K. T. WEBER, R. A. RATSHIN, C. E. RACKLEY AND R. 0. RUSSELL, JR. 
175 
1201 
20 
0 5 10 15 20 25 30 35 
E DP 
Figure 4. — Angiotensin stress curves following sub- 
acute microsphere infusion. The control observations 
for each animal are shown in the speckled area. The 
low (Group I) and high (Group II) dose groups are 
also represented. 
90 mmHg or less and an elevated LVEDP of 15 
mmHg or more; (b) reductions in CI of 40% 
or more; (c) an elevated PVR; and (d) a mod- 
erate tachycardia. In addition to these hemody- 
namic features, the preparation should be free 
of complicating ventricular arrhythmias which 
make successful data collection and interpreta- 
tion difficult. The shortcomings of anesthesia 
and thoracotomy need only be cited for com- 
pleteness. The percent of myocardial damage or 
infarction seen at autopsy in patients with 
shock has been reported as 40% to 60%.^^"^'^ 
Clearly, to experimentally evaluate an aggres- 
sive intervention such as the intra-aortic bal- 
loon in an animal model simulating the low 
mortality shock subgroup (CI greater than 2.1) 
would tend to lead to falsely optimistic conclu- 
sions. Several experimental cardiogenic 
shock preparations which have appeared in the 
literature are listed in Table VI. -''"^^ 
Ventricular failure (without shock) in the 
ischemic heart is another major area of concern. 
Here, chronicity or the time period following 
infarction and the amount of compensatory 
change (i.e., wall thickness, chamber dilatation 
and increased rate of viable fiber shortening) 
is important in determining the level of impair- 
ment. The influence of these changes has been 
clearly demonstrated both clinically ^^"-^ and 
experimentally.-^-'^'' Also, the response to phar- 
macological agents, such as digitalis, will be 
variable for these reasons. Design criteria for 
a failure model would appear to include (a) re- 
ductions in coronary flow at a subacute rate ^-^^ 
so as to permit coronary hyperemia and electro- 
mechanical stability during the induction pe- 
riod; (b) persistent elevations in LVEDP; (c) 
Table V. — Published Hemodynamic Data In Patients With Cardiogenic Shock 
HR 
SI 
CI 
TPR 
LVPP 
Aufhor 
No. of Pts. 
beats/min 
cc/m- 
L/min/m- 
dyne-sec-cm—' 
mmHg 
Scheldt 
19 
109 
11 
1.1 
2600 
22* 
Smith 
14 
98 
17 
1.6 
1586 
"Weil _ 
20 
95 
14 
1.3 
2042 
Gunnar 
12 
101 
13 
1.3 
1688 
Bradley 
5 
102 
17 
1.8 
1448 
21 
Mueller 
18 
102 
16 
1.4 
1575 
Cohn ..... 
14 
101 
18 
1.8 
2386 
23 
MacKenzie 
6 
108 
15 
1.7 
3016 
Weber 
45 
98 
18 
1.6 
2704 
25 
Avprn gp 
102 
15 
1.5 
2116 
22 
*7 pts.; — = Not reported. 
