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...
