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Hello,
An interesting question came up few days ago. If a patient requering
inotropic support due to septic shock and also being haemofiltered
(CVVHF) due to kidney failure, how does this process change the serum
cathetcolamin level? My clinical experience shows no changes was ever
necesssary in cathecolamin doses. But pharmacokinetic point of view does
the haemofiltration change the serum level?
Thanks, Laszlo
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The following message was posted to: PharmPK
The first question I would ask, Laszlo, would be the drug used for
support. Adrenaline/epinephrine and noradr/norepi. have a very short
half-life and would not be detectably affected. Probably the same for
dopamine or dobutamine. Milrinone with its 3 hr + t1/2 and renal
excretion would reflect the relative loss of elimination and would reach
a higher than expected level at steady state after a much longer than
normal time for equilibration.
Tom Torda
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The following message was posted to: PharmPK
Dear Thomas,
>The first question I would ask, Laszlo, would be the drug used for
support.
>Adrenaline/epinephrine and noradr/norepi. have a very short half-life
and
>would not be detectably affected. Probably the same for dopamine or
Thank you for your answer. I meant, how the haemofiltration would
effect the epinephrine's pharmacokinetic when it was used to support the
circulation in patient with septic shock - hyperdynamic circulation with
vasodilatation, but with renal failure. I have never seen case when
inotropic support would have needed adjustment due to haemofiltartion,
but found nothing in literature about it.
Thanks again, Laszlo
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Thomas and Laszlo,
While it is an interesting academic question, this drug and many others
like it are titrated to patient hemodynamic parameters, and are weaned
to minimum effect dose whenever possible. Therefore empiric dose
adjustments based on population kinetics is less important. We have from
3-7 critically ill patients, who are treated with CVVHDF daily, and have
never faced a dilemma in dosing for titrated agents. Our concern mainly
resides in those drugs without objective endpoints or were toxicity is
potentially subtle and drug or metabolite related. This second scenario
is potentially the case with vasopressors, but the option to avoid this
class of medications is usually unlikely. Similar questions arise with
the use of vasopressors, antiarrhythmics, neuromuscular blocking agents
(specifically those with toxic metabolites), sedatives. We rely heavily
on kinetic information for antibiotics due to unclear objective
continuous outcome parameters (ie hemodynamics), especially when assays
are not readily available to determine drug levels (meropenem, imipenem,
pip/tazo).
Lance J. Oyen, PharmD, BCPS
Specialist in Critical Care
1216 2nd St SW
Mayo Clinic, Rochester
Rochester, MN 55902
email: oyen.lance.aaa.mayo.edu
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The following message was posted to: PharmPK
Dear Laszlo,
Consider the fraction of the cardiac output which passes via the
heamofiltration. I suspect that this is so small in comparison to the
total cardiac output that it is negligible. If you have data for noradr.
levels in mixed venous or even better arterial blood, why not compare it
with blood at the exit of the filter?
I have not noted any difference in practice, either. Tom T
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