Serum potassium elevation and acute respiratory acidosis during thoracoscopic esophagectomy with intrathoracic carbon dioxide insufflation: a multicenter retrospective observational study
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Background
Thoracoscopic esophagectomy with intrathoracic carbon dioxide insufflation and lung collapse, usually performed in the prone position, can markedly alter respiratory physiology and acid-base balance. Serum potassium elevation is often observed during acute respiratory acidosis in these procedures, despite the conventional view that respiratory acidosis has little effect on potassium. We quantified the intraoperative potassium change and explored associated factors.
Methods
This multicenter retrospective study included adults undergoing thoracoscopic esophagectomy with carbon dioxide insufflation in the prone or lateral decubitus position during 2022–2024. Arterial blood gas variables were evaluated after anesthesia induction and at the time of the lowest arterial pH during carbon dioxide insufflation. The primary outcome was the paired difference in serum potassium. Sensitivity, subgroup, and regression analyses were performed.
Results
All 131 patients were included: 117 in the prone position and 14 in the lateral decubitus position. Serum potassium increased from 3.96 ± 0.38 to 4.59 ± 0.63 mEq/L (mean increase, 0.64 mEq/L; 95% confidence interval, 0.55–0.73; p < 0.001). During the same period, pH decreased from 7.387 to 7.247 and arterial carbon dioxide tension increased from 41.48 to 58.60 mmHg. After excluding marked metabolic acidosis, the increase remained significant and similar in magnitude (0.618 mEq/L). In the centered multivariable model, lactate change was independently associated with potassium change (β = 0.303; p = 0.004), whereas arterial carbon dioxide change and preoperative renal function were not. The intercept remained significantly positive.
Conclusions
A clinically meaningful potassium increase was observed during thoracoscopic esophagectomy with carbon dioxide insufflation, while acute respiratory acidosis developed during the same period. The increase persisted after excluding marked metabolic acidosis and may not be explained solely by metabolic stress. Arterial blood gas assessment, including potassium measurement, is warranted during significant hypercapnia, and potential electrolyte consequences should be considered when permissive hypercapnia is accepted.
