A P2G1 diabetic woman is at risk of delivering at 29 weeks gestation. Her obstetrician counsels her that there is a risk the baby could have significant pulmonary distress after it is born. However, she states she will give the mother corticosteroids, which will help prevent this from occurring. Additionally, the obstetrician states she will perform a test on the amniotic fluid which will indicate the likelihood of the infant being affected by this syndrome. Which of the following ratios would be most predictive of the infant having pulmonary distress?

lecithin:phosphatidylserine < 1.5

lecithin:phosphatidylserine > 3.0

A P1G0 diabetic woman is at risk of delivering at 30 weeks gestation. Her obstetrician counsels her that there is a risk the baby could have significant pulmonary distress after it is born. However, she states she will administer a drug to the mother to help prevent this from occurring. By what action will this drug prevent respiratory distress in the premature infant?

Increasing the secretory product of type II alveolar cells

Promoting increased surface tension of alveoli

Suppressing the neonatal immune system

Preventing infection of immature lungs

Reducing the secretory product of type II alveolar cells

A 19-year-old primigravid woman at 32 weeks' gestation comes to the physician because of a 2-day history of headache and blurred vision. She has had no prenatal care. She is diagnosed with pre-eclampsia. Amniocentesis shows a lecithin-sphingomyelin ratio of 0.7. If delivery is induced at this time, the newborn is most likely to show which of the following findings?

Decreased functional residual capacity

Increased diffusion capacity for carbon monoxide

Decreased right ventricular afterload

Increased anatomical dead space

Two days after undergoing left hemicolectomy for a colonic mass, a 62-year-old man develops shortness of breath. His temperature is 38.1°C (100.6°F), pulse is 80/min, respirations are 22/min, and blood pressure is 120/78 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 88%. Cardiopulmonary examination shows decreased breath sounds and decreased fremitus at both lung bases. Arterial blood gas analysis on room air shows: pH 7.35 PaO2 70 mm Hg PCO2 40 mm Hg An x-ray of the chest shows a collapse of the bases of both lungs. Which of the following is the most likely underlying mechanism of this patient's hypoxemia?

Decreased ratio of ventilated alveoli

Decreased hemoglobin oxygen-binding capacity

Decreased chest wall compliance

A 68-year-old man with both severe COPD (emphysema) and newly diagnosed idiopathic pulmonary fibrosis presents with worsening dyspnea. His pressure-volume curve shows a complex pattern with features of both diseases. Static compliance measured at mid-lung volumes is 120 mL/cm H2O. His pulmonologist must decide on optimal management. Synthesizing the pathophysiology of both conditions, what represents the most significant clinical challenge in managing his combined disease?

The opposing effects on compliance create a pseudonormal total respiratory compliance masking disease severity

Pulmonary rehabilitation cannot address the opposing mechanical derangements

The increased compliance from emphysema completely negates decreased compliance from fibrosis

Emphysema treatment with bronchodilators will worsen fibrosis progression

Oxygen therapy beneficial for COPD will accelerate fibrotic changes

A 42-year-old woman with systemic sclerosis develops both pulmonary fibrosis and chest wall restriction from skin thickening. Her measured total respiratory system compliance is 30 mL/cm H2O. Testing with complete paralysis and positive pressure ventilation shows isolated lung compliance of 50 mL/cm H2O. She is being considered for immunosuppressive therapy versus supportive care. Evaluate which intervention would provide the greatest improvement in her respiratory mechanics.

Combined therapy targeting lung disease with chest wall mobilization

Supportive care only, as both components contribute equally and irreversibly

Aggressive immunosuppression targeting both lung and skin disease

Lung-directed therapy only, as it contributes more to total compliance reduction

Chest wall-directed physical therapy, as it is the primary limiting factor

A 58-year-old man with end-stage pulmonary fibrosis is being evaluated for lung transplantation. His current static compliance is 25 mL/cm H2O (normal: 200 mL/cm H2O). He also has mild obesity (BMI 32) and ankylosing spondylitis affecting chest wall mobility. Post-transplant, assuming successful bilateral lung transplant with normal donor lungs, what would be the expected change in his total respiratory system compliance?

Improved but still reduced compliance due to persistent chest wall restriction

Improved lung compliance but worsened chest wall compliance from surgery

Worse compliance initially due to transplant rejection and denervation

Return to completely normal respiratory compliance matching healthy individuals

No significant change because the primary problem is muscular weakness

A research study compares two patients with different lung pathologies but identical functional residual capacity (FRC) of 3.0 L. Patient A has pulmonary fibrosis with FRC above the steep portion of the compliance curve. Patient B has emphysema with FRC on the flat upper portion of the curve. Both attempt to inhale the same tidal volume. Analyzing their work of breathing, which statement best characterizes the difference?

Patient B does more elastic work due to hyperinflation beyond optimal compliance

Patient B does less work because emphysematous lungs are more compliant

Patient A does less work because fibrotic lungs have increased elastic recoil assisting inspiration

Patient A does more elastic work; Patient B does more resistive work

Both do equal work because FRC and tidal volumes are identical

Surface tension effects on compliance | Compliance

Surface Tension & Compliance - The Bubble Trouble

The thin fluid layer lining alveoli creates surface tension, an inward-pulling force that opposes lung inflation (↓ compliance) and promotes collapse (atelectasis).
Law of Laplace: Describes this collapsing pressure as $P = 2T/r$ (Pressure = 2 × Tension / radius).
- This implies smaller alveoli (↓ radius) are more prone to collapse than larger ones.
Pulmonary Surfactant: Secreted by Type II pneumocytes, primarily dipalmitoylphosphatidylcholine (DPPC).
- It disrupts the cohesive forces between water molecules, reducing surface tension.
- This action increases compliance and stabilizes alveoli, preventing atelectasis.

⭐ In Neonatal Respiratory Distress Syndrome (NRDS), a deficiency of surfactant leads to high surface tension, causing widespread alveolar collapse and severe breathing difficulty.

Laplace's Law and Surfactant in Alveoli

Pulmonary Surfactant - Soapy Super-Stabilizer

Composition & Source: A lipoprotein complex, rich in dipalmitoylphosphatidylcholine (DPPC). Synthesized and secreted by Type II pneumocytes.
Primary Function: Reduces surface tension at the air-liquid interface within alveoli.
- Disrupts the hydrogen bonds between water molecules.
- Results in ↑ pulmonary compliance and ↓ work of breathing.
- Prevents alveolar collapse (atelectasis), especially during expiration.
Law of Laplace & Stability: $P = 2T/r$
- P=Collapsing pressure, T=Surface tension, r=Radius.
- Without surfactant, smaller alveoli (↓r) would have ↑P and empty into larger ones.
- Surfactant's effect is radius-dependent; it reduces T more in smaller alveoli, equalizing pressures and stabilizing them.

⭐ In Neonatal Respiratory Distress Syndrome (NRDS), surfactant deficiency in premature infants causes high alveolar surface tension, leading to diffuse atelectasis and respiratory failure. Antenatal corticosteroids are a key intervention.

Clinical Correlates - When the Bubble Bursts

Neonatal Respiratory Distress Syndrome (NRDS)
- Cause: Prematurity (< 35 weeks gestation) → insufficient surfactant production by Type II pneumocytes.
- Pathophysiology: ↑ surface tension → widespread alveolar collapse (atelectasis) → ↓ lung compliance, ↓ Functional Residual Capacity (FRC), and severe V/Q mismatch.
- Tx: Antenatal corticosteroids to mother; exogenous surfactant to infant.
Acute Respiratory Distress Syndrome (ARDS)
- Cause: Lung injury (sepsis, pneumonia, trauma) damages pneumocytes and inactivates surfactant.
- Pathophysiology: Protein-rich edema fluid enters alveoli, disrupting the surfactant layer → ↑ surface tension, non-cardiogenic pulmonary edema, and stiff, poorly compliant lungs.

⭐ The lecithin-to-sphingomyelin (L/S) ratio in amniotic fluid assesses fetal lung maturity. A ratio > 2.0 indicates low risk of NRDS.

Chest X-ray: ARDS with diffuse ground-glass opacities

High‑Yield Points - ⚡ Biggest Takeaways

Pulmonary surfactant, secreted by Type II pneumocytes, profoundly reduces alveolar surface tension.

This reduction increases lung compliance, making it easier to inflate the lungs, and prevents atelectasis (collapse).

Its primary component is dipalmitoylphosphatidylcholine (DPPC).

Per the Law of Laplace, surfactant's effect is greatest in smaller alveoli, preventing them from collapsing into larger ones.

A deficiency causes Neonatal Respiratory Distress Syndrome (NRDS).