Module 6: Bronchopulmonary Dysplasia Flashcards
What are 2 major factors contributing to the etiology of BPD?
- prematurity and
- mechanical ventilation
What are 4 major risk factors of BPD?
- preterm birth,
- the need for supplemental oxygen and positive pressure ventilation,
- patent ductus arterious (PDA) and
- pre- and postnatal infection
**these risk factors trigger a systemic and pulmonary inflammatory response
What are the two major forms of BPD?
- “classic/old” or severe and
- “new” or mild.
**old BPD is more severe
What is the classic “old” BPD?
The severe form of chronic lung disease is seen less frequently due to the current treatment and management of infants suffering from respiratory distress (surfactant replacement, CPAP and ventilation, limiting hyperoxia).
Injury to relatively immature and surfactant-deficient lung is inflicted secondary to?
- high inspired oxygen concentrations (through production of free radicals) and
- high positive airway pressures (causing pulmonary barotrauma).
What are 2 things chronic lung disease characterized by?
- increased airway resistance resulting from airway inflammation, and
- to bronchial hyperresponsivenes.
What are two conditions infants with severe chronic lung disease develop?
- tracheomalacia and/or bronchomalacia,
- resulting in atelectasis and/or hyperinflation due to dynamic airway obstruction.
What does infant with “new” or mild form of BPD require?
- only low or moderate concentrations of oxygen and mechanical ventilation with low pressures, and usually respond favorably to the administration of surfactant
What is the lung development at 24-28 weeks of gestation?
- (the canalicular stage of human lung development extends to 26-28 weeks gestation) the lung is just beginning to develop into a gas exchanging organ.
- In the saccular (primitive alveolar) stage the distal saccules are alveolarised with parallel development of the alveolar capillary bed;
- alveoli are present at approximately 32 weeks.
Why is that the most important pathogenetic factors of infants who develop new BPD is not oxidant injury and mechanical ventilation?
- premature birth with initiation of pulmonary gas exchange interrupts normal alveolar development.
What are the lungs of infants with new BPD is characterized by?
- minimal alveolarisation,
- less airway epithelial disease,
- less severe vascular disease, and
- less interstitial fibrosis compared with lungs with alternating zones of overdistention and atelectasis in infants with severe BPD.
What is the new BPD understood to be reflect of?
- is understood to reflect extreme lung immaturity with an arrest of alveolar growth and development and
- an inflammatory response to treatment induced injury that leads to cycles of lung injury and repair.
What is the characteristic of old BPD
GA: 32 weeks
Infants at risk: more mature
BW: 1900g
- Airway injury: severe
- Interstitial fibrosis: severe
- Alveoli: Well developed in regions without fibrosis
- Causes: Oxygen toxicity and mechanical ventilation
What is the characteristic of new BPD
GA: 24-26 weeks
Infants at risk: LGA
BW: 600g
- Airway injury: mild to none
- Interstitial fibrosis: minimal
- Alveoli: Disruption in lung development (Vascular and alveolar impairment, Large simplified alveoli, Dysmorphic capillary configuration)
- Causes: interference with lung development
What are 2 primary culprits in the development of BPD?
- birth weight and gestational age
- although family predisposition to asthma, PDA, etc. have been associated with development of BPD
What is the relationship between free oxygen radicals and the development of BPD?
- We know that premature infants are prone to hypoxia.
- Under these hypoxic conditions, these infants often require oxygen therapy.
- However, not only can the rate of production of these (free oxygen radicals) exceed the capacity of these protective systems but also the systems themselves are immature and functioning at a lower level than those of the adult.
- Further, these free radicals have a direct toxic effect on pulmonary epithelial cells, causing cell membrane injury, enzyme inactivation and structural protein damage.
- Because of these damaging effects of free oxygen radicals, oxygen is not a harmless drug!
- Unfortunately, infants with BPD need supplemental oxygen … this supplemental oxygen, in turn, contributes to the ongoing damage to infants’ lungs.
What is the relationship between capillary leak syndrome and BPD?
- Capillary leak syndrome refers to the damage done to pulmonary capillaries, partly as a result of free oxygen radicals and partly due to the inflammatory process occurring in damaged lungs.
- Capillary leak syndrome results in loss of integrity of the pulmonary capillary walls.
- This enables fluid and protein that is normally confined to the vascular bed to leak into the lung tissue.
- This results in pulmonary edema and further lung damage.
Use your own words to describe the damage that occurs in the lungs of a premature infant who is receiving both positive pressure mechanical ventilation and supplemental oxygen.
- premature infants who require mechanical ventilation incur pulmonary damage because their immature lungs cannot withstand the damaging effects of oxygen toxicity (free radicals) and barotrauma (high inflating pressure).
- The result is alveolar and bronchiolar inflammation, edema, necrosis, atelectasis, overdistention, fibrotic scarring, and loss of elasticity.
- Unfortunately, all of this damage often means that further oxygen and ventilation support is required … and a vicious cycle of damage to lung tissue is established.
How can nurses either prevent or minimize BPD?
- Ultimately, preventing preterm birth would prevent BPD!
- Failing that, preventing the initial respiratory distress due to RDS that preterm infants develop would help to prevent and/or minimize BPD.
- Failing that, understanding the vicious cycle of BPD and providing care aimed at breaking the cycle would help to prevent and minimize BPD.
- Specifically, it is helpful for nurses to aim their care at both supporting infants’ normal ventilation and minimizing infants’ oxygen needs.
For example:
- minimizing pain, stress, and handling would serve to decrease oxygen consumption.
- Maintaining thermal regulation would decrease oxygen consumption.
- Maintaining Sp02 within target parameters, helps to prevent hypoxia and hyperoxia.
- Proper positioning can both decrease stress for infants and can serve to support normal breathing.
Reflect also upon resuscitation of these vulnerable infants.
Ensuring adequate, effective resuscitation with maintenance of body temperature is essential for reducing the incidence and severity of this disease.
What does infant with BPD is very labile?
meaning that it can change quickly without much warning.
What is one reason for the lability of infant with BPD?
- one of the reasons for this lability is that the lungs of infants with BPD are often damaged to the extent that there is very little in the way of respiratory reserve.
- Minor changes in an infant’s condition, such as a small amount of pulmonary edema, a small amount of secretions, fluid overload, a slight increase in atelectasis - any of these changes can cause an infant with BPD to decompensate.
What is another reason for labile respiratory status of infants with BPD?
- relates to the effect of hypoxia on pulmonary blood vessels.
- Hypoxia causes pulmonary vasoconstriction.
- This, in turn, leads to decreased pulmonary perfusion.
- Decreased perfusion leads to further hypoxia, which increases pulmonary vasoconstriction.
- A vicious cycle of hypoxia and pulmonary vasoconstriction can become established in these infants.
What the range of O2 saturation be for infant with BPD?
- 88-92% if < 36 weeks gestation and
- 90-94% if > 36 weeks gestation,
***while being mindful that hyperoxia is detrimental as well.
How does BPD affect infants blood gases?
- Typically, pCO2 is elevated; accumulation of CO2 is a result of decreased elimination, owing to damaged (inflamed, scarred, atelectatic, hyperinflated) alveoli. - Initially, the elevated pCO2 produces an acidotic pH, often below 7.30.
- Over time, the kidneys compensate for the chronic respiratory acidosis by retaining HCO3, a base.
- The combination of excess CO2 (acid) and increased HCO3 (base) results in a neutralized pH.
- In other words, over time, the pH returns to normal.
- This process is known as compensation and, in infants with BPD, results in a compensated respiratory acidosis.