Control of cardiac output by systemic vessels: Circulatory adjustments to acute and chronic respiratory failure and the effect of therapeutic interventions

Abstract

The circulation requires the heart to pump blood from the venous to the arterial bed. The factors that determine venous flow into the heart are mean pressure in the systemic vasculature, right atrial pressure and the resistance to venous return. The mean pressure in the systemic vasculature is a function of the stressed vascular volume and the systemic vascular compliance. Right atrial pressure depends on many factors. These include the contractile state of the right and left ventricles, the load on the right and left ventricles, the presence or absence of pericardial effusion, and alterations in pleural pressure that might occur with positive pressure ventilation. The resistance to venous return tends to stay remarkably constant, but can be reduced by significant arteriovenous shunting. The right ventricle has a relatively high diastolic compliance. Because of this, changes in volume of the right ventricle are associated with only modest increases in right atrial pressure. Therefore, as load on the right ventricle increases, mean systemic vascular pressure needs to increase only a small amount to maintain cardiac output. If right atrial pressure increases sufficiently as a result of a greatly increased load on the right ventricle, as in pulmonary embolism, hypoxic pulmonary vasoconstriction or chronic respiratory failure, the increase in mean systemic vascular pressure necessary to maintain normal venous return, and therefore cardiac output, may lead to signs of right heart failure, with no change in the slope of the right heart function curves. The implications of this phenomenon are important in managing patients with acute and chronic respiratory failure. Positive pressure ventilation, diuretic agents, cardiac glycosides and other inotropic or vasoactive drugs will influence the relation between the mean systemic pressure and right atrial pressure. Therefore, these treatment modalities may unexpectedly alter cardiac output if the systemic vascular effects are not kept in mind.