74 DONALD D. VAN SLYKE 



air with reduced oxygen percentage is breathed at sea level pressure. 



The process by which the state of compensated CO 2 deficit is reached 

 has been outlined in the discussion of the" condition represented by Areas 

 2 and 3. 



The final effect, lowered bicarbonate with normal pH, is the same as 

 in compensated alkali deficit caused by retention of non-volatile acids. 

 The primary cause in compensated CO 2 deficit, however, is not acid re- 

 tention, but loss of an acid (carbonic), which is subsequently compensated 

 by a reduction of the blood alkali. 



Area 7-8. Uncompensated C0 2 Excess. In this condition respiratory 

 excretion of C0 2 is retarded, either by physical hindrance or by deadening 

 of the respiratory center, so that H 2 CO 3 of the blood is raised. In con- 

 sequence the BHCO 3 : H 2 CO 3 ratio and the pH are lowered. The actual 

 blood reaction becomes less alkaline than normal. 



This condition has been caused experimentally by breathing air which 

 contains 3 to 5 per cent of CO 2 (Hasselbalch and Lundsgaard, 1912; 

 Davies, Haldane, and Kennaway, 1920). It appears to be caused also 

 when the respiratory center is deadened by morphin narcosis (Henderson 

 and Haggard, 1917, a). 



Clinically Means, Bock, and Woodwell (1921) report observation of 

 the condition in a cyanotic pneumonia patient. 



The physiological effects are seen in an accelerated excretion of am- 

 monia and titratable acid by the urine, the same effects observed when the 

 acid-base balance is upset by retention of non-volatile acids. Davies, 

 Haldane, and Kennaway (1920) observed a doubling of the rate of am- 

 monia and titratable acid excretion after breathing air containing up to 

 5 per cent of CO 2 . There is also, as in non-volatile acid retention, an 

 increase in the minute volume of air expired, in the apparent attempt to 

 get rid of the excess of H 2 CO 3 unless the respiratory center is deadened 

 (as by morphin). 



The first effect of CO 2 retention on the blood is to increase the H 2 C0 3 

 and H + of the blood, without changing the buffer alkali content (condition 

 represented by Area 8). Thus Davies, Haldane, and Kennaway found 

 after breathing for an hour air containing CO 2 in amounts gradually in- 

 creasing up to 5 per cent, there was no change in the CO 2 capacity of the 

 blood (unchanged total buffer alkali). Henderson and Haggard (1917) 

 found that in dogs a rise of 2 or more volumes per cent in CO 2 capacity of 

 the blood within a half hour after injecting morphin, or breathing air 

 containing 5 or more per cent of CO 2 . 



This increase in the blood alkali secondary to H 2 CO 3 increase is com- 

 pensatory in its nature, it tends to raise the BHCO 3 :H 2 CO 3 ratio back to 

 normal by increasing the BHCO 3 to balance the increased H 2 CO 3 . In 

 consequence the blood condition tends to shift from Area 8 to Area 7 



