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

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.

Estimation of myocardial performance in CABG patients.

Myocardial performance index (MPI) permits a relative easy estimation of global left ventricular (LV) systolic and diastolic function. It was shown that MPI inversely correlated strongly with the maximum derivative of LV pressure with respect to time (+dP/dtmax). The current study evaluated the change of MPI during and immediately after coronary artery bypass surgery (CABG) surgery and analyzed the relationship between MPI and hydraulic energy (exemplified by preload adjusted maximal power-PAMP) during that same period. The study was conducted in 45 patients undergoing CABG. After induction of anaesthesia, 10 min after revascularization and 2 h postoperatively, haemodynamics were assessed. Preload was characterized by LV end-diastolic area indexed for BSA (LVEDAI); afterload was estimated by arterial elastance (Ea) and indexed systemic vascular resistance (SVRI). Global myocardial performance was indicated in terms of MPI and contractility was achieved by PAMP. Myocardial performance index increased postoperatively (0.44 +/- 0.13, 0.37 +/- 0.17 and 0.50 +/- 0.16, respectively; P < 0.001). Preload adjusted maximal power did not alter significantly (1.90 +/- 1.24, 2.02 +/- 1.34 and 2.12 +/- 1.00 W cm(-2)*10(4), respectively). Left ventricular enddiastolic area indexed did not change. Arterial elastance augmented to 0.76 +/- 0.39, 0.80 +/- 0.40 and 1.01 +/- 0.43 mmHg ml(-1), respectively; P < 0.001. Systemic vascular resistance did not change. A relationship was found between 1-MPI/LVEDAI2 and PAMP (R2 = 0.50). This study shows that in the setting of CABG surgery, MPI appears to be a good measure of global LV function.