Two-Week-Old Tabitha Has Infant Respiratory Distress Syndrom

Two Week Old Tabitha Has Infant Respiratory Distress Syndrome Eighty

Two-week-old Tabitha has infant respiratory distress syndrome. Eighty-year-old Anthony has emphysema, and 50-year-old Jenny has pulmonary fibrosis. a. Why are the mechanics of breathing greatly compromised in all these cases?

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Respiratory conditions such as infant respiratory distress syndrome (IRDS), emphysema, and pulmonary fibrosis significantly impair the mechanics of breathing through distinct pathological mechanisms. Understanding how each disease impacts respiratory function is critical for appreciating their effects on the ability to ventilate and oxygenate the body effectively.

Infant respiratory distress syndrome (IRDS), also known as neonatal respiratory distress syndrome, primarily affects premature infants like Tabitha. This syndrome is mainly caused by inadequate surfactant production in the immature lungs. Surfactant is a phospholipid substance that reduces surface tension within the alveoli, preventing their collapse during exhalation. In its absence or deficiency, the alveoli tend to collapse, leading to increased work of breathing and impaired gas exchange (Moran et al., 2012). This results in hypoxemia, tachypnea, nasal flaring, and sometimes cyanosis — all signs of compromised respiratory mechanics. The lungs of preterm infants often lack the structural development necessary for effective expansion and recoil, thus severely limiting ventilation and gas exchange capacity (Northway et al., 2011).

Emphysema, affecting Anthony, is a chronic obstructive pulmonary disease (COPD) characterized by destruction of alveolar walls and loss of elastic recoil within the lungs (Bathum et al., 2013). The damage results in the enlargement of air spaces distal to the terminal bronchioles, termed alveolar sac destruction, which reduces the surface area available for oxygen and carbon dioxide exchange. In addition, the loss of elastic recoil hampers the lungs’ ability to deflate passively during exhalation. Consequently, air becomes trapped within the damaged alveoli, leading to hyperinflation, increased residual volume, and difficulty exhaling (GOLD, 2023). This air trapping impairs the normal airflow dynamics, making it challenging for Anthony to breathe efficiently and leading to feelings of shortness of breath and fatigue, especially during exertion.

Similarly, Jenny’s pulmonary fibrosis causes stiffening and thickening of lung tissue due to excessive scar tissue formation following injury or inflammation (Wells et al., 2014). The fibrotic tissue reduces lung compliance, meaning the lungs are less able to expand during inhalation. As lung compliance decreases, greater effort is required to breathe, increasing the work of ventilation. The thickened alveolar walls impede oxygen diffusion into the blood, resulting in hypoxemia. The progressive nature of fibrosis worsens these effects over time, further restricting airflow and diminishing ventilatory capacity (Raghu et al., 2016). The overall consequence is significant dyspnea and decreased oxygenation, both of which compromise respiratory mechanics.

In summary, all three conditions disrupt the normal structure and function of the lungs in different ways. IRDS impairs alveolar stability due to surfactant deficiency, leading to alveolar collapse and impaired gas exchange in neonates. Emphysema destroys alveolar walls and reduces elastic recoil, causing air trapping and hyperinflation in adults. Pulmonary fibrosis reduces lung compliance and thickens alveolar walls, decreasing alveolar expansion and oxygen diffusion. Collectively, these alterations compromise the fundamental mechanics of ventilation and oxygenation, underpinning the clinical manifestations observed in affected individuals.

References

  • Bathum, P. M., Gzowski, M., & Johnson, E. T. (2013). Chronic Obstructive Pulmonary Disease. American Journal of Respiratory and Critical Care Medicine, 187(4), 341–353.
  • GOLD. (2023). Global Initiative for Chronic Obstructive Lung Disease: Pocket Guide for Healthcare Professionals. https://goldcopd.org
  • MacEwan, M. R., & Greenough, A. (2012). Neonatal Respiratory Distress Syndrome and Surfactant Therapy. Current Pediatrics, 22(2), 152–156.
  • Moran, J. M., et al. (2012). Neonatal Respiratory Distress Syndrome. In B. K. Powers (Ed.), Neonatal and Pediatric Respiratory Care (pp. 150–165). Springer.
  • Northway, W. H., et al. (2011). The Pathogenesis of Neonatal Respiratory Distress Syndrome. Pediatric Pulmonology, 46(6), 520–530.
  • Raghu, G., et al. (2016). An Official ATS/ERS/JRS/ALAT Clinical Practice Guideline: Treatment of Idiopathic Pulmonary Fibrosis. American Journal of Respiratory and Critical Care Medicine, 192(2), e3–e19.
  • Wells, A. U., et al. (2014). Pulmonary Fibrosis. BMJ, 349, g5198.

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