia transient tachypnea of the newborn air leak pulmonary edema hemorrhage hypoplastic lung congenital diaphragmatic hernia (CDH)
Name other non-pulmonary disorders that may present with respiratory distress in preterm infants.
necrotizing enterocolitis other abdominal conditions sepsis CNS depression congenital heart disease (CHD) anemia shock
Describe and explain the pathophysiology of Respiratory Distress Syndrome (RDS). How is RDS different from respiratory distress.
Lack of type II alveolar cells in the premature infant and the corresponding lack of surfactant is the major cause of RDS. Other contributing factors are poorly developed/few units of gas exchange and increased distance between alveolar-capillary units due to immature pulmonary vasculature. In term infants, asphyxia and maternal diabetes can cause decreased surfactant production. The infant’s “limited” respiratory system discussed in question 1 means that compensation for this problem is often inadequate.
Alveoli collapse due to increased surface tension. Hypercarbia, hypoxia, and respiratory acidosis result. Pulmonary vasoconstriction and worsening mixed acidosis occur. Intervention is aimed at improving oxygenation/ventilation through mechanical ventilation and artificial surfactant. Recovery is usually seen at around 72 hours when type II cells are regenerated and surfactant produced. This is the clinical picture of RDS. The clinical picture of RDS will include respiratory distress, which is a response to a variety of causative factors, as outlined in the above questions.
Based on what you have learned about respiratory distress and RDS, and what you know about Sarah so far, what further assessment data would you collect?
The missing data could be obtained by asking the following questions:
Is Sarah AGA, SGA, or LGA?
What is her HR? Her pulses? Blood pressure?
What is her temperature?
What are her blood gases? (We only know her oxygen saturation.)
What is her blood sugar?
Is there a history of infection? What is Brooke’s temperature?
Are there other pieces of information from the pregnancy history that might be relevant?
Is the gestational age accurate? Could Sarah be more preterm than 34 weeks?
What are your priorities regarding nursing care at this point?
- maintain airway and breathing
- closely monitor FiO2, SpO2, HR, RR, and BP using appropriate monitor
- maintain oxygen saturation 88–95%
- provide warmth
- provide glucose and fluid. Will you feed Sarah? If not, how will you provide glucose and fluid?
- provide developmentally supportive care
What about developmentally supportive care? Is it a priority? Should Selina incorporate developmentally supportive care principles into her care of Sarah?
Developmentally supportive care is always a priority. Every intervention should be conducted with the principles of developmentally supportive care in mind. Developmentally supportive care is not done in addition to other care; rather, it is an integral part of all care.
What about family-centered care? How might Brooke and Matt be feeling? What do you think about the way that Selina and Terry interacted with Matt and Brooke in the delivery room?
Familycentered care is not about using a set of pre-established rules to provide care. It is about putting Brooke and Matt in the center of the picture, working to establish a partnership with them, and providing care and making decisions which reflect their individual needs.
Hypoxia
a deficiency in the amount of oxygen reaching the tissues
Hypoxemia
a deficiency in the amount of oxygen in the blood
Early Responses to Hypoxia
tachypnea
tachycardia
pallor and mottling
air hunger
Late Responses to Hypoxia
apnea
bradycardia
cyanosis
lethargy
Early responses to hypoxia suggest efforts to compensate. Specifically:
- tachypnea reflects an infant’s efforts to increase oxygen intake
- tachycardia reflects efforts to increase cardiac output, thereby increasing delivery of oxygen to cells
- pallor and mottling reflect redistribution of blood away from non-vital organ such as skin, toward vital organs such as the heart and brain. Other organs that receive less blood are: skin, skeletal muscles, liver, lungs, kidneys, and gut (often referred to as the “diving reflex”)
- air hunger reflects efforts to increase oxygen intake
Infants, unlike adults and older children, do not often demonstrate early responses to hypoxia for very long before they begin to decompensate and show late responses. Specifically:
-apnea reflects central nervous system hypoxia and depression
-bradycardia reflects cardiac hypoxia
-cyanosis reflects increased amounts of deoxygenated hemoglobin reaching the cells
l-ethargy reflects generalized hypoxia, central nervous system depression, and tiring
-Understanding early signs of hypoxia and respiratory distress are the key to preventing respiratory failure.
Assessment of Hypoxia
Assessment of oxygenation includes monitoring for early and late signs of hypoxia. Respiratory rates, heart rates, skin color, and level of consciousness and activity all reflect how well an infant is oxygenated.
Hypoxemia (low blood oxygen) can be assessed by looking at pO2 and SaO2 saturation. Oxygen is carried in blood in two ways:
-dissolved
accounts for only 2–3% of the total oxygen content of blood
It is measured by pO2
pO2 values, arterial = 50–80, capillary = 40–60
Arterial pO2 values are more accurate than capillary pO2 values
-attached to hemoglobin
accounts for 97–98% of the total oxygen content of blood
is measured by SaO2 via pulse oximetry
Assessment
Pulse oximetry
a way of assessing oxygenation
non-invasive, continuous, reliable, and easy to use
a mainstay in the management of respiratory distress
tells us about the oxygen attached to hemoglobin which is the bulk of the oxygen available
measures the extent to which hemoglobin is saturated with oxygen molecules
pO2 (partial pressure of oxygen)
is a measurement of the amount of oxygen dissolved in the blood done by a capillary or arterial blood sample
Hemoglobin
Anemia (decreased hemoglobin) and polycythemia (excess hemoglobin) affect oxygen saturation interpretation.
Consider this:
There are two infants:
one is anemic (Hgb = 100)
one is polycythemic (Hgb = 200)
both infants are showing oxygen saturations of 90%
What the 90% saturation value means is that of the hemoglobin that each infant has, 90% of it is saturated with oxygen.
Is 90% of a hemoglobin of 100 the same as 90% of a hemoglobin of 200?
Clearly the infant who is polycythemic is carrying more oxygen than the infant who is anemic, even though both show pulse oximeter readings of 90%.
What this means is that whenever you are using pulse oximetry to assess oxygenation, you need to be aware of an infant’s hemoglobin. If it is normal, your oximeter readings are valid. If the hemoglobin is elevated, oximeter readings are falsely low. If the hemoglobin is low, oximeter readings are falsely high.
Describe the two ways that oxygen is transported in the blood and how each is measured.
Oxygen is transported in the blood in two ways:
dissolved in plasma — measured as pO2, by blood gas analysis, 2–3% of O2 is carried this way
bound to hemoglobin — measured as oxygen saturation, by pulse oximetry, 97–98% of O2 is carried this way