Respiratory Flashcards
All infants <30wks should automatically be started on CPAP in the DR
Benefits of CPAP
-deters alveolar collapse
-increases end-expiratory lung volumes
-maintains functional residual capacity (FRC).
Indications for nitric oxide
> 34wks, PaO2<100 on 100% O2 and OI >20
Literature suggests there is no difference in oxygenation response between 20 ppm and 5-6 ppm, though 20ppm is associated with an improved pulmonary-systemic blood flow ratio
Response to nitric oxide
-PaO2 increase by >20mmHg or 20% from baseline
-increase O2 sats by 10%
**assess after 30mins
20/20/20 rule
concerning methemoglobin level
If >5%
Can begin weaning FiO2 after 4 hours of iNO by 5% per hour
fetal absorption of fluid
- 1/3 absorbed prenatally during labor
- 1/3 absorbed during vaginal delivery
- 1/3 absorbed after delivery
Mechanism of fluid absorption
-Onset of labor, maternal epinephrine, and glucocorticoids activate the ENaC on the apical membranes of type II pneumocytes.
-Sodium in the alveolus is transported passively across the ENaC proteins which in turn is actively transported back to the interstitium by the Na+/K+-ATPase pump
-An osmotic gradient is created which allows chloride and water to follow and be absorbed into pulmonary circulation and lymphatics.
if placenta undergoes stress might increase innate steroid release for baby and result less severe RDS vs chorioamnioitis results in diffuse inflammation response and worsening RDS
Diabetes and surfactant
hyperglycemia and hyperinsulinemia can disrupt surfactant lipid and protein synthesis, causing delayed maturation in surfactant in IDM
TTN time frame
symptomatic for 12 to 24 hours, but signs may persist as long as 72 hours
RDS peak time
48-72hrs
hyperoxia does not enhance pulmonary vasodilation-> increased free radius that increase pulmonary arterial contractility and impairs vasodilation effects of iNO
Atelectotrauma
repeated alveoli deflation and decreased lung volumes
-look at flow volume loop should see immediate increase upon a breath
volutrauma
inflation of lungs to volumes that approach the total lung capacity
barotrauma
overinflation and shearing stressed due to high PIPs
Minimal tidal volume: <1kg: 5ml/kg, >1kg: 4.5ml/kg
causes of pulmonary edema
-too much blood/fluid going to the lungs
-increase leaking at capillary (sepsis, hypoxemia, hypoxia, RDS)
-increase resistance to blood leaving lungs (TAPVR, tamponade)
Avoid caffeine in preterm infants likely to remain mechanically ventilated beyond 10 post natal days
CAP trial
The use of caffeine was associated with decreased risk of bronchopulmonary dysplasia (anti-inflammatory effect) and cerebral palsy at 2 years
VitA criteria
<28wks, >28wks + <1kg +needs for mechanical ventilation or supplemental oxygen at 24hrs of life
-outborn qualifies if first dose given by 96hrs of life
Benefits of VitA
-reduce the incidence of death or BPD at 36 weeks
-reduction in oxygen requirement at one month of age and a marginal reduction in oxygen use at 36 weeks
-reductions in periventricular leukomalacia and any grade of ROP
Early postnatal (<8days) corticosteroid treatment adverse effects
-gastrointestinal bleeding, intestinal perforation, hyperglycemia, hypertension, hypertrophic cardiomyopathy and growth failure.
- increased risk of abnormal neurological examination and cerebral palsy
Late postnatal (>8days) DART therapy
may reduce neonatal mortality without significantly increasing the risk of adverse long-term neurodevelopmental outcomes
Threshold for DART therapy
> 65% risk for BPD: lower risk for death or CP (less harm)
<35% risk for BPD: increase risk of death or CP, neurodevelopment impairment
Causes of BPD
-Prematurity
-Positive pressure ventilation
-prolonged oxygen exposure-free oxygen radicals
-protracted use of ET tubes
-pulmonary edema (PDA, over hydration, delayed diuresis)
-pulmonary air leak (PTX, PIE)
-proinflammatory cascade
these variable affect the growth and development of the lungs + injury->inflammation +
younger the infant at birth the higher change the lungs not develop properly since more development takes place outside womb
Vit A mechanism
needed for lung growth and keep epithelial cells of respiratory tract functioning
BPD outcomes
-more likely to have respiratory symptoms (WOB, wheezing, tachypnea)
-increase re-hospitalzization and infections
-neurodevelopmental delay (cognitive/motor)
-cor pulmonale 2/2 pulmonary hypertension
-growth failure
goal of management in BPD
-once stability is met, reduce respiratory support and medications in a way that maintains stability and growth while avoiding unnecessary stress (affect levels of inflammation-> affect progress, growth, development)
-provide adequate respiratory support in all states to allow infant to grow, develop and slowly gain improving respiratory function
PFTs for infants with severe BPD
-91% had obstructive or obstructive/restrictive mixed lung disease (obstruction was mostly moderate or severe)
-heterogenous lung disease (area of atelectasis, and hyperinflation)
-chronic airway inflammation
-dynamic airway collapse
PIP settings for severe BPD
-higher PIP to overcomes increased airway resistance and allow recruitment
-should have good air exchange and visible chest rise correlates with good air flow
Optimal Tidal Volume
-10-12mL/kg during stable states
-higher in inflammatory states. (15-18mL/kg).
Lower rates and increase i-time
-supports lung recruitment and allow time for emptying
0.55-0.6: rr 25
0.6-0.65: rr 20
0.65-0.7: rr 18
0.8: rr 15
Steady linear growth in severe BPD
-Has recently been shown to predict improved tolerance and success to respiratory support decreases
-improved survival, developmental outcomes
A stable respiratory status generally
allows tolerance of movement (improve muscle tone/strength allows weaning of the ventilator), improving neuro-regulation and engagement, and steady linear growth.
long-term use of diuretics and low mobility combined, substantially increases
the risk of poor bone mineralization
high levels of NaCl replacements may lead to fluid retention
management of severe BPD
-optimize vent
-inhaled steroids
-bronchodilators (75%/63% of obstructive/mixed group were responsive), improved airflow, decrease in needed PIP to delivery goal tidal volumes
-nutrition
-diuretics
-systemic steroids (acute source of inflammation, regain stability, 3-10 days prevent adrenal suppression)
Recruitment, decrease V/Q mismatch, adequate air flow and emptying->less “air hunger”
As inflammation subsides, and linear growth resumes, gradually see decreasing oxygen needs and improving C02.
DART Trial
-faciliate extubation in preterm infants
-first 4-6 weeks of life
Other factors to focus on when weaning medications in severe BPD
- NAS score
-impact of the stress of weaning on ability to maintain stability of respiratory status and engage with their environment
Higher PEEP in severe BPD
-Can worsen ability to get air flow in due to more pressure must overcome
-can worsen the area of lung that is over inflated
-range: 8-9
Using atelectasis, hyperinflation, and air trapping to assess rate and i_time
If atelectasis: drop the rate to give pressure more time to get air in
if hyperinflation or air trapping either drop the time or the rate
The issue with high pressure support in distress
tachypneic and infant has large tidal volume (taking good breath plus high pressure support) leads to inadequate expiration time
-can sometimes give sedation and drop the PS to help
-goal: 10-14
The issue with high pressure support in distress
tachypneic and infant has large tidal volume (taking good breath plus high pressure support) leads to inadequate expiration time
-can sometimes give sedation and drop the PS to help
-goal: 10-14
lasix has ventilator (via prostaglandin pathway) and diuretic effects
SUPPORT Trial
-CPAP vs surfactant and intubation
-No difference in death of BPD
-CPAP group:Less frequently required intubation or postnatal corticosteroids for bronchopulmonary dysplasia, required fewer days of mechanical ventilation, and were more likely to be alive and free from the need for mechanical ventilation by day 7
-Study support consideration of CPAP as an alternative to intubation and surfactant in preterm infants
Prenatal growth of CPAM
- increase in size until 26 – 28 weeks’ gestation
-after many plateau or even decrease
CVR (CPAM volume ratio) measurement, CPAM
-size of lung lesion in relation to size of baby (head circumference)
>1.6 increase risk for developing heart failure
CPAM +hydrops
-large lesions shift the heart and impair venous return or compression of lymphatic structure-> fetal heart failure (hydrops-skin edema, pleural effusion, ascites, pericardial)
Complications of CPAM
in utero: compression of lungs (lead to pulmonary hypoplasia), displacement heart, hydrops
infections, malignancy (pleuropulmonary blastoma)
lungs grow best when they are expanded
PPH can be due to increase vascular or increase flow
PPHN worse in first 72hrs
