Related Experiment Videos
Pulmonary vascular response to oxygen in infants with severe bronchopulmonary dysplasia
Insights
Infants with bronchopulmonary dysplasia (BPD) and pulmonary hypertension showed responsive pulmonary vascular beds to oxygen. Continuous oxygen therapy may help treat this condition in BPD patients.
Area of Science:
- Pediatric Cardiology
- Neonatology
- Pulmonary Medicine
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in infants.
- Persistent pulmonary hypertension is a common complication of BPD.
- Infants with BPD often have prolonged oxygen requirements and right ventricular hypertrophy.
Purpose of the Study:
- To investigate the pulmonary vascular bed's responsiveness to oxygen tension in infants with BPD and pulmonary hypertension.
- To assess the efficacy of supplemental oxygen in reducing pulmonary artery pressure in these infants.
Main Methods:
- Retrospective review of cardiac catheterization data from six infants with BPD.
- Measurement of mean pulmonary artery pressure (mPAP) in room air and with varying levels of inspired oxygen (FiO2).
- Assessment of mPAP changes with low-flow nasal cannula oxygen therapy.
Main Results:
- All infants had elevated mPAP in room air (mean 48 mm Hg).
- High FiO2 (greater than 80%) significantly reduced mPAP (mean 25 mm Hg, P < .005).
- Most of this reduction occurred at lower, outpatient-level oxygen flow rates via nasal cannula.
Conclusions:
- Infants with BPD and pulmonary hypertension generally exhibit reactive pulmonary vascular beds.
- Supplemental oxygen, even at low flow rates, can effectively reduce pulmonary artery pressure.
- Continuous oxygen therapy via nasal cannula may be a beneficial treatment for pulmonary hypertension associated with BPD.
Abstract:
The cardiac catheterization data of six infants with bronchopulmonary dysplasia (BPD) were reviewed to examine the responsiveness of their pulmonary vascular beds to changes in oxygen tension. The infants were studied because of slow recovery from their oxygen requirements and clinical evidence of persistent pulmonary hypertension. All were receiving home oxygen therapy and had abnormal chest radiographs and right ventricular hypertrophy by ECG at the time of catheterization (mean age, 25 months). All infants had mean pulmonary artery pressure greater than 25 mm Hg in room air, with a mean of 48 mm Hg. All decreased mean pulmonary artery pressure by at least 10 mm Hg when placed in high levels of inspired oxygen (FiO2 greater than 80), with a mean pulmonary artery pressure of 25 mm Hg. This represented a significant decrease in mean pulmonary artery pressure from room air pressures (P less than .005). Mean pulmonary artery pressure was also measured in three infants who were breathing supplemental oxygen by nasal cannula at flow rates similar to levels used for outpatient therapy. Most of the reduction in mean pulmonary artery pressure that occurred at high FiO2 occurred at these lower flow rates of supplemental oxygen. It is concluded that infants with bronchopulmonary dysplasia who have pulmonary hypertension generally have reactive pulmonary vascular beds, responsive to supplemental oxygen. Continuous oxygen therapy by nasal cannula may be useful in the treatment of pulmonary hypertension associated with bronchopulmonary dysplasia.