Which of the following is an anticipated cardiovascular effect of CO2 pneumoperitoneum that informs prophylaxis?

Which of the following is an anticipated cardiovascular effect of CO2 pneumoperitoneum that informs prophylaxis?

• A. Increased venous stasis due to peritoneal pressure requiring VTE prophylaxis
• B. Decreased systemic vascular resistance
• C. Hyperkalemia due to acidosis
• D. Increased left ventricular ejection fraction

Answer: (A)

CO2 pneumoperitoneum raises intra-abdominal pressure, which compresses abdominal and pelvic veins and reduces venous return from the lower body. This creates venous stasis in the legs, a key factor that increases the risk of deep vein thrombosis during laparoscopy. Because of this stasis, venous thromboembolism prophylaxis (mechanical measures or pharmacologic anticoagulation as appropriate) is guided by the expected cardiovascular effect of the insufflation. The other options don’t fit this primary concern: decreased systemic vascular resistance is not the typical result of pneumoperitoneum ( vascular resistance often increases with CO2 insufflation due to sympathetic activation); hyperkalemia from acidosis is not a defining or consistent consequence in this context; and an increased left ventricular ejection fraction would not be expected since preload tends to be reduced with higher intra-abdominal pressures.

CO2 pneumoperitoneum raises intra-abdominal pressure, which compresses abdominal and pelvic veins and reduces venous return from the lower body. This creates venous stasis in the legs, a key factor that increases the risk of deep vein thrombosis during laparoscopy. Because of this stasis, venous thromboembolism prophylaxis (mechanical measures or pharmacologic anticoagulation as appropriate) is guided by the expected cardiovascular effect of the insufflation.

The other options don’t fit this primary concern: decreased systemic vascular resistance is not the typical result of pneumoperitoneum ( vascular resistance often increases with CO2 insufflation due to sympathetic activation); hyperkalemia from acidosis is not a defining or consistent consequence in this context; and an increased left ventricular ejection fraction would not be expected since preload tends to be reduced with higher intra-abdominal pressures.