CARDIAC OUTPUT AND TOTAL PERIPHERAL RESISTANCE IN POST-HEMORRHAGIC HYPOTENSION AND SHOCK

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Abstract
Utilizing a "modified Stewart method" for determining cardiac output, variations of the latter and of total peripheral resistance (TPR) were studied during the course of standardized hemorrhagic shock in relation to other cardiodynamic events and hematocrit changes. During a 90 min. period of 50 mm. of Hg hypotension and a subsequent 45 min. period at 30 mm. of Hg, cardiac output and stroke vol. were reduced to 29-45% of the control flow. Although they were restored to normal in the majority of expts. immediately after reinfusion, in some the recovery was only to 45-85% of control values. During the 3 hrs. succeeding reinfusion, cardiac output decreased rapidly and was the chief cause of the declining arterial blood pressure. In the final stages cardiac output stabilized at low levels and the continued fall of blood pressure was occasioned chiefly by peripheral factors. Slowing and failure of the heart was often the ultimate step in the series of cardiodynamic events leading to death. Hematocrit readings indicated a hemodilution during the periods of hypotension and a tendency toward conc. following reinfusion of the blood. The course of events in standardized hemorrhagic shock is, therefore, similar to that described in other exptl. types in that hemoconc. occurs, and progressive reduction of cardiac output is chiefly responsible for the progressive decline of arterial pressures after reinfusion. Despite the universally fatal outcome, changes in the total peripheral resistance were extremely variable during the periods of post-hemorrhagic hypotension and during circulatory failure which developed after reinfusion of blood. The different trends are analyzed. Arguments are advanced that physical factors concerned in such changes can be evaluated and that an estimate of directional changes in vasomotor tone can be made. Supplementary evidence is cited from which the conclusion is reached that humoral or metabolic factors play a considerable role in these changes. In the method for producing shock by holding mean arterial pressures at successive levels of 50 and 30 mm. of Hg for specified intervals of time, cardiac output was reduced to 29-45% of the original blood flow. Such ranges of reduction indicate that the procedure recommended for the rather regular production of hemorrhagic shock does not result in equivalent reductions of circulatory values when applied to different animals. Of course, the possibility that other factors may enter cannot be excluded.

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