Clinical Snapshot

A 45-year-old male with end-stage renal disease (ESRD) due to IgA nephropathy, body mass index (BMI) of 26, was scheduled for renal transplantation. His main preoperative concern was persistent hyperkalemia greater than 5.4 mmol/L. The nephrologist prescribed salbutamol nebulization every six hours to reduce serum potassium. Heparin exposure likely contributed to type IV renal tubular acidosis (RTA), which had since been addressed by discontinuing heparin.

Induction of anesthesia was smooth, with no post-induction hypotension. Ventilation was set with a tidal volume of 520 mL, respiratory rate of 12 breaths per minute, PEEP of 5 cm H₂O, and an FiO₂ of 50%. Monitoring showed EtCO₂ of 33 mmHg, PaCO₂ of 44 mmHg, inspiratory EtO₂ 46%, expiratory EtO₂ 42%.

Arterial blood gas analysis revealed:

• pH 7.37
• PaCO₂ 44 mmHg
• PaO₂ 102 mmHg
• HCO₃⁻ 25.4 mmol/L
• Lactate 3.2 mmol/L
• Potassium 5.0 mmol/L
• Hemoglobin 10.9 g/dL

The EtCO₂–PaCO₂ gap was 11 mmHg.

Interpretation: Normocapnia was present, along with mild hyperlactatemia, borderline hyperkalemia, and evidence of ventilation–perfusion (V/Q) mismatch.

Hyperkalemia and Salbutamol

• What: The patient’s persistent hyperkalemia, initially above 5.4 mmol/L, was reduced to 5.0 mmol/L after repeated salbutamol nebulizations.
• Why: Salbutamol, a selective β2-adrenergic agonist, stimulates Na⁺/K⁺ ATPase activity in skeletal muscle, promoting intracellular potassium uptake without affecting total body potassium.
• How: At the molecular level, β2 receptor stimulation increases intracellular cAMP, which activates Na⁺/K⁺ ATPase. This facilitates potassium influx into cells. The onset occurs within 15–30 minutes, lasting one to two hours. Heparin-related suppression of aldosterone production from the adrenal zona glomerulosa may have contributed to persistent hyperkalemia.

Clinical insight: Salbutamol provides a rapid but temporary reduction in potassium levels. Rebound hyperkalemia is likely if the underlying aldosterone dysfunction is not corrected.

Lactic Acidosis Without Hypotension

• What: Lactate was elevated at 3.2 mmol/L, despite stable hemodynamics and no hypoxemia.
• Why: This was most likely caused by a β2-mediated glycolytic surge rather than impaired tissue perfusion.
• How: Salbutamol and endogenous catecholamines enhance glycolysis, producing excess pyruvate that is converted to lactate via lactate dehydrogenase. In ESRD, both hepatic and renal lactate clearance are reduced, amplifying the elevation.

Clinical insight: In ESRD, lactate levels may rise due to adrenergic stimulation or stress rather than tissue hypoperfusion. Monitoring the trend in lactate is more useful than reacting to a single absolute value.

Oxygenation and V/Q Mismatch

• What: PaO₂ was 102 mmHg on FiO₂ 0.5, which is lower than expected for this oxygen fraction.
• Why: Possible causes included post-induction atelectasis, uremic interstitial lung changes, and reduced functional residual capacity (FRC) in the supine position.
• How: Ventilation–perfusion mismatch occurs when alveolar ventilation or perfusion is impaired. High FiO₂ can also lead to nitrogen washout and atelectasis. The inspiratory-to-expiratory EtO₂ gradient (46% vs 42%) and the widened alveolar–arterial oxygen gradient supported this mechanism.

Clinical insight: Recruitment maneuvers and optimizing PEEP should be considered early after induction to stabilize alveoli and improve oxygenation in ESRD patients.

EtCO₂–PaCO₂ Gap

• What: The EtCO₂ was 33 mmHg compared to PaCO₂ of 44 mmHg, giving a difference of 11 mmHg.
• Why: This discrepancy reflects increased alveolar dead space ventilation or possible subclinical bronchospasm.
• How: While salbutamol may have improved bronchial tone, an elevated gradient indicates uneven ventilation, air trapping, or altered pulmonary vascular perfusion. In ESRD, chronic uremic changes and fluid overload may contribute.

Clinical insight: Vigilance is required for dynamic hyperinflation and bronchospasm. Lung auscultation, adjustment of the inspiratory-to-expiratory ratio, and flow rate optimization may be necessary.

Anesthesia Implications

• Borderline hyperkalemia (5.0 mmol/L) was lowered with β2-agonist therapy. Potassium should be monitored hourly intraoperatively, and succinylcholine avoided.
• Elevated lactate likely reflects adrenergic stimulation rather than hypoperfusion; fluid administration should be guided by hemodynamics rather than lactate alone.
• Low PaO₂ on FiO₂ 0.5 suggests V/Q mismatch and atelectasis; recruitment and lung-protective ventilation strategies are advised.
• The widened EtCO₂–PaCO₂ gap suggests dead space or bronchospasm; ventilatory adjustments should be made as needed.
• In ESRD, renally excreted anesthetic drugs should be avoided. Cisatracurium is preferred, and potassium-containing fluids should be avoided.

Conclusion

This case illustrates how integration of arterial blood gas interpretation with ventilatory, pharmacologic, and metabolic physiology is essential in anesthetic management of renal transplant candidates. The molecular effects of salbutamol, mechanisms of lactate elevation, and challenges of oxygenation in ESRD highlight the need for precision-based, physiology-driven anesthetic care.