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J Thorac Cardiovasc Surg 2001;121:0116-0124
© 2001 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Effect of acutely increased left ventricular afterload on work output from the right ventricle in conscious dogs

Mohanraj K. Karunanithi, BE, MBiomedE, Jerzy Michniewicz, MBBS, MBA, Jason A. Young, BE, MBiomedE, Michael P. Feneley, MD, FACC

From The Victor Chang Cardiac Research Institute and Cardiology Department, St Vincent's Hospital, Sydney, Australia.

Supported by a Project Grant from the National Health and Medical Research Council of Australia.

Received for publication Jan 18, 2000. Revisions requested March 14, 2000; revisions received May 1, 2000. Accepted for publication Aug 7, 2000. Address for reprints: Michael P. Feneley, MD, FRACP, FACC, Cardiology Department, St Vincent's Hospital, Darlinghurst, NSW 2010, Australia (E-mail: M.Karunanithi{at}unsw.edu.au).

Objective: To determine the effect of acute increments in left ventricular afterload on the stroke work output of the right ventricle in vivo.
Methods: After pharmacologic attenuation of autonomic reflexes, left and right ventricular pressure-volume data were obtained in 9 conscious dogs during vena caval occlusions performed before and during aortic constriction.
Results: The relationship between right ventricular stroke work and end-diastolic volume during vena caval occlusion was highly linear (r = 0.97 ± 0.02), but the slope decreased by 20% ± 13% during aortic constriction sufficient to increase left ventricular mean ejection pressure by 25% ± 14% (P < .05). The volume-axis intercept remained constant. Similarly, the slope of the linear relationship between right ventricular free wall regional segment work and end-diastolic segment length declined by 22% ± 10% during aortic constriction (P < .05), without significant change in the length-axis intercept. The reduction in both global and regional right ventricular stroke work at any given preload with increased left ventricular afterload was due entirely to decreased right ventricular stroke volume and free wall shortening, because right ventricular mean ejection pressure was unchanged. Additional experiments were performed in 5 open-chest dogs to produce a greater reduction in left ventricular free wall shortening than observed with aortic constriction by transient constriction of the left circumflex coronary artery. However, this intervention had no effect on right ventricular free wall segment work output.
Conclusion: Increased left ventricular afterload decreases global and regional right ventricular stroke work at any given preload, a direct, negative systolic ventricular interaction.






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