270 Discussion 



attempt to corapensate them artificially by getting their serum bicar- 

 bonate levels up. We treated a 50-year-old man with acute respiratory 

 acidosis whose initial bicarbonate figure was 40 m-equiv./l. and the 

 blood pH, breathing room air, about 7 • 28. When he went into oxygen 

 he became unconscious rather quickly, presumably due to the decrease 

 in ventilation from the relief of anoxia. He was removed from oxygen 

 and over the next 18 hours dialysed through a cellophan bag in his 

 stomach, using a fluid containing 50 m-equiv./l. sodium bicarbonate 

 in 5 per cent glucose. The dialysis elevated his serum bicarbonate to 

 64 m-equiv./l. despite a negative sodium balance of 200 m-equiv. The 

 sodium was lost mainly in the urine. The high serum bicarbonate ele- 

 vated his blood pH, breathing room air, to 7-55. When he again went 

 into oxygen his blood pH fell to 7 • 45 and he did not become unconscious. 

 His anoxia disappeared despite the fact that his ventilatory rate slowed 

 from 9 litres per minute to 3 litres per minute. During the next 72 hours 

 his kidneys sustained his serum bicarbonate level above 60 m-equiv./l. 

 by excreting a normal amount of ammonia and titratable acidity. 



Experience in this patient suggests that so-called "CO 2 narcosis" is 

 actually due to the low pH rather than the high pCOg. The results also 

 suggest that despite the high serum bicarbonate renal compensation for 

 the respiratory acidosis may be incomplete in this acute situation. 

 Gastrodialysis makes it possible to treat the acidosis without resorting 

 to sodium administration, which is contraindicated because of the heart 

 failure from cor pulmonale. 



