178 
CARDIAC MODELS 
that different animals have different pressures ; 
that in dogs, even the arresting pressure is 
higher than in humans. I don't know whether 
you can rely on systolic blood pressure as a 
criteria. I certainly agree with everything else 
you say about blood pressure. 
K. T. Weber, Jr. : I must admit that the ma- 
jority of the conscious animals that we have 
experimented with were calves. Their blood 
pressure, however, is within the range seen 
clinically for humans as we have previously re- 
ported. I understand from the conscious canine 
model series in the literature, that one does 
not see the hypertension and tachycardia which 
accompanies barbiturate anesthesia and thora- 
cotomy. This may likewise influence the total 
peripheral resistance changes which are seen in 
some of the cardiac models, namely drops in 
peripheral resistance resulting in "warm" cardi- 
ogenic shock rather than the typical "cold" type 
of shock. 
Chairman: The left ventricle end diastolic 
pressures are certainly very important: unless 
you have these, you probably have a hypovo- 
lemic animal. This is one of the important 
points when you should know whether or not 
you have a hypovolemic animal. 
R. E. Clark, Washington University, St. 
Louis, Mo. : I rise to emphasize Dr. Weber's 
figures on his patients. When the index was less 
than 2.1 liters per minute per meter squared, 
the mortality rate was very high. Most of our 
patients do not have the availability of the left 
ventricular pressure, particularly when we are 
concerned with the low pump syndrome follow- 
ing open heart surgery. We frequently do not 
have a left atrial pressure, and we are left with 
arterial pressure. Although we need more pa- 
tients for a complete statistical anlysis, I think 
we have been able to document reasonably that, 
using a method of simultaneous dye and ther- 
mal cardiac output, the approximate cutoff in 
patients is at about 2 liters per minute. With 
an index of 2 liters per minute per meter 
squared, in our operative patients, we get a 
mortality rate of nearly 100%. Accordingly, at 
least the clinical data in surgery patients seems 
to correlate with the data you get in calves and 
in your myocardial infarction patients. 
M. W. Osborne, Hoffman-Laroche, Inc., Nut- 
ley, N.J. : Could you describe the angiotensin 
stress test briefly, please. I am not acquainted 
with it. 
K. T. Weber: Yes. The angiotensin stress 
response was reported by Drs. Ross and Braun- 
wald some years ago ; it involves the intravenous 
administration of angiotensin or Hypertensin® 
to elevate systemic resistance (afterload) and 
evaluate ventricular function. The drip rate 
can be controlled and you can easily control the 
pressure level against which the heart has to 
pump. It is possible to analyze peak systolic 
pressures all the way up to 200 mm of mercury 
or more, if you decide to do so. Another at- 
tractive feature of this stress test is that the 
angiotensin effect does not persist for more than 
five minutes. 
W. Erlich: (Question: partially inaudible, 
concerns the survival rate and the compensat- 
ing mechanism.) 
K. T. Weber : I agree that at first the peri- 
pheral bed responds to inadequate profusion 
with vasoconstriction. However, the choice of 
pharmacological vasodilators versus vasocon- 
strictors in these patients is not diflficult. When 
we're dealing with blood pressures of 90 mm of 
mercury or less to begin with and cardiac in- 
dexes of less than 2.1 (and often as low as 0.6) 
it is difficult to justify the use of a vasodilator. 
Coronary perfusion pressure is already critical- 
ly reduced. The major concern in infarction 
shock should be with the heart and not the peri- 
phery. 
We are currently attempting to assess, with 
three-dimensional analysis, the influence of pe- 
ripheral resistance, filling pressure, and cardiac 
index in predicting both prognostic and thera- 
peutic hemodynamics sub-groups. 
