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Infant Transport Team > Neonatal Respiratory > Flashcards

Neonatal Respiratory Flashcards

1
Q

what does type 2 pneunmocyte do

A

provides surfactant. acts to reduce surface tension

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2
Q

Neonate Mech Ventilation approach

A

VE/VT = RR
60s/RR = TCT
Once obtain TCT/3 FOR I:E 1:2, for I:E 1:1 divide by 2

VE = 200-300ml/kg/min
VT = 4-6ml/kg

Upper limit PIP/Plat neo 25cmH20

VT= 4-6
RR = 40-60
Ti = .35-.55
PEEP 5-8
VE = 200-300ml/kg/min
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3
Q

Persistent pulmonary HTN of the newborn definition

A

PPHN occurs when the PVR remains abnormally elevated after birth. resulting in right to left shunting of blood through the fetal circulatory pathways.

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4
Q

Common causes of PPHN

A

MAC, PNA, RDS, CDH, Pulmonary hypoplasia, idiopathic.

can be categorized as underdeveloped, maldevelopment, (MAS, NSAIDS)
or maladaptive (GBS, infections
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5
Q

DDx of PPHN

A 
CHD
CDH
RDS
TTN
PNA
MAS
Sepsis
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6
Q

Treatment pillars of PPHN

A
  1. Treat underlining etiology
  2. optimize ventilation and oxygenation
  3. Improve PVR
  4. Optimize RV function with optimal cardiac output
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7
Q

7 steps of PPHN mgmt

A
  1. oxygen
  2. ventilation
  3. sedation
  4. circulatory support
  5. correction of acidosis
  6. surfactant
  7. interventions for severe cases (iNO)
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8
Q

Oxygen in PPHN

A
  • oxygen is a pulmonary vasodilatory and it should be initially administered in a concentration of 100% to patients with PPHN in attempt to reverse vasoconstriction to target spo2 >95. remembering that pao2 >50 or Fio2 >.5 won’t pulmonary vasodialtor effect
  • titrate to spo2 90-95% preductal
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9
Q

Ventilation in PPHN

A

Allow a permissive hypercapnia 40-50mmHg to minimize lung injury

-gentle ventilation. optmial PEEP low inflation/VT

-

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10
Q

Sedation in PPHN

A

Pain and agitation causes catecholamine release, resulting in increased PVR and increased right to left shunting. in addition, agitation may result in vent dysynchrony.

IV morphine or fentanyl can be used

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11
Q

Circulatory support in PPHN

A

right to left increased CO but eventually LV fails and SBP falls.

SBP target are set at upper limits of normal (SBP 50-70) because patients with PPHN is at or near normal systemic levels

vasopressors of choice:

dobutamine, milrinone, and vasopressin

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12
Q

Surfactant in PPHN

A

surfactant doesn’t appear to be effective in PPHN unless associated with parnychmeal lung damage (RDS/MAS)

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13
Q

iNO mechanism of action

A

MOA:
-iNO diffuses to vascular smooth muscle layer from the alveoli. It stimulates gluanylate cyclase and increases cGMP, creating pulmonary vasodilation vasodilation

Endogenous NO regulates vascular tone by causing relaxation of vascular smooth muscle.

Exogenous iNO is a selective pulmonary vasodilator that acts by decreasing the pulmonary artery pressure. Oxygenation improves as vessels are dilated in well-ventilated lung regions, redistributing blood from regions with decreased ventilation and reducing intrapulmonary shunting.

Not only does iNO improve alveolar oxygen exchange, but it also improves RV failure with the reduction in PA pressure

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14
Q

iNO onset

A

response is usually seen within 15-20 minutes and is considered successful when there is at least an increase of 20% of the previous PaO2/SaO2

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15
Q

GA of neonates in saccular phase

A

GA 24-36 weeks

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16
Q

When do alveoli actually develop

A

36 weeks

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17
Q

what does the type 1 pneunmocyte do

A

involves gas exchange, covers 95% of alveolar surface

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18
Q

Extrauterine transition of clearing fluids

A
  1. prenatal
    - decreased formation and secretion of fluids
    -chloride secretion decreases and sodium increases
    -
  2. active labour
    -mechanical compressions and catecholamine surge increase Na transport
  3. post natal
    - lungs are distended increasing transpulmonary pressure. crying and increased intrathoracic pressure
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19
Q

Staged approach to respiratory support

A 
noninvasive:
-low flow
-high flow
-CPAP
-BiPAP
-NAVA
Invasive:
-conventional
-HFOV
-HFJV
-NAVA
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20
Q

When is NAVA used?

A

is used by BCCH NICU commonly for increased comfort of mechanical ventilation when a baby is nearing extubation

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21
Q

How does Jet ventilation remove CO2

A

HFJV - is a jet of air that is ejected down the ETT that essentially washes out CO2 by blowing the CO2 up and around the jet stream of air.

High frequency does have a higher overall MAP than CMV, but the PIP is attenuated by the tube/proximal airways which theoretically helps prevent VILI

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22
Q

How does the fetal lung transition in life?

A

With the onset of respiration after delivery, the lungs expand and the systemic oxygen saturation rises, resulting in pulmonary vasodilatation and a drop in pulmonary vascular resistance.

Systemic resistance rises at the same time with placental removal after cutting the umbilical cord.

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23
Q

Acute reversible pulmonary aetiologies of PPHN

A 
RDS
TTN
MAS
CDH
PNA
GDM
Pulmonary hypoplasia
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24
Q

Acute reversible non-pulmonary causes of PPHN

A

HIE
AVM
Rx (NSAIDs/SSRI)
Metabolic (Hypoglycemia/polycythemia)

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25
Q

How much cardiac output goes to the lungs in utero?

A

5-10%

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26
Q

Hemodynamic effects of PPHN in the context of ventricular pathophysiology

A

An increase in PVR (RV afterload) causes RV dysfunction, which decreases pulmonary BF worsening hypoxemia/acidosis and VQ mismatching. Decreasing LV preload which causes LV dysfunction and decrease in LV out put

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27
Q

How to dx PPHN

A
  • clinical presentation/hx
  • resp distress + cyanosis
  • pre/post diff of 10%
  • Hyperoxia test
  • labs, ABG
  • CXR
  • Echo
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28
Q

Why is iNO an ideal pulmonary vasodilator?

A
  • selective pulmonary vasodilator at doses <100ppm
  • confined to the pulmonary vascular bed (due to the rapid inactivation by hemoglobin in the pulmonary circulation)
  • vasodilator effect is not altered by extra-pulmonary shunts
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29
Q

What does oxygen do in the setting of PPHN

A

oxygen acts as a pulmonary vasodilator. Higher level of alveolar pO2 may contribute to secondary lung parenchymal damage

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30
Q

what does sedation do in the setting of PPHN

A
  • used for hypoxia associated with agitation
  • achieve vent synchrony
  • reduced metabolic demands
  • fentanyl less likely to induced systemic hypotension
31
Q

ABG targets in PPHN

A

pH 7.35-7.45
pco2 35-45
sats >92-96%

32
Q

When do you add in pulmonary vasodilator medications in neonates in PPHN

A

Vasodilators can be considered once RV performance and ductal potency have been optimized

33
Q

When do alveoli develop?

A

36 weeks to 3 yrs

34
Q

Whats significant about saccular phase

A

25-36 weeks, large primitive alveoli capable of gas exchange develop from terminal bronchioles, increasing surface area.

35
Q

What happens during alveolar development phase

A

number of alveoli increase from 0-100million and 300million in adults

36
Q

What are the epithelial sodium channels (ENaC) in alveoli responsible for?

A

The production of ENaC in the alveoli rises consistently towards term. ENaC are responsible for 1/3 of fetal lung fluid clearance.

37
Q

What cell type does surfactant come from

A

Pneumocyte type 2

38
Q

What are the roles of surfactant and properties of surfactant

A
  • Has both hydrophobic and hydrophilic properties.
  • Decreases surface tension, requiring less pressure to keep alveoli open. When you start to expand, the surfactant will dissipate therefore maintains a higher FRCs
  • Surfactant not only decrease surface tension but acts as a barrier to prevent the reentry of fluid into the alveolus.
39
Q

When will a fetus produce more surfactant

A

The fetus has increased surfactant production when stressed. Babies with IUGR or born to mothers with maternal HTN actually have accelerated lung maturation from stress. Similar mechanism as to why steroids assist with growth.

Steroids effectively assist in the release of surfactant from the type 2 alveolar cells.

40
Q

What can decrease the activation of surfactant

A

Meconium increase the inactivation of surfactant. And also decrease the synthesis of surfactant. Meconium also creates physical occlusion of the small airways

Hyperinsulinemia

41
Q

Why is fetal lung fluid important?

A

Fetal lung fluid is important for lung development. Oligohydraminos can result in a degree of pulmonary hypoplasia.

42
Q

Discuss HFOV

A

HFOV Primairly used for oxygenation.

In HFOV a ventilator piston creates + and - pressure oscillations to deliver small VTs on a set mean airway pressure (MAP).

Expiration is an active process with HFOV, unlike conventional.

The frequencies used are typically 480-900 Breaths/min (HZ 480-900)

43
Q

Discuss how HFJV works

A

HFJV uses a pinch valve to interrupt gas flow and produces small volume pulses of gas at a high frequency, which are delivered through a port on a specialized ETT adapter.

This is applied in parallel to a conventional ventilator that provides PEEP and delivered sigh breaths. Typically 2-10/min when additional lung recruitment is desired.

44
Q

How do you move someone from HFJV to conventional

A

Aim for a MAP approx 2 above MAP in JET

-MAP = (iT x F) / 60 x (PIP-PEEP) + PEEP

45
Q

How do you transition some from HFOV

A

Aim for a MAP that is approx 1/2 the MAP on the oscillator

MAP = (iT x f) / 60 x (PIP- PEEP) + PEEP

46
Q

Ideal oxygenation saturations in neonates is:

A

88-95% - avoiding hypoxic ischemic vents such as HIE and gut ischemic but also preventing free radical generation

47
Q

What is fetal lung fluid?

A

Its an ultra-filtrate of pulmonary capillary blood - it is not amniotic fluid

48
Q

Discuss pulmonary/chest wall compliance in neonates vs adults

A

Comparing chest walls, neonates have more compliant chest wall but neonate has less compliant alveoli. This can explain the increased incidence of pneumothoraces in infants

49
Q

Discuss respiratory volumes in neonates compared to adults

A
  • less respiratory reserve volumes
  • decrease FRC
  • increased closing capacity
  • decreased expiratory reserve volumes
  • increased residual volume
50
Q

Why do neonate have increased minute ventilation

A

they have increased MV due to their high basal metabolic rate with higher CO2 production.

Their intrinsic higher rate is due to limitations of VT with a more compliant chest wall, increased anatomic dead space, decreased lung compliance due to insufficiency surfactant, and flattened diaphragm/weak intercostal muscles putting the respiratory muscles at disadvantage

51
Q

In the context of RSI why is it important to put your RSI meds on a pump infusion

A

Neonates <32 weeks GA have an immature germinal matrix, meaning they have a poor ability to control swings in BP, particularly during induction.
These boluses are at risk of IVH when boluses with IVF

52
Q

Whats closing capacity

A

Is the max lung volume at which airway closure can be detected in dependent parts of the lung (comprised of residual volume and closing volume)

53
Q

In relation to the time settings, what helps differentiate TTN vs RDS

A

When differentiating RDS vs TTN consider that the clinical course of TTN generally improves over 24-72 hours.
While RDS typically worsens in 24-72 hours before beginning to improve

54
Q

Discuss how GDM has an influence on RDS

A

RDS increases from poorly controlled GDM. This is because high serum insulin during fetal growth which inhibits the production of surfactant

55
Q

Indications for BLES

A
  • FiO2 > 30 and CPAP of 7cmH20
  • Significant WOB
  • CXR consisted with RDS
  • MAS with RDS
56
Q

TTN MGMT

A
  1. Neutral thermal environment
  2. High Flow 1-2LPM/KG
  3. nCPAP 5-7cmH20
  4. Intubation if failing CPAP
57
Q

Complications of surfactant administrations

A

intermittent risk of airway obstruction/aspiration with application of surfactant

58
Q

Synopsis of CDH

A

CDH is the developmental defect in the diaphragm that allows abdominal viscera to herniate into the chest. Thereby compressing the lung and interfering with normal lung development

Corresponds with decrease in bronchial and pulmonary arterial branching resulting in increasing degrees of lung hypoplasia and pulmonary arterial hyperplasia (Pulmonary HTN)

59
Q

Which side is generally insulted with CDH

A

Left sided more common

60
Q

Common clinical manifestations of CDH

A

Barrel shaped chest
Scaphoid-appearing abdominal from less abdominal contents (going into chest)
Absent breath sounds on the ipsilateral side

61
Q

How is CDH Dx?

A

Prenatally- US
Postnatally - AXR/CXR
Measurement of the lung to head ratio predicts the severity of pulmonary hypoplasia

62
Q

CDH MGMT Pillars

A
  1. VENTILATION
    - intubate immediately after birth
    - NG tube to decompress the stomach
    - avoid BVM/NIPPV
    - preductal 85-95%
    - gentle ventilation
    - avoid sedation
  2. HD Support
    - cautious use of lfuids
    - steroids
    - inotropic support
    - ECHO
  3. Pulmonary HTN
    - oxygen
    - sedation
    - iNO
    - Sildenafil
    - prostaglandin
    - vasopressin
    - milirinone
    - ECMO
63
Q

three types of apnea

A

Central, obstructives, mixed

64
Q

Whats the differences in time frames from AOP and periodic breathing

A

AOP >20s

preiodic <20s

65
Q

Bronchopulmonary Dysplasia is also known as

A

Neonatal chronic lung disease

66
Q

BPD commonly occurs secondary to

A

CDH
Oliohydramnios
Low birth weight
prolonged mech vent or high FiO2 requirements

67
Q

What is pulmonary interstitial emphysema

A

PIE the collection of air around the alveoli, associated to over-ventilation.
CXR presents similar to BPD or emphysema.

68
Q

RSI for neonates

A

1mcg/kg atropine
3mcg/kg fentanyl
2mcg/kg suc

69
Q

When does a fetus secrete and stop secreting pulmonary Na

A

The fetal lung secrete Na and fluid to cause the lungs to expand and promote growth during development.

During birth the bronchopulmonary epithelial Na channels change from secretion to absorption of Na and fluid. This is unregulated with catecholamines and glucocorticoids. The squeeze of birth cannel aids in compressing the chest and dispersing more fluid.

70
Q

how long does it take for a baby to achieve ideal FRC in SVD or C-section

A

2-3 hours in SVD (FRC of 30ml/kg)

5-6 hr in C-Section

71
Q

TTN definition

A

Transient tachypnea of the newborn is a lung disorder characterized by pulmonary edema resulting from delayed resorption and clearance of fetal alveolar fluid.

72
Q

TTN pathophysiology synopsis

A

Delayed resorption of fetal lung is thought to be the underlying cause of TTN.

Fluid fills the airspaces and manifests to the interstium, where it pools in the perivascular tissues and interloper fissures until its eventually cleared by the lymphatic or absorbed into small blood vessel.

Tachypnea develops to compensate for reduced compliance

73
Q

RDS patho

A

In the premature lung, inadequate surfactant activity results in high-surface tension leading to instability of the lung at end-expiration, low lung volumes and decrease compliance.

These changes in lung function causes hypoxemia due to V/Q mismatch due to collapse of large portions of the lungs with additional contributions of V/Q mismatching from intrapulmonary and extrapulmonary R-L shunts

Surfactant deficiency also leads to lung inflammation and respiratory epithelium injury which may result in pulmonary edema and increase airway resistance.

74
Q

MAS definition and patho

A

Defied as respiratory distress in newborn infants though meconium stained amniotic fluid who’s symptoms can be otherwise explained

Perinatal aspiration of meconium leading to small airway obstruction, pneumonititis, surfactant inactivation and VQ mismatching

Infant Transport Team (14 decks)

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