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Clinical and Experimental Circulation

Differentiation of cardiovascular effects of phenylephrine by noninvasive advanced hemodynamic monitoring


Kalmar, A. F.; Poterman, M.; Van der Velde, M. I.; Struys, M. M.R.F.; Scheeren, T. W.L.

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European Journal of Anaesthesiology (EJA): June 2013 - Volume 30 - Issue - p 62-62
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Background and Goal of Study: Phenylephrine(PHE) is a pure α-adrenergic agonist, which is widely used to treat hypotension. PHE acts mainly via an increase of the peripheral arterial vascular resistance, which often induces reflex bradycardia thus decreasing cardiac output. On the other hand, venous vasoconstriction by PHE may improve venous return, increase cardiac preload and thus partly compensate for abovementioned hemodynamic suppression. We therefore performed a beat-to-beat analysis of blood pressure(MAP), heart rate(HR), cardiac output(CO), stroke volume variation(SVV) and pulse pressure variation(PPV) obtained noninvasively with the Nexfin® device (Edwards Lifesciences) to differentiate these cardiovascular effects.

Materials and Methods: After local IRB approval, hemodynamic variables of 15 patients under general anesthesia for ophthalmic surgery were recorded. Euvolaemia was pursued (500ml colloids) and methylatropine 500μg was administered in anticipation of vagal stimulating ophthalmic interventions. If the MAP decreased below 80% of baseline value for >1 minute, PHE 100μg was administered.

Results and Discussion: The figure shows the evolution of the average curves from 60 seconds before to 300 seconds after (T300) PHE administration and mean(SD) values at T0 and at T120 (*p< 0.05).

[Hemodynamic effects of Phenylephrine]

A single bolus of PHE in these euvolemic, atropinised patients resulted in a significantly increased MAP with preserved CO and HR. A significant decrease in SVV and PPV together with a preserved CO convincingly reflects an increased preload due to increased venous return. The maximal effect on MAP (reflecting arterial vasoconstriction) occurred at T70, while the maximal effect on SVV and PPV (reflecting venoconstriction) occurred at T120.

Conclusions: PHE has the potential to increase venous return and thus cardiac preload and render increased blood pressure with preserved cardiac output in a selected patient population. The time delay of maximal effects after a single administration reflects different effect sites of PHE within the circulation. The availability of noninvasive continuous advanced haemodynamic monitoring allows for superior haemodynamic management.

© 2013 European Society of Anaesthesiology