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Ann Thorac Surg 1987;43:478-483
© 1987 The Society of Thoracic Surgeons

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Articles

Preload Dependence of Right Ventricular Blood How: I. The Normal Right Ventricle

From the Department of Surgery, Duke University Medical Center, Durham, NC

^* Address reprint requests to Dr. Wechsler, Box 3174, Duke University Medical Center, Durham, NC 27710

Right ventricular (RV) failure is commonly treated with intravascular volume expansion to increase the RV–left atrial pressure gradient and improve left-sided filling. As RV pressure rises, chamber distention occurs and wall tension increases. These studies were designed to determine if increased wall tension might impede RV myocardial blood flow in the normal canine right ventricle and thus contribute to RV failure. Hemodynamic data, the septal–RV free wall dimension, and RV myocardial blood flow were obtained at low and high levels of preload and in both the autoregulated and vasodilated (adenosine, 2 mg per kilogram of body weight per minute) states. Elevated filling pressure decreased RV myocardial blood flow in both the autoregulated (0.85 ± 0.18 to 0.67 ± 0.15 ml/min/gm; p < .05) and vasodilated (2.25 ± 0.50 to 0.85 ± 0.25 ml/min/gm; p < .05) states but did not change the transmural distribution of blood flow to the right ventricle. Vasodilator reserve was markedly impaired in the high-preload state. These observations suggest that preload is an important determinant of RV myocardial blood flow. Volume loading to treat RV dysfunction may be limited by impairment of RV myocardial blood flow.