Phenylephrine increases cardiac output by raising cardiac preload in patients with anesthesia induced hypotension

Abstract

Induction of general anesthesia frequently induces arterial hypotension, which is often treated with a vasopressor, such as phenylephrine. As a pure α-agonist, phenylephrine is conventionally considered to solely induce arterial vasoconstriction and thus increase cardiac afterload but not cardiac preload. In specific circumstances, however, phenylephrine may also contribute to an increase in venous return and thus cardiac output (CO). The aim of this study is to describe the initial time course of the effects of phenylephrine on various hemodynamic variables and to evaluate the ability of advanced hemodynamic monitoring to quantify these changes through different hemodynamic variables. In 24 patients, after induction of anesthesia, during the period before surgical stimulus, phenylephrine 2 µg kg-1 was administered when the MAP dropped below 80% of the awake state baseline value for > 3 min. The mean arterial blood pressure (MAP), heart rate (HR), end-tidal CO2 (EtCO2), central venous pressure (CVP), stroke volume (SV), CO, pulse pressure variation (PPV), stroke volume variation (SVV) and systemic vascular resistance (SVR) were recorded continuously. The values at the moment before administration of phenylephrine and 5(T5) and 10(T10) min thereafter were compared. After phenylephrine, the mean(SD) MAP, SV, CO, CVP and EtCO2 increased by 34(13) mmHg, 11(9) mL, 1.02(0.74) L min-1, 3(2.6) mmHg and 4.0(1.6) mmHg at T5 respectively, while both dynamic preload variables decreased: PPV dropped from 20% at baseline to 9% at T5 and to 13% at T10 and SVV from 19 to 11 and 14%, respectively. Initially, the increase in MAP was perfectly aligned with the increase in SVR, until 150 s after the initial increase in MAP, when both curves started to dissociate. The dissociation of the evolution of MAP and SVR, together with the changes in PPV, CVP, EtCO2 and CO indicate that in patients with anesthesia-induced hypotension, phenylephrine increases the CO by virtue of an increase in cardiac preload.

Keywords: Cardiac output; Fluid responsiveness; Hemodynamic monitoring; Phenylephrine; Pulse pressure variation.

Conflict of interest statement

Conflict of interest

Thomas W.L. Scheeren received honoraria for consulting and lecturing from Edwards Lifesciences and from Masimo Inc. (Irvine, CA, USA). TWLS received honoraria from Pulsion Medical Systems SE for giving lectures. TWLS is associate editor of the Journal of Clinical Monitoring and Computing, but has no role in the handling of this paper. For the remaining authors none were declared.

Ethical approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed consent

Informed consent was obtained from all individual participants included in the study.

Figures

Fig. 1

Flow chart of the patients’ inclusion and analysis

Fig. 2

The evolution of individual patient variables. The evolution in individual patients (thin lines) and average (thick line) values of the main preload-dependent variables over the period from 1 min before till 12 min after the increase in initial blood pressure following the administration of phenylephrine. All measurements are synchronized at the moment (T0) of 10 mmHg increase in MAP following phenylephrine administration

Fig. 3

The course of the hemodynamic variables after administration of phenylephrine. The MAP, CVP, HR, PPV, SVV, SV, SVR, end-tidal CO2-concentration (EtCO2), mean systemic filling pressure (Pmsa), CO and resistance to vascular return (RVR) are shown. The graphs are the averages of the individual patient measurements, synchronized at the moment (T0) of 10 mmHg increase in MAP after phenylephrine administration