32 
CARDIAC MODELS 
was offset by the fact that cathodal current did 
not cause the electrolytic deposition of heavy 
metal salts from the wire within the artery. In 
5 experiments in which 6 external electrodes 
were arranged circumferentially around the 
thorax, only 2 occluding thrombi were produced 
after delivery of an average electrical energy of 
675 mw sec. Sixteen experiments in which the 
intracoronary electrode was paired with a sin- 
gle external electrode located on the chest over- 
lying the anterior surface of the heart, culmi- 
nated in 13 occluding thrombi after an average 
energy delivery of 317 mw sec. The latter tech- 
nique was therefore selected for all subsequent 
experiments. 
The total energy delivered between the intra- 
coronary electrode and the external electrode to 
a tissue load of approximately 500 ohms, 
ranged from 18 to 2067 mw sec. We have found 
that the production of arterial wall damage and 
thrombosis depended in each individual experi- 
ment upon attaining the prerequisite amount of 
blood flow reduction. In the experiment cited 
above where 2067 mw sec. of total energy was 
delivered, blood flow could not be reduced suffi- 
ciently to allow either arterial wall damage or 
thrombosis to occur. In contrast, where a good 
reduction in blood flow was attained, as little as 
54 mw sec. of total electrical energy produced 
intimal damage and complete occlusion by 
thrombus. In any given dog, continuation of 
electric current caused increasingly persistent 
manifestations of ischemia on the electrocar- 
diogram. Therefore, in each experiment the ter- 
mination of electric current delivery depended 
upon electrocardiographic changes which were 
sustained for 20 minutes or more without fur- 
ther electric current. The average amount of en- 
ergy required for thrombotic occlusion was 
about 400 mw sec, and the magnitude of the 
curents ranged from 0.2 to 1.0 milliamperes, 
and averaged 0.8 milliamperes delivered for an 
average of 20 minutes. 
In contrast to the dimensions of electric cur- 
rent described above, 9 experiments were per- 
formed utilizing a specially constructed current 
generator which delivered impulses 11 msec in 
duration and up to 320 ma strength. The total 
energy delivered ranged from 1 to 5120 mw sec, 
and in 1 experiment 60,000 mw sec were deliv- 
ered. Despite the fact that the current pulses 
were synchronized to occur during the refrac- 
tory period of the ventricular myocardium, 2 
dogs died with ventricular fibrillation immedi- 
ately following delivery of current. A third dog 
died of ventricular fibrillation 15 minutes after 
electric current delivery. In the experiment in 
which the energy dose was 60,000 mw sec, an 
intimal lesion and a partially occluding throm- 
bus were found at autopsy. In only one other 
heart was a minor intimal lesion found accom- 
panied by a totally occluding thrombus, and in a 
third heart a partially occluding thrombus was 
found but no evidence of intimal damage. The 
remaining 6 hearts showed neither intimal 
damage nor thrombus formation. In addition to 
the obvious conclusion that this method of ar- 
terial injury was inferior to the former one, the 
fact that the electric energy was delivered over 
a much shorter period of time mitigated against 
the possibility that the mechanism of arterial 
injury was a thermal one. Since the average ad- 
ministered electrical energy of 400 mw sec cited 
above, has a heat equivalent of 0.1 calorie, it 
was also felt on a theoretical basis that the 
mechanism of arterial injury was not a thermal 
one. 
Pathophysiologic Consequences 
The electrocardiographic manifestations of 
acute myocardial infarction followed the same 
sequence as the classical changes observed in 
man. Very transient peaking of T waves was 
followed by S-T segment elevations of varying 
magnitudes. All S-T segment displacements re- 
turned to the baseline. Progressive loss of R 
wave amplitude, increasingly deep and wide Q 
waves and terminal inversion of T waves pro- 
ceeded simultaneously. The distribution of these 
changes led to interpretations ranging from an- 
teroseptal to anterolateral locations of the acute 
infarct, in agreement with the fact that the oc- 
clusion were located in the mid left anterior de- 
scending coronary artery or one of its major 
branches, in all of our experiments. 
We found surprising uniformity between ex- 
periments in the electrocardiographic manifes- 
tations of infarction, in contrast to the wide 
and varied deviations from the so-called "text- 
book picture" of myocardial infarction seen in 
