Intravenous anesthetics causes depression of ventilatory response to hypercapnea. Doxapram stimulates ventilation via peripheral and central chemoreceptors. This study was aimed to evaluate the effect of doxapram on ventilation during total intravenous anesthesia (TIVA).

60 patients undergoing operation under spontaneous ventilation via laryngeal mask airwaywere randomly divided into 3 groups: Control group received 5% dextrous infusion, D-2 group received doxapram injection of 1 mg/kg followed by continuous infusion of 2 mg/kg/hr, and D-4 group received doxapram injection of 2 mg/kg followed by continuous infusion of 4 mg/kg/hr. Anesthesia was induced and maintained with propofol and remifentanil. Respiratory rate, tidal volume (V_T) and arterial carbon dioxide tension (PaCO₂) were measured before and 15 min after induction of anesthesia, 0(15 min after start of operation), 1, 2, 3, 5, 15, 30, 45, and 60 min after start of doxapram infusion during TIVA.

V_T was significantly increased 1 min after start of doxapram infusion and returned to the value of pre-doxapram infusion immediately. In D-4 group, V_T was significantly (P < 0.05) increased again 5 min after doxapram infusion compared with the value of pre-doxapram infusion and control group. PaCO₂ was decreased 1 min after start of doxapram infusion and then increased again 2 min after doxapram infusion. In D-4 group, the degree of increase of PaCO₂ was significantly (P < 0.05) less than those of D-2 group.

Doxapram injection of 2 mg/kg followed by continuous infusion of 4 mg/kg/hr improved the depression of ventilatory response during TIVA.