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Apnea of Prematurity and BPD Flashcards

1
Q

Premature infants and Periodic Respirations

A

Premature infants will have periodic respiration which comprise of sequential short apneic episode of 5-10 seconds followed by 10-15 seconds of rapid respirations

Apneic spells are abnormal when they last longer than 15 seconds or are associated with cyanosis, pallor, hypotonia, or bradycardia

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2
Q

Central Apnea

A

If no effort to breathe occurs during a apnea spell then it is known as a central apnea

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3
Q

Obstructive Apnea

A

If there is breathing effort but an obstruction is preventing the airflow than it is known as an obstructive apnea

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4
Q

Mixed Apnea

A

Mixed apnea is a combination of the central and obstructive types that start as obstructive and then will develop into being central

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5
Q

Primary Apnea

A

Apnea and bradycardia where the baby recovers with tactile stimulation

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6
Q

Secondary Apnea

A

Apnea and Bradycardia, does not recover with tactile stimulation, requires PPV to recover

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7
Q

What is babies respond to CO2 in babies

A

When there is an increase in CO2 babies will slow down their breathing and take bigger breaths to try and compensate

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8
Q

Premature Infants and Control of Respiration

A

Premature infants have immature control of respiratory drive in response to O2 and carbon dioxide (CO2).

In mature animals, an increase in alveolar PaCO2 elicits an increase in VT and respiratory rate. A decrease in FiO2 below room air also triggers an increase in VT.

In premature animals, an increase in PaCO2 temporarily increases VT but does not increase respiratory rate. A decrease in FiO2 below room air decreases VT and respiratory rate. This effect can lead to apnea in a premature infant.

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9
Q

External causes of apnea

A

Temperature, suction, vagal stimulation

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10
Q

Apneas can Lead to

A

Apneas can lead to bradycardia, arrythmias, and respiratory arrest

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11
Q

Frequent Apneas can lead to

A

Frequent apneas can lead to cerebral hypoxia and ischemic brain injury

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12
Q

Clinical Manifestation of Apnea

A

Snoring, choking, gasping
Cyanosis
Bradycardia
Hypoxia

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13
Q

Apnea that is secondary to prematurity should be treated with

A

methylxanthines, especially theophylline and caffeine.

These agents stimulate the central nervous system and increase the infant’s responsiveness to CO2.

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14
Q

CPAP for Apnea

A

CPAP also can be used to manage infant apnea.
CPAP probably increases FRC and improves arterial partial pressure of oxygen (PaO2) and PaCO2. CPAP may stimulate vagal receptors in the lung, increasing the output of the brainstem respiratory centers. Severe or recurrent apnea that is unresponsive to these interventions may necessitate mechanical ventilatory support.

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15
Q

Resolution of Apnea of prematurity

A

Apneic spells begin to disappear by weeks 37 to 44 of postmenstrual age with no apparent long-term effects. Infants who have apnea of prematurity are not at higher risk for sudden infant death syndrome (SIDS) than other infants.

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16
Q

bronchopulmonary dysplasia (BPD).

A

Infants, especially preterm infants, with severe respiratory failure in the first few weeks of life may develop a chronic pulmonary condition called bronchopulmonary dysplasia (BPD).

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17
Q

4 factors in BPD Pathogenesis

A

Lung immaturity
Respiratory failure
Oxygen supplementation
Mechanical ventilation

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18
Q

bpd vs rds

A

BPD IS an obstructive disease and RDS is a restrictive disease

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19
Q

The New BPD Diagnosis Criteria

A

The Diagnosis of bPD is based on how long the baby need oxygen and how much oxygen is needed

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20
Q

initiatin Fators in bPD

A

• The initiating factors are related to atelectrauma (lung collapse) and volutrauma (large tidal volume [VT]). Factors such as hyperoxia and hypoxia, mechanical forces, vascular maldevelopment, inflammation, nutrition, and genetics contribute to the abnormal development of the lung and lead to BPD.

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21
Q

Atelectrauma

A

Atelectrauma is a term coined to describe loss of alveolar volume that is both a result and a cause of lung injury. Atelectrauma leads to derecuitment (e.g., areas of alveolar collapse) of the lung.

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22
Q

Volutrauma

A

o Volutrauma is the term used to describe local overinflation (and stretch) of airways and alveoli. Volutrauma leads to damage to airways, pulmonary capillary endothelium, alveolar and airway epithelium, and basement membranes.

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23
Q

what is the result of atelectrauma and volutrauma

A

Both atelectrauma and volutrauma cause a need for increased supplemental O2 concentrations. whichleads to overproduction of superoxide, hydrogen peroxide, and perhydroxyl radicals. Preterm infants are particularly susceptible to O2 radicals because the antioxidant systems develop in the last trimester of pregnancy. Prolonged hyperoxia begins a sequence of lung injury that leads to inflammation, diffuse alveolar damage, pulmonary dysfunction, and death.

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24
Q

The response of the lungs to the combination of trauma and O2 toxicity

A

The response of the lungs to the combination of trauma and O2 toxicity is the production and release of soluble mediators. These mediators probably are released from granulocytes residing in the lung. The release of these mediators can injure the alveolar-capillary barrier and cause an inflammatory response.

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25
BPD Progression
CXR in the first day of life shows a mild ground glass appearance consistent with RDS CXR at 2 weeks of age with early BPD changes CXR at 1 month of age showing progressive BPD with pulmonary edema and atelectasis
26
Diganosis of BPD
Diagnosis is based on clinical manifestation and CXR, but these are not specific.
27
What needs to be rules out before BPD can be diagnosed
``` o Congenital heart disease o Pulmonary lymphangiectasia o Pneumonitis o Cystic Fibrosis o Surfactant protein deficiency ```
28
Chest X-ray for BPD
• The chest radiograph in severe disease shows areas of atelectasis, emphysema, and fibrosis diffusely intermixed throughout the lung
29
ABG in BPD
• ABG measurements reveal varying degrees of hypoxemia and hypercapnia secondary to airway obstruction, air trapping, pulmonary fibrosis, and atelectasis. There is a marked increase in airway resistance with an overall decrease in lung compliance.
30
Clinical Manifestations of BPD
Respiratory distress o Tachypnea o Cyanosis o Intercostal retraction o Nasal flaring • Auscultation: fine crackles and expiratory wheeze • Increased airway resistance and sensitivity (bronchospasms) • Increased FRC and Hyperinflation associated with severe BPD
31
What is the best treatment for BPD
The best treatment is prevention Prevention of atelectrauma and volutrauma begins in the delivery room, with the establishment of an optimal FRC without over- stretching the lung r Surfactant should be delivered early in the course of treatment. o Other methods of prevention include  Nasal Positive Pressure Ventilation  Mechanical ventilation with permissive hypercapnia  Oxygen therapy to maintain targeted oxygen saturations  iNO for certain cases (PPHN)  Adequate nutrition  Corticosteroids  Caffeine or methylxanthines
32
Prevention of Minimizing Additional Lung Injury
Supplemental O2 can help decrease the pulmonary hypertension that is common with BPD Diuretics are given as needed to decrease pulmonary edema; antibiotics are given to manage existing pulmonary infection. o Chest physical therapy may help mobilize secretions and prevent further atelectasis. o Bronchodilator therapy may help decrease airway resistance. o Steroid therapy with dexamethasone can produce substantial short-term improvement in lung function, often allowing rapid weaning from ventilatory support. However, steroid therapy has little effect on long-term outcome such as mortality and duration of O2 therapy. Steroid therapy also has been implicated in decreased alveolarization and increased developmental delay. Although steroids are still given in clinical practice, they should be used cautiously and only after the risks have been thoroughly explained to the parents. The use of NO to prevent or improve BPD is controversial.
33
What is characterized by cycles of hyperventilation followed by short apneic pauses of less than 3 seconds?
Periodic breathing.
34
What is the purpose of central chemoreceptors?
They increase ventilation in response to low cerebral spinal fluid pH.
35
How is apnea of prematurity defined clinically?
Cessation of breathing for >20 seconds with bradycardia and hypoxemia for >10 seconds.
36
Which of the following are considered detrimental consequences of apnea in neonates?
Hypoxemia, hypercarbia, and bradycardia.
37
What long-term treatments are available to treat or prevent apnea of premature?
Methylxanthine, Nasal cannula, Blood transfusions, NCPAP, and Caffeine citrate.
38
At what age do most infants resolve apnea issues?
37 weeks postmenstrual age.
39
What risk factors increase the likelihood for more severe bronchopulmonary dysplasia?
Surfactant therapy and Nosocomial infection.
40
Which of the following are strategies to consider for the treatment of respiratory distress syndrome to minimize the risk of bronchopulmonary dysplasia?
Arterial oxygen tension >90mmHg, Surfactant administration prior to MV, Extubating to NIPPV in the first month of life.
41
What is essential for the optimal growth of cells and tissues?
Vitamin A.
42
What is the diuretic of choice for ventilator-dependent infants with evolving or established bronchopulmonary dysplasia (BPD)?
Thiazide.
43
What is apnea of prematurity (AOP)?
A sudden cessation of breathing that lasts for at least 20 secs or is accompanied by bradycardia or oxygen desaturation in an infant younger than 37 weeks gestation.
44
What are the causes of apnea in premature infants?
Incorrect neural signaling and airway obstruction.
45
What is periodic breathing?
A benign, abnormal form of breathing with cycles of hyperventilation followed by short apneic pauses of <3 seconds.
46
What 2 things can stimulate apnea of prematurity?
High humidity cannula and caffeine.
47
When is CPAP indicated?
For obstruction like tonsils pushing it out of the way.
48
What are the 3 classifications of Adverse Outcome Passage (AOP)?
Central, obstructive, and mixed apnea.
49
What is the cause of central apnea?
A dysfunction of the nerve centers in the brainstem to send signals to the muscles of respiration, and no attempt at inspiration can be observed.
50
How would you fix central apnea?
With caffeine.
51
What is the characteristics of obstructive apnea?
Some attempt to ventilate, resulting in chest wall movement but without gas entry, usually caused by an upper airway obstruction.
52
What is the airway like in obstructive apnea and the treatment?
Airway is floppy, and treatment is CPAP.
53
What is mixed apnea?
It consists of obstructive respiratory efforts, usually following central pauses, and is probably the most common type of apnea.
54
What is the treatment for mixed apnea?
Caffeine and CPAP.
55
What is the primary role of the respiratory control system?
To regulate ventilation to supply the O2 needs of the body and to remove CO2.
56
Where does control of ventilation occur?
At the brainstem.
57
What is the dysfunction of the respiratory control system?
It is the primary cause of the central apnea component of AOP.
58
What kind of medications are used to treat apnea of prematurity?
Methylxanthines mostly caffeine.
59
What do methylxanthines do?
It stimulates respiratory drive, increases diaphragmatic activity, increases VE, enhances chemoreceptor sensitivity to CO2, reduces periodic breathing, reduces hypoxic respiratory depression, increases metabolic rate, increases O2 consumption, and stimulates diuresis.
60
What can alleviate anemia that can cause irregular breathing in preterm infants?
Blood transfusions because blood carries oxygen.
61
How is a nasal cannula used to prevent obstructive apnea?
Mild positive pressure in the upper airway to prevent it.
62
How does a nasal cannula prevent central apnea?
It uses tactile simulation in the nares as a way to prevent it.
63
What does noninvasive ventilation do for apnea of prematurity?
NCPAP and NIPPV provide positive pressure that reduces the likelihood of upper airway collapse.
64
What is neurocognitive dysfunction?
BPD is a major predictor of poor neurodevelopment outcomes. It increased rate of cerebral palsy. Its developmental delays and poor neuromotor outcomes at 6 months of age.
65
What are respiratory exacerbations?
Infants with BPD have frequent & recurrent respiratory symptoms & infections. It requires subspecialty care: pulmonologists, neonatologists. Medications: O2, diuretics, & respiratory meds
66
What are the spirometry values that are consistently lower with BPD?
FEV1, FVC, forced expiratory flow at 25 % to 75% of the FVC, and shows substantial airway obstruction & alveolar hyperinflation.
67
Patients with BPD may typically have repeat what?
Hospitalizations, abnormal pulmonary function results & the need for home supplemental O2.
68
What do infants with BPD exhibit?
Obstructive lung disease that can persist into adolescence & young adulthood.
69
What is the prognosis for individual patients with BPD?
It is unpredictable & the course can vary widely.
70
What are the management & treatment of BPD?
Guaranteed prevention premature birth prevention, minimal O2 use, exogenous surfactant, open lung ventilation & gentle ventilation strategies, corticosteroids, caffeine citrate, mast cell stabilizers, vitamin A, inositol, antioxidants, inhaled NO, treatment of pulmonary edema, fluid restriction, diuretics. And bronchodilators.
71
What are the pulmonary vasculature characteristics of BPD?
Thickening of the basement membrane, subsequently increasing A-C membrane distance, decreased vasculature, and lower A-C membrane area.
72
What are the alveoli characteristics for BPD?
Fibrosis of alveolar tissue, emphysematic changes, heterogeneous pattern of atelectasis & over inflation, alveolar hypoplasia, fewer & larger, and less evidence of direct damage to alveolar tissue.
73
What are the airway characteristics for BPD?
Fibroproliferative airway injury, smooth muscle hyperplasia, varying amounts of smooth muscles, and minimal damage present.
74
What are the risks factors for the development of BPD?
Gestational age = 28 weeks, birth weight = 1,000 grams, hypothermia &/or Hypotension at admission, RDS, need for prolonged MV, hypercarbia (paCO2 >50 mmHg), need for exogenous surfactant therapy, higher fluid therapy, nosocomial infection, more than two blood transfusions, chorioamnionitis, preeclampsia, acidosis at admission, surfactant therapy, nosocomial infections, PDA, oligohydramnios, and Apgar Score <6 at 5 mins.
75
How can body positioning help in apnea of prematurity?
Prone positioning can improve thoraco-abdominal synchrony and stabilize the chest wall.
76
What are the treatments for apnea of prematurity?
Blood transfusions, nasal cannula, noninvasive ventilation, body positioning, and stimulation.
77
What is the NICU’s observation period prior to discharge for an apnea-free time?
Usually 3-8 days and after discontinuing caffeine citrate.
78
Can premature infants be sent home with caffeine citrate?
Yes, it provided with a home cardiorespiratory monitor.
79
What is essential prior to discharge of an apnea of prematurity baby?
Family education and training are provided with basic life support course.
80
What is bronchopulmonary dysplasia?
A type of chronic lung disease, currently defined as the need for supplemental oxygen for at least 28 days after birth, assessed at discharge or when the baby is close to their estimated full-term age.
81
What does intubation cause?
Slower lung development.
82
No supplemental O2 required at the time of evaluation (28 days after birth).
What constitutes mild bronchopulmonary dysplasia?
83
What constitutes moderate bronchopulmonary dysplasia?
FIO2 <30% and/or PPV or NCPAP at time of evaluation. 42. What constitutes severe bronchopulmonary dysplasia (BPD)? FIO2>30% and/or PPV or NCPAP at time of evaluation.
84
What does dysplasia mean?
It causes airways to grow differently.
85
Describe the development of new BPD?
Gestational age <28, birth weight <1000 grams, hypothermia at admission, hypotension at admission, RDS, need for prolonged MV, hypercarbia, need for surfactant therapy, higher fluid therapy, nosocomial infection, more than 2 blood transfusions, and preeclampsia.
86
What do infants with BPD exhibit?
Some degree of obstructive lung disease that can persist into adolescence and young adulthood.
87
What do BPD patients often have?
Repeat hospitalizations, abnormal PFT results, and the need for home supplemental O2.
88
How are spirometry values in survivors with BPD?
Consistently lower.
89
What do infants with BPD have frequently?
Respiratory exacerbations, recurrent respiratory symptoms and infections.
90
What are the BPD meds?
Oxygen, diuretics, and respiratory medications.
91
What is neurocognitive dysfunction?
BPD is a major predictor of poor neurodevelopmental outcomes, increased rate of cerebral palsy, developmental delays, and poor neuromotor outcomes at 6 months of age.
92
What is Apnea of Prematurity?
It is a sudden cessation of breathing that lasts for at least 20 secs or is accompanied by bradycardia or oxygen desaturation in an infant younger than 37 weeks gestation.
93
What are the causes of apnea in premature infants?
Incorrect neural signaling and airway obstruction.
94
What is AOP caused by?
The physiological immaturity of the neurological & chemical receptor systems of the body that regulate respiration & respond to hypoxemia & hypercapnia.
95
What is Periodic breathing?
A benign, abnormal form of breathing w/ cycles of hyperventilation followed by short apneic pauses of <3 secs.
96
How can AOP be classified?
Central, obstructive or mixed.
97
What is central apnea?
It caused by a dysfunction of the nerve centers in the brainstem to send signals to the muscles of respiration & no attempt at inspiration can be observed.
98
What is obstructive apnea?
It is characterized by some attempt to ventilate, resulting in chest wall movement but without gas entry, usually caused by an upper airway obstruction.
99
What is mixed apnea?
It consists of obstructed respiratory efforts, usually following central pauses, and is probably the most common type of apnea.
100
What does the control of ventilation occur?
The brainstem with central & peripheral chemoreceptors helping plays a role.
101
What is the primary cause of the central apnea component of AOP?
Dysfunction of the respiratory control system.
102
What is a nasal cannula?
Mild positive pressure in the upper airway to prevent obstructive apnea & tactile stimulation in the nares as a way to prevent central apnea.
103
What is noninvasive ventilation?
NCPAP & NIPPV provides positive pressure that reduces the likelihood of upper airway collapse.
104
How does body positioning play a role?
Prone positioning can improve thoracic abdominal synchrony & stabilize the chest wall.
105
What is the major developmental milestone of premature infants?
Resolution of apnea & establishment of a normal respiratory pattern.
106
How long is the NICU’s required observation period prior to discharge?
Usually 3 to 8 days and after discontinuing caffeine citrate.
107
What is bronchopulmonary dysplasia (BPD)?
A type of chronic lung disease, currently defined as the need for supplemental O2 for at least 28 days after birth, assessed at discharge or when the baby is close to his or her estimated full age.`
108
When to evaluate BPD?
At 36 weeks postmenstrual age or discharge to home (whichever comes first), and at >28 days but <56 days post-natal age or discharge to home (whichever comes first).
109
What is mild BPD? | No supplemental O2 requirement at time of evaluation.
No supplemental O2 requirement at time of evaluation.
110
What is moderate BPD?
Need for FiO2 < or = 0.30 &/or PPV or NCPAP at time of evaluation.
111
What is severe BPD? Need for >0.30 fio2 &/or PPV or NCPAP at time of evaluation.
Need for >0.30 fio2 &/or PPV or NCPAP at time of evaluation.

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