THE CONTROL OF THE RESPIRATION 365 



Increase in P n (diminished H-ion concentration). 



3. Addition of excess of alkali to the Hood, either by intravenous in- 

 jection of carbonate solutions, or by overdosing with bicarbonates or 

 phosphates. There is a great excess of total C0 2 as shown in area V of 

 chart, - When the alkalosis is extreme, symptoms of tetany supervene 

 (page 805). The compensation in this case involves the following: (a) 

 Diminished excretion of C0 2 brought about by lessened breathing (-the" 

 percentage of-GG 2 in the alveolar air is however increased because of 

 the curtailment in the amount of air breathed), (b) Liberation of lactic 

 acid into the blood, (Macleod and Knapp). (c) Increased excretion of 

 alkali (as bicarbonate) and diminished excretion of ammonia in the 

 urine. When compensation is adequate the blood picture shifts to area II 

 (the same position as for compensated C0 2 excess). 



4. Removal of excess of H 2 CO & (free C0 2 ) from the body. This results 

 from increased breathing, being readily induced either voluntarily or 

 as a result of stimulation of the respiratory center by anoxemia (page 

 378) or by excitation of afferent respiratory nerves. H 2 C0 3 being re- 

 duced, there is a relative excess of BHC0 3 making the condition one akin 

 to that following alkali administration (i.e., a true alkalosis, although 

 the absolute amount of alkali is much less) and being accompanied by 

 the same symptoms (tetany) and compensated byv the same mechanisms 

 (increased excretion of alkali by the urine, disappearance of ammonia 

 and probably production of lactic acid) as when excess of alkali is admin- 

 istered. The blood condition immediately after the removal of the C0 2 

 corresponds to that of area VI on the chart, it then shifts to that of 

 area IV (the same as in compensated alkali deficit). This form of al- 

 kalosis is particularly important from the clinical standpoint since it 

 must tend to be produced in all forms of hyperpnea not due to actual 

 addition or accumulation of acids in the organism. It is the condition 

 established in mountain sickness' (page 415). 



In all the above cases if compensation proceeds satisfactorily the blood 

 condition ultimately returns to area VII on the chart, i.e., P H lies between 

 7.30 and 7.50 with the vol. of combined C0 2 between 43 and 55 when 

 the blood is exposed to 40 mm. C0 2 pressure. 



Finally it should be pointed out that analysis of the percentage of 

 C0 2 in the alveolar air and of the percentage of C0 2 in arterial blood 

 (simultaneously collected), or of P H and the total C0 2 of blood, will 

 give us the necessary data to find the actual blood condition from the 

 chart, provided only that the breathing is normal. If the conditions be 

 uncompensated, the alveolar C0 2 will be either too high or too low ac- 

 cording to whether there is hypnea or hyperpnea. 



