Apnea of Prematurity and BPD Flashcards
Premature infants and Periodic Respirations
Premature infants will have periodic respiration which comprise of sequential short apneic episode of 5-10 seconds followed by 10-15 seconds of rapid respirations
Apneic spells are abnormal when they last longer than 15 seconds or are associated with cyanosis, pallor, hypotonia, or bradycardia
Central Apnea
If no effort to breathe occurs during a apnea spell then it is known as a central apnea
Obstructive Apnea
If there is breathing effort but an obstruction is preventing the airflow than it is known as an obstructive apnea
Mixed Apnea
Mixed apnea is a combination of the central and obstructive types that start as obstructive and then will develop into being central
Primary Apnea
Apnea and bradycardia where the baby recovers with tactile stimulation
Secondary Apnea
Apnea and Bradycardia, does not recover with tactile stimulation, requires PPV to recover
What is babies respond to CO2 in babies
When there is an increase in CO2 babies will slow down their breathing and take bigger breaths to try and compensate
Premature Infants and Control of Respiration
Premature infants have immature control of respiratory drive in response to O2 and carbon dioxide (CO2).
In mature animals, an increase in alveolar PaCO2 elicits an increase in VT and respiratory rate. A decrease in FiO2 below room air also triggers an increase in VT.
In premature animals, an increase in PaCO2 temporarily increases VT but does not increase respiratory rate. A decrease in FiO2 below room air decreases VT and respiratory rate. This effect can lead to apnea in a premature infant.
External causes of apnea
Temperature, suction, vagal stimulation
Apneas can Lead to
Apneas can lead to bradycardia, arrythmias, and respiratory arrest
Frequent Apneas can lead to
Frequent apneas can lead to cerebral hypoxia and ischemic brain injury
Clinical Manifestation of Apnea
Snoring, choking, gasping
Cyanosis
Bradycardia
Hypoxia
Apnea that is secondary to prematurity should be treated with
methylxanthines, especially theophylline and caffeine.
These agents stimulate the central nervous system and increase the infant’s responsiveness to CO2.
CPAP for Apnea
CPAP also can be used to manage infant apnea.
CPAP probably increases FRC and improves arterial partial pressure of oxygen (PaO2) and PaCO2. CPAP may stimulate vagal receptors in the lung, increasing the output of the brainstem respiratory centers. Severe or recurrent apnea that is unresponsive to these interventions may necessitate mechanical ventilatory support.
Resolution of Apnea of prematurity
Apneic spells begin to disappear by weeks 37 to 44 of postmenstrual age with no apparent long-term effects. Infants who have apnea of prematurity are not at higher risk for sudden infant death syndrome (SIDS) than other infants.
bronchopulmonary dysplasia (BPD).
Infants, especially preterm infants, with severe respiratory failure in the first few weeks of life may develop a chronic pulmonary condition called bronchopulmonary dysplasia (BPD).
4 factors in BPD Pathogenesis
Lung immaturity
Respiratory failure
Oxygen supplementation
Mechanical ventilation
bpd vs rds
BPD IS an obstructive disease and RDS is a restrictive disease
The New BPD Diagnosis Criteria
The Diagnosis of bPD is based on how long the baby need oxygen and how much oxygen is needed
initiatin Fators in bPD
• The initiating factors are related to atelectrauma (lung collapse) and volutrauma (large tidal volume [VT]). Factors such as hyperoxia and hypoxia, mechanical forces, vascular maldevelopment, inflammation, nutrition, and genetics contribute to the abnormal development of the lung and lead to BPD.
Atelectrauma
Atelectrauma is a term coined to describe loss of alveolar volume that is both a result and a cause of lung injury. Atelectrauma leads to derecuitment (e.g., areas of alveolar collapse) of the lung.
Volutrauma
o Volutrauma is the term used to describe local overinflation (and stretch) of airways and alveoli. Volutrauma leads to damage to airways, pulmonary capillary endothelium, alveolar and airway epithelium, and basement membranes.
what is the result of atelectrauma and volutrauma
Both atelectrauma and volutrauma cause a need for increased supplemental O2 concentrations. whichleads to overproduction of superoxide, hydrogen peroxide, and perhydroxyl radicals. Preterm infants are particularly susceptible to O2 radicals because the antioxidant systems develop in the last trimester of pregnancy. Prolonged hyperoxia begins a sequence of lung injury that leads to inflammation, diffuse alveolar damage, pulmonary dysfunction, and death.
The response of the lungs to the combination of trauma and O2 toxicity
The response of the lungs to the combination of trauma and O2 toxicity is the production and release of soluble mediators. These mediators probably are released from granulocytes residing in the lung. The release of these mediators can injure the alveolar-capillary barrier and cause an inflammatory response.
BPD Progression
CXR in the first day of life shows a mild ground glass appearance consistent with RDS
CXR at 2 weeks of age with early BPD changes
CXR at 1 month of age showing progressive BPD with pulmonary edema and atelectasis
Diganosis of BPD
Diagnosis is based on clinical manifestation and CXR, but these are not specific.
What needs to be rules out before BPD can be diagnosed
o Congenital heart disease o Pulmonary lymphangiectasia o Pneumonitis o Cystic Fibrosis o Surfactant protein deficiency
Chest X-ray for BPD
• The chest radiograph in severe disease shows areas of atelectasis, emphysema, and fibrosis diffusely intermixed throughout the lung
ABG in BPD
• ABG measurements reveal varying degrees of hypoxemia and hypercapnia secondary to airway obstruction, air trapping, pulmonary fibrosis, and atelectasis. There is a marked increase in airway resistance with an overall decrease in lung compliance.
Clinical Manifestations of BPD
Respiratory distress
o Tachypnea
o Cyanosis
o Intercostal retraction
o Nasal flaring
• Auscultation: fine crackles and expiratory wheeze
• Increased airway resistance and sensitivity (bronchospasms)
• Increased FRC and Hyperinflation associated with severe BPD
What is the best treatment for BPD
The best treatment is prevention
Prevention of atelectrauma and volutrauma begins in the delivery room, with the establishment of an optimal FRC without over- stretching the lung r
Surfactant should be delivered early in the course of treatment.
o Other methods of prevention include
Nasal Positive Pressure Ventilation
Mechanical ventilation with permissive hypercapnia
Oxygen therapy to maintain targeted oxygen saturations
iNO for certain cases (PPHN)
Adequate nutrition
Corticosteroids
Caffeine or methylxanthines
Prevention of Minimizing Additional Lung Injury
Supplemental O2 can help decrease the pulmonary hypertension that is common with BPD
Diuretics are given as needed to decrease pulmonary edema; antibiotics are given to manage existing pulmonary infection.
o Chest physical therapy may help mobilize secretions and prevent further atelectasis.
o Bronchodilator therapy may help decrease airway resistance.
o Steroid therapy with dexamethasone can produce substantial short-term improvement in lung function, often allowing rapid weaning from ventilatory support. However, steroid therapy has little effect on long-term outcome such as mortality and duration of O2 therapy. Steroid therapy also has been implicated in decreased alveolarization and increased developmental delay. Although steroids are still given in clinical practice, they should be used cautiously and only after the risks have been thoroughly explained to the parents. The use of NO to prevent or improve BPD is controversial.
What is characterized by cycles of hyperventilation followed by short apneic pauses of less than 3 seconds?
Periodic breathing.
What is the purpose of central chemoreceptors?
They increase ventilation in response to low cerebral spinal fluid pH.
How is apnea of prematurity defined clinically?
Cessation of breathing for >20 seconds with bradycardia and hypoxemia for >10 seconds.
Which of the following are considered detrimental consequences of apnea in neonates?
Hypoxemia, hypercarbia, and bradycardia.
What long-term treatments are available to treat or prevent apnea of premature?
Methylxanthine, Nasal cannula, Blood transfusions, NCPAP, and Caffeine citrate.
At what age do most infants resolve apnea issues?
37 weeks postmenstrual age.
What risk factors increase the likelihood for more severe bronchopulmonary dysplasia?
Surfactant therapy and Nosocomial infection.
Which of the following are strategies to consider for the treatment of respiratory distress syndrome to minimize the risk of bronchopulmonary dysplasia?
Arterial oxygen tension >90mmHg, Surfactant administration prior to MV, Extubating to NIPPV in the first month of life.
What is essential for the optimal growth of cells and tissues?
Vitamin A.
What is the diuretic of choice for ventilator-dependent infants with evolving or established bronchopulmonary dysplasia (BPD)?
Thiazide.
What is apnea of prematurity (AOP)?
A sudden cessation of breathing that lasts for at least 20 secs or is accompanied by bradycardia or oxygen desaturation in an infant younger than 37 weeks gestation.
What are the causes of apnea in premature infants?
Incorrect neural signaling and airway obstruction.
