MEASUREMENT OF THE CARDIAC OUTPUT 



363 



5 10 15 20 2b 30 35 



FIG. 8. Relation of stroke volume as calculated from the 

 Fick or dye dilution methods and that calculated from the 

 pulse contour, showing discrepant pulses (X). [From Reming- 

 ton (109).] 



Increase in the air pressure, i.e., the force of accelera- 

 tion, increased the recoil, whether the stroke volume 

 was large (long-lasting ejection) or small. The recoil 

 curve thus responded only to the initial acceleration 

 of "blood" and not to the steady ejection. A cardiac 

 contraction therefore, acting against a low aortic 

 pressure, may give an early systolic surge of blood 

 which, in shock (19) produces large deflections, in- 

 dicating a stroke volume that is greater than normal 

 instead of the known small stroke volume. On the 

 other hand, in hypertension where the stroke volume 

 is nearly normal, the initial ballistocardiographic de- 

 flections are small because the ejection is relatively 

 slow and long maintained, giving small acceleration 

 components and prolonged ejection at a relatively 

 steady rate (i 1 1) which is silent for the ballistocardio- 

 gram. 



Perhaps the most important basis for the ballisto- 

 cardiogram's failure to have a simple quantitative re- 

 lation to the forces of cardiac ejection is the fact that 

 during systole there are many forces generated at the 

 same time, which are contrary to each other and tend 

 to cancel one another out. If there were none of these 

 contrary forces operating during systole we could 

 think of there being in the body two reservoirs: one, 

 the heart which empties during systole, accelerates 

 blood out into the arteries, and produces a recoil that 

 is equal and opposite; and the other, a peripheral 



reservoir located at a place in the body which repre- 

 sents the center of gravity of the blood, being the 

 source of a steady return to the heart through the 

 veins. Knowing the distensibility of the major seg- 

 ments of the arterial tree (iii, 112) it is possible to 

 calculate the ma.ss movements of blood from the 

 heart (59). On the a.ssumption that blood returns 

 through the veins in a steady stream, there would be 

 no accelerative forces connected with movement of 

 venous blood and the arterial recoil forces would be 

 alone in producing the ballistocardiogram. 



Unfortunately, this is not true because when the 

 forces which move the ejected blood out into and 

 through the aorta are calculated in detail (59), it is 

 seen that there are two important differences between 

 the calculated and the recorded force curve. The cal- 

 culated force curve begins much earlier and is very 

 much larger (.see fig. 10). 



Two of the more important forces which may re- 

 duce and delay the recorded ballistocardiogram are 

 accelerations of the venous stream and movements 

 of the ventricular wall. The idea that the venous 

 blood returns to the heart in a steady stream is not 

 tenable. The measurements of Brecher show that 

 there is a decided acceleration of the venous stream 

 during systole (10). If this were not true there would 

 be a volume of 50 or 60 ml less of blood in the thorax 

 at the end of systole than at its beginning. On the 

 assumption that there are 2.5 liters of air in the chest, 

 systolic expulsion of 50 ml of blood from the thorax 

 would lower the air pressure in the chest by 14 or 15 

 mm Hg if the airway were closed, or would cause a 

 movement of 50 ml of air through the open trachea 

 with each heart beat. There are, of course, no such 

 changes of either pressure or volume. Measurement 

 of the pressure change in normal man (W. F. H.) 

 show that it is less than 0.2 mm Hg (56, 60). It con- 

 sists of a lowering of pressure in early systole which is 

 reversed by a rise in intrathoracic pressure in mid 

 systole that cancels part or all of the lowering in early 

 systole (see fig 11). This indicates exit of Ijlood in 

 early systole which is made up for before mid systole 

 either wholly or in part. The very small air pressure 

 change mentioned above would correspond to a 

 volume change of 1.75 ml if the chest walls were rigid. 

 Calculation of the equivalent elasticity of the chest 

 walls from records made when known volume of air 

 was added to the closed system in which the cardio- 

 pneumogram was recorded indicated that the volume 

 change might be as high as 7.50 ml if the chest walls 

 had the same elastic properties as air. Since the chest 

 walls have a large mass and cannot fully respond to 



