Neonatal Respiratory Flashcards
what does type 2 pneunmocyte do
provides surfactant. acts to reduce surface tension
Neonate Mech Ventilation approach
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
Persistent pulmonary HTN of the newborn definition
PPHN occurs when the PVR remains abnormally elevated after birth. resulting in right to left shunting of blood through the fetal circulatory pathways.
Common causes of PPHN
MAC, PNA, RDS, CDH, Pulmonary hypoplasia, idiopathic.
can be categorized as underdeveloped, maldevelopment, (MAS, NSAIDS) or maladaptive (GBS, infections
DDx of PPHN
CHD CDH RDS TTN PNA MAS Sepsis
Treatment pillars of PPHN
- Treat underlining etiology
- optimize ventilation and oxygenation
- Improve PVR
- Optimize RV function with optimal cardiac output
7 steps of PPHN mgmt
- oxygen
- ventilation
- sedation
- circulatory support
- correction of acidosis
- surfactant
- interventions for severe cases (iNO)
Oxygen in PPHN
- 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
Ventilation in PPHN
Allow a permissive hypercapnia 40-50mmHg to minimize lung injury
-gentle ventilation. optmial PEEP low inflation/VT
-
Sedation in PPHN
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
Circulatory support in PPHN
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
Surfactant in PPHN
surfactant doesn’t appear to be effective in PPHN unless associated with parnychmeal lung damage (RDS/MAS)
iNO mechanism of action
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
iNO onset
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
GA of neonates in saccular phase
GA 24-36 weeks
When do alveoli actually develop
36 weeks
what does the type 1 pneunmocyte do
involves gas exchange, covers 95% of alveolar surface
Extrauterine transition of clearing fluids
- prenatal
- decreased formation and secretion of fluids
-chloride secretion decreases and sodium increases
- - active labour
-mechanical compressions and catecholamine surge increase Na transport - post natal
- lungs are distended increasing transpulmonary pressure. crying and increased intrathoracic pressure
Staged approach to respiratory support
noninvasive: -low flow -high flow -CPAP -BiPAP -NAVA Invasive: -conventional -HFOV -HFJV -NAVA
When is NAVA used?
is used by BCCH NICU commonly for increased comfort of mechanical ventilation when a baby is nearing extubation
How does Jet ventilation remove CO2
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
How does the fetal lung transition in life?
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.
Acute reversible pulmonary aetiologies of PPHN
RDS TTN MAS CDH PNA GDM Pulmonary hypoplasia
Acute reversible non-pulmonary causes of PPHN
HIE
AVM
Rx (NSAIDs/SSRI)
Metabolic (Hypoglycemia/polycythemia)
How much cardiac output goes to the lungs in utero?
5-10%
Hemodynamic effects of PPHN in the context of ventricular pathophysiology
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
How to dx PPHN
- clinical presentation/hx
- resp distress + cyanosis
- pre/post diff of 10%
- Hyperoxia test
- labs, ABG
- CXR
- Echo
Why is iNO an ideal pulmonary vasodilator?
- 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
What does oxygen do in the setting of PPHN
oxygen acts as a pulmonary vasodilator. Higher level of alveolar pO2 may contribute to secondary lung parenchymal damage
what does sedation do in the setting of PPHN
- used for hypoxia associated with agitation
- achieve vent synchrony
- reduced metabolic demands
- fentanyl less likely to induced systemic hypotension
ABG targets in PPHN
pH 7.35-7.45
pco2 35-45
sats >92-96%
When do you add in pulmonary vasodilator medications in neonates in PPHN
Vasodilators can be considered once RV performance and ductal potency have been optimized
When do alveoli develop?
36 weeks to 3 yrs
Whats significant about saccular phase
25-36 weeks, large primitive alveoli capable of gas exchange develop from terminal bronchioles, increasing surface area.
What happens during alveolar development phase
number of alveoli increase from 0-100million and 300million in adults
What are the epithelial sodium channels (ENaC) in alveoli responsible for?
The production of ENaC in the alveoli rises consistently towards term. ENaC are responsible for 1/3 of fetal lung fluid clearance.
What cell type does surfactant come from
Pneumocyte type 2
What are the roles of surfactant and properties of surfactant
- 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.
When will a fetus produce more surfactant
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.
What can decrease the activation of surfactant
Meconium increase the inactivation of surfactant. And also decrease the synthesis of surfactant. Meconium also creates physical occlusion of the small airways
Hyperinsulinemia
Why is fetal lung fluid important?
Fetal lung fluid is important for lung development. Oligohydraminos can result in a degree of pulmonary hypoplasia.
Discuss HFOV
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)
Discuss how HFJV works
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.
How do you move someone from HFJV to conventional
Aim for a MAP approx 2 above MAP in JET
-MAP = (iT x F) / 60 x (PIP-PEEP) + PEEP
How do you transition some from HFOV
Aim for a MAP that is approx 1/2 the MAP on the oscillator
MAP = (iT x f) / 60 x (PIP- PEEP) + PEEP
Ideal oxygenation saturations in neonates is:
88-95% - avoiding hypoxic ischemic vents such as HIE and gut ischemic but also preventing free radical generation
What is fetal lung fluid?
Its an ultra-filtrate of pulmonary capillary blood - it is not amniotic fluid
Discuss pulmonary/chest wall compliance in neonates vs adults
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
Discuss respiratory volumes in neonates compared to adults
- less respiratory reserve volumes
- decrease FRC
- increased closing capacity
- decreased expiratory reserve volumes
- increased residual volume
Why do neonate have increased minute ventilation
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
In the context of RSI why is it important to put your RSI meds on a pump infusion
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
Whats closing capacity
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)
In relation to the time settings, what helps differentiate TTN vs RDS
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
Discuss how GDM has an influence on RDS
RDS increases from poorly controlled GDM. This is because high serum insulin during fetal growth which inhibits the production of surfactant
Indications for BLES
- FiO2 > 30 and CPAP of 7cmH20
- Significant WOB
- CXR consisted with RDS
- MAS with RDS
TTN MGMT
- Neutral thermal environment
- High Flow 1-2LPM/KG
- nCPAP 5-7cmH20
- Intubation if failing CPAP
Complications of surfactant administrations
intermittent risk of airway obstruction/aspiration with application of surfactant
Synopsis of CDH
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)
Which side is generally insulted with CDH
Left sided more common
Common clinical manifestations of CDH
Barrel shaped chest
Scaphoid-appearing abdominal from less abdominal contents (going into chest)
Absent breath sounds on the ipsilateral side
How is CDH Dx?
Prenatally- US
Postnatally - AXR/CXR
Measurement of the lung to head ratio predicts the severity of pulmonary hypoplasia
CDH MGMT Pillars
- VENTILATION
- intubate immediately after birth
- NG tube to decompress the stomach
- avoid BVM/NIPPV
- preductal 85-95%
- gentle ventilation
- avoid sedation - HD Support
- cautious use of lfuids
- steroids
- inotropic support
- ECHO - Pulmonary HTN
- oxygen
- sedation
- iNO
- Sildenafil
- prostaglandin
- vasopressin
- milirinone
- ECMO
three types of apnea
Central, obstructives, mixed
Whats the differences in time frames from AOP and periodic breathing
AOP >20s
preiodic <20s
Bronchopulmonary Dysplasia is also known as
Neonatal chronic lung disease
BPD commonly occurs secondary to
CDH
Oliohydramnios
Low birth weight
prolonged mech vent or high FiO2 requirements
What is pulmonary interstitial emphysema
PIE the collection of air around the alveoli, associated to over-ventilation.
CXR presents similar to BPD or emphysema.
RSI for neonates
1mcg/kg atropine
3mcg/kg fentanyl
2mcg/kg suc
When does a fetus secrete and stop secreting pulmonary Na
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.
how long does it take for a baby to achieve ideal FRC in SVD or C-section
2-3 hours in SVD (FRC of 30ml/kg)
5-6 hr in C-Section
TTN definition
Transient tachypnea of the newborn is a lung disorder characterized by pulmonary edema resulting from delayed resorption and clearance of fetal alveolar fluid.
TTN pathophysiology synopsis
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
RDS patho
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.
MAS definition and patho
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
