Phenylephrine Administration Increases Cardiac Output in Parasympathically Blocked Patients

A.F. Kalmar, Marieke Poterman, Thomas Scheeren

Research output: Contribution to conferenceAbstractAcademic


Introduction: Phenylephrine (PHE), a pure α1-agonist, is widely used to treat hypotension in anesthetized patients although controversy on its beneficial versus deleterious effects on blood flow and tissue perfusion is still vivid. Conventionally, PHE is considered to increase the arterial blood pressure (ABP) by isolated arterial vasoconstriction, thereby increasing ventricular afterload and thus decreasing cardiac output (CO). However, the potential of PHE to increase cardiac preload by unloading splanchnic capacitance vessels resulting in an increase in CO was recently demonstrated in an animal hemorrhage model1. Induction of anesthesia results in vasodilation and therefore relative hypovolemia. Hence, PHE may induce a significant release of splanchnic blood volume and thus contribute to an increased CO. Three major effects of PHE occur simultaneously - increased cardiac preload, increased ventricular afterload and reflex bradycardia - with opposing affects on CO. To eliminate reflex bradycardia, we investigated the contribution of parasympathetic blockade with atropine on the hemodynamic effect of PHE on post-induction hypotension during propofol/remifentanil anesthesia.
Methods: After IRB approval and written IC, 20 patients received either saline or atropine 500μg at induction of propofol/remifentanil anesthesia in this randomized controlled prospective study. Hemodynamics were continuously monitored using the Nexfin® monitor. When MAP decreased below 80% of baseline, PHE 100μg was administered.

Results: The figure shows the mean values of 10 parasympathically-blocked and 10 non-parasympathically-blocked patients. All curves are synchronized with T0 at the moment of PHE administration. At 120 seconds after T0, we observed a significant (p<0.05) and equal increase in MAP in both groups, and an equal increase in stroke volume(SV) compared to baseline. Correspondingly, the stroke volume variation (SVV) and pulse pressure variation (PPV) decreased in both groups to a comparable amount. However, in the atropine group, PHE caused a slight decrease in HR and a trend to increase in CO, while in the no-atropine group, PHE induced a clinically significant decrease in both HR and CO.

Discussion: The PHE-induced increase in CO in the atropine group confirms that the increase in SV cannot be solely attributed to changes in heart rate. In addition, the simultaneous decrease in SVV and PPV demonstrates a shift to the right of the position of the heart on the Frank-Starling relationship, which conceivably reflects a recruitment of blood volume from capacitance vessels. Inversely, in the no-atropine group, despite equivalent effects on SV, SVV and PPV, PHE decreased CO.

These observations illustrate that a moderate administration of PHE in parasympathically-blocked patients delivers an increased perfusion pressure with concomitant rise in CO. However, as higher doses of PHE are well known to suppress CO, and since these effects are dependent on complex cardiovascular interactions, we strongly suggest using advanced (noninvasive) hemodynamic monitoring during administration of this vasopressor in clinical practice.

1. Cannesson, J Appl Physiol 2012; 113:281-289
Original languageEnglish
Publication statusPublished - 15-Oct-2013
EventANESTHESIOLOGY™ 2013 annual meeting - San Francisco, United States
Duration: 12-Oct-201316-Oct-2013


ConferenceANESTHESIOLOGY™ 2013 annual meeting
CountryUnited States
CitySan Francisco
Internet address

Cite this