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Volume 29, Issue 5, Pages 568-573 (May 2010)


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Induced pulsation of a continuous-flow total artificial heart in a mock circulatory system

Hassan A. Khalil, BSab, Daniel T. Kerr, BSa, Mark A. Schusterman II, BSa, William E. Cohn, MDa, O.H. Frazier, MDabCorresponding Author Informationemail address, Branislav Radovancevic, MDab

published online 16 February 2010.

Background

We studied the hemodynamic effects of inducing an artificial pulse in a continuous-flow total artificial heart consisting of 2 axial-flow pumps in a mock circulatory system.

Methods

We varied the amplitude (maximum minus minimum speed), beat rate and systolic duration of the left pump, right pump or both. Mean left and right pump speeds were maintained at 11 and 8 krpm, respectively. Flow rates and arterial and filling pressures were measured in the systemic and pulmonary portions of the mock circulation. Pulse pressure, pulse flow, pulsatility index and surplus hemodynamic energy (SHE) were calculated. The percent change in mean left atrial pressure (LAP) during each induced pulsatility condition was compared with that observed during continuous flow.

Results

Systemic pulse pressures of 17 to 61 mm Hg were attained when the left pump was pulsed, regardless of right pump pulsatility settings. The pulse pressure was directly related to the systolic duration and inversely related to the left pump beat rate. SHE ranged from 0.1 to 3.0 mm Hg, and its changes were comparable to those in pulse pressure. The LAP was reduced by left pump pulsation, but a maximal reduction (≤77%) relative to continuous flow was achieved when the two pumps were copulsed or counterpulsed at a slow rate (10 bpm).

Conclusions

This approach provided maximal flow pulsatility and an adequate reduction in LAP, which may be elevated in recipients of a cardiac replacement device. Further bench and in vivo experiments are needed to assess pump synchronization modes.

a Cardiovascular Surgical Research Laboratories, Texas Heart Institute at St. Luke's Episcopal Hospital, Houston, Texas

b The University of Texas Medical School at Houston, Houston, Texas

Corresponding Author InformationReprint requests: O.H. Frazier, MD, Department of Cardiovascular Surgery, Texas Heart Institute, P.O. Box 20345, MC 3-147, Houston, TX 77225-0345. Telephone: 832-355-3000. Fax: 832-355-6798

PII: S1053-2498(09)01525-3

doi:10.1016/j.healun.2009.12.004


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