> Talk to your ITU bods.......... dobutamine is a Beta 1
> chronotrope and inotrope
> as well as an alpha 1 and beta 2 venoDILATOR. Apparently the
> dilatation out
> weighs the small inotrope effect The result pharamcologically
> speaking should
> be an increased rate but a DROP in BP!!
> Epi, oh alright, adrenaline is more beta 1 (but is not clean
> either)so causes
> a positive inotropic effect on balance (Though it can cause a
> drop in diastolic).
A few maxims about pharmacology of catecholamines in critical illness:
1. There is no such thing as a pure agonist
2. There is no such thing as a pure antagonist
3. Drugs have different effects in animals, healthy volunteers and
critically ill patients
4. The only relevant end point is functional survival
You can't predict what will happen- any catecholamine or equivalent is a
positive and negative intrope, chrontrope and dromotrope as well as a
vasodilator and constrictor given the right circustances. If you use drugs,
suck it and see. Measurement of cardiac output whether by ultrasound or
thermodilution; or of oxygen uptake would be useful to know what was
happening (although goal directed therapy arguably not shown to influence
outcome favourably- I don't believe Shoemakers metanalysis in Crit Care Med
this month as it seems a bit selective and the funnel plot points to
selection bias).
Another point: assuming you want to maximise left ventricular work (and it's
a big assumption in a patient with myocardial ischaemia), how prepared are
you to trade off BP for output or vice versa (in other words, how
constricted to you want the blood vessels)? Individual patient judgement,
not well evidence based.
BTW, anyone tried using cardiac glycosides in cardiogenic shock- well if you
want an intrope with no vasodilator effects, why not? Using them in ITU I've
seen rises of around 25% in left ventricular work.
Matt Dunn
Warwick
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