Effects of buffering in hypercapnia and hypercapnic hypoxemia

Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (PaCO2 approximately 20 kPa) at FiO2 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 +/- 0.01 vs 7.01 +/- 0.01 (mean +/- s.e.mean, P < 0.01). Serum osmolality and PaCO2 did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 +/- 6 vs 189 +/- 12 min-1 (P < 0.01), mean arterial pressure (MAP) 109 +/- 4 vs 124 +/- 4 mmHg (14.5 +/- 0.5 vs 16.5 +/- 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16 +/- 1 vs 23 +/- 1 mmHg (2.1 +/- 0.1 vs 3.1 +/- 0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 +/- 21 vs 343 +/- 20 dyn s.cm-5 (2490 +/- 210 vs 3430 +/- 200 microN.s.cm-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in FiO2 (0.15, 0.10, 0.05) at 30-min intervals, while FiCO2 was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At FiO2 0.15, buffered animals had higher arterial oxygen saturation (73 +/- 5%) than the controls (55 +/- 5%), (P < 0.05).