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.
Highlights
The ultimate goal of hemodynamic management is to maintain adequate tissue oxygen delivery to the different end-organs [1]
Our hypothesis was on the contrary, that if a relative hypovolemia is present due to anesthesia-induced excessive vasodilation of the capacitance vessels, this could be corrected by phenylephrine, inducing an improved centralization of the available blood, eventually resulting in an increase in cardiac output (CO)
The main finding of this prospective study was that in patients with anesthesia-induced hypotension and preload dependency—defined as pulse pressure variation (PPV) > 12%, phenylephrine increases CO by virtue of an increase in return function. This is reflected in multiple distinct indices, all indicating an increase in CO, owing to a rightward shift in the position of the heart on the Frank–Starling relationship: the dissociation of mean arterial blood pressure (MAP) and systemic vascular resistance (SVR) at T1, central venous pressure (CVP), PPV, CO, and EtCO2
Summary
The ultimate goal of hemodynamic management is to maintain adequate tissue oxygen delivery to the different end-organs [1]. Surgical patients often suffer relative hypovolemia owing to a combination of epidural analgesia, general anesthesia and patient positioning. The principal aim of goal-directed fluid therapy is to optimize the position of the heart on the Frank–Starling curve by increasing cardiac preload. This is conventionally pursued by administration of fluids to increase total blood volume and can improve patient outcome by reducing postoperative complications and length of hospital stay [2]. Phenylephrine is a direct α-adrenergic receptor agonist, predominantly α1, increasing the systemic vascular resistance (SVR) and arterial pressure [3].
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