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A servomechanism has been designed and built for controlling the output of an artificial ventricle. Venous pressure was selected as the primary parameter of control because of experimental and clinical studies which report this mechanism to assume control under certain conditions in which neural and/or hormonal control mechanisms are attenuated. In this control system, venous pressure, as measured with a pressure transducer, is compared to an “ideal” venous pressure, usually 0 mm Hg. An error signal is thus generated, amplified, and integrated with respect to time. The integrated error signal is fed into a programable d-c power supply. The power supply output runs a small, positive-displacement artificial ventricle. The pump output is controlled by setting the venous pressure. Studies in a mock circulation setup in which venous return was varied over a wide range demonstrated how either blood loss or pooling of blood in the periphery will lead to a diminished ventricular output while the venous pressure is maintained at the same level. This situation has its clinical analogues. It is anticipated that the use of two such venous pressure-controlled artificial ventricles as a heart replacement in the experimental animal will permit changes in heart output in accord with tissue demands both at rest and during exercise. venous pressure regulation Submitted on February 28, 1963

Supported in part by U.S. Public Health Service Grants HE-7207 and HE-06352, and grants from the Delaware and Northeastern Chapter of the Pennsylvania Heart Associations.

The existence of the complication of arterial dissection or rupture caused by the arterial perfusing cannula used for extracorporeal systems has been recognized for some time but has been infrequently referred to in the literature. Jones et al reported a 3.2% major complication rate directly related to arterial cannulation. 1 Included in their analysis of 125 patients was a case of retrograde dissection of the aorta with rupture at the time of operation into the pericardium. The occurrence of a case of retrograde dissection with subsequent spontaneous decompression by rerupture into the thoracic aorta but with catastrophic occlusion of the celiac, left renal, superior mesenteric, and inferior mesenteric arteries has prompted us to describe this case in some detail in order to further focus attention upon this complication and its possible prevention. Report of Case A 51-year-old man was admitted to the Hospital of the University of Pennsylvania on Oct