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J Thorac Cardiovasc Surg 2000;120:379-386
© 2000 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Maximizing hemodynamic effectiveness of biventricular assistance by direct cardiac compression studied in ex vivo and in vivo canine models of acute heart failure

From the Department of Surgery, Division of Cardiothoracic Surgery,^a and the Department of Medicine, Division of Circulatory Physiology,^b College of Physicians and Surgeons, Columbia University, New York, NY.

This research was sponsored in part by an unrestricted grant from Cardio Technologies Inc, Pine Brook, NJ. Daniel Burkhoff and Jie Wang received grant support through Columbia University.

Address for reprints: Dan Burkhoff, MD, PhD, Department of Medicine, Division of Circulatory Physiology, College of Physicians and Surgeons, Columbia University, MHB 5-435, 177 Fort Washington Ave, New York, NY 10032 (E-mail: db59{at}columbia.edu ).

Objective: Direct cardiac compression improves effective ventricular contractility. However, associated reductions in filling volumes and increases in arterial pressure occurring at the onset of direct cardiac compression limit the degree to which cardiac output is augmented. We tested the hypothesis that active preload and afterload control maximizes the hemodynamic effectiveness of direct cardiac compression.
Methods and results: Studies in isolated canine hearts loaded with a computer-controlled volume servo system that mimicked heart failure were used to clearly define the hemodynamic effects of direct cardiac compression. Immediately on initiation of direct cardiac compression, ventricular end-diastolic pressure and volume decreased substantially, arterial pressure increased, but stroke volume did not change significantly. When end-diastolic pressure was restored to about 20 mm Hg, stroke volume doubled; decreasing afterload resistance further increased stroke volume by about 30%. Such load adjustments were then tested in vivo in a canine model of acute heart failure induced by coronary artery microembolizations titrated to decrease cardiac output to 33% ± 9% of control as end-diastolic pressure rose to 20.6 ± 2.2 mm Hg. Direct cardiac compression decreased end-diastolic pressure to 11.4 ± 2.6 mm Hg while increasing cardiac output from 0.8 ± 0.2 to 1.4 ± 0.5 L/min (to only ~55% of normal). Restoring end-diastolic pressure to 19.6 ± 2.2 mm Hg by infusions of saline solution increased cardiac output to 1.9 ± 0.5 L/min. Afterload reduction (nitroprusside), while maintaining end-diastolic pressure at 19.8 ± 1.3 mm Hg, increased cardiac output to its baseline, 2.8 ± 1.1 L/min.
Conclusions: Direct cardiac compression significantly improves ventricular pumping capacity and can restore cardiac output to about 60% of normal in the setting of acute heart failure. When combined with active preload and afterload manipulations, direct cardiac compression can restore cardiac output to normal.

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				M. R. Williams and J. H. Artrip Direct cardiac compression for cardiogenic shock with the CardioSupport system Ann. Thorac. Surg., March 1, 2001; 71 (2007): S188 - S189. [Abstract] [Full Text] [PDF]