64 
CARDIAC MODELS 
this is flushed by 2 ml isotonic saline. The inner 
catheter is then withdrawn and removed while 
the outer catheter is left in place. 
Soon after the injection of mercury electro- 
cardiographic changes of injury pattern occur 
and all hemodynamic measurements deterio- 
rate. The animals usually do not show any sign 
of pain or only occasionally become somewhat 
restless. In such case, additional morphine is 
given. The measurements are then repeated se- 
rially for several hours and, depending upon the 
experimental protocol, are continued during the 
entire day, until the death of the animal, or 
until termination of the experiment. 
RESULTS 
We have used this animal model to study the 
hemodynamic and biochemical changes in the 
cardiogenic shock and attempted to determine 
prognostic factors for early death. 
In another series of experiments we have 
studied the role of vagal afferents originating in 
the left heart in the mechanism of shock state. 
It has been known for sometime that reflexes 
originate in the heart and these reflexes may be 
both chemoceptor and baroceptor in nature. 
Since these experiments involved recording of 
nerve action potentials from the aortic barocep- 
tor, the vagal alferent nerves and post- 
ganglionic sympathetic nerves, the animals were 
kept in general anesthesia for this experiment 
using chloralose urethan. 
In another series of experiments we have 
tested the effect of sympathetic beta and alpha 
stimulator and blocking agents in order to de- 
termine the best drug or combination treatment 
of the hemodynamic and metabolic derrange- 
ments of cardiogenic shock. The results of these 
studies are briefly described. 
Hemodynamics of 
Experimental Cardiogenic Shock 
In a total of 25 mongrel dogs the hemody- 
namics and biochemical changes in experimental 
cardiogenic shock were studied in the awake se- 
dated animal. The purpose was to determine 
which hemodynamic and biochemical variables 
describe more closely the dc rrangements in ex- 
perimental cardiogenic shock and which can be 
used to arrive at a prognostic index of early 
death. Further, we have tested, by subsequent 
autopsy examinations, the question of how this 
index relates to the size of anatomical damage 
of the left ventricular free wall.'^ 
Of the 25 dogs thus studied, seven developed 
ventricular fibrillation within a few minutes 
after injection of mercury and could not be re- 
suscitated. The remaining 18 dogs were contin- 
uously monitored for the entire day. Seven of 
them (39%) died 2-12 hours after injection 
while eleven (61%) survived 2-11 days. Since 
the circumflex artery of the dog supplies the 
posterior inferior wall of the left ventricle, the 
changes in the electrocardiogram were reflected 
in leads 2, 3, and AVF. These changes were 
marked ST segment elevation leading eventu- 
ally to Q wave development and T wave inver- 
sion. The mercury droplets blocked the smaller 
and medium vessels of the circumflex coronary 
artery and produced an infarction of the poste- 
rior-inferior wall of the left ventricle. The aver- 
age heart weight of the total group was 154.17 
± 15.7 grams and the average infarct weight 
36.44 ± 8.2 grams. This latter represented 42% 
of the weight of the left ventricular free wall. 
All hemodynamic variables showed a signifi- 
cant impairment consisting of decrease of the 
mean blood pressure, the cardiac output, left 
ventricular dP/dt max and an increase of the 
heart rate and peripheral resistence as well as 
of the left ventricular end-diastolic pressure. 
These changes occurred during the first hour of 
the shock and continued to become worse in the 
subsequent hours (Figures 3 and 4) . 
In our attempt to determine the prognostic 
indices which could predict an early death or 
survival of the initial insult of infarction, we 
arbitrarily separated the animals into two 
groups : one which died within 48 hours and the 
other which survived beyond 48 hours. We then 
compared the hemodynamic and biochemical 
variables in the two groups. It can be seen in 
Figures 3 and 4 that heart rate increased in 
both groups simultaneously while mean blood 
pressure decreased to moderately low levels. 
There was no statistical significance between 
the two groups. Left ventricular end-diastolic 
pressure increased in both, somewhat more in 
