Dear Editor,A 69-year-old, 179 cm, 101 kg male, with coronary artery disease, ischemic cardiomyopathy and a 25% ejection fraction, underwent coronary artery bypass grafting (CABG). Past medical history included hypertension, hyperlipidemia, pulmonary fibrosis, and stroke. Anesthetic induction was uneventful. Anesthesia was maintained with isoflurane in 100% oxygen. Monitoring included standard ASA monitors, invasive arterial blood pressure, pulmonary artery catheter placement, transesophageal echocardiography, and foley catheter.The baseline arterial blood gas (ABG) was pH 7.343, PaCO2 was 30.6 mmHg, PaO2 was 86.6 mmHg, bicarbonate 16.2 mM/L, and potassium 4.7 mM/L on FiO2 1.0 on SIMV 10, Tidal Volume (TV) 700 ml, peep 5 cm H2 O and pressure support 5 cm H2 O and minute ventilation (MV) 6 L/min. Median sternotomy incision was made concurrently with endoscopic saphenous vein harvesting using carbon dioxide insufflation (initiated flow of 3 L/min with insufflation pressure of 12 mm Hg—normal flow rate and pressure). End-tidal CO2 progressively increased during the harvest (over 45 minutes). A follow-up ABG demonstrated a pH of 7.11, PaCO2 66.8 mmHg, PaO2 248 mmHg, bicarbonate 20.3 mM/L, potassium 5.5 mM/L. MV was increased to 12 L/min with a resultant ABG of pH 7.15, PaCO2 56.6 mmHg, PaO2 263 mmHg, bicarbonate 19.3 mM/L, and potassium 5.6 mM/L.The MV was eventually adjusted to 20 L/min with a consequent ABG of pH 7.11, PaCO2 65.1 mmHg, PaO2 250 mmHg, and bicarbonate 19.9 mM/L. The heart rate reached 120 beats/min and the blood pressure was as low as 90/60 mm Hg. Pulmonary artery pressure increased from 40/20 mmHg to 50/30 mm Hg. Urine output remained unaffected and the patient remained afebrile.There was no evidence of increased bleeding, vessel injury or equipment malfunction. Transesophageal echocardiography revealed no abnormalities. When the saphenectomy was completed, and insufflation discontinued, the acidemia resolved (over 90 minutes). The saphenectomy time was prolonged at 59 minutes and the surgery was completed uneventfully. The patient was transferred to the intensive care unit (ICU) and extubated on post-operative day one and discharged on the sixth day.The prolonged saphenectomy time contributed to the hypercapnea. Additionally, a sealed anesthesia system was used as opposed to an open system, and this too may have contributed to the hypercapnea/acid base disorder. Endoscopic saphenectomy is an alternative to conventional open vein vessel harvesting. Its advantages include better wound healing, reduced pain and better cosmesis. Endoscopy with carbon dioxide insufflation allows better operative field visualization and easier tissue plane identification, and improved hemostasis without needing retraction.[1]This technique's disadvantages, besides hypercapnea with hemodynamic perturbations, include CO2 embolization through a patent foramen ovale, as well as occasional poor visibility which requires increased insufflation pressures thereby allowing CO2 circulatory access.[23]Several differential diagnoses need consideration, including lighter planes of anesthesia, malignant hyperthermia, thyroid storm, and neurolept malignant syndrome. Endoscopic saphenectomy associated with hypercapnea secondary to CO2 insufflation during venous conduit acquisition is rare. We report this case to our colleagues in order to demonstrate the importance of vigilance on the surgeon/anesthesiologist's part in regard to the occurrence and differential diagnosis of hypercapnea in this setting.