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J Thorac Cardiovasc Surg 1994;107:1496-1502
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Left-to-right ventricular interaction with a noncontracting right ventricle

Bronx, N.Y., and Stanford and Palo Alto, Calif.

Supported in part by National Institutes of Health grant HL-49614.

Received for publication March 24, 1993. Accepted for publication Sept. 7, 1993. Address for reprints: Srdjan D. Nikolic, PhD, Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305.

Abstract

Left ventricular systole is known to contribute to generation of right ventricular pressure and stroke volume. To study the interactions in a dilated noncontractile right ventricle after cardiopulmonary bypass we created a variable volume, neo-right ventricle by excision and replacement of the right ventricular free wall with a xenograft pericardial patch. We investigated the interactions in eight dogs with neo-right ventricle, instrumented to measure cardiac pressures and cardiac output in control conditions ( n = 69) and during partial pulmonary artery occlusion ( n = 50). Results: The size of the neo-right ventricle was increased from original right ventricular volume V ₀ to V ₁ (V ₁ = V ₀ + 54 ± 23 ml), V ₂ (V ₂ = V ₀ + 124 ± 85 ml), and V ₃ (V ₃ = V ₀ + 223 ± 162 ml). Cardiac output increased with increasing left ventricular end-diastolic pressure, indicating that the Frank-Starling mechanism was operating in the left ventricle. However, cardiac output decreased with increasing neo-right ventricular size ( p < 0.001) and during pulmonary artery occlusion ( p < 0.001). Maximal neo-right ventricular pressure was a linear function of the maximal left ventricular pressure at each neo-right ventricular size and decreased with the increase in neo-right ventricular size ( p < 0.001), both in control conditions and during pulmonary artery occlusion ( p < 0.004). Stroke work of the neo-right ventricle and left ventricle decreased with increasing neo-right ventricular size ( p < 0.002). The relationship between neo-right ventricular stroke work and left ventricular stroke work at different neo-right ventricular sizes was linear both in control conditions and during pulmonary artery occlusion: in control Y = 0.24X ( r = 0.968, n = 69); in pulmonary artery occlusion Y = 0.35X ( r = 0.986, n = 50). In both conditions the intercept of the linear relationship was not significantly different from zero ( p < 0.974 in control; p < 0.614 in pulmonary artery occlusion). The slope was significantly increased in pulmonary artery occlusion ( p < 0.001). Conclusion: Left ventricular contraction contributes 24% of left ventricular stroke work to the generation of right ventricular stroke work via the septum in the absence of a contracting right ventricle; this increases to 35% in the face of increased pulmonary afterload. This mechanism can maintain adequate global cardiac function in the case of a noncontracting right ventricle while right ventricular volume is kept small and afterload is not increased. The interventricular interaction of the ventricles must be considered when patients with postbypass right ventricular failure are treated. (J T HORAC C ARDIOVASC S URG 1994;107:1496-1502)

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