Figure 8. — End-diastolic (left) and end-systolic (right) frames from a biplane angiogram re- 
corded in a normal, control calf (above; see also Figure 1), and in a calf after induction 
of left ventricular myocardial failure by coronary microsphere infarction. (Distortion in de- 
scending thoracic aorta, calf C-50, caused by substituted vascular prosthesis with flocked 
dacron fibril blood-material interface; an early study. )-^ 
rectly for filling volume. The earlier inexplic- 
ability of the phenomenon of reduced ventricu- 
lar stroke volume but increased "cardiac 
output" in the face of a closed aortic valve 
finally yielded to the data in Table II (Figure 
6). 
Note the column headed COatr : it represents 
that fraction of total output which is not solely 
left ventricular (COlv), but is included in the 
total measured output of the ventricular bypass 
pump (COp). Not only in these two instances 
in the calf whose data are tabulated in Table II 
(pumping in normal and in failure states), but 
in almost every study of LV, RV, or biventricu- 
lar pumps, the total cardiac output increased 
during pumping. The aortic valve being closed 
(note equivalent LV pressures in Table I), 
there, are only 4 possible sources of blood for 
the pump : the left ventricle, the left atrium, 
the LV-coronary anastamoses, and the aortic 
end of the pump. That there is no significant 
retrograde flow into the pump has been proven 
on many occasions by electromagnetic flow 
probe monitoring. The volume available through 
the LV-coronary asastomoses is extremely small 
(no more than 10 ml/min). The source of the 
increased cardiac output must, then, be left 
atrial. Thus, the left ventricular blood pump 
tends to unload the left atrium both directly and 
indirectly. The same phenomenon has proven 
true during pure RV bypass : cardiac output in - 
