Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neo/Ped > ch 22 > Flashcards

ch 22 Flashcards

1
Q

what are possible predisposing factors of AOP

A
  1. immaturity and depressed central respiratory drive to respiratory muscles
  2. temperature instability (hypo/hyperthermia)
  3. neurological (birth trauma, ICH, perinatal asphyxia, drugs)
  4. pulmonary (RDS, pneumonia, BPD, pneumothorax)
  5. cardiac (congenital, hypo/hypertension, CHF, PDA)
  6. infection (sepsis, NEC)
  7. GI (GERD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe central apnea

A

absent inspiratory efforts, no obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe obstructive apnea

A

persistent inspiratory efforts, no obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe mixed apnea

A

airway obstruction with inspiratory efforts precedes or follows central apnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the clinical presentations of AOP in the first 24 hours

A
  1. not simple AOP
  2. infant or maternal condition
  3. neonatal sepsis
  4. hypoglycemia
  5. ICH
  6. maternal antepartum Mg treatment
  7. maternal narcotic exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the clinical presentations of AOP after the first 24 hours

A
  1. classified as AOP if no other pathological condition exists
  2. present post prolonged ventilatory support
  3. associated with intermittent hypoxia 2nd degree hypoventilation or atelectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the signs of apnea

A
  1. no chest movement
  2. staring gaze
  3. red or blue color to face
  4. stiff posture
  5. pale white or blue colored lips
  6. sudden loss of strength
  7. loss of consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe monitoring process for diagnosis of AOP

A
  1. look at all preterm infants
  2. presence of apnea associated with bradycardia and hypoxemia
  3. detailed H&P
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe general measures for treatment of AOP

A
  1. tactile stimulation (careful suction of pharynx, avoid oral feeding, gentle stimulation)
  2. maintain stable thermal environment (temp controlled radiant warmer, incubator)
  3. positioning (prevent extreme flexion or extension)
  4. oxygenation (<29 wk 85-92%; >29 wk 85-95%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe CPAP treatment for AOP

A
  1. applied using sialistic nasal prongs
  2. initiated at 4-6 cmH2O
  3. flow rates 4-5L/min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe pharmacological treatments of AOP

A
  1. methylxanthine (caffeine, theophylline)

2. doxapram (respiratory stimulant of carotid chemoreceptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the primary cause of RDS

A

pulmonary surfactant deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the physiological development of RDS

A
  1. surfactant deficiency
  2. alveolar cellular damage
  3. inadequate surface area
  4. reduction of effective ventilation
  5. thickened a-c membrane
  6. insufficient vascularization
  7. inflammation
  8. genetic disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

who is at risk of developing RDS

A
  1. preterm infants
  2. happens in 1% of pregnancies
  3. 60-80% in infants <28 weeks
  4. 15-30% in infants between 26-32 weeks
  5. rarely in infants >37 weeks
  6. highest in preterm white males
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the risk factors for term infants with RDS

A
  1. maternal diabetes
  2. multiple births
  3. C-sections
  4. fetal asphyxia
  5. cold stress
  6. maternal previous history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the presentation of RDS

A
  1. tachypnea (>60 bpm)
  2. grunt
  3. nasal flaring
  4. retractions
  5. cyanosis
  6. chest/abdomen asynchrony
  7. hypothermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how can RDS be prevented

A
  1. avoid unnecessary or poorly timed C-section
  2. antenatal and intrapartum fetal monitoring
  3. maternal (antenatal) steroid therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how can RDS be prevented

A
  1. avoid unnecessary or poorly timed C-section
  2. antenatal and intrapartum fetal monitoring
  3. maternal (antenatal) asteroid therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the possible treatments for RDS

A
  1. surfactant instalation
  2. oxygen therapy
  3. CPAP
  4. mechanical ventilation
  5. pressure ventilator
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the goal of surfactant instillation for RDS

A

asssist in preventing or improving RDS status and decrease morbidity and mortality rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the goal of surfactant instillation for RDS

A

assist in preventing or improving RDS status and decrease morbidity and mortality rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the goal of oxygen therapy for RDS

A

to maintain PaO2 between 50-80 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the goal of oxygen therapy for RDS

A
  1. to maintain PaO2 between 50-80 mmHg
  2. PaCO2 between 40-55 mmHg
  3. pH <7.25
  4. FiO2 increased in increments of 10% while evaluating with POx or ABG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the goal of CPAP therapy for RDS

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
what is the goal of CPAP therapy for RDS
to stabilize infant and prevent intubation to reduce risk of pneumothorax, PIE and mortality
25
what are possible complications of RDS treatment therapies
1. oxygen toxicity 2. IVH 3. ROP 4. Necrotizing enterocolitis 5. DIC 6. infection 7. air leaks 8. barotrauma 9. PDA R-L shunt
26
what is the treatment focus for RDS
1. hydration and electrolyte balance 2. neutral thermal environment 3. dexamethasone 4. minimize infection/sepsis 5. albuterol and Atrovent MDI
27
what is BPD
neonatal chronic lung disease (CLD) where infant is O2 dependent post 28 days of age with abnormal CXR
28
NIH divides BPD into 3 categories: mild, moderate and severe based on what
1. duration of oxygen therapy | 2. level of O2 therapy
29
describe the atypical or "new" BPD
milder form of CLD that is present in preterm infants who have minimal or no ventilator support and low FiO2
30
who does BPD effect
usually present after RDS in preterm and ELBW infants where it is marked by the inflammation of the airways and the CXR appears with diffuse lung infiltrates
31
what are the 4 major factors for BPD
1. lung maturity 2. respiratory failure 3. oxygen supplementation 4. positive pressure mechanical ventilation
32
what are the pathophysiological pathways for BPD
1. prematurity 2. ventilator-induced lung injury 3. hypoxia or hyperoxia induced lung injury 4. inflammation 5. nutrition 6. PDA 7. genetics 8. vascular
33
how does BPD present
MV and O2 dependent beyond 10-14 days
33
how does BPD present
MV and O2 dependent beyond 10-14 days
34
how does BPD present
1. MV and O2 dependent beyond 10-14 days | 2. "new" BPD affects ELBW infants (400-1000g)
35
what are the physical findings of BPD
1. tachypnea 2. mild to severe retractions 3. scattered crackles 4. intermittent expiratory wheezes
36
describe a BPD CXR
diffusely hazy (reflecting inflammation and/or pulmonary edema), low lung volumes (or normal), hyperinflation, pulmonary edema (apparent during acute exacerbations), may be areas of atelectasis that alternate with airtrapping related to airway obstruction from secretions, streaky densities or cystic areas may be prominent corresponding to fibrotic changes
37
describe stage 1 of BPD 2-3 days
1. signs of RDS (cyanosis, tachypnea, grunting, nasal flaring) 2. severe hypoxemia with supplemental O2 3. CXR has ground glass appearance
38
describe stage 2 of BPD 4-10 days
1. CXR is radiopaque with obscured heart borders 2. diffuse atelectasis with fluid accumulation progressing to pulmonary edema 3. reopening of PDA 4. pink frothy secretions
39
describe stage 3 of BPD 10-20 days
1. transition from acute to chronic condition 2. significant O2 requirement 3. hypercarbia 4. weaning is not possible
40
describe stage 4 of BPD >30 days
1. healing phase (months to years) 2. CXR has minimal improvement (diffuse fibrosis, hyperinflation, streaky densities, cardiomegaly) 3. tracheostomy may be indicated for long term ventilation
41
how do you prevent BPD
1. lung protective vent strategies (low Vt and permissive hypercapnia) 2. O2 therapy (allow lower saturations) 3. antioxidants 4. inhaled NO (reduced lung inflammation) 5. nutrition 6. corticosteroids 7. methylxanthine
42
what is the treatment for BPD
1. oxygenation (92%) 2. MV 3. fluid management 4. drug therapy 5. nutrition
43
what are the goals of treatment for BPD
1. minimize further lung injury (baro/volutrauma, oxygen toxicity, inflammation) 2. maximize nutrition and diminish O2 consumption
44
what are the complications of BPD
1. infection 2. reactive airway disease 3. cor pulmonale 4. pulmonary hypertension 5. neurodevelopmental and neurological delay 6. growth failure 7. psychomotor retardation
45
what is MAS
respiratory disorder caused by inhalation of meconium in amniotic fluid into tracheobronchial tree
46
what is meconium
infants thick, green-tinged bowel contents usually passed within 48 hours
47
what is the ball valve effect
a mechanical airway obstruction or partial airway obstruction
48
what is the cause of MAS
interuterine stress or hypoxia in utero
49
who is at risk for MAS
preterm infants because they lack anal sphincter tone
50
what is the pathophysiology of MAS
1. degree of obstruction is dependent on amount, viscosity and dilution of meconium 2. chemical pneumonitis 3. surfactant hinderance 4. pulmonary vasocontriction
51
how is MAS diagnosed
CXR
52
description of MAS initial CXR
streaky, linear densities similar to neonatal pneumonia
53
description of progression CXR of MAS
lung appear hyperinflated with flattening of diaphragm
54
description of progression CXR of MAS
1. lung appear hyperinflated with flattening of diaphragm | 2. diffuse patchy densities
55
what is the general goal for MV therapy treatment for MAS
1. maintain low MAP (low PIP, PEEP, Ti and flow) 2. maintain PaCO2 25-35 3. PaO2 high to normal range
56
what are complication of MAS
1. barotrauma (volutrama) 2. intraventricular hemorrhage 3. PPHN
57
what is the underlying cause of barotrauma regarding MAS
1. Results with atelectasis and airtrapping with level of obstruction 2. Barotrauma may result in atelectasis or airtrapping depending on how the airway is obstructed
58
what is the underlying cause of IVH in regard to MAS
1. MV increases intrathoracic pressure which increases ICP | 2. as mechanical ventilation increases intrathoracic pressure and thus transcends into the head as an increased ICP
59
what is the underlying cause of PPHN in regards to MAS
1. Occurs in 1/3 of MAS cases 2. Contributes to mortality rate 3. Perform ECHO (degree of R-L shunting & exclude CHD as cause for PPHN)
60
what is the underlying cause of TTN
common after C-section without labor
61
who is at risk of developing TTN and why
infants between 37-42 weeks (term) who do not go through vaginal canal
62
what is the clinical presentation of TTN
1. tachypnea 2. cyanosis 3. grunting 4. retractions 5. nasal flaring 6. ABG - resp acid with mild to mod hypox 7. CXR
63
describe a CXR of TTN
1. PV congestion 2. peripheral streaking 3. hyperexpansion 4. flat diaphragms 5. mild cardiomegaly 6. pleural effusions
64
what are the supportive measures regarding TTN
1. maintain oxygenation 2. nutrition via OG 3. neutral thermal environment 4. administration of antibiotics 5. lasix
65
what are possible complications of TTN
1. resolves in 12-24 hours 2. RA infant usually within 48 hours 3. complication are rare
66
who is at risk for air leaks
1. preterm infants 2. infants with underlying causes 3. infants who need resuscitation and PPV support
67
what are causes of air leaks
1. overdistention of terminal air space or airways 2. uneven alveolar ventilation 3. inappropriate use of PPV
68
how does pneumothorax present
1. signs of RDS 2. sudden decrease in voltage of QRS complex 3. asymmetrical chest movement 4. decreased breath sounds of affected side 5. shift PMI away from affected side 6. decreased C.O.
69
how do you diagnose pneumothorax
CXR or transilumination
70
describe CXR of pneumothorax
1. air in the pleural space 2. flattening of diaphragm 3. shift of mediastinum away
71
what are the treatments for penumothorax
1. thoracentesis | 2. chest tube
72
how does pneumomediastinum clinically present
1. most cases are asymptomatic 2. tachypnea 3. cyanosis 4. distant heart sound
73
how do you diagnosis pneumomediastinum
CXR
74
describe CXR of pneumomediastinum
halo around hear and spinniker sail sign
75
what are the treatments for pneumomediastinum
1. usually resolves spontaneously 2. requires no specific treatment 3. observed closely for other air leaks
76
how does PIE clinically present
1. affects MV ELBW infants 2. involve one or both lungs 3. usually presents 96 hours after birth with worsening hypoxia 4. overdistention 5. may precede development of pneumothorax
77
describe CXR of PIE
air trapped in perivascular tissue of lung
78
how do you treat PIE
1. Provide adequate gas exchange 2. Minimizing risk of further air leak 3. Decreasing mean airway pressure (MAP) 4. If unilateral – lateral decubitus position – “bad lung down” 5. High frequency ventilation (HFV)
79
how does a pneumopericardium clinically present
1. Abrupt onset of hemodynamic compromise (cardiac tamponade) 2. Hypotension 3. Decreased/narrow pulse pressure 4. Bradycardia 5. Tachycardia with increased respiratory distress 6. Cyanosis 7. Muffled or distant heart sounds 8. Pericardial knock – millwheel like murmur 9. ECG – low voltage with small QRS complex
80
how do you diagnose pneumopericardium
1. CXR 2. transilumination 3. therapeutic pericardiocentesis
81
describe the CXR of pneumopericardium
air surrounding heart shadow within pericardium
82
how do you treat asymptomatic pneumopericardium
1. close observation of VS, pulse pressures and CXR | 2. if on MV: minimize pressures
83
how do you treat symptomatic pnuemopericardium
1. pericardial drainage | 2. pericardiocentesis
84
define transillumination
high intensity fiberoptic light source may be helpful while awaiting a chest radiograph
85
when is the spinniker sail sign seen
in pneumomediastinum
86
How does the management of PIE differ from the other air leak syndromes
1. It is only supportive because there is no definitive treatment for PIE. 2. It is directed at providing pulmonary air leak in the newborn with adequate gas exchange and minimizing the risk of further air leak
87
define PPHN based on characteristics
1. sustained elevated PVR after birth 2. R-L shunting (FO or PDA) 3. severe hypoxemia
88
define PPHN based off clinical presentation
1. infant with ECHO confirmed normal heart has severe hypoxemia (PaO2 37.5-45 mmHg) on 1.0 FiO2 (and IPPV if necessary) 2. mild lung disease with severe hypoxemia 3. evidence of R-L shunting 4. pre/post ductal difference of >20 mmHg
89
Who is at high risk and what is the prognosis for PPHN
1. 1-2 per 1000 live births 2. most common in full/post term infants 3. high risk of mortality
90
what are 3 types of PPHN
1. maladaptation 2. maldevelopment 3. underdevelopment
91
describe maladaptation PPHN
1. Normally developed pulmonary vascular bed 2. Interference of decrease in PVR due to active vasoconstriction due to parenchymal lung disease (MAS, RDS, Group B strep pneumonia) 3. In maladaptation, the pulmonary vascular bed is normally developed. However, adverse perinatal conditions cause active vasoconstriction and interfere with the normal postnatal fall in PVR. These conditions include perinatal depression, pulmonary parenchymal diseases, and bacterial infections, especially those caused by group B strep (GBS). 4. The mechanism of increased PVR in newborn lambs, pulm. HTN was induced by infusion of cardiolipin and phosphatidylglycerol, phospholipids located primarily in the cell wall of GBS.
92
describe maldevelopment PPHN
1. Normal lung development 2. Remodeled pulmonary vasculature (Thickened smooth muscle cells; Muscle extension into small vessels) Factors (Increased pulmonary blood flow into utero; hypoxia; hyperoxia; vasculature mediators (endotheline-1, inhibition of cGMP and NO))
93
describe underdevelopment PPHN
1. Reduction of cross-sectional area of pulmonary vasculature 2. Resulting in fixed elevated PVR 3. Factors: congenital diaphragmatic hernia (CDH); oligohydramnios 4. Mortality risk is greatest in this category of patient
94
when should PPHN diagnosis be considered
in any infant w/severe cyanosis. In affected patients, little improvement in PaO2 to 100% FiO2, increased mean airway pressure with CPAP or high PIPs with mechanical ventilation. Other diagnoses that must be considered include uncomplicated pulmonary parenchymal disease, infection, structural heart disease and myocardia dysfunction.
95
how is PPHN diagnosed
1. CXR – heart is normal or slightly enlarged 2. ECG – elevated ST segments 3. ABG – PaO2 <100 mmHg on 1.0 FiO2; difference in pre/post ductal saturation 4. ECHO (definitive) – R-L shunting predominately via FO rather than PD
96
what are the treatments for PPHN
1. oxygen - 1.0 FiO2, PaO2 50-90 2. assisted ventilation - PaCO2 40-50, minimize MAP, HFOV 3. pharmacotherapy 4. ECMO
97
what are the possible pharmacotherapy for PPHN
1. Surfactant (administer in RDS, sepsis, pneumonia, MAS) 2. sedation and analgesics (block stress response to release of catecholamine and “bucking” ventilator) 3. circulatory support – maintenance of C.O and B/P (avoid hypotension/hypovolemia 4. increase contractility of heart: dopamine, dobutamine, epinephrine, norepinephrine) 5. antioxidant therapy (increase availability of endogenous NO and iNO, reduce oxidative stress and limit lung injury) 6. pulmonary vasodilators (iNO, MgSO, sildenafil (Viagra))
98
What is the recommendation given by the American Academy of Pediatrics for iNO?
* Care of patients in centers with personnel experience with multiple modes of respiratory support, rescue therapies and use of iNO * Availability of ECMO at center or an established mechanism for timely transfer of infants to an ECMO center * Performance of n echocardiogram to exclude the diagnosis of congenital heart disease
99
What is the calculation for the oxygen index and what does the OI assess?
OI = (mean airway pressure x 100 x FiO2) / PaO2
100
When should iNO be considered?
• A OI ≥25 indicates severe hypoxemic respiratory failure, and a term or late preterm infant should receive care in a center where HFOV, iNO and ECMO are readily available
101
What is the initial dose, typical course and at what rate should it be decreased?
* Initial dose: 20 parts per million (ppm) * Typical course: 3-4 days * Rate to decrease slowly with improvement of PaO2 and SpO2
102
Briefly describe the goal of ECMO, initial criteria, and weaning.
* Goal: maintain adequate tissue oxygen delivery and avoid irreversible lung injury; decrease PVR and resolve pulmonary HTN * Initial criteria: OI ≥40 if conventional ventilation; ≥60 if HFVO is used * Weaning: weaned after 5-7 days; occasionally 2 or more weeks is necessary
103
What are the main complications of PPHN discussed and mortality rate?
* Survivors have increased risk of (about 5%): (Developmental delay (speech), motor disability, hearing deficits) * Neurodevelopmental monitoring for: (6–12-month intervals, hearing test prior to hospital discharge and at 18-24 months corrected age, Today mortality rate at about 20%)
104
How does PVR decrease?
* Increase in PaO2 and pH * Air expanding the lung * Release of vasoactive substances (bradykinin, prostaglandins, and endogenous nitric oxide)

Neo/Ped (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions