BACKGROUND
During minimally invasive thoracic surgery with intrathoracic carbon dioxide (CO₂) insufflation, an abrupt rise in end-tidal CO₂ (EtCO₂) alone cannot distinguish true hypercapnia from artifactual or exogenous CO₂ contamination. We report 2 contrasting cases in which the direction of the arterial-to-end-tidal CO₂ gradient, Δ(PaCO₂−EtCO₂), guided differential diagnosis.
CASE REPORT
Case 1: A 62-year-old man undergoing robot-assisted right lower lobectomy developed an abrupt EtCO₂ rise from 40 to 130 mm Hg immediately after CO2 insufflation, with severe hypotension and bradycardia. Arterial blood gas (ABG) analysis showed pH 6.79, PaCO2 228.0 mm Hg, and Δ(PaCO₂−EtCO₂) +98.0 mm Hg, suggesting a possible contribution of low cardiac output to the widened gradient. Insufflation was stopped, 2-lung ventilation resumed, and surgery completed without re-insufflation. Case 2: A 77-year-old man undergoing thoracoscopic subtotal esophagectomy developed an EtCO₂ rise from 54 to 99 mm Hg while hemodynamically stable. After excluding circuit and sampling-line artifacts, ABG analysis showed pH 7.21, PaCO₂ 72.5 mm Hg, and Δ(PaCO₂−EtCO₂) -26.5 mm Hg, suggesting exogenous CO₂ contamination of expiratory gas rather than systemic retention alone. Surgical exploration confirmed a partial injury to the left main bronchus.
CONCLUSIONS
During abrupt EtCO₂ surges under 1-lung ventilation with capnothorax, the direction of Δ(PaCO₂–EtCO₂) on prompt ABG analysis may help prioritize the differential diagnosis between systemic retention and exogenous contamination, provided hemodynamics and circuit integrity are concurrently assessed. A markedly positive gradient during shock may indicate systemic CO₂ loading with reduced pulmonary perfusion, whereas a negative gradient after artifact exclusion suggests pleuro-airway communication or peri-device leakage. This hypothesis-generating approach remains unvalidated as a standalone diagnostic tool.

Keywords: One-Lung Ventilation; Hypercapnia