Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome

Objective: To measure the effects of rapid permissive hypercapnia on hemodynamics and gas exchange in patients with acute respiratory distress syndrome (ARDS). Design: Prospective study. Setting: 18-bed, medical intensive care unit, university hospital. Patients: 11 mechanically ventilated ARDS patients. Intervention: Patients were sedated and ventilated in the controlled mode. Hypercapnia was induced over a 30-60 min period by decreasing tidal volume until pH decreased to 7.2 and/or P-50 increased by 7.5 mmHg. Settings were then maintained for 2 h. Results: Minute ventilation was reduced from 13.5 +/- 6.1 to 8.2 +/- 4.11/min (mean +/- SD), PaCO2 increased (40.3 +/- 6.6 to 59.3 +/- 7.2 mmHg), pH decreased (7.40 +/- 0.05 to 7.26 +/- 0.05), and P-50 increased (26.3 +/- 2.02 to 31.1 +/- 2.2 mmHg) (p < 0.05). Systemic vascular resistance decreased (865 +/- 454 to 648 +/- 265 dyne . s . cm(-5), and cardiac index (CI) increased (4 +/- 2.4 to 4.7 +/- 2.4 l/min/m(2)) (p < 0.05). Mean systemic arterial pressure was unchanged. Pulmonary vascular resistance was unmodified, and mean pulmonary artery pressure (MPAP) increased (29 +/- 5 to 32 +/- 6 mmHg, p < 0.05). PaO2 remained unchanged, while saturation decreased (93 +/- 3 to 90 +/- 3%, p < 0.05), requiring an increase in FIO2 from 0.56 to 0.64 in order to maintain an SaO(2) > 90%. PvO(2) increased (36.5 +/- 5.7 to 43.2 +/- 6.1 mmHg, p < 0.05), while saturation was unmodified. The arteriovenous O-2 content difference was unaltered. Oxygen transport (DO2) increased (545 +/- 240 to 621 +/- 274 ml/min/m(2), p < 0.05), while the O-2 consumption and extraction ratio did not change significantly. Venous admixture (Q(va)/Q(t)) increased (26.3 +/- 12.3 to 32.8 +/- 13.2, p < 0.05). Conclusions: These data indicate that acute hypercapnia increases DO2 and O-2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O-2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined. Furthermore, even though hypercapnia was well tolerated, the increase in Q(va)/Q(t), CI, and MPAP should prompt caution in patients with severe hypoxemia, as well as in those with depressed cardiac function and/or severe pulmonary hypertension.