phenylephrine mechanism of action

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.....In these patients, as alpha-1 receptors in the venous capacitance vessels get hit with phenylephrine they get squeezed down on and have an immediate push into the venous circulation and consequently into the right heart. Still, at this piont, arteriolar vasoconstriction is dominant, but with a venous return component.

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Acutely, administration of PHE may lead to increase in preload, with increased venous return to the heart, which may (as discussed above) help increase stroke volume somewhat. Importantly, however, this effect is only transient, and over the long run the increase in venous resistance will decrease venous return (and thus preload).
https://www.openanesthesia.org/chf_frank_starl_curve_phenylephrine/
To eliminate reflex changes in vascular tone, eight dogs received ganglionic blockade with trimethaphan. After ganglionic blockade phenylephrine increased cardiac output, systemic vascular resistance, mean circulatory filling pressure, pressure gradient for venous return and central blood volume (P < .025). Thus, in conscious dogs, phenylephrine reduces peripheral vascular capacitance and shifts blood from the venous circulation to the central and arterial vascular compartments.
https://arizona.pure.elsevier.com/e...ontrol-of-the-venous-circulation-in-intact-do

I hope everybody's happy now. Will somebody close this thread, please, before we play ETT vs LMA again?
 
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The volume-dependent effect of phenylephrine on cardiac output in patients under general anesthesia.
(2013) Yeung, M.H.

Background:
Phenylephrine, an α1-adrenergic agonist, is widely used during surgery and intensive care settings for its antihypotensive effect. Nevertheless, the effects of phenylephrine are not completely understood yet. In some patients phenylephrine may cause a decrease in cardiac output (CO) due to an increase in afterload through vasoconstriction in the arterioles. In other patients phenylephrine may cause an increase in cardiac output due to an increase in preload through an increase in venous return. These inconsistent effects may be dependent on the volume status of a patient.
Objectives:
In this pilot study, we wanted to observe the volume dependent effect of phenylephrine on cardiac output in patients under general anesthesia.
Materials & methods:
Hemodynamic variables (cardiac output, mean arterial pressure, stroke volume, heart rate and systemic vascular resistance) were measured in a non-invasive way with the Nexfin® monitor. In our study protocol, phenylephrine (100μg) and Voluven® (6% hydroxyethyl starch) were used according to normal clinical management. Patients who had elective surgery and underwent general anesthesia were included if phenylephrine and Voluven® were used in the sequence of our study protocol. The effects of a bolus of phenylephrine (100μg) on the hemodynamic variables were analyzed. Furthermore, the hemodynamic changes induced by phenylephrine between two different volume statuses in one patient were compared.
Results:
Ten patients were eligible to be included in our data analysis. Before Voluven® administration, phenylephrine significantly increased CO (0,51 ± 0,57 L/min; P < 0,006). After Voluven® administration, phenylephrine also significantly increased CO (00,47 ± 0,33 L/min; P < 0,009). The increase in CO before Voluven® administration did not significantly differ from the increase in CO after Voluven® administration (difference of 0,04 ± 0,63 L/min; P = 0,844).
Conclusions:
This pilot study showed that a bolus of phenylephrine administration (100μg) significantly increased CO in patients who had elective surgery and underwent general anesthesia. We conclude that the beneficial effect of increase in preload is higher than the negative effect of increase in afterload. However, there was no significant difference in increase in CO between before and after Voluven® administration, suggesting that the effects of phenylephrine are not dependent on volume status.
 
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Under a volatile anesthetic with vasodilation, your coronary bloodflow is already maximal and your myocardial oxygen demand is minimal since you're typically not tachycardic due to diminished baroceptor reflexes. Increasing your DBP won't improve myocardial performance unless your MAP was critically low (like less than 50), or you have severe LVH, CAD, AS etc



My entire point is that phenylephrine's effects vary based on the volume status of the patient. Yes, it's a pig study (https://www.ncbi.nlm.nih.gov/pubmed/22556399) but preload (IVC flow), stroke volume, and CO increase when the heart is preload dependent. When preload indepdent, MAP may still go up but CO goes down.

I think I've made this point enough times, up to you all whether you think it's a believable mechanism.

I agree with you. Please see the next post to postulate on the effects of a BOLUS vs an INFUSION.

  1. The physiologic effect of a phenylephrine bolus is not necessarily the same as a phenylephrine infusion. For example, Cannesson 2012 found in pigs that when volume loaded (and preload-independent), a phenylephrine bolus reduced cardiac output. However, in this same setting a phenylephrine infusion had a positive/neutral effect on cardiac output. The response to a phenylephrine bolus represents the body’s initial response, but may not represent the new equilibrium state that is eventually reached when ongoing phenylephrine exposure occurs in the form of an infusion. This post is focused on phenylephrine infusions. In general it seems that the response to phenylephrine boluses is less favorable than infusions. It is possible that studies of phenylephrine boluses may have contributed to phenylephrine’s bad reputation.
 
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