A study in Anesthesiology looks at how common pressors could affect hemodynamics in septis. It is a small animal study but confirms current research and thinking.  Importantly, it reminds us to think before using pure α-agonists. A lot of the time, all they do is give us nice numbers for our case-sheets, but screw with the hemodynamics.

A few years ago we were told only about 25% of adult sepsis patients had myocardial depression. It is probably a lot more common than that. Recent studies put the number of sepsis patients with left ventricular hypokinesia to around 60%. Other research tell us how 10-20% of sepsis patients will have hearts that are so toxic and cardiodepressed that sepsis will mimic cardiogenic shock.

Getting our pressors right is just as important as figuring out the fluid loading.

Recently pure α-agonists have come under fire. There is no evidence of them actually improving perfusion or global hemodynamics despite improving blood pressure. Blood pressure is not blood perfusion.

The study
The study in Anesthesiology compares the hemodynamic effects of α/β-agonists adrenaline and noradrenaline with pure α-agonist phenylephrine. It is a small rat study where experimental septic peritonitis was created by perforating the rat coecum.

After 18 hours, adrenaline, noradrenaline and phenylephrin were titrated to a dose that increased MAP by 20% over baseline values. At this stage all pressors had equally improved blood pressure. But what of the other parameters?


Take-home message
According to this animal study adrenaline and noradrenaline, in this setting, increases cardiac output while phenylephrin kills hemodynamics. It is year another reminder of how blood pressure is not the same as perfusion.

Pure α-agonist increase arterial tone, but for hemodynamics to actually improve, these patients need β1-agonism too. This phenomenon, where isolated increased vessel tone without increased isotropy results in deteriorating hemodynamics, is called ventriculoarterial uncoupling.

This is a small animal study and it comes with all the usual disclaimers. However, it fits nicely with current discussions around the dangers of  pure α-agonism in emergency medicine or critical care.

I struggle more and more to come up with scenarios where pure α-agonists have a place in critically ill patients.

Comparison of Equipressor Doses of Norepinephrine, Epinephrine, and Phenylephrine on Septic Myocardial Dysfunction., Ducrocq N, Kimmoun A, Furmaniuk A, Hekalo Z et al
Anesthesiology, 2012 May;116(5):1083-1091.

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  1. nfkb says:

    Hello !

    Thank you for this note.

    There was another article in the BJA in 2012 comparing phenylephrine and ephedrine on cerebral hemodynamic. There is the same observation that good figures is not adequate perfusion.

    Differential effect of phenylephrine and ephedrine on cerebral haemodynamics before carotid cross-clamping during carotid endarterectomy

    C. W. A. Pennekamp,
    R. V. Immink,
    F. L. Moll,
    W. F. Buhre and
    G. J. de Borst*
    Utrecht, The Netherlands
    ↵*E-mail: g.j.deborst-2{at}
    Editor—Internal carotid artery stenosis is often associated with impaired cerebral autoregulation, implying that cerebral blood flow depends on arterial pressure. To preserve cerebral perfusion and to prevent ‘watershed’ stroke during carotid endarterectomy (CEA), hypotension before and during cross-clamping needs to be avoided. Several short-acting agents, such as phenylephrine or ephedrine, are commonly used to correct intraoperative hypotension, but have different haemodynamic effects. Phenylephrine, an α-agonist, increases arterial pressure by arterial vasoconstriction, whereas ephedrine, an α- and β-agonist, increases arterial pressure by arterial vasoconstriction combined with an increase in heart rate and cardiac output (CO). In healthy anaesthetized subjects with intact cerebral autoregulation, frontal lobe cerebral tissue oxygenation (rSO2) declined after phenylephrine while it was preserved after ephedrine.

    • E Paul says:

      Hi-I’d like more information on this subject especially in the presence of burns and sepsis. Do you have any more information?
      Thank you.

  2. Thomas D says:

    Thanks for that other reference, Rémi! It’s always good with more input.

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