BACKGROUND: Although the use of inhaled nitric oxide offers certain advantages over more traditional pulmonary vasodilators, concerns have emerged because of reports of acute pulmonary edema during nitric oxide administration in patients with chronic heart failure. It is unclear whether the pulmonary vasodilating action of nitric oxide could, by itself, cause venous pressures to rise in the lung and why patients with preexisting chronic heart failure are at greatest risk for the development of pulmonary edema during inhaled nitric oxide therapy.
METHODS: The cardiovascular system was modeled as time-varying elastances; the pulmonary and systemic vascular systems were each modeled as a series of resistive and compliance elements. Protocols were devised to examine the effects of a decrease in pulmonary vascular resistance on pulmonary venous pressure under different conditions of contractile state and volume status.
RESULTS: Under all conditions studied, pulmonary venous pressure increased as pulmonary vascular resistance decreased. Increases in pulmonary venous pressure were caused by volume shifts between pulmonary arterial and venous compartments. These volume shifts were accentuated by high volume status. The impact of alterations in contractile state was minimal.
CONCLUSIONS: Pulmonary vasodilation by itself can lead to an increase in pulmonary venous pressure that is mediated by shifts of blood between arterial and venous compartments of the pulmonary bed. Furthermore, impairment in ventricular contractile state by itself has relatively little effect on pulmonary venous pressure. The magnitude of the increase in pulmonary venous pressure is largely determined by the volume status and the initial value of pulmonary vascular resistance.
Tags: heart failure, model, NO, simulation