If you’re ready to learn about the Diseases of Full-term infants, then this is the study guide for you. As you will see below, this post is loaded with practice questions that are designed to teach you everything you need to know about the different diseases of full-term infants.
As a Respiratory Therapist is information that you will definitely need to know, especially if you’re potentially interested in working in a NICU someday. So let’s go ahead and dive right in, shall we?
Disease of Full-term Infants Practice Questions:
1. What is the most common underlying diagnosis of persistent pulmonary hypertension of the newborn?
Meconium aspiration syndrome.
2. A change from fetal circulation to adult circulation requires what to occur?
A drop in PVR and a significant increase in SVR.
3. What change in the blood gas, sensed by chemoreceptors in the aorta and carotid artery, causes a chemical message to be sent to the brain stem to increase ventilation?
A drop in PaO2.
4. Which of the following describes cardiomegaly in infants?
A heart silhouette occupying >60% of the thoracic diameter.
5. Which of the following are considered proper management of persistent pulmonary hypertension of the newborn?
Decrease pulmonary vascular resistance and Minimize ventilator-induced lung injury.
6. What is the most frequently used pulmonary vasodilator for neonates?
Inhaled nitric oxide.
7. Complications of extracorporeal life support include which of the following?
IVH, Cardia dysrhythmias, Infection, and Bleeding.
8. What are the advantages of using venovenous ECMO support?
Spares the carotid artery and Potential emboli remain on the venous side of the patient.
9. What factors show an increased risk for meconium aspiration syndrome?
Maternal, hypertension, and Fetal distress.
10. Which of the following is NOT an indication for intubation and ventilation in neonates with meconium aspiration syndrome?
11, What is Persistent Pulmonary Hypertension of the Newborn (PPHN)?
A syndrome with severe hypoxemia and high pulmonary artery pressures that occurs when the pulmonary vascular resistance (PVR), normally high in utero, fails to decrease at birth.
12. When does PPHN usually present?
At birth or shortly after.
13. What is PPHN characterized by?
By a failure to establish adequate pulmonary and systemic oxygenation.
14. What happens if PPHN goes without treatment?
It can cause severe cardiac dysfunction, multiorgan dysfunction, and death.
15. Where is a PDA located and what issue does it cause?
It is in the aorta and pulmonary artery and causes a lack of O2 to get to the rest of the body because it is not being picked up by the lungs.
16. What happens if normal pulmonary vasculature is impeded?
It can result in sustained high pulmonary artery pressure.
17. What is the result of persistent PPHN?
Hypoxemia and cyanosis.
18. What is preductal SPO2?
Oxygen saturation is taken from an area where arterial blood supply comes prior to ductus arteriosus. Primarily the right hand.
19. What is post ductal SPO2?
Oxygen saturation taken from an area where arterial blood supply comes after ductus arteriosus which is typically placed on the lower limbs.
20. When is PPHN suspected?
When the preductal SPO2 and the post ductal SPO2 shows greater than a 10% difference.
21. What does the ABG show in PPHN?
When PaO2 has a 15mm difference between pre and post ductal.
22. What is the oxygen index equation (OI)?
Paw x FIO2 x 100/PaO2.
23. What happens when there is a higher OI number?
It worsens the patient’s ability to oxygenate despite high levels of support.
24. What is an Oxygen Index greater than 20 an indication for?
Inhaled Nitric Oxide (iNO).
25. What is an Oxygen Index greater than 40 an indication for?
Extracorporeal Membrane Oxygenation (ECMO).
26. What is the management and treatment for PPHN?
O2 therapy (maintain PaO2 90-120), conventional mechanical ventilation (CMV), HFOV when CMV pressures or rates are too high, pulmonary vasodilators such as iNO
maintain HCT at 35% to 45%, and ECMO for pts who are unresponsive to above therapeutic measures w an OI >40.
27. What is nitric oxide?
It Is a substance produced by nearly every cell and organ in the human body.
28. What are the functions of nitric oxide?
Vasodilation, platelet inhibition, immune regulation, enzyme regulation
29. What is nitric oxides main use in the medical environment?
For smooth muscle relaxation of the pulmonary vascular bed.
30. What does inhaled nitric oxide do?
Selectively dilates the pulmonary vasculature adjacent to open lung units.
31. What is general usage for iNO?
A failure of ventilation to restore normal PVR.
32. Why do we want vasodilation?
Because everything is constricted.
33. iNO only works where?
It only works where the blood flow goes it has a short 1/2 life and only works w open alveoli.
34. What is the recommended starting dose for nitric oxide?
35. How long is the half-life of iNO?
Less than 5 seconds.
36. What does iNO combine with?
Hb and methemoglobinemia and nitrate.
37. What is a positive response to iNO therapy?
It is evident by an increase in oxygenation (SpO2 and PaO2) as well as a decrease in the preductal and postductal SpO2 gradient.
38. What are the 2 most common side effects of iNO?
Rebound hypoxemia and methemoglobinemia.
39. How do you prevent rebound hypoxemia?
iNO weaning is done in increments which avoids abrupt discontinuation of iNO.
40. What problems cause a need for iNO?
Swallowed meconium, severe resp distress, or something that has caused.
41. What will not benefit from iNO?
Atelectatic or fluid-filled lungs due to no uptake of gas.
42. When will iNO have improved outcomes?
If more reaches capillary endothelium by opening collapsed alveoli which will increase the degree of vasodilation.
43. What is the responsiveness to iNO enhanced by?
The use of PEEP and high-frequency ventilation.
44. What shows responsiveness after using iNO?
46. Where is iNO bled into the vent circuit?
Before the humidifier.
47. How do you analyze iNO and NO2 concentrations?
Gas is read at the sample line placed prior to the patient-circuit interface.
48. What happens when nitric oxide is combined with oxygen
It produces NO2 which is toxic.
49. What factors influence NO2?
Oxygen concentration, NO concentration and the time they are in contact.
50. Who is at highest risk of NO2?
Those that are receiving high O2 concentrations and low ventilator flow rates.
51. What is extracorporeal membrane oxygenation (ECMO)?
A technique used to support the heart and/or lungs externally when the native heart and/or lungs are no longer able to provide adequate support.
52. What is the lung goal when using ECMO?
To prevent nitrogenic damage caused by high mean airway pressure.
53. What is the heart goal when using ECMO?
To prevent the use of high doses of toxic medications to keep the heart functioning.
54. What is the patient criteria for using ECMO?
55. What are the 2 types of ECMO support?
Venovenous that take blood out of right atrium and put back there and venoarterial which take blood out of right atrium and put back into the aorta.
56. What can be done with the ventilator once ECMO has been initiated and the patient is stabilized?
Ventilator settings can be reduced.
57. What kind of vent settings is appropriate when ECMO is providing respiratory support?
PIP 20, PEEP 10, RR 10, and FiO2 30%-40%.
58. What does ECMO stand for?
Extracorporeal life support (ECLS).
59. What is the purpose of ECMO?
To minimize the ventilation support to avoid damage to the lungs while allowing disease process to run its course.
60. What is the major pathophysiologic condition that ECMO treats?
Persistent pulmonary hypertension of the newborn (PPHN).
61. What neonatal conditions can hypoxic states result from?
Meconium aspiration syndrome, diaphragmatic hernia, sepsis, and RDS.
62. What does ECMO interrupt?
The cycle of PPHN minimizes the need for excessive ventilation, while the underlying condition is resolved.
63. What is meconium aspiration syndrome?
Respiratory distress occurring soon after delivery in a meconium-stained infant.
64. Who are mostly affected by MAS (meconium aspiration syndrome)?
Term and post-term infants.
65. What are the factors associated with increased risk of MAS?
Post-term pregnancy (greater than 42 weeks), preeclampsia or eclampsia, maternal hypertension, maternal diabetes, intrauterine growth retardation, abnormal biophysical profile, oligohydramnios, maternal heavy smoking, abnormal fetal HR, the presence of fetal distress, low 5 min Apgar
Ethnicity, and home birth.
66. Meconium is the byproduct of what?
Metabolic waste of gestation.
67. What is meconium like?
Sticky, viscous, consistency like tar, odorless and almost sterile.
68. What happens when amniotic fluid is stained with meconium?
Gasping or deep irregular respirations can result in aspiration.
69. What does meconium inhibit?
Surfactant function and is directly toxic to the pulmonary epithelium.
70. What are the 3 levels of meconium airway obstruction?
Partial obstruction, ball valve obstruction, and total obstruction.
71. What is partial obstruction?
It allows some air passage into and out of the alveoli.
72. What is the ball valve obstruction?
It allows air in the alveoli during inspiration but closes during expiration. causes air trapping.
73. What is total obstruction?
It will not allow air in during inhalation or exhalation and leads to atelectasis and hypoventilation.
74. What are symptoms of meconium aspiration?
Abnormal respiratory rate may manifest as tachypnea, but w fatigue may deteriorate to apnea. Increase resp effort, grunting, nasal flaring and retractions. Cyanosis and auscultation may reveal diminished or unequal breath sounds, rales, rhonchi or wheezing. Increased AP diameter of the chest if the newborn has air trapping. Asymmetry of the chest is also common if air leaks develop.
75. What is the management and treatment of Meconium Aspiration Syndrome (MAS)?
Supplemental O2 via nasal cannula to MV, HFOV, and ECMO.
76. What is Transient Tachypnea of the Newborn (TTN)?
A condition of
77. What is TTN caused by?
Failure to clear fetal lung fluid prior to delivery.
78. When does TTN resolved by?
Within 48 to 72 hours of life.
79. What are the main risk factors of TTN?
Delivery via C-section, macrosomia (birth weight above the 90th percentile), maternal asthma, maternal diabetes, and male gender.
80. What are the clinical manifestation of TTN?
Respiratory distress within 6 hours of birth, RR >60, grunting, nasal flaring, and retractions.
81. What is the management and treatment of TTN?
O2 therapy: O2 hood or nasal cannula connected to an air oxygen blender to maintain O2 sat 90-96, CPAP 4-6 to resolve moderate respiratory distress, withholding of enteral feeds, administration of intravenous fluids, administration of antibiotics, and of thermoregulation (keep warm).
So there you have it. That wraps up our study guide about the diseases of full-term infants. I hope this information was helpful and I hope you can use these practice questions as tools to help you ace your exams. Thank you for much for reading and as always, breathe easy my friend.