Arterial pressure allows monitoring the changes in cardiac output induced by volume expansion but not by norepinephrine

Abstract

Objective: To evaluate to which extent the systemic arterial pulse pressure could be used as a surrogate of cardiac output for assessing the effects of a fluid challenge and of norepinephrine.

Design: Observational study.

Setting: Medical intensive care unit.

Patients: Patients with an acute circulatory failure who received a fluid challenge (228 patients, group 1) or in whom norepinephrine was introduced or increased (145 patients, group 2).

Interventions: We measured the systolic, diastolic, and mean arterial pressure, pulse pressure, and the transpulmonary thermodilution cardiac output before and after the therapeutic interventions.

Main results: In group 1, the fluid challenge significantly increased cardiac output by 24% ± 25%. It significantly increased cardiac output by ≥15% (+35% ± 27%) in 142 patients ("responders"). The fluid-induced changes in cardiac output were correlated with the changes in pulse pressure (r = .56, p < .0001), systolic arterial pressure (r = .55, p < .0001), diastolic arterial pressure (r = .37, p < .0001), and mean arterial pressure (r = .52, p < .0001). At multivariate analysis, changes in pulse pressure were significantly related to changes in stroke volume (multiple r = .52) and to age (r = .12). A fluid-induced increase in pulse pressure of ≥17% allowed detecting a fluid-induced increase in cardiac output of ≥15% with a sensitivity of 65[56-72]% and a specificity of 85[76-92]%. The area under the receiver operating characteristic curves for the fluid-induced changes in mean arterial pressure and in diastolic arterial pressure was significantly lower than for pulse pressure. In group 2, the introduction/increase of norepinephrine significantly increased cardiac output by 14% ± 18%. The changes in cardiac output induced by the introduction/increase in the dose of norepinephrine were correlated with the changes in pulse pressure and systolic arterial pressure (r = .21 and .29, respectively, p = .001) but to a significantly lesser extent than in group 1.

Conclusions: Pulse pressure and systolic arterial pressure could be used for detecting the fluid-induced changes in cardiac output, in spite of a significant proportion of false-negative cases. By contrast, the changes in pulse pressure and systolic arterial pressure were unable to detect the changes in cardiac output induced by norepinephrine.