MEASUREMENT OF THE CARDIAC OUTPUT 



571 



measure the gas content of arterial blood. From the 

 arteriovenous difference thus determined, and the 

 gas exchange, the cardiac output could be calculated. 



The procedure of Loewi and \on Schrotter was 

 cumbersome and difficult, but it could not be 

 criticized on theoretical grounds. It was possible for 

 them to make measurements in a steady state and 

 allow time for complete equilibrium between lung 

 blood and lung air to occur. Nonetheless, the method 

 has never been tried again. 



The difficulties of the Loewi and von Schrotter 

 procedure were surmounted by making certain rather 

 doubtful assumptions and using a simpler technique. 

 The new technique was to rebreathe, or hold in the 

 lungs, gas mixtures, the strength of which did not 

 change on being exposed to lung blood. Such mixtures 

 could be made up by trial and error until one was 

 found, the tension of which did not change on breath 

 holding (23). A simple way to make up such mixtures 

 was to repeatedly rebreathe oxygen (to assure 

 oxygenation of lung blood). After several rebreath- 

 ings, each lasting 15 sec, the CO2 tension of the re- 

 breathed air came to a constant figure which was 

 said to be that of mixed venous blood (74). 



Originally, analyses were made of the general 

 volume of 3 or 4 liters of rebreathed air as sampled 

 from the rebreathing bag. Results obtained in this 

 way may be stultified by incomplete mixing of lung 

 air and bag air, and may further be stultified by the 

 slowing of the evolution of CO-2 from the venous lung 

 blood as the rebreathed air tension asymptotically 

 approaches that of the venous blood (57). These 

 difficulties can be avoided by insuring that the sample 

 of rebreathed air be taken from the depths of the 

 lung — an end expiratory or alveolar sample. Doing 

 this uncovers other difficulties (61). 



By going through the process of repeated rebreath- 

 ing for 1 5 sec the alveolar samples reach a constant 

 value after 3 or 4 episodes of rebreathing. If the tension 

 reached by this plateau is that of the mixed venous 

 blood, and that of the normal alveolar air is the ten- 

 sion of the arterial blood, we have established an A-V 

 CO2 tension difference from which the A-V content 

 difference can readily be derived. Knowing this and 

 the COo production the cardiac output can be cal- 

 culated by the Fick equation. 



Unfortunately, however, the "A-V difference" 

 levels off at different heights depending on how long 

 the rebreathing time is made. If the repeated episodes 

 of rebreathing are 8 sec in duration the A-V differ- 

 ence is 79 ± 0.9 per cent of that at 16 sec. If re- 

 breathing episodes last 24 sec, the A-V difference is 



1 1 7 ± 1.7 per cent of that at 16 sec. Moreover, it has 

 been statistically shown (68) that it would be im- 

 possible to prove the existence of a plateau of 

 rebreathed gas tension plotted against time of re- 

 breathing during the period before recirculation (15 

 sec after the start of rebreathing). This is true, whether 

 or not enough CO2 has been added to the mixture to 

 compensate for the diluting effect of residual 

 (alveolar) air, added to the system at the beginning of 

 each rebreathing episode. 



Due to the high diffusibility of CO2 it cannot be 

 said that there is a failure of the CO2 in the alveoli to 

 reach equilibrium with the walls of the alveoli. There 

 must be, therefore, in addition to the mixed venous 

 blood perfusing the lungs, an appreciable quantity of 

 arterialized fluid (blood plasma or other fluid) which 

 remains in the lungs during the rebreathing process 

 and absorbs CO2 from the virtual venous inspired 

 mixture. This has been quantitatively measured (57) 

 and it is found that during the first 4 sec of rebreathing 

 the stagnant arterialized fluids of the lungs absorb 

 not only the CO2 brought to the lungs by the venous 

 blood but, in addition, 13 ml of inspired CO2. At the 

 end of 8 sec of rebreathing the lungs have absorbed 

 the CO2 entering the lungs together with about i ml 

 of inspired CO2. Assuming, as we must, that there is a 

 CO2 equilibrium between the lung and alveolar air, 

 we have to think that the C.O2 has diffused into ar- 

 terialized lung fluids. 



This has been confirmed recently by Dubois et al. 

 (28), who have shown that the fluid of the lung tissues 

 combines with CO2 in amounts similar to blood. The 

 movement of CO2 into the lung fluids was shown to 

 cause the PCO2 in the alveolar air to rise during 

 breath holding much more slowly than would be pre- 

 dicted from the volume of air in the lungs and the 

 rate of CO2 output. To put the matter in other words, 

 the amount of CO2 required to raise the PCO2 of the 

 lung air (3 liters) by i mm Hg is 3.95 ml, whereas 

 that required to raise both the lung air and lung tissue 

 by I mm Hg is 4. 75 ml. These experiments were done 

 in lungs washed free of blood. The natural lung con- 

 tains stagnant blood, and blood flowing backward 

 (cf 61). In addition to this, there is more plasma 

 (about 30% more) in the lungs than would be ex- 

 pected from their erythrocyte content (46). More- 

 over, a large part of this plasma is sequestered prob- 

 ably in capillaries where it remains stagnant and 

 capable of adding to the CO2 combining power of 

 lung tissue. It is believed to be stagnant because only 

 a small part of the "extra plasma," about 5 per cent, 

 can be accounted for by laminar flow and longer 



