In critically ill patients, alterations in pulmonary vasomotor tone profoundly influence right ventricular (RV) function. An increase in end-diastolic volume (EDV) follows elevations in the RV afterload, this increase in preload probably subserving the increased RV stroke work (SW) required to ensure unchanged RV pump function. The maintenance of a normal left ventricular (LV) preload is essential in the cardiovascular adaptation to an acute illness. With volume overload of the RV consequent upon pulmonary artery hypertension (PAH), leftward septal shift occurs and reduces LV diastolic compliance. With extremely high levels of RV loading conditions, a depression in RV contractility and reduced RV pump function are eventually seen, both of which then become partially responsible for LV pump failure. Hence, abnormalities in RV function will have a marked clinical influence on the circulatory response seen in critically ill patients. Future investigation should be directed toward the effects of augmenting or improving RV function with pharmacologic agents in this patient population.