Question

A newborn exhibits signs of respiratory distress due to the lack of surfactant. She has signs of low oxygen and high carbon dioxide.Explain why the lack of surfactant would result in respiratory distress. Furthermore, what type of acid-base disorder might she develop and how would her body compensate. Be detailed in your explanation and support your answer with facts from your textbook, research, and articles from scholarly journals. In addition, remember to add references in APA format to your posts to avoid plagiarism.

Answer 1

The absence of surfactant in a newborn causes respiratory distress syndrome by preventing alveoli from inflating, leading to hypoxia and acidosis. The body compensates by increasing respiratory rate and kidney function to balance pH. Pulmonary surfactant therapy is a critical treatment that has significantly reduced RDS mortality.

Step-by-step explanation:

Respiratory distress syndrome (RDS) in newborns can be attributed to the lack of pulmonary surfactant, which is vital for reducing surface tension and facilitating alveolar inflation. Without surfactant, the alveoli collapse, creating a condition where it's arduous to reopen the air sacs with each breath; this condition is known as infant respiratory distress syndrome (IRDS). The presence of surfactant is necessary because it minimizes the effort required to expand the lungs during inhalation and prevents alveolar collapse during exhalation, ensuring that oxygen can be appropriately exchanged for carbon dioxide in the blood.

Without sufficient surfactant, the newborn's lungs struggle to inflate, leading to hypoxia (low oxygen in the blood) and the potential build-up of carbon dioxide, making the blood more acidic— a condition known as acidosis. This acid-base imbalance can result in a disorder known as respiratory acidosis, where the body tries to compensate by increasing the respiratory rate to blow off excess carbon dioxide and by the kidneys increasing the secretion of hydrogen ions to reabsorb bicarbonate, buffering the acidity.

Medical interventions for RDS include administration of exogenous pulmonary surfactant, use of nasal continuous positive airway pressure (CPAP), and ventilation support if necessary. The introduction of surfactant therapy has reduced mortality due to RDS by 50%.

Answer 2

- The pulmonary surfactant decreases the surface tension in the lungs

- Protein-lipid interactions at air-liquid interfaces are influenced by pH changes, and therefore alter pulmonary surfactant function.

- Mutations in the surfactant associated proteins SP-C may lead to respiratory acidosis

Step-by-step explanation:

The pulmonary surfactant is a surface-active lipoprotein complex (phospholipoprotein) produced by type II alveolar pneumocytes that act to decrease the surface tension between gaseous-aqueous interphase in the lungs. Pulmonary surfactant is composed of 90% lipids and 10% of four lipid-associated proteins, SP-A, SPB, SP-C, and SP-D (Veldhuizen et al. 1998, Dieudonné et al. 2001). Protein-lipid interactions at the air-liquid interphase are influenced by pH changes, and therefore they may alter pulmonary surfactant function (Amirkhanian and Merritt, 1995). Surfactant dysfunction may be caused by mutations in one of the protein-encoding genes SFTPB, SFTPC, and ABCA3, which are involved in surfactant production (Peca et al. 2011). Respiratory acidosis is an acid-base disorder characterized by the failure of ventilation and an accumulation of carbon dioxide (Patel and Sharma 2020). It has been shown that one mutation in the surfactant protein C gene (SP-C) leads to neonatal respiratory failure associated with respiratory acidosis (Soraisham et al. 2006).

References (APA format)

1. Amirkhanian, J. D., & Merritt, T. A. (1995). The influence of pH on surface properties of lung surfactants. Lung, 173(4), 243-254.

2. Dieudonné, D., Mendelsohn, R., Farid, R. S., & Flach, C. R. (2001). Secondary structure in lung surfactant SP-B peptides: IR and CD studies of bulk and monolayer phases. Biochimica et Biophysica Acta (BBA)-Biomembranes, 1511(1), 99-112.

3.Patel, S., & Sharma, S. (2020). Respiratory acidosis. StatPearls.

4. Peca, D., Petrini, S., Tzialla, C., Boldrini, R., Morini, F., Stronati, M., ... & Danhaive, O. (2011). Altered surfactant homeostasis and recurrent respiratory failure secondary to TTF-1 nuclear targeting defect. Respiratory research, 12(1), 1-8.

5. Soraisham, A. S., Tierney, A. J., & Amin, H. J. (2006). Neonatal respiratory failure associated with mutation in the surfactant protein C gene. Journal of perinatology, 26(1), 67-70.

6. Veldhuizen, R., Nag, K., Orgeig, S., & Possmayer, F. (1998). The role of lipids in pulmonary surfactant. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1408(2-3), 90-108.