Renal transplant recipients with coexisting bronchiectasis and fibro-interstitial lung disease exhibit complex respiratory physiology that fundamentally alters perioperative gas exchange. Arterial blood gas (ABG) interpretation in such patients must integrate basic sciences—alveolar diffusion theory, V/Q matching, dead-space physiology, structural lung disease mechanics, ESRD acid–base chemistry, hemoglobin dissociation kinetics, and cardiopulmonary interactions—together with real-time clinical variables.
This article analyzes three perioperative ABGs (preoperative, intraoperative, and post-extubation) in a 61-year-old male with bronchiectasis, fibrocalcific TB sequelae, ground-glass opacities, pleural thickening, and mild pulmonary hypertension. The analysis highlights how CT-documented structural disease shapes oxygenation, ventilation, diffusion, acid–base status, and metabolic response in renal transplant anesthesia.

Bronchiectasis and ESRD each distort fundamental components of respiratory and acid–base physiology:

1.1 Disrupted Airway Geometry & Dead Space

Bronchiectasis enlarges conducting airways.
These do not participate in gas exchange, increasing physiological dead space (VD):

↑VD/Vt → ↑ wasted ventilation → potential for CO₂ retention, especially after extubation.

1.2 Impaired V/Q Matching

Structural distortion → some regions ventilated but poorly perfused (high V/Q), others perfused but poorly ventilated (low V/Q).
This increases A–a gradient, even on high FiO₂.

1.3 Reduced Diffusion Capacity (DLCO)

Ground-glass opacities and fibro-interstitial changes thicken the alveolar–capillary membrane.
By Fick’s law:

Membrane thickening (↑T) → diffusion limitation → PaO₂ rises suboptimally even on high FiO₂.

1.4 ESRD Acid–Base Constraints

• Chronic metabolic acidosis due to loss of renal bicarbonate regeneration

• Increased chloride retention

• Reduced phosphate/ammonia buffering

• Impaired compensation during acute metabolic stress

1.5 Interaction Between Bronchiectasis and ESRD

ESRD requires hyperventilatory compensation,
but bronchiectasis limits this ability → risk of rapid acidosis under stress.

This fundamental physiology frames all ABG interpretations in this case.

2.1 Fibrocalcific Sequelae of Prior TB

• Loss of alveolar surface area (↓A)

• Formation of noncompliant fibrotic zones

• Contributes to chronic shunt physiology

2.2 Traction Bronchiectasis

• Dilated bronchi = ↑ anatomic dead space

• Turbulent airflow increases resistance (Reynolds number)

• Impaired mucus clearance → mucus plugging risk

• V/Q mismatch is chronic and fixed

2.3 Bilateral Ground-Glass Opacities

• Represent interstitial thickening (↑T in Fick’s law)

• Reduce DLCO

• Create diffusion-limited oxygen transport

• Flatten the PaO₂ vs FiO₂ curve

2.4 Pleural Thickening

• Reduced chest wall compliance

• Lower FRC → collapse of dependent alveoli

• Increased risk of postoperative atelectasis

2.5 Pulmonary Artery Enlargement (32 mm)

• Suggests early pulmonary hypertension

• ↑ RV afterload

• ↓ perfusion to...